Systematic approach to EKG - use it EVERY SINGLE TIME

Determine rhythm last… quickly answer regular vs. irregular

RhythmIs there p waveIs there QRSRelationship of P:QRSIs it regular or irregular

Systematic approach to EKG - use it EVERY SINGLE TIME

Determine rhythm last… quickly answer regular vs. irregular

RhythmIs there p waveIs there QRSRelationship of P:QRSIs it regular or irregular

Small box 40 ms, large box 200 msSmall box is 0.04 sec, large is 0.2 sec

Rhythm:Is the P waveIs there QRSWhat is relationshipIs it regular

REGULAR rhythms● Rate = 300 / number of LARGE squares between consecutive R waves.

Very FAST rhythms:● Rate = 1500 / number of SMALL squares between consecutive R waves.

SLOW or IRREGULAR rhythms:● Rate = Number of R waves X 6● The number of complexes (count R waves) on the rhythm strip gives the

average rate over a ten-second period. This is multiplied by 6 (10 seconds x 6 = 1 minute) to give the average Beats per minute (bpm)

Upward deflection occurs when charge moves toward lead in depolarizationNormal axis is -30-90

Why does axis matter?- Reflects overall electrical activity in the heart- See changes with hypertrophy (enlargement)- See with changes in conduction (bundle and hemi-blocks)

Quick look method with eval of leads I and avF

Typically expect lead II to be most positive because size of L ventricle

Can also look to see which lead is most isoelectric lead and calculate perpendicular values; axis is whichever one is upward deflection-Vector going towards I and II so the EKG has upward reflection-Vector is going away from aVR so the EKG has a downward reflection

No onto waves and intervals...

● Present? (esp check II and V1)● Amplitude + duration: normal <3mm high and wide (LAE/RAE/Biatrial)● Contour: normal — inverted aVR, biphasic V1, upright I,II, aVF, V2-V6

-One p wave precedes each QRS complex-Do all p waves look the same?

Look in all leads for presence of q waves (normal in V5/V5 - left leads)R is first upward deflection; ventricular depolarizationAbnormalities

- Low voltage R waves? (V1-6 R waves are all less than 10mm tall or I/II/III R waves are all less than 5mm tall)? No

- High voltage R waves (are the R waves in V1-6 excessively tall)? No - progression?

Peaked. Early STEMI-Inverted. Ischemia, BBB, ventricular hypertrophy, PE, HCM, raised ICP-Biphasic. Ischemia (Wellens syndrome), hypokalemia.-Camel hump. Severe hypokalemia (U wave fused to T wave), heart block (p wave embedded in T wave)-Flat. Ischemia, hypokalemia.

Abnormal U waves are prominent or inverted-Prominent. More than 2 mm or 25% height of T wave. Bradycardia, severe hypokalemia, hypo Ca, Hypo Mag, Hypothermia, raised ICP, Digoxin toxicity-Giant U waves may precede Torsades in those with Long QT syndrome-Inverted. Highly specific for heart disease. CAD, htn, valvular, congenital, cardiomyopathy.

Epsilon wave: buried in the end of the QRS complex. Epsilon waves are caused by postexcitation of the myocytes in the right ventricle. Epsilon waves are the most characteristic finding in arrhythmogenic right ventricular dysplasia (ARVD/C).

No onto intervals...

-Four Intervals-PR 120-200 ms-QRS 70-100 ms-ST segment. Elevated or depressed.-QTc. Upper limit of normal is 440 ms for men and 460 ms for women. 500 is easier to remember.

