Arrhythmias

Sinus bradycardia

Sinus bradycardia is simply a slowing of the normal heart rhythm below 60 bpm. It can be physiologic, result from damage to the SA node, ie by ischemia or cardiomyopathy, or caused by drugs or metabolic causes (ie hypothyroidism).

Intrinsic SA node dysfunction is called sick sinus syndrome can cause dizziness, syncope, or confusion.

If the SA node is sufficiently impaired, escape rhythms can emerge from the AV node, bundle of His, or ventricles. Junctional escape beats have no P waves and have normal, narrow QRS complexes, with a rate of 40-60 bpm. Retrograde P waves can sometimes be observed. Ventricular escape rhythms are slow - 30-40 bpm - and have widened QRS complexes. Morphology depends on area of origin.

First Degree AV block

With first degree block, there is a delay of over 0.2 sec (5 boxes) between the PR interval. However, the 1:1 relationship is maintained between atrial and ventricular contractions. Impairment is usally in the AV node. Reversible causes include heightened vagal tone, ischemia, and drugs that suppress conduction, ie digitalis, beta blockers, calcium channel antagonists, and other antiarrhythmic medications. Structural causes include myocardial infarction and chronic degenerative changes.

Second degree AV block

Second degree heart block is the intermittent failure of AV conduction, resulting in some P waves not being followed by a QRS complex.

In Mobitz Type I block (also known as Wenckebach), there is a gradual lengthening of PR interval until an impulse is completely blocked. It is usally benign and is commonly seen in athletes, children, and people with high vagal tone.

Mobitz type II block is characterized by the sudden intermittent loss of AV conduction, without a gradual PR lengthening. The block may persist for two or more atrial beats. It is usually caused by block distal to the AV node. It usually indicates severe disease.

Third degree AV block

In third degree block, there is complete failure of conduction between the atria and ventricles. P waves and QRS complexes occur independently of each other, and the QRS shape and rate depend on the site of origin.

Complete heart block can occur in children following maternal transfer of Rho antibody, ie as occurs with SLE.

Sinus Tachycardia or Supraventricular Tachycardia

Sinus tachycardia is an SA discharge rate above 100 bpm, with normal P waves and QRS complexes. It most often results from increased sympathetic tone, as occurs during exercise. It can also be caused by fever, hypoxemia, hyperthyroidism, hypovolemia, and anemia.

SVT is the most common sustained dysrhythmia in children. It is not life-threatening, but can be symptomatic.

Treatment includes valsava maneuver, adenosine, digoxin, beta blockers, or cardioversion if unstable.

Premature Atrial Contractions

Premature atrial contractions (PACs) are common in healthy and diseased hearts. They originate from automaticity or reentry in an atrial site, and can be exacerbated by sympathetic stimulation, caffeine, alcohol, and stress. They are usually asymptomatic but can cause palpitations. PACs are abnormal P waves and are followed by normal QRS complexes, unless it falls during the refractory period. Beta blockers are the preferred treatment if needed.

Atrial Flutter

Atrial flutter is characterized by regular atrial activity at a rate of 180-350 bpm. Many of these fall during the ventricular refractory period, resulting in a much slower heart rate. Atrial flutter is typically caused by a large rentry circuit. P waves often have asinusoidal or sawtooth appearance. It generally occurs with heart disease, and can can be transient, persistent, or permanent. Antiarrhythmic medications can make the situation more dangerous by slowing the atria enough to allow 1:1 ventricular contraction, speeding up the ventricles. Flutter can be treated with cardioversion, implantable burst pacing, catheter ablation, or antiarrhythmic drugs, ie beta-blockers, calcium channel blockers, or digoxin.

Atrial Fibrillation

Atrial fibrillation is so common and potentially dangerous it merits its own page.

Premature Ventricular Contractions

PVCs arise when an ectopic ventricular focus fires an action potential. This appears as a widened QRS complex, as the impulse travels in an altered path.If every alternating beat is a PVC, it is called bigeminy. Consecutive PVCs are called couplets, and three are triplets.

PVCs are common in healthy people, particularly adolescents. Benign PVcs are single, uniform, disappear with exercise, and have no structural abnormalities present.

Ominous PVCs can also occur with underlying conditions and can lead to severe dysrhythmias or sudden death.

Ventricular Tachycardia

Ventricular tachycardia is a run of three or more PVCs. QRS complexes are wide, and occur at rates of 100-200, or sometimes faster. These wide QRS complexes distinguish ventricular tachycardia from supraventricular causes. Sustained VT lasts linger than 30 seconds, can induce syncope, or requires termination by drugs or cardioversion. V tach is commonly seen in patients with structural heart disease, including myocardial infarction, heart failure, hypertrophy, electrical diseases, valvular heart diseases, and congenital heart diseases. Reentry circuits are most commonly old scars.

Ventricular tachycardia is an emergency, as it can quickly deteriorate into ventricular fibrillation. Cardioversion is normally done, or drugs such as amiodarone, procainamide, or lidocaine can be used. Underlying facotrs need to be sought, and pacemakers are very useful for future episodes. Idiopathic VT exists and is rarely life-threatening.

Torsades de Pointes

Torsades de pointes is a form of ventricular tachycardia with varying amplitudes of QRS waves. It sis commonly caused by drugs, electrolyte imbalances (hypokalemia or hypomagnesemia), on top of prolonged QT intervals. It is usually symptomatic but frequently self-limiting.

Ventricular Fibrillation

Ventricular fibrillation is an emergency. Its significance merits its own page.