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 of specific rhythms that fit these characteristics, including AV nodal reentrant tachycardia (AVNRT), AV reentrant tachycardia (AVRT), and some types of atrial tachycardia. Other causes of narrow-complex tachycardia are listed in Table 30-1.

TABLE 30-1 Differential Diagnosis for a Narrow-Complex Tachycardia

13 What is multifocal atrial tachycardia? When is it seen?

Multifocal atrial tachycardia (MAT) is a supraventricular rhythm (SVT) rhythm with heart rate greater than 100 when there are at least three different P wave morphologies. MAT is commonly seen in patients with significant lung disease or high catecholamine states.

14 What is the main contraindication to adenosine?

Bronchospasm. Despite its short half-life, adenosine can provoke severe exacerbations of bronchospasm, and it should be used with caution in patients with a history of asthma or reactive chronic obstructive pulmonary disease.

15 A patient suddenly develops an irregular rhythm with heart rate of 170. A 12-lead electrocardiogram shows no P waves. What is the likely rhythm? How should it be managed?

The patient has probably developed atrial fibrillation with rapid ventricular response. If the patient is unstable, electrical cardioversion would be appropriate. If symptoms are mild, hemodynamics may improve with reduction in heart rate (rate control) with agents such as diltiazem or β-blockers. Of note, rate control via initiation of moderate doses of β-blockers is contraindicated in patients with significant left ventricular dysfunction who are not already on β-blockers. Some patients are candidates for chemical cardioversion with agents such as amiodarone, procainamide, or ibutilide. This may be followed by electrical cardioversion if the antiarrhythmic agent does not convert the rhythm on its own.

Patients with intractable rapid atrial fibrillation who require a pressor should receive an agent that does not increase tachycardia further. In most of these cases phenylephrine is generally preferable to dopamine if a pressor must be used.

16 Is adenosine useful for the treatment of atrial fibrillation?

No. Adenosine does not convert atrial fibrillation, and the half-life is so short (seconds) that reduction of the heart rate is quite brief. For atrial flutter adenosine may occasionally make the diagnosis more clear if it is not already evident from the baseline tracing. Adenosine causes transient slowing of the RR interval, which makes flutter waves easier to identify.

17 What should be done to reduce the risk of stroke in a patient with chronic or paroxysmal atrial fibrillation?

Anticoagulation should generally be undertaken in cases of atrial fibrillation when it is not contraindicated. For a patient who recently underwent an invasive procedure, the surgeon should be involved in the decision regarding the risk of bleeding posed by anticoagulation.

Stable patients who have been in atrial fibrillation for more than 48 hours should not undergo cardioversion unless they have been anticoagulated for 3 weeks or have had a transesophageal echocardiogram to exclude atrial clot.

18 What is a wide-complex tachycardia? What is in the differential diagnosis?

A wide-complex tachycardia is a fast (>100 beats/min) rhythm in which the QRS duration is greater than 120 milliseconds. The differential diagnosis includes VT, SVT with aberrant conduction, and conduction from the atria to the ventricles via an accessory pathway (Wolff-Parkinson-White [WPW] syndrome).

19 A 60-year-old man with a history of prior anterior myocardial infarction develops a monomorphic wide complex tachycardia after noncardiac surgery. What is the most likely diagnosis, and which treatments would be appropriate or inappropriate?

In the setting of structural heart disease, a wide-complex tachycardia should be assumed to be VT until proven otherwise. In unstable patients electrical cardioversion is appropriate.

For stable patients a 12-lead electrocardiogram (ECG) should be obtained to aid definitive diagnosis. Amiodarone, procainamide, and lidocaine are reasonable therapeutic choices for monomorphic VT.

Tragic outcomes may occur when VT is unrecognized and mistakenly treated as SVT. Diltiazem and verapamil (which depress contractility and lower blood pressure) may be life threatening in these patients.

20 What characteristics of a wide-complex tachycardia suggest ventricular tachycardia rather than supraventricular tachycardia with aberrancy?

AV dissociation, if present, confirms the diagnosis of VT.

The ability of a P wave to conduct to the ventricle and capture the rhythm with a narrow QRS complex is diagnostic for VT.

Concordance (QRS entirely above the baseline in all precordial leads or below the baseline in all precordial leads) is seen in a minority of cases of VT. When present, concordance strongly suggests VT. However, the absence of concordance is common with VT and does not imply that a wide-complex tachycardia is SVT with aberrancy.

When the interval from the beginning of the QRS to the nadir of the S wave is greater than 100 milliseconds in any precordial lead, VT is suggested.

The QRS in patients with SVT with aberrancy usually looks like a typical right or left bundle-branch block. If it does not look like either one, the rhythm is usually VT.

