Arrhythmia

Atrial fibrillation (AF or Afib) is a supraventricular tachyarrhythmia and the most common kind of arrhythmia. It is caused by rapid, uncontrolled atrial contractions and uncoordinated ventricular responses. There are many conditions that can cause AF, usually damage to the heart (e.g., coronary artery disease, previous myocardial infarction). Diagnosis is confirmed by an electrocardiogram that will show an “irregularly irregular” heartbeat with no distinct P waves and narrow QRS complexes. AF increases the risk of thromboembolic events. Treatment is primarily based on ventricular rate and rhythm control, which can be achieved through drugs and/or cardioversion. Anticoagulation (AC) is administered if the patient is at significant risk for thromboembolic events.

Long QT syndrome (LQTS) is a disorder of ventricular myocardial repolarization that produces QT prolongation on electrocardiogram (ECG). Long QT syndrome is associated with an increased risk of developing life-threatening cardiac arrhythmias, specifically torsades de pointes. The condition may be congenital or acquired. Congenital LQTS is attributed to genetic mutations affecting cardiac ion channels. Acquired LQTS usually results from drug therapy or electrolyte abnormalities. Patients can be asymptomatic or present with palpitations, syncope, seizures, and even sudden cardiac death. Diagnosis is established with ECG along with medical and family history, laboratory workup, and other cardiac tests. Treatment is determined by etiology. Acquired LQTS requires removal of the offending drug or drug combinations and correction of electrolyte abnormalities. Congenital LQTS management involves beta blockers, aggressive treatment of electrolyte imbalances, avoidance of medications that prolong the QT interval, and placement of an implantable cardioverter–defibrillator (ICD).

Atrioventricular (AV) block is a bradyarrhythmia caused by delay, or interruption, in the electrical conduction between the atria and the ventricles. Atrioventricular block occurs due to either anatomic or functional impairment and is classified into 3 types. The 1st-degree block is due to delayed conduction through the AV node. The 2nd-degree block is characterized by progressive conduction delay or intermittently blocked conduction. The 3rd-degree block involves total interruption in conduction between the atria and ventricles, causing complete AV dissociation. Patients may be asymptomatic or may present with syncope, chest pain, dyspnea, and bradycardia depending on the severity of the block. Electrocardiography (ECG) establishes the diagnosis, and treatment is based on the type of block and hemodynamic stability of the patient.

A complex system of coordinated electrical circuitry within the heart governs cardiac muscle activity. The heart generates its own electrical impulses within its pacemaker cells. The signal then travels through specialized myocytes, which act as electrical wiring, distributing the signal throughout the heart. Once the signal “leaves” the specialized conduction system, it passes to each myocyte through channels called gap junctions (which connect myocytes to each other) and causes them to contract. An electrical impulse is created by the opening and closing of ion channels, allowing the flow of charged particles across the myocardial cell membrane. The flow of charged particles changes the voltage across the membrane and opens up additional voltage-gated channels, allowing the signal to propagate throughout the heart.

A tachyarrhythmia is a rapid heart rhythm, regular or irregular, with a rate > 100 beats/min. Tachyarrhythmia may or may not be accompanied by symptoms of hemodynamic change. Pathologic tachyarrhythmias resulting in hemodynamic instability can be caused by intrinsic cardiac abnormalities, systemic diseases, or medication toxicity. Supraventricular arrhythmias are called narrow-complex tachycardias and originate in the sinoatrial (SA) node, atrial myocardium, or atrioventricular (AV) node. Ventricular arrhythmias originate below the AV node and are characterized by a wide QRS complex. Diagnosis is made by physical exam and ECG. Management is directed toward the type of tachyarrhythmia present and its underlying cause.

Long QT syndrome (LQTS) is a disorder of ventricular myocardial repolarization that produces QT prolongation on electrocardiogram (ECG). Long QT syndrome is associated with an increased risk of developing life-threatening cardiac arrhythmias, specifically torsades de pointes. The condition may be congenital or acquired. Congenital LQTS is attributed to genetic mutations affecting cardiac ion channels. Acquired LQTS usually results from drug therapy and/or electrolyte abnormalities. Patients can be asymptomatic or present with palpitations, syncope, seizures, and even sudden cardiac death. Diagnosis is established with ECG along with medical and family history, laboratory workup, and other cardiac tests. Treatment is determined by etiology. Acquired LQTS requires removal of the offending drug and correction of electrolyte abnormalities. Congenital LQTS management involves avoidance of triggers of arrhythmia, intake of beta-blockers, and placement of an implantable cardioverter-defibrillator (ICD).

Atrioventricular (AV) block is a bradyarrhythmia caused by delay, or interruption, in the electrical conduction between the atria and the ventricles. Atrioventricular block occurs due to either anatomic or functional impairment, and is classified into 3 types. The 1st-degree block is due to delayed conduction through the AV node. The 2nd-degree block is characterized by progressive conduction delay or intermittently blocked conduction. The 3rd-degree block involves total interruption in conduction between the atria and ventricles, causing complete AV dissociation. Patients may be asymptomatic or may present with syncope, chest pain, dyspnea, and bradycardia depending on the severity of the block. Electrocardiography (ECG) establishes the diagnosis, and treatment is based on the type of block and hemodynamic stability of the patient.

An electrocardiogram (ECG) is a graphic representation of the electrical activity of the heart plotted against time. Electrocardiograms are simple, inexpensive, noninvasive, and readily obtained. Adhesive electrodes are affixed to the skin surface allowing measurement of cardiac impulses from many angles. The ECG provides 3-dimensional information about the conduction system of the heart, the myocardium, and other cardiac structures. In the healthy state, an ECG records predictable, reproducible waves and complexes, which correspond to electromechanically coupled physiologic events in the heart. Under pathologic conditions, the ECG can detect arrhythmias, ischemia, inflammation, and more.

Cardiac arrest is the sudden, complete cessation of cardiac output with hemodynamic collapse. Patients present as pulseless, unresponsive, and apneic. Rhythms associated with cardiac arrest are ventricular fibrillation/tachycardia, asystole, or pulseless electrical activity. The treatment of cardiac arrest begins with basic life support (BLS) when out-of-hospital and advanced cardiac life support (ACLS) when in-hospital. Basic life support comprises checking the patient’s mental status, activating the emergency response system, and cardiopulmonary resuscitation (CPR). An automated external defibrillator (AED) should be used once available. High-quality CPR (with early defibrillation in shockable rhythms) is crucial to survival in cardiac arrest. Advanced cardiac life support includes CPR, securing the airway, administering medications (such as epinephrine), and identifying and treatment of the cause of cardiac arrest. Post-cardiac arrest care follows return of spontaneous circulation (ROSC).

Supraventricular tachycardias are related disorders in which the elevation in heart rate is driven by pathophysiology in the atria. This group falls under the larger umbrella of tachyarrhythmias and includes paroxysmal supraventricular tachycardias (PSVTs), ventricular pre-excitation syndromes (i.e. Wolff-Parkinson-White syndrome), atrial flutter, multifocal atrial tachycardia, and atrial fibrillation. Sinus tachycardia (> 100/min) is not a pathologic arrhythmia. The diagnosis of these conditions can be made using electrocardiogram (ECG), and treatment differs depending on the condition.

Bradyarrhythmia is a rhythm in which the heart rate is less than 60/min. Bradyarrhythmia can be physiologic, without symptoms or hemodynamic change. Pathologic bradyarrhythmia results in reduced cardiac output and hemodynamic instability causing syncope, dizziness, or dyspnea. Bradyarrhythmia is due to dysfunction in the sinoatrial (SA) node, atrioventricular (AV) node, or the lower conduction system. Bradyarrhythmia can be associated with an intrinsic cardiac abnormality or with medications, electrolyte imbalances, and systemic diseases. Arrhythmia is detected by electrocardiogram (ECG). Additional tests such as event recorders are performed if symptoms are less frequent and require a longer observation period. There are bradyarrhythmias requiring no intervention. In symptomatic or life-threatening conduction abnormalities such as complete heart block, permanent pacemaker placement is the mainstay of treatment.

Atrial fibrillation (AF or Afib) is a supraventricular tachyarrhythmia and the most common kind of arrhythmia. It is caused by rapid, uncontrolled atrial contractions and uncoordinated ventricular responses. There are many conditions that can cause AF, usually damage to the heart (e.g., coronary artery disease, previous myocardial infarction). Diagnosis is confirmed by an electrocardiogram that will show an “irregularly irregular” heartbeat with no distinct P waves and narrow QRS complexes. AF increases the risk of thromboembolic events. Treatment is primarily based on ventricular rate and rhythm control, which can be achieved through drugs and/or cardioversion. Anticoagulation is administered if the patient is at significant risk for thromboembolic events.