Ventricular tachycardia cardioversion

DCC, direct current cardioversion HF, heart failure LVEF, left ventricular ejection fraction VT, ventricular tachycardia. (Algorithm adapted with permission fromTisdaleJE, Moser LR. Tachyarrhythmias. In Mueller BA, Bertch KE, DunsworthTS, et al. (eds.) Pharmacotherapy Self-Assessment Program, 4th ed. Kansas City American College of Clinical Pharmacy 2001 21 7-267.)50... 

Implantable cardioverter-defibrillator (ICD) A device implanted into the heart transvenously with a generator implanted subcutaneously in the pectoral area that provides internal electrical cardioversion of ventricular tachycardia or defibriUation of ventricular fibrillation. 

FIGURE 6-2. Algorithm for the treatment of acute (top portion) paroxysmal supraventricular tachycardia and chronic prevention of recurrences (bottom portion). Note For empiric bridge therapy prior to radiofrequency ablation procedures, calcium channel blockers (or other atrioventricular [AV] nodal blockers) should not be used if the patient has AV reentry with an accessory pathway. (AAD, antiarrhythmic drugs AF, atrial fibrillation AP, accessory pathway AVN, atrioventricular nodal AVNRT, atrioventricular nodal reentrant tachycardia AVRT, atrioventricular reentrant tachycardia DCC, direct-current cardioversion ECG, electrocardiographic monitoring EPS, electrophysiologic studies PRN, as needed VT, ventricular tachycardia.)... 

Cardiovascular Effects. In a recent report on the clinical treatment of phenol poisoning, Langford et al. (1998) provide a summary of a case report in which a woman accidentally consumed an ounce of 89% phenol which had been mistakenly been given to her in preparation for an in-office procedure. Her immediate reaction upon consuming the phenol was to clutch her throat and collapse, and within 30 minutes she was comatose and had gone into respiratory arrest. Treatment was initiated with an endotracheal intubation. Ventilation with a bag and mask led to the detection of a lamp oil odor. Within an hour she developed ventricular tachycardia which responded to cardioversion however, she subsequently developed (in the first 24 hours) supraventricular and ventricular dysrhythmias, metabolic acidosis, and experienced a grand mal seizure. After a 15-day hospital stay, she was completely recovered with no evidence of impaired motility or compromised gastrointestinal or cardiovascular systems. 

Lidocaine is the agent of choice for termination of ventricular tachycardia and prevention of ventricular fibrillation after cardioversion in the setting of acute ischemia. However, routine prophylactic use of lidocaine in this setting may actually increase total mortality, possibly by increasing the incidence of asystole, and is not the standard of care. Most physicians administer IV lidocaine only to patients with arrhythmias. 

Supraventricular tachycardia is the major arrhythmia indication for verapamil. Adenosine or verapamil are preferred over older treatments (propranolol, digoxin, edrophonium, vasoconstrictor agents, and cardioversion) for termination. Verapamil can also reduce the ventricular rate in atrial fibrillation and flutter. It only rarely converts atrial flutter and fibrillation to sinus rhythm. Verapamil is occasionally useful in ventricular arrhythmias. However, intravenous verapamil in a patient with sustained ventricular tachycardia can cause hemodynamic collapse. 

Lidocaine Sodium channel (INa) blockade Blocks activated and inactivated channels with fast kinetics does not prolong and may shorten action potential Terminate ventricular tachycardias and prevent ventricular fibrillation after cardioversion IV first-pass hepatic metabolism reduce dose in patients with heart failure or liver disease Toxicity Neurologic symptoms... 

Some of the beneficial effects of fish oils after acute myocardial infarction have been attributed to an antidysr-hythmic effect on the heart (5). However, the results of a randomized trial in 200 patients with implantable cardioverter defibrillators are at variance with this the rate of cardioversion was higher in those taking fish oils 1.8 g/day than in a control group who took olive oil (6). The lack of benefit and the suggestion that fish oil supplementation may increase the risk of ventricular tachycardia or ventricular fibrillation in some patients with implantable cardioverter defibrillators can reasonably be interpreted as evidence that the routine use of fish oil supplementation in patients with implantable cardioverter defibrillators and recurrent ventricular dysrhythmias should be avoided. 

Therapeutic uses Quinidine is used in the treatment of a wide variety of arrhythmias, including atrial, AV junctional, and ventricular tachyarrhythmias. Quinidine is used to maintain sinus rhythm after direct current cardioversion of atrial flutter or fibrillation and to prevent frequent ventricular tachycardia. 

A 34-year-old man developed palpitation, shortness of breath, and chest pain. He had smoked a quarter to a half an ounce of marijuana per week and had taken it 3 hours before the incident. He had ventricular tachycardia at a rate of 200/minute with a right bundle branch block pattern. Electrical cardioversion restored sinus rhythm. Angiography showed a significant reduction in left anterior descending coronary artery flow rate, which was normalized by intra-arterial verapamil 200 micrograms. 

An 86-year-old woman was given adenosine 12 mg intravenously for sustained supraventricular tachycardia, which terminated but was followed by atrial fibrillation and paroxysmal ventricular tachycardia (24). Cardioversion was unsuccessful, but normal sinus rhythm was obtained with procainamide. This followed an anteroseptal myocardial infarction. 

In a comparison of intravenous dofetihde (8 micrograms/kg n = 48), amiodarone (5mg/kg n=50), or placebo (n = 52) in converting atrial fibrillation or flutter to sinus rhythm in 150 patients, two patients given dofetilide had non-sustained ventricular tachycardias four had torsade de pointes, in one case requiring electrical cardioversion (53). 

