chapter12 clinical aspects of arrhythmias

5 basic questions to consider when encountering a patient with arrhythmia

identification, pathogenesis, precipitating factors, clinical presentation, treatment

Types of bradyarrhythmias

SA node, escape rhythms, AV conduction system

Sinus bradycardia

slowing of the normal R, as a result of decreased firing of the SA node less than 60 bpm

When is sinus bradycardia normal?

at rest and during sleep

When is sinus bradycardia pathologic?

intrinsic SA node disease (IHD, CM) or extrinsic factors that affect the node (medication)

What is the clinical presentation of Sinus bradycardia?

fatigue, dizziness, syncope due to fall in CO

Sick Sinus Syndrome (SSS)

intrinsic SA node dysfunction that causes periods of inappropriate bradycardia

SSS has similar symptoms as sinus bradycardia, such as-

dizziness, confusion, syncope

What is the treatment for SSS?

IV anticholinergic drugs (atropine) of beta-adrenergic agonists (isoproterenol), or pacemaker implant in chronic cases

SSS is common in elderly patients, and is susceptible to -

SVT, especially Afib

Bradycardia-tachycardia syndrome

result of atrial fibrosis that impairs function of SA node and predisposes to Afib or Aflutter. During the rhythm, overdrive suppression of SA node occurs and the tachycardia is followed by bradycardia

Treatment of Bradycardia-tachycardia syndrome

antiarrhythmic drugs for tachycardia + pacemaker to prevent bradycardia

Escape rhythms

rhythms that emerge from the latent pacemakers when the SA node is impaired or conduction impulse from the SA node is blocked

Junctional escape rhythm

arise from the AV bundle at a rate of 40-60 bpm, normal narrow QRS, no P-waves or inverted P-waves

Why are P-waves hidden or inverted in Junctional escape rhythms?

because the impulse originates below the atria, and an impulse more distal propagates retrograde toward the atria

Ventricular escape rhythms

characterized by slower rate at 30-40 bpm and WIDENDED QRS

LBB causes a RBBB QRS pattern because

the impulse depolarizes the LV first and then spreads more slowly to the RV

RBB causes a LBBB QRS pattern because

the RV depolarizes first then the impulse spreads more slowly to the LV

Escape rhythms that originate more distally in the LV myocardium causes…

even wider QRS complexes

Impaired conduction between the atria and the ventricles can result in…

3 types of AV conduction blocks

First degree AV block

PRI is lengthened (>.20sec), every P-wave has an QRS complex

In First degree AV block, AV node can be:

reversible: increased vagal tone, transient nodal ischemia, drugs or structural: MI, degenerative disease of conduction system with age

Wenckebach is seen in -

children, young athletes, sleep

Second degree AV block

intermittent failure of AV conduction, with some P-waves NOT followed by QRS complex

Type 1 second degree block

PRI gradually increases with each beat until an impulse is completely blocked, there is no QRS after the P-wave

Type II second degree block

more serious, sudden intermittent loss of AV conduction without preceding gradual lengthening of PRI (consistent PRI)

High grade AV block

when Mobitz II block persists for 2 or more beats

What causes Mobitz II?

conduction block distal to the AV node and the QRS is often widened

Third degree AV block

complete failure of conduction between atria and ventricles caused by MI or degeneration of conduction pathways with advanced age

EKG of complete AV block

electrically disconnects the atria and the ventricles, so there is no relationship between P-waves and QRS complexes

AV dissociation

when atria and ventricles beat independently without relationship between P-waves and QRS complexes

Tachyarrhythmias

when HR is more than 100 bpm for more than 3 beats and result from enhanced automaticity, reentry, or triggered activity

Sinus tachycardia response to vagal maneuvers

atrial rate may slow

Reentrant SVT response to vagal maneuvers

abruptly terminate

WAP response to vagal maneuvers

AV block may increase, doesn't usually revert

Atrial Flutter response to vagal maneuvers

AV block may increase

Sinus Tachycardia

SA node discharge rate of over 100 bpm with normal P-waves and QRS complexes resulting from increased sympathetic or decreased vagal tone

Sinus tach is a normal response to

exercise

Pathologic conditions of Sinus tachycardia

fever, hypoxemia, hyperthyroidism, hypovolemia, anemia

Camel hump

P-waves are very close T-waves in sinus tachycardia

Premature Atrial Complexes (PAC)/ Atrial Premature Beats (APB)

originate from automaticity or reentry in atrial focus outside the SA node and are often exacerbated by sympathetic stimulation

EKG of PAC

earlier than expected P-wave with abnormal shape, followed by normal QRS

Blocked APB

when P-wave is not followed by QRS due to PAC falling during absolute refractory period of the AV node and it cannot conduct to ventricles

APB with aberrant conduction

when P-wave is followed by abnormally wide QRS (RBBB)

Atrial Flutter

rapid, regular atrial activity at a rate of 180-350 bpm, with fast impulses reaching the AV node in its refractory period and NOT conduction to ventricles

Atrial flutter is caused by…

reentry over large anatomically fixed circuit, more commonly the right atrial tissue along TV annulus

EKG of A Flutter

saw-toothed F-waves, followed by normal QRS at a fraction rate of 2:1, 3:1, 4:1 due to AV conduction blocking atrial impulses

Symptoms of A Flutter

palpitations, dyspnea, or weakness at higher rates

Why are antiarrhythmic medications paradoxically more dangerous in A flutter?

it allows the AV conduction to recover between impulses, conducting at a 1:1 rate and therefore producing very high ventricular rates

