Management of a case of rhythm disturbance in ICCU supra-ventricular supra-ventricular

tachyarrhythmia tachyarrhythmia

Dr Jayanta paul

Final year PGT Medicine dept

Burdwan medical college

Atrial fibrillation

ECG Diagnosis Of Atrial Fibrillation

bull Irregularly irregular RR intervals

bull Absence of P waves

bull Irregular fibrillatory wave forms (best seen in V1)

Atrial fibrillation with rapid ventricular response in a 76-year-old man with breathlessness

Note the irregularly irregular ventricular rhythm Sometimes on first look the

rhythm may appear regular but on closer inspection it is clearly irregular

Atrial fibrillation with pre-existing LBBB in a 60-year-old woman with hypertension

Sometimes this can be confused with ventricular tachycardia but closer inspection can identify the irregularity

The irregularly irregular rhythm suggests AF Features of typical left bundle branch block include wide QRS (gt 120 ms) no secondary R wave in lead V1 and no lateral Q waves

Wolff-Parkinson-White syndrome with atrial fibrillation in a 47-year-old man with a long history of palpitations and lately blackouts

Note the irregularly irregular wide complex tachycardia

Impulses from the atria are conducted to the ventricles via either both the AV node and accessory pathway (producing a broad fusion complex) or just the AV node (producing a narrow complex without a delta wave) or just the accessory pathway (producing a very broad ldquopurerdquo delta wave)

People who develop this rhythm and have very short RR intervals are at higher risk of VF

Laboratory Tests ---

1 Thyroid Studies

2 Complete Blood Count

3 Drug Levels

4 Coagulation Studies

5 Cardiac Markers

7 Tests For Pulmonary Embolism

6Echocardiography

Digoxin toxicity (but not digoxin use) is a relative contraindication to electrical cardioversiondefibrillationas case reports of asystole after such attempts to treat tachydysrhythmias in this setting have occurred40

Obtain a protime (PT) and international normalized ratio (INR) if the patient is on warfarin

Up to 20 of patients who present with acute MI will develop AF in close proximity to the acute MI

hellipECG changes suspicious for ischemia or underlyingheart disease hellipSignificant risk factors for CAD

hellippossible angina (chest pain pressure significant dyspnea CHF etc)

It is important to note that a transthoracic echo is inadequate for the exclusion of clot as it cannot visualize the left atrialappendage very well

a screening TSH should be obtained in older patients (gt 55) with NOAF

classic signs and symptoms (like buggy eyessweating tremors or diarrhea)

RATE VERSUS RHYTHM CONTROL

WHICH IS SUPERIOR

AFFIRM Trial

RACE Trail

AF-CHF Trail

STAF Trail

PIAF trail

Management of atrial fibrillation

N Engl J Med 2002 Dec 5347(23)1825-33

A comparison of rate control and rhythm control in patients with atrial fibrillationWyse DG Waldo AL DiMarco JP Domanski MJ Rosenberg Y Schron EB Kellen JC Greene HL Mickel MC Dalquist JE Corley SD Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) InvestigatorsSourceAFFIRM Clinical Trial Center Axio Research 2601 4th Ave Ste 200 Seattle WA 98121 USA

Abstract

BACKGROUNDThere are two approaches to the treatment of atrial fibrillation one is cardioversion and treatment with antiarrhythmic drugs to maintain sinus rhythm and the other is the use of rate-controlling drugs allowing atrial fibrillation to persist In both approaches the use of anticoagulant drugs is recommendedMETHODSWe conducted a randomized multicenter comparison of these two treatment strategies in patients with atrial fibrillation and a high risk of stroke or death The primary end point was overall mortalityRESULTSA total of 4060 patients (mean [+-SD] age 697+-90 years) were enrolled in the study 708 percent had a history of hypertension and 382 percent had coronary artery disease Of the 3311 patients with echocardiograms the left atrium was enlarged in 647 percent and left ventricular function was depressed in 260 percent There were 356 deaths among the patients assigned to rhythm-control therapy and 310 deaths among those assigned to rate-control therapy (mortality at five years 238 percent and 213 percent respectively hazard ratio 115 [95 percent confidence interval 099 to 134] P=008) More patients in the rhythm-control group than in the rate-control group were hospitalized and there were more adverse drug effects in the rhythm-control group as well In both groups the majority of strokes occurred after warfarin had been stopped or when the international normalized ratio was subtherapeuticCONCLUSIONSManagement of atrial fibrillation with the rhythm-control strategy offers no survival advantage over the rate-control strategy and there are potential advantages such as a lower risk of adverse drug effects with the rate-control strategy Anticoagulation should be continued in this group of high-risk patients

Atrial fibrillation

ECG Diagnosis Of Atrial Fibrillation

bull Irregularly irregular RR intervals

bull Absence of P waves

bull Irregular fibrillatory wave forms (best seen in V1)

Atrial fibrillation with rapid ventricular response in a 76-year-old man with breathlessness

Note the irregularly irregular ventricular rhythm Sometimes on first look the

rhythm may appear regular but on closer inspection it is clearly irregular

Atrial fibrillation with pre-existing LBBB in a 60-year-old woman with hypertension

Sometimes this can be confused with ventricular tachycardia but closer inspection can identify the irregularity

The irregularly irregular rhythm suggests AF Features of typical left bundle branch block include wide QRS (gt 120 ms) no secondary R wave in lead V1 and no lateral Q waves

Wolff-Parkinson-White syndrome with atrial fibrillation in a 47-year-old man with a long history of palpitations and lately blackouts

Note the irregularly irregular wide complex tachycardia

Impulses from the atria are conducted to the ventricles via either both the AV node and accessory pathway (producing a broad fusion complex) or just the AV node (producing a narrow complex without a delta wave) or just the accessory pathway (producing a very broad ldquopurerdquo delta wave)

People who develop this rhythm and have very short RR intervals are at higher risk of VF

Laboratory Tests ---

1 Thyroid Studies

2 Complete Blood Count

3 Drug Levels

4 Coagulation Studies

5 Cardiac Markers

7 Tests For Pulmonary Embolism

6Echocardiography

Digoxin toxicity (but not digoxin use) is a relative contraindication to electrical cardioversiondefibrillationas case reports of asystole after such attempts to treat tachydysrhythmias in this setting have occurred40

Obtain a protime (PT) and international normalized ratio (INR) if the patient is on warfarin

Up to 20 of patients who present with acute MI will develop AF in close proximity to the acute MI

hellipECG changes suspicious for ischemia or underlyingheart disease hellipSignificant risk factors for CAD

hellippossible angina (chest pain pressure significant dyspnea CHF etc)

It is important to note that a transthoracic echo is inadequate for the exclusion of clot as it cannot visualize the left atrialappendage very well

a screening TSH should be obtained in older patients (gt 55) with NOAF

classic signs and symptoms (like buggy eyessweating tremors or diarrhea)

RATE VERSUS RHYTHM CONTROL

WHICH IS SUPERIOR

AFFIRM Trial

RACE Trail

AF-CHF Trail

STAF Trail

PIAF trail

Management of atrial fibrillation

N Engl J Med 2002 Dec 5347(23)1825-33

A comparison of rate control and rhythm control in patients with atrial fibrillationWyse DG Waldo AL DiMarco JP Domanski MJ Rosenberg Y Schron EB Kellen JC Greene HL Mickel MC Dalquist JE Corley SD Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) InvestigatorsSourceAFFIRM Clinical Trial Center Axio Research 2601 4th Ave Ste 200 Seattle WA 98121 USA

Abstract

BACKGROUNDThere are two approaches to the treatment of atrial fibrillation one is cardioversion and treatment with antiarrhythmic drugs to maintain sinus rhythm and the other is the use of rate-controlling drugs allowing atrial fibrillation to persist In both approaches the use of anticoagulant drugs is recommendedMETHODSWe conducted a randomized multicenter comparison of these two treatment strategies in patients with atrial fibrillation and a high risk of stroke or death The primary end point was overall mortalityRESULTSA total of 4060 patients (mean [+-SD] age 697+-90 years) were enrolled in the study 708 percent had a history of hypertension and 382 percent had coronary artery disease Of the 3311 patients with echocardiograms the left atrium was enlarged in 647 percent and left ventricular function was depressed in 260 percent There were 356 deaths among the patients assigned to rhythm-control therapy and 310 deaths among those assigned to rate-control therapy (mortality at five years 238 percent and 213 percent respectively hazard ratio 115 [95 percent confidence interval 099 to 134] P=008) More patients in the rhythm-control group than in the rate-control group were hospitalized and there were more adverse drug effects in the rhythm-control group as well In both groups the majority of strokes occurred after warfarin had been stopped or when the international normalized ratio was subtherapeuticCONCLUSIONSManagement of atrial fibrillation with the rhythm-control strategy offers no survival advantage over the rate-control strategy and there are potential advantages such as a lower risk of adverse drug effects with the rate-control strategy Anticoagulation should be continued in this group of high-risk patients

ECG Diagnosis Of Atrial Fibrillation

bull Irregularly irregular RR intervals

bull Absence of P waves

bull Irregular fibrillatory wave forms (best seen in V1)

Atrial fibrillation with rapid ventricular response in a 76-year-old man with breathlessness

Note the irregularly irregular ventricular rhythm Sometimes on first look the

rhythm may appear regular but on closer inspection it is clearly irregular

Atrial fibrillation with pre-existing LBBB in a 60-year-old woman with hypertension

Sometimes this can be confused with ventricular tachycardia but closer inspection can identify the irregularity

The irregularly irregular rhythm suggests AF Features of typical left bundle branch block include wide QRS (gt 120 ms) no secondary R wave in lead V1 and no lateral Q waves

Wolff-Parkinson-White syndrome with atrial fibrillation in a 47-year-old man with a long history of palpitations and lately blackouts

Note the irregularly irregular wide complex tachycardia

Impulses from the atria are conducted to the ventricles via either both the AV node and accessory pathway (producing a broad fusion complex) or just the AV node (producing a narrow complex without a delta wave) or just the accessory pathway (producing a very broad ldquopurerdquo delta wave)

People who develop this rhythm and have very short RR intervals are at higher risk of VF

Laboratory Tests ---

1 Thyroid Studies

2 Complete Blood Count

3 Drug Levels

4 Coagulation Studies

5 Cardiac Markers

7 Tests For Pulmonary Embolism

6Echocardiography

Digoxin toxicity (but not digoxin use) is a relative contraindication to electrical cardioversiondefibrillationas case reports of asystole after such attempts to treat tachydysrhythmias in this setting have occurred40

Obtain a protime (PT) and international normalized ratio (INR) if the patient is on warfarin

Up to 20 of patients who present with acute MI will develop AF in close proximity to the acute MI

hellipECG changes suspicious for ischemia or underlyingheart disease hellipSignificant risk factors for CAD

hellippossible angina (chest pain pressure significant dyspnea CHF etc)

It is important to note that a transthoracic echo is inadequate for the exclusion of clot as it cannot visualize the left atrialappendage very well

a screening TSH should be obtained in older patients (gt 55) with NOAF

classic signs and symptoms (like buggy eyessweating tremors or diarrhea)

RATE VERSUS RHYTHM CONTROL

WHICH IS SUPERIOR

AFFIRM Trial

RACE Trail

AF-CHF Trail

STAF Trail

PIAF trail

Management of atrial fibrillation

N Engl J Med 2002 Dec 5347(23)1825-33

A comparison of rate control and rhythm control in patients with atrial fibrillationWyse DG Waldo AL DiMarco JP Domanski MJ Rosenberg Y Schron EB Kellen JC Greene HL Mickel MC Dalquist JE Corley SD Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) InvestigatorsSourceAFFIRM Clinical Trial Center Axio Research 2601 4th Ave Ste 200 Seattle WA 98121 USA

Abstract

BACKGROUNDThere are two approaches to the treatment of atrial fibrillation one is cardioversion and treatment with antiarrhythmic drugs to maintain sinus rhythm and the other is the use of rate-controlling drugs allowing atrial fibrillation to persist In both approaches the use of anticoagulant drugs is recommendedMETHODSWe conducted a randomized multicenter comparison of these two treatment strategies in patients with atrial fibrillation and a high risk of stroke or death The primary end point was overall mortalityRESULTSA total of 4060 patients (mean [+-SD] age 697+-90 years) were enrolled in the study 708 percent had a history of hypertension and 382 percent had coronary artery disease Of the 3311 patients with echocardiograms the left atrium was enlarged in 647 percent and left ventricular function was depressed in 260 percent There were 356 deaths among the patients assigned to rhythm-control therapy and 310 deaths among those assigned to rate-control therapy (mortality at five years 238 percent and 213 percent respectively hazard ratio 115 [95 percent confidence interval 099 to 134] P=008) More patients in the rhythm-control group than in the rate-control group were hospitalized and there were more adverse drug effects in the rhythm-control group as well In both groups the majority of strokes occurred after warfarin had been stopped or when the international normalized ratio was subtherapeuticCONCLUSIONSManagement of atrial fibrillation with the rhythm-control strategy offers no survival advantage over the rate-control strategy and there are potential advantages such as a lower risk of adverse drug effects with the rate-control strategy Anticoagulation should be continued in this group of high-risk patients

Atrial fibrillation with rapid ventricular response in a 76-year-old man with breathlessness

Note the irregularly irregular ventricular rhythm Sometimes on first look the

rhythm may appear regular but on closer inspection it is clearly irregular

Atrial fibrillation with pre-existing LBBB in a 60-year-old woman with hypertension

Sometimes this can be confused with ventricular tachycardia but closer inspection can identify the irregularity

The irregularly irregular rhythm suggests AF Features of typical left bundle branch block include wide QRS (gt 120 ms) no secondary R wave in lead V1 and no lateral Q waves

Wolff-Parkinson-White syndrome with atrial fibrillation in a 47-year-old man with a long history of palpitations and lately blackouts

Note the irregularly irregular wide complex tachycardia

Impulses from the atria are conducted to the ventricles via either both the AV node and accessory pathway (producing a broad fusion complex) or just the AV node (producing a narrow complex without a delta wave) or just the accessory pathway (producing a very broad ldquopurerdquo delta wave)

People who develop this rhythm and have very short RR intervals are at higher risk of VF

Laboratory Tests ---

1 Thyroid Studies

2 Complete Blood Count

3 Drug Levels

4 Coagulation Studies

5 Cardiac Markers

7 Tests For Pulmonary Embolism

6Echocardiography

Digoxin toxicity (but not digoxin use) is a relative contraindication to electrical cardioversiondefibrillationas case reports of asystole after such attempts to treat tachydysrhythmias in this setting have occurred40

Obtain a protime (PT) and international normalized ratio (INR) if the patient is on warfarin

Up to 20 of patients who present with acute MI will develop AF in close proximity to the acute MI

hellipECG changes suspicious for ischemia or underlyingheart disease hellipSignificant risk factors for CAD

hellippossible angina (chest pain pressure significant dyspnea CHF etc)

It is important to note that a transthoracic echo is inadequate for the exclusion of clot as it cannot visualize the left atrialappendage very well

a screening TSH should be obtained in older patients (gt 55) with NOAF

classic signs and symptoms (like buggy eyessweating tremors or diarrhea)

RATE VERSUS RHYTHM CONTROL

WHICH IS SUPERIOR

AFFIRM Trial

RACE Trail

AF-CHF Trail

STAF Trail

PIAF trail

Management of atrial fibrillation

N Engl J Med 2002 Dec 5347(23)1825-33

A comparison of rate control and rhythm control in patients with atrial fibrillationWyse DG Waldo AL DiMarco JP Domanski MJ Rosenberg Y Schron EB Kellen JC Greene HL Mickel MC Dalquist JE Corley SD Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) InvestigatorsSourceAFFIRM Clinical Trial Center Axio Research 2601 4th Ave Ste 200 Seattle WA 98121 USA

Abstract

BACKGROUNDThere are two approaches to the treatment of atrial fibrillation one is cardioversion and treatment with antiarrhythmic drugs to maintain sinus rhythm and the other is the use of rate-controlling drugs allowing atrial fibrillation to persist In both approaches the use of anticoagulant drugs is recommendedMETHODSWe conducted a randomized multicenter comparison of these two treatment strategies in patients with atrial fibrillation and a high risk of stroke or death The primary end point was overall mortalityRESULTSA total of 4060 patients (mean [+-SD] age 697+-90 years) were enrolled in the study 708 percent had a history of hypertension and 382 percent had coronary artery disease Of the 3311 patients with echocardiograms the left atrium was enlarged in 647 percent and left ventricular function was depressed in 260 percent There were 356 deaths among the patients assigned to rhythm-control therapy and 310 deaths among those assigned to rate-control therapy (mortality at five years 238 percent and 213 percent respectively hazard ratio 115 [95 percent confidence interval 099 to 134] P=008) More patients in the rhythm-control group than in the rate-control group were hospitalized and there were more adverse drug effects in the rhythm-control group as well In both groups the majority of strokes occurred after warfarin had been stopped or when the international normalized ratio was subtherapeuticCONCLUSIONSManagement of atrial fibrillation with the rhythm-control strategy offers no survival advantage over the rate-control strategy and there are potential advantages such as a lower risk of adverse drug effects with the rate-control strategy Anticoagulation should be continued in this group of high-risk patients

Atrial fibrillation with pre-existing LBBB in a 60-year-old woman with hypertension

Sometimes this can be confused with ventricular tachycardia but closer inspection can identify the irregularity

The irregularly irregular rhythm suggests AF Features of typical left bundle branch block include wide QRS (gt 120 ms) no secondary R wave in lead V1 and no lateral Q waves

Wolff-Parkinson-White syndrome with atrial fibrillation in a 47-year-old man with a long history of palpitations and lately blackouts

Note the irregularly irregular wide complex tachycardia

Impulses from the atria are conducted to the ventricles via either both the AV node and accessory pathway (producing a broad fusion complex) or just the AV node (producing a narrow complex without a delta wave) or just the accessory pathway (producing a very broad ldquopurerdquo delta wave)

People who develop this rhythm and have very short RR intervals are at higher risk of VF

Laboratory Tests ---

1 Thyroid Studies

2 Complete Blood Count

3 Drug Levels

4 Coagulation Studies

5 Cardiac Markers

7 Tests For Pulmonary Embolism

6Echocardiography

Digoxin toxicity (but not digoxin use) is a relative contraindication to electrical cardioversiondefibrillationas case reports of asystole after such attempts to treat tachydysrhythmias in this setting have occurred40

Obtain a protime (PT) and international normalized ratio (INR) if the patient is on warfarin

Up to 20 of patients who present with acute MI will develop AF in close proximity to the acute MI

hellipECG changes suspicious for ischemia or underlyingheart disease hellipSignificant risk factors for CAD

hellippossible angina (chest pain pressure significant dyspnea CHF etc)

It is important to note that a transthoracic echo is inadequate for the exclusion of clot as it cannot visualize the left atrialappendage very well

a screening TSH should be obtained in older patients (gt 55) with NOAF

classic signs and symptoms (like buggy eyessweating tremors or diarrhea)

RATE VERSUS RHYTHM CONTROL

WHICH IS SUPERIOR

AFFIRM Trial

RACE Trail

AF-CHF Trail

STAF Trail

PIAF trail

Management of atrial fibrillation

N Engl J Med 2002 Dec 5347(23)1825-33

A comparison of rate control and rhythm control in patients with atrial fibrillationWyse DG Waldo AL DiMarco JP Domanski MJ Rosenberg Y Schron EB Kellen JC Greene HL Mickel MC Dalquist JE Corley SD Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) InvestigatorsSourceAFFIRM Clinical Trial Center Axio Research 2601 4th Ave Ste 200 Seattle WA 98121 USA

Abstract

BACKGROUNDThere are two approaches to the treatment of atrial fibrillation one is cardioversion and treatment with antiarrhythmic drugs to maintain sinus rhythm and the other is the use of rate-controlling drugs allowing atrial fibrillation to persist In both approaches the use of anticoagulant drugs is recommendedMETHODSWe conducted a randomized multicenter comparison of these two treatment strategies in patients with atrial fibrillation and a high risk of stroke or death The primary end point was overall mortalityRESULTSA total of 4060 patients (mean [+-SD] age 697+-90 years) were enrolled in the study 708 percent had a history of hypertension and 382 percent had coronary artery disease Of the 3311 patients with echocardiograms the left atrium was enlarged in 647 percent and left ventricular function was depressed in 260 percent There were 356 deaths among the patients assigned to rhythm-control therapy and 310 deaths among those assigned to rate-control therapy (mortality at five years 238 percent and 213 percent respectively hazard ratio 115 [95 percent confidence interval 099 to 134] P=008) More patients in the rhythm-control group than in the rate-control group were hospitalized and there were more adverse drug effects in the rhythm-control group as well In both groups the majority of strokes occurred after warfarin had been stopped or when the international normalized ratio was subtherapeuticCONCLUSIONSManagement of atrial fibrillation with the rhythm-control strategy offers no survival advantage over the rate-control strategy and there are potential advantages such as a lower risk of adverse drug effects with the rate-control strategy Anticoagulation should be continued in this group of high-risk patients

Wolff-Parkinson-White syndrome with atrial fibrillation in a 47-year-old man with a long history of palpitations and lately blackouts

Note the irregularly irregular wide complex tachycardia

Impulses from the atria are conducted to the ventricles via either both the AV node and accessory pathway (producing a broad fusion complex) or just the AV node (producing a narrow complex without a delta wave) or just the accessory pathway (producing a very broad ldquopurerdquo delta wave)

People who develop this rhythm and have very short RR intervals are at higher risk of VF

Laboratory Tests ---

1 Thyroid Studies

2 Complete Blood Count

3 Drug Levels

4 Coagulation Studies

5 Cardiac Markers

7 Tests For Pulmonary Embolism

6Echocardiography

Digoxin toxicity (but not digoxin use) is a relative contraindication to electrical cardioversiondefibrillationas case reports of asystole after such attempts to treat tachydysrhythmias in this setting have occurred40

Obtain a protime (PT) and international normalized ratio (INR) if the patient is on warfarin

Up to 20 of patients who present with acute MI will develop AF in close proximity to the acute MI

hellipECG changes suspicious for ischemia or underlyingheart disease hellipSignificant risk factors for CAD

hellippossible angina (chest pain pressure significant dyspnea CHF etc)

It is important to note that a transthoracic echo is inadequate for the exclusion of clot as it cannot visualize the left atrialappendage very well

a screening TSH should be obtained in older patients (gt 55) with NOAF

classic signs and symptoms (like buggy eyessweating tremors or diarrhea)

RATE VERSUS RHYTHM CONTROL

WHICH IS SUPERIOR

AFFIRM Trial

RACE Trail

AF-CHF Trail

STAF Trail

PIAF trail

Management of atrial fibrillation

N Engl J Med 2002 Dec 5347(23)1825-33

A comparison of rate control and rhythm control in patients with atrial fibrillationWyse DG Waldo AL DiMarco JP Domanski MJ Rosenberg Y Schron EB Kellen JC Greene HL Mickel MC Dalquist JE Corley SD Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) InvestigatorsSourceAFFIRM Clinical Trial Center Axio Research 2601 4th Ave Ste 200 Seattle WA 98121 USA

Abstract

BACKGROUNDThere are two approaches to the treatment of atrial fibrillation one is cardioversion and treatment with antiarrhythmic drugs to maintain sinus rhythm and the other is the use of rate-controlling drugs allowing atrial fibrillation to persist In both approaches the use of anticoagulant drugs is recommendedMETHODSWe conducted a randomized multicenter comparison of these two treatment strategies in patients with atrial fibrillation and a high risk of stroke or death The primary end point was overall mortalityRESULTSA total of 4060 patients (mean [+-SD] age 697+-90 years) were enrolled in the study 708 percent had a history of hypertension and 382 percent had coronary artery disease Of the 3311 patients with echocardiograms the left atrium was enlarged in 647 percent and left ventricular function was depressed in 260 percent There were 356 deaths among the patients assigned to rhythm-control therapy and 310 deaths among those assigned to rate-control therapy (mortality at five years 238 percent and 213 percent respectively hazard ratio 115 [95 percent confidence interval 099 to 134] P=008) More patients in the rhythm-control group than in the rate-control group were hospitalized and there were more adverse drug effects in the rhythm-control group as well In both groups the majority of strokes occurred after warfarin had been stopped or when the international normalized ratio was subtherapeuticCONCLUSIONSManagement of atrial fibrillation with the rhythm-control strategy offers no survival advantage over the rate-control strategy and there are potential advantages such as a lower risk of adverse drug effects with the rate-control strategy Anticoagulation should be continued in this group of high-risk patients

Laboratory Tests ---

1 Thyroid Studies

2 Complete Blood Count

3 Drug Levels

4 Coagulation Studies

5 Cardiac Markers

7 Tests For Pulmonary Embolism

6Echocardiography

Digoxin toxicity (but not digoxin use) is a relative contraindication to electrical cardioversiondefibrillationas case reports of asystole after such attempts to treat tachydysrhythmias in this setting have occurred40

Obtain a protime (PT) and international normalized ratio (INR) if the patient is on warfarin

Up to 20 of patients who present with acute MI will develop AF in close proximity to the acute MI

hellipECG changes suspicious for ischemia or underlyingheart disease hellipSignificant risk factors for CAD

hellippossible angina (chest pain pressure significant dyspnea CHF etc)

It is important to note that a transthoracic echo is inadequate for the exclusion of clot as it cannot visualize the left atrialappendage very well

a screening TSH should be obtained in older patients (gt 55) with NOAF

classic signs and symptoms (like buggy eyessweating tremors or diarrhea)

RATE VERSUS RHYTHM CONTROL

WHICH IS SUPERIOR

AFFIRM Trial

RACE Trail

AF-CHF Trail

STAF Trail

PIAF trail

Management of atrial fibrillation

N Engl J Med 2002 Dec 5347(23)1825-33

A comparison of rate control and rhythm control in patients with atrial fibrillationWyse DG Waldo AL DiMarco JP Domanski MJ Rosenberg Y Schron EB Kellen JC Greene HL Mickel MC Dalquist JE Corley SD Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) InvestigatorsSourceAFFIRM Clinical Trial Center Axio Research 2601 4th Ave Ste 200 Seattle WA 98121 USA

Abstract

BACKGROUNDThere are two approaches to the treatment of atrial fibrillation one is cardioversion and treatment with antiarrhythmic drugs to maintain sinus rhythm and the other is the use of rate-controlling drugs allowing atrial fibrillation to persist In both approaches the use of anticoagulant drugs is recommendedMETHODSWe conducted a randomized multicenter comparison of these two treatment strategies in patients with atrial fibrillation and a high risk of stroke or death The primary end point was overall mortalityRESULTSA total of 4060 patients (mean [+-SD] age 697+-90 years) were enrolled in the study 708 percent had a history of hypertension and 382 percent had coronary artery disease Of the 3311 patients with echocardiograms the left atrium was enlarged in 647 percent and left ventricular function was depressed in 260 percent There were 356 deaths among the patients assigned to rhythm-control therapy and 310 deaths among those assigned to rate-control therapy (mortality at five years 238 percent and 213 percent respectively hazard ratio 115 [95 percent confidence interval 099 to 134] P=008) More patients in the rhythm-control group than in the rate-control group were hospitalized and there were more adverse drug effects in the rhythm-control group as well In both groups the majority of strokes occurred after warfarin had been stopped or when the international normalized ratio was subtherapeuticCONCLUSIONSManagement of atrial fibrillation with the rhythm-control strategy offers no survival advantage over the rate-control strategy and there are potential advantages such as a lower risk of adverse drug effects with the rate-control strategy Anticoagulation should be continued in this group of high-risk patients

RATE VERSUS RHYTHM CONTROL

WHICH IS SUPERIOR

AFFIRM Trial

RACE Trail

AF-CHF Trail

STAF Trail

PIAF trail

Management of atrial fibrillation

N Engl J Med 2002 Dec 5347(23)1825-33

A comparison of rate control and rhythm control in patients with atrial fibrillationWyse DG Waldo AL DiMarco JP Domanski MJ Rosenberg Y Schron EB Kellen JC Greene HL Mickel MC Dalquist JE Corley SD Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) InvestigatorsSourceAFFIRM Clinical Trial Center Axio Research 2601 4th Ave Ste 200 Seattle WA 98121 USA

