Chapter 23: Treatment of Cardiac Arrhythmias Flashcards by Pauline Mendoza

A disturbance of heart rate or
rhythm caused by an abnormal rate of electrical impulse
generation by the SA node or by the abnormal conduction
of impulses

Arrhythmia (Dysrhythmia)

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Arrhythmias are classified by
1. Origin:
2. Pattern
3. Speed/Rate

Origin: Ventricular, Supraventricular (Atrial)

Pattern: Fibrillation or flutter

Speed/Rate: Tachycardia or bradycardia

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Etiology of Arrhythmias

● Congenital
● Hypertension
● previous MI
● Heart failure
● Valvular heart disease
● irritability after surgery
● degeneration of conductive
tissue (sick sinus syndrome)

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Arrhythmia Risk Factors

● Diabetes
● Obstructive sleep apnea
● smoking
● alcohol
● increased pulse pressure
● family history
● LVH
● increased BMI

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Pathogenesis & Clinical Manifestations of Arrhythmias

● can be changes in either the heart’s rate
or its cardiac conduction pattern
● some arrhythmias will affect rate only, some rhythm
only, some affect both rate and rhythm

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Normal Heart Rate

60-100 beats/min
(an arrhythmia is considered to be any significant deviation
from the normal range)

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More than 110 beats/min;
Increased sympathetic stimulation (fear, pain, emotional stress, exertion, exercise, caffeine, nicotine, amphetamines), exercise (transient physiologic state)

Tachycardia

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Less than 50 beat/min
■ normal in well trained athletes, in individuals taking beta blockers, pts with TBI or brain tumors, and increased vagal stimulation to the pacemaker of the heart
■ Organic disease of the sinus node, heart disease
■ Symptoms: fatigue, dyspnea, syncope, dizziness, angina, diaphoresis
■ Medical intervention is not usually necessary unless symptoms interfere with
function, low cardiac output, drug or angina induced.
■ Atropine or Mechanical pacemaker can be used to reestablish normal rhythm

Bradycardia

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Detected when patients become symptomatic or during monitoring for
another cardiac condition.
Symptoms: Asymptomatic, syncope or near syncope, dizziness, chest
pain, dyspnea, palpitations
sudden cardiac death
Altered cardiac output -> impaired perfusion of the brain or
myocardium

Arrhythmias as variations from the normal rhythm of the heart

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● Irregular rhythm that may be a normal variation in athletes,
children, and older people or may be caused by and alteration in vagal stimulation.
● May be respiratory or
nonrespiratory, associated with
infection, drug toxicity, or fever
● Treatment for the respiratory type
of sinus arrhythmia is not necessary; all others sinus arrhythmias are treated by providing intervention for the
underlying cause

Sinus Arrhythmia

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● Most common type of supraventricular tachycardia (SVT) or chronic arrhythmia
● SVT is also called paroxysmal SVT or paroxysmal atrial tachycardia
● Irregularly irregular
● No P waves
● Absence of isoelectric baseline

Atrial Fibrillation

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SVT is also called

Paroxysmal SVT or paroxysmal atrial tachycardia

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Self-terminating episode <7 days

Paroxysmal AF

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not self-terminating, >7 days

Persistent AF

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> 1 year

Long-standing Persistent AF

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> 1 year, wherein rhythm control interventions are not pursued or are
unsuccessful

Permanent (accepted) AF

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Irregular contraction of the atrial myocardium

Quivering

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Atrial Fibrillation

● blood remains in the atria after they contract and the ventricles do not fill properly
● as the heart rate increases, there is less time for passive ventricular filling from
the atria
● blood flow from the heart diminshes, creating a drop in oxygen levels
● Sx: SOB, palpitations, fatigue, fainting

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Rheumatic heart disease, dilated cardiomyopathy, atrial septal defect, hypertension, mitral valve prolapse, recurrent cardiac surgery, after MI,
hypertrophic cardiomyopathy, hyperthyroidism, medications, diabetes, obesity, pneumonia, alcohol intoxication/withdrawal

Secondary AF

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People with AF are prone to:

blood clots

(because blood components remain in the atria and aggregate and attract other
components, triggering clot formation.)

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AF can result in:

HF, cardiac ischemia, and
arterial emboli that can result in ischemic
stroke

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An electrical phenomenon that results in INVOLUNTARY, UNCOORDINATED MUSCULAR CONTRACTIONS of the
VENTRICULAR MUSCLE
A FREQUENT CAUSE OF CARDIAC ARREST
Treatment is directed toward DEPOLARIZING the muscle, thus ending the irregular contraction and allowing the heart to resume normal regular contractions.

Ventricular Fibrillation

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Interruption in the passage of impulses through the heart’s electrical system. This may occur because the SA node misfires or the impulses it generated are not properly transmitted through the heart’s conduction system.

