Ventricular tachycardia

Ventricular tachycardia (VT) is a potentially life-threatening cardiac arrhythmia originating from the ventricles. It is characterized by a rapid heart rate and can lead to hemodynamic instability or sudden cardiac death if not promptly recognized and managed. Understanding its classification and clinical features is crucial for effective diagnosis and treatment.

Definition and Classification

Definition

Ventricular tachycardia is defined as a series of three or more consecutive ventricular beats occurring at a rate exceeding 100 beats per minute. The rhythm originates from abnormal electrical activity within the ventricles rather than the sinoatrial node, often resulting in inefficient cardiac output.

Classification

• Monomorphic Ventricular Tachycardia: QRS complexes are uniform in morphology, usually indicating a single ventricular focus or reentry circuit.
• Polymorphic Ventricular Tachycardia: QRS complexes vary in shape and amplitude, often associated with acute ischemia or electrolyte abnormalities.
• Torsades de Pointes: A specific form of polymorphic VT characterized by twisting of QRS complexes around the isoelectric line, commonly linked to prolonged QT interval.
• Non-sustained VT: VT episodes lasting less than 30 seconds, often asymptomatic but may indicate underlying heart disease.
• Sustained VT: VT lasting more than 30 seconds or causing hemodynamic compromise, requiring urgent intervention.
• Idiopathic VT: Occurs in structurally normal hearts, usually with a benign course.
• Secondary VT: Associated with underlying structural heart disease, ischemia, or inherited arrhythmia syndromes.

Etiology and Risk Factors

Structural Heart Disease

• Ischemic heart disease, including prior myocardial infarction and scar-related reentry circuits
• Cardiomyopathies such as dilated, hypertrophic, or restrictive forms
• Valvular heart disease contributing to ventricular remodeling

Electrolyte and Metabolic Disorders

• Hypokalemia and hypomagnesemia
• Acid-base disturbances including acidosis or alkalosis

Drug-Induced Causes

• Antiarrhythmic medications with proarrhythmic potential
• QT-prolonging drugs such as certain antibiotics or antipsychotics
• Stimulants, including cocaine and amphetamines

Genetic and Inherited Conditions

• Long QT syndrome
• Brugada syndrome
• Catecholaminergic polymorphic ventricular tachycardia

Pathophysiology

Ventricular tachycardia arises from abnormal electrical activity within the ventricles. The underlying mechanisms vary depending on the etiology and can significantly affect the severity and management of the arrhythmia.

• Reentry Circuits: The most common mechanism, often occurring around areas of scar tissue from prior myocardial infarction, where a circulating electrical impulse causes continuous ventricular activation.
• Triggered Activity: Early or delayed afterdepolarizations in ventricular myocytes can initiate VT, often linked to electrolyte imbalances or drug effects.
• Abnormal Automaticity: Ectopic ventricular pacemaker cells spontaneously generate impulses at an increased rate, overriding normal sinus rhythm.

Clinical Presentation

Symptoms

• Palpitations or awareness of rapid heartbeat
• Syncope or presyncope due to transient cerebral hypoperfusion
• Chest pain or discomfort, particularly in ischemic VT
• Dyspnea or shortness of breath from reduced cardiac output
• Sudden cardiac arrest in severe, untreated cases

Signs

• Tachycardia detected on pulse or cardiac monitoring
• Hypotension due to impaired ventricular filling and output
• Signs of heart failure, such as pulmonary congestion or peripheral edema
• Altered mental status if cerebral perfusion is compromised

Diagnostic Evaluation

Electrocardiography (ECG)

• 12-lead ECG is the primary tool for diagnosing VT, showing wide QRS complexes and regular or irregular rapid ventricular rhythm.
• Distinguishing VT from supraventricular tachycardia with aberrancy is critical for appropriate management.

Holter Monitoring and Event Recorders

Ambulatory monitoring may be used to capture intermittent or non-sustained VT episodes that are not seen on standard ECG.

Electrophysiological Studies

Invasive testing may be indicated to map the origin of VT, assess inducibility, and guide catheter ablation therapy.

Imaging Studies

• Echocardiography to evaluate structural heart disease, ventricular function, and valvular abnormalities.
• Cardiac MRI to detect myocardial scar, fibrosis, or infiltrative processes that predispose to VT.

Laboratory Tests

• Electrolytes including potassium, magnesium, and calcium levels
• Cardiac biomarkers if ischemia is suspected
• Genetic testing in cases suggestive of inherited arrhythmia syndromes

Management

Acute Management

• Hemodynamically unstable VT requires immediate synchronized cardioversion.
• Hemodynamically stable VT may be managed with intravenous antiarrhythmic medications such as amiodarone, lidocaine, or procainamide.

Chronic Management

• Implantable cardioverter-defibrillator (ICD) for secondary prevention or high-risk patients.
• Long-term oral antiarrhythmic medications for rhythm control in selected cases.
• Catheter ablation to eliminate arrhythmogenic foci or reentry circuits, particularly in recurrent VT.

Management of Underlying Causes

• Correction of electrolyte disturbances and metabolic imbalances.
• Optimal treatment of ischemic heart disease, cardiomyopathy, or heart failure.
• Avoidance of proarrhythmic drugs and careful medication review.

Prognosis

The prognosis of ventricular tachycardia depends on the underlying heart condition, VT type, and timeliness of treatment. Patients with structural heart disease or sustained VT are at higher risk of sudden cardiac death.

• Risk of sudden cardiac death is greatest in patients with ischemic cardiomyopathy or prior myocardial infarction.
• Factors influencing outcomes include left ventricular function, frequency of VT episodes, and response to therapy.
• Long-term survival improves significantly with implantable cardioverter-defibrillators and appropriate medical management.

Prevention

• Primary and Secondary Prevention: ICD placement is recommended for high-risk patients or those with a history of sustained VT or cardiac arrest.
• Lifestyle Modifications: Avoiding stimulants, managing stress, and optimizing cardiovascular risk factors can reduce arrhythmia triggers.
• Medical Therapy: Long-term antiarrhythmic medications may be used in selected patients to prevent recurrence.
• Management of Underlying Conditions: Effective treatment of ischemic heart disease, heart failure, and electrolyte disturbances is crucial for VT prevention.

Complications

• Sudden Cardiac Arrest: Sustained VT can degenerate into ventricular fibrillation, leading to sudden cardiac death if not promptly treated.
• Heart Failure Exacerbation: Rapid ventricular rates can reduce cardiac output and precipitate acute heart failure in vulnerable patients.
• Thromboembolic Events: Prolonged VT may contribute to intracardiac thrombus formation, increasing the risk of stroke or systemic embolism.
• Medication-Related Adverse Effects: Antiarrhythmic drugs may cause proarrhythmia, organ toxicity, or other side effects requiring close monitoring.

References

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