Arrhythmias
last authored: April 2012, David LaPierre
last reviewed:
Introduction
Arrhythmias are disruptions normal electrical rhythm of the heart, resulting from alterations in impulse formation, conduction, or both. Arrhythmias may arise from altered impulse at the SA node, the AV node, Purkinje fibres, or regions of cardiac muscle. Abnormally slow heart rates are called bradycardias, while fast rhythms are called tachycardias.
Arrhythmias they can be transient or permanent. They are often caused by damage to the heart, as can follow ischemia and acute coronary syndromes. Drug toxicity, electrolyte imbalance, or infection can also cause arrhythmias, while congenital causes are also possible.
Arrhythmias can be normal. Sinus arrhythmia is a phasic change with respiration. It is seen in most children. Sinus tachycardia is seen during exercise or times of stress. Premature atrial contractions (PACs) can be normal or caused by electrolyte imbalance, hyperthyroidism, surgery, or digoxin toxicity.
Many arrhythmias do not require treatment, but medications, pacemakers, and catheter ablation can all be used.
When an arrhythmia produces severe hypotension or cardiac arrest, immediate action is required. Electrical cardioversion (defibrillation), cardiac pacing, or medications can all be used.
Tachyarrhythmias
- sinus
tachycardia - premature atrial
contractions - atrial
flutter - atrial
fibrillation - premature vent.
contractions - ventricular
tachycardia - torsades
des pointes - ventricular
fibrillation
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.
Accessory-Mediated SVT
- caffeine, nicotine, or other stimulants
- stress, anxiety, sleep deprivation
- numerous medications
SVT is the most common sustained dysrrhythmia in children. It is not life-threatening, but can be symptomatic.
Treatment includes carotid massage, valsava maneuver, adenosine, calcium channel blockers, beta blockers, digoxin, or cardioversion if unstable.
Catheter ablation can be used to destroy distinct rentry foci, mapped using electrophysiologic techniques.
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 a common, potentially life-threatening condition meriting 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 factors 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 is 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 a life-threatening emergency. Its significance merits its own page.
Treatment
Treatment of tachyarrhythmias is to mitigate the underlying cause of abnormal rhythm and protect against lethal consequences. Medications must be used with caution due to the high risk of further arrhythmic complications and death.
Electrical cardioversion and defibrillation is used to depolarize the bulk of myocardial tissue, interrupting rentry and allow the sinus node to regain pacemaker control. Implantable cardioverters can be used to automatically cardiovert or defibrillate a heart.
Altered Impulse Formation
Escape Rhythms
If the SA node becomes suppressed and fires less frequently than normal, latent pacemakers can escape overdrive suppression and initiate an escape beat. This can occur durng very strong parasympathetic activity.
Ectopic Rhythms
If an area of tissue develops an intrinsic rate of firing faster than that of the SA node, ectopic (premature) beats can occur. They can occur due to high catecholamine concentrations, hypoxemia, ischemia, electrolyte disturbances, and drugs such as digitalis.
Abnormal Automaticity
Injured cardiomyocytes can acquire automaticity and spontaneously depolarize, though means not fully understood, but is likely due to slow calcium current.
Triggered Activity
Under certain conditions, action potentials can trigger abnormal depolarizations that result in extra heart beats or rapid arrhythmias. Afterdepolarizations appear as oscillations and can be early, during repolarization, or delayed. Early afterdepoloarizations are most common during conditions that prolong APs, such as long GT syndrome.
Conduction Blocks
Conduction blocks can be transient or permanent, and can be unidirectional or bidirectional. They typically cause bradyarrhythmias. Various conditions can cause conduction block, including ischemia, fibrosis, inflammation, and certain drugs.
Reentry
Reentry occurs when impulses circuluate around a unidirectional conduction block, recurrently depolarizing a region of cardiac tissue. This can lead to tachyarrhythmias. Reentry around distinct anatomic pathways usually appears as monomorphic tachycardia on an ECG, while fibrillation is likely caused by multiple circulation reentry wave fronts.
Resources and References
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