Ventricular Tachycardia

Ventricular Tachycardia

Definition Ventricular tachycardia (VT) is defined as three or more consecutive premature ventricular contractions (PVCs). Associated Clinical Features 1. Ventricular tachycardia is uncommon in the pediatric age group. 2. Heart rate in VT varies from near normal to more than 200 bpm. 3. Stroke volume and cardiac output may become compromised with rapid ventricular rates, and VT may deteriorate into pulseless VT or VF. 4. Presenting signs and symptoms of VT include: a. Sudden onset of rapid heartbeat and palpitations b. Chest pain c. With slower tachycardia: fatigue, lethargy, or symptoms of CHF d. Syncope e. Occasionally asymptomatic f. Cardiac arrest g. Signs of circulatory impairment (poor end-organ perfusion) 1) Skin perfusion: color pale, cyanotic, or mottled, cool extremities, prolonged capillary refill 2) Peripheral pulses: rapid, thready, weak, or absent 3) Discrepancy in volume between peripheral and central pulses 4) CNS: irritable, lethargic, confused, or decrease in level of consciousness 5) Diminished response to pain 6) Respiratory difficulty 7) Pulse pressure decrease of >20 mmHg 8) Hypotension (decompensated shock) 9) Decreased or no urine output 5. Electrocardiographic findings of VT include: a. P waves usually not identifiable b. If P waves are present, they are not related to the QRS complex (AV dissociation; P wave slower than the QRS rate) c. Ventricular rate at least 120 bpm (usually 120 to 200 bpm) d. Ventricular rate regular e. Wide QRS complex (>0.08 second [QRS width is age dependent in children]; Fig. 5-15) f. T waves usually opposite in polarity to QRS complex 6. Radiographic findings seen in VT are related to the presence of underlying heart disease. View Large Figure 5-15. Ventricular Tachycardia Add to 'My Saved Images' Ventricular rhythm is rapid and regular. Note QRS widening of >0.08 second and absence of atrial depolarization. Consultation Cardiology (usually after initial stabilization) Emergency Department Treatment and Disposition 1. Assess and support ABCs as needed (provide 100% oxygen, ventilation as needed, continuous cardiac and pulse oximetry monitoring) 2. During evaluation identify and treat possible contributory causes (see Box 5-1 for "H"s and "T"s of CPR). 3. VT with palpable pulses and adequate perfusion: a. Consult a pediatric cardiologist. b. Synchronized cardioversion: 0.5 to 1 joule/kg (consider sedation; may double dose if initial dose ineffective) or c. Consider alternative medications (any of the following; do not give amiodarone and procainamide together): 1) Amiodarone given intravenously at a loading dose of 5 mg/kg over 20 to 60 minutes followed by a continuous infusion at rates of 5 to 10 g/kg per minute (5 to 10 mg/kg per day) or 2) Procainamide given IV at a loading dose of 15 mg/kg over 30 to 60 minutes followed by a continuous infusion of 30 to 50 g/kg per minute (rate of infusion directed by measurement of serum levels) or 3) Lidocaine (easiest and safest drug) given as an IV bolus at a dose of 1 mg/kg followed by a continuous infusion of 30 to 50 g/kg per minute (rate of infusion directed by measurement of serum levels [2 to 5 g/mL]) 4. VT with palpable pulses and poor systemic perfusion: a. Immediate synchronized cardioversion (same as above; do not delay cardioversion for sedation) or b. Consider alternative medications (amiodarone, procainamide, or lidocaine; same as above) 5. VT without palpable pulses and poor systemic perfusion (pulseless VT): a. Begin CPR and attempt defibrillation. b. Treatment same as for ventricular fibrillation/pulseless arrest (see Box 5-29) 6. Following stabilization, all patients require hospitalization in the PICU for continuous monitoring and subsequent management. Clinical Pearls: Ventricular Tachycardia 1. Ventricular tachycardia may degenerate into ventricular fibrillation. 2. Aberrant SVT presents with a wide QRS complex and may resemble VT. If uncertain, all wide-complex tachycardias are assumed to be VT unless proved otherwise. 3. Both amiodarone and procainamide prolong the QT interval, and when given rapidly together can cause vasodilatation, hypotension, and increase the risk of heart block and polymorphic VT. Box 5-25. Etiology of Ventricular Tachycardia Structural congenital heart disease or post–cardiac surgery (most common etiologies)    (1) Tetralogy of Fallot    (2) Eisenmenger's syndrome    (3) Aortic stenosis    (4) Transposition of the great arteries    (5) Anomalies of coronary arteries Cardiac catheterization (mechanical irritation) Prolonged QT syndrome (see Fig. 5-7) Myocarditis (e.g., viral) Cardiomyopathy (e.g., dilated, hypertrophic) Pulmonary hypertension Arrhythmogenic RV dysplasia Cardiac tumors Drugs or poisons (see Box 5-26) Possible contributory causes: "H"s and "T"s of CPR (see Box 5-1) Box 5-26. Drugs That Cause Ventricular Tachycardia and Supraventricular Tachycardia    (1) Anticholinergics    (2) Antihistamines    (3) Catecholamine infusion    (4) Digitalis toxicity    (5) Tricyclic antidepressants    (6) Phenothiazines    (7) Sympathomimetics (e.g., beta-agonists, alpha-agonists, cocaine, amphetamines, phencyclidine)    (8) Sedative hypnotics (e.g., chloral hydrate, ethanol)    (9) Antidysrhythmics (classes I through IV)    (10) Thyroid hormone    (11) Carbamazepine Box 5-27. Differential Diagnosis of Ventricular Tachycardia Supraventricular tachycardia (SVT) with aberrant conduction (due to bundle-branch block or WPW syndrome)    (1) Seen in 10% of children with SVT    (2) Presents with wide QRS complex and may resemble VT    (3) The ability to terminate tachycardia with vagal maneuvers does not distinguish SVT from VT.    (4) Hemodynamic stability also does not predict SVT versus VT (e.g., a patient without signs of circulatory impairment with a wide-complex tachycardia is more likely to have VT, and should not be assumed to have SVT).    (5) Erroneously treating VT as SVT can be devastating (VT deteriorates into pulseless VT/VF).