Heart Block

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Heart block causes, symptoms, and treatment:

● Causes: coronary artery disease, hypertension, myocarditis, acute MI
overdose of cardiac meds
● Symptoms: fatigue, dizziness, fainting

● can affect any people at any age, but primarily affects older people

● Treatment: mild cases do not require treatment, Medications, pacemakers

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● Or brady-tachy syndrome ● complex cardiac arrhythmia and conduction disturbance ○ bradycardia alone, bradycardia alternating with tachycardia, or bradycardia with atrioventricular block (AV) block ● associated with advanced age, CAD, HF, or drug therapy ● Degeneration of conductive tissue necessary to maintain normal heart rhythm ● symptoms: light-headedness, dizziness, near or true syncope

Sick Sinus Syndrome

Rapid depolarization; no influx

PHASE 0

Brief period of repolarization: K channels open, K leaves the cell

PHASE 1

Plateau phase: Ca channels open, slow, prolonged, influx of Ca, K still leaves the cell. No net change in cell charge

PHASE 2

Repolarization is complete: closing of Ca+ channels, stops Ca influx. Unopposed exit of K ions

PHASE 3

Slow spontaneous depolarization: membrane ions allow continuous leak of sodium ions into the cell, gradual decrease in K exit from the cell; intracellular Ca release from SR; net change is accumulation of positive cell charge, reaching threshold and phase 0 again

PHASE 4

Normal conduction of Cardiac Action Potential

SA Node > Atrial Conduction Pathways > AV Node > Bundle of His > Right and Left bundle branches > Purkinje Fibers

Mechanisms of Cardiac Arrhythmias

Any factor can disrupt the normal cardiac excitation process leading to arrhythmic contractions: ○ metabolic and electrolyte imbalances ○ abnormal autonomic influence ○ toxicity to other drugs ○ psychological distress ○ myocardial ischemia ○ infarction ○ heart failure, hypertension ○ genetic factors ● Abnormal impulse generation ● Abnormal impulse conduction ● Simultaneous abnormalities of impulse generation

Type of arrhythmia with: Fibrillatory waves ● MC sustained cardiac arrhythmia in older adults ● Atrial rate >300-350 bpm; ventricular rate varies ● Rhythm: irregularly irregular ● P waves: no discernable P wave ● QRS: normal

Atrial Fibrillation

Type of arrhythmia with: Sawtooth pattern ● Macroreentrant atrial tachycardia ● Organized reentry creates organized but rapid atriala activity ● Rate: atrial rate is 250-350bpm; ventricular rate varies ● Rhythm: variable ● P-waves: saw-tooth appearance ● QRS: usually normal

Atrial Flutter

Atrioventricular Junctional Arrhythmias

Junctional Rhythm: 40-55 bpm Junctional Tachycardia: 100-200 bpm

Pacemaker: AV junction with ventricular rate of 40-60bpm P wave may appear, after or buried within QRS complex Rhythm: regular QRS: narrow

Junctional (Atrioventricular) Rhythm

Variable Conduction Disturbances

- Atrioventricular block - Bundle branch block - Fascicular block

Ventricular Arrhythmias

Premature ventricular contractions - variable Ventricular tachycardia - 140-200 bpm Ventricular fibrillation - Irregular; totally uncoordinated rhythm

-prematurely occurring QRS complex which is wide and bizarre-looking - no preceding p-wave -T wave is opposite in deflection compared to the bizarre QRS complex

Premature ventricular complex

-continuous irregular activation with no discrete QRS complexes - chaotic or fine undulations -no Pwaves - no effective cardiac output (CO)

Ventricular Fibrillation

● Bind to membrane sodium channels ● Class I drugs normalize the rate of sodium entry into the cardiac tissues and thereby help control cardiac excitation and conduction ● Sodium influx plays an important role during phase 0 of cardiac action potential generation ● Inhibition of Sodium channels decrease membrane excitability ● Class I drugs stabilize the cardiac cell membrane and normalize the rate of cardiac cell firing.

Class I - Sodium Channel Blockers

● Produce a MODERATE slowing of phase 0 depolarization and moderate slowing of action potential propagation through the myocardium ● Prolong repolarization of the cardiac cell, thus lengthening the interval before a second action potential can occur - increases the effective refractory period

Class IA

Slows the upstroke, slows conduction, prolongs QRS by blockade of sodium channels

Quinidine (Class IA)

○ Same as quinidine; also prolongs the action potential duration (a Class 3 action). ○ Ganglion blocking properties: reduces peripheral vasoconstriction ○ AE: hypotension ○ Uses: Ventricular tachyarrhythmis

Procainamide (Class IA)

○ Effects similar to quinidine ○ Negative inotropic effects (depresses contractility) ○ Uses: atrial flutter, atrial fibrillation, hypertrophic cardiomyopathy ○ AE: anticholinergic actions - precipitation of glaucoma, constipation, dry mouth, urinary retention, Torsades de pointes

Disopyramide (Class IA)