Abstract

BACKGROUNDThere are two approaches to the treatment of atrial fibrillation one is cardioversion and treatment with antiarrhythmic drugs to maintain sinus rhythm and the other is the use of rate-controlling drugs allowing atrial fibrillation to persist In both approaches the use of anticoagulant drugs is recommendedMETHODSWe conducted a randomized multicenter comparison of these two treatment strategies in patients with atrial fibrillation and a high risk of stroke or death The primary end point was overall mortalityRESULTSA total of 4060 patients (mean [+-SD] age 697+-90 years) were enrolled in the study 708 percent had a history of hypertension and 382 percent had coronary artery disease Of the 3311 patients with echocardiograms the left atrium was enlarged in 647 percent and left ventricular function was depressed in 260 percent There were 356 deaths among the patients assigned to rhythm-control therapy and 310 deaths among those assigned to rate-control therapy (mortality at five years 238 percent and 213 percent respectively hazard ratio 115 [95 percent confidence interval 099 to 134] P=008) More patients in the rhythm-control group than in the rate-control group were hospitalized and there were more adverse drug effects in the rhythm-control group as well In both groups the majority of strokes occurred after warfarin had been stopped or when the international normalized ratio was subtherapeuticCONCLUSIONSManagement of atrial fibrillation with the rhythm-control strategy offers no survival advantage over the rate-control strategy and there are potential advantages such as a lower risk of adverse drug effects with the rate-control strategy Anticoagulation should be continued in this group of high-risk patients

N Engl J Med 2002 Dec 5347(23)1825-33

A comparison of rate control and rhythm control in patients with atrial fibrillationWyse DG Waldo AL DiMarco JP Domanski MJ Rosenberg Y Schron EB Kellen JC Greene HL Mickel MC Dalquist JE Corley SD Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) InvestigatorsSourceAFFIRM Clinical Trial Center Axio Research 2601 4th Ave Ste 200 Seattle WA 98121 USA

Abstract

BACKGROUNDThere are two approaches to the treatment of atrial fibrillation one is cardioversion and treatment with antiarrhythmic drugs to maintain sinus rhythm and the other is the use of rate-controlling drugs allowing atrial fibrillation to persist In both approaches the use of anticoagulant drugs is recommendedMETHODSWe conducted a randomized multicenter comparison of these two treatment strategies in patients with atrial fibrillation and a high risk of stroke or death The primary end point was overall mortalityRESULTSA total of 4060 patients (mean [+-SD] age 697+-90 years) were enrolled in the study 708 percent had a history of hypertension and 382 percent had coronary artery disease Of the 3311 patients with echocardiograms the left atrium was enlarged in 647 percent and left ventricular function was depressed in 260 percent There were 356 deaths among the patients assigned to rhythm-control therapy and 310 deaths among those assigned to rate-control therapy (mortality at five years 238 percent and 213 percent respectively hazard ratio 115 [95 percent confidence interval 099 to 134] P=008) More patients in the rhythm-control group than in the rate-control group were hospitalized and there were more adverse drug effects in the rhythm-control group as well In both groups the majority of strokes occurred after warfarin had been stopped or when the international normalized ratio was subtherapeuticCONCLUSIONSManagement of atrial fibrillation with the rhythm-control strategy offers no survival advantage over the rate-control strategy and there are potential advantages such as a lower risk of adverse drug effects with the rate-control strategy Anticoagulation should be continued in this group of high-risk patients

Management Choosing longterm rate versus rhythm control

1 Rate control has less drug-related adverse effects

2 Rate control has equivalent efficacy to rhythm controlSame survival benefitSame Cerebrovascular Accident risk

3 Rhythm control may offer benefit in age lt65 years

RATE CONTROL STRATEGIES

Rate control with pharmacological therapy is the main stay of

therapy for persistent amp permanent cases of atrial fibrillation

Target HR - 80 to 100 bpm

Precautions --Beware agents which may cardiovert Atrial Fib gt48 hours Risk of embolic complications

Protocol Rate control if Ejection Fraction lt40 (No WPW)

GeneralRisk of embolus if rhythm cardiovertsConsider Atrial Fibrillation Anticoagulation

Recommended agentsDigoxin Amiodarone

Digitalis is more effective in controling the resting heart rateBeta blocker or diltiazem or verapamil may be combined with digitalis

Rate control if Heart function preserved (No WPW)

GeneralRisk of embolus if rhythm cardiovertsConsider Atrial Fibrillation Anticoagulation

Recommended agents

Beta BlockerPropranolol Esmolol Metoprolol

Calcium Channel BlockerVerapamil Diltiazem - preferred

Rate Control if WPW Syndrome present

Risk of embolus if rhythm cardiovertsConsider Atrial Fibrillation Anticoagulation

Recommended agents (Use only 1 agent)

Electrical Synchronized Cardioversion if unstableClass IA Agents

ProcainamideClass IC Agents

Propafenone Flecainide

Class III AgentsAmiodarone Sotalol

Rhythm control

Am J Cardiol 2003 Mar 2091(6A)15D-26D

Old and new antiarrhythmic drugs for converting and maintaining sinus rhythm in atrial fibrillation comparative efficacy and results of trials

Naccarelli GV Wolbrette DL Khan M Bhatta L Hynes J Samii S Luck J

SourceDivision of Cardiology and the Penn State Cardiovascular Center Penn State University College of Medicine The Milton S Hershey Medical Center Hershey Pennsylvania 17033 USA gnaccarellipsuedu

Am J Cardiol 2003 Mar 2091(6A)15D-26D

Old and new antiarrhythmic drugs for converting and maintaining sinus rhythm in atrial fibrillation comparative efficacy and results of trials

Naccarelli GV Wolbrette DL Khan M Bhatta L Hynes J Samii S Luck J

SourceDivision of Cardiology and the Penn State Cardiovascular Center Penn State University College of Medicine The Milton S Hershey Medical Center Hershey Pennsylvania 17033 USA gnaccarellipsuedu

Abstract

In managing atrial fibrillation (AF) the main therapeutic strategies include rate control termination of the arrhythmia and the prevention of recurrences and thromboembolic events Safety and efficacy considerations are important in optimizing the choice of an antiarrhythmic drug for the treatment of AF Recently approved antiarrhythmics such as dofetilide and promising investigational drugs such as azimilide and dronedarone may change the treatment landscape for AF

For medical conversion of recent-onset AF class IC antiarrhythmic drugs administered as an oral bolus have been demonstrated to be the most efficacious pharmacologic conversion agents

Intravenous ibutilide and oral dofetilide both have efficacies superior to placebo in controlled trials for converting persistent AF

Comparative trials in paroxysmal AF have demonstrated that flecainide propafenone quinidine and sotalol are equally effective in preventing recurrences of AF

Amiodarone has been demonstrated to be more efficacious than propafenone or sotalol in the Canadian Trial of Atrial Fibrillation

In persistent AF twice-daily dofetilide has been shown to be as or more effective than low-dose sotalol given twice daily for the maintenance of sinus rhythm in patients with AF Trials have demonstrated that subjective adverse effects are less frequent with class IC drugs sotalol and dofetilide compared with such drugs as quinidine

In patients without structural heart disease flecainide propafenone and DL-sotalol are the initial drugs of choice given their reasonable efficacy low incidence of subjective side effects and lack of significant end-organ toxicity

Treating AF in patients with left ventricular dysfunction can be difficult because of associated electrophysiologic derangements potential proarrhythmic concerns and negative inotropic effects of antiarrhythmics

Some data exist suggesting that angiotensin-converting enzyme inhibitors and angiotensin receptor blockers can prevent AF either by preventing atrial dilation and stretch-induced arrhythmias or by blocking the renin-angiotensin system

In post-myocardial infarction patients DL-sotalol dofetilide and amiodarone-and in congestive heart failure patients amiodarone and dofetilide-have demonstrated neutral effects on survival in controlled trials

In the Congestive Heart Failure Survival Trial of Antiarrhythmic Therapy (CHF-STAT) amiodarone lowered the frequency of AF development and improved left ventricular ejection fraction over time In CHF-STAT there was lower mortality in patients who converted from AF to sinus rhythm

Dofetilide decreased rehospitalization for congestive heart failure in the Danish Investigations of Arrhythmia and Mortality on Dofetilide (DIAMOND) trials

Neutral effects on survival and favorable hemodynamics have positioned amiodarone and dofetilide as the antiarrhythmics of choice in patients with left ventricular dysfunction

In post-myocardial infarction patients sotalol is an additional agent to consider for treatment of AF in this setting

External defibrillation

Termination of AF by electrical defibrillator

acutely may be warranted based on clinical parameters andor hemodynamic status

Confirmation of appropriate anticoagulation must be documented unless symptoms and clinical status warrant emergent intervention

Direct current transthoracic cardioversion during short-acting anesthesia is a reliable way to terminate AF

Conversion rates using a 200-J biphasic shock delivered synchronously with the QRS complex typically are gt90

Recurrence after external defibrillation

J Am Coll Cardiol 2007 Apr 1749(15)1642-8 Epub 2007 Apr 2

Association between C-reactive protein and recurrence of atrial fibrillation after successful electrical cardioversion a meta-analysisLiu T Li G Li L Korantzopoulos PSourceDepartment of Cardiology Tianjin Institute of Cardiology Second Hospital of Tianjin Medical University Tianjin Peoples Republic of ChinaAbstract

OBJECTIVESWe conducted a systematic review and meta-analysis of observational studies to examine the association between baseline C-reactive protein (CRP) levels and the recurrence of atrial fibrillation (AF) after successful electrical cardioversion (EC)BACKGROUNDCurrent evidence links AF to the inflammatory state Inflammatory indexes such as CRP have been related to the development and persistence of AF However inconsistent results have been published with regard to the role of CRP in predicting sinus rhythm maintenance after successful ECMETHODSUsing PubMed the Cochrane clinical trials database and EMBASE we searched for literature published June 2006 or earlier In addition a manual search was performed using all review articles on this topic reference lists of papers and abstracts from conference reports Of the 225 initially identified studies 7 prospective observational studies with 420 patients (229 with and 191 without AF relapse) were finally analyzedRESULTSOverall baseline CRP levels were greater in patients with AF recurrence The standardized mean difference in the CRP levels between the patients with and those without AF was 035 units (95 confidence interval 001 to 069) test for overall effect z-score = 200 (p = 005) The heterogeneity test showed that there were significant differences between individual studies (p = 002 I(2) = 602) Further analysis revealed that differences between the CRP assays possibly account for this heterogeneityCONCLUSIONSOur meta-analysis suggests that increased CRP levels are associated with greater risk of AF recurrence although there was significant heterogeneity across the studies The use of CRP levels in predicting sinus rhythm maintenance appears promising but requires further study

Treating AF in patients with left ventricular dysfunction can be difficult because of associated electrophysiologic derangements potential proarrhythmic concerns and negative inotropic effects of antiarrhythmics

Some data exist suggesting that angiotensin-converting enzyme inhibitors and angiotensin receptor blockers can prevent AF either by preventing atrial dilation and stretch-induced arrhythmias or by blocking the renin-angiotensin system

In post-myocardial infarction patients DL-sotalol dofetilide and amiodarone-and in congestive heart failure patients amiodarone and dofetilide-have demonstrated neutral effects on survival in controlled trials

In the Congestive Heart Failure Survival Trial of Antiarrhythmic Therapy (CHF-STAT) amiodarone lowered the frequency of AF development and improved left ventricular ejection fraction over time In CHF-STAT there was lower mortality in patients who converted from AF to sinus rhythm

Dofetilide decreased rehospitalization for congestive heart failure in the Danish Investigations of Arrhythmia and Mortality on Dofetilide (DIAMOND) trials

Neutral effects on survival and favorable hemodynamics have positioned amiodarone and dofetilide as the antiarrhythmics of choice in patients with left ventricular dysfunction

In post-myocardial infarction patients sotalol is an additional agent to consider for treatment of AF in this setting

External defibrillation

Termination of AF by electrical defibrillator

acutely may be warranted based on clinical parameters andor hemodynamic status

Confirmation of appropriate anticoagulation must be documented unless symptoms and clinical status warrant emergent intervention

Direct current transthoracic cardioversion during short-acting anesthesia is a reliable way to terminate AF

Conversion rates using a 200-J biphasic shock delivered synchronously with the QRS complex typically are gt90

Recurrence after external defibrillation

J Am Coll Cardiol 2007 Apr 1749(15)1642-8 Epub 2007 Apr 2

Association between C-reactive protein and recurrence of atrial fibrillation after successful electrical cardioversion a meta-analysisLiu T Li G Li L Korantzopoulos PSourceDepartment of Cardiology Tianjin Institute of Cardiology Second Hospital of Tianjin Medical University Tianjin Peoples Republic of ChinaAbstract

OBJECTIVESWe conducted a systematic review and meta-analysis of observational studies to examine the association between baseline C-reactive protein (CRP) levels and the recurrence of atrial fibrillation (AF) after successful electrical cardioversion (EC)BACKGROUNDCurrent evidence links AF to the inflammatory state Inflammatory indexes such as CRP have been related to the development and persistence of AF However inconsistent results have been published with regard to the role of CRP in predicting sinus rhythm maintenance after successful ECMETHODSUsing PubMed the Cochrane clinical trials database and EMBASE we searched for literature published June 2006 or earlier In addition a manual search was performed using all review articles on this topic reference lists of papers and abstracts from conference reports Of the 225 initially identified studies 7 prospective observational studies with 420 patients (229 with and 191 without AF relapse) were finally analyzedRESULTSOverall baseline CRP levels were greater in patients with AF recurrence The standardized mean difference in the CRP levels between the patients with and those without AF was 035 units (95 confidence interval 001 to 069) test for overall effect z-score = 200 (p = 005) The heterogeneity test showed that there were significant differences between individual studies (p = 002 I(2) = 602) Further analysis revealed that differences between the CRP assays possibly account for this heterogeneityCONCLUSIONSOur meta-analysis suggests that increased CRP levels are associated with greater risk of AF recurrence although there was significant heterogeneity across the studies The use of CRP levels in predicting sinus rhythm maintenance appears promising but requires further study

External defibrillation

Termination of AF by electrical defibrillator

acutely may be warranted based on clinical parameters andor hemodynamic status

Confirmation of appropriate anticoagulation must be documented unless symptoms and clinical status warrant emergent intervention

Direct current transthoracic cardioversion during short-acting anesthesia is a reliable way to terminate AF

Conversion rates using a 200-J biphasic shock delivered synchronously with the QRS complex typically are gt90

Recurrence after external defibrillation

J Am Coll Cardiol 2007 Apr 1749(15)1642-8 Epub 2007 Apr 2

Association between C-reactive protein and recurrence of atrial fibrillation after successful electrical cardioversion a meta-analysisLiu T Li G Li L Korantzopoulos PSourceDepartment of Cardiology Tianjin Institute of Cardiology Second Hospital of Tianjin Medical University Tianjin Peoples Republic of ChinaAbstract

OBJECTIVESWe conducted a systematic review and meta-analysis of observational studies to examine the association between baseline C-reactive protein (CRP) levels and the recurrence of atrial fibrillation (AF) after successful electrical cardioversion (EC)BACKGROUNDCurrent evidence links AF to the inflammatory state Inflammatory indexes such as CRP have been related to the development and persistence of AF However inconsistent results have been published with regard to the role of CRP in predicting sinus rhythm maintenance after successful ECMETHODSUsing PubMed the Cochrane clinical trials database and EMBASE we searched for literature published June 2006 or earlier In addition a manual search was performed using all review articles on this topic reference lists of papers and abstracts from conference reports Of the 225 initially identified studies 7 prospective observational studies with 420 patients (229 with and 191 without AF relapse) were finally analyzedRESULTSOverall baseline CRP levels were greater in patients with AF recurrence The standardized mean difference in the CRP levels between the patients with and those without AF was 035 units (95 confidence interval 001 to 069) test for overall effect z-score = 200 (p = 005) The heterogeneity test showed that there were significant differences between individual studies (p = 002 I(2) = 602) Further analysis revealed that differences between the CRP assays possibly account for this heterogeneityCONCLUSIONSOur meta-analysis suggests that increased CRP levels are associated with greater risk of AF recurrence although there was significant heterogeneity across the studies The use of CRP levels in predicting sinus rhythm maintenance appears promising but requires further study

Termination of AF by electrical defibrillator

acutely may be warranted based on clinical parameters andor hemodynamic status

Confirmation of appropriate anticoagulation must be documented unless symptoms and clinical status warrant emergent intervention

Direct current transthoracic cardioversion during short-acting anesthesia is a reliable way to terminate AF

Conversion rates using a 200-J biphasic shock delivered synchronously with the QRS complex typically are gt90

Recurrence after external defibrillation

J Am Coll Cardiol 2007 Apr 1749(15)1642-8 Epub 2007 Apr 2

Association between C-reactive protein and recurrence of atrial fibrillation after successful electrical cardioversion a meta-analysisLiu T Li G Li L Korantzopoulos PSourceDepartment of Cardiology Tianjin Institute of Cardiology Second Hospital of Tianjin Medical University Tianjin Peoples Republic of ChinaAbstract

OBJECTIVESWe conducted a systematic review and meta-analysis of observational studies to examine the association between baseline C-reactive protein (CRP) levels and the recurrence of atrial fibrillation (AF) after successful electrical cardioversion (EC)BACKGROUNDCurrent evidence links AF to the inflammatory state Inflammatory indexes such as CRP have been related to the development and persistence of AF However inconsistent results have been published with regard to the role of CRP in predicting sinus rhythm maintenance after successful ECMETHODSUsing PubMed the Cochrane clinical trials database and EMBASE we searched for literature published June 2006 or earlier In addition a manual search was performed using all review articles on this topic reference lists of papers and abstracts from conference reports Of the 225 initially identified studies 7 prospective observational studies with 420 patients (229 with and 191 without AF relapse) were finally analyzedRESULTSOverall baseline CRP levels were greater in patients with AF recurrence The standardized mean difference in the CRP levels between the patients with and those without AF was 035 units (95 confidence interval 001 to 069) test for overall effect z-score = 200 (p = 005) The heterogeneity test showed that there were significant differences between individual studies (p = 002 I(2) = 602) Further analysis revealed that differences between the CRP assays possibly account for this heterogeneityCONCLUSIONSOur meta-analysis suggests that increased CRP levels are associated with greater risk of AF recurrence although there was significant heterogeneity across the studies The use of CRP levels in predicting sinus rhythm maintenance appears promising but requires further study

Recurrence after external defibrillation

J Am Coll Cardiol 2007 Apr 1749(15)1642-8 Epub 2007 Apr 2

Association between C-reactive protein and recurrence of atrial fibrillation after successful electrical cardioversion a meta-analysisLiu T Li G Li L Korantzopoulos PSourceDepartment of Cardiology Tianjin Institute of Cardiology Second Hospital of Tianjin Medical University Tianjin Peoples Republic of ChinaAbstract

OBJECTIVESWe conducted a systematic review and meta-analysis of observational studies to examine the association between baseline C-reactive protein (CRP) levels and the recurrence of atrial fibrillation (AF) after successful electrical cardioversion (EC)BACKGROUNDCurrent evidence links AF to the inflammatory state Inflammatory indexes such as CRP have been related to the development and persistence of AF However inconsistent results have been published with regard to the role of CRP in predicting sinus rhythm maintenance after successful ECMETHODSUsing PubMed the Cochrane clinical trials database and EMBASE we searched for literature published June 2006 or earlier In addition a manual search was performed using all review articles on this topic reference lists of papers and abstracts from conference reports Of the 225 initially identified studies 7 prospective observational studies with 420 patients (229 with and 191 without AF relapse) were finally analyzedRESULTSOverall baseline CRP levels were greater in patients with AF recurrence The standardized mean difference in the CRP levels between the patients with and those without AF was 035 units (95 confidence interval 001 to 069) test for overall effect z-score = 200 (p = 005) The heterogeneity test showed that there were significant differences between individual studies (p = 002 I(2) = 602) Further analysis revealed that differences between the CRP assays possibly account for this heterogeneityCONCLUSIONSOur meta-analysis suggests that increased CRP levels are associated with greater risk of AF recurrence although there was significant heterogeneity across the studies The use of CRP levels in predicting sinus rhythm maintenance appears promising but requires further study

J Am Coll Cardiol 2007 Apr 1749(15)1642-8 Epub 2007 Apr 2

Association between C-reactive protein and recurrence of atrial fibrillation after successful electrical cardioversion a meta-analysisLiu T Li G Li L Korantzopoulos PSourceDepartment of Cardiology Tianjin Institute of Cardiology Second Hospital of Tianjin Medical University Tianjin Peoples Republic of ChinaAbstract

OBJECTIVESWe conducted a systematic review and meta-analysis of observational studies to examine the association between baseline C-reactive protein (CRP) levels and the recurrence of atrial fibrillation (AF) after successful electrical cardioversion (EC)BACKGROUNDCurrent evidence links AF to the inflammatory state Inflammatory indexes such as CRP have been related to the development and persistence of AF However inconsistent results have been published with regard to the role of CRP in predicting sinus rhythm maintenance after successful ECMETHODSUsing PubMed the Cochrane clinical trials database and EMBASE we searched for literature published June 2006 or earlier In addition a manual search was performed using all review articles on this topic reference lists of papers and abstracts from conference reports Of the 225 initially identified studies 7 prospective observational studies with 420 patients (229 with and 191 without AF relapse) were finally analyzedRESULTSOverall baseline CRP levels were greater in patients with AF recurrence The standardized mean difference in the CRP levels between the patients with and those without AF was 035 units (95 confidence interval 001 to 069) test for overall effect z-score = 200 (p = 005) The heterogeneity test showed that there were significant differences between individual studies (p = 002 I(2) = 602) Further analysis revealed that differences between the CRP assays possibly account for this heterogeneityCONCLUSIONSOur meta-analysis suggests that increased CRP levels are associated with greater risk of AF recurrence although there was significant heterogeneity across the studies The use of CRP levels in predicting sinus rhythm maintenance appears promising but requires further study

Factors Associated With Failed Cardioversion

bull Underlying illnessmdashcongestive heart failure thyrotoxicosis valvular disease

bull Dilated left atrium

bull Longer duration of atrial fibrillation

bull Too low energy

bull Technique

bull Other patient factors

J Interv Card Electrophysiol 2005 Aug13 Suppl 161-6Internal defibrillation where we have been and where we should be goingLeacutevy S

SourceDivision of Cardiology School of Medicine University of Marseille Chemin des Bourrellys Marseille France samuelsamuel-levycom

AbstractInternal cardioversion has been developed as an alternative technique for patients who are resistant to external DC cardioversion of atrial fibrillation (AF) and was found to be associated with higher success rates It used initially high energies (200-300 J) delivered between an intracardiac catheter and a backplate Subsequent studies have shown that it is possible to terminate with energies of 1 to 6 Joules paroxysmal or induced AF in 90 percent of patients and persistent AF in 75 percent of patients using biphasic shocks delivered between a right atrium-coronary sinus vectors Consequently internal atrial defibrillation can be performed under sedation only without the need for general anesthesia Recently developed external defibrillators capable of delivering biphasic shocks have increased the success rates of external cardioversion and reduced the need for internal cardioversion However internal defibrillation is still useful in overweight or obese patients in patients with chronic obstructive pulmonary disease or asthma who are more difficult to defibrillate and in patients with implanted devices which may be injured by high energy shocks Low energy internal defibrillation has also proven to be safe and this has prompted the development of implantable devices for terminating AF The first device used was the Metrix system a stand-alone atrial defibrillator (without ventricular defibrillation) which was found to be safe and effective in selected groups of patients Unfortunately this device is no longer being marketed Only double chamber defibrillators with pacing capabilities are presently available the Medtronic GEM III AT an updated version of the Jewel AF and the Guidant PRIZM AVT These devices can be patient-activated or programmed to deliver automatically ounce atrial tachyarrhythmias are detected therapies including pacing orand shocks Attempts to define the group of patients who might benefit from these devices are described but the respective role of atrial defibrillators versus other non-pharmacologic therapies for AF such as surgery and radiofrequency catheter ablation remains to be determined Advantages and limitations or atrial defibrillators and approaches to reduce shock related discomfort which may be a concern in some patients are reviewed Studies have shown that despite shock discomfort quality of life was improved in patients with atrial defibrillators and the need for repeated hospitalizations was reduced The cost of these devices remains a concern for the treatment of a non-lethal arrhythmia Attention that atrial defibrillators will receive from cardiologists and from the industry in the future will depend of the long-term results of other non-pharmacological options and of the identification of the group of AF patients which will require restoration and maintenance of sinus rhythm But there is no doubt that selected subsets of patients with AF could benefit from atrial defibrillation

J Interv Card Electrophysiol 2005 Aug13 Suppl 161-6Internal defibrillation where we have been and where we should be goingLeacutevy S

SourceDivision of Cardiology School of Medicine University of Marseille Chemin des Bourrellys Marseille France samuelsamuel-levycom

AbstractInternal cardioversion has been developed as an alternative technique for patients who are resistant to external DC cardioversion of atrial fibrillation (AF) and was found to be associated with higher success rates It used initially high energies (200-300 J) delivered between an intracardiac catheter and a backplate Subsequent studies have shown that it is possible to terminate with energies of 1 to 6 Joules paroxysmal or induced AF in 90 percent of patients and persistent AF in 75 percent of patients using biphasic shocks delivered between a right atrium-coronary sinus vectors Consequently internal atrial defibrillation can be performed under sedation only without the need for general anesthesia Recently developed external defibrillators capable of delivering biphasic shocks have increased the success rates of external cardioversion and reduced the need for internal cardioversion However internal defibrillation is still useful in overweight or obese patients in patients with chronic obstructive pulmonary disease or asthma who are more difficult to defibrillate and in patients with implanted devices which may be injured by high energy shocks Low energy internal defibrillation has also proven to be safe and this has prompted the development of implantable devices for terminating AF The first device used was the Metrix system a stand-alone atrial defibrillator (without ventricular defibrillation) which was found to be safe and effective in selected groups of patients Unfortunately this device is no longer being marketed Only double chamber defibrillators with pacing capabilities are presently available the Medtronic GEM III AT an updated version of the Jewel AF and the Guidant PRIZM AVT These devices can be patient-activated or programmed to deliver automatically ounce atrial tachyarrhythmias are detected therapies including pacing orand shocks Attempts to define the group of patients who might benefit from these devices are described but the respective role of atrial defibrillators versus other non-pharmacologic therapies for AF such as surgery and radiofrequency catheter ablation remains to be determined Advantages and limitations or atrial defibrillators and approaches to reduce shock related discomfort which may be a concern in some patients are reviewed Studies have shown that despite shock discomfort quality of life was improved in patients with atrial defibrillators and the need for repeated hospitalizations was reduced The cost of these devices remains a concern for the treatment of a non-lethal arrhythmia Attention that atrial defibrillators will receive from cardiologists and from the industry in the future will depend of the long-term results of other non-pharmacological options and of the identification of the group of AF patients which will require restoration and maintenance of sinus rhythm But there is no doubt that selected subsets of patients with AF could benefit from atrial defibrillation

ANTI - COAGULATION THERAPY

CHADS2 score (2001) CHA2DS2-VASc(2010)

C-- Cardiac failureH-- HypertensionA-- Age D-- DiabetesS-- Stroke Vndash vascular disease( prior myocardial infarction perferal vascular disease aortic plaque )Sc -- sex category

Score = 0-1 Score = 2 or more than 2

Target INR-- 2-3

Others risk factors for embolism

1 Valvular heart diseases

2 Age 65-74 yrs

3 Female sex

4 Coronary artery disease

5 Mechanical prosthetic valve

6 Systemic embolism

7 Marked left atrial enlargement (gt50 cm)

High risk catagories

1 Valvular heart disease

2 Prior ischemic stroke

3 ho systemic embolism

4 Mechanical prosthetic valve

ANTI COAGULATION THERAPY IN SPECIAL CONDITIONS

1 Age gt 85

2 Stroke and TIA

3 Pregnancy

4 Dental or surgical procedures

5 After Coronary revascularization

DRUGS USED IN ANTI COAGULATION THERAPY

1 Vitamine K antagonist----- warfarin

2 Direct thrombine inhibitors----

RE-LY study

3 factor Xa inhibitors-----

apixaban endoxaban

AVERROES study

betrixaban

dabigatran Ximelagatran

Direct thrombin inhibition

RE-LY (Randomized Evaluation of Long-term Anticoagulation Therapy) is an international multicenter study (18113 patients from 967 centers in 44 countries) that demonstrated the ability of dabigatran to reduce the occurrence of both stroke and hemorrhage in patients who had atrial fibrillation (AF) with high risks of stroke compared with patients who received warfarin From Japan 326 patients were randomized in RE-LY

