Ventricular tachycardia acute

Ventricular tachycardia (VT) is defined by three or more repetitive PVCs occurring at a rate greater than 100 beats/min. It occurs most commonly in acute myocardial infarction (MI) other causes are severe electrolyte abnormalities (e.g., hypokalemia), hypoxemia, and digitalis toxicity. The chronic recurrent form is almost always associated with underlying organic heart disease (e.g., idiopathic dilated cardiomyopathy or remote MI with left ventricular [LV] aneurysm). 

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.)... 

Severe - Leukopenia (less than 1000/mm ) 2.8% hypoglycemia (less than 25 mg/dL) 2.4% thrombocytopenia (less than 20,000/mm ) 1.7% hypotension (less than 60 mm Hg systolic) 0.9% acute renal failure (serum creatinine greater than 6 mg/dL) 0.5% hypocalcemia (0.2%) Stevens-Johnson syndrome and ventricular tachycardia (0.2%) fatalities caused by severe hypotension, hypoglycemia, and cardiac arrhythmias. 

Procainamide can decrease the occurrence of all types of active ventricular dysrhythmias in patients with acute myocardial infarction who are free from A-V dissociation, serious ventricular failure, and cardiogenic shock. About 90% of patients with ventricular premature contractions and 80% of patients with ventricular tachycardia respond to procainamide administration. 

Unlabeled Uses Acute alcohol withdrawal, arrhythmia (especially supraventricular and ventricular tachycardia), improved survival in diabetics with heart disease, mild to moderately severe CHF (adjunct) prevention of migraine, thyrotoxicosis, tremors treatment of hypertrophic cardiomyopathy, pheochromocytoma, and syndrome of mitral valve prolapse... 

Contraindications Phenylephrine HCl injection should not be used with patients with severe hypertension, ventricular tachycardia or fibrillation, acute myocardial infarction (Ml), atrial flutter or fibrillation, cardiac arrhythmias, cardiac disease, cardiomyopathy, closed-angle glaucoma, coronary artery disease, patients who have a known hypersensitivity to phenylephrine, sulfites, or to any one of its components. 

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. 

Venodilators Releases nitric oxide (NO) activates guanylyl cyclase (see Chapter 12) Venodilation reduces preload and ventricular stretch Acute and chronic heart failure angina Oral 4-6 h duration Toxicity Postural hypotension, tachycardia, headache Interactions Additive with other vasodilators and synergistic with phosphodiesterase type 5 inhibitors... 

Vomiting is common in patients with digitalis overdose. Hyperkalemia may be caused by acute digitalis overdose or severe poisoning, whereas hypokalemia may be present in patients as a result of long-term diuretic treatment. (Digitalis does not cause hypokalemia.) A variety of cardiac rhythm disturbances may occur, including sinus bradycardia, AV block, atrial tachycardia with block, accelerated junctional rhythm, premature ventricular beats, bidirectional ventricular tachycardia, and other ventricular arrhythmias. 

Of 86 cirrhotic patients treated with terlipressin 10 developed a tachycardia, four developed atrial fibrillation, and one developed ventricular tachycardia. Four patients in the same study developed hypertension (11). In another study, tachycardia occurred in 23% of patients randomized to pitressin for acute variceal bleeding and 8% developed transient hypertension (12). 

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. 

In addition to sinus tachycardia and tremor, vomiting is common after overdose. Hypotension, tachycardia, hypokalemia, and hyperglycemia may occur, probably due to -adrenergic activation. The cause of this activation is not fully understood, but the effects can be ameliorated by the use of B-blockers (see below). Cardiac arrhythmias include atrial tachycardias, premature ventricular contractions, and ventricular tachycardia. In severe poisoning (eg, acute overdose with serum level > 100 mg/L), seizures often occur and are usually resistant to common anticonvulsants. Toxicity may be delayed in onset for many hours after ingestion of sustained-release tablet formulations. 

As noted above, the antiarrhythmic drugs can modify impulse generation and conduction. More than a dozen such drugs that are potentially useful in treating arrhythmias are currently available. However, only a limited number of these agents are clinically beneficial in the treatment of selected arrhythmias. For example, the acute termination of ventricular tachycardia by lidocaine or supraventricular tachycardia by adenosine or verapamil are examples in which antiarrhythmic therapy results in decreased morbidity. In contrast, many of the antiarrhythmic agents are now known to have lethal proarrhythmic actions, that is, to cause arrhythmias. 

A breakdown of actual cardiac symptoms for OP poisoning in hospital admissions is given by