Time to r wave peak

Typically say < 120

Isoelectric line which to base ST changes of is TP interval no electrical activity

J point in a) normal; b) c) J point (ST) elevation; d) J point (ST) depression; e) with J wave (Osborn wave)

Primarily looking for prolongation (QTc>500) is increased risk torsades

What is your interpretation of the EKG? History/Clinical Picture—age and possible anginal equivalent symptoms Rate—66 (11 x 6) or ~66 (>5 large boxes) Rhythm—Sinus Rhythm Axis—Normal, positive in I & aVF

P Waves—normal Q/R/S Waves— Q Waves II, III, aVF T Waves—T wave Inversion in I, aVL U Waves—No pathologic U waves noted

PR Interval—Normal at ~140ms QRS Width—Narrow ST Segment—ST elevation in II, III, and aVF with reciprocal ST depression in I, aVL,QT Interval—Normal

Diagnosis—This EKG is consistent with an Inferior STEMI

The vast majority (~80%) of inferior STEMIs are due to occlusion of the dominant right coronary artery (RCA).

What 2 conditions are frequently associated with this EKG pattern? How frequently do

they occur?

Significant bradycardia resulting from 2nd or 3rd degree AV block occurs 20% of the

time with inferior MIs.

Right ventricular infarction occurs concurrently with inferior MIs 40% of the time.

● Ischaemia of the AV node due to impaired blood flow via the AV nodal artery.

This artery arises from the RCA 80% of the time, hence its involvement in

inferior STEMI due to RCA occlusion.

● Bezold-Jarisch reflex = increased vagal tone secondary to ischaemia.

What EKG pattern is frequently associated?

The following are associated with concomitant RV infarct: ST elevation in lead III that

is greater than lead II, reciprocal depression in I, and ST elevation in V1.

Signs of right ventricular infarction: STE in V1 and V4R

How can you confirm? Right sided EKG—remember only 0.5mm STE in a single lead

rules in STEMI (except men < 30 =1mm)

What medication is relatively contraindicated with this EKG pattern? Why?

Nitroglycerin can cause severe hypotension when given to patients with RV

infarctions so it is critical that you rule it out first (decrease preload)

History/Clinical Picture— 20 yo F presents with palpitationsRate— ~70Rhythm— sinus rhythmAxis— right axis deviationP Waves— presentQ, R, S Waves— large S waves in I and aVL, large R waves in V1-6. QRS complexes with sloping upstrokeT Waves— T-wave inversion V1-3U Waves— not presentPR Interval— narrow at just under 120 msQRS Width— narrow, but appears prolonged due to sloping of R-waveST Segment— slight depressions in V1-3QT Interval— normal

Diagnosis: Sinus rhythm with pre-excitation (Wolff-Parkinson-White)

Discussion: The presence of a narrow PR-interval and sloping upstroke to the QRS complex suggests the presence of an accessory pathway. Symptomatic tachy-arrhythmias in the presence of an accessory pathway constitute the Wolff-Parkinson White syndrome. An accessory pathway is an abnormal congenital electrical pathway that connects the atria to the ventricles, allowing supraventricular impulses to conduct to the ventricles without travelling through the AV-node. The presence of

the bypass tract makes possible the development of re-entrant circuits (and re-entrant tachycardias) between the atria andventricles. AV nodal re-entrant tachycardia (AVRT) is the name for the rhythm that occurs when a re-entrant impulse beginsto self-propagate by travelling back to the atria via either the AV-node or the accessory pathway and triggering anotherround of depolarization.

The presence of a narrow PR-interval and sloping upstroke to the QRS complex suggests the presence of an accessory pathway. Symptomatic tachy-arrhythmias in the presence of an accessory pathway constitute the Wolff-Parkinson White syndrome. An accessory pathway is an abnormal congenital electrical pathway that connects the atria to the ventricles, allowing supraventricular impulses to conduct to the ventricles without travelling through the AV-node. The presence of the bypass tract makes possible the development of re-entrant circuits (and re-entrant tachycardias) between the atria and ventricles.

AV nodal re-entrant tachycardia (AVRT) is the name for the rhythm that occurs when a re-entrant impulse begins to self-propagate by travelling back to the atria via either the AV-node or the accessory pathway and triggering another round of depolarization.