A P wave before each wide QRS suggests SVT with aberrancy.

In some cases a previous 12-lead ECG from the patient shows the same wide QRS morphology without tachycardia, suggesting SVT rather than VT.

21 Why is it important to distinguish between polymorphic and monomorphic ventricular tachycardia?

The differential diagnosis and treatment for each are somewhat different. Monomorphic VT is common in patients with structural heart disease (such as a previous Q wave myocardial infarction), but it is generally not caused by acute ischemia. Polymorphic VT may be seen in a variety of settings. Patients may have a long QT interval associated with polymorphic VT, commonly referred to as torsades de pointes. This may arise from medications, electrolyte derangements, a congenital predisposition (long QT syndrome), severe bradycardia, or myocardial ischemia (Figure 30-1).

Figure 30-1 Torsades de pointes.

(From Olgin JE, Zipes DP: Specific arrhythmias: diagnosis and treatment. In Libby P et al: Braunwald’s heart disease: a textbook of cardiovascular medicine, ed 8, Philadelphia, 2008, Saunders.)

22 How is torsades de pointes treated?

If the patient is unstable with ongoing VT, electrical cardioversion is warranted.

If an offending drug (such as procainamide) is suspected as the cause, the drug should be discontinued immediately.

Magnesium should generally be given even if the patient’s serum levels are normal. Look for and correct other electrolyte abnormalities such as hypokalemia.

Acute myocardial ischemia should be considered and treated if present.

In certain cases isoproterenol or temporary pacing (to avoid bradycardia) may be life saving. Pacing is the treatment of choice when torsades is the consequence of a severe bradyarrhythmia such as complete heart block.

23 How are patients with congenital long QT syndrome and syncope treated?

Syncope in these individuals may be a consequence of torsades de pointes, a type of VT. If not recognized and treated, a fatal recurrence of torsades could develop. Treatment is generally with β-blockers and a pacemaker/ defibrillator. Relatives of the affected individuals should be screened for congenital long QT syndrome.

24 Are implantable cardioverter-defibrillators curative for ventricular arrhythmias?

No. They merely treat the episodes with shock or overdrive pacing. A patient with intractable VT must be stabilized before being considered for such a device. Many patients with such a device need adjunctive pharmacologic therapy to minimize VT (and firing of the device).

25 Do all patients with an accessory pathway have a delta wave (WPW pattern) on their baseline electrocardiogram?

No. Many accessory pathways conduct only in a retrograde fashion (from ventricle to atrium) or have very slow antegrade (atrial to ventricular) conduction.

These patients may or may not have narrow-complex SVT (AVRT). In contrast, some patients have a delta wave on the baseline ECG with no clinical symptoms. In many cases these asymptomatic patients do not need pharmacologic treatment or invasive electrophysiologic testing.

26 A 25-year-old patient presenting with palpitations is noted to have a wide-complex, irregular tachycardia at a rate of 260. The upstroke of the QRS is slurred. The blood pressure is normal, and the patient appears well. What is the most likely diagnosis? What treatments are indicated? What treatments are potentially harmful?

This is probably a case of atrial fibrillation with WPW syndrome (Figure 30-2). The wide QRS is a result of conduction down the accessory pathway from the atrium to the ventricular myocardium. In an unstable patient electrical cardioversion is warranted. In a stable patient amiodarone or procainamide would be reasonable. In these patients avoid using digoxin, calcium blockers, adenosine, and β-blockers. Heart rate may actually increase, and ventricular fibrillation has been reported from AV nodal blocking agents. Elective radiofrequency ablation of the pathway is indicated. This is a percutaneous catheter-based approach that is performed by a cardiac electrophysiologist.

Figure 30-2 Irregularly irregular wide complex tachycardia in a young patient with Wolff-Parkinson-White syndrome and atrial fibrillation. The QRS complex is wide because the ventricles are activated via an accessory pathway rather than the atrioventricular (AV) node. Drugs that primarily block the AV node such as digoxin, diltiazem, verapamil, β-blockers, and adenosine are contraindicated in this situation because they may precipitate ventricular fibrillation.

27 Why is it important to save electrocardiogram tracings that document an arrhythmia?

A cardiologist or cardiac electrophysiologist will be able to give much more meaningful advice if the arrhythmia can be properly diagnosed. The initiation and termination of the event may help to determine the specific type of arrhythmia. General descriptions of the arrhythmia such as bradycardia, or wide complex tachycardia may not be enough to enable specific treatment.

Artifact cannot be diagnosed unless the actual tracing is available for analysis. Finally, third-party payers (such as insurance companies) may be reluctant to reimburse for devices such as pacemakers and defibrillators unless there is proof of an arrhythmia.