Clinical Aspects of Cardiac Arrhythmias (Coromilas) - 11/9/16

Question 1

Sinus Bradycardia

Answer 1

Slowing of normal heart rhythm as a result of decreasing firing of SA node

Rate < 60 bpm

SB at rest or during sleep, or for trained athletes = normal/benign

Conversely, pathologic SB –> result from:

• intrinsic SA node disease
  
  • ​ischemic heart disease
  • cardiomyopathy
• extrinsic factors that affect the node
  
  • ​meds (beta-blockers, certain calcium channel blockers)
  • metabolic causes (e.g. hypothyroidism)

Question 2

Sick Sinus Syndrome (SSS)

Answer 2

Intrinsic SA node dysfunction causing bradycardia

Treatment: anticholinergic drugs (e.g. atropine) or beta-adrenergic agents (e.g. isoproterenol) –> transiently accelerate HR

If problem is chronic and not corrected by removal of aggravating factors –> permanent pacemaker required

SSS most common in elderly patients who also are susceptible to atrial fibrillation

Question 3

Escape rhythms (2)

Answer 3

If SA node activity becomes impaired or if there is conduction block of impulse from SA node, escape rhythms can emerge from the more distal latent pacemakers

1. Junctional escape rhythm
   
   1. arise from AV node or proximal bundle of His
   2. Normal, narrow QRS (appear at rate of 40-60 bpm)
   3. QRS complexes not preceeded by normal P waves b/c impulse originates below the atria
   4. Retrograde P waves may be observed as impulse propagates from more distal pacemaker backward to atrium
   5. Abnormally inverted (negative deflection) in II, III, and aVF –> activation of atria from inferior direction
2. Ventricular escape rhythm
   
   1. Even slower rates (30-40 bpm)
   2. Abnormally widened QRS complexes (ventricles not depolarized by normal rapid simultaneous conduction over RBB and LBB but rather from more distal point in conduction system)
   3. Escape rhythm originating from LBB will cause RBBB QRS pattern b/c impulse depolarizes LV first and then spreads more slowly through RV

Junctional and ventricular escape rhythms = protective backup mechanisms that maintain a heartbeat and CO when sinus node or normal AV conduction fails

Treatment similar to SSS

Question 4

Impaired conduction b/w atria and ventricles can result in 3 degrees of AV conduction block.

First-degree AV block

Answer 4

Prolonged delay between atrial and ventricular depolarization - slowed conduction in AV node

PR interval is prolonged (>0.2 sec, >5 small boxes)

usually asymptoic

Question 5

Impaired conduction b/w atria and ventricles can result in 3 degrees of AV conduction block.

Second-degree AV block (Type I)

Answer 5

2nd-degree AV block: intermittent failure of AV conduction

Result: some P waves that are not followed by QRS

Type I (wenckebach): degree of AV delay gradually increases with each beat until an impulse is completely blocked, such that there is no QRS after P wave for a single beat

Less severe than Type II

Question 6

Impaired conduction b/w atria and ventricles can result in 3 degrees of AV conduction block.

Second-degree AV block (Type II)

Answer 6

Sudden intermittent loss of AV conduction, without preceding gradual lengthing of PR interval

Block may persist for two or more beats (i.e. two sequential P waves not followed by QRS complexes)

Permanent structural damage in His-Purkinje system

Treatment: pacemaker

Question 7

Impaired conduction b/w atria and ventricles can result in 3 degrees of AV conduction block.

Third-degree AV block (Complete)

Answer 7

Complete failure of conduction b/w atria and ventricles

No relationship b/w P waves and QRS complexes b/c the atria depolarize in response to SA node activity, while a more distal escape rhythm drives ventricles independently

Question 8

Tachyarrhythmias

Answer 8

when HR is > 100 bpm for three beats or more

Result from one of three mechanisms:

• • enhanced automaticity
• • reentry
• • triggered activity

Categorized into those that arise above ventricles (supraventricular) and those that arise within ventricle

Question 9

Sinus tachycardia

Answer 9

SA node discharge rate greater than 100 bpm

Normal P wave

Normal QRS complexes

Rhythm results from increased sympathetic and/or decreased vagal tone

Physiologic response to exercise

Pathologic response to fever, hypoxemia, hyperthyroidism, hypovolemia, anemia

Question 10

Atrial flutter

Answer 10

Rapid, regular atrial activity

rate 180-350 bpm

Many of the fast impulses reach AV node during refractory period and do not conduct to ventricles –> slower ventricular rate….

Thus, atrial rate is 300 bpm and 2:1 block occurs at AV node (every other atrial impulse finds AV node refractory), ventricular rate is 150 bpm

Usually caused by reentry over large anatomically fixed circuit (since large area being depolarized… leads to “sawtooth” appearance)

Question 11

Atrial fibrillation

Answer 11

Chaotic rhythm with atrial rate so fast (350-600) that distinct P waves are indiscernible on ECG

As with atrial flutter, many of atrial impulses encounter refractory tissue at AV node, allowing only some of depolarizations to be conducted to ventricles in a very irregular fashion (“irregularly irregular” rhythm)

Avg ventricular rate in untreated AF = 140-160 bpm