● During tachyarrythmias the features of pre-excitation are lost as the accessory pathway forms part of the reentry circuit.

● AVRT often triggered by premature atrial or premature ventricular beats.● AVRT are further divided in to orthodromic or antidromic conduction

based on direction of reentry conduction and ECG morphology.

● Atrial fibrillation can occur in up to 20% of patients with WPW.● Atrial flutter can occur in up to 7% of patients with WPW.● The accessory pathway allows for rapid conduction directly to the ventricles

bypassing the AV node.● Rapid ventricular rates may result in degeneration to VT or VF.

The normal AV nodal delay protects the ventricle from excessively fast stimulation however some accessory pathways are extremely fast and have essentially no delay. Considering the lack of delay it is easy to understand how atrial fibrillation or atrial flutter with their 260-300bpm electrical signals can trigger ventricular fibrillation when they are transmitted directly to the ventricle via the accessory pathway.Atrial fibrillation still causes an irregularly irregular rhythm in AVRT but you may have to look very closely because the rate is so fast. Atrial flutter is more difficult and may not be possible to identify prior to conversion. Procainamide should be used for irregular AVRT because it directly acts to slow the speed of the accessory pathway.

History/Clinical Picture—young age and family history of early CADRate—100 (22 x 6) or ~130-140 (>2 large boxes)Rhythm—Sinus TachycardiaAxis—Normal, I positive, aVF positiveP Waves—normalQ, R, S Waves—No pathologic QsT Waves—no inversionsU Waves—no clear U waves however possibly present in V4PR Interval—approximately 120ms, significant PR elevation in aVR, significant PR depression in I,II,V2-V^QRS Width—narrow, ~90msST Segment—ST segment elevation is defined in relation to the T-P segment during which the heart is electrically inactive.ST elevation: ~1mm above T-P segment in I,II, V2-V6QT Interval—not prolonged

What’s your differential? What is most likely?

Diagnosis: Acute pericarditis

Moderate pericardial effusion

How To Recognise PericarditisWidespread concave ST elevation and PR depression throughout most of the limb leads (I, II, III, aVL, aVF) and precordial leads (V2-6).Reciprocal ST depression and PR elevation in lead aVR (± V1).Sinus tachycardia is also common in acute pericarditis due to pain and/or pericardial effusion.

Stages of PericarditisPericarditis is classically associated with ECG changes that evolve through four stages.

● Stage 1 – widespread STE and PR depression with reciprocal changes in aVR (occurs during the first two weeks)

● Stage 2 – normalisation of ST changes; generalised T wave flattening (1 to 3 weeks)

● Stage 3 – flattened T waves become inverted (3 to several weeks)● Stage 4 – ECG returns to normal (several weeks onwards)

NB. Less than 50% of patients progress through all four classical stages and evolution of changes may not follow this typical pattern.

At least two of the four clinical features (chest pain, pericardial friction rub, ECG changes, and pericardial effusion) should be present to make the diagnosis. Pericarditis should also be suspected in a patient with persistent fever and either a pericardial effusion or new unexplained cardiomegaly.

Pericarditis vs STEMIClassic teaching of generalised concave up ST elevation and PR elevation in aVR is not reliable for distinguishing pericarditis from ST elevation myocardial infarction (STEMI).

● Pericarditis can cause localised ST elevation but there should be no reciprocal ST depression (except in AVR and V1).

● STEMI, like pericarditis, can also cause concave up ST elevation.● Only STEMI causes convex up or horizontal ST elevation.● ST elevation greater in III than II strongly suggests a STEMI.● PR segment depression is only reliably seen in viral pericarditis, not by other

causes. It is often only an early transient phenomenon (lasting only hours). MI can also cause PR segment depression due to atrial infarction (or PR segment elevation in aVR).