RE-LY (Randomized Evaluation of Long-term Anticoagulation Therapy) study

1 For any bleeding the relative risk of dabigatran at 110mg and 150mg twice

daily over warfarin was 079 and 106

2 In RE-LY the efficacy and safety profiles of dabigatran for Japanese AF patients

at high risk of stroke were essentially the same as for the study population

overall

Circ J 2011 Mar 2575(4)800-805 Epub 2011 Mar 19

Efficacy and Safety of Dabigatran vs Warfarin in Patients With Atrial FibrillationHori M Connolly SJ Ezekowitz MD Reilly PA Yusuf S Wallentin L the RE-LY Investigators

SourceOsaka Medical Center for Cancer and Cardiovascular Diseases

CHADS2 score (2001) CHA2DS2-VASc(2010)

C-- Cardiac failureH-- HypertensionA-- Age D-- DiabetesS-- Stroke Vndash vascular disease( prior myocardial infarction perferal vascular disease aortic plaque )Sc -- sex category

Score = 0-1 Score = 2 or more than 2

Target INR-- 2-3

Others risk factors for embolism

1 Valvular heart diseases

2 Age 65-74 yrs

3 Female sex

4 Coronary artery disease

5 Mechanical prosthetic valve

6 Systemic embolism

7 Marked left atrial enlargement (gt50 cm)

High risk catagories

1 Valvular heart disease

2 Prior ischemic stroke

3 ho systemic embolism

4 Mechanical prosthetic valve

ANTI COAGULATION THERAPY IN SPECIAL CONDITIONS

1 Age gt 85

2 Stroke and TIA

3 Pregnancy

4 Dental or surgical procedures

5 After Coronary revascularization

DRUGS USED IN ANTI COAGULATION THERAPY

1 Vitamine K antagonist----- warfarin

2 Direct thrombine inhibitors----

RE-LY study

3 factor Xa inhibitors-----

apixaban endoxaban

AVERROES study

betrixaban

dabigatran Ximelagatran

Direct thrombin inhibition

RE-LY (Randomized Evaluation of Long-term Anticoagulation Therapy) is an international multicenter study (18113 patients from 967 centers in 44 countries) that demonstrated the ability of dabigatran to reduce the occurrence of both stroke and hemorrhage in patients who had atrial fibrillation (AF) with high risks of stroke compared with patients who received warfarin From Japan 326 patients were randomized in RE-LY

RE-LY (Randomized Evaluation of Long-term Anticoagulation Therapy) study

1 For any bleeding the relative risk of dabigatran at 110mg and 150mg twice

daily over warfarin was 079 and 106

2 In RE-LY the efficacy and safety profiles of dabigatran for Japanese AF patients

at high risk of stroke were essentially the same as for the study population

overall

Circ J 2011 Mar 2575(4)800-805 Epub 2011 Mar 19

Efficacy and Safety of Dabigatran vs Warfarin in Patients With Atrial FibrillationHori M Connolly SJ Ezekowitz MD Reilly PA Yusuf S Wallentin L the RE-LY Investigators

SourceOsaka Medical Center for Cancer and Cardiovascular Diseases

Others risk factors for embolism

1 Valvular heart diseases

2 Age 65-74 yrs

3 Female sex

4 Coronary artery disease

5 Mechanical prosthetic valve

6 Systemic embolism

7 Marked left atrial enlargement (gt50 cm)

High risk catagories

1 Valvular heart disease

2 Prior ischemic stroke

3 ho systemic embolism

4 Mechanical prosthetic valve

ANTI COAGULATION THERAPY IN SPECIAL CONDITIONS

1 Age gt 85

2 Stroke and TIA

3 Pregnancy

4 Dental or surgical procedures

5 After Coronary revascularization

DRUGS USED IN ANTI COAGULATION THERAPY

1 Vitamine K antagonist----- warfarin

2 Direct thrombine inhibitors----

RE-LY study

3 factor Xa inhibitors-----

apixaban endoxaban

AVERROES study

betrixaban

dabigatran Ximelagatran

Direct thrombin inhibition

RE-LY (Randomized Evaluation of Long-term Anticoagulation Therapy) is an international multicenter study (18113 patients from 967 centers in 44 countries) that demonstrated the ability of dabigatran to reduce the occurrence of both stroke and hemorrhage in patients who had atrial fibrillation (AF) with high risks of stroke compared with patients who received warfarin From Japan 326 patients were randomized in RE-LY

RE-LY (Randomized Evaluation of Long-term Anticoagulation Therapy) study

1 For any bleeding the relative risk of dabigatran at 110mg and 150mg twice

daily over warfarin was 079 and 106

2 In RE-LY the efficacy and safety profiles of dabigatran for Japanese AF patients

at high risk of stroke were essentially the same as for the study population

overall

Circ J 2011 Mar 2575(4)800-805 Epub 2011 Mar 19

Efficacy and Safety of Dabigatran vs Warfarin in Patients With Atrial FibrillationHori M Connolly SJ Ezekowitz MD Reilly PA Yusuf S Wallentin L the RE-LY Investigators

SourceOsaka Medical Center for Cancer and Cardiovascular Diseases

High risk catagories

1 Valvular heart disease

2 Prior ischemic stroke

3 ho systemic embolism

4 Mechanical prosthetic valve

ANTI COAGULATION THERAPY IN SPECIAL CONDITIONS

1 Age gt 85

2 Stroke and TIA

3 Pregnancy

4 Dental or surgical procedures

5 After Coronary revascularization

DRUGS USED IN ANTI COAGULATION THERAPY

1 Vitamine K antagonist----- warfarin

2 Direct thrombine inhibitors----

RE-LY study

3 factor Xa inhibitors-----

apixaban endoxaban

AVERROES study

betrixaban

dabigatran Ximelagatran

Direct thrombin inhibition

RE-LY (Randomized Evaluation of Long-term Anticoagulation Therapy) is an international multicenter study (18113 patients from 967 centers in 44 countries) that demonstrated the ability of dabigatran to reduce the occurrence of both stroke and hemorrhage in patients who had atrial fibrillation (AF) with high risks of stroke compared with patients who received warfarin From Japan 326 patients were randomized in RE-LY

RE-LY (Randomized Evaluation of Long-term Anticoagulation Therapy) study

1 For any bleeding the relative risk of dabigatran at 110mg and 150mg twice

daily over warfarin was 079 and 106

2 In RE-LY the efficacy and safety profiles of dabigatran for Japanese AF patients

at high risk of stroke were essentially the same as for the study population

overall

Circ J 2011 Mar 2575(4)800-805 Epub 2011 Mar 19

Efficacy and Safety of Dabigatran vs Warfarin in Patients With Atrial FibrillationHori M Connolly SJ Ezekowitz MD Reilly PA Yusuf S Wallentin L the RE-LY Investigators

SourceOsaka Medical Center for Cancer and Cardiovascular Diseases

ANTI COAGULATION THERAPY IN SPECIAL CONDITIONS

1 Age gt 85

2 Stroke and TIA

3 Pregnancy

4 Dental or surgical procedures

5 After Coronary revascularization

DRUGS USED IN ANTI COAGULATION THERAPY

1 Vitamine K antagonist----- warfarin

2 Direct thrombine inhibitors----

RE-LY study

3 factor Xa inhibitors-----

apixaban endoxaban

AVERROES study

betrixaban

dabigatran Ximelagatran

Direct thrombin inhibition

RE-LY (Randomized Evaluation of Long-term Anticoagulation Therapy) is an international multicenter study (18113 patients from 967 centers in 44 countries) that demonstrated the ability of dabigatran to reduce the occurrence of both stroke and hemorrhage in patients who had atrial fibrillation (AF) with high risks of stroke compared with patients who received warfarin From Japan 326 patients were randomized in RE-LY

RE-LY (Randomized Evaluation of Long-term Anticoagulation Therapy) study

1 For any bleeding the relative risk of dabigatran at 110mg and 150mg twice

daily over warfarin was 079 and 106

2 In RE-LY the efficacy and safety profiles of dabigatran for Japanese AF patients

at high risk of stroke were essentially the same as for the study population

overall

Circ J 2011 Mar 2575(4)800-805 Epub 2011 Mar 19

Efficacy and Safety of Dabigatran vs Warfarin in Patients With Atrial FibrillationHori M Connolly SJ Ezekowitz MD Reilly PA Yusuf S Wallentin L the RE-LY Investigators

SourceOsaka Medical Center for Cancer and Cardiovascular Diseases

DRUGS USED IN ANTI COAGULATION THERAPY

1 Vitamine K antagonist----- warfarin

2 Direct thrombine inhibitors----

RE-LY study

3 factor Xa inhibitors-----

apixaban endoxaban

AVERROES study

betrixaban

dabigatran Ximelagatran

Direct thrombin inhibition

RE-LY (Randomized Evaluation of Long-term Anticoagulation Therapy) is an international multicenter study (18113 patients from 967 centers in 44 countries) that demonstrated the ability of dabigatran to reduce the occurrence of both stroke and hemorrhage in patients who had atrial fibrillation (AF) with high risks of stroke compared with patients who received warfarin From Japan 326 patients were randomized in RE-LY

RE-LY (Randomized Evaluation of Long-term Anticoagulation Therapy) study

1 For any bleeding the relative risk of dabigatran at 110mg and 150mg twice

daily over warfarin was 079 and 106

2 In RE-LY the efficacy and safety profiles of dabigatran for Japanese AF patients

at high risk of stroke were essentially the same as for the study population

overall

Circ J 2011 Mar 2575(4)800-805 Epub 2011 Mar 19

Efficacy and Safety of Dabigatran vs Warfarin in Patients With Atrial FibrillationHori M Connolly SJ Ezekowitz MD Reilly PA Yusuf S Wallentin L the RE-LY Investigators

SourceOsaka Medical Center for Cancer and Cardiovascular Diseases

Direct thrombin inhibition

RE-LY (Randomized Evaluation of Long-term Anticoagulation Therapy) is an international multicenter study (18113 patients from 967 centers in 44 countries) that demonstrated the ability of dabigatran to reduce the occurrence of both stroke and hemorrhage in patients who had atrial fibrillation (AF) with high risks of stroke compared with patients who received warfarin From Japan 326 patients were randomized in RE-LY

RE-LY (Randomized Evaluation of Long-term Anticoagulation Therapy) study

1 For any bleeding the relative risk of dabigatran at 110mg and 150mg twice

daily over warfarin was 079 and 106

2 In RE-LY the efficacy and safety profiles of dabigatran for Japanese AF patients

at high risk of stroke were essentially the same as for the study population

overall

Circ J 2011 Mar 2575(4)800-805 Epub 2011 Mar 19

Efficacy and Safety of Dabigatran vs Warfarin in Patients With Atrial FibrillationHori M Connolly SJ Ezekowitz MD Reilly PA Yusuf S Wallentin L the RE-LY Investigators

SourceOsaka Medical Center for Cancer and Cardiovascular Diseases

RE-LY (Randomized Evaluation of Long-term Anticoagulation Therapy) is an international multicenter study (18113 patients from 967 centers in 44 countries) that demonstrated the ability of dabigatran to reduce the occurrence of both stroke and hemorrhage in patients who had atrial fibrillation (AF) with high risks of stroke compared with patients who received warfarin From Japan 326 patients were randomized in RE-LY

RE-LY (Randomized Evaluation of Long-term Anticoagulation Therapy) study

1 For any bleeding the relative risk of dabigatran at 110mg and 150mg twice

daily over warfarin was 079 and 106

2 In RE-LY the efficacy and safety profiles of dabigatran for Japanese AF patients

at high risk of stroke were essentially the same as for the study population

overall

Circ J 2011 Mar 2575(4)800-805 Epub 2011 Mar 19

Efficacy and Safety of Dabigatran vs Warfarin in Patients With Atrial FibrillationHori M Connolly SJ Ezekowitz MD Reilly PA Yusuf S Wallentin L the RE-LY Investigators

SourceOsaka Medical Center for Cancer and Cardiovascular Diseases

1 For any bleeding the relative risk of dabigatran at 110mg and 150mg twice

daily over warfarin was 079 and 106

2 In RE-LY the efficacy and safety profiles of dabigatran for Japanese AF patients

at high risk of stroke were essentially the same as for the study population

overall

Circ J 2011 Mar 2575(4)800-805 Epub 2011 Mar 19

Efficacy and Safety of Dabigatran vs Warfarin in Patients With Atrial FibrillationHori M Connolly SJ Ezekowitz MD Reilly PA Yusuf S Wallentin L the RE-LY Investigators

SourceOsaka Medical Center for Cancer and Cardiovascular Diseases

1 Ximelagatran was as effective as warfarin in reducing strokesystemic emboli in the elderly (223y with ximelagatran vs 227y with warfarin) as in younger patients (125y vs 128y)

2 Total bleeds were significantly lower with ximelagatran compared with warfarin in elderly (40 vs 45 P=001) and younger (27 vs 35 Plt0001) patients

3 Raised alanine aminotransferase values (gt3-fold elevation) among ximelagatran patients were more common in older (75 old vs 53 young) patients particularly women (95 elderly women vs 61 elderly men)

4 In high-risk elderly AF patients ximelagatran is as effective as warfarin with less bleeding but alanine aminotransferase elevations are common particularly in elderly women Oral DTIs for stroke prevention show promise in elderly patients

Stroke 2007 Nov38(11)2965-71 Epub 2007 Sep 20

Direct thrombin inhibition and stroke prevention in elderly patients with atrial fibrillation experience from the SPORTIF III and V TrialsFord GA Choy AM Deedwania P Karalis DG Lindholm CJ Pluta W Frison L Olsson SB SPORTIF III V Investigators

SourceInstitute for Ageing and Health University of Newcastle upon Tyne Newcastle upon Tyne England

When compared with men with AF women in these studies were older and had more

stroke risk factors Women were more prone to anticoagulant-related bleeding the

higher rate of thrombo-embolism among women was related to more frequent

interruption of anticoagulant therapy

Eur Heart J 2006 Aug27(16)1947-53 Epub 2006 Jun 14

Anticoagulation in women with non-valvular atrial fibrillation in the stroke prevention using an oral thrombin inhibitor (SPORTIF) trialsGomberg-Maitland M Wenger NK Feyzi J Lengyel M Volgman AS Petersen P Frison L Halperin JL

SourceDepartment of Medicine Section of Cardiology University of Chicago Hospitals University of Chicago 5841 S Maryland Avenue MC2016 Chicago IL 60637 USA mgombergmedicinebsduchicagoedu

Antiarrhythmic effect of statin therapy

1 Atrial fibrillation (AF) is the most common clinical arrhythmia Recent investigations have suggested that inflammation might have a role in the pathophysiology of AF

2 In this review the association between inflammation and AF and the effects of several agents that have anti-inflammatory actions such as statins polyunsaturated fatty acids corticosteroids and angiotensin-converting enzyme inhibitors and angiotensin receptor blockers have been investigated

World J Cardiol 2010 Aug 262(8)243-50

Atrial fibrillation and inflammationOzaydin M

SourceMehmet Ozaydin Department of Cardiology School of Medicine Suleyman Demirel University 32040 Isparta Turkey

1 Atrial fibrillation (AF) is the most common clinical arrhythmia Recent investigations have suggested that inflammation might have a role in the pathophysiology of AF

2 In this review the association between inflammation and AF and the effects of several agents that have anti-inflammatory actions such as statins polyunsaturated fatty acids corticosteroids and angiotensin-converting enzyme inhibitors and angiotensin receptor blockers have been investigated

World J Cardiol 2010 Aug 262(8)243-50

Atrial fibrillation and inflammationOzaydin M

SourceMehmet Ozaydin Department of Cardiology School of Medicine Suleyman Demirel University 32040 Isparta Turkey

1 Inflammation appears to play a significant role in the initiation and perpetuation of AF as well as the prothrombotic state associated with AF

2 Inflammatory biomarkers (C-reactive protein and interleukin-6) have been shown to be associated with the future development recurrence and burden of AF and the likelihood of successful cardioversion

3 Animal and clinical studies have evaluated statins angiotensin-converting enzyme inhibitorsangiotensin-II receptor blockers and corticosteroids for the treatment or prevention of AF

J Cardiovasc Electrophysiol 2010 Sep21(9)1064-70 doi 101111j1540-8167201001774x

Update on the association of inflammation and atrial fibrillationPatel P Dokainish H Tsai P Lakkis N

SourceSection of Cardiology Baylor College of Medicine Houston Texas USA

1 Overall the use of statins was significantly associated with a decreased risk of AF compared with control (odds ratio [OR] 039 95 confidence interval [CI] 018 to 085 p = 002)

2 Benefit of statin therapy seemed more marked in secondary prevention of AF (OR 033 95 CI 010 to 103 p = 006) than for new-onset or postoperative AF (OR 060 95 CI 027 to 137 p = 023)

3 Use of statins was significantly associated with a decreased risk of incidence or recurrence of AF in patients in sinus rhythm with a history of previous AF or undergoing cardiac surgery or after acute coronary syndrome

J Am Coll Cardiol 2008 Feb 2651(8)828-35

Antiarrhythmic effect of statin therapy and atrial fibrillation a meta-analysis of randomized controlled trialsFauchier L Pierre B de Labriolle A Grimard C Zannad N Babuty D

SourceCardiologie Centre Hospitalier Universitaire Trousseau Tours France lfaumeduniv-toursfr

Our meta-analysis suggests that increased CRP levels are associated with greater risk of AF recurrence although there was significant heterogeneity across the studies The use of CRP levels in predicting sinus rhythm maintenance appears promising but requires further study

J Am Coll Cardiol 2007 Apr 1749(15)1642-8 Epub 2007 Apr 2

Association between C-reactive protein and recurrence of atrial fibrillation after successful electrical cardioversion a meta-analysisLiu T Li G Li L Korantzopoulos P

SourceDepartment of Cardiology Tianjin Institute of Cardiology Second Hospital of Tianjin Medical University Tianjin Peoples Republic of China

Angiotensin-converting enzyme inhibitors and angiotensin receptor blocker in

atrial fibrillation

ACEIsARBs are effective for primary prevention and secondary prevention of AF They decrease the incidence of AF especially in patients with hypertension patients with chronic heart failure and those with AF

Eur J Clin Invest 2011 Jan 20 doi 101111j1365-2362201002460x [Epub ahead of print]

Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers decrease the incidence of atrial fibrillation a meta-analysisHuang G Xu JB Liu JX He Y Nie XL Li Q Hu YM Zhao SQ Wang M Zhang WY Liu XR Wu T Arkin A Zhang TJ

ACEIsARBs are effective for primary prevention and secondary prevention of AF They decrease the incidence of AF especially in patients with hypertension patients with chronic heart failure and those with AF

Eur J Clin Invest 2011 Jan 20 doi 101111j1365-2362201002460x [Epub ahead of print]

Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers decrease the incidence of atrial fibrillation a meta-analysisHuang G Xu JB Liu JX He Y Nie XL Li Q Hu YM Zhao SQ Wang M Zhang WY Liu XR Wu T Arkin A Zhang TJ

new drug to treat patients with acute onset atrial fibrillation

Dronedarone was approved by the US Food and Drug Administration on July 2 2009

1 It is a deiodinated derivative of amiodarone that has no organ toxicity

2 Its use will likely extend to both atrial and ventricular arrhythmias

3 Dronedarone has multiple actions (all 4 Von Williams class effects)

4 Unlike amiodarone it does not have the iodine moiety

5 The lack of iodination may offer a better side-effect profile Dronedarone has been shown to (1) have antiadrenergic effects (2) prolong atrial and ventricular refractory periods and (3) prolong atrioventricular node conduction as well as the paced QRS complex

5 In animal models dronedarone has been shown to decrease ischemia-induced ventricular arrhythmias

6 The clinical effects of dronedarone are currently being examined in patients with atrial fibrillation and in patients with ICDs

1 Vernakalant is a sodium and ultra-rapid potassium channel blocker with atrial selective effects In 2 clinical studies evaluating use of intravenous vernakalant in cardioversion of patients with recent-onset AF

2 vernakalant improved the chance of restoration of normal sinus rhythm (combined results 51 vs 38 with placebo p lt 0001)

3 In postoperative AF intravenous vernakalant also improved the chance of restoration of normal sinus rhythm (45 vs 15 with placebo p = 00002)

4 Early Phase 2 studies demonstrated that oral vernakalant 300 mg or 600 mg twice daily successfully maintained sinus rhythm compared with placebo

5No proarrhythmias relating to vernakalant have been reported to date Common adverse effects include dysgeusia sneezing and paresthesia

Ann Pharmacother 2008 Apr42(4)533-42 Epub 2008 Mar 11

Vernakalant in the management of atrial fibrillationCheng JW

SourceMassachusetts College of Pharmacy and Health Sciences Brigham and Womens Hospital Boston MA 02115 USA judychengmcphsedu

1 Vernakalant is available in both intravenous and oral forms In phase II and III trials intravenous vernakalant has been shown to be effective in terminating acute onset atrial fibrillation whose duration is gt3 hours and lt7 days ( 50 efficiency vs 10 for placebo) sim

2 It does not appear to be effective for atrial fibrillation whose duration is gt7 days nor does it appear to be effective for atrial flutter

3 Studies with oral vernakalant have been designed to evaluate its efficacy and safety in the prevention of atrial fibrillation recurrence Studies to date have shown that 51 of patients were able to maintain sinus rhythm after 90 days of using oral vernakalant 50 mgkg twice daily compared with 37 of patients receiving placebo

4 In the clinical trials there were minimal drug-induced ventricular arrhythmias observed

Cardiol Rev 2011 Jan-Feb19(1)41-4

Vernakalant a new drug to treat patients with acute onset atrial fibrillationTian D Frishman WH

SourceDepartment of Medicine Johns Hopkins Medical School Johns Hopkins Hospital Baltimore MD USA

Catheter and Surgical Ablative Therapy to Prevent Recurrent AF

Ablation therapy is currently considered an alternative to pharmacologic therapy in patients with recurrent symptomatic AF

Elimination of AF in 50ndash80 of patients with a catheter-based ablation procedure should be anticipated depending on the chronicity of the AF

Catheter ablative therapy also holds promise in patients with more persistent forms of AF and even those with severe atrial dilatation

If its efficacy is confirmed with additional study it may also afford an important alternative to His bundle ablation and pacemaker insertion

Risks pulmonary vein stenosis

atrioesophageal fistula

systemic embolic events

perforationtamponade

Surgical ablation of AF is typically performed at the time of other cardiac valve or

coronary artery surgery and less commonly as a stand-alone procedure

view of the left atrium depicting the isolating lesions delivered by catheter ablation around each set of pulmonary veins-

AV nodal re entry tachycardia

55 yo female with no cardiac history but allegedly one similar episode 10 years

ago when her heart ldquowent crazyrdquo for 20 minutes When EMS arrives Sudden

onset of strong palpitations dizziness chest pain paleness and mild diaphoresis

Blood pressure is 13292 and the the patient has a rapid regular pulse at around

180 beats min A 12 lead ECG is obtained

ECG description

Regular narrow-complex tachycardia

150 bpm

No visible P waves preceding QRS

Retrograde P waves with an RP interval of 120ms Inverted in inferior leads II III aVF and upright in aVR and right precordial leads V1 and V2 Also called pseudo S-waves (inferior leads) or pseudo R-waves (right precordial)

Cardiac axis is normal at approx 50deg

Interpretation

A narrow-complex tachycardia is most likely to be supraventricular in origin as this indicates normal His-Purkinje impulse propagation and simultaneous ventricular activation

However there is no P wave preceding the QRS complex to indicate that a sinoatrial origin of the propagated impulse

The regularity rules out atrial fibrillation and the fact that the P waves are not visible could of course just be due to the tachycardic rate At a first glance we can only conclude that this is a supraventricular tachycardia A natural next move would be to perform carotid pressure or other vagal manuevres to induce atrioventricular block in order to help us differentiate this rhythm

With the same intentions and if carotid pressure doesnrsquot work adenosine would be the drug of choice here

A closer look

However differentiation stop here as the diagnosis lies right in front of us clearly visible in both the ECGs

Although there is no sign of atrial activity preceding the QRS take a look after the QRS complex

In all inferior leads II III and aVF an inverted P wave with an RP interval of 120 ms followes each QRS complex

The same P wave with the same RP interval can be spotted in the right precordial leads V1 and V2 as well as in aVR

Logially the P wave is upright in these leads This means that the atrias are depolarized in a retrograde fashion after ventricular

Adenosine effect

Atrioventricular Nodal Reentry Tachycardia (AVNRT) Treatment amp Management

AVNRT

Patient condition

Hemodynamic ally

stable Hemodynamic ally

unstble

Vagal maneuver

adenosine calcium channel blockers (eg diltiazem verapamil) beta-blockers and digitalis

Direct current (DC) synchronized cardioversion

To prevent recurrence

Drugs

Multifocal Atrial Tachycardia

A 52 years old male COPD patient presented with palpitation shortness of

breath chest pain and syncopal history On examination pulse is rapid

irregular amp 1st heart sound is variable

1 Irregular ventricular rate greater than 100 bpm

2 Organized and discrete P waves with at least 3 different morphologies in the same electrocardiographic lead

3 Irregular PP PR and RR intervals with an isoelectric baseline between the P waves

Treatment of MAT

Administer oxygen to maintain the saturation greater than 90 but avoid excessive oxygen in patients with known significant chronic obstructive pulmonary disease (COPD) This will avoid the theoretical problem of removing the hypoxic drive for ventilation which can result in increased carbon dioxide retention

Establish cardiac monitor blood pressure monitor and pulse oximetry

Assess for and treat the underlying cardiopulmonary process theophylline toxicity or metabolic abnormality

Administer bronchodilators and oxygen for treatment of decompensated COPD

activated charcoal andor charcoal hemoperfusion is the therapy for theophylline toxicity

When magnesium sulfate is administered to correct hypokalemia most patients convert to normal sinus rhythm

Avoid sedatives

Diltiazem and verapamil decrease the atrial activity and slow atrioventricular (AV) nodal conduction thereby decreasing ventricular rate but they do not return all patients to normal sinus rhythm

Diltiazem may be used as a 20-45 mg intravenous bolus and then as a 10-25 mgh continuous infusion

high-dose magnesium causes a significant decrease in the patients heart rate and conversion to normal sinus rhythm The dosage is 2 g intravenously over 1 minute followed by 2 gh infusion over 5 hours

Amiodarone (300 mg PO tid or 450-1500 mg IV over 2-24 h) has been used and has been reported to be associated with conversion to normal sinus rhythm The success rate was 40 at 3 days with oral dosing and 75 on day 1 with intravenous dosing however this has been evaluated in a very small number of patients

Cardioversion in MAT

Cardioversion is contraindicated in MAT Due to the multiple atrial foci direct

current (DC) cardioversion is not effective in restoring normal sinus rhythm

and can precipitate more dangerous arrhythmias

Surgical care

In patients who have persistent and recurrent episodes of MAT and problems with

rate control the AV node may be ablated using radiofrequency energy and a

permanent pacemaker implanted[22] This approach should be considered both for

symptomatic and hemodynamic improvement and to prevent the development of

tachycardia-mediated cardiomyopathy

Atrial flutter

A 50 years old diabetic hypertensive hyperthyroid male patient presented

with palpitation fatigue or poor exercise tolerance mild dyspneaand

presyncope On psysical examination pulse rate 150 min

Note negative sawtooth pattern of flutter waves in leads II III and aVF

Emergency Department Care

Assess airway breathing and circulation Hemodynamic concerns will dictate initial treatment

Treatment options for atrial flutter include the following

Antiarrhythmic drugsnodal agents

Direct-current (DC) cardioversion

Rapid atrial pacing to terminate atrial flutter

Blood pressure can be supported and rate controlled with medication

Anti coagulation therapy

Look for underlying causes At times treatment of the underlying disorder (eg thyroid disease valvular heart disease) is necessary to effect conversion to sinus rhythm

Cardioversion for unstable patients

If the patient is unstable (eg hypotension poor perfusion) synchronous direct-current (DC) cardioversion is commonly the initial treatment of choice

Cardioversion may be successful with energies as low as 25 Joules but since 100 Joules is virtually always successful this may be a reasonable initial shock strength

If the electrical shock results in atrial fibrillation (AF) a second shock at a higher energy level is used to restore normal sinus rhythm (NSR)

