17.1 Introduction to Dysrhythmias

Overview of Cardiac Dysrhythmias

Cardiac dysrhythmias are disruptions in the heart's normal rhythm that cause irregular, too-fast, or too-slow heartbeats. They can originate in the atria, the ventricles, or the conduction system itself. Understanding the types, mechanisms, and management of dysrhythmias is foundational for pharmacology because the drug you choose depends entirely on where the problem starts and what's going wrong electrically.

Types of Cardiac Dysrhythmias

Dysrhythmias are grouped by where they originate and how dangerous they are.

Atrial dysrhythmias originate in the atria and disrupt normal heart rhythm:

• Atrial fibrillation (AF) is the most common sustained dysrhythmia. The atria fire rapid, disorganized electrical signals, producing an irregularly irregular ventricular response. AF significantly increases stroke risk because blood can pool and clot in the fibrillating atria.
• Atrial flutter produces rapid but regular atrial contractions, typically around 300 bpm, with a characteristic "sawtooth" pattern on ECG. The ventricles usually respond at a fixed ratio (e.g., 2:1 or 4:1 block).
• Supraventricular tachycardia (SVT) is a rapid heart rate originating above the ventricles, often involving a reentry circuit through or near the AV node.

Ventricular dysrhythmias originate in the ventricles and can be life-threatening:

• Ventricular tachycardia (VT) involves rapid, regular ventricular contractions (typically >100 bpm) that may compromise cardiac output. Sustained VT can deteriorate into VF.
• Ventricular fibrillation (VF) produces chaotic, uncoordinated ventricular activity. The heart cannot pump blood effectively, resulting in cardiac arrest. VF is a medical emergency requiring immediate defibrillation.

Conduction disorders affect the heart's electrical conduction system:

• Heart block involves delayed or blocked impulse transmission through the AV node or bundle branches. It ranges from first-degree (prolonged PR interval) to third-degree (complete block requiring pacemaker).
• Sinus node dysfunction refers to abnormalities in the SA node that can produce inappropriate bradycardia, tachycardia, or alternating between the two (tachy-brady syndrome).

Clinical consequences of dysrhythmias include reduced cardiac output, poor tissue perfusion, and symptoms such as palpitations, dizziness, syncope, and shortness of breath. AF in particular carries a significant risk of thromboembolic events, including stroke.

Cardiac Conduction System

To understand dysrhythmias, you need to know the normal pathway an electrical impulse follows through the heart.

1. The sinoatrial (SA) node initiates each heartbeat. It's the heart's natural pacemaker, firing at a normal rate of 60–100 bpm.
2. The impulse spreads across the atria, causing atrial contraction.
3. The atrioventricular (AV) node receives the impulse and deliberately slows conduction. This brief delay allows the ventricles to fill with blood before they contract.
4. The impulse then travels down the bundle of His, splits into the left and right bundle branches, and spreads through the Purkinje fibers, which rapidly depolarize the ventricles for a coordinated contraction.

A few key concepts tie into how dysrhythmias develop:

• The cardiac action potential represents the electrical cycle of an individual cardiac cell, including depolarization and repolarization. Different phases of the action potential are targeted by different drug classes.
• Reentry is one of the most common mechanisms behind sustained dysrhythmias. It occurs when an electrical impulse loops back through cardiac tissue instead of dying out, creating a self-perpetuating circuit. Many antidysrhythmic drugs work by interrupting reentry pathways.
• The electrocardiogram (ECG) records the heart's electrical activity from the body surface and is the primary tool for diagnosing dysrhythmias.

Management of Dysrhythmias

Treatment depends on the type of dysrhythmia, its severity, and the patient's overall condition. Management falls into three broad categories.

Non-pharmacological approaches directly restore rhythm or prevent dangerous episodes:

• Cardioversion delivers a synchronized electrical shock timed to the cardiac cycle to convert an abnormal rhythm back to normal sinus rhythm.
• Ablation uses radiofrequency energy or cryotherapy to destroy the abnormal cardiac tissue responsible for initiating or maintaining the dysrhythmia.
• Implantable devices such as pacemakers (for bradydysrhythmias) and implantable cardioverter-defibrillators (ICDs, for life-threatening ventricular dysrhythmias) continuously monitor and treat abnormal rhythms.

Pharmacological approaches use antidysrhythmic drugs matched to the specific dysrhythmia and patient characteristics. The goals of drug therapy are to:

• Restore and maintain normal sinus rhythm
• Control ventricular rate (particularly in AF and atrial flutter)
• Prevent recurrence of dysrhythmias

Supportive measures address root causes and complications:

• Correcting underlying triggers such as electrolyte imbalances (especially potassium and magnesium) and myocardial ischemia
• Initiating anticoagulation in patients with AF to reduce thromboembolic risk
• Monitoring for adverse effects of antidysrhythmic drugs, many of which are themselves proarrhythmic (meaning they can cause new dysrhythmias)

Classes of Antidysrhythmic Drugs

The Vaughan Williams classification organizes antidysrhythmic drugs into four classes based on their primary mechanism of action. This is the framework you'll use throughout this unit.

Class I: Sodium Channel Blockers slow the influx of sodium during phase 0 of the action potential, reducing the speed of depolarization. They're subdivided by how strongly they block sodium channels and their effect on action potential duration (APD):

• Subclass IA (quinidine, procainamide): Moderate sodium channel blockade. They prolong APD and the QT interval. Used for both atrial and ventricular dysrhythmias.
• Subclass IB (lidocaine, mexiletine): Fast-on/fast-off sodium channel blockade. They shorten APD. Primarily used for ventricular dysrhythmias, especially in acute settings like post-MI.
• Subclass IC (flecainide, propafenone): Strong sodium channel blockade with minimal effect on APD. Potent rhythm control agents, but reserved for patients without structural heart disease due to proarrhythmic risk.

Class II: Beta-Blockers (propranolol, metoprolol) block sympathetic stimulation of the heart. They decrease heart rate, slow AV conduction, and reduce myocardial oxygen demand. Beta-blockers are particularly useful for rate control and for suppressing dysrhythmias triggered by excess catecholamines.

Class III: Potassium Channel Blockers (amiodarone, sotalol) block potassium efflux during repolarization, which prolongs APD and the refractory period. This makes cardiac tissue less susceptible to reentry. Effective for both atrial and ventricular dysrhythmias. Amiodarone is one of the most widely used antidysrhythmics but has significant long-term toxicities (thyroid, pulmonary, hepatic).

Class IV: Calcium Channel Blockers (verapamil, diltiazem) block L-type calcium channels, slowing conduction through the AV node. They're primarily used for rate control in atrial dysrhythmias (AF, atrial flutter) and for terminating SVTs that involve the AV node.

Miscellaneous Agents don't fit neatly into the Vaughan Williams system:

• Adenosine transiently blocks AV node conduction and is the first-line drug for acute termination of SVT. It's given as a rapid IV push because its half-life is under 10 seconds.
• Digoxin increases vagal tone and slows AV nodal conduction. It's used for rate control in AF, particularly in patients with heart failure.
• Ivabradine selectively inhibits the $I_f$ ("funny") current in the SA node, reducing heart rate without affecting contractility or blood pressure. It's used in heart failure and inappropriate sinus tachycardia.