● You can’t rely on history either — STEMI can also cause positional or pleuritic pain. A pericardial friction rub

Steps to distinguish pericarditis from STEMI:1. Is there ST depression in a lead other than AVR or V1? This is a STEMI2. Is there convex up or horizontal ST elevation? This is a STEMI3. Is there ST elevation greater in III than II? This is a STEMI4. Now look for PR depression in multiple leads… this suggests pericarditis

(especially if there is a friction rub!)

Retrocardiac airspace disease _ concenring for pna

Malignant involvement of the pericardium can manifest as painful pericarditis, pericardial effusion, cardiac tamponade, or constrictive pericarditis. Among patients known to have an underlying malignancy who present with pericardial effusion requiring drainage, between 50 and 60 percent will have a malignant effusion

History/Clinical Picture— 240 yoF presents with ICD firingRhythm— wide, complex regular tachycardiaAxis— ?? LAD?P Waves— not visibleQ, R, S Waves— broad/ wide-complex; ? possible RBBB morphologyT Waves— unable to assesU Waves— unable to assesPR Interval— no consistent PR intervalQRS Width— wide, regularST Segment— unable to assesQT Interval— unable to asses

Diagnosis: Wide complex tachcardia

History/Clinical Picture— 240 yoF presents with ICD firingRhythm— wide, complex regular tachycardiaAxis— ?? LAD?P Waves— not visibleQ, R, S Waves— broad/ wide-complex; ? possible RBBB morphologyT Waves— unable to assesU Waves— unable to assesPR Interval— no consistent PR intervalQRS Width— wide, regularST Segment— unable to assesQT Interval— unable to asses

Diagnosis: Wide complex tachcardia

Features common to any broad complex tachycardia

Rapid heart rate (> 100 bpm).Broad QRS complexes (> 120 ms).Features suggestive of VT

Very broad complexes (>160ms).Absence of typical RBBB or LBBB morphology.Extreme axis deviation (“northwest axis”) — QRS is positive in aVR and negative in I

+ aVF.AV dissociation (P and QRS complexes at different rates).Capture beats — occur when the sinoatrial node transiently ‘captures’ the ventricles, in the midst of AV dissociation, to produce a QRS complex of normal duration.Fusion beats — occur when a sinus and ventricular beat coincide to produce a hybrid complex of intermediate morphology.Positive or negative concordance throughout the chest leads, i.e. leads V1-6 show entirely positive (R) or entirely negative (QS) complexes, with no RS complexes seen.Brugada’s sign – The distance from the onset of the QRS complex to the nadir of the S-wave is > 100ms.Josephson’s sign – Notching near the nadir of the S-wave.RSR’ complexes with a taller “left rabbit ear”. This is the most specific finding in favour of VT. This is in contrast to RBBB, where the right rabbit ear is taller.

“I dont want to be shocked”

150 amio x 2

2 mg magProcainamide 50 mg/min; after 2 minutes

He feels better after all!

History/Clinical Picture— 240 yoF presents with ICD firingRhythm— wide, complex regular tachycardiaAxis— ?? LAD?P Waves— not visibleQ, R, S Waves— broad/ wide-complex; ? possible RBBB morphologyT Waves— unable to assesU Waves— unable to assesPR Interval— no consistent PR intervalQRS Width— wide, regularST Segment— unable to assesQT Interval— unable to asses

Diagnosis: Wide complex tachcardia

Features common to any broad complex tachycardia

Rapid heart rate (> 100 bpm).Broad QRS complexes (> 120 ms).Features suggestive of VT

Very broad complexes (>160ms).Absence of typical RBBB or LBBB morphology.Extreme axis deviation (“northwest axis”) — QRS is positive in aVR and negative in I

+ aVF.AV dissociation (P and QRS complexes at different rates).Capture beats — occur when the sinoatrial node transiently ‘captures’ the ventricles, in the midst of AV dissociation, to produce a QRS complex of normal duration.Fusion beats — occur when a sinus and ventricular beat coincide to produce a hybrid complex of intermediate morphology.Positive or negative concordance throughout the chest leads, i.e. leads V1-6 show entirely positive (R) or entirely negative (QS) complexes, with no RS complexes seen.Brugada’s sign – The distance from the onset of the QRS complex to the nadir of the S-wave is > 100ms.Josephson’s sign – Notching near the nadir of the S-wave.RSR’ complexes with a taller “left rabbit ear”. This is the most specific finding in favour of VT. This is in contrast to RBBB, where the right rabbit ear is taller.