AV-His Bundle ablation

In patients who have failed antiarrhythmic therapy or who have failed RFA and who

are symptomatic palliative therapy with AV-His Bundle ablation can eliminate rapid

ventricular rates but it does require a permanent pacemaker to be placed as this

procedure creates third-degree heart block

Questions

• Slide 1
• Slide 2
• Slide 3
• Slide 4
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• Slide 10
• Slide 11
• Rate versus rhythm control which is superior
• Slide 13
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• Slide 18
• Slide 19
• Slide 20
• Slide 21
• Slide 22
• Slide 23
• Slide 24
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• Anti - coagulation therapy
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• Slide 42
• Slide 43
• Slide 44
• Slide 45
• Slide 46
• Slide 47
• Slide 48
• Slide 49
• Slide 50
• Slide 51
• Slide 52
• Slide 53
• Slide 54
• Slide 55
• Slide 56
• Slide 57
• Slide 58
• Slide 59
• Slide 60
• Slide 61
• Slide 62
• Slide 63
• Slide 64
• Slide 65
• Slide 66
• Slide 67
• Slide 68
• Slide 69
• Slide 70
• Slide 71
• Slide 72
• Slide 73
• Slide 74
• Slide 75
• Slide 76
• Slide 77
• Slide 78
• Slide 79
• Slide 80
• Slide 81

Dronedarone was approved by the US Food and Drug Administration on July 2 2009

1 It is a deiodinated derivative of amiodarone that has no organ toxicity

2 Its use will likely extend to both atrial and ventricular arrhythmias

3 Dronedarone has multiple actions (all 4 Von Williams class effects)

4 Unlike amiodarone it does not have the iodine moiety

5 The lack of iodination may offer a better side-effect profile Dronedarone has been shown to (1) have antiadrenergic effects (2) prolong atrial and ventricular refractory periods and (3) prolong atrioventricular node conduction as well as the paced QRS complex

5 In animal models dronedarone has been shown to decrease ischemia-induced ventricular arrhythmias

6 The clinical effects of dronedarone are currently being examined in patients with atrial fibrillation and in patients with ICDs

1 Vernakalant is a sodium and ultra-rapid potassium channel blocker with atrial selective effects In 2 clinical studies evaluating use of intravenous vernakalant in cardioversion of patients with recent-onset AF

2 vernakalant improved the chance of restoration of normal sinus rhythm (combined results 51 vs 38 with placebo p lt 0001)

3 In postoperative AF intravenous vernakalant also improved the chance of restoration of normal sinus rhythm (45 vs 15 with placebo p = 00002)

4 Early Phase 2 studies demonstrated that oral vernakalant 300 mg or 600 mg twice daily successfully maintained sinus rhythm compared with placebo

5No proarrhythmias relating to vernakalant have been reported to date Common adverse effects include dysgeusia sneezing and paresthesia

Ann Pharmacother 2008 Apr42(4)533-42 Epub 2008 Mar 11

Vernakalant in the management of atrial fibrillationCheng JW

SourceMassachusetts College of Pharmacy and Health Sciences Brigham and Womens Hospital Boston MA 02115 USA judychengmcphsedu

1 Vernakalant is available in both intravenous and oral forms In phase II and III trials intravenous vernakalant has been shown to be effective in terminating acute onset atrial fibrillation whose duration is gt3 hours and lt7 days ( 50 efficiency vs 10 for placebo) sim

2 It does not appear to be effective for atrial fibrillation whose duration is gt7 days nor does it appear to be effective for atrial flutter

3 Studies with oral vernakalant have been designed to evaluate its efficacy and safety in the prevention of atrial fibrillation recurrence Studies to date have shown that 51 of patients were able to maintain sinus rhythm after 90 days of using oral vernakalant 50 mgkg twice daily compared with 37 of patients receiving placebo

4 In the clinical trials there were minimal drug-induced ventricular arrhythmias observed

Cardiol Rev 2011 Jan-Feb19(1)41-4

Vernakalant a new drug to treat patients with acute onset atrial fibrillationTian D Frishman WH

SourceDepartment of Medicine Johns Hopkins Medical School Johns Hopkins Hospital Baltimore MD USA

Catheter and Surgical Ablative Therapy to Prevent Recurrent AF

Ablation therapy is currently considered an alternative to pharmacologic therapy in patients with recurrent symptomatic AF

Elimination of AF in 50ndash80 of patients with a catheter-based ablation procedure should be anticipated depending on the chronicity of the AF

Catheter ablative therapy also holds promise in patients with more persistent forms of AF and even those with severe atrial dilatation

If its efficacy is confirmed with additional study it may also afford an important alternative to His bundle ablation and pacemaker insertion

Risks pulmonary vein stenosis

atrioesophageal fistula

systemic embolic events

perforationtamponade

Surgical ablation of AF is typically performed at the time of other cardiac valve or

coronary artery surgery and less commonly as a stand-alone procedure

view of the left atrium depicting the isolating lesions delivered by catheter ablation around each set of pulmonary veins-

AV nodal re entry tachycardia

55 yo female with no cardiac history but allegedly one similar episode 10 years

ago when her heart ldquowent crazyrdquo for 20 minutes When EMS arrives Sudden

onset of strong palpitations dizziness chest pain paleness and mild diaphoresis

Blood pressure is 13292 and the the patient has a rapid regular pulse at around

180 beats min A 12 lead ECG is obtained

ECG description

Regular narrow-complex tachycardia

150 bpm

No visible P waves preceding QRS

Retrograde P waves with an RP interval of 120ms Inverted in inferior leads II III aVF and upright in aVR and right precordial leads V1 and V2 Also called pseudo S-waves (inferior leads) or pseudo R-waves (right precordial)

Cardiac axis is normal at approx 50deg

Interpretation

A narrow-complex tachycardia is most likely to be supraventricular in origin as this indicates normal His-Purkinje impulse propagation and simultaneous ventricular activation

However there is no P wave preceding the QRS complex to indicate that a sinoatrial origin of the propagated impulse

The regularity rules out atrial fibrillation and the fact that the P waves are not visible could of course just be due to the tachycardic rate At a first glance we can only conclude that this is a supraventricular tachycardia A natural next move would be to perform carotid pressure or other vagal manuevres to induce atrioventricular block in order to help us differentiate this rhythm

With the same intentions and if carotid pressure doesnrsquot work adenosine would be the drug of choice here

A closer look

However differentiation stop here as the diagnosis lies right in front of us clearly visible in both the ECGs

Although there is no sign of atrial activity preceding the QRS take a look after the QRS complex

In all inferior leads II III and aVF an inverted P wave with an RP interval of 120 ms followes each QRS complex

The same P wave with the same RP interval can be spotted in the right precordial leads V1 and V2 as well as in aVR

Logially the P wave is upright in these leads This means that the atrias are depolarized in a retrograde fashion after ventricular

Adenosine effect

Atrioventricular Nodal Reentry Tachycardia (AVNRT) Treatment amp Management

AVNRT

Patient condition

Hemodynamic ally

stable Hemodynamic ally

unstble

Vagal maneuver

adenosine calcium channel blockers (eg diltiazem verapamil) beta-blockers and digitalis

Direct current (DC) synchronized cardioversion

To prevent recurrence

Drugs

Multifocal Atrial Tachycardia

A 52 years old male COPD patient presented with palpitation shortness of

breath chest pain and syncopal history On examination pulse is rapid

irregular amp 1st heart sound is variable

1 Irregular ventricular rate greater than 100 bpm

2 Organized and discrete P waves with at least 3 different morphologies in the same electrocardiographic lead

3 Irregular PP PR and RR intervals with an isoelectric baseline between the P waves

Treatment of MAT

Administer oxygen to maintain the saturation greater than 90 but avoid excessive oxygen in patients with known significant chronic obstructive pulmonary disease (COPD) This will avoid the theoretical problem of removing the hypoxic drive for ventilation which can result in increased carbon dioxide retention

Establish cardiac monitor blood pressure monitor and pulse oximetry

Assess for and treat the underlying cardiopulmonary process theophylline toxicity or metabolic abnormality

Administer bronchodilators and oxygen for treatment of decompensated COPD

activated charcoal andor charcoal hemoperfusion is the therapy for theophylline toxicity

When magnesium sulfate is administered to correct hypokalemia most patients convert to normal sinus rhythm

Avoid sedatives

Diltiazem and verapamil decrease the atrial activity and slow atrioventricular (AV) nodal conduction thereby decreasing ventricular rate but they do not return all patients to normal sinus rhythm

Diltiazem may be used as a 20-45 mg intravenous bolus and then as a 10-25 mgh continuous infusion

high-dose magnesium causes a significant decrease in the patients heart rate and conversion to normal sinus rhythm The dosage is 2 g intravenously over 1 minute followed by 2 gh infusion over 5 hours

Amiodarone (300 mg PO tid or 450-1500 mg IV over 2-24 h) has been used and has been reported to be associated with conversion to normal sinus rhythm The success rate was 40 at 3 days with oral dosing and 75 on day 1 with intravenous dosing however this has been evaluated in a very small number of patients

Cardioversion in MAT

Cardioversion is contraindicated in MAT Due to the multiple atrial foci direct

current (DC) cardioversion is not effective in restoring normal sinus rhythm

and can precipitate more dangerous arrhythmias

Surgical care

In patients who have persistent and recurrent episodes of MAT and problems with

rate control the AV node may be ablated using radiofrequency energy and a

permanent pacemaker implanted[22] This approach should be considered both for

symptomatic and hemodynamic improvement and to prevent the development of

tachycardia-mediated cardiomyopathy

Atrial flutter

A 50 years old diabetic hypertensive hyperthyroid male patient presented

with palpitation fatigue or poor exercise tolerance mild dyspneaand

presyncope On psysical examination pulse rate 150 min

Note negative sawtooth pattern of flutter waves in leads II III and aVF

Emergency Department Care

Assess airway breathing and circulation Hemodynamic concerns will dictate initial treatment

Treatment options for atrial flutter include the following

Antiarrhythmic drugsnodal agents

Direct-current (DC) cardioversion

Rapid atrial pacing to terminate atrial flutter

Blood pressure can be supported and rate controlled with medication

Anti coagulation therapy

Look for underlying causes At times treatment of the underlying disorder (eg thyroid disease valvular heart disease) is necessary to effect conversion to sinus rhythm

Cardioversion for unstable patients

If the patient is unstable (eg hypotension poor perfusion) synchronous direct-current (DC) cardioversion is commonly the initial treatment of choice

Cardioversion may be successful with energies as low as 25 Joules but since 100 Joules is virtually always successful this may be a reasonable initial shock strength

If the electrical shock results in atrial fibrillation (AF) a second shock at a higher energy level is used to restore normal sinus rhythm (NSR)

AV-His Bundle ablation

In patients who have failed antiarrhythmic therapy or who have failed RFA and who

are symptomatic palliative therapy with AV-His Bundle ablation can eliminate rapid

ventricular rates but it does require a permanent pacemaker to be placed as this

procedure creates third-degree heart block

Questions

• Slide 1
• Slide 2
• Slide 3
• Slide 4
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• Slide 10
• Slide 11
• Rate versus rhythm control which is superior
• Slide 13
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• Slide 18
• Slide 19
• Slide 20
• Slide 21
• Slide 22
• Slide 23
• Slide 24
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• Anti - coagulation therapy
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• Slide 42
• Slide 43
• Slide 44
• Slide 45
• Slide 46
• Slide 47
• Slide 48
• Slide 49
• Slide 50
• Slide 51
• Slide 52
• Slide 53
• Slide 54
• Slide 55
• Slide 56
• Slide 57
• Slide 58
• Slide 59
• Slide 60
• Slide 61
• Slide 62
• Slide 63
• Slide 64
• Slide 65
• Slide 66
• Slide 67
• Slide 68
• Slide 69
• Slide 70
• Slide 71
• Slide 72
• Slide 73
• Slide 74
• Slide 75
• Slide 76
• Slide 77
• Slide 78
• Slide 79
• Slide 80
• Slide 81

1 Vernakalant is a sodium and ultra-rapid potassium channel blocker with atrial selective effects In 2 clinical studies evaluating use of intravenous vernakalant in cardioversion of patients with recent-onset AF

2 vernakalant improved the chance of restoration of normal sinus rhythm (combined results 51 vs 38 with placebo p lt 0001)

3 In postoperative AF intravenous vernakalant also improved the chance of restoration of normal sinus rhythm (45 vs 15 with placebo p = 00002)

4 Early Phase 2 studies demonstrated that oral vernakalant 300 mg or 600 mg twice daily successfully maintained sinus rhythm compared with placebo

5No proarrhythmias relating to vernakalant have been reported to date Common adverse effects include dysgeusia sneezing and paresthesia

Ann Pharmacother 2008 Apr42(4)533-42 Epub 2008 Mar 11

Vernakalant in the management of atrial fibrillationCheng JW

SourceMassachusetts College of Pharmacy and Health Sciences Brigham and Womens Hospital Boston MA 02115 USA judychengmcphsedu

1 Vernakalant is available in both intravenous and oral forms In phase II and III trials intravenous vernakalant has been shown to be effective in terminating acute onset atrial fibrillation whose duration is gt3 hours and lt7 days ( 50 efficiency vs 10 for placebo) sim

2 It does not appear to be effective for atrial fibrillation whose duration is gt7 days nor does it appear to be effective for atrial flutter

3 Studies with oral vernakalant have been designed to evaluate its efficacy and safety in the prevention of atrial fibrillation recurrence Studies to date have shown that 51 of patients were able to maintain sinus rhythm after 90 days of using oral vernakalant 50 mgkg twice daily compared with 37 of patients receiving placebo

4 In the clinical trials there were minimal drug-induced ventricular arrhythmias observed

Cardiol Rev 2011 Jan-Feb19(1)41-4

Vernakalant a new drug to treat patients with acute onset atrial fibrillationTian D Frishman WH

SourceDepartment of Medicine Johns Hopkins Medical School Johns Hopkins Hospital Baltimore MD USA

Catheter and Surgical Ablative Therapy to Prevent Recurrent AF

Ablation therapy is currently considered an alternative to pharmacologic therapy in patients with recurrent symptomatic AF

Elimination of AF in 50ndash80 of patients with a catheter-based ablation procedure should be anticipated depending on the chronicity of the AF

Catheter ablative therapy also holds promise in patients with more persistent forms of AF and even those with severe atrial dilatation

If its efficacy is confirmed with additional study it may also afford an important alternative to His bundle ablation and pacemaker insertion

Risks pulmonary vein stenosis

atrioesophageal fistula

systemic embolic events

perforationtamponade

Surgical ablation of AF is typically performed at the time of other cardiac valve or

coronary artery surgery and less commonly as a stand-alone procedure

view of the left atrium depicting the isolating lesions delivered by catheter ablation around each set of pulmonary veins-

AV nodal re entry tachycardia

55 yo female with no cardiac history but allegedly one similar episode 10 years

ago when her heart ldquowent crazyrdquo for 20 minutes When EMS arrives Sudden

onset of strong palpitations dizziness chest pain paleness and mild diaphoresis

Blood pressure is 13292 and the the patient has a rapid regular pulse at around

180 beats min A 12 lead ECG is obtained

ECG description

Regular narrow-complex tachycardia

150 bpm

No visible P waves preceding QRS

Retrograde P waves with an RP interval of 120ms Inverted in inferior leads II III aVF and upright in aVR and right precordial leads V1 and V2 Also called pseudo S-waves (inferior leads) or pseudo R-waves (right precordial)

Cardiac axis is normal at approx 50deg

Interpretation

A narrow-complex tachycardia is most likely to be supraventricular in origin as this indicates normal His-Purkinje impulse propagation and simultaneous ventricular activation

However there is no P wave preceding the QRS complex to indicate that a sinoatrial origin of the propagated impulse

The regularity rules out atrial fibrillation and the fact that the P waves are not visible could of course just be due to the tachycardic rate At a first glance we can only conclude that this is a supraventricular tachycardia A natural next move would be to perform carotid pressure or other vagal manuevres to induce atrioventricular block in order to help us differentiate this rhythm

With the same intentions and if carotid pressure doesnrsquot work adenosine would be the drug of choice here

A closer look

However differentiation stop here as the diagnosis lies right in front of us clearly visible in both the ECGs

Although there is no sign of atrial activity preceding the QRS take a look after the QRS complex

In all inferior leads II III and aVF an inverted P wave with an RP interval of 120 ms followes each QRS complex

The same P wave with the same RP interval can be spotted in the right precordial leads V1 and V2 as well as in aVR

Logially the P wave is upright in these leads This means that the atrias are depolarized in a retrograde fashion after ventricular

Adenosine effect

Atrioventricular Nodal Reentry Tachycardia (AVNRT) Treatment amp Management

AVNRT

Patient condition

Hemodynamic ally

stable Hemodynamic ally

unstble

Vagal maneuver

adenosine calcium channel blockers (eg diltiazem verapamil) beta-blockers and digitalis

Direct current (DC) synchronized cardioversion

To prevent recurrence

Drugs

Multifocal Atrial Tachycardia

A 52 years old male COPD patient presented with palpitation shortness of

breath chest pain and syncopal history On examination pulse is rapid

irregular amp 1st heart sound is variable

1 Irregular ventricular rate greater than 100 bpm

2 Organized and discrete P waves with at least 3 different morphologies in the same electrocardiographic lead

3 Irregular PP PR and RR intervals with an isoelectric baseline between the P waves

Treatment of MAT

Administer oxygen to maintain the saturation greater than 90 but avoid excessive oxygen in patients with known significant chronic obstructive pulmonary disease (COPD) This will avoid the theoretical problem of removing the hypoxic drive for ventilation which can result in increased carbon dioxide retention

Establish cardiac monitor blood pressure monitor and pulse oximetry

Assess for and treat the underlying cardiopulmonary process theophylline toxicity or metabolic abnormality

Administer bronchodilators and oxygen for treatment of decompensated COPD

activated charcoal andor charcoal hemoperfusion is the therapy for theophylline toxicity

When magnesium sulfate is administered to correct hypokalemia most patients convert to normal sinus rhythm

Avoid sedatives

Diltiazem and verapamil decrease the atrial activity and slow atrioventricular (AV) nodal conduction thereby decreasing ventricular rate but they do not return all patients to normal sinus rhythm

Diltiazem may be used as a 20-45 mg intravenous bolus and then as a 10-25 mgh continuous infusion

high-dose magnesium causes a significant decrease in the patients heart rate and conversion to normal sinus rhythm The dosage is 2 g intravenously over 1 minute followed by 2 gh infusion over 5 hours

Amiodarone (300 mg PO tid or 450-1500 mg IV over 2-24 h) has been used and has been reported to be associated with conversion to normal sinus rhythm The success rate was 40 at 3 days with oral dosing and 75 on day 1 with intravenous dosing however this has been evaluated in a very small number of patients

Cardioversion in MAT

Cardioversion is contraindicated in MAT Due to the multiple atrial foci direct

current (DC) cardioversion is not effective in restoring normal sinus rhythm

and can precipitate more dangerous arrhythmias

Surgical care

In patients who have persistent and recurrent episodes of MAT and problems with

rate control the AV node may be ablated using radiofrequency energy and a

permanent pacemaker implanted[22] This approach should be considered both for

symptomatic and hemodynamic improvement and to prevent the development of

tachycardia-mediated cardiomyopathy

Atrial flutter

A 50 years old diabetic hypertensive hyperthyroid male patient presented

with palpitation fatigue or poor exercise tolerance mild dyspneaand

presyncope On psysical examination pulse rate 150 min

Note negative sawtooth pattern of flutter waves in leads II III and aVF

Emergency Department Care

Assess airway breathing and circulation Hemodynamic concerns will dictate initial treatment

Treatment options for atrial flutter include the following

Antiarrhythmic drugsnodal agents

Direct-current (DC) cardioversion

Rapid atrial pacing to terminate atrial flutter

Blood pressure can be supported and rate controlled with medication

Anti coagulation therapy

Look for underlying causes At times treatment of the underlying disorder (eg thyroid disease valvular heart disease) is necessary to effect conversion to sinus rhythm

Cardioversion for unstable patients

If the patient is unstable (eg hypotension poor perfusion) synchronous direct-current (DC) cardioversion is commonly the initial treatment of choice

Cardioversion may be successful with energies as low as 25 Joules but since 100 Joules is virtually always successful this may be a reasonable initial shock strength

If the electrical shock results in atrial fibrillation (AF) a second shock at a higher energy level is used to restore normal sinus rhythm (NSR)

AV-His Bundle ablation

In patients who have failed antiarrhythmic therapy or who have failed RFA and who

are symptomatic palliative therapy with AV-His Bundle ablation can eliminate rapid

ventricular rates but it does require a permanent pacemaker to be placed as this

procedure creates third-degree heart block

Questions

• Slide 1
• Slide 2
• Slide 3
• Slide 4
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• Slide 10
• Slide 11
• Rate versus rhythm control which is superior
• Slide 13
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• Slide 18
• Slide 19
• Slide 20
• Slide 21
• Slide 22
• Slide 23
• Slide 24
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• Anti - coagulation therapy
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• Slide 42
• Slide 43
• Slide 44
• Slide 45
• Slide 46
• Slide 47
• Slide 48
• Slide 49
• Slide 50
• Slide 51
• Slide 52
• Slide 53
• Slide 54
• Slide 55
• Slide 56
• Slide 57
• Slide 58
• Slide 59
• Slide 60
• Slide 61
• Slide 62
• Slide 63
• Slide 64
• Slide 65
• Slide 66
• Slide 67
• Slide 68
• Slide 69
• Slide 70
• Slide 71
• Slide 72
• Slide 73
• Slide 74
• Slide 75
• Slide 76
• Slide 77
• Slide 78
• Slide 79
• Slide 80
• Slide 81

1 Vernakalant is available in both intravenous and oral forms In phase II and III trials intravenous vernakalant has been shown to be effective in terminating acute onset atrial fibrillation whose duration is gt3 hours and lt7 days ( 50 efficiency vs 10 for placebo) sim

2 It does not appear to be effective for atrial fibrillation whose duration is gt7 days nor does it appear to be effective for atrial flutter

3 Studies with oral vernakalant have been designed to evaluate its efficacy and safety in the prevention of atrial fibrillation recurrence Studies to date have shown that 51 of patients were able to maintain sinus rhythm after 90 days of using oral vernakalant 50 mgkg twice daily compared with 37 of patients receiving placebo

4 In the clinical trials there were minimal drug-induced ventricular arrhythmias observed

Cardiol Rev 2011 Jan-Feb19(1)41-4

Vernakalant a new drug to treat patients with acute onset atrial fibrillationTian D Frishman WH

SourceDepartment of Medicine Johns Hopkins Medical School Johns Hopkins Hospital Baltimore MD USA

Catheter and Surgical Ablative Therapy to Prevent Recurrent AF

Ablation therapy is currently considered an alternative to pharmacologic therapy in patients with recurrent symptomatic AF

Elimination of AF in 50ndash80 of patients with a catheter-based ablation procedure should be anticipated depending on the chronicity of the AF

Catheter ablative therapy also holds promise in patients with more persistent forms of AF and even those with severe atrial dilatation

If its efficacy is confirmed with additional study it may also afford an important alternative to His bundle ablation and pacemaker insertion

Risks pulmonary vein stenosis

atrioesophageal fistula

systemic embolic events

perforationtamponade

Surgical ablation of AF is typically performed at the time of other cardiac valve or

coronary artery surgery and less commonly as a stand-alone procedure

view of the left atrium depicting the isolating lesions delivered by catheter ablation around each set of pulmonary veins-

AV nodal re entry tachycardia

55 yo female with no cardiac history but allegedly one similar episode 10 years

ago when her heart ldquowent crazyrdquo for 20 minutes When EMS arrives Sudden

onset of strong palpitations dizziness chest pain paleness and mild diaphoresis

Blood pressure is 13292 and the the patient has a rapid regular pulse at around

180 beats min A 12 lead ECG is obtained

ECG description

Regular narrow-complex tachycardia

150 bpm

No visible P waves preceding QRS

Retrograde P waves with an RP interval of 120ms Inverted in inferior leads II III aVF and upright in aVR and right precordial leads V1 and V2 Also called pseudo S-waves (inferior leads) or pseudo R-waves (right precordial)

Cardiac axis is normal at approx 50deg

Interpretation

A narrow-complex tachycardia is most likely to be supraventricular in origin as this indicates normal His-Purkinje impulse propagation and simultaneous ventricular activation

However there is no P wave preceding the QRS complex to indicate that a sinoatrial origin of the propagated impulse

The regularity rules out atrial fibrillation and the fact that the P waves are not visible could of course just be due to the tachycardic rate At a first glance we can only conclude that this is a supraventricular tachycardia A natural next move would be to perform carotid pressure or other vagal manuevres to induce atrioventricular block in order to help us differentiate this rhythm

With the same intentions and if carotid pressure doesnrsquot work adenosine would be the drug of choice here

A closer look

However differentiation stop here as the diagnosis lies right in front of us clearly visible in both the ECGs

Although there is no sign of atrial activity preceding the QRS take a look after the QRS complex

In all inferior leads II III and aVF an inverted P wave with an RP interval of 120 ms followes each QRS complex

The same P wave with the same RP interval can be spotted in the right precordial leads V1 and V2 as well as in aVR

Logially the P wave is upright in these leads This means that the atrias are depolarized in a retrograde fashion after ventricular

Adenosine effect

Atrioventricular Nodal Reentry Tachycardia (AVNRT) Treatment amp Management

AVNRT

Patient condition

Hemodynamic ally

stable Hemodynamic ally

unstble

Vagal maneuver

adenosine calcium channel blockers (eg diltiazem verapamil) beta-blockers and digitalis

Direct current (DC) synchronized cardioversion

To prevent recurrence

Drugs

Multifocal Atrial Tachycardia

A 52 years old male COPD patient presented with palpitation shortness of

breath chest pain and syncopal history On examination pulse is rapid

irregular amp 1st heart sound is variable

1 Irregular ventricular rate greater than 100 bpm

2 Organized and discrete P waves with at least 3 different morphologies in the same electrocardiographic lead

3 Irregular PP PR and RR intervals with an isoelectric baseline between the P waves

Treatment of MAT

Administer oxygen to maintain the saturation greater than 90 but avoid excessive oxygen in patients with known significant chronic obstructive pulmonary disease (COPD) This will avoid the theoretical problem of removing the hypoxic drive for ventilation which can result in increased carbon dioxide retention

Establish cardiac monitor blood pressure monitor and pulse oximetry

Assess for and treat the underlying cardiopulmonary process theophylline toxicity or metabolic abnormality

Administer bronchodilators and oxygen for treatment of decompensated COPD

activated charcoal andor charcoal hemoperfusion is the therapy for theophylline toxicity

When magnesium sulfate is administered to correct hypokalemia most patients convert to normal sinus rhythm

Avoid sedatives

Diltiazem and verapamil decrease the atrial activity and slow atrioventricular (AV) nodal conduction thereby decreasing ventricular rate but they do not return all patients to normal sinus rhythm

Diltiazem may be used as a 20-45 mg intravenous bolus and then as a 10-25 mgh continuous infusion

high-dose magnesium causes a significant decrease in the patients heart rate and conversion to normal sinus rhythm The dosage is 2 g intravenously over 1 minute followed by 2 gh infusion over 5 hours

Amiodarone (300 mg PO tid or 450-1500 mg IV over 2-24 h) has been used and has been reported to be associated with conversion to normal sinus rhythm The success rate was 40 at 3 days with oral dosing and 75 on day 1 with intravenous dosing however this has been evaluated in a very small number of patients

Cardioversion in MAT

Cardioversion is contraindicated in MAT Due to the multiple atrial foci direct

current (DC) cardioversion is not effective in restoring normal sinus rhythm

and can precipitate more dangerous arrhythmias

Surgical care

In patients who have persistent and recurrent episodes of MAT and problems with

rate control the AV node may be ablated using radiofrequency energy and a

permanent pacemaker implanted[22] This approach should be considered both for

symptomatic and hemodynamic improvement and to prevent the development of

tachycardia-mediated cardiomyopathy

Atrial flutter

A 50 years old diabetic hypertensive hyperthyroid male patient presented

with palpitation fatigue or poor exercise tolerance mild dyspneaand

presyncope On psysical examination pulse rate 150 min

Note negative sawtooth pattern of flutter waves in leads II III and aVF

Emergency Department Care

Assess airway breathing and circulation Hemodynamic concerns will dictate initial treatment

Treatment options for atrial flutter include the following

Antiarrhythmic drugsnodal agents

Direct-current (DC) cardioversion

Rapid atrial pacing to terminate atrial flutter

Blood pressure can be supported and rate controlled with medication

Anti coagulation therapy

Look for underlying causes At times treatment of the underlying disorder (eg thyroid disease valvular heart disease) is necessary to effect conversion to sinus rhythm