Conversion of atrial flutter to sinus rhythm

electrical synchronized cardioversion, temporary or permanent pacemaker, pharmacologic therapy, catheter ablation

Atrial Fibrillation

chaotic rhythm with a fast atrial rate of 350-600 discharges/min, allowing only some of the depolarization to reach the ventricles in a very irregular fashion

EKG of A Fib

no P-waves, only low amplitude undulations followed by QRS complexes and T-waves

Mechanism of A fib

multiple wandering reentrant circuits within the atria with the rhythm repetitively shifting between fibrillation and flutter

Paroxysmal A fib

initiated by rapid firing of foci in sleeves of atrial muscle that extend into pulmonary veins

How does enlarged atrium affect Atrial fibrillation

increases the potential of reentrant foci are needed to sustain Afib

Diseases that increase LA size and pressure that promote Afib

HR, MV disease, HTN, thyrotoxicosis, alcohol consumption

3 aspects of treatment for A fib

ventricular rate control, assessment for need of anticoagulants, consider methods to restore sinus rhythm

Antiarrhythmic drugs for Afib

betablockers, calcium channel antagonists

Anticoagulant drugs for Afib

to reduce risk of thromboembolism in LAA and stroke

Chads-Vasc

criteria for long-term anticoagulant therapy : Congestive HF, HTN, Age, Diabetes, prior Stroke, Vascular disease, Sex

Cardioversion

attempted chemically with antiarrhythmics first and then electrical cardioversion to sinus rhythm

Maze procedure

surgical option that places multiple incision in the LA and RA to disrupt formation of reentry circuits

Percutaneous catheter ablation

applying radio frequency or cryothermal energy delivered by intracardiac catheters to areas of the LA and Pv

Catheter ablation of AV node

causing complete AV block followed by pacemaker implant

LAA ligation or occlusion

exclude the appendage from the circulation to prevent thrombus formation in patients intolerant to anticoagulation

Paroxysmal Supraventricular Tachycardia (PSVT)

manifested by sudden onset and termination, atrial rates of 140-250 bpm, narrow and normal QRS complexes unless aberrantly conducted

Mechanism of PSVT

reentry involving AV node, atrium, accessory pathway → AVNRT, AVRT, WPW, concealed accessory pathways

AVNRT

most common form of PSVT

EKG for AVNRT

shows regular tachycardia with narrow QRS and hidden P-waves or retrograde P-waves (atypical)

Symptoms of AVNRT

palpitations, light headedness, dyspnea or syncope, angina, pulmonary edema

Treatment of AVNRT

vagal maneuvers, adenosine, beta-blockers, calcium channel antagonists, catheter ablation

AVRT

one limb of the reentrant loop is constituted by an accessory pathway

Bypass tract

abnormal band of myocytes that spans the AV groove and connects the atrial and ventricular tissue separately from normal conduction pathway

Antegrade

atria to ventricles

Retrograde

ventricles to atria

Patients with WPW syndrome are predisposed to PSVTs because the accessory pathway can provide a potential limb of reentrant loop with 2 forms: and

orthodromic and Antidromic

Orthodromic AVRT

impulse travels antegrade down AV node to ventricles, then retrogradely up accessory tract to atria → no delta wave, negative P-wave AFTER QRS

Antidromic AVRT

impulse travels antegrade down accessory path and retrogradely up the AV node → wide QRS, no P-wave

Lown-Ganong-Levine syndrome

pre-excitation syndrome with PSVT due to AV nodal reentry → short PRI but normal, narrow QRS

Treatment for AVRT

sodium and potassium channel blockers, catheter ablation

Concealed accessory pathways are only capable of…

retrograde conduction, with ventricles depolarized normally thru AV node

Focal Atrial Tachycardia

results from automaticity of an atrial ectopic site or reentry

EKG of AT

appearance of Sinus tachycardia, but P-wave morphology is different, indicating depolarization from abnormal location

Treatment of AT

beta-blockers, calcium channel blockers, Class IA, IC, and III antiarrhythmics, ablation

Multifocal Atrial Tachycardia

irregular rhythm with multiple (at least 3) P-wave morphology and average HR over 100 bpm

MAT is caused by:

abnormal automaticity in SEVERAL foci in atria or triggered activity, common in pulmonary disease or hypoxemia

Ventricular arrhythmias

more dangerous than SVT rhythm disorders, causing sudden cardiac death

Ventricular Premature Complexes

arise when ventricular ectopic focus fires an action potential

EKG for PVC

widened QRS complex, no P-waves

PVCS are caused by:

electrolyte abnormalities, caffeine, beta-adrenergic medications, MI

Ventricular Tachycardia

series of 3 or more PVCs

Sustained VT

lasts more than 30 sec → syncope, requires termination via cardioversion or drugs

Non-sustained VT

lasts less than 30 sec → self-terminating

Monophorphic VT vs polymorphic VT

in PVT, rate and morphology changes from beat to beat, caused by acute MI and inherited predisposition to PVT (long Q-T and Brugada syndrome)

Treatment of VT

antiarrhythmics, electric cardioversion, ICD

Treatment of idiopathic VT

betablockers, calcium channel clockers or catheter ablation

Torsades de Pointes

a form of polymorphic VT with various amplitudes linked to long Q-T interval caused by hypokalemia, hypomagnesemia, persistent bradycardia, drugs, or long Q-T prolongation

Ventricular Fibrillation

life-threatening arrhythmia with disordered, rapid stimulation of ventricles with no coordinated contraction, use electro cardioversion (defibrillation)