Magnet on pacemaker vs ICD- Placing a magnet on a pacemaker will switch the pacemaker to asynchronous

(fixed rate) pacing with no sensing and no inhibition. Placing a magnet on an ICD will stop the ICD from delivering shocks. It will have no effect on the ICD’s pacing capabilities.

- Determined that patient was in v tach → appropriate ICD firing

Stable Vtach → VSS w/ good perfusion, no anginal equivalents- stableventriculartachycardia(SBP>/=90mmHg,absenceofdyspneaat

rest,absenceofperipheralhypoperfusionandnosevereanginalsymptoms).

Amiodarone is a class III antidysrhythmic first released for human use in 1962. As with other drugs in this class, amiodarone acts by blocking potassium channels thus prolonging the action potential. This, in turn, leads to a lengthening of depolarization of the atria and ventricles.

The PROCAMIO study compared amiodarone to procainamide in a randomized open-label trial with a primary endpoint of major adverse cardiac events and a secondary endpoint of efficacy (Ortiz 2016). Procainamide won on both endpoints. Procainamide (10 mg/kg over 20 min) had a lower frequency of adverse events (9% vs. 41% OR 0.1 NNH = 3) as well as a superior termination rate (67% vs. 38% OR 3.3 NNT = 3.3) in comparison to amiodarone (5 mg/kg over 20 min). The rate of adverse events in the group of patients with structural heart disease was lower in the procainamide group as well. Though it’s only one study, it represents the best quality of evidence we have to date.

Once again, electrical cardioversion is the superior approach for tachydysrhythmia termination. In the PROCAMIO study, only 33/62 patients converted when given either procainamide or amiodarone – almost half of the patients needed to proceed to electricity for termination. Though some patients will remain in hemodynamically stable VT for prolonged periods of time, the risk of decompensation to unstable VT or VF is always present. All of this underscores the need to always have defibrillator pads applied to the patient and have a plan for failed chemical cardioversion in place. Based on the overall low rate of chemical cardioversion, electing to go directly to electricity is a reasonable and possibly superior approach.

● Primary Endpoint: Major Cardiac Adverse Events○ Overall: 24% (15/62)○ Procainamide = 9% vs. Amiodarone = 41%

○ Absolute difference = 32% NNH = 3○ OR = 0.1 (95% CI 0.03 – 0.6)

● Secondary Endpoints:○ Tachycardia Termination within 40 min

■ Overall: 53% (33/62)■ Procainamide = 67% vs. Amiodarone = 38%■ Absolute difference 29% NNT = 3.3■ OR = 3.3 (95% CI 1.2 – 9.3)

○ Adverse Events in Following 24 Hours■ Procainamide = 18% vs. Amiodarone = 31%■ Absolute difference = 13% NNH = 7.5■ OR = 0.49 (95% CI 0.15 – 1.61)

History/Clinical Picture— 69 M w/ ESRD; syncope and bradycardia Rate— ~36 (QRS x 6)Rhythm— sinus w/ IVCD. possible AV blockAxis— LADP Waves— present? Not always conduction a QRSQ, R, S Waves— widemed, RBBB pattern in V1, fluctuationT Waves— peaked V3-V4U Waves— not present?PR Interval— very prolongedQRS Width— slightly wideST Segment— normalQT Interval— long

Rhythm: slow junctional rhythm w/ IVCD?Bradycardia w/ IVCD

Suspect hyperkalaemia in any patient with a new bradyarrhythmia or AV block, especially patients with renal failure, on haemodialysis or taking any combination of ACE inhibitors, potassium-sparing diuretics and potassium supplements.