● MINIMAL ability to slow phase 0 depolarization; MINIMAL slowing of cardiac conduction ● Shorten cardiac repolarization - Effective refractory period is decreased

Class IB

○ Lidocaine is a local anesthetic; useful in the acute IV therapy of ventricular arrhythmias ○ Blocks both open and inactivated cardiac Na channels ○ Decreases automaticity by reducing the slope of phase 4 and altering the threshold for excitability ○ AE: seizures in large IV rapid doses; tremor, dysarthria, altered level of consciousness in maintenance therapy ■ Nystagmus is an early sign of lidocaine toxicity

Lidocaine (Class IB)

○ Analogue of lidocaine that has been modified to reduce first-pass hepatic metabolism ○ AE: dose related: nausea, tremor; minimized by taking the drug with food

Mexiletine (Class IB)

Indications: ventricular tachycardia, premature ventricular contractions (PVCs) Tocainide

Class IB

● Marked decrease in the rate of phase 0 depolarization ● Marked slowing of cardiac conduction; little effect on repolarization

Class IC

○ Blocks Na channel; blocks K channels ○ AE: dose-related blurred vision; exacerbation of CHF, provocation or exacerbation of potentially lethal arrhythmias, heart block

Flecainide (Class IC)

○ Blocks Na channel; blocks K channels ○ B adrenergic blockade ○ Major effect: to slow conduction in fast-response tissues ○ Prolongs PR and QRS duration ○ Indication: maintains sinus rhythm in patients c SVTs including Atrial Fibrillation; ventricular arrhythmias ○ AE: acceleration of ventricular response in atrial flutter ○ Increased severity of reentrant vtach, exacerbates HF; b adrenergic: sinus bradycardia and bronchospasm

Propafenone (Class IC)

Indications: ventricular tachycardia and PVCs

Class IC

● Mainstay in arrhythmia treatment ● Beta blockers decrease excitatory effects of the SNS and related catecholamines on the heart (NE, Epi) ○ Decrease cardiac automaticity ○ Prolongs the effective refractory period - slowing the heart rate ○ Controls the function of the AV node

Class II - Beta Blockers

Class II Indications

Atrial tachycardia, ventricular tachycardia

Class II (Beta Blockers) example

Acetabulol, atenolol, emsolol, metoprolol, nadolol, propranolol, sotalol, timolol AE: for nonselective beta blockers, bronchoconstriction in patients with BA and COPD, excessive slowing of cardiac conduction

● Drugs that prolong ERP by prolonging the Action Potential (AP) ● These drugs prolong the action potential by blocking the potassium channels or by enhancing inward current through sodium channels

Class III: Drugs that Prolong Repolarization

Class III Effects and Indications

○ Limits potassium efflux during phase 2 and 3 of the AP ○ lengthens time interval before a subsequent AP can be initiated Indication: ventricular tachycardia, ventricular fibrillation, SVTs, post-op Afib

○ Class I,II,III IV effect ○ Indication: supraventricular arrhythmias, atrial fibrillation ○ AE: pulmonary toxicity, thyroid problems, liver damage, bradycardia, heart block in preexisting sinus or AV node dse.

Amiodarone (Class III)

○ Class III effect; 100% bioavailable ○ Indications: maintenance of sinus rhythm in atrial fibrillation

Dofetilide (Class III)

○ analog of amiodarone that lacks iodine atoms ○ for treatment of atrial flutter and fibrillation ○ no pulmonary toxicity and thyroid dysfunction in short-term studies;

Dronedarone (Class III)

Ibutilide

Class III

Class III Adverse Effects

proarrhythmic: torsades de pointes

● Selective ability to block calcium entry into myocardial and vascular smooth-muscle cells ● Inhibit calcium influx by binding to specific channels during phase 2 -> alter the excitability and conduction of cardiac tissues Effects: ○ Decrease rate of discharge of SA node ○ Inhibit conduction velocity through the AV node

Class IV: Calcium Channel Blockers

Class IV indications

SVT, Afib

○ Used to treat CHF, A fib, paroxysmal AV nodal reentrant tachycardia

Digitalis glycosides

Class IV Drugs; both normalize heart rate by reducing calcium effects on the SA and AV nodes

Verapamil, Diltiazem

Class IV Adverse Effects

bradycardia (<50bpm), peripheral vasodilation -> headache and dizziness

○ Ventricular arrhythmias (ie. Torsades de pointes)

Magnesium

○ Used to terminate severe arrhythmias (ie. reentrant supraventricular tachycardia) ○ Binds to adenosine receptors and affects heart rate by decreasing calcium entry into myocardial tissues

Adenosine

○ Help control atrial and ventricular arrhythmias with minimal proarrhthmic effect

Ranolazine

Nonpharmacologic treatment

● Implants: ○ Pacemakers ○ Cadiovert defibrillators ● Surgical: ○ Electrode catheter ablation