arrhythmia

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ELECTRICAL CONDUCTION SYSTEM OF THE HEART:

Composed of the following: Sino atrial (SA) node Internodal atrial conduction tracts and Interatrial conduction tract (Bachmann’s bundle) Atrioventricular (AV) junction

- AV node- Bundle of His

Right bundle branch, left bundle branch, left anterior and left posterior fascicles Purkinje network

Sinoatrial Node: Transmit minute electrical impulses from the SA node to the atria and ventricles SA Node – consist of pacemaker cells 3 Internodal atrial conduction tracts – from the walls of the RA

Atrioventricular Node: in the interatrial septum, upper part of the intraventricular septum Relay electrical impulses from the atria to the ventricles

Bundle of His: lies in the upper part of the intraventricular septum Connects AV node with the 2 bundle branches Right and left common bundle branch straddle the interventricular septum and down the

sides of the septum Bundle branch divide into fascicles Smallest fascicles connect with Purkinje fibers Purkinje fibers spread beneath the endocardium Ends of Purkinje fibers end at myocardial cells

Electrophysiology of the Heart: Cardiac cells are responsible for the contraction and relaxation of myocardial cells Caused by brief but rapid flow of positively charged ions back and forth across the cardiac

cell membrane Electrical potential (voltage) – difference in the concentration of ions across cell membrane;

measured in millivolts (mV)Polarization:

Negative Electrical Potential• Na ions (+ ions) outside of cell membrane• K ions (- ions) inside the cell • Polarization – ions are aligned

Depolarization: Membrane becomes permeable Allow Na to flow into cell (fast channels in the myocardial cells) K ions flow out of the cell Allow Na-Ca ions to flow into cell (slow channels of the SA and AV nodes) Act as an impulse on adjacent cells to cause depolarization P wave and QRS complex

Repolarization: Cells return to its resting, polarized state Complex exchange of sodium, calcium and potassium exchange across cell membrane T wave

Ma. Christina B. Celdran – Oraa, RN MAN

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Threshold Potential: The level to which cell must be repolarized before it can be depolarized again Cardiac cell cannot generate or conduct an electrical impulse or be stimulated to contract

until it has been repolarized to its threshold potential

CARDIAC ACTION POTENTIAL:

PHASE 0 Membrane reaches action potential Sharp tall upstroke Triggers fast Na channels to open Cell depolarizes and begin to contract

PHAE 1 Early rapid repolarization phase Fast Na channels close Loss of K ions from the cell

PHASE 2 Plateau phase Prolonged phase of slow repolarization Allow cell to finish contracting and begin relaxing Ca enters the cell K leave cell

PHASE 3 Terminal phase of rapid repolarization Inside of the cell is markedly negative Repolarization is completed

PHASE 4 Period between action potentials Membrane returned to resting potential Excess Na inside; excess K outside Na-K pump is activated

Refractory and Supernormal Periods: Time between the onset of depolarization and end of repolarization Divided into periods which cardiac cells can or cannot be stimulated to depolarize

REFRACTORY PERIOD: Begin with the onset of Phase O and ends just before Phase 3 ECG: onset of QRS to just about end of T wave

- ARP: onset of Phase 0 and midway through Phase 3 Complete depolarization of cardiac cells

- RRP: second half of Phase 3 cardiac cells ready to be stimulatedExcitability and Automaticity:

Excitability – ability of the cardiac cells to depolarize


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Automaticity – ability of the cardiac cells to depolarize completely without being externally stimulated (self excitation)

Depends on the ability of the cell membrane to be permeable to NaPacemakers:

SA NODE: Dominant pacemaker Primary pacemaker Highest level of automaticity

AV NODE: Escape pacemaker

INHERENT FIRING RATE: Pacemaker normally generates electrical impulse

Mechanism of Abnormal Electrical Impulse Formation: Ectopic pacemakers – generate extraneous electrical impulses Result to ectopic beats and rhythmsIdentified according to location:

- atrial- junctional- ventricular

3 Basic Mechanisms:- enhanced automaticity- reentry- triggered activity

Enhanced Automaticity: Abnormal condition latent pacemaker cells firing rate beyond inherent rate Cell membranes abnormally permeable to Na (Phase 4) Cause atrial, junctional and ventricular ectopic beats and rhythmsCauses:

Catecholamines digitalis toxicity atropine administration myocardial ischemia myocardial infarction cardiomegaly Hypokalemia Hypocalcemia heat and cold

Reentry: Blocked or delayed progression of electrical

impulse Delayed antegrade or retrograde conduction of

electrical impulses into cardiac cells which have been depolarized normally

If cardiac cells have repolarized, delayed electrical impulse depolarizes them prematurely

Produce ectopic beats and rhythms (atrial and ventricular tachycardias)

Triggered Activity: Cells depolarize more than once after stimulation by a single electrical impulse Called afterdepolarization occur immediately after depolarization in Phase 3 Delayed afterdepolarization – occur late in Phase 4 Ectopic beats:

- singly- groups of 2 (paired; coupled beats)- groups of 3 (paroxysms of beats; tachycardia)


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AUTONOMIC NERVOUS SYSTEM Sympathetic nervous system (cardioaccelerator) Parasympathetic nervous system (cardioinhibitor) Cause changes in BP and CO (HR and SV)

Stimulation of the SNS:Adrenergic effects on the heart:

automaticity (firing rate of SA node, escape and ectopic pacemakers)

conductivity through atria and ventricles force of atrial and ventricular contractionsAccomplished by:

- epinehprine- norepinephrine

Effects:- CO, BP and HR

Stimulation of the PNS:Cholinergic (Vagal) effects on the heart: automaticity (firing rate of SA, escape and ectopic pacemakers) Slow conduction of electrical impulses through AV node

ATROPINE – effectively blocks PNS activityEffects: CO, BP & HRBODILY FUNCTIONS STIMULATE PNS:

- pressure on the carotid sinus- valsalva maneuver- straining to move bowels- distention of urinary bladder- N & V- bronchial spasms- sweating; hypersalivation- faintness

ELECTROCARDIOGRAM: Graphic recording of the electrical activity generated by the depolarization and repolarization

of atria and ventriclesComponents of Electrocardiogram:

Depolarization and repolarization is detected by electrodes Displayed on an oscilloscope Recorded on ECG paper as waves and complexes Non invasive test Determining cardiac rhythm, pattern variation may reveal pathologic processes (MI &

Ischemia, electrolyte & acid base balance, chamber enlargement) Wave forms are called deflections relative to an isoelectric line (determined by looking at

the T-P interval)


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P wave – first positive deflection; atrial depolarization Q wave – first negative deflection after the P wave R wave is the first positive deflection after the P wave S wave – negative deflection after the R wave QRS wave – generally regarded as a unit; ventricular depolarization T wave – joined to the QRS complex by the ST segment T wave – represents the return of ions to the appropriate side of the cell membrane; signifies

relaxation; repolarization of the ventricles atrial T wave (Ta) – normally occurs during ventricular depolarization; buried in the QRS

complex QT interval – time between the Q wave and T wave

Artifacts: Abnormal waves and spikes in ECG Causes:

- muscle tremors- alternating current interference- loose electrodes- biotelemetry interference- external chest compressions


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ECG Paper:• Allow measurement of time (seconds) and distance (mm) along horizontal lines• Measure voltage (mV) along vertical lines• Grid:

- dark vertical lines are 0.20 sec (5mm) apart- light vertical lines are 0.04 sec (1mm) apart- dark horizontal lines are 5mm apart- light horizontal lines are 1mm apart- One large square is 5 X 5 mm- One small square is 1 X 1 mm

• Sensitivity of the ECG machine is standardized at 1 mV electrical signal produces 10mm deflection on ECG• Time lines – regularly spaced short, vertical lines denoting intervals of time

- 75 mm (3 sec) – distance between 2 consecutive short vertical lines- 150 mm (6 sec) – between every 3rd short vertical line

ECG Leads: Record of electrical activity sensed by either one of 2 ways:

- Bipolar lead - 2 electrodes of opposite polarity (+ -)- Unipolar lead - 1 (+) electrode and an “indifferent” zero reference point

12 Lead ECG: 3 standard (bipolar) limb leads -lead I, II and III 3 augmented (unipolar) leads – leads aVR, aVL, and aVF And 6 precordial (unipolar) leads – V1, V2, V3, V4, V5, V6

