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Management of bradydysrhythmias

available during a patient’s emergency depart- ment course, they are of use to the physician who admits the patient or sees the patient in follow-up.

Drug levels

A digoxin level should be obtained in patients taking this medication. Digoxin toxicity should be suspected if the patient presents with sympto- matic bradycardia, high-grade AV block, atrial tachycardias with block, or bidirectional VT. A urine toxicology screen should also be obtained, especially from those patients in whom illicit sympathomimetic substance abuse is suspected.

Management of

Sinoatrial block (sinus exit block)

Sinoatrial (SA) block is characterized by the absence of atrial depolarization. This can occur due to the SA node’s failure to generate an impulse or failure of the SA nodal impulse to con- duct to the atria. On the ECG, P waves are typically

absent. The most common factors that predispose to SA block are ischemia, hyperkalemia, excessive vagal tone or negative chronotropic drugs.

Typically, an alternate region of myocardium becomes the dominant pacemaker and manifests an escape rhythm. Junctional escape rhythms are

Cardiac dysrhythmias

Serious signs or symptoms?

Due to the bradycardia?

Yes

Yes No

No

Type II second-degree AV block or

Third-degree AV block?

• Prepare for transvenous pacer

• If symptoms develop, use transcutaneous pacemaker until transvenous pacer placed Observe

• Assess secondary ABCs (invasive airway management needed?)

• Oxygen–IV access–monitor–fluids

• Vital signs, pulse oximeter, monitor BP

• Obtain and review 12-lead ECG

• Obtain and review portable chest X-ray

• Problem-focused history

• Problem-focused physical examination

• Consider causes (differential diagnoses)

• Assess ABCs

• Secure airway non-invasively

• Ensure monitor/defibrillator is available Primary ABCD survey

Secondary ABCD survey or

Bradycardias

Relatively slow (rate less than expected relative to underlying condition or cause)

Slow (absolute bradycardia = rate 60 bpm)

Atropine 0.5–1.0 mg

Transcutaneous pacing if available

Dopamine 5–20 mcg/kg/minute

Epinephrine 2–10 mcg/minute

Isoproterenol 2–10 mcg/minute Intervention sequence

Figure 4.3

Bradycardias. bpm: beats per minute; ABCD: Airway, Breathing, Circulation, Defibrillation. Reproduced with permission, ACLS Provider Manual, © 2001, Copyright American Heart Association.

usually narrow-complex rhythms at 45–60 beats per minute, while escape rhythms originating from the His–Purkinje system are wide-complex with a rate of 30–45 beats per minute. Treatment of SA block with escape rhythms is indicated based on the patient’s symptoms.

Sick sinus syndrome

Sick sinus syndrome is a syndrome of abnormal- ities in cardiac impulse formation and AV con- duction that manifest as combinations of tachydysrhythmias and bradydysrhythmias. It is also referred to as tachy–brady syndrome. Most patients present to the emergency department with symptomatic bradydysrhythmias and a his- tory of episodic palpitations. The ECG manifes- tations include SA block, sinus or atrial bradycardia with bursts of an atrial tachydys- rhythmia (usually atrial fibrillation). Treatment of this syndrome is directed towards the specific manifestation of the syndrome – either augmen- tation of rate with atropine if the patient has bradycardia or rate control of an atrial tachydys- rhythmia with a beta-blocker, calcium channel blocker, or digoxin. One must exercise caution with these agents, as they may lead to excessive tachycardia or bradycardia. In the long term, most patients require a permanent pacemaker for support during excessive sinus bradycardia and an antidysrhythmic medication to suppress tachydysrhythmias.

First-degree atrioventricular block

AV block is divided into three grades, based on the ECG characteristics and the degree of the block. AV block is the result of impaired conduc- tion through the atria, AV node, or His–Purkinje system.

First-degree AV block is defined as prolonged AV conduction without loss of conduction of any single atrial impulse. On the ECG, it is manifested by a PR interval greater than 0.20 seconds. In first- degree AV block, the ventricular rate is not slow unless there is concomitant sinus bradycardia.

No specific treatment is indicated. Negatively chronotropic medications should be used with caution in these patients.

Second-degree atrioventricular block

In second-degree AV block, most but not all atrial impulses are conducted to the ventricles. It is divided into two subtypes based on the ECG appearance and the underlying pathophysiology.