Quick exam: rales, JVD, noncompliant w/ renal diet but takijg meds

Intrinsic pacemaker rates in heart

Junctional is at AV node junction w/ intrinsic rate 40-60l usually fairly narrow

Push atropine → no change

Pt report placement; Attempt pacing but only with intermittent capture

The ventricles are pacing the heart at their inherent rate of 20-40 beats per minute as higher pacemakers (the sinus node and AV node) have failed. Emergent treatment of this hemodynamically unstable bradycardia include medications (atropine, isoproterenol, dopamine, epinephrine), and if these fail, transcutaneous or transvenous pacing. The emergency physician should seek to identify any reversible precipitants of the bradycardia, such as: ischemia, hyperkalemia, and medication overdose (beta-blockers, calcium channel blockers, and digoxin). Reversible causes should be treated, and if the bradycardia persists, the patient should be admitted to an ICU for cardiology consult and consideration of a permanent pacemaker.

Suspect hyperkalaemia in any patient with a new bradyarrhythmia or AV block, especially patients with renal failure, on haemodialysis or taking any combination of ACE inhibitors, potassium-sparing diuretics and potassium supplements.

History/Clinical Picture— 69 M w/ ESRD; syncope and bradycardia Rate— 75 Rhythm— sinus w/ IVCD. possible AV blockAxis— LADP Waves— present. monomorphicQ, R, S Waves—narrow; RBBB pattern in V1/V2 T Waves— normalU Waves— not presentPR Interval— wnlQRS Width— narrowST Segment— normalQT Interval— normal

Calcium use:Routine use: 1 gram of 10% calcium gluconate (i.e. 10 ml mixed with 100cc of D5W or NS ina mini-bag) over 5-10 minutes. Repeat as needed to achieve QRS &lt;100ms and p waves re-appear.Arrest or Pre-arrest: Push 1 amp (1 gram) of 10% calcium chloride through a large borewell-running peripheral IV or central line (preferable). Repeat as needed to achieve QRS

&lt;100ms and p waves re-appear.

○ Stabilizecardiacmembrane>calcium■ 3amps(30ml)ofcalciumgluconateisequivalentto1amp

(10ml)ofcalciumchloride■ MonitortheECGcontinuously.YoushouldseeECG

improvementwithin3minutes.Dosecanberepeatedifthereisnoimprovement.Calciumchloridecontainsthreetimestheconcentrationofelementalcalciumcomparedwithcalciumgluconate(13.6versus4.6mEqin10mLofa10percentsolution

■ ThedoseofeitherformulationcanberepeatedafterfiveminutesiftheECGchangespersistorrecur.Administrationofcalciumcanberepeatedevery30to60minutesifthehyperkalemicemergencypersistsandtheserumcalciumdoesnotbecomeelevated.

Calcium changes occur rapidly → redose every 5 minutes as needed. Or start a drip!

AEIUO

What treatment options do you have for this patient and how do they work? Stabilize Myocardium—Calcium is the only option that stabilizes the cardiac membrane Intracellular Relocation—Insulin/Dextrose, Bicarb, & Albuterol work to activate Na/K pump to move K into the intracellular space Elimination—Dialysis (most effective), Normal Saline with/without Furosemide (increased urinary excretion), Kayexylate (unclear efficacy but thought to trap K in the gut)

Bradycardia not always a primary cardiac issue such as sick sinus syndrome,atrioventricular block, or myocardial ischemia → consider secondary causessuch as hyperkalemia, hypothyroidism, hypothermia, or overdose with beta-blockers, calcium channel blockers, digitalis, clonidine, or otherAntiarrhythmics.