Lead 1 ECG: Limb leads measure cardiac depolarization in the frontal (coronal) plane (-) electrode - RIGHT ARM (+) electrode - LEFT ARM axis is 0 degrees action potential starts on the right and proceeds toward the left side of the heart, a positive

inflection will be seen in lead 1 Whenever a current proceeds toward a positive electrode, an upright inflection is seen on the

EKG tracing

Lead II ECG: Normal rhythms present with a prominant P wave and a tall QRS (-) electrode - RIGHT ARM (+) electrode - LEFT LEG


POSITIVE ELECTRODE: attached to the R or L arm, left leg or one of the several locations on the anterior chest wall

-;

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axis is +60 degrees In all the limb leads, the electrodes may be positioned close to the torso

Indications for ECG: MI, CAD Cardiac dysrhythmias Cardiac enlargement Electrolyte imbalances (Ca & K) Inflammatory diseases Effects of drugs in the heart

COMPONENTS OF ECG:P WAVE:

Represents atrial depolarization Electrical impulse progress from SA node through the internodal atrial conduction tracts and

most of AV node P wave occurs during ventricular diastole

Normal Sinus P Wave: Onset: first abrupt or gradual deviation from baseline End: point where the wave flattens out to return to baseline, joining with the P-R

segment Direction: positive (upright) in lead II Duration: 0.10 seconds or less Amplitude: 0.5 to 2.5 mm in lead II Shape: smooth and rounded PR Interval: 0.12 to 0.20 sec

Abnormal Sinus P Wave: Pacemaker site: SA node Represents depolarization of altered, damaged or

abnormal atria Onset, end, direction and duration may be normal Amplitude: may be normal or greater than 2.5 mm Shape: tall and symmetrically peaked; may be wide

and notched PR Interval may be normal or greater Tall and symmetrically peaked P wave (P pulmonale)

- atrial dilatation- status asthmaticus- acute PE- sinus tachycardia

Wide and notched P wave- HPN- MI- valvular disease- delay/blocked impulses

Ectopic P wave: Pacemaker site: ectopic pacemaker in the atria outside of the SA node or AV

junction or ventricles Depolarization of atria in abnormal sequence or direction Onset and end is the same with sinus P wave Direction:

- either (+) or (-) if ectopic pacemaker is in the atria- (-) if ectopic pacemaker is in the junction or ventricles- (-) if pacemaker is in LA or lower RA

Duration: 0.10 sec or less Amplitude: less than 2.5 mm in lead II; but may be greater


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Shape: smooth and rounded, peaked or dimple-shaped P wave-QRS complex: P wave may precede, buried or follow QRS complex;

superimposed in the preceding T wave PR Interval: usually less than 0.12 sec

Normal QRS Complex: Represents depolarization of right and left ventricles Pacemaker site: SA node, ectopic or escape pacemaker in the atria or AV junction Onset: point where the first wave of the complex begins to deviate from baseline End: last wave of the complex begins to flatten out R wave – first (+) deflection Q wave – first (-) deflection; not preceded by an R wave S wave – first (-) deflection that extends below baseline following an R waveNOTE:

Although there may only be one Q wave, there can be more than R and S wave Direction: predominantly (+) or (-) or equiphasic Duration: between 0.06 to 0.10 sec Amplitude:

- Q – less than 3 mm- R – 5 to 10 mm

Shape: narrow and sharply pointed

Abnormal QRS Complex: Represents abnormal depolarization of ventricles Pacemaker site: SA node, escape or ectopic pacemaker in the atria, AV junction,

bundle branches, purkinje network or ventricular myocardium Onset and end: - the same with normal QRS complex Duration: >0.10 sec Direction: predominantly positive (upright), predominantly negative (inverted) or

equiphasic Amplitude: from 1-2 mm to 20 mm or more Shape: varies widely in shape, from normal to narrow and sharply pointed, wide and

bizarre, slurred and notched

Normal T Wave: Represents normal repolarization of the ventricles Occurs during the last part of the ventricular systole Resting state of cardiac work Onset: first abrupt or gradual deviation from the ST segment (if ST segment is absent, T

wave begins at the end of the QRS complex) End: T wave returns to baseline Direction: (+), upright Duration: 0.10 to 0.25 sec or > Amplitude: 5 mm Shape: sharply or bluntly rounded, slightly asymmetrical

Abnormal T Wave:


EXAMPLES OF ECTOPIC P WAVE:• Wandering atrial pacemaker• PACs• Paroxysmal atrial tachycardia• Premature junctional contractions• Paroxysmal junctional tachycardia• PVCs

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Represents abnormal ventricular repolarization May result from:

- MI- ischemia- myocarditis- pericarditis- ventricular hypertrophy

- electrolyte imbalance- drugs (quinidine)- persons who are hyperventilating (athletes)

Onset and end: the same with normal T wave Direction: ay be (+) and abnormally tall or low (-), inverted or biphasic T wave may or may not be in the same direction as the QRS complex Amplitude: varies Duration: 0.10 to 0.25 sec or > Shape: rounded, blunt, sharply peaked, wide or notched

U Wave: Represents the final stage of ventricular repolarization Onset: first abrupt or gradual deviation from the baseline or the downward slope of the T

wave End: point where U wave returns to baseline or the downward slope of the T wave Direction: may be (+) or (-) Duration: not determined routinely Amplitude: <2mm Shape: rounded and symmetrical Represents repolarization of a small segment of ventricles such as the papillary muscles or septum) U wave is best seen when the heart rate is slow

PR Interval: Represents the time of progression of the electrical impulse from the SA node or

ectopic/escape pacemaker in the AV junction to the ventricular myocardium, including the depolarization of the atria

Onset and end: from the onset of the P wave and ends with the onset of QRS complex Duration: 0.12 to 0.20 sec

HR – taller PR interval HR – shorter PR interval

Abnormal PR Interval: Onset and end: the same as the normal Duration: > 0.20 sec or < 0.12 sec Prolong PR interval – delayed progression of impulses through the AV node Short PR Interval – impulses originates from ectopic pacemaker in the atria near AV

node or in the AV junction

QT Interval: Represents the time between the onset of depolarization and the termination of

repolarization of the ventricles Onset: point where the first wave of the QRS complex begins to deviate from the baseline End: point where the T wave returns to the baseline


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Duration: - HR – short QT Interval (0.29 sec)- HR – long QT Interval (0.39 sec)

Abnormally prolonged QT Interval: Electrolyte imbalance Drug overdose MI LV hypertrophy Hypothermia CNS disorders

Short QT Interval: Digitalis therapy hypercalcemia

RR Interval: Represents the time between two successive ventricular depolarizations Onset: considered to be the peak of one R wave End: peak of the succeeding R wave Duration:

- HR – short RR interval- HR – prolonged RR Interval

ST Segment: Represents the early part of repolarization of the right and left ventricles Onset and end: begins with the end of QRS complex and ends with the onset of the T wave “J” point – junction Duration: 0.20 sec or less Amplitude: flat but may be slightly elevated or depressed Appearance: flat, concave or arched

Abnormal ST Segment: Signifies abnormal ventricular depolarization Onset and end: same with normal Duration: 0.20 sec or less Amplitude: abnormal when it is elevated (1mm or more) 0.08 sec (2 small squares) Appearance: concave or arched, downsloping or upsloping Present in:

- MI- ventricular fibrosis aneurysm- pericarditis

PR Segment: Represents the time of progression of impulse from AV node through Bundle of His, bundle branches, Purkinje network to ventricular

myocardium Onset and end: begins with the end of P wave and ends with the onset of QRS complex


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Duration: 0.02 to 0.10 sec Amplitude: flat (isoelectric)

TP Segment: Interval between 2 successive P-QRST complexes during which electrical activity of the

heart is absent Onset and end: begins with the end of the T wave and ends with the onset of the following P

wave Duration: 0.0 to 0.40 sec or greater; dependent on the HR Amplitude: usually flat (isoelectric)

NURSING RESPONSIBILITIES IN ECG: Provide privacy ECG takes about 10 minutes and cause no discomfort Patient must lie still, relax and breathe normally Place leads on chest and limbs as labeled using water soluble gel or any conductive material

ARRHYTHMIA DETERMINATION

Step One: Identify and Analyze QRS Complex: Identify QRS complexes Note the duration and shape of QRS complexes Compare the QRS complexes