Type I second-degree

Type I second-degree AV block (referred to as the Wenckebach phenomenon or Mobitz Type I block) is caused by a conduction defect within the AV node itself (Figure 4.4). On the ECG there is progressive lengthening of the PR interval on successive cardiac cycles until eventually a P wave is not conducted (“dropped”). This results in an irregular rhythm with “grouped beating,”

usually in pairs or triplets, but occasionally larger groups. Progressive lengthening of the PR intervals occurs because each successive atrial impulse arrives earlier and earlier in the refrac- tory period of the AV node, and therefore takes longer and longer to conduct to the ventricle.

Another feature is a progressive shortening of the RR interval in the grouped beats preceding the dropped beat. Type I second-degree AV block can occur following inferior wall myocardial infarction, and occasionally requires temporary pacing in this setting. In the majority of cases, however, it is asymptomatic and requires no treatment.

Cardiac dysrhythmias

Figure 4.4

Second-degree AV block, Mobitz Type I. From Da Costa D, Brady WJ, Edhouse J.

Bradycardias and atrioventricular conduction block.Br Med J2002;324(7336):

535–538. Printed with permission.

Type II second-degree

Type II second-degree AV block (or Mobitz Type II block) suggests a conduction block below the level of the AV node (Figure 4.5). This finding is much more ominous than Type I block, as there is a significant risk of progression to complete heart block. It is caused by degenerative disease of the conduction system, termed Lev orLenegre disease.

On the ECG there is preservation of a constant PR interval on conducted beats with sudden loss of P wave conduction. There is often a concomitant bundle branch block or baseline first-degree AV block reflecting underlying conduction system disease. Patients with this form of AV block can present with symptomatic bradydysrhythmias or syncope. As parasympathetic innervation is absent below the level of the AV node, atropine is not effective in treating bradycardia associated with this type of conduction block. Permanent pacemaker placement is indicated.

2 : 1 block

A third type of AV block exists that cannot be definitively classified as Type I or Type II. It is termed as 2 : 1 block and is characterized by two

P waves for every QRS complex. The location of the block cannot be determined with certainty based on the ECG alone, as it may represent a 2 : 1 Mobitz Type I block or high-grade conduction system disease. This type of conduction block can occur with digoxin toxicity or AV nodal ischemia.

Further invasive electrophysiologic (EP) testing involving measurement of H–V conduction times is necessary to clarify the location of the block and determine further treatment.

Third-degree atrioventricular block

Third-degree AV block occurs when there is absolutely no conduction of atrial impulses to the ventricle (Figure 4.6). Atrial and ventricular impulses may be present, but each occur inde- pendent of the other. This phenomenon is also termed AV dissociation. With third-degree AV block, a secondary pacemaker below the AV node assumes control and produces an escape rhythm.

This escape pacemaker can originate from low in the AV node or from the His–Purkinje system.

This is usually evident from the width of the QRS complex. On the ECG, there are visible P waves with a constant PP interval that continuously

Cardiac dysrhythmias

Figure 4.5

Second-degree AV block, Mobitz Type II. From Da Costa D, Brady WJ, Edhouse J.

Bradycardias and atrioventricular conduction block.Br Med J2002;324(7336):

535–538. Printed with permission.

Figure 4.6

Third-degree AV Block. From Da Costa D, Brady WJ, Edhouse J. Bradycardias and atrioventricular conduction block.

Br Med J2002;324(7336):535–538. Printed with permission.

marches through the strip. In addition, there are visible QRS complexes with a constant RR interval that also marches through. As there is AV dissoci- ation, and the atria and ventricles beat independ- ent of each other, the PR interval is variable. In some instances, it may be difficult to identify AV dissociation as the atrial and ventricular rates may be similar (termed isorhythmic AV dissocia- tion), and longer rhythm strips may be necessary.

Management of third-degree AV block depends on the patient’s clinical status. Drugs that can cause AV nodal block should be reversed. If there is evidence of significant hemodynamic compromise, transcutaneous or transvenous pacemaker placement is indicated. Unless a clearly reversible cause of third-degree block is present, most patients will require permanent pacemaker placement. With all forms of AV block, the patient should be questioned regarding risk factors for Lyme disease, myocarditis, endocar- ditis, or lupus erythematosus, as these systemic illnesses can contribute to disease of the cardiac conduction system.

Management of