Peaked T wave (K approx 5.5-6.5) >Peaked T waves reflect faster repolarization of the myosite.Prolonged PR interval and flattening or disappearance of the P wave (K approx 6.5-7.5) > The resting potential of myosite becomes more positive which slows depolarization.Widening of the QRS > The increasingly positive membrane potential leads to

progressively slowed depolarization and widening of the QRS.Sine Wave: pre-terminal rhythm > As the depolarization slows, the widening QRS begins to merge with the T wave. This is a pre-terminal rhythm which can deteriorate rapidly into Ventricular Fibrillation.

70yM with history of CAD, HTN, HL presents after a syncopal episode while walking. An EKG from 1 year ago shows NSR with a right bundle branch block.

History/Clinical Picture—elderly man with lightheadednessRate—42Rhythm—Unclear. As demonstrated in the ladder diagram below QRS complexes 6/7 seem to have a consistent PRinterval but none of the other QRS other complexes are preceded by P waves.Axis—Mild Left Axis Deviation (I pos, aVF neg, II neg)P Waves—normal morphology, more P waves than QRS complexes (as seen below in ladder diagram)Q, R, S Waves—non-pathologic Q waves in I & aVL, R & S waves normalT Waves—T wave inversion in V1/2 and III.U Waves—NonePR Interval—no consistent PR intervalQRS Width—normalST Segment—no ST elevation or depressionQT Interval—normal

Regular p-waves; more than QRS complees

Regular QRS complexes; consistent morphology

Presuming the patient is maintaining his triage blood pressure of 100/60 you are unlikely to need to pace themimmediately so while preparing to pace if needed try to figure out why they are in a 3rd degree block

● IV, O2, Monitor● Place defibrillation/transcutaneous pacing pads● Transvenous Pacer kit to the bedside● Send complete set of labs including CBC, BMP, Magnesium, Phosphorus,

Ionized Calcium, Troponin, BNP with a● VBG or iStat to facilitate rapid assessment of the potassium level if possible● Focused cardiac and medication history as well as screening for Lyme or

hypothyroidism● Complete head to toe exam with a special focus on tissue perfusion and metal

status● Consult cardiology

Look for etiology and easily reversible causes:

Pathologic – Myocardial ischemia (acute or chronic) involving the conduction system, cardiomyopathy (eg, amyloidosis, sarcoidosis), myocarditis (eg, Lyme disease), endocarditis with abscess formation, hyperkalemia, and hypervagotonia.

Iatrogenic – Medication-related (AV nodal blocking medications), post-cardiac

surgery, post-catheter ablation, post-transcatheter aortic valve implantation.

If the patient becomes unstable attempt transcutaneous pacing and then transvenous if necessary

What is your interpretation of the EKG?History/Clinical Picture— middle aged woman presents with palpitations for 72 hoursRate— 140-160Rhythm— irregularly, irregular → atrial fibrillationAxis— normalP Waves— absentQ, R, S Waves— normalT Waves— no notable abnormalitiesU Waves— absentPR Interval— not applicableQRS Width— normalST Segment— no notable deviationQT Interval— difficult to assess given degree of tachycardia but grossly normalDiagnosis: Atrial fibrillation with rapid ventricular rate

Atrial Fibrillation (AF) is the most common sustained arrhythmia. Characterized by disorganized atrial electrical activity and contraction.

ECG Features of Atrial Fibrillation● Irregularly irregular rhythm.● No P waves.● Absence of an isoelectric baseline.● Variable ventricular rate.

● QRS complexes usually < 120 ms unless pre-existing bundle branch block, accessory pathway, or rate related aberrant conduction.

● Fibrillatory waves may be present and can be either fine (amplitude < 0.5mm) or coarse (amplitude >0.5mm).

● Fibrillatory waves may mimic P waves leading to misdiagnosis

The incidence and prevalence of AF is increasing. Lifetime risk over the age of 40 years is ~25%. Complications of AF include haemodynamic instability, cardiomyopathy, cardiac failure, and embolic events such as stroke.

he ventricular response and thus ventricular rate in AF is dependent on several factors including vagal tone, other pacemaker foci, AV node function, refractory period, and medications.Commonly AF is associated with a ventricular rate ~ 110 – 160.AF is often described as having ‘rapid ventricular response’ once the ventricular rate is > 100 bpm.

In the hemodynamically unstable patient, synchronized cardioversion should be done emergently. Hemodynamically stable patients may be managed medically. Rhythm control with medications (amiodarone, flecainide, or ibutilide, among others) or with elective synchronized cardioversion can be considered in patients who have been in atrial fibrillation for ≤ 48 hours.

In patients in whom the duration of atrial fibrillation is ˃ 48 hours or unknown, rhythm control should be avoided due to the risk of thromboembolism. In these patients, the focus should be on rate control with beta-blockers (generally metoprolol) or nondihydropyridine calcium channel blockers (diltiazem or verapamil).

The ED physician should search for an underlying cause for the atrial fibrillation (PE, hyperthyroidism, medication side effect) with appropriate diagnostics. All patients in atrial fibrillation should have their thromboembolic risk assessed in the ED using the CHA2DS2-VASc score and anticoagulation should be started for a score ≥ 2, assuming no contraindications.

In the emergency department and observation,

options include Diltiazem, 0.25mg/kg IV x1 if SBP>100 mm Hg followed by 30mg PO

q6h if rate adequately controlled.

Also, Lopressor, 5-10mg IV x1 if SBP>100 mm Hg followed by 25mg PO q6h if rate

adequately controlled (preferred agent for patients already on a β blocker).

If rate is not controlled and SBP<100 mm Hg consider

Diltiazem drip (start at 10 mg/hr IV, titrate at 5mg/hr increments to max of 25mg/hr to

HR<100).

Adequate rate control for discharge home defined as resting HR<100bpm and

ambulatory HR<110bpm with tolerable symptoms.

Discharge rate control for patients sent home in atrial fib/flutter should be lowest dose

equivalent of long acting oral medication (i.e., if the patient did well on 30mg PO

Diltiazem q6h, discharge patient with 120mg of long-acting Diltiazem once daily, first

dose due 6h from previous).

In the absence of an acute trigger, risk factors leading to the development of

AF include (but are not limited to) the following conditions: advanced age,

hypertension, diabetes, obstructive sleep apnea, obesity, heart failure, valvular

heart disease, cardiomyopathies, chronic kidney disease, family history, etc

Many patients with new onset AF evaluated in an emergency room may not need to

be hospitalized. However, indications for hospitalization in these patients include:

●Patients in whom ablation of an accessory pathway is being considered, particularly if the AF was highly symptomatic and associated with hemodynamic collapse and rapid ventricular response rate.●Severe bradycardia or prolonged pauses.●Patients with severe bradycardia or prolonged pauses after cardioversion. (See "Sinus node dysfunction: Epidemiology, etiology, and natural history".)●Treatment of an associated medical problem, which is often the reason for the arrhythmia. Examples include the treatment of hypertension, infection, exacerbation of chronic obstructive pulmonary disease, pulmonary embolism, persistent myocardial ischemia, or acute pericarditis. Patients may be placed in an observation protocol to rule out acute myocardial infarction, and hospitalization is no longer required unless there is ongoing ischemia or suspected acute coronary syndrome that requires intervention. AF alone is not an indication to rule out myocardial infarction. The "rule-out" should be done only if other factors suggest the presence of unstable coronary artery disease.●Further management of heart failure or hypotension after control of the rhythm or rate●Initiation of antiarrhythmic drug therapy. Ultimately, the decision to hospitalize needs to take into account patient and drug characteristics. ●Difficult-to-control ventricular rates with evidence of ischemia, congestive heart failure symptoms or signs, and severe symptoms are indications for at least a 24-hour admission.