Step Two: Determine Heart Rate:A. THE 6-SECOND COUNT METHOD

count the number of QRS complexes within a 6 sec time interval multiply the complexes by a factor of 10 Counting the QRS complex is only applicable for rhythms occurring at normal

intervals Irregular rhythms are counted for one full minute for accuracy

B. R-R INTERVAL METHOD Rhythm must be regular Different ways


1. Measure the distance in seconds between the peaks of 2 consecutive R waves and divide this number into 60example: If the distance between 2 consecutive R

waves is 0.56 sec

2. Count the large squares (0.20 sec spaces) between 2 consecutive R waves- divide the number into 300 to obtain HR- 300 large blocks represent 1 minute on the ECG paper- example: If there are 2.5 large squares between 2 R

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C. TRIPLICATE METHOD For regular rhythm Select an R wave that lines up with a dark vertical line and label it “A” Number the next 6 vertical lines consecutively from L-R, “300”, “150”, “100”, “75”, “60”, “50” --- these numbers represent heart rate in beats/minute Identify the first R wave to the right of the R wave labeled “A”, and label this R wave “B” Identify the numbered dark vertical lines on either side of the R wave labeled “B” Estimate the distance of the R wave labeled “B” from the nearest of the 2 adjacent numbered

dark vertical lines with respect to the total distance between them Estimate the heart rate by equating the estimated distance of the R wave labeled “B” from

the nearest adjacent numbered, dark vertical line to beats/minute

Step Three: Determine the Ventricular Rhythm Use ECG calipers or count the number of blocks between QRS complexes to determine

regularity Examine each wave and segment for abnormalities Find the P waves

- present/absent- replaced by other wave forms?- identical/well formed?- change in shape?

Measure P-R interval- prolonged PR may be a precursor to heart blocks or MI

Look for pathologic Q waves- greater than 0.04 sec; more than 3 mm in depth; higher than R wave

Measure the QRS complex- do they fall early?- wide and bizarre?

Examine S-T segments- elevated ST (initial change in acute MI)- ST depression (ischemia)- ST changes (Ca and K changes)

Examine T wave- positive or negative?- deflected or peaked?- inverted T waves (ischemia)

Measure Q-T interval- should be less than the R-R interval- prolonged Q-T interval indicate digitalis toxicity, long term procainamide,

quinidine or magnesemia

Step Four: Determine Site of Origin of Arrhythmia DETERMINING PACEMAKER SITE OF ARRHYTHMIAS WITH P WAVES


3. Count the small squares (0.04 sec spaces) between 2 R waves and divide the number into 1500 to obtain HR- example: If there are 19 small squares between 2 R waves

1500 19

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ASSOCIATED WITH QRS COMPLEXES- P waves associated with QRS complexes regularly precede or follow QRS

Complexes- site of origin of the arrhythmia is the P wave

Pacemaker Site Direction of P Wave P-QRS Relationship PR IntervalSA node orAtria

Lower atria orProximal AV junction

Distal AV junction or Ventricles

(+) upright

(-) inverted

(-) inverted

P precedes QRScomplex

P precedes QRS complex

P follows QRS complex

0.12 – 0.20 secor <0.12 sec

<0.12 sec

none

- QRS complexes have no set relationship to the P waves, occurs at a different rate or if P wave is absent

- electrical impulses originate in an ectopic or escape pacemaker in the AV junction or ventricles

Cardiac Rhythm: Pattern or pace of heartbeat Affect the heart’s ability to pump blood efficiently Sinus rhythm – normal cardiac rhythm

Dysrhythmia; Conduction disorder Abnormally slow or rapid heart rate Does not proceed through the conduction system

Common Causes of Dysrhythmias: Myocardial ischemia Drug therapy Electrolyte imbalances Metabolic acidosis Hypothermia Degenerative age-related diseases

DYSRHYTHMIAS ORIGINATING IN THE SINOATRIAL (SA) NODE:1. Normal Sinus Rhythm (NSR):

Rhythm: atrial and ventricular rhythms are essentially regular Pacemaker site: SA node Heart rate: 60 – 100 beats/minute P waves: are identical and precede QRS complex; (+), upright PR Intervals: 0.12 to 0.20 sec R-R Intervals: may be equal or vary slightly QRS complexes: typically follow each P wave

2. Sinus Arrhythmia Rhythm: atrial and ventricular rhythms are regularly irregular


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Hear rate: 60 – 100 beats/minute; gradually increases during inspiration and slows during expiration; changes in rate occur in cycles

Pacemaker site: SA node P waves:

- identical and precede each QRS complex; (+), upright- difference between longest and shortest P-P or R-R interval is >0.16 sec

