30: Cardiac Dysrhythmias

CHAPTER 30 Cardiac Dysrhythmias

William A. Baker, MD, Christopher M. Lowery, MD

1 Name some of the causes of sinus bradycardia

Causes include high vagal tone, medications, hypoxia, hypothyroidism, intrinsic sinus node dysfunction, electrolyte abnormalities, and hypothermia.

2 A postoperative patient develops light-headedness with sinus bradycardia and a heart rate of 36. Systolic blood pressure is 83 mm Hg. What treatment should be undertaken?

Atropine, 0.5 mg intravenously, may be effective in increasing heart rate. In addition, search for clues to the etiology of the bradycardia such as those listed in Question 1.

3 How is first-degree atrioventricular block identified?

The PR interval is abnormally prolonged (>0.20 second), but all of the P waves conduct (i.e., they are followed by a QRS complex).

4 Describe the types of second-degree atrioventricular block

Mobitz type I (Wenckebach): Involves progressive lengthening of the PR interval followed by a nonconducted P wave, followed by a conducted P wave with a shorter PR interval. When lengthening of the PR is difficult to identify, comparing the PR duration before and after the blocked P wave may confirm Wenckebach. The level of block is usually in the atrioventricular (AV) node with Mobitz I.

Mobitz type II: Far less common than Wenckebach. With Mobitz II block there is no progressive prolongation of the PR interval, which for the first conducted beat is the same as the PR interval before the nonconducted beat. The level of the AV block is generally below the AV node with Mobitz II, as suggested by a wide QRS complex. Permanent pacing is usually indicated in patients with Mobitz II block.

2:1 AV block: A rhythm in which every other P wave is conducted. Because there is no opportunity to evaluate successive conducted beats, 2:1 AV block is neither Mobitz I nor Mobitz II.

5 What is third-degree atrioventricular block?

This is also known as complete heart block, with no P waves conducted to the ventricles. The RR interval is regular unless there are premature ventricular complexes. The level of the block may be either at the AV node (usually with a narrow QRS) or below the node (with a wide QRS and a particularly slow heart rate).

Complete heart block is one form, but not the only form, of AV dissociation. Not infrequently a patient will have a rhythm in which only occasional P waves conduct, as indicated by a transient shortening of the RR interval. Officially this does not constitute complete heart block since a P wave does get through the AV node to the ventricles. This incomplete AV dissociation is commonly referred to as high-degree AV block.

6 In addition to complete heart block, what are some other causes of atrioventricular dissociation?

Other causes include accelerated junctional rhythm and ventricular tachycardia (VT).

7 What are some of the causes of atrioventricular block?

As with sinus node dysfunction, causes of AV block may be intrinsic (associated with structural heart disease) or extrinsic (related to external factors).

Extrinsic causes: include medications, electrolyte abnormalities, hypothyroidism, hypoxia, and increased vagal tone

Intrinsic conduction abnormalities: may arise in a patient with coronary artery disease (sometimes as a complication of acute myocardial infarction), ventricular hypertrophy, myocarditis, sarcoidosis, recent cardiac surgery (especially valve surgery), or calcific degeneration of the conduction system

8 Your patient exhibits transient evidence of both sinoatrial node and atrioventricular node dysfunction with simultaneous slowing of the sinus rate and second-degree atrioventricular block, type I. What is going on?

Simultaneous sinoatrial and AV nodal blockade is commonly seen with increased vagal tone, often in a sleeping patient or a patient with vagally mediated syncope. Another consideration is a pharmacologic effect such as that seen with β-blockers or adenosine.

9 Which antihypertensive agents are to be avoided in patients with significant bradycardia or heart block?

β-Blockers such as metoprolol and esmolol, nondihydropyridine calcium blockers (verapamil and diltiazem), and central sympatholytics such as clonidine should be avoided. In addition, lithium and some anticonvulsants may cause bradycardia.

10 Name some of the arrhythmias seen with digoxin toxicity

Sinus bradycardia, AV block, atrial tachycardia with 2:1 block, accelerated junctional rhythm, and VT are seen with digoxin toxicity.

11 Is it always appropriate to treat sinus tachycardia with β-blockers?

Not always. Sinus tachycardia may be a response to many insults, and the best approach is to identify why the patient is tachycardic and treat the underlying cause. In some cases such as myocardial ischemia from hypertension, β-blockers may be a useful adjunct. In other cases (e.g., acute bronchospasm, pulmonary edema, tamponade, and hypovolemia) β-blockers can be harmful. Pain, fever, volume shifts, and anemia are all important causes of tachycardia to consider in a postoperative patient.

12 What is meant by the term paroxysmal supraventricular tachycardia?

Paroxysmal supraventricular tachycardia (PSVT) is a regular tachycardia with sudden onset and offset that usually has a narrow complex. It may be aborted with vagal maneuvers such as carotid sinus massage or Valsalva. Generally PSVT is responsive to agents such as adenosine, β-blockers, or verapamil if the rhythm is AV nodal dependent. PSVT is actually a family

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