Week 5: Cardiology Part 1/5: Dysrhythmias, Syncope, & AICDs

Brief (usually less than 10 seconds) tonic–clonic seizure activity can accompany syncope of any etiology. This activity is not accompanied by postictal disorientation, and it does not represent true seizure activity. For cerebrovascular disease to cause a loss of consciousness, either both cerebral hemispheres or the brainstem must be deprived of blood flow. Therefore transient ischemic attacks and stroke are rarely the cause of syncope. Screening laboratory studies have been shown to add little to establishing a cause of syncope. In most cases, hypoglycemia is clinically suspected and abnormal electrolytes rarely account for a loss of consciousness. Anemia from bleeding is usually clinically evident. Tilt-table testing reveals abnormalities in 20% to 70% of patients whose emergency department evaluation leaves them without a diagnosis.

Although the definition of abnormal ECG varies among the many studies examining their role in the diagnosis of syncope, particular attention should be paid to any nonsinus rhythm, signs of ischemia, or conduction abnormalities.

Syncope is defined as an interruption in cerebral perfusion causing a transient loss of consciousness. Syncopal events should last less than 5 minutes and patients should return immediately to their baseline mental status as cerebral perfusion is restored. Lateral tongue biting is more commonly associated with seizure, and the most specific sign for a seizure, while anterior tongue biting can be seen with syncope. Urinary incontinence is frequently seen in seizure patients, but would be unusual following syncope.

A is incorrect, because the R-R interval classically shortens as the PR interval lengthens. B describes a first-degree AV block, not a second-degree AV block. C is correct. D is incorrect, because Mobitz type II blocks more commonly feature a prolonged QRS complex than Mobitz type I AV blocks.

The sinoatrial (SA) node is innervated by both the sympathetic and parasympathetic nerves, which alter its discharge rate. The SA node is the normal pacemaker of the heart with an inherent rate of 60 to 100 beats per minute. The arterial supply for the SA node is either the right coronary artery (55%) or the circumflex artery (45%). The atrioventricular (AV) node is usually supplied by the right coronary artery 90% of the time with the remaining 10% originating from the circumflex. The inherent rate of the AV node is 30 to 40 beats per minute, which is primarily used as an escape rhythm if the primary pacemaker of the heart, the SA node, fails.

Lidocaine, which may abolish the ventricular rhythm completely, is contraindicated because it may cause cardiac standstill. Atropine, due to its vagolytic properties, enhances sinus node automaticity and AV nodal conduction. Isoproterenol, a beta-adrenergic agonist, has both inotropic and chronotropic effects. Isoproterenol increases myocardial oxygen demand and should be used with caution in ischemic myocardium. Glucagon has been shown to be useful in the treatment of bradyarrhythmias secondary to beta-adrenergic blocking agents and calcium antagonists. Glucagon stimulates the SA node directly giving some mild increase in heart rate. Glucagon also increases cardiac contractility.

In wide-complex atrial fibrillation, any drug that slows conduction through the AV node can cause ventricular fibrillation from rapidly conducted impulses via the accessory pathway. Adenosine, calcium channel blockers, and beta blockers are all contraindicated in this setting. Though procainamide is considered first-line pharmacotherapy in the stable patient with wide-complex atrial fibrillation, electrical cardioversion is more effective. Amiodarone is also less effective and carries the risk of slowing AV conduction.

As per the 2010 AHA guidelines, CPR should only take place until the defibrillator is ready, and defibrillation at 200 J should be performed as soon as possible in VF arrest. Escalating doses of 50–100–150 J are no longer recommended and 200 J should be used for biphasic defibrillators. Though epinephrine is recommended as part of ACLS, it should not take precedence over defibrillation and has not shown long-term benefit in the treatment of cardiac arrest.

This patient represents stable atrial fibrillation (AF) with a rapid ventricular rate. For patients presenting with AF and a rapid ventricular response, treatment is directed at slowing the ventricular rate. Calcium channel blockers, in particular diltiazem, slow ventricular response within the first few minutes of IV administration. Beta blockers such as atenolol or metoprolol are about as effective as calcium channel blockers for rate control, but are seldom used because of a higher incidence of hypotension. Neither calcium channel blockers nor beta blockers are particularly effective at producing cardioversion to sinus rhythm. Digoxin is no better than placebo in the first few hours of rate control for rapid atrial fibrillation. Stable patients do not need cardioversion in the ED. This patient has an unknown time period since the atrial fibrillation has manifested. Anticoagulation is an important management issue for patients with AF. Not only are patients with AF that lasts more than several days at risk for systemic embolization, but recent evidence suggests that even shorter periods of AF may carry a risk of embolization, particularly following conversion to sinus rhythm. Patients should be considered for anticoagulation prior to cardioversion for all presentations of atrial fibrillation that is stable. Amiodarone slows ventricular rate and increases the frequency of conversion to sinus rhythm after greater than 24 hours. There is no difference between placebo and amiodarone in the first 8 hours. Amiodarone thus has little utility in the new-onset stable patient with AF and a rapid rate.

Placement of a magnet over a pacemaker will cause synchronous pacing at model-specific rates.