Cardioversion for unstable patients

If the patient is unstable (eg hypotension poor perfusion) synchronous direct-current (DC) cardioversion is commonly the initial treatment of choice

Cardioversion may be successful with energies as low as 25 Joules but since 100 Joules is virtually always successful this may be a reasonable initial shock strength

If the electrical shock results in atrial fibrillation (AF) a second shock at a higher energy level is used to restore normal sinus rhythm (NSR)

AV-His Bundle ablation

In patients who have failed antiarrhythmic therapy or who have failed RFA and who

are symptomatic palliative therapy with AV-His Bundle ablation can eliminate rapid

ventricular rates but it does require a permanent pacemaker to be placed as this

procedure creates third-degree heart block

Questions

• Slide 1
• Slide 2
• Slide 3
• Slide 4
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• Slide 10
• Slide 11
• Rate versus rhythm control which is superior
• Slide 13
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• Slide 18
• Slide 19
• Slide 20
• Slide 21
• Slide 22
• Slide 23
• Slide 24
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• Anti - coagulation therapy
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• Slide 42
• Slide 43
• Slide 44
• Slide 45
• Slide 46
• Slide 47
• Slide 48
• Slide 49
• Slide 50
• Slide 51
• Slide 52
• Slide 53
• Slide 54
• Slide 55
• Slide 56
• Slide 57
• Slide 58
• Slide 59
• Slide 60
• Slide 61
• Slide 62
• Slide 63
• Slide 64
• Slide 65
• Slide 66
• Slide 67
• Slide 68
• Slide 69
• Slide 70
• Slide 71
• Slide 72
• Slide 73
• Slide 74
• Slide 75
• Slide 76
• Slide 77
• Slide 78
• Slide 79
• Slide 80
• Slide 81

Catheter and Surgical Ablative Therapy to Prevent Recurrent AF

Ablation therapy is currently considered an alternative to pharmacologic therapy in patients with recurrent symptomatic AF

Elimination of AF in 50ndash80 of patients with a catheter-based ablation procedure should be anticipated depending on the chronicity of the AF

Catheter ablative therapy also holds promise in patients with more persistent forms of AF and even those with severe atrial dilatation

If its efficacy is confirmed with additional study it may also afford an important alternative to His bundle ablation and pacemaker insertion

Risks pulmonary vein stenosis

atrioesophageal fistula

systemic embolic events

perforationtamponade

Surgical ablation of AF is typically performed at the time of other cardiac valve or

coronary artery surgery and less commonly as a stand-alone procedure

view of the left atrium depicting the isolating lesions delivered by catheter ablation around each set of pulmonary veins-

AV nodal re entry tachycardia

55 yo female with no cardiac history but allegedly one similar episode 10 years

ago when her heart ldquowent crazyrdquo for 20 minutes When EMS arrives Sudden

onset of strong palpitations dizziness chest pain paleness and mild diaphoresis

Blood pressure is 13292 and the the patient has a rapid regular pulse at around

180 beats min A 12 lead ECG is obtained

ECG description

Regular narrow-complex tachycardia

150 bpm

No visible P waves preceding QRS

Retrograde P waves with an RP interval of 120ms Inverted in inferior leads II III aVF and upright in aVR and right precordial leads V1 and V2 Also called pseudo S-waves (inferior leads) or pseudo R-waves (right precordial)

Cardiac axis is normal at approx 50deg

Interpretation

A narrow-complex tachycardia is most likely to be supraventricular in origin as this indicates normal His-Purkinje impulse propagation and simultaneous ventricular activation

However there is no P wave preceding the QRS complex to indicate that a sinoatrial origin of the propagated impulse

The regularity rules out atrial fibrillation and the fact that the P waves are not visible could of course just be due to the tachycardic rate At a first glance we can only conclude that this is a supraventricular tachycardia A natural next move would be to perform carotid pressure or other vagal manuevres to induce atrioventricular block in order to help us differentiate this rhythm

With the same intentions and if carotid pressure doesnrsquot work adenosine would be the drug of choice here

A closer look

However differentiation stop here as the diagnosis lies right in front of us clearly visible in both the ECGs

Although there is no sign of atrial activity preceding the QRS take a look after the QRS complex

In all inferior leads II III and aVF an inverted P wave with an RP interval of 120 ms followes each QRS complex

The same P wave with the same RP interval can be spotted in the right precordial leads V1 and V2 as well as in aVR

Logially the P wave is upright in these leads This means that the atrias are depolarized in a retrograde fashion after ventricular

Adenosine effect

Atrioventricular Nodal Reentry Tachycardia (AVNRT) Treatment amp Management

AVNRT

Patient condition

Hemodynamic ally

stable Hemodynamic ally

unstble

Vagal maneuver

adenosine calcium channel blockers (eg diltiazem verapamil) beta-blockers and digitalis

Direct current (DC) synchronized cardioversion

To prevent recurrence

Drugs

Multifocal Atrial Tachycardia

A 52 years old male COPD patient presented with palpitation shortness of

breath chest pain and syncopal history On examination pulse is rapid

irregular amp 1st heart sound is variable

1 Irregular ventricular rate greater than 100 bpm

2 Organized and discrete P waves with at least 3 different morphologies in the same electrocardiographic lead

3 Irregular PP PR and RR intervals with an isoelectric baseline between the P waves

Treatment of MAT

Administer oxygen to maintain the saturation greater than 90 but avoid excessive oxygen in patients with known significant chronic obstructive pulmonary disease (COPD) This will avoid the theoretical problem of removing the hypoxic drive for ventilation which can result in increased carbon dioxide retention

Establish cardiac monitor blood pressure monitor and pulse oximetry

Assess for and treat the underlying cardiopulmonary process theophylline toxicity or metabolic abnormality

Administer bronchodilators and oxygen for treatment of decompensated COPD

activated charcoal andor charcoal hemoperfusion is the therapy for theophylline toxicity

When magnesium sulfate is administered to correct hypokalemia most patients convert to normal sinus rhythm

Avoid sedatives

Diltiazem and verapamil decrease the atrial activity and slow atrioventricular (AV) nodal conduction thereby decreasing ventricular rate but they do not return all patients to normal sinus rhythm

Diltiazem may be used as a 20-45 mg intravenous bolus and then as a 10-25 mgh continuous infusion

high-dose magnesium causes a significant decrease in the patients heart rate and conversion to normal sinus rhythm The dosage is 2 g intravenously over 1 minute followed by 2 gh infusion over 5 hours

Amiodarone (300 mg PO tid or 450-1500 mg IV over 2-24 h) has been used and has been reported to be associated with conversion to normal sinus rhythm The success rate was 40 at 3 days with oral dosing and 75 on day 1 with intravenous dosing however this has been evaluated in a very small number of patients

Cardioversion in MAT

Cardioversion is contraindicated in MAT Due to the multiple atrial foci direct

current (DC) cardioversion is not effective in restoring normal sinus rhythm

and can precipitate more dangerous arrhythmias

Surgical care

In patients who have persistent and recurrent episodes of MAT and problems with

rate control the AV node may be ablated using radiofrequency energy and a

permanent pacemaker implanted[22] This approach should be considered both for

symptomatic and hemodynamic improvement and to prevent the development of

tachycardia-mediated cardiomyopathy

Atrial flutter

A 50 years old diabetic hypertensive hyperthyroid male patient presented

with palpitation fatigue or poor exercise tolerance mild dyspneaand

presyncope On psysical examination pulse rate 150 min

Note negative sawtooth pattern of flutter waves in leads II III and aVF

Emergency Department Care

Assess airway breathing and circulation Hemodynamic concerns will dictate initial treatment

Treatment options for atrial flutter include the following

Antiarrhythmic drugsnodal agents

Direct-current (DC) cardioversion

Rapid atrial pacing to terminate atrial flutter

Blood pressure can be supported and rate controlled with medication

Anti coagulation therapy

Look for underlying causes At times treatment of the underlying disorder (eg thyroid disease valvular heart disease) is necessary to effect conversion to sinus rhythm

Cardioversion for unstable patients

If the patient is unstable (eg hypotension poor perfusion) synchronous direct-current (DC) cardioversion is commonly the initial treatment of choice

Cardioversion may be successful with energies as low as 25 Joules but since 100 Joules is virtually always successful this may be a reasonable initial shock strength

If the electrical shock results in atrial fibrillation (AF) a second shock at a higher energy level is used to restore normal sinus rhythm (NSR)

AV-His Bundle ablation

In patients who have failed antiarrhythmic therapy or who have failed RFA and who

are symptomatic palliative therapy with AV-His Bundle ablation can eliminate rapid

ventricular rates but it does require a permanent pacemaker to be placed as this

procedure creates third-degree heart block

Questions

• Slide 1
• Slide 2
• Slide 3
• Slide 4
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• Slide 10
• Slide 11
• Rate versus rhythm control which is superior
• Slide 13
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• Slide 18
• Slide 19
• Slide 20
• Slide 21
• Slide 22
• Slide 23
• Slide 24
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• Anti - coagulation therapy
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• Slide 42
• Slide 43
• Slide 44
• Slide 45
• Slide 46
• Slide 47
• Slide 48
• Slide 49
• Slide 50
• Slide 51
• Slide 52
• Slide 53
• Slide 54
• Slide 55
• Slide 56
• Slide 57
• Slide 58
• Slide 59
• Slide 60
• Slide 61
• Slide 62
• Slide 63
• Slide 64
• Slide 65
• Slide 66
• Slide 67
• Slide 68
• Slide 69
• Slide 70
• Slide 71
• Slide 72
• Slide 73
• Slide 74
• Slide 75
• Slide 76
• Slide 77
• Slide 78
• Slide 79
• Slide 80
• Slide 81

Ablation therapy is currently considered an alternative to pharmacologic therapy in patients with recurrent symptomatic AF

Elimination of AF in 50ndash80 of patients with a catheter-based ablation procedure should be anticipated depending on the chronicity of the AF

Catheter ablative therapy also holds promise in patients with more persistent forms of AF and even those with severe atrial dilatation

If its efficacy is confirmed with additional study it may also afford an important alternative to His bundle ablation and pacemaker insertion

Risks pulmonary vein stenosis

atrioesophageal fistula

systemic embolic events

perforationtamponade

Surgical ablation of AF is typically performed at the time of other cardiac valve or

coronary artery surgery and less commonly as a stand-alone procedure

view of the left atrium depicting the isolating lesions delivered by catheter ablation around each set of pulmonary veins-

AV nodal re entry tachycardia

55 yo female with no cardiac history but allegedly one similar episode 10 years

ago when her heart ldquowent crazyrdquo for 20 minutes When EMS arrives Sudden

onset of strong palpitations dizziness chest pain paleness and mild diaphoresis

Blood pressure is 13292 and the the patient has a rapid regular pulse at around

180 beats min A 12 lead ECG is obtained

ECG description

Regular narrow-complex tachycardia

150 bpm

No visible P waves preceding QRS

Retrograde P waves with an RP interval of 120ms Inverted in inferior leads II III aVF and upright in aVR and right precordial leads V1 and V2 Also called pseudo S-waves (inferior leads) or pseudo R-waves (right precordial)

Cardiac axis is normal at approx 50deg

Interpretation

A narrow-complex tachycardia is most likely to be supraventricular in origin as this indicates normal His-Purkinje impulse propagation and simultaneous ventricular activation

However there is no P wave preceding the QRS complex to indicate that a sinoatrial origin of the propagated impulse

The regularity rules out atrial fibrillation and the fact that the P waves are not visible could of course just be due to the tachycardic rate At a first glance we can only conclude that this is a supraventricular tachycardia A natural next move would be to perform carotid pressure or other vagal manuevres to induce atrioventricular block in order to help us differentiate this rhythm

With the same intentions and if carotid pressure doesnrsquot work adenosine would be the drug of choice here

A closer look

However differentiation stop here as the diagnosis lies right in front of us clearly visible in both the ECGs

Although there is no sign of atrial activity preceding the QRS take a look after the QRS complex

In all inferior leads II III and aVF an inverted P wave with an RP interval of 120 ms followes each QRS complex

The same P wave with the same RP interval can be spotted in the right precordial leads V1 and V2 as well as in aVR

Logially the P wave is upright in these leads This means that the atrias are depolarized in a retrograde fashion after ventricular

Adenosine effect

Atrioventricular Nodal Reentry Tachycardia (AVNRT) Treatment amp Management

AVNRT

Patient condition

Hemodynamic ally

stable Hemodynamic ally

unstble

Vagal maneuver

adenosine calcium channel blockers (eg diltiazem verapamil) beta-blockers and digitalis

Direct current (DC) synchronized cardioversion

To prevent recurrence

Drugs

Multifocal Atrial Tachycardia

A 52 years old male COPD patient presented with palpitation shortness of

breath chest pain and syncopal history On examination pulse is rapid

irregular amp 1st heart sound is variable

1 Irregular ventricular rate greater than 100 bpm

2 Organized and discrete P waves with at least 3 different morphologies in the same electrocardiographic lead

3 Irregular PP PR and RR intervals with an isoelectric baseline between the P waves

Treatment of MAT

Administer oxygen to maintain the saturation greater than 90 but avoid excessive oxygen in patients with known significant chronic obstructive pulmonary disease (COPD) This will avoid the theoretical problem of removing the hypoxic drive for ventilation which can result in increased carbon dioxide retention

Establish cardiac monitor blood pressure monitor and pulse oximetry

Assess for and treat the underlying cardiopulmonary process theophylline toxicity or metabolic abnormality

Administer bronchodilators and oxygen for treatment of decompensated COPD

activated charcoal andor charcoal hemoperfusion is the therapy for theophylline toxicity

When magnesium sulfate is administered to correct hypokalemia most patients convert to normal sinus rhythm

Avoid sedatives

Diltiazem and verapamil decrease the atrial activity and slow atrioventricular (AV) nodal conduction thereby decreasing ventricular rate but they do not return all patients to normal sinus rhythm

Diltiazem may be used as a 20-45 mg intravenous bolus and then as a 10-25 mgh continuous infusion

high-dose magnesium causes a significant decrease in the patients heart rate and conversion to normal sinus rhythm The dosage is 2 g intravenously over 1 minute followed by 2 gh infusion over 5 hours

Amiodarone (300 mg PO tid or 450-1500 mg IV over 2-24 h) has been used and has been reported to be associated with conversion to normal sinus rhythm The success rate was 40 at 3 days with oral dosing and 75 on day 1 with intravenous dosing however this has been evaluated in a very small number of patients

Cardioversion in MAT

Cardioversion is contraindicated in MAT Due to the multiple atrial foci direct

current (DC) cardioversion is not effective in restoring normal sinus rhythm

and can precipitate more dangerous arrhythmias

Surgical care

In patients who have persistent and recurrent episodes of MAT and problems with

rate control the AV node may be ablated using radiofrequency energy and a

permanent pacemaker implanted[22] This approach should be considered both for

symptomatic and hemodynamic improvement and to prevent the development of

tachycardia-mediated cardiomyopathy

Atrial flutter

A 50 years old diabetic hypertensive hyperthyroid male patient presented

with palpitation fatigue or poor exercise tolerance mild dyspneaand

presyncope On psysical examination pulse rate 150 min

Note negative sawtooth pattern of flutter waves in leads II III and aVF

Emergency Department Care

Assess airway breathing and circulation Hemodynamic concerns will dictate initial treatment

Treatment options for atrial flutter include the following

Antiarrhythmic drugsnodal agents

Direct-current (DC) cardioversion

Rapid atrial pacing to terminate atrial flutter

Blood pressure can be supported and rate controlled with medication

Anti coagulation therapy

Look for underlying causes At times treatment of the underlying disorder (eg thyroid disease valvular heart disease) is necessary to effect conversion to sinus rhythm

Cardioversion for unstable patients

If the patient is unstable (eg hypotension poor perfusion) synchronous direct-current (DC) cardioversion is commonly the initial treatment of choice

Cardioversion may be successful with energies as low as 25 Joules but since 100 Joules is virtually always successful this may be a reasonable initial shock strength

If the electrical shock results in atrial fibrillation (AF) a second shock at a higher energy level is used to restore normal sinus rhythm (NSR)

AV-His Bundle ablation

In patients who have failed antiarrhythmic therapy or who have failed RFA and who

are symptomatic palliative therapy with AV-His Bundle ablation can eliminate rapid

ventricular rates but it does require a permanent pacemaker to be placed as this

procedure creates third-degree heart block

Questions

• Slide 1
• Slide 2
• Slide 3
• Slide 4
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• Slide 10
• Slide 11
• Rate versus rhythm control which is superior
• Slide 13
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• Slide 18
• Slide 19
• Slide 20
• Slide 21
• Slide 22
• Slide 23
• Slide 24
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• Anti - coagulation therapy
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• Slide 42
• Slide 43
• Slide 44
• Slide 45
• Slide 46
• Slide 47
• Slide 48
• Slide 49
• Slide 50
• Slide 51
• Slide 52
• Slide 53
• Slide 54
• Slide 55
• Slide 56
• Slide 57
• Slide 58
• Slide 59
• Slide 60
• Slide 61
• Slide 62
• Slide 63
• Slide 64
• Slide 65
• Slide 66
• Slide 67
• Slide 68
• Slide 69
• Slide 70
• Slide 71
• Slide 72
• Slide 73
• Slide 74
• Slide 75
• Slide 76
• Slide 77
• Slide 78
• Slide 79
• Slide 80
• Slide 81

Surgical ablation of AF is typically performed at the time of other cardiac valve or

coronary artery surgery and less commonly as a stand-alone procedure

view of the left atrium depicting the isolating lesions delivered by catheter ablation around each set of pulmonary veins-

AV nodal re entry tachycardia

55 yo female with no cardiac history but allegedly one similar episode 10 years

ago when her heart ldquowent crazyrdquo for 20 minutes When EMS arrives Sudden

onset of strong palpitations dizziness chest pain paleness and mild diaphoresis

Blood pressure is 13292 and the the patient has a rapid regular pulse at around

180 beats min A 12 lead ECG is obtained

ECG description

Regular narrow-complex tachycardia

150 bpm

No visible P waves preceding QRS

Retrograde P waves with an RP interval of 120ms Inverted in inferior leads II III aVF and upright in aVR and right precordial leads V1 and V2 Also called pseudo S-waves (inferior leads) or pseudo R-waves (right precordial)

Cardiac axis is normal at approx 50deg

Interpretation

A narrow-complex tachycardia is most likely to be supraventricular in origin as this indicates normal His-Purkinje impulse propagation and simultaneous ventricular activation

However there is no P wave preceding the QRS complex to indicate that a sinoatrial origin of the propagated impulse

The regularity rules out atrial fibrillation and the fact that the P waves are not visible could of course just be due to the tachycardic rate At a first glance we can only conclude that this is a supraventricular tachycardia A natural next move would be to perform carotid pressure or other vagal manuevres to induce atrioventricular block in order to help us differentiate this rhythm

With the same intentions and if carotid pressure doesnrsquot work adenosine would be the drug of choice here

A closer look

However differentiation stop here as the diagnosis lies right in front of us clearly visible in both the ECGs

Although there is no sign of atrial activity preceding the QRS take a look after the QRS complex

In all inferior leads II III and aVF an inverted P wave with an RP interval of 120 ms followes each QRS complex

The same P wave with the same RP interval can be spotted in the right precordial leads V1 and V2 as well as in aVR

Logially the P wave is upright in these leads This means that the atrias are depolarized in a retrograde fashion after ventricular

Adenosine effect

Atrioventricular Nodal Reentry Tachycardia (AVNRT) Treatment amp Management

AVNRT

Patient condition

Hemodynamic ally

stable Hemodynamic ally

unstble

Vagal maneuver

adenosine calcium channel blockers (eg diltiazem verapamil) beta-blockers and digitalis

Direct current (DC) synchronized cardioversion

To prevent recurrence

Drugs

Multifocal Atrial Tachycardia

A 52 years old male COPD patient presented with palpitation shortness of

breath chest pain and syncopal history On examination pulse is rapid

irregular amp 1st heart sound is variable

1 Irregular ventricular rate greater than 100 bpm

2 Organized and discrete P waves with at least 3 different morphologies in the same electrocardiographic lead

3 Irregular PP PR and RR intervals with an isoelectric baseline between the P waves

Treatment of MAT

Administer oxygen to maintain the saturation greater than 90 but avoid excessive oxygen in patients with known significant chronic obstructive pulmonary disease (COPD) This will avoid the theoretical problem of removing the hypoxic drive for ventilation which can result in increased carbon dioxide retention

Establish cardiac monitor blood pressure monitor and pulse oximetry

Assess for and treat the underlying cardiopulmonary process theophylline toxicity or metabolic abnormality

Administer bronchodilators and oxygen for treatment of decompensated COPD

activated charcoal andor charcoal hemoperfusion is the therapy for theophylline toxicity

When magnesium sulfate is administered to correct hypokalemia most patients convert to normal sinus rhythm

Avoid sedatives

Diltiazem and verapamil decrease the atrial activity and slow atrioventricular (AV) nodal conduction thereby decreasing ventricular rate but they do not return all patients to normal sinus rhythm

Diltiazem may be used as a 20-45 mg intravenous bolus and then as a 10-25 mgh continuous infusion

high-dose magnesium causes a significant decrease in the patients heart rate and conversion to normal sinus rhythm The dosage is 2 g intravenously over 1 minute followed by 2 gh infusion over 5 hours

Amiodarone (300 mg PO tid or 450-1500 mg IV over 2-24 h) has been used and has been reported to be associated with conversion to normal sinus rhythm The success rate was 40 at 3 days with oral dosing and 75 on day 1 with intravenous dosing however this has been evaluated in a very small number of patients

Cardioversion in MAT

Cardioversion is contraindicated in MAT Due to the multiple atrial foci direct

current (DC) cardioversion is not effective in restoring normal sinus rhythm

and can precipitate more dangerous arrhythmias

Surgical care

In patients who have persistent and recurrent episodes of MAT and problems with

rate control the AV node may be ablated using radiofrequency energy and a

permanent pacemaker implanted[22] This approach should be considered both for

symptomatic and hemodynamic improvement and to prevent the development of

tachycardia-mediated cardiomyopathy

Atrial flutter

A 50 years old diabetic hypertensive hyperthyroid male patient presented

with palpitation fatigue or poor exercise tolerance mild dyspneaand

presyncope On psysical examination pulse rate 150 min

Note negative sawtooth pattern of flutter waves in leads II III and aVF

Emergency Department Care

Assess airway breathing and circulation Hemodynamic concerns will dictate initial treatment

Treatment options for atrial flutter include the following

Antiarrhythmic drugsnodal agents

Direct-current (DC) cardioversion

Rapid atrial pacing to terminate atrial flutter

Blood pressure can be supported and rate controlled with medication

Anti coagulation therapy

Look for underlying causes At times treatment of the underlying disorder (eg thyroid disease valvular heart disease) is necessary to effect conversion to sinus rhythm

Cardioversion for unstable patients

If the patient is unstable (eg hypotension poor perfusion) synchronous direct-current (DC) cardioversion is commonly the initial treatment of choice

Cardioversion may be successful with energies as low as 25 Joules but since 100 Joules is virtually always successful this may be a reasonable initial shock strength

If the electrical shock results in atrial fibrillation (AF) a second shock at a higher energy level is used to restore normal sinus rhythm (NSR)

AV-His Bundle ablation

In patients who have failed antiarrhythmic therapy or who have failed RFA and who

are symptomatic palliative therapy with AV-His Bundle ablation can eliminate rapid

ventricular rates but it does require a permanent pacemaker to be placed as this

procedure creates third-degree heart block

Questions

• Slide 1
• Slide 2
• Slide 3
• Slide 4
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• Slide 10
• Slide 11
• Rate versus rhythm control which is superior
• Slide 13
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• Slide 18
• Slide 19
• Slide 20
• Slide 21
• Slide 22
• Slide 23
• Slide 24
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• Anti - coagulation therapy
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• Slide 42
• Slide 43
• Slide 44
• Slide 45
• Slide 46
• Slide 47
• Slide 48
• Slide 49
• Slide 50
• Slide 51
• Slide 52
• Slide 53
• Slide 54
• Slide 55
• Slide 56
• Slide 57
• Slide 58
• Slide 59
• Slide 60
• Slide 61
• Slide 62
• Slide 63
• Slide 64
• Slide 65
• Slide 66
• Slide 67
• Slide 68
• Slide 69
• Slide 70
• Slide 71
• Slide 72
• Slide 73
• Slide 74
• Slide 75
• Slide 76
• Slide 77
• Slide 78
• Slide 79
• Slide 80
• Slide 81

AV nodal re entry tachycardia

55 yo female with no cardiac history but allegedly one similar episode 10 years

ago when her heart ldquowent crazyrdquo for 20 minutes When EMS arrives Sudden

onset of strong palpitations dizziness chest pain paleness and mild diaphoresis

Blood pressure is 13292 and the the patient has a rapid regular pulse at around

180 beats min A 12 lead ECG is obtained

ECG description

Regular narrow-complex tachycardia

150 bpm

No visible P waves preceding QRS

Retrograde P waves with an RP interval of 120ms Inverted in inferior leads II III aVF and upright in aVR and right precordial leads V1 and V2 Also called pseudo S-waves (inferior leads) or pseudo R-waves (right precordial)

Cardiac axis is normal at approx 50deg

Interpretation

A narrow-complex tachycardia is most likely to be supraventricular in origin as this indicates normal His-Purkinje impulse propagation and simultaneous ventricular activation

However there is no P wave preceding the QRS complex to indicate that a sinoatrial origin of the propagated impulse

The regularity rules out atrial fibrillation and the fact that the P waves are not visible could of course just be due to the tachycardic rate At a first glance we can only conclude that this is a supraventricular tachycardia A natural next move would be to perform carotid pressure or other vagal manuevres to induce atrioventricular block in order to help us differentiate this rhythm

With the same intentions and if carotid pressure doesnrsquot work adenosine would be the drug of choice here

A closer look

However differentiation stop here as the diagnosis lies right in front of us clearly visible in both the ECGs

Although there is no sign of atrial activity preceding the QRS take a look after the QRS complex

In all inferior leads II III and aVF an inverted P wave with an RP interval of 120 ms followes each QRS complex

The same P wave with the same RP interval can be spotted in the right precordial leads V1 and V2 as well as in aVR

Logially the P wave is upright in these leads This means that the atrias are depolarized in a retrograde fashion after ventricular

Adenosine effect

Atrioventricular Nodal Reentry Tachycardia (AVNRT) Treatment amp Management

AVNRT

Patient condition

Hemodynamic ally

stable Hemodynamic ally

unstble

Vagal maneuver

adenosine calcium channel blockers (eg diltiazem verapamil) beta-blockers and digitalis

Direct current (DC) synchronized cardioversion

To prevent recurrence

Drugs

Multifocal Atrial Tachycardia

A 52 years old male COPD patient presented with palpitation shortness of

breath chest pain and syncopal history On examination pulse is rapid

irregular amp 1st heart sound is variable

1 Irregular ventricular rate greater than 100 bpm

2 Organized and discrete P waves with at least 3 different morphologies in the same electrocardiographic lead

3 Irregular PP PR and RR intervals with an isoelectric baseline between the P waves

Treatment of MAT

Administer oxygen to maintain the saturation greater than 90 but avoid excessive oxygen in patients with known significant chronic obstructive pulmonary disease (COPD) This will avoid the theoretical problem of removing the hypoxic drive for ventilation which can result in increased carbon dioxide retention

Establish cardiac monitor blood pressure monitor and pulse oximetry

Assess for and treat the underlying cardiopulmonary process theophylline toxicity or metabolic abnormality

Administer bronchodilators and oxygen for treatment of decompensated COPD

activated charcoal andor charcoal hemoperfusion is the therapy for theophylline toxicity

When magnesium sulfate is administered to correct hypokalemia most patients convert to normal sinus rhythm

Avoid sedatives

Diltiazem and verapamil decrease the atrial activity and slow atrioventricular (AV) nodal conduction thereby decreasing ventricular rate but they do not return all patients to normal sinus rhythm

Diltiazem may be used as a 20-45 mg intravenous bolus and then as a 10-25 mgh continuous infusion

high-dose magnesium causes a significant decrease in the patients heart rate and conversion to normal sinus rhythm The dosage is 2 g intravenously over 1 minute followed by 2 gh infusion over 5 hours

Amiodarone (300 mg PO tid or 450-1500 mg IV over 2-24 h) has been used and has been reported to be associated with conversion to normal sinus rhythm The success rate was 40 at 3 days with oral dosing and 75 on day 1 with intravenous dosing however this has been evaluated in a very small number of patients