PR Intervals: normal and consistent RR Intervals: unequal QRS complex: normally follow each P wave Cause of Arrhythmia:

- normal phenomenon in children, adults and elderly- inhibitory vagal (parasympathetic) effect of respiration on the SA node- post MI- digitalis- morphine

Clinical Significance: does not require treatment; cause dizziness, palpitations, syncope

3. Sinus Bradycardia Dysrhythmia that proceeds normally through the conduction pathway but slower than usual 60 beats/minute or less May be pathologic in patients with:

- heart disorders- ICP- hypothyroidism- digitalis toxicity

May be insufficient to maintain CO DOC: Atropine SO4 IV

Clinical Significance: HR between 50-59 bpm - May be asymptomatic bradycardia HR between 30-45 bpm – marked sinus bradycardia symptomatic bradycardia – treated with atropine or transcutaneous pacemaker

- hypotension- CO- organ perfusion

4. Sinus Arrest and SA Exit Block: SINUS ARREST - Arrhythmia caused by episodes of failure in the automaticity of the SA

node, resulting in bradycardia, asystole or both SA EXIT BLOCK – arrhythmia caused by a block in the conduction of impulse from SA

node to the atria resulting to sinus arrest, bradycardia, asystole, or both Heart rate: 60 – 100 bpm or less Rhythm: irregular Pacemaker site: SA node P waves: identical and precede each QRS complex

- sinus arrest – not generated by SA node; no depolarization; dropped P wave

- SA exit block – no P wave; long P-P interval PR Interval: may be normal or abnormal RR Interval: unequal QRS complexes: normal unless there is intraventricular conduction disturbance; may be

absent when P wave does not occur

Cause of Arrhythmia:- block in the conduction pathway- parasympathetic stimulation


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- hypoxia- hyperkalemia- digitalis and propanolol overdose

Clinical Significance: Transient ventricular asystole Lightheadedness Syncope Slow HR

5. Sinus Tachycardia Dysrhythmia that proceeds normally through the conduction pathway but faster than usual 100-150 beats/min May be a physiologic response:

- strenuous activities- anxiety- fear and pain- fever- hyperthyroidism- hemorrhage- shock- hypoxemia

Clinical Significance: Benign arrhythmia in healthy individuals workload and oxygen requirement of the heart myocardial ischemia Treatment should be directed to the underlying cause of arrhythmia

6. Premature Atrial Contractions (PACs) Atrial conduction system initiates an early electrical impulse Impulse is initiated somewhere in the atria rather than the SA node P wave may look similar or differ slightly to other conducted impulses Contractions occur earlier than expected

CAUSES OF PACs:- Caffeine- Nicotine or SNS stimulants- Response to heart disease metabolic disorders (hyperthyroidism)

• Ectopic sites – may lead to supraventricular tachycardia

Clinical Significance: May occur in healthy individuals In heart disease:

- enhanced automaticity of the atria- reentry mechanism- may initiate supraventricular arrhythmia

7. Supraventricular Tachycardia Heart rate has a consistent rhythm but beats dangerously 150 beats/min Shortened diastole CO; heart failure CAD and SVT may have chest pain

DOC: Digitalis, ABs, CCBsTreatment:

- valsalva maneuver


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- unilateral carotid massage- immersion of face in ice water- IV adenosine- cardioversion- radiofrequency ablation

8. Atrial Flutter Single irritable atrial impulse outside the SA node causes atrial contraction at a rapid rate P wave is called F wave 200-400 beats/min AV nodes conducts some impulse to the ventricle Ventricular rate is slower than atrial rate

Cause of Arrhythmia:- In people with RHD- mitral or tricuspid valve disorders- CAD; HPN- cardiomyopathy- thyrotoxicosis- hypoxia- CHF

Clinical Significance:2:1 Atrial Flutter

- atria do not regularly contract and empty before each ventricular contraction, filling the ventricles during the last part of diastole - Loss of “atrial kick” results in incomplete filling of the ventricles before they contract

- CO reduced by 25% ECG: saw-toothed pattern Treatment:

- cardioversion- digitalis- quinidine- propanolol- verapamil

9. Atrial Fibrillation Several areas in the RA initiate impulses Disorganized, rapid activity atria quiver rather than contract Ventricles respond to atrial stimulus randomly Causes irregular ventricular heart rate CO DOC: Chemical Cardioversion

