Ventricular premature beats Supraventricular premature beats Ventricular tachycardia
Ventricular premature beats Supraventricular premature beats Ventricular tachycardia Dr. Jamal Dabbas Interventional cardiologist & internist
Ventricular premature beats
Summary Ventricular premature beats (VPBs) are extra, abnormal heartbeats caused by ectopic foci within the ventricles. VPBs are very common and most individuals are asymptomatic, but select patients may present with symptoms such as dizziness or palpitations.
Typical ECG findings of VPBs include broad QRS complexes, compensatory pauses, and axis deviation, and may be random or have consistent patterns, such as couplets or bigeminy.
Most patients do not require treatment. However, any underlying condition, e. g. , myocarditis, must be managed appropriately. Patients with frequent VPBs that cause significant symptoms should receive antiarrhythmic drugs or possibly catheter ablation, as they are at risk for sudden cardiac death.
Etiology § Idiopathic § Cardiovascular disease (e. g. , CAD, myocarditis) § Electrolyte imbalances (e. g. , hypokalemia, hypomagnesemia) § Side effect of certain drugs (e. g. , digoxin, psychiatric medications) § Caffeine, alcohol
Classification § Monomorphic VPB: Each VPB has the same configuration → identical origin § Polymorphic VPB: VPBs have different configurations → multiple foci
Clinical features § Most patients are asymptomatic. § Skipped beat § If frequent VPBs, possibly → lightheadedness, dizziness, palpitations, irregular heart beat
Diagnostics If patient suspected of VPBs → evaluate with ECG → if confirmed, rule out underlying disease (e. g. , echocardiography, exercise treadmill stress test) with further procedures
ECG findings • Common ECG characteristics • QRS duration ≥ 120 ms with a block-like QRS morphology • VPBs are often followed by a compensatory pause
§ May be random or adhere to a specific pattern, including: § Single VPBs § Couplet: two VPBs in a row § Triplet: three VPBs in a row § Bigeminy: one extrasystole after every single sinus beat § Trigeminy: one extrasystole after every two sinus beats
VPBs are a common incidental finding on routine ECGs. The detection of them does not require any further workup in patients who are asymptomatic!
Additional procedures • Only indicated in case of frequent, symptomatic VPBs • 24 -hour Holter monitor • Exercise stress test • Echocardiography
Treatment • Most patients do not require any treatment • Treat any underlying disease (e. g. , CAD, myocarditis) • Only treat frequent and significantly symptomatic VPBs • Antiarrhythmic therapy • Catheter ablation if antiarrhythmic therapy fails
Supraventricular premature beats
Summary Supraventricular premature beats are atrial contractions triggered by ectopic foci rather than the sinoatrial node. They arise within the atria (atrial premature beats).
Premature beats may be found in healthy individuals as well as patients with underlying heart disease. Certain triggers, e. g. , alcohol, smoking or electrolyte imbalances, may also contribute to the condition.
Premature beats do not significantly impair cardiac output on their own; however, they may lead to more severe forms of arrhythmia such as atrial fibrillation. Unless patients exhibit severe symptoms (e. g. , tachycardia), those experiencing premature beats do not require treatment.
Etiology • Idiopathic • Potential triggers: smoking, alcohol, coffee • Cardiovascular disease or electrolyte imbalances (e. g. , hypokalemia)
Classification Atrial premature beats • Definition: extrasystole that originates in the atrial myocardium and occurs prior to the expected QRS complex • Typical findings on ECG
• P-wave abnormalities or absent P waves • Altered PR interval in the premature beats (compared to the normal beats) • QRS complex may be normal, aberrant (widened), or absent • No full compensatory pause
Junctional premature beats • Definition: premature beat that occurs prior to the expected QRS complex and that originates between the atria and ventricles • Typical findings on ECG
• Negative P wave • Narrow QRS complex • No compensatory pause • Usually asymptomatic • Palpitations
Diagnostics • ECG: identify supraventricular premature beats (SPBs) • Echocardiography: to rule out structural heart disease and evaluate cardiac structure and function if SPBs are identified on ECG or Holter monitor
Treatment • Treatment is not required in asymptomatic individuals without underlying structural heart defects. • Underlying conditions, e. g. , electrolyte imbalances, should be treated. • Symptomatic patients • Advise patients to reduce potential triggers like caffeine, alcohol, stress and smoking. • Beta blockers or catheter ablation in patients with persistent symptoms
Ventricular tachycardia
Summary Ventricular tachycardia (VT) is a potentially lifethreatening arrhythmia originating in the cardiac ventricles. Usually, VT results from underlying cardiac diseases such as myocardial infarction or cardiomyopathy, but it can also be idiopathic or iatrogenic.
Clinical manifestations range from palpitations and syncope to cardiogenic shock and sudden cardiac death. The characteristic ECG findings of VT are broad QRS complexes (> 120 ms) and tachycardia (> 120 bpm).
In the acute setting, management of VT may require immediate cardioversion, defibrillation, or administration of antiarrhythmic drugs. Most patients who develop symptomatic, sustained VT require long-term antiarrhythmic therapy involving medication, intracardiac devices, or catheter ablation.
Etiology • Cardiac scars (usually due to infarction; also iatrogenic, e. g. , postoperative) • Conduction disorders • Drugs (e. g. , digitalis, antiarrhythmics)
• Long-QT syndrome • Congenital long-QT syndrome • Acquired long-QT syndrome • Drugs • Antiarrhythmics • Class Ia (e. g. , quinidine, disopyramide) • Class III (e. g. , sotalol, amiodarone) • Antibiotics (e. g. , macrolides, fluoroquinol ones) • Antidepressants (most tricyclic and tetracyclic antidepressants, lithium) • Antipsychotics (e. g. , haloperidol) • Anticonvulsants (fosphenytoin, felbamate)
• Electrolyte imbalances (hypokalemia, hypomagnesemia, hypocalcemia) • Ischemic stroke or intracranial hemorrhage • Endocrine disorders (e. g. , hypothyroidism) • Nutritional disorders (e. g. , anorexia nervosa) • In rare cases, VT can occur in healthy individuals.
Pathophysiology • Monomorphic VT (all QRS complexes look similar) • Increased automaticity • Re-entry circuit • Polymorphic VT (dissimilar QRS complexes): caused by abnormal ventricular repolarization (e. g. , long QT syndrome, drug toxicity, electrolyte abnormalities) • Decreased cardiac output: asynchronous atrial and ventricular beats + rapid ventricular rhythm → ↓ blood flow into the ventricle during diastole → ↓ CO • → hemodynamic compromise → symptoms of syncope, MI, angina
Clinical features • Often asymptomatic, especially if nonsustained • Common symptoms of sustained VT include: • Palpitations • Hypotension • Syncope
• In more severe cases: • Chest pain/pressure (often in conjunction with MI) • Cardiogenic shock • Loss of consciousness • Progression to ventricular fibrillation • Sudden cardiac death
Subtypes and variants Torsades de pointes • Polymorphic ventricular tachycardia with QRS complexes that appear to twist around the isoelectric line • Most severe complication: progression to lifethreatening ventricular arrhythmia • Cause: prolonged QT interval caused by congenital disease, electrolyte abnormalities , and drugs • Treatment • If hemodynamically unstable → defibrillation • If hemodynamically stable → IV magnesium sulfate
Diagnostics • ECG • 3 or more consecutive premature ventricular beats (i. e. , widened QRS) • Heart rate > 120 bpm • Duration • Nonsustained: < 30 s • Sustained: > 30 s
• Morphology • Monomorphic: all QRS complexes look similar (identical origin) • Polymorphic: QRS complexes are different (multiple origins)
• Other possible ECG findings • AV-dissociation: no relationship between P waves and QRS complexes (in VT, ventricular rhythm is often faster than atrial rhythm) • Fusion complex: atrial and ventricular impulses occur simultaneously • Capture beats: Occasionally, a supraventricular impulse may reach AV node and produce a subsequent ventricular beat (similar to a beat in sinus rhythm).
Other diagnostic tests • Holter monitor: useful for diagnosing intermittent VT which may not be present on a single ECG • Patient-activated (manual) event recorder • Echocardiography: provides information about possible etiologies of VT (e. g. structural heart disease, prior MI) and is thus a useful tool for evaluation of VT
Differential diagnoses Confirming the diagnosis of VT can be challenging and, in some cases, impossible. However, VT accounts for nearly 80% of widecomplex tachycardias. • Supraventricular tachycardia with aberrancy (RBBB, LBBB, Wolff-Parkinson-White) • It is important to make the distinction between SVT with aberrancy and VT because treatment of the two conditions differs and sometimes the wrong treatment can lead to hemodynamic instability (e. g. , using AVnodal blocking drugs in patient with VT).
• Signs and symptoms that suggest VT rather than SVT are: • Age > 35 (high PPV) • History of structural heart defects or past MI • AV dissociation, fusion beats, and capture beats
• Signs and symptoms that suggest SVT with aberrancy rather than VT are: • Bundle branch block on prior ECG • History of SVT • Evidence of WPW (e. g. , delta wave) • If there is any doubt regarding the diagnosis, assume VT rhythm and treat accordingly.
Treatment • Initial therapy • If patient is hemodynamically unstable (hypotension, loss of consciousness): • VT with pulse → cardioversion • VT without pulse → defibrillation • “Advanced cardiac life support”
• If patient is hemodynamically stable: • Antiarrhythmics (typically lidocaine, procain amide, amiodarone) • Cardioversion if medical therapy fails
• In all patients, look for and address possible causes of VT such as: • Electrolyte abnormalities (e. g. , hypokalemia) → correct any electrolyte imbalances • Medication-induced QT prolongation → remove any offending medication, digoxin immune fab (fragment antigen-binding) for digoxin toxicity
• Long-term therapy • Intracardiac devices (ICD) (most effective treatment for reducing mortality): indicated in case of VT that does not respond to therapy • Catheter ablation • Antiarrhythmics (usually class I or III)
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