Cardioversion in MAT

Cardioversion is contraindicated in MAT Due to the multiple atrial foci direct

current (DC) cardioversion is not effective in restoring normal sinus rhythm

and can precipitate more dangerous arrhythmias

Surgical care

In patients who have persistent and recurrent episodes of MAT and problems with

rate control the AV node may be ablated using radiofrequency energy and a

permanent pacemaker implanted[22] This approach should be considered both for

symptomatic and hemodynamic improvement and to prevent the development of

tachycardia-mediated cardiomyopathy

Atrial flutter

A 50 years old diabetic hypertensive hyperthyroid male patient presented

with palpitation fatigue or poor exercise tolerance mild dyspneaand

presyncope On psysical examination pulse rate 150 min

Note negative sawtooth pattern of flutter waves in leads II III and aVF

Emergency Department Care

Assess airway breathing and circulation Hemodynamic concerns will dictate initial treatment

Treatment options for atrial flutter include the following

Antiarrhythmic drugsnodal agents

Direct-current (DC) cardioversion

Rapid atrial pacing to terminate atrial flutter

Blood pressure can be supported and rate controlled with medication

Anti coagulation therapy

Look for underlying causes At times treatment of the underlying disorder (eg thyroid disease valvular heart disease) is necessary to effect conversion to sinus rhythm

Cardioversion for unstable patients

If the patient is unstable (eg hypotension poor perfusion) synchronous direct-current (DC) cardioversion is commonly the initial treatment of choice

Cardioversion may be successful with energies as low as 25 Joules but since 100 Joules is virtually always successful this may be a reasonable initial shock strength

If the electrical shock results in atrial fibrillation (AF) a second shock at a higher energy level is used to restore normal sinus rhythm (NSR)

AV-His Bundle ablation

In patients who have failed antiarrhythmic therapy or who have failed RFA and who

are symptomatic palliative therapy with AV-His Bundle ablation can eliminate rapid

ventricular rates but it does require a permanent pacemaker to be placed as this

procedure creates third-degree heart block

Questions

• Slide 1
• Slide 2
• Slide 3
• Slide 4
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• Slide 10
• Slide 11
• Rate versus rhythm control which is superior
• Slide 13
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• Slide 18
• Slide 19
• Slide 20
• Slide 21
• Slide 22
• Slide 23
• Slide 24
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• Anti - coagulation therapy
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• Slide 42
• Slide 43
• Slide 44
• Slide 45
• Slide 46
• Slide 47
• Slide 48
• Slide 49
• Slide 50
• Slide 51
• Slide 52
• Slide 53
• Slide 54
• Slide 55
• Slide 56
• Slide 57
• Slide 58
• Slide 59
• Slide 60
• Slide 61
• Slide 62
• Slide 63
• Slide 64
• Slide 65
• Slide 66
• Slide 67
• Slide 68
• Slide 69
• Slide 70
• Slide 71
• Slide 72
• Slide 73
• Slide 74
• Slide 75
• Slide 76
• Slide 77
• Slide 78
• Slide 79
• Slide 80
• Slide 81

55 yo female with no cardiac history but allegedly one similar episode 10 years

ago when her heart ldquowent crazyrdquo for 20 minutes When EMS arrives Sudden

onset of strong palpitations dizziness chest pain paleness and mild diaphoresis

Blood pressure is 13292 and the the patient has a rapid regular pulse at around

180 beats min A 12 lead ECG is obtained

ECG description

Regular narrow-complex tachycardia

150 bpm

No visible P waves preceding QRS

Retrograde P waves with an RP interval of 120ms Inverted in inferior leads II III aVF and upright in aVR and right precordial leads V1 and V2 Also called pseudo S-waves (inferior leads) or pseudo R-waves (right precordial)

Cardiac axis is normal at approx 50deg

Interpretation

A narrow-complex tachycardia is most likely to be supraventricular in origin as this indicates normal His-Purkinje impulse propagation and simultaneous ventricular activation

However there is no P wave preceding the QRS complex to indicate that a sinoatrial origin of the propagated impulse

The regularity rules out atrial fibrillation and the fact that the P waves are not visible could of course just be due to the tachycardic rate At a first glance we can only conclude that this is a supraventricular tachycardia A natural next move would be to perform carotid pressure or other vagal manuevres to induce atrioventricular block in order to help us differentiate this rhythm

With the same intentions and if carotid pressure doesnrsquot work adenosine would be the drug of choice here

A closer look

However differentiation stop here as the diagnosis lies right in front of us clearly visible in both the ECGs

Although there is no sign of atrial activity preceding the QRS take a look after the QRS complex

In all inferior leads II III and aVF an inverted P wave with an RP interval of 120 ms followes each QRS complex

The same P wave with the same RP interval can be spotted in the right precordial leads V1 and V2 as well as in aVR

Logially the P wave is upright in these leads This means that the atrias are depolarized in a retrograde fashion after ventricular

Adenosine effect

Atrioventricular Nodal Reentry Tachycardia (AVNRT) Treatment amp Management

AVNRT

Patient condition

Hemodynamic ally

stable Hemodynamic ally

unstble

Vagal maneuver

adenosine calcium channel blockers (eg diltiazem verapamil) beta-blockers and digitalis

Direct current (DC) synchronized cardioversion

To prevent recurrence

Drugs

Multifocal Atrial Tachycardia

A 52 years old male COPD patient presented with palpitation shortness of

breath chest pain and syncopal history On examination pulse is rapid

irregular amp 1st heart sound is variable

1 Irregular ventricular rate greater than 100 bpm

2 Organized and discrete P waves with at least 3 different morphologies in the same electrocardiographic lead

3 Irregular PP PR and RR intervals with an isoelectric baseline between the P waves

Treatment of MAT

Administer oxygen to maintain the saturation greater than 90 but avoid excessive oxygen in patients with known significant chronic obstructive pulmonary disease (COPD) This will avoid the theoretical problem of removing the hypoxic drive for ventilation which can result in increased carbon dioxide retention

Establish cardiac monitor blood pressure monitor and pulse oximetry

Assess for and treat the underlying cardiopulmonary process theophylline toxicity or metabolic abnormality

Administer bronchodilators and oxygen for treatment of decompensated COPD

activated charcoal andor charcoal hemoperfusion is the therapy for theophylline toxicity

When magnesium sulfate is administered to correct hypokalemia most patients convert to normal sinus rhythm

Avoid sedatives

Diltiazem and verapamil decrease the atrial activity and slow atrioventricular (AV) nodal conduction thereby decreasing ventricular rate but they do not return all patients to normal sinus rhythm

Diltiazem may be used as a 20-45 mg intravenous bolus and then as a 10-25 mgh continuous infusion

high-dose magnesium causes a significant decrease in the patients heart rate and conversion to normal sinus rhythm The dosage is 2 g intravenously over 1 minute followed by 2 gh infusion over 5 hours

Amiodarone (300 mg PO tid or 450-1500 mg IV over 2-24 h) has been used and has been reported to be associated with conversion to normal sinus rhythm The success rate was 40 at 3 days with oral dosing and 75 on day 1 with intravenous dosing however this has been evaluated in a very small number of patients

Cardioversion in MAT

Cardioversion is contraindicated in MAT Due to the multiple atrial foci direct

current (DC) cardioversion is not effective in restoring normal sinus rhythm

and can precipitate more dangerous arrhythmias

Surgical care

In patients who have persistent and recurrent episodes of MAT and problems with

rate control the AV node may be ablated using radiofrequency energy and a

permanent pacemaker implanted[22] This approach should be considered both for

symptomatic and hemodynamic improvement and to prevent the development of

tachycardia-mediated cardiomyopathy

Atrial flutter

A 50 years old diabetic hypertensive hyperthyroid male patient presented

with palpitation fatigue or poor exercise tolerance mild dyspneaand

presyncope On psysical examination pulse rate 150 min

Note negative sawtooth pattern of flutter waves in leads II III and aVF

Emergency Department Care

Assess airway breathing and circulation Hemodynamic concerns will dictate initial treatment

Treatment options for atrial flutter include the following

Antiarrhythmic drugsnodal agents

Direct-current (DC) cardioversion

Rapid atrial pacing to terminate atrial flutter

Blood pressure can be supported and rate controlled with medication

Anti coagulation therapy

Look for underlying causes At times treatment of the underlying disorder (eg thyroid disease valvular heart disease) is necessary to effect conversion to sinus rhythm

Cardioversion for unstable patients

If the patient is unstable (eg hypotension poor perfusion) synchronous direct-current (DC) cardioversion is commonly the initial treatment of choice

Cardioversion may be successful with energies as low as 25 Joules but since 100 Joules is virtually always successful this may be a reasonable initial shock strength

If the electrical shock results in atrial fibrillation (AF) a second shock at a higher energy level is used to restore normal sinus rhythm (NSR)

AV-His Bundle ablation

In patients who have failed antiarrhythmic therapy or who have failed RFA and who

are symptomatic palliative therapy with AV-His Bundle ablation can eliminate rapid

ventricular rates but it does require a permanent pacemaker to be placed as this

procedure creates third-degree heart block

Questions

• Slide 1
• Slide 2
• Slide 3
• Slide 4
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• Slide 10
• Slide 11
• Rate versus rhythm control which is superior
• Slide 13
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• Slide 18
• Slide 19
• Slide 20
• Slide 21
• Slide 22
• Slide 23
• Slide 24
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• Anti - coagulation therapy
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• Slide 42
• Slide 43
• Slide 44
• Slide 45
• Slide 46
• Slide 47
• Slide 48
• Slide 49
• Slide 50
• Slide 51
• Slide 52
• Slide 53
• Slide 54
• Slide 55
• Slide 56
• Slide 57
• Slide 58
• Slide 59
• Slide 60
• Slide 61
• Slide 62
• Slide 63
• Slide 64
• Slide 65
• Slide 66
• Slide 67
• Slide 68
• Slide 69
• Slide 70
• Slide 71
• Slide 72
• Slide 73
• Slide 74
• Slide 75
• Slide 76
• Slide 77
• Slide 78
• Slide 79
• Slide 80
• Slide 81

ECG description

Regular narrow-complex tachycardia

150 bpm

No visible P waves preceding QRS

Retrograde P waves with an RP interval of 120ms Inverted in inferior leads II III aVF and upright in aVR and right precordial leads V1 and V2 Also called pseudo S-waves (inferior leads) or pseudo R-waves (right precordial)

Cardiac axis is normal at approx 50deg

Interpretation

A narrow-complex tachycardia is most likely to be supraventricular in origin as this indicates normal His-Purkinje impulse propagation and simultaneous ventricular activation

However there is no P wave preceding the QRS complex to indicate that a sinoatrial origin of the propagated impulse

The regularity rules out atrial fibrillation and the fact that the P waves are not visible could of course just be due to the tachycardic rate At a first glance we can only conclude that this is a supraventricular tachycardia A natural next move would be to perform carotid pressure or other vagal manuevres to induce atrioventricular block in order to help us differentiate this rhythm

With the same intentions and if carotid pressure doesnrsquot work adenosine would be the drug of choice here

A closer look

However differentiation stop here as the diagnosis lies right in front of us clearly visible in both the ECGs

Although there is no sign of atrial activity preceding the QRS take a look after the QRS complex

In all inferior leads II III and aVF an inverted P wave with an RP interval of 120 ms followes each QRS complex

The same P wave with the same RP interval can be spotted in the right precordial leads V1 and V2 as well as in aVR

Logially the P wave is upright in these leads This means that the atrias are depolarized in a retrograde fashion after ventricular

Adenosine effect

Atrioventricular Nodal Reentry Tachycardia (AVNRT) Treatment amp Management

AVNRT

Patient condition

Hemodynamic ally

stable Hemodynamic ally

unstble

Vagal maneuver

adenosine calcium channel blockers (eg diltiazem verapamil) beta-blockers and digitalis

Direct current (DC) synchronized cardioversion

To prevent recurrence

Drugs

Multifocal Atrial Tachycardia

A 52 years old male COPD patient presented with palpitation shortness of

breath chest pain and syncopal history On examination pulse is rapid

irregular amp 1st heart sound is variable

1 Irregular ventricular rate greater than 100 bpm

2 Organized and discrete P waves with at least 3 different morphologies in the same electrocardiographic lead

3 Irregular PP PR and RR intervals with an isoelectric baseline between the P waves

Treatment of MAT

Administer oxygen to maintain the saturation greater than 90 but avoid excessive oxygen in patients with known significant chronic obstructive pulmonary disease (COPD) This will avoid the theoretical problem of removing the hypoxic drive for ventilation which can result in increased carbon dioxide retention

Establish cardiac monitor blood pressure monitor and pulse oximetry

Assess for and treat the underlying cardiopulmonary process theophylline toxicity or metabolic abnormality

Administer bronchodilators and oxygen for treatment of decompensated COPD

activated charcoal andor charcoal hemoperfusion is the therapy for theophylline toxicity

When magnesium sulfate is administered to correct hypokalemia most patients convert to normal sinus rhythm

Avoid sedatives

Diltiazem and verapamil decrease the atrial activity and slow atrioventricular (AV) nodal conduction thereby decreasing ventricular rate but they do not return all patients to normal sinus rhythm

Diltiazem may be used as a 20-45 mg intravenous bolus and then as a 10-25 mgh continuous infusion

high-dose magnesium causes a significant decrease in the patients heart rate and conversion to normal sinus rhythm The dosage is 2 g intravenously over 1 minute followed by 2 gh infusion over 5 hours

Amiodarone (300 mg PO tid or 450-1500 mg IV over 2-24 h) has been used and has been reported to be associated with conversion to normal sinus rhythm The success rate was 40 at 3 days with oral dosing and 75 on day 1 with intravenous dosing however this has been evaluated in a very small number of patients

Cardioversion in MAT

Cardioversion is contraindicated in MAT Due to the multiple atrial foci direct

current (DC) cardioversion is not effective in restoring normal sinus rhythm

and can precipitate more dangerous arrhythmias

Surgical care

In patients who have persistent and recurrent episodes of MAT and problems with

rate control the AV node may be ablated using radiofrequency energy and a

permanent pacemaker implanted[22] This approach should be considered both for

symptomatic and hemodynamic improvement and to prevent the development of

tachycardia-mediated cardiomyopathy

Atrial flutter

A 50 years old diabetic hypertensive hyperthyroid male patient presented

with palpitation fatigue or poor exercise tolerance mild dyspneaand

presyncope On psysical examination pulse rate 150 min

Note negative sawtooth pattern of flutter waves in leads II III and aVF

Emergency Department Care

Assess airway breathing and circulation Hemodynamic concerns will dictate initial treatment

Treatment options for atrial flutter include the following

Antiarrhythmic drugsnodal agents

Direct-current (DC) cardioversion

Rapid atrial pacing to terminate atrial flutter

Blood pressure can be supported and rate controlled with medication

Anti coagulation therapy

Look for underlying causes At times treatment of the underlying disorder (eg thyroid disease valvular heart disease) is necessary to effect conversion to sinus rhythm

Cardioversion for unstable patients

If the patient is unstable (eg hypotension poor perfusion) synchronous direct-current (DC) cardioversion is commonly the initial treatment of choice

Cardioversion may be successful with energies as low as 25 Joules but since 100 Joules is virtually always successful this may be a reasonable initial shock strength

If the electrical shock results in atrial fibrillation (AF) a second shock at a higher energy level is used to restore normal sinus rhythm (NSR)

AV-His Bundle ablation

In patients who have failed antiarrhythmic therapy or who have failed RFA and who

are symptomatic palliative therapy with AV-His Bundle ablation can eliminate rapid

ventricular rates but it does require a permanent pacemaker to be placed as this

procedure creates third-degree heart block

Questions

• Slide 1
• Slide 2
• Slide 3
• Slide 4
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• Slide 10
• Slide 11
• Rate versus rhythm control which is superior
• Slide 13
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• Slide 18
• Slide 19
• Slide 20
• Slide 21
• Slide 22
• Slide 23
• Slide 24
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• Anti - coagulation therapy
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• Slide 42
• Slide 43
• Slide 44
• Slide 45
• Slide 46
• Slide 47
• Slide 48
• Slide 49
• Slide 50
• Slide 51
• Slide 52
• Slide 53
• Slide 54
• Slide 55
• Slide 56
• Slide 57
• Slide 58
• Slide 59
• Slide 60
• Slide 61
• Slide 62
• Slide 63
• Slide 64
• Slide 65
• Slide 66
• Slide 67
• Slide 68
• Slide 69
• Slide 70
• Slide 71
• Slide 72
• Slide 73
• Slide 74
• Slide 75
• Slide 76
• Slide 77
• Slide 78
• Slide 79
• Slide 80
• Slide 81

Interpretation

A narrow-complex tachycardia is most likely to be supraventricular in origin as this indicates normal His-Purkinje impulse propagation and simultaneous ventricular activation

However there is no P wave preceding the QRS complex to indicate that a sinoatrial origin of the propagated impulse

The regularity rules out atrial fibrillation and the fact that the P waves are not visible could of course just be due to the tachycardic rate At a first glance we can only conclude that this is a supraventricular tachycardia A natural next move would be to perform carotid pressure or other vagal manuevres to induce atrioventricular block in order to help us differentiate this rhythm

With the same intentions and if carotid pressure doesnrsquot work adenosine would be the drug of choice here

A closer look

However differentiation stop here as the diagnosis lies right in front of us clearly visible in both the ECGs

Although there is no sign of atrial activity preceding the QRS take a look after the QRS complex

In all inferior leads II III and aVF an inverted P wave with an RP interval of 120 ms followes each QRS complex

The same P wave with the same RP interval can be spotted in the right precordial leads V1 and V2 as well as in aVR

Logially the P wave is upright in these leads This means that the atrias are depolarized in a retrograde fashion after ventricular

Adenosine effect

Atrioventricular Nodal Reentry Tachycardia (AVNRT) Treatment amp Management

AVNRT

Patient condition

Hemodynamic ally

stable Hemodynamic ally

unstble

Vagal maneuver

adenosine calcium channel blockers (eg diltiazem verapamil) beta-blockers and digitalis

Direct current (DC) synchronized cardioversion

To prevent recurrence

Drugs

Multifocal Atrial Tachycardia

A 52 years old male COPD patient presented with palpitation shortness of

breath chest pain and syncopal history On examination pulse is rapid

irregular amp 1st heart sound is variable

1 Irregular ventricular rate greater than 100 bpm

2 Organized and discrete P waves with at least 3 different morphologies in the same electrocardiographic lead

3 Irregular PP PR and RR intervals with an isoelectric baseline between the P waves

Treatment of MAT

Administer oxygen to maintain the saturation greater than 90 but avoid excessive oxygen in patients with known significant chronic obstructive pulmonary disease (COPD) This will avoid the theoretical problem of removing the hypoxic drive for ventilation which can result in increased carbon dioxide retention

Establish cardiac monitor blood pressure monitor and pulse oximetry

Assess for and treat the underlying cardiopulmonary process theophylline toxicity or metabolic abnormality

Administer bronchodilators and oxygen for treatment of decompensated COPD

activated charcoal andor charcoal hemoperfusion is the therapy for theophylline toxicity

When magnesium sulfate is administered to correct hypokalemia most patients convert to normal sinus rhythm

Avoid sedatives

Diltiazem and verapamil decrease the atrial activity and slow atrioventricular (AV) nodal conduction thereby decreasing ventricular rate but they do not return all patients to normal sinus rhythm

Diltiazem may be used as a 20-45 mg intravenous bolus and then as a 10-25 mgh continuous infusion

high-dose magnesium causes a significant decrease in the patients heart rate and conversion to normal sinus rhythm The dosage is 2 g intravenously over 1 minute followed by 2 gh infusion over 5 hours

Amiodarone (300 mg PO tid or 450-1500 mg IV over 2-24 h) has been used and has been reported to be associated with conversion to normal sinus rhythm The success rate was 40 at 3 days with oral dosing and 75 on day 1 with intravenous dosing however this has been evaluated in a very small number of patients

Cardioversion in MAT

Cardioversion is contraindicated in MAT Due to the multiple atrial foci direct

current (DC) cardioversion is not effective in restoring normal sinus rhythm

and can precipitate more dangerous arrhythmias

Surgical care

In patients who have persistent and recurrent episodes of MAT and problems with

rate control the AV node may be ablated using radiofrequency energy and a

permanent pacemaker implanted[22] This approach should be considered both for

symptomatic and hemodynamic improvement and to prevent the development of

tachycardia-mediated cardiomyopathy

Atrial flutter

A 50 years old diabetic hypertensive hyperthyroid male patient presented

with palpitation fatigue or poor exercise tolerance mild dyspneaand

presyncope On psysical examination pulse rate 150 min

Note negative sawtooth pattern of flutter waves in leads II III and aVF

Emergency Department Care

Assess airway breathing and circulation Hemodynamic concerns will dictate initial treatment

Treatment options for atrial flutter include the following

Antiarrhythmic drugsnodal agents

Direct-current (DC) cardioversion

Rapid atrial pacing to terminate atrial flutter

Blood pressure can be supported and rate controlled with medication

Anti coagulation therapy

Look for underlying causes At times treatment of the underlying disorder (eg thyroid disease valvular heart disease) is necessary to effect conversion to sinus rhythm

Cardioversion for unstable patients

If the patient is unstable (eg hypotension poor perfusion) synchronous direct-current (DC) cardioversion is commonly the initial treatment of choice

Cardioversion may be successful with energies as low as 25 Joules but since 100 Joules is virtually always successful this may be a reasonable initial shock strength

If the electrical shock results in atrial fibrillation (AF) a second shock at a higher energy level is used to restore normal sinus rhythm (NSR)

AV-His Bundle ablation

In patients who have failed antiarrhythmic therapy or who have failed RFA and who

are symptomatic palliative therapy with AV-His Bundle ablation can eliminate rapid

ventricular rates but it does require a permanent pacemaker to be placed as this

procedure creates third-degree heart block

Questions

• Slide 1
• Slide 2
• Slide 3
• Slide 4
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• Slide 10
• Slide 11
• Rate versus rhythm control which is superior
• Slide 13
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• Slide 18
• Slide 19
• Slide 20
• Slide 21
• Slide 22
• Slide 23
• Slide 24
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• Anti - coagulation therapy
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• Slide 42
• Slide 43
• Slide 44
• Slide 45
• Slide 46
• Slide 47
• Slide 48
• Slide 49
• Slide 50
• Slide 51
• Slide 52
• Slide 53
• Slide 54
• Slide 55
• Slide 56
• Slide 57
• Slide 58
• Slide 59
• Slide 60
• Slide 61
• Slide 62
• Slide 63
• Slide 64
• Slide 65
• Slide 66
• Slide 67
• Slide 68
• Slide 69
• Slide 70
• Slide 71
• Slide 72
• Slide 73
• Slide 74
• Slide 75
• Slide 76
• Slide 77
• Slide 78
• Slide 79
• Slide 80
• Slide 81

A closer look

However differentiation stop here as the diagnosis lies right in front of us clearly visible in both the ECGs

Although there is no sign of atrial activity preceding the QRS take a look after the QRS complex

In all inferior leads II III and aVF an inverted P wave with an RP interval of 120 ms followes each QRS complex

The same P wave with the same RP interval can be spotted in the right precordial leads V1 and V2 as well as in aVR

Logially the P wave is upright in these leads This means that the atrias are depolarized in a retrograde fashion after ventricular

Adenosine effect

Atrioventricular Nodal Reentry Tachycardia (AVNRT) Treatment amp Management

AVNRT

Patient condition

Hemodynamic ally

stable Hemodynamic ally

unstble

Vagal maneuver

adenosine calcium channel blockers (eg diltiazem verapamil) beta-blockers and digitalis

Direct current (DC) synchronized cardioversion

To prevent recurrence

Drugs

Multifocal Atrial Tachycardia

A 52 years old male COPD patient presented with palpitation shortness of

breath chest pain and syncopal history On examination pulse is rapid

irregular amp 1st heart sound is variable

1 Irregular ventricular rate greater than 100 bpm

2 Organized and discrete P waves with at least 3 different morphologies in the same electrocardiographic lead

3 Irregular PP PR and RR intervals with an isoelectric baseline between the P waves

Treatment of MAT

Administer oxygen to maintain the saturation greater than 90 but avoid excessive oxygen in patients with known significant chronic obstructive pulmonary disease (COPD) This will avoid the theoretical problem of removing the hypoxic drive for ventilation which can result in increased carbon dioxide retention

Establish cardiac monitor blood pressure monitor and pulse oximetry

Assess for and treat the underlying cardiopulmonary process theophylline toxicity or metabolic abnormality

Administer bronchodilators and oxygen for treatment of decompensated COPD

activated charcoal andor charcoal hemoperfusion is the therapy for theophylline toxicity

When magnesium sulfate is administered to correct hypokalemia most patients convert to normal sinus rhythm

Avoid sedatives

Diltiazem and verapamil decrease the atrial activity and slow atrioventricular (AV) nodal conduction thereby decreasing ventricular rate but they do not return all patients to normal sinus rhythm

Diltiazem may be used as a 20-45 mg intravenous bolus and then as a 10-25 mgh continuous infusion

high-dose magnesium causes a significant decrease in the patients heart rate and conversion to normal sinus rhythm The dosage is 2 g intravenously over 1 minute followed by 2 gh infusion over 5 hours

Amiodarone (300 mg PO tid or 450-1500 mg IV over 2-24 h) has been used and has been reported to be associated with conversion to normal sinus rhythm The success rate was 40 at 3 days with oral dosing and 75 on day 1 with intravenous dosing however this has been evaluated in a very small number of patients

Cardioversion in MAT

Cardioversion is contraindicated in MAT Due to the multiple atrial foci direct

current (DC) cardioversion is not effective in restoring normal sinus rhythm

and can precipitate more dangerous arrhythmias

Surgical care

In patients who have persistent and recurrent episodes of MAT and problems with

rate control the AV node may be ablated using radiofrequency energy and a

permanent pacemaker implanted[22] This approach should be considered both for

symptomatic and hemodynamic improvement and to prevent the development of

tachycardia-mediated cardiomyopathy

Atrial flutter

A 50 years old diabetic hypertensive hyperthyroid male patient presented

with palpitation fatigue or poor exercise tolerance mild dyspneaand

presyncope On psysical examination pulse rate 150 min

Note negative sawtooth pattern of flutter waves in leads II III and aVF

Emergency Department Care

Assess airway breathing and circulation Hemodynamic concerns will dictate initial treatment

Treatment options for atrial flutter include the following

Antiarrhythmic drugsnodal agents

Direct-current (DC) cardioversion

Rapid atrial pacing to terminate atrial flutter

Blood pressure can be supported and rate controlled with medication

Anti coagulation therapy

Look for underlying causes At times treatment of the underlying disorder (eg thyroid disease valvular heart disease) is necessary to effect conversion to sinus rhythm

Cardioversion for unstable patients

If the patient is unstable (eg hypotension poor perfusion) synchronous direct-current (DC) cardioversion is commonly the initial treatment of choice

Cardioversion may be successful with energies as low as 25 Joules but since 100 Joules is virtually always successful this may be a reasonable initial shock strength

If the electrical shock results in atrial fibrillation (AF) a second shock at a higher energy level is used to restore normal sinus rhythm (NSR)

AV-His Bundle ablation

In patients who have failed antiarrhythmic therapy or who have failed RFA and who

are symptomatic palliative therapy with AV-His Bundle ablation can eliminate rapid

ventricular rates but it does require a permanent pacemaker to be placed as this

procedure creates third-degree heart block

Questions

• Slide 1
• Slide 2
• Slide 3
• Slide 4
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• Slide 10
• Slide 11
• Rate versus rhythm control which is superior
• Slide 13
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• Slide 18
• Slide 19
• Slide 20
• Slide 21
• Slide 22
• Slide 23
• Slide 24
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• Anti - coagulation therapy
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• Slide 42
• Slide 43
• Slide 44
• Slide 45
• Slide 46
• Slide 47
• Slide 48
• Slide 49
• Slide 50
• Slide 51
• Slide 52
• Slide 53
• Slide 54
• Slide 55
• Slide 56
• Slide 57
• Slide 58
• Slide 59
• Slide 60
• Slide 61
• Slide 62
• Slide 63
• Slide 64
• Slide 65
• Slide 66
• Slide 67
• Slide 68
• Slide 69
• Slide 70
• Slide 71
• Slide 72
• Slide 73
• Slide 74
• Slide 75
• Slide 76
• Slide 77
• Slide 78
• Slide 79
• Slide 80
• Slide 81

Adenosine effect

Atrioventricular Nodal Reentry Tachycardia (AVNRT) Treatment amp Management

AVNRT

Patient condition

Hemodynamic ally

stable Hemodynamic ally

unstble

Vagal maneuver

adenosine calcium channel blockers (eg diltiazem verapamil) beta-blockers and digitalis

Direct current (DC) synchronized cardioversion

To prevent recurrence

Drugs

Multifocal Atrial Tachycardia

A 52 years old male COPD patient presented with palpitation shortness of

breath chest pain and syncopal history On examination pulse is rapid

irregular amp 1st heart sound is variable

1 Irregular ventricular rate greater than 100 bpm

2 Organized and discrete P waves with at least 3 different morphologies in the same electrocardiographic lead

3 Irregular PP PR and RR intervals with an isoelectric baseline between the P waves

Treatment of MAT

Administer oxygen to maintain the saturation greater than 90 but avoid excessive oxygen in patients with known significant chronic obstructive pulmonary disease (COPD) This will avoid the theoretical problem of removing the hypoxic drive for ventilation which can result in increased carbon dioxide retention

Establish cardiac monitor blood pressure monitor and pulse oximetry

Assess for and treat the underlying cardiopulmonary process theophylline toxicity or metabolic abnormality

Administer bronchodilators and oxygen for treatment of decompensated COPD

activated charcoal andor charcoal hemoperfusion is the therapy for theophylline toxicity

When magnesium sulfate is administered to correct hypokalemia most patients convert to normal sinus rhythm

Avoid sedatives

Diltiazem and verapamil decrease the atrial activity and slow atrioventricular (AV) nodal conduction thereby decreasing ventricular rate but they do not return all patients to normal sinus rhythm

Diltiazem may be used as a 20-45 mg intravenous bolus and then as a 10-25 mgh continuous infusion

high-dose magnesium causes a significant decrease in the patients heart rate and conversion to normal sinus rhythm The dosage is 2 g intravenously over 1 minute followed by 2 gh infusion over 5 hours

Amiodarone (300 mg PO tid or 450-1500 mg IV over 2-24 h) has been used and has been reported to be associated with conversion to normal sinus rhythm The success rate was 40 at 3 days with oral dosing and 75 on day 1 with intravenous dosing however this has been evaluated in a very small number of patients

Cardioversion in MAT

Cardioversion is contraindicated in MAT Due to the multiple atrial foci direct

current (DC) cardioversion is not effective in restoring normal sinus rhythm

and can precipitate more dangerous arrhythmias

Surgical care

In patients who have persistent and recurrent episodes of MAT and problems with

rate control the AV node may be ablated using radiofrequency energy and a

permanent pacemaker implanted[22] This approach should be considered both for

symptomatic and hemodynamic improvement and to prevent the development of

tachycardia-mediated cardiomyopathy

Atrial flutter

A 50 years old diabetic hypertensive hyperthyroid male patient presented

with palpitation fatigue or poor exercise tolerance mild dyspneaand

presyncope On psysical examination pulse rate 150 min

Note negative sawtooth pattern of flutter waves in leads II III and aVF

Emergency Department Care

Assess airway breathing and circulation Hemodynamic concerns will dictate initial treatment

Treatment options for atrial flutter include the following

Antiarrhythmic drugsnodal agents

Direct-current (DC) cardioversion

Rapid atrial pacing to terminate atrial flutter

Blood pressure can be supported and rate controlled with medication

Anti coagulation therapy

Look for underlying causes At times treatment of the underlying disorder (eg thyroid disease valvular heart disease) is necessary to effect conversion to sinus rhythm

Cardioversion for unstable patients

If the patient is unstable (eg hypotension poor perfusion) synchronous direct-current (DC) cardioversion is commonly the initial treatment of choice

Cardioversion may be successful with energies as low as 25 Joules but since 100 Joules is virtually always successful this may be a reasonable initial shock strength

If the electrical shock results in atrial fibrillation (AF) a second shock at a higher energy level is used to restore normal sinus rhythm (NSR)

AV-His Bundle ablation

In patients who have failed antiarrhythmic therapy or who have failed RFA and who

are symptomatic palliative therapy with AV-His Bundle ablation can eliminate rapid

ventricular rates but it does require a permanent pacemaker to be placed as this

procedure creates third-degree heart block

Questions

• Slide 1
• Slide 2
• Slide 3
• Slide 4
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• Slide 10
• Slide 11
• Rate versus rhythm control which is superior
• Slide 13
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• Slide 18
• Slide 19
• Slide 20
• Slide 21
• Slide 22
• Slide 23
• Slide 24
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• Anti - coagulation therapy
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• Slide 42
• Slide 43
• Slide 44
• Slide 45
• Slide 46
• Slide 47
• Slide 48
• Slide 49
• Slide 50
• Slide 51
• Slide 52
• Slide 53
• Slide 54
• Slide 55
• Slide 56
• Slide 57
• Slide 58
• Slide 59
• Slide 60
• Slide 61
• Slide 62
• Slide 63
• Slide 64
• Slide 65
• Slide 66
• Slide 67
• Slide 68
• Slide 69
• Slide 70
• Slide 71
• Slide 72
• Slide 73
• Slide 74
• Slide 75
• Slide 76
• Slide 77
• Slide 78
• Slide 79
• Slide 80
• Slide 81

Atrioventricular Nodal Reentry Tachycardia (AVNRT) Treatment amp Management

AVNRT

Patient condition

Hemodynamic ally

stable Hemodynamic ally

unstble

Vagal maneuver

adenosine calcium channel blockers (eg diltiazem verapamil) beta-blockers and digitalis

Direct current (DC) synchronized cardioversion

To prevent recurrence

Drugs

Multifocal Atrial Tachycardia

A 52 years old male COPD patient presented with palpitation shortness of

breath chest pain and syncopal history On examination pulse is rapid

irregular amp 1st heart sound is variable

1 Irregular ventricular rate greater than 100 bpm

2 Organized and discrete P waves with at least 3 different morphologies in the same electrocardiographic lead

3 Irregular PP PR and RR intervals with an isoelectric baseline between the P waves

Treatment of MAT

Administer oxygen to maintain the saturation greater than 90 but avoid excessive oxygen in patients with known significant chronic obstructive pulmonary disease (COPD) This will avoid the theoretical problem of removing the hypoxic drive for ventilation which can result in increased carbon dioxide retention

Establish cardiac monitor blood pressure monitor and pulse oximetry

Assess for and treat the underlying cardiopulmonary process theophylline toxicity or metabolic abnormality

Administer bronchodilators and oxygen for treatment of decompensated COPD

activated charcoal andor charcoal hemoperfusion is the therapy for theophylline toxicity

When magnesium sulfate is administered to correct hypokalemia most patients convert to normal sinus rhythm

Avoid sedatives

Diltiazem and verapamil decrease the atrial activity and slow atrioventricular (AV) nodal conduction thereby decreasing ventricular rate but they do not return all patients to normal sinus rhythm

Diltiazem may be used as a 20-45 mg intravenous bolus and then as a 10-25 mgh continuous infusion

high-dose magnesium causes a significant decrease in the patients heart rate and conversion to normal sinus rhythm The dosage is 2 g intravenously over 1 minute followed by 2 gh infusion over 5 hours

Amiodarone (300 mg PO tid or 450-1500 mg IV over 2-24 h) has been used and has been reported to be associated with conversion to normal sinus rhythm The success rate was 40 at 3 days with oral dosing and 75 on day 1 with intravenous dosing however this has been evaluated in a very small number of patients

Cardioversion in MAT

Cardioversion is contraindicated in MAT Due to the multiple atrial foci direct

current (DC) cardioversion is not effective in restoring normal sinus rhythm

and can precipitate more dangerous arrhythmias

Surgical care

In patients who have persistent and recurrent episodes of MAT and problems with

rate control the AV node may be ablated using radiofrequency energy and a

permanent pacemaker implanted[22] This approach should be considered both for

symptomatic and hemodynamic improvement and to prevent the development of

tachycardia-mediated cardiomyopathy

Atrial flutter

A 50 years old diabetic hypertensive hyperthyroid male patient presented

with palpitation fatigue or poor exercise tolerance mild dyspneaand

presyncope On psysical examination pulse rate 150 min

Note negative sawtooth pattern of flutter waves in leads II III and aVF

Emergency Department Care

Assess airway breathing and circulation Hemodynamic concerns will dictate initial treatment

Treatment options for atrial flutter include the following

Antiarrhythmic drugsnodal agents

Direct-current (DC) cardioversion

Rapid atrial pacing to terminate atrial flutter

Blood pressure can be supported and rate controlled with medication

Anti coagulation therapy

Look for underlying causes At times treatment of the underlying disorder (eg thyroid disease valvular heart disease) is necessary to effect conversion to sinus rhythm

Cardioversion for unstable patients

If the patient is unstable (eg hypotension poor perfusion) synchronous direct-current (DC) cardioversion is commonly the initial treatment of choice

Cardioversion may be successful with energies as low as 25 Joules but since 100 Joules is virtually always successful this may be a reasonable initial shock strength

If the electrical shock results in atrial fibrillation (AF) a second shock at a higher energy level is used to restore normal sinus rhythm (NSR)

AV-His Bundle ablation

In patients who have failed antiarrhythmic therapy or who have failed RFA and who

are symptomatic palliative therapy with AV-His Bundle ablation can eliminate rapid

ventricular rates but it does require a permanent pacemaker to be placed as this

procedure creates third-degree heart block

Questions

• Slide 1
• Slide 2
• Slide 3
• Slide 4
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• Slide 10
• Slide 11
• Rate versus rhythm control which is superior
• Slide 13
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• Slide 18
• Slide 19
• Slide 20
• Slide 21
• Slide 22
• Slide 23
• Slide 24
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• Anti - coagulation therapy
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• Slide 42
• Slide 43
• Slide 44
• Slide 45
• Slide 46
• Slide 47
• Slide 48
• Slide 49
• Slide 50
• Slide 51
• Slide 52
• Slide 53
• Slide 54
• Slide 55
• Slide 56
• Slide 57
• Slide 58
• Slide 59
• Slide 60
• Slide 61
• Slide 62
• Slide 63
• Slide 64
• Slide 65
• Slide 66
• Slide 67
• Slide 68
• Slide 69
• Slide 70
• Slide 71
• Slide 72
• Slide 73
• Slide 74
• Slide 75
• Slide 76
• Slide 77
• Slide 78
• Slide 79
• Slide 80
• Slide 81

AVNRT

Patient condition

Hemodynamic ally

stable Hemodynamic ally

unstble

Vagal maneuver

adenosine calcium channel blockers (eg diltiazem verapamil) beta-blockers and digitalis

Direct current (DC) synchronized cardioversion

To prevent recurrence

Drugs

Multifocal Atrial Tachycardia

A 52 years old male COPD patient presented with palpitation shortness of

breath chest pain and syncopal history On examination pulse is rapid

irregular amp 1st heart sound is variable

1 Irregular ventricular rate greater than 100 bpm

2 Organized and discrete P waves with at least 3 different morphologies in the same electrocardiographic lead

3 Irregular PP PR and RR intervals with an isoelectric baseline between the P waves

Treatment of MAT

Administer oxygen to maintain the saturation greater than 90 but avoid excessive oxygen in patients with known significant chronic obstructive pulmonary disease (COPD) This will avoid the theoretical problem of removing the hypoxic drive for ventilation which can result in increased carbon dioxide retention

Establish cardiac monitor blood pressure monitor and pulse oximetry

Assess for and treat the underlying cardiopulmonary process theophylline toxicity or metabolic abnormality

Administer bronchodilators and oxygen for treatment of decompensated COPD

activated charcoal andor charcoal hemoperfusion is the therapy for theophylline toxicity

When magnesium sulfate is administered to correct hypokalemia most patients convert to normal sinus rhythm

Avoid sedatives

Diltiazem and verapamil decrease the atrial activity and slow atrioventricular (AV) nodal conduction thereby decreasing ventricular rate but they do not return all patients to normal sinus rhythm

Diltiazem may be used as a 20-45 mg intravenous bolus and then as a 10-25 mgh continuous infusion

high-dose magnesium causes a significant decrease in the patients heart rate and conversion to normal sinus rhythm The dosage is 2 g intravenously over 1 minute followed by 2 gh infusion over 5 hours

Amiodarone (300 mg PO tid or 450-1500 mg IV over 2-24 h) has been used and has been reported to be associated with conversion to normal sinus rhythm The success rate was 40 at 3 days with oral dosing and 75 on day 1 with intravenous dosing however this has been evaluated in a very small number of patients

Cardioversion in MAT

Cardioversion is contraindicated in MAT Due to the multiple atrial foci direct

current (DC) cardioversion is not effective in restoring normal sinus rhythm

and can precipitate more dangerous arrhythmias

Surgical care

In patients who have persistent and recurrent episodes of MAT and problems with

rate control the AV node may be ablated using radiofrequency energy and a

permanent pacemaker implanted[22] This approach should be considered both for

symptomatic and hemodynamic improvement and to prevent the development of

tachycardia-mediated cardiomyopathy

Atrial flutter

A 50 years old diabetic hypertensive hyperthyroid male patient presented

with palpitation fatigue or poor exercise tolerance mild dyspneaand

presyncope On psysical examination pulse rate 150 min

Note negative sawtooth pattern of flutter waves in leads II III and aVF

Emergency Department Care

Assess airway breathing and circulation Hemodynamic concerns will dictate initial treatment

Treatment options for atrial flutter include the following

Antiarrhythmic drugsnodal agents

Direct-current (DC) cardioversion

Rapid atrial pacing to terminate atrial flutter

Blood pressure can be supported and rate controlled with medication

Anti coagulation therapy

Look for underlying causes At times treatment of the underlying disorder (eg thyroid disease valvular heart disease) is necessary to effect conversion to sinus rhythm

Cardioversion for unstable patients

If the patient is unstable (eg hypotension poor perfusion) synchronous direct-current (DC) cardioversion is commonly the initial treatment of choice

Cardioversion may be successful with energies as low as 25 Joules but since 100 Joules is virtually always successful this may be a reasonable initial shock strength

If the electrical shock results in atrial fibrillation (AF) a second shock at a higher energy level is used to restore normal sinus rhythm (NSR)

AV-His Bundle ablation

In patients who have failed antiarrhythmic therapy or who have failed RFA and who

are symptomatic palliative therapy with AV-His Bundle ablation can eliminate rapid

ventricular rates but it does require a permanent pacemaker to be placed as this

procedure creates third-degree heart block

Questions

• Slide 1
• Slide 2
• Slide 3
• Slide 4
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• Slide 10
• Slide 11
• Rate versus rhythm control which is superior
• Slide 13
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• Slide 18
• Slide 19
• Slide 20
• Slide 21
• Slide 22
• Slide 23
• Slide 24
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• Anti - coagulation therapy
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• Slide 42
• Slide 43
• Slide 44
• Slide 45
• Slide 46
• Slide 47
• Slide 48
• Slide 49
• Slide 50
• Slide 51
• Slide 52
• Slide 53
• Slide 54
• Slide 55
• Slide 56
• Slide 57
• Slide 58
• Slide 59
• Slide 60
• Slide 61
• Slide 62
• Slide 63
• Slide 64
• Slide 65
• Slide 66
• Slide 67
• Slide 68
• Slide 69
• Slide 70
• Slide 71
• Slide 72
• Slide 73
• Slide 74
• Slide 75
• Slide 76
• Slide 77
• Slide 78
• Slide 79
• Slide 80
• Slide 81

Multifocal Atrial Tachycardia

A 52 years old male COPD patient presented with palpitation shortness of

breath chest pain and syncopal history On examination pulse is rapid

irregular amp 1st heart sound is variable

1 Irregular ventricular rate greater than 100 bpm

2 Organized and discrete P waves with at least 3 different morphologies in the same electrocardiographic lead

3 Irregular PP PR and RR intervals with an isoelectric baseline between the P waves

Treatment of MAT

Administer oxygen to maintain the saturation greater than 90 but avoid excessive oxygen in patients with known significant chronic obstructive pulmonary disease (COPD) This will avoid the theoretical problem of removing the hypoxic drive for ventilation which can result in increased carbon dioxide retention

Establish cardiac monitor blood pressure monitor and pulse oximetry

Assess for and treat the underlying cardiopulmonary process theophylline toxicity or metabolic abnormality

Administer bronchodilators and oxygen for treatment of decompensated COPD

activated charcoal andor charcoal hemoperfusion is the therapy for theophylline toxicity

When magnesium sulfate is administered to correct hypokalemia most patients convert to normal sinus rhythm

Avoid sedatives

Diltiazem and verapamil decrease the atrial activity and slow atrioventricular (AV) nodal conduction thereby decreasing ventricular rate but they do not return all patients to normal sinus rhythm

Diltiazem may be used as a 20-45 mg intravenous bolus and then as a 10-25 mgh continuous infusion

high-dose magnesium causes a significant decrease in the patients heart rate and conversion to normal sinus rhythm The dosage is 2 g intravenously over 1 minute followed by 2 gh infusion over 5 hours

Amiodarone (300 mg PO tid or 450-1500 mg IV over 2-24 h) has been used and has been reported to be associated with conversion to normal sinus rhythm The success rate was 40 at 3 days with oral dosing and 75 on day 1 with intravenous dosing however this has been evaluated in a very small number of patients

Cardioversion in MAT

Cardioversion is contraindicated in MAT Due to the multiple atrial foci direct

current (DC) cardioversion is not effective in restoring normal sinus rhythm

and can precipitate more dangerous arrhythmias

Surgical care

In patients who have persistent and recurrent episodes of MAT and problems with

rate control the AV node may be ablated using radiofrequency energy and a

permanent pacemaker implanted[22] This approach should be considered both for

symptomatic and hemodynamic improvement and to prevent the development of

tachycardia-mediated cardiomyopathy

Atrial flutter

A 50 years old diabetic hypertensive hyperthyroid male patient presented

with palpitation fatigue or poor exercise tolerance mild dyspneaand

presyncope On psysical examination pulse rate 150 min

Note negative sawtooth pattern of flutter waves in leads II III and aVF

Emergency Department Care

Assess airway breathing and circulation Hemodynamic concerns will dictate initial treatment

Treatment options for atrial flutter include the following

Antiarrhythmic drugsnodal agents

Direct-current (DC) cardioversion

Rapid atrial pacing to terminate atrial flutter

Blood pressure can be supported and rate controlled with medication

Anti coagulation therapy

Look for underlying causes At times treatment of the underlying disorder (eg thyroid disease valvular heart disease) is necessary to effect conversion to sinus rhythm

Cardioversion for unstable patients

If the patient is unstable (eg hypotension poor perfusion) synchronous direct-current (DC) cardioversion is commonly the initial treatment of choice

Cardioversion may be successful with energies as low as 25 Joules but since 100 Joules is virtually always successful this may be a reasonable initial shock strength

If the electrical shock results in atrial fibrillation (AF) a second shock at a higher energy level is used to restore normal sinus rhythm (NSR)

AV-His Bundle ablation

In patients who have failed antiarrhythmic therapy or who have failed RFA and who

are symptomatic palliative therapy with AV-His Bundle ablation can eliminate rapid

ventricular rates but it does require a permanent pacemaker to be placed as this

procedure creates third-degree heart block

Questions

• Slide 1
• Slide 2
• Slide 3
• Slide 4
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• Slide 10
• Slide 11
• Rate versus rhythm control which is superior
• Slide 13
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• Slide 18
• Slide 19
• Slide 20
• Slide 21
• Slide 22
• Slide 23
• Slide 24
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• Anti - coagulation therapy
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• Slide 42
• Slide 43
• Slide 44
• Slide 45
• Slide 46
• Slide 47
• Slide 48
• Slide 49
• Slide 50
• Slide 51
• Slide 52
• Slide 53
• Slide 54
• Slide 55
• Slide 56
• Slide 57
• Slide 58
• Slide 59
• Slide 60
• Slide 61
• Slide 62
• Slide 63
• Slide 64
• Slide 65
• Slide 66
• Slide 67
• Slide 68
• Slide 69
• Slide 70
• Slide 71
• Slide 72
• Slide 73
• Slide 74
• Slide 75
• Slide 76
• Slide 77
• Slide 78
• Slide 79
• Slide 80
• Slide 81

A 52 years old male COPD patient presented with palpitation shortness of

breath chest pain and syncopal history On examination pulse is rapid

irregular amp 1st heart sound is variable

1 Irregular ventricular rate greater than 100 bpm

2 Organized and discrete P waves with at least 3 different morphologies in the same electrocardiographic lead

3 Irregular PP PR and RR intervals with an isoelectric baseline between the P waves

Treatment of MAT

Administer oxygen to maintain the saturation greater than 90 but avoid excessive oxygen in patients with known significant chronic obstructive pulmonary disease (COPD) This will avoid the theoretical problem of removing the hypoxic drive for ventilation which can result in increased carbon dioxide retention

Establish cardiac monitor blood pressure monitor and pulse oximetry

Assess for and treat the underlying cardiopulmonary process theophylline toxicity or metabolic abnormality

Administer bronchodilators and oxygen for treatment of decompensated COPD

activated charcoal andor charcoal hemoperfusion is the therapy for theophylline toxicity

When magnesium sulfate is administered to correct hypokalemia most patients convert to normal sinus rhythm

Avoid sedatives

Diltiazem and verapamil decrease the atrial activity and slow atrioventricular (AV) nodal conduction thereby decreasing ventricular rate but they do not return all patients to normal sinus rhythm

Diltiazem may be used as a 20-45 mg intravenous bolus and then as a 10-25 mgh continuous infusion

high-dose magnesium causes a significant decrease in the patients heart rate and conversion to normal sinus rhythm The dosage is 2 g intravenously over 1 minute followed by 2 gh infusion over 5 hours

Amiodarone (300 mg PO tid or 450-1500 mg IV over 2-24 h) has been used and has been reported to be associated with conversion to normal sinus rhythm The success rate was 40 at 3 days with oral dosing and 75 on day 1 with intravenous dosing however this has been evaluated in a very small number of patients

Cardioversion in MAT

Cardioversion is contraindicated in MAT Due to the multiple atrial foci direct

current (DC) cardioversion is not effective in restoring normal sinus rhythm

and can precipitate more dangerous arrhythmias

Surgical care

In patients who have persistent and recurrent episodes of MAT and problems with

rate control the AV node may be ablated using radiofrequency energy and a

permanent pacemaker implanted[22] This approach should be considered both for

symptomatic and hemodynamic improvement and to prevent the development of

tachycardia-mediated cardiomyopathy

Atrial flutter

A 50 years old diabetic hypertensive hyperthyroid male patient presented

with palpitation fatigue or poor exercise tolerance mild dyspneaand

presyncope On psysical examination pulse rate 150 min

Note negative sawtooth pattern of flutter waves in leads II III and aVF

Emergency Department Care

Assess airway breathing and circulation Hemodynamic concerns will dictate initial treatment

Treatment options for atrial flutter include the following

Antiarrhythmic drugsnodal agents

Direct-current (DC) cardioversion

Rapid atrial pacing to terminate atrial flutter

Blood pressure can be supported and rate controlled with medication

Anti coagulation therapy

Look for underlying causes At times treatment of the underlying disorder (eg thyroid disease valvular heart disease) is necessary to effect conversion to sinus rhythm

Cardioversion for unstable patients

If the patient is unstable (eg hypotension poor perfusion) synchronous direct-current (DC) cardioversion is commonly the initial treatment of choice

Cardioversion may be successful with energies as low as 25 Joules but since 100 Joules is virtually always successful this may be a reasonable initial shock strength

If the electrical shock results in atrial fibrillation (AF) a second shock at a higher energy level is used to restore normal sinus rhythm (NSR)

AV-His Bundle ablation

In patients who have failed antiarrhythmic therapy or who have failed RFA and who

are symptomatic palliative therapy with AV-His Bundle ablation can eliminate rapid

ventricular rates but it does require a permanent pacemaker to be placed as this

procedure creates third-degree heart block

Questions

• Slide 1
• Slide 2
• Slide 3
• Slide 4
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• Slide 10
• Slide 11
• Rate versus rhythm control which is superior
• Slide 13
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• Slide 18
• Slide 19
• Slide 20
• Slide 21
• Slide 22
• Slide 23
• Slide 24
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• Anti - coagulation therapy
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• Slide 42
• Slide 43
• Slide 44
• Slide 45
• Slide 46
• Slide 47
• Slide 48
• Slide 49
• Slide 50
• Slide 51
• Slide 52
• Slide 53
• Slide 54
• Slide 55
• Slide 56
• Slide 57
• Slide 58
• Slide 59
• Slide 60
• Slide 61
• Slide 62
• Slide 63
• Slide 64
• Slide 65
• Slide 66
• Slide 67
• Slide 68
• Slide 69
• Slide 70
• Slide 71
• Slide 72
• Slide 73
• Slide 74
• Slide 75
• Slide 76
• Slide 77
• Slide 78
• Slide 79
• Slide 80
• Slide 81

1 Irregular ventricular rate greater than 100 bpm

2 Organized and discrete P waves with at least 3 different morphologies in the same electrocardiographic lead

3 Irregular PP PR and RR intervals with an isoelectric baseline between the P waves

Treatment of MAT

Administer oxygen to maintain the saturation greater than 90 but avoid excessive oxygen in patients with known significant chronic obstructive pulmonary disease (COPD) This will avoid the theoretical problem of removing the hypoxic drive for ventilation which can result in increased carbon dioxide retention

Establish cardiac monitor blood pressure monitor and pulse oximetry

Assess for and treat the underlying cardiopulmonary process theophylline toxicity or metabolic abnormality

Administer bronchodilators and oxygen for treatment of decompensated COPD

activated charcoal andor charcoal hemoperfusion is the therapy for theophylline toxicity

When magnesium sulfate is administered to correct hypokalemia most patients convert to normal sinus rhythm

Avoid sedatives

Diltiazem and verapamil decrease the atrial activity and slow atrioventricular (AV) nodal conduction thereby decreasing ventricular rate but they do not return all patients to normal sinus rhythm

Diltiazem may be used as a 20-45 mg intravenous bolus and then as a 10-25 mgh continuous infusion

high-dose magnesium causes a significant decrease in the patients heart rate and conversion to normal sinus rhythm The dosage is 2 g intravenously over 1 minute followed by 2 gh infusion over 5 hours

Amiodarone (300 mg PO tid or 450-1500 mg IV over 2-24 h) has been used and has been reported to be associated with conversion to normal sinus rhythm The success rate was 40 at 3 days with oral dosing and 75 on day 1 with intravenous dosing however this has been evaluated in a very small number of patients

Cardioversion in MAT

Cardioversion is contraindicated in MAT Due to the multiple atrial foci direct

current (DC) cardioversion is not effective in restoring normal sinus rhythm

and can precipitate more dangerous arrhythmias

Surgical care

In patients who have persistent and recurrent episodes of MAT and problems with

rate control the AV node may be ablated using radiofrequency energy and a

permanent pacemaker implanted[22] This approach should be considered both for

symptomatic and hemodynamic improvement and to prevent the development of

tachycardia-mediated cardiomyopathy

Atrial flutter

A 50 years old diabetic hypertensive hyperthyroid male patient presented

with palpitation fatigue or poor exercise tolerance mild dyspneaand

presyncope On psysical examination pulse rate 150 min

Note negative sawtooth pattern of flutter waves in leads II III and aVF

Emergency Department Care

Assess airway breathing and circulation Hemodynamic concerns will dictate initial treatment

Treatment options for atrial flutter include the following

Antiarrhythmic drugsnodal agents

Direct-current (DC) cardioversion

Rapid atrial pacing to terminate atrial flutter

Blood pressure can be supported and rate controlled with medication

Anti coagulation therapy

Look for underlying causes At times treatment of the underlying disorder (eg thyroid disease valvular heart disease) is necessary to effect conversion to sinus rhythm

Cardioversion for unstable patients

If the patient is unstable (eg hypotension poor perfusion) synchronous direct-current (DC) cardioversion is commonly the initial treatment of choice

Cardioversion may be successful with energies as low as 25 Joules but since 100 Joules is virtually always successful this may be a reasonable initial shock strength

If the electrical shock results in atrial fibrillation (AF) a second shock at a higher energy level is used to restore normal sinus rhythm (NSR)

AV-His Bundle ablation

In patients who have failed antiarrhythmic therapy or who have failed RFA and who

are symptomatic palliative therapy with AV-His Bundle ablation can eliminate rapid

ventricular rates but it does require a permanent pacemaker to be placed as this

procedure creates third-degree heart block

Questions

• Slide 1
• Slide 2
• Slide 3
• Slide 4
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• Slide 10
• Slide 11
• Rate versus rhythm control which is superior
• Slide 13
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• Slide 18
• Slide 19
• Slide 20
• Slide 21
• Slide 22
• Slide 23
• Slide 24
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• Anti - coagulation therapy
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• Slide 42
• Slide 43
• Slide 44
• Slide 45
• Slide 46
• Slide 47
• Slide 48
• Slide 49
• Slide 50
• Slide 51
• Slide 52
• Slide 53
• Slide 54
• Slide 55
• Slide 56
• Slide 57
• Slide 58
• Slide 59
• Slide 60
• Slide 61
• Slide 62
• Slide 63
• Slide 64
• Slide 65
• Slide 66
• Slide 67
• Slide 68
• Slide 69
• Slide 70
• Slide 71
• Slide 72
• Slide 73
• Slide 74
• Slide 75
• Slide 76
• Slide 77
• Slide 78
• Slide 79
• Slide 80
• Slide 81

Treatment of MAT

Administer oxygen to maintain the saturation greater than 90 but avoid excessive oxygen in patients with known significant chronic obstructive pulmonary disease (COPD) This will avoid the theoretical problem of removing the hypoxic drive for ventilation which can result in increased carbon dioxide retention

Establish cardiac monitor blood pressure monitor and pulse oximetry

Assess for and treat the underlying cardiopulmonary process theophylline toxicity or metabolic abnormality

Administer bronchodilators and oxygen for treatment of decompensated COPD

activated charcoal andor charcoal hemoperfusion is the therapy for theophylline toxicity

When magnesium sulfate is administered to correct hypokalemia most patients convert to normal sinus rhythm

Avoid sedatives

Diltiazem and verapamil decrease the atrial activity and slow atrioventricular (AV) nodal conduction thereby decreasing ventricular rate but they do not return all patients to normal sinus rhythm

Diltiazem may be used as a 20-45 mg intravenous bolus and then as a 10-25 mgh continuous infusion

high-dose magnesium causes a significant decrease in the patients heart rate and conversion to normal sinus rhythm The dosage is 2 g intravenously over 1 minute followed by 2 gh infusion over 5 hours

Amiodarone (300 mg PO tid or 450-1500 mg IV over 2-24 h) has been used and has been reported to be associated with conversion to normal sinus rhythm The success rate was 40 at 3 days with oral dosing and 75 on day 1 with intravenous dosing however this has been evaluated in a very small number of patients

Cardioversion in MAT

Cardioversion is contraindicated in MAT Due to the multiple atrial foci direct

current (DC) cardioversion is not effective in restoring normal sinus rhythm

and can precipitate more dangerous arrhythmias

Surgical care

In patients who have persistent and recurrent episodes of MAT and problems with

rate control the AV node may be ablated using radiofrequency energy and a

permanent pacemaker implanted[22] This approach should be considered both for

symptomatic and hemodynamic improvement and to prevent the development of

tachycardia-mediated cardiomyopathy

Atrial flutter

A 50 years old diabetic hypertensive hyperthyroid male patient presented

with palpitation fatigue or poor exercise tolerance mild dyspneaand

presyncope On psysical examination pulse rate 150 min

Note negative sawtooth pattern of flutter waves in leads II III and aVF

Emergency Department Care

Assess airway breathing and circulation Hemodynamic concerns will dictate initial treatment

Treatment options for atrial flutter include the following

Antiarrhythmic drugsnodal agents

Direct-current (DC) cardioversion

Rapid atrial pacing to terminate atrial flutter

Blood pressure can be supported and rate controlled with medication

Anti coagulation therapy

Look for underlying causes At times treatment of the underlying disorder (eg thyroid disease valvular heart disease) is necessary to effect conversion to sinus rhythm

Cardioversion for unstable patients

If the patient is unstable (eg hypotension poor perfusion) synchronous direct-current (DC) cardioversion is commonly the initial treatment of choice

Cardioversion may be successful with energies as low as 25 Joules but since 100 Joules is virtually always successful this may be a reasonable initial shock strength

If the electrical shock results in atrial fibrillation (AF) a second shock at a higher energy level is used to restore normal sinus rhythm (NSR)

AV-His Bundle ablation

In patients who have failed antiarrhythmic therapy or who have failed RFA and who

are symptomatic palliative therapy with AV-His Bundle ablation can eliminate rapid

ventricular rates but it does require a permanent pacemaker to be placed as this

procedure creates third-degree heart block

Questions

• Slide 1
• Slide 2
• Slide 3
• Slide 4
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• Slide 10
• Slide 11
• Rate versus rhythm control which is superior
• Slide 13
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• Slide 18
• Slide 19
• Slide 20
• Slide 21
• Slide 22
• Slide 23
• Slide 24
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• Anti - coagulation therapy
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• Slide 42
• Slide 43
• Slide 44
• Slide 45
• Slide 46
• Slide 47
• Slide 48
• Slide 49
• Slide 50
• Slide 51
• Slide 52
• Slide 53
• Slide 54
• Slide 55
• Slide 56
• Slide 57
• Slide 58
• Slide 59
• Slide 60
• Slide 61
• Slide 62
• Slide 63
• Slide 64
• Slide 65
• Slide 66
• Slide 67
• Slide 68
• Slide 69
• Slide 70
• Slide 71
• Slide 72
• Slide 73
• Slide 74
• Slide 75
• Slide 76
• Slide 77
• Slide 78
• Slide 79
• Slide 80
• Slide 81

Diltiazem and verapamil decrease the atrial activity and slow atrioventricular (AV) nodal conduction thereby decreasing ventricular rate but they do not return all patients to normal sinus rhythm

Diltiazem may be used as a 20-45 mg intravenous bolus and then as a 10-25 mgh continuous infusion

high-dose magnesium causes a significant decrease in the patients heart rate and conversion to normal sinus rhythm The dosage is 2 g intravenously over 1 minute followed by 2 gh infusion over 5 hours

Amiodarone (300 mg PO tid or 450-1500 mg IV over 2-24 h) has been used and has been reported to be associated with conversion to normal sinus rhythm The success rate was 40 at 3 days with oral dosing and 75 on day 1 with intravenous dosing however this has been evaluated in a very small number of patients

Cardioversion in MAT

Cardioversion is contraindicated in MAT Due to the multiple atrial foci direct

current (DC) cardioversion is not effective in restoring normal sinus rhythm

and can precipitate more dangerous arrhythmias

Surgical care

In patients who have persistent and recurrent episodes of MAT and problems with

rate control the AV node may be ablated using radiofrequency energy and a

permanent pacemaker implanted[22] This approach should be considered both for

symptomatic and hemodynamic improvement and to prevent the development of

tachycardia-mediated cardiomyopathy

Atrial flutter

A 50 years old diabetic hypertensive hyperthyroid male patient presented

with palpitation fatigue or poor exercise tolerance mild dyspneaand

presyncope On psysical examination pulse rate 150 min

Note negative sawtooth pattern of flutter waves in leads II III and aVF

Emergency Department Care

Assess airway breathing and circulation Hemodynamic concerns will dictate initial treatment

Treatment options for atrial flutter include the following

Antiarrhythmic drugsnodal agents

Direct-current (DC) cardioversion

Rapid atrial pacing to terminate atrial flutter

Blood pressure can be supported and rate controlled with medication

Anti coagulation therapy

Look for underlying causes At times treatment of the underlying disorder (eg thyroid disease valvular heart disease) is necessary to effect conversion to sinus rhythm

Cardioversion for unstable patients

If the patient is unstable (eg hypotension poor perfusion) synchronous direct-current (DC) cardioversion is commonly the initial treatment of choice

Cardioversion may be successful with energies as low as 25 Joules but since 100 Joules is virtually always successful this may be a reasonable initial shock strength

If the electrical shock results in atrial fibrillation (AF) a second shock at a higher energy level is used to restore normal sinus rhythm (NSR)

AV-His Bundle ablation

In patients who have failed antiarrhythmic therapy or who have failed RFA and who

are symptomatic palliative therapy with AV-His Bundle ablation can eliminate rapid

ventricular rates but it does require a permanent pacemaker to be placed as this

procedure creates third-degree heart block

Questions

• Slide 1
• Slide 2
• Slide 3
• Slide 4
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• Slide 10
• Slide 11
• Rate versus rhythm control which is superior
• Slide 13
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• Slide 18
• Slide 19
• Slide 20
• Slide 21
• Slide 22
• Slide 23
• Slide 24
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• Anti - coagulation therapy
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• Slide 42
• Slide 43
• Slide 44
• Slide 45
• Slide 46
• Slide 47
• Slide 48
• Slide 49
• Slide 50
• Slide 51
• Slide 52
• Slide 53
• Slide 54
• Slide 55
• Slide 56
• Slide 57
• Slide 58
• Slide 59
• Slide 60
• Slide 61
• Slide 62
• Slide 63
• Slide 64
• Slide 65
• Slide 66
• Slide 67
• Slide 68
• Slide 69
• Slide 70
• Slide 71
• Slide 72
• Slide 73
• Slide 74
• Slide 75
• Slide 76
• Slide 77
• Slide 78
• Slide 79
• Slide 80
• Slide 81

Cardioversion in MAT

Cardioversion is contraindicated in MAT Due to the multiple atrial foci direct

current (DC) cardioversion is not effective in restoring normal sinus rhythm

and can precipitate more dangerous arrhythmias

Surgical care

In patients who have persistent and recurrent episodes of MAT and problems with

rate control the AV node may be ablated using radiofrequency energy and a

permanent pacemaker implanted[22] This approach should be considered both for

symptomatic and hemodynamic improvement and to prevent the development of

tachycardia-mediated cardiomyopathy

Atrial flutter

A 50 years old diabetic hypertensive hyperthyroid male patient presented

with palpitation fatigue or poor exercise tolerance mild dyspneaand

presyncope On psysical examination pulse rate 150 min

Note negative sawtooth pattern of flutter waves in leads II III and aVF

Emergency Department Care

Assess airway breathing and circulation Hemodynamic concerns will dictate initial treatment

Treatment options for atrial flutter include the following

Antiarrhythmic drugsnodal agents

Direct-current (DC) cardioversion

Rapid atrial pacing to terminate atrial flutter

Blood pressure can be supported and rate controlled with medication

Anti coagulation therapy

Look for underlying causes At times treatment of the underlying disorder (eg thyroid disease valvular heart disease) is necessary to effect conversion to sinus rhythm

Cardioversion for unstable patients

If the patient is unstable (eg hypotension poor perfusion) synchronous direct-current (DC) cardioversion is commonly the initial treatment of choice

Cardioversion may be successful with energies as low as 25 Joules but since 100 Joules is virtually always successful this may be a reasonable initial shock strength

If the electrical shock results in atrial fibrillation (AF) a second shock at a higher energy level is used to restore normal sinus rhythm (NSR)

AV-His Bundle ablation

In patients who have failed antiarrhythmic therapy or who have failed RFA and who

are symptomatic palliative therapy with AV-His Bundle ablation can eliminate rapid

ventricular rates but it does require a permanent pacemaker to be placed as this

procedure creates third-degree heart block

Questions

• Slide 1
• Slide 2
• Slide 3
• Slide 4
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• Slide 10
• Slide 11
• Rate versus rhythm control which is superior
• Slide 13
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• Slide 18
• Slide 19
• Slide 20
• Slide 21
• Slide 22
• Slide 23
• Slide 24
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• Anti - coagulation therapy
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• Slide 42
• Slide 43
• Slide 44
• Slide 45
• Slide 46
• Slide 47
• Slide 48
• Slide 49
• Slide 50
• Slide 51
• Slide 52
• Slide 53
• Slide 54
• Slide 55
• Slide 56
• Slide 57
• Slide 58
• Slide 59
• Slide 60
• Slide 61
• Slide 62
• Slide 63
• Slide 64
• Slide 65
• Slide 66
• Slide 67
• Slide 68
• Slide 69
• Slide 70
• Slide 71
• Slide 72
• Slide 73
• Slide 74
• Slide 75
• Slide 76
• Slide 77
• Slide 78
• Slide 79
• Slide 80
• Slide 81

Surgical care

In patients who have persistent and recurrent episodes of MAT and problems with

rate control the AV node may be ablated using radiofrequency energy and a

permanent pacemaker implanted[22] This approach should be considered both for

symptomatic and hemodynamic improvement and to prevent the development of

tachycardia-mediated cardiomyopathy

Atrial flutter

A 50 years old diabetic hypertensive hyperthyroid male patient presented

with palpitation fatigue or poor exercise tolerance mild dyspneaand

presyncope On psysical examination pulse rate 150 min

Note negative sawtooth pattern of flutter waves in leads II III and aVF

Emergency Department Care

Assess airway breathing and circulation Hemodynamic concerns will dictate initial treatment

Treatment options for atrial flutter include the following

Antiarrhythmic drugsnodal agents

Direct-current (DC) cardioversion

Rapid atrial pacing to terminate atrial flutter

Blood pressure can be supported and rate controlled with medication

Anti coagulation therapy

Look for underlying causes At times treatment of the underlying disorder (eg thyroid disease valvular heart disease) is necessary to effect conversion to sinus rhythm

Cardioversion for unstable patients

If the patient is unstable (eg hypotension poor perfusion) synchronous direct-current (DC) cardioversion is commonly the initial treatment of choice

Cardioversion may be successful with energies as low as 25 Joules but since 100 Joules is virtually always successful this may be a reasonable initial shock strength

If the electrical shock results in atrial fibrillation (AF) a second shock at a higher energy level is used to restore normal sinus rhythm (NSR)

AV-His Bundle ablation

In patients who have failed antiarrhythmic therapy or who have failed RFA and who

are symptomatic palliative therapy with AV-His Bundle ablation can eliminate rapid

ventricular rates but it does require a permanent pacemaker to be placed as this

procedure creates third-degree heart block

Questions

• Slide 1
• Slide 2
• Slide 3
• Slide 4
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• Slide 10
• Slide 11
• Rate versus rhythm control which is superior
• Slide 13
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• Slide 18
• Slide 19
• Slide 20
• Slide 21
• Slide 22
• Slide 23
• Slide 24
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• Anti - coagulation therapy
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• Slide 42
• Slide 43
• Slide 44
• Slide 45
• Slide 46
• Slide 47
• Slide 48
• Slide 49
• Slide 50
• Slide 51
• Slide 52
• Slide 53
• Slide 54
• Slide 55
• Slide 56
• Slide 57
• Slide 58
• Slide 59
• Slide 60
• Slide 61
• Slide 62
• Slide 63
• Slide 64
• Slide 65
• Slide 66
• Slide 67
• Slide 68
• Slide 69
• Slide 70
• Slide 71
• Slide 72
• Slide 73
• Slide 74
• Slide 75
• Slide 76
• Slide 77
• Slide 78
• Slide 79
• Slide 80
• Slide 81

Atrial flutter

A 50 years old diabetic hypertensive hyperthyroid male patient presented

with palpitation fatigue or poor exercise tolerance mild dyspneaand

presyncope On psysical examination pulse rate 150 min

Note negative sawtooth pattern of flutter waves in leads II III and aVF

Emergency Department Care

Assess airway breathing and circulation Hemodynamic concerns will dictate initial treatment

Treatment options for atrial flutter include the following

Antiarrhythmic drugsnodal agents

Direct-current (DC) cardioversion

Rapid atrial pacing to terminate atrial flutter

Blood pressure can be supported and rate controlled with medication

Anti coagulation therapy

Look for underlying causes At times treatment of the underlying disorder (eg thyroid disease valvular heart disease) is necessary to effect conversion to sinus rhythm

Cardioversion for unstable patients

If the patient is unstable (eg hypotension poor perfusion) synchronous direct-current (DC) cardioversion is commonly the initial treatment of choice

Cardioversion may be successful with energies as low as 25 Joules but since 100 Joules is virtually always successful this may be a reasonable initial shock strength

If the electrical shock results in atrial fibrillation (AF) a second shock at a higher energy level is used to restore normal sinus rhythm (NSR)

AV-His Bundle ablation

In patients who have failed antiarrhythmic therapy or who have failed RFA and who

are symptomatic palliative therapy with AV-His Bundle ablation can eliminate rapid

ventricular rates but it does require a permanent pacemaker to be placed as this

procedure creates third-degree heart block

Questions

• Slide 1
• Slide 2
• Slide 3
• Slide 4
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• Slide 10
• Slide 11
• Rate versus rhythm control which is superior
• Slide 13
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• Slide 18
• Slide 19
• Slide 20
• Slide 21
• Slide 22
• Slide 23
• Slide 24
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• Anti - coagulation therapy
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• Slide 42
• Slide 43
• Slide 44
• Slide 45
• Slide 46
• Slide 47
• Slide 48
• Slide 49
• Slide 50
• Slide 51
• Slide 52
• Slide 53
• Slide 54
• Slide 55
• Slide 56
• Slide 57
• Slide 58
• Slide 59
• Slide 60
• Slide 61
• Slide 62
• Slide 63
• Slide 64
• Slide 65
• Slide 66
• Slide 67
• Slide 68
• Slide 69
• Slide 70
• Slide 71
• Slide 72
• Slide 73
• Slide 74
• Slide 75
• Slide 76
• Slide 77
• Slide 78
• Slide 79
• Slide 80
• Slide 81

A 50 years old diabetic hypertensive hyperthyroid male patient presented

with palpitation fatigue or poor exercise tolerance mild dyspneaand

presyncope On psysical examination pulse rate 150 min

Note negative sawtooth pattern of flutter waves in leads II III and aVF

Emergency Department Care

Assess airway breathing and circulation Hemodynamic concerns will dictate initial treatment

Treatment options for atrial flutter include the following

Antiarrhythmic drugsnodal agents

Direct-current (DC) cardioversion

Rapid atrial pacing to terminate atrial flutter

Blood pressure can be supported and rate controlled with medication

Anti coagulation therapy

Look for underlying causes At times treatment of the underlying disorder (eg thyroid disease valvular heart disease) is necessary to effect conversion to sinus rhythm

Cardioversion for unstable patients

If the patient is unstable (eg hypotension poor perfusion) synchronous direct-current (DC) cardioversion is commonly the initial treatment of choice

Cardioversion may be successful with energies as low as 25 Joules but since 100 Joules is virtually always successful this may be a reasonable initial shock strength

If the electrical shock results in atrial fibrillation (AF) a second shock at a higher energy level is used to restore normal sinus rhythm (NSR)

AV-His Bundle ablation

In patients who have failed antiarrhythmic therapy or who have failed RFA and who

are symptomatic palliative therapy with AV-His Bundle ablation can eliminate rapid

ventricular rates but it does require a permanent pacemaker to be placed as this

procedure creates third-degree heart block

Questions

• Slide 1
• Slide 2
• Slide 3
• Slide 4
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• Slide 10
• Slide 11
• Rate versus rhythm control which is superior
• Slide 13
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• Slide 18
• Slide 19
• Slide 20
• Slide 21
• Slide 22
• Slide 23
• Slide 24
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• Anti - coagulation therapy
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• Slide 42
• Slide 43
• Slide 44
• Slide 45
• Slide 46
• Slide 47
• Slide 48
• Slide 49
• Slide 50
• Slide 51
• Slide 52
• Slide 53
• Slide 54
• Slide 55
• Slide 56
• Slide 57
• Slide 58
• Slide 59
• Slide 60
• Slide 61
• Slide 62
• Slide 63
• Slide 64
• Slide 65
• Slide 66
• Slide 67
• Slide 68
• Slide 69
• Slide 70
• Slide 71
• Slide 72
• Slide 73
• Slide 74
• Slide 75
• Slide 76
• Slide 77
• Slide 78
• Slide 79
• Slide 80
• Slide 81

Note negative sawtooth pattern of flutter waves in leads II III and aVF

Emergency Department Care

Assess airway breathing and circulation Hemodynamic concerns will dictate initial treatment

Treatment options for atrial flutter include the following

Antiarrhythmic drugsnodal agents

Direct-current (DC) cardioversion

Rapid atrial pacing to terminate atrial flutter

Blood pressure can be supported and rate controlled with medication

Anti coagulation therapy

Look for underlying causes At times treatment of the underlying disorder (eg thyroid disease valvular heart disease) is necessary to effect conversion to sinus rhythm

Cardioversion for unstable patients

If the patient is unstable (eg hypotension poor perfusion) synchronous direct-current (DC) cardioversion is commonly the initial treatment of choice

Cardioversion may be successful with energies as low as 25 Joules but since 100 Joules is virtually always successful this may be a reasonable initial shock strength

If the electrical shock results in atrial fibrillation (AF) a second shock at a higher energy level is used to restore normal sinus rhythm (NSR)

AV-His Bundle ablation

In patients who have failed antiarrhythmic therapy or who have failed RFA and who

are symptomatic palliative therapy with AV-His Bundle ablation can eliminate rapid

ventricular rates but it does require a permanent pacemaker to be placed as this

procedure creates third-degree heart block

Questions

• Slide 1
• Slide 2
• Slide 3
• Slide 4
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• Slide 10
• Slide 11
• Rate versus rhythm control which is superior
• Slide 13
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• Slide 18
• Slide 19
• Slide 20
• Slide 21
• Slide 22
• Slide 23
• Slide 24
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• Anti - coagulation therapy
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• Slide 42
• Slide 43
• Slide 44
• Slide 45
• Slide 46
• Slide 47
• Slide 48
• Slide 49
• Slide 50
• Slide 51
• Slide 52
• Slide 53
• Slide 54
• Slide 55
• Slide 56
• Slide 57
• Slide 58
• Slide 59
• Slide 60
• Slide 61
• Slide 62
• Slide 63
• Slide 64
• Slide 65
• Slide 66
• Slide 67
• Slide 68
• Slide 69
• Slide 70
• Slide 71
• Slide 72
• Slide 73
• Slide 74
• Slide 75
• Slide 76
• Slide 77
• Slide 78
• Slide 79
• Slide 80
• Slide 81

Emergency Department Care

Assess airway breathing and circulation Hemodynamic concerns will dictate initial treatment

Treatment options for atrial flutter include the following

Antiarrhythmic drugsnodal agents

Direct-current (DC) cardioversion

Rapid atrial pacing to terminate atrial flutter

Blood pressure can be supported and rate controlled with medication

Anti coagulation therapy

Look for underlying causes At times treatment of the underlying disorder (eg thyroid disease valvular heart disease) is necessary to effect conversion to sinus rhythm

Cardioversion for unstable patients

If the patient is unstable (eg hypotension poor perfusion) synchronous direct-current (DC) cardioversion is commonly the initial treatment of choice

Cardioversion may be successful with energies as low as 25 Joules but since 100 Joules is virtually always successful this may be a reasonable initial shock strength

If the electrical shock results in atrial fibrillation (AF) a second shock at a higher energy level is used to restore normal sinus rhythm (NSR)

AV-His Bundle ablation

In patients who have failed antiarrhythmic therapy or who have failed RFA and who

are symptomatic palliative therapy with AV-His Bundle ablation can eliminate rapid

ventricular rates but it does require a permanent pacemaker to be placed as this

procedure creates third-degree heart block

Questions

• Slide 1
• Slide 2
• Slide 3
• Slide 4
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• Slide 10
• Slide 11
• Rate versus rhythm control which is superior
• Slide 13
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• Slide 18
• Slide 19
• Slide 20
• Slide 21
• Slide 22
• Slide 23
• Slide 24
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• Anti - coagulation therapy
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• Slide 42
• Slide 43
• Slide 44
• Slide 45
• Slide 46
• Slide 47
• Slide 48
• Slide 49
• Slide 50
• Slide 51
• Slide 52
• Slide 53
• Slide 54
• Slide 55
• Slide 56
• Slide 57
• Slide 58
• Slide 59
• Slide 60
• Slide 61
• Slide 62
• Slide 63
• Slide 64
• Slide 65
• Slide 66
• Slide 67
• Slide 68
• Slide 69
• Slide 70
• Slide 71
• Slide 72
• Slide 73
• Slide 74
• Slide 75
• Slide 76
• Slide 77
• Slide 78
• Slide 79
• Slide 80
• Slide 81

Cardioversion for unstable patients

If the patient is unstable (eg hypotension poor perfusion) synchronous direct-current (DC) cardioversion is commonly the initial treatment of choice

Cardioversion may be successful with energies as low as 25 Joules but since 100 Joules is virtually always successful this may be a reasonable initial shock strength

If the electrical shock results in atrial fibrillation (AF) a second shock at a higher energy level is used to restore normal sinus rhythm (NSR)

AV-His Bundle ablation

In patients who have failed antiarrhythmic therapy or who have failed RFA and who

are symptomatic palliative therapy with AV-His Bundle ablation can eliminate rapid

ventricular rates but it does require a permanent pacemaker to be placed as this

procedure creates third-degree heart block

Questions

• Slide 1
• Slide 2
• Slide 3
• Slide 4
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• Slide 10
• Slide 11
• Rate versus rhythm control which is superior
• Slide 13
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• Slide 18
• Slide 19
• Slide 20
• Slide 21
• Slide 22
• Slide 23
• Slide 24
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• Anti - coagulation therapy
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• Slide 42
• Slide 43
• Slide 44
• Slide 45
• Slide 46
• Slide 47
• Slide 48
• Slide 49
• Slide 50
• Slide 51
• Slide 52
• Slide 53
• Slide 54
• Slide 55
• Slide 56
• Slide 57
• Slide 58
• Slide 59
• Slide 60
• Slide 61
• Slide 62
• Slide 63
• Slide 64
• Slide 65
• Slide 66
• Slide 67
• Slide 68
• Slide 69
• Slide 70
• Slide 71
• Slide 72
• Slide 73
• Slide 74
• Slide 75
• Slide 76
• Slide 77
• Slide 78
• Slide 79
• Slide 80
• Slide 81

AV-His Bundle ablation

In patients who have failed antiarrhythmic therapy or who have failed RFA and who

are symptomatic palliative therapy with AV-His Bundle ablation can eliminate rapid

ventricular rates but it does require a permanent pacemaker to be placed as this

procedure creates third-degree heart block

Questions

• Slide 1
• Slide 2
• Slide 3
• Slide 4
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• Slide 10
• Slide 11
• Rate versus rhythm control which is superior
• Slide 13
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• Slide 18
• Slide 19
• Slide 20
• Slide 21
• Slide 22
• Slide 23
• Slide 24
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• Anti - coagulation therapy
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• Slide 42
• Slide 43
• Slide 44
• Slide 45
• Slide 46
• Slide 47
• Slide 48
• Slide 49
• Slide 50
• Slide 51
• Slide 52
• Slide 53
• Slide 54
• Slide 55
• Slide 56
• Slide 57
• Slide 58
• Slide 59
• Slide 60
• Slide 61
• Slide 62
• Slide 63
• Slide 64
• Slide 65
• Slide 66
• Slide 67
• Slide 68
• Slide 69
• Slide 70
• Slide 71
• Slide 72
• Slide 73
• Slide 74
• Slide 75
• Slide 76
• Slide 77
• Slide 78
• Slide 79
• Slide 80
• Slide 81

Questions

• Slide 1
• Slide 2
• Slide 3
• Slide 4
• Slide 5
• Slide 6
• Slide 7
• Slide 8
• Slide 9
• Slide 10
• Slide 11
• Rate versus rhythm control which is superior
• Slide 13
• Slide 14
• Slide 15
• Slide 16
• Slide 17
• Slide 18
• Slide 19
• Slide 20
• Slide 21
• Slide 22
• Slide 23
• Slide 24
• Slide 25
• Slide 26
• Slide 27
• Slide 28
• Slide 29
• Slide 30
• Slide 31
• Anti - coagulation therapy
• Slide 33
• Slide 34
• Slide 35
• Slide 36
• Slide 37
• Slide 38
• Slide 39
• Slide 40
• Slide 41
• Slide 42
• Slide 43
• Slide 44
• Slide 45
• Slide 46
• Slide 47
• Slide 48
• Slide 49
• Slide 50
• Slide 51
• Slide 52
• Slide 53
• Slide 54
• Slide 55
• Slide 56
• Slide 57
• Slide 58
• Slide 59
• Slide 60
• Slide 61
• Slide 62
• Slide 63
• Slide 64
• Slide 65
• Slide 66
• Slide 67
• Slide 68
• Slide 69
• Slide 70
• Slide 71
• Slide 72
• Slide 73
• Slide 74
• Slide 75
• Slide 76
• Slide 77
• Slide 78
• Slide 79
• Slide 80
• Slide 81