- Ibutilide (covert into sinus rhythm)- flecainamide, amiodarone- propafenone- anticoagulant

Elective cardioversion or digitalis (for not too slow ventricular rate) Maze procedure (not responsive to chemical cardioversion) – creates a new conduction

pathway Continue to experience episodic events

DYARHYTHMIAS ORIGINATING IN THE ATRIVENTRICULAR (AV) NODE:

1. Heart Block Interference in the transmission of impulses from the SA node through the AV node to the

ventricles


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1st and 2nd degree HB – impulse is delayed Complete HB – atrial impulse does not get through; ventricles develop own rhythm

independently Ventricular rate: 30-40 beats/min Treatment: Pacemaker

2. Premature Ventricular Contractions (PACs): Ventricular contractions occur early and independently Before SA node initiates electrical impulse Originates in the His-Purkinje system No P wave precedes the wide, bizarre-looking QRS complex If HR is very , the ventricles can repolarize after a PVC to receive atrial stimulation when it

is due PVCs cause “flip-flop” sensation in the chest (fluttering) s/s: pallor, nervousness, sweating, faintness Occassional PVCs related to: anxiety, stress, fatigue, alcohol withdrawal

PVCs as precursor of lethal dysrhythmias: 6 or more PVCs per minute Runs of bigeminy (every other beat is a PVC) Couplets (2 PVCs in a row) Runs of PVC (3 or more in a row) Multifocal PVCs (originating from more than one focus) R on T phenomenon (R wave falls on the T wave of the preceding complex)

Clinical Significance: PVCs in patients with no underlying heart disease require no treatment PVCs in patients with heart disease – indicate presence of enhanced ventricular

automaticity, reentry High risk for ventricular tachycardia or fibrillation All PVCs should be treated IMMEDIATELY

3. Ventricular Tachycardia Caused by a single irritable focus in the ventricle that initiates heartbeat Ventricular beat: 150-250 beats/minute CO May loss consciousness and become pulseless May progress to ventricular fibrillation

Clinical Significance: Aggravate existing AP, MI, CHF Loss of “atrial kick” Reduced CO May initiate ventricular tachycardia Treatment:

- Defibrillation if pulseless- cardioversion

DOC: lidocaine, procainamide, bretylium

4. Ventricular Fibrillation Rhythm of a dying heart From multiple sites within the ventricles Ventricular tachycardia can precipitate Ventricles do not contract effectively No CO Treatment: CPR; immediate defibrillation preceded by or followed with epinephrine Result from myocardial ischemia secondary to CAD, CHF, shock Disturbances from anxiety, pain, endocrine disorders, valvular diseases, invasive cath, drugs


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Affect pumping ability of the heart Affect CO

Signs & Symptoms: Weak, tired, faintness Anginal pain Palpitations, flutterings in the chest bp Irregular pulse; difficult to palpate Unusually fast or slow Apical and radial pulses differ

DRUG THERAPY FOR DYSRHYTHMIAS:

1. LIDOCAINE HYDROCHLORIDE (Xylocaine) ventricular excitability Suppress dysrhythmias S/E:

- dizziness, fatigue- drowsiness, nausea- vision changes- seizures, hypotension

Monitor cardiac rhythm Keep LSS available

2. PROCAINAMIDE HCL (Pronestyl) electrical conduction

3. BRETYLIUM TOSYLATE (Bretylol) Inhibit the release of norepinephrine Used in dysrhythmias resistant to other drugs Monitor pain at IV site Keep patient recumbent

4. VERAPAMIL HCL (Calan) Inhibit movement of calcium across cell membranes S/E:

- bradycardia- hypotension- heart block

Keep patient flat for 1 hour after administration

5. ADENOSINE (Adenocard) Slow rapid conduction through AV node S/E:

- facial flushing- chest pain

Monitor those with COPD

6. VASOPRESSORSEPINEPHRINE HCL (Adrenalin)

HR BP; force of contraction Used in asystole S/E:

- HPN- oliguria


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Give every 5 mins during cardiac resuscitation

7. CHOLINERGIC ANTAGONISTSATROPINE SULFATE

Block the effects of vagus nerve stimulation HR Use for bradydysrhythmias S/E:

- palpitations- tachycardia- urinary retention

Check HR before and after administration

8. CALCIUM CHLORIDE cardiac contraction in case of standstill Improve ineffective myocardial contractions when epinephrine fails S/E:

- HR- tingling- hypotension with rapid administration

Given IV Avoid extravasation

Elective Electrical Cardioversion None emergency procedure done by rapid (not necessarily) life-threatening dysrhythmias Delivers discharge after the physician To stop appearance of R wave Prevents disrupting the heart during critical period of ventricular repolarization Patient is sedated Electrodes are lubricated with special gel or moist saline pads are applied to the chest Electrical energy is released when the ventricles are depolarized Electrical current completely depolarizes the entire myocardium The heart repolarizes, pacemaker regains control and restore normal conduction through the

heart

Cardiac Pacing: Electronic device that delivers direct stimulation to the heart Initiate and maintain the heart rate May be a permanent implantable system, or Temporary system with an external pulse generator and percutaneously threaded leads, or Transcutaneous external system with electrode pads on chest

Clinical Indications: Symptomatic bradydysrhythmias Symptomatic heart blocks Prophylaxis

- after acute MI- pre or post cardiac

surgery- pre diagnostic tests

tachydysrhythmias


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Defibrillation: Only treatment for life-threatening dysrhythmias Same effect as cardioversion

Indications for Defibrillation: None functional ventricular contraction Pulseless ventricular tachycardia Ventricular fibrillation Asystole (cardiac arrest) – no R wave

Comparison of Defibrillation and Cardioversion:

Automatic Implantable Cardiac Defibrillator:

Candidates: Survived at least 1 episode of cardiac arrest due to ventricular dysrhythmia Experience recurrent episodes of ventricular tachycardia At risk for sudden cardiac death due to structural heart disease

Ex: cardiomyopathy (poor ventricular function) Generator with battery and 1 or 2 electrical leads that resembles a wire Lead wire is transvenously inserted through the subclavian or cephalic vein to the apex or

septum of RA Lead senses the cardiac rhythm and transmits to the generator Generator delivers electrical shock through the lead to restore cardiac rhythm, records and

resets itself Client perceives the shock as a “kick” to the chest AICDs may obliterate tachydysrhythmias and perform low-energy cardioversion AICDs are checked every 3-4 months

Stored information are retrieved by passing a wand over the generator AICDs lasts for 3-6 years Client must avoid devices with magnetic field

- lithotripsy machines- cautery devices- nerve stimulators - welding equipments- industrial electrical motors- signals from digital cellular cellphomes can mimic an abnormal heart

rhythm- electrical razors- remote controlled cars- metal detectors

NURSING PROCESS:ASSESSMENT

• Review client history


• schedule procedure in advance• eliminate atrial dysrhythmias• client is sedated before procedure• use less electrical energy

(50-100 joules) but levels can be administered delivers energy when machin senses the R wave in the ECG

• emergency procedure during emergency• eliminate ventricular dysrhythmias• client is not sedated but unresponsive• more electrical energy (200-360 joules)• delivers electrical energy whenever the

buttons on the paddles are pressed

ARRHYTHMIA

• General cardiovascular assessment• Trends in HR, BP, cardiac rhythm, LOC, UO, physiologic changes in response to activities• Results of hemodynamic monitoring devices (CVPs) and measurements of CO• Signs and symptoms• Level of knowledge

NURSING DIAGNOSIS: CO related to ineffective heart contractions secondary to dysrhythmia or ineffective response to treatment measures.

EXPECTED OUTCOME:Client will maintain adequate CO as evidenced by stable VS, no chest pain, dizziness or syncope and UO at least 1500 ml in 24 hours.

INTERVENTIONS:• Maintain physical and emotional rest ( tachycardia)• Provide supplemental oxygen for dyspnea, chestpain or syncope ( oxygen available for cellular metabolism)

EXPECTED OUTCOME:The nurse will monitor to detect dysrhythmias and manage and minimize any that occur.

INTERVENTIONS:• Monitor cardiac rhythm continuously• Ensure a patent IV access (emergency meds)• Administer antidysrhythmic drugs as prescribed (restore normal sinus)• Prepare for elective cardioversion or the use of temporary pacemaker• ACLS measures to be prepared


arrhythmia

Documents

dark vertical

ventricular

qrs complex

qrs complexes

av node

purkinje network

electrical

limb leads