A 65-year-old woman, who had had normal preoperative serum electrolytes and a normal QT interval with sinus rhythm, received hydroxyzine and atropine premedication followed by thiopental and vecuronium for anesthetic induction. Endotracheal intubation was difficult and precipitated atrial fibrillation, which was refractory to disopyramide 100 mg. Anesthesia was then maintained with sevoflurane 2% and nitrous oxide 50%. Ten minutes later ventricular tachycardia ensued, refractory to intravenous lidocaine, disopyramide, and magnesium. DC cardioversion resulted in a change to a supraventricular tachycardia, which then deteriorated to torsade de pointes. External cardiac massage and further DC cardioversion were initially unsuccessful, but the cardiac rhythm reverted to atrial fibrillation 10 minutes after the sevoflurane was switched off. Two weeks later she had her operation under combined epidural and general anesthesia, with no changes in cardiac rhythm. 

Sustained ventricular tachycardia is defined as consecutive premature ventricular contractions lasting more than 30 seconds. Nonsustained ventricular tachycardia (VT) usually self-terminates and lasts for less than 30 seconds. The acute treatment of SuVT depends on the hemodynamic stability and symptoms of the patient. Unstable patients should receive immediate cardioversion. If patients are stable with mild symptoms, they can be treated with IV antiarrhythmics. 

Patients with hemodynamically significant ventricular tachycardia or ventricular fibrillation not associated with an acute Ml who are resuscitated successfully (electrical cardioversion, pressors, amiodarone) are at high risk for death and should receive implantation of an internal cardioverter-defibrillator. 

Synchronized cardioversion is used for new-onset atrial fibrillation or unstable ventricular tachycardia. 

Ventricular tachycardia (VT) is the result of uncontrolled electrical activity in the ventricle. This activity may be coordinated or uncoordinated. The definitive therapy for Ventricular is external stimulation by an electric field sufficiently large to reset the electrical activity of most ventricular cells. This ends the previous (uncontrolled) electrical activity and allows the reestablishment of normal cardiac activity. As explained earlier, this requires depolarization of a critical mass of tissue by a high-voltage discharge. When high-voltage therapy is delivered, an attempt is made to synchronize the delivery with a detected R-wave. A synchronized shock is termed cardioversion, whereas an unsynchronized shock is termed defibrillation because VF has no coherent electrical activity, and therefore no basis for synchronization (Figure 15.6). 

The introduction and manipulation of pacing leads are frequently associated with both tachyarrhythmias and bradyarrhythmias as a lead negotiates the chambers of the right heart. Ventricular tachycardia is extremely common as the pacing electrode or guidewire contacts the right ventricular myocardium. Simple withdrawal of these objects usually terminates the arrhythmia. In extreme cases, sustained monomorphic ventricular tachycardia and even ventricular fibrillation may occur. Some institutions have instituted a policy of placing external defibrillation pads prophylactically in anticipation of required cardioversion. 

Fig. 20.2 Detection and therapy parameters for an ICD. Top Detection parameters. As programmed the ICD defines ventricular tachycardia (VT) as 12 beats greater than 150 bpm and ventricular fibrillation (VF) as 12 of 16 beats greater than 188 bpm. An optional fast ventricular tachycardia (FVT) zone has not been programmed on. Bottom Therapies for ventricular fibrillation are a first shock at 24 J and subsequent shocks at 35 J. Therapies for ventricular tachycardia are two pacing sequences followed by cardioversion attempts at 15,35,35, and 35 J. Pacing for bradycardia is set at 40 bpm.

Cardiovascular Intravenous procainamide had a prodysrhythmic effect when it was given as a single 1000 mg bolus during an electrophysiological study in a patient with myotonic dystrophy type 1 [SO J. During ventricular pacing, ventricular tachycardia and fibrillation occurred and required DC cardioversion. By slowing cardiac conduction, procainamide, as do other sodium channel blockers, worsens abnormalities already present in the hearts of patients with myotonic dystrophy t)q)e 1. 

Cardioversion is an appropriate, immediate treatment for stable ventricular tachycardia (VT). Alternatives to this treatment depend on the type of VT, the patient s cardiac function, and the configuration of the QT interval. In monomorphic VT, QRS complexes keep the same form or appearance. In polymorphic VT, QRS complexes occur in more than one form, varying in appearance. 

Treatment of atrial fibrillation is initiated to relieve patient symptoms and prevent the complications of thromboembolism and tachycardia-induced heart failure, the result of prolonged uncontrolled heart rates. The initial treatment objective is control of the ventricular response. This is usually achieved by use of a calcium channel-blocking drug alone or in combination with a 13-adrenergic blocker. Digoxin may be of value in the presence of heart failure. A second objective is a restoration and maintenance of normal sinus rhythm. Several studies show that rate control (maintenance of ventricular rate in the range of 60-80 bpm) has a better benefit-to-risk outcome than rhythm control (conversion to normal sinus rhythm) in the long-term health of patients with atrial fibrillation. If rhythm control is deemed desirable, sinus rhythm is usually restored by DC cardioversion in the USA in... 

Arruodarone is used in chronic ventricular arrhythmias in atrial fibrillation it both slows the ventricular response and may restore sinus rhythm it may be used to maintain sinus rhythm after cardioversion for atrial fibrillation or flutter. Amiodarone should no longer be used for the management of reentrant supraventricular tachycardias associated with the Wolff-Parkinson-White syndrome as radiofrequency ablation is preferable. 

A 52-year-old woman with a wide-complex tachycardia was given adenosine 6,12, and another 12 mg as intravenous bolus doses immediately after the third dose she developed ventricular fibrillation (27). She recovered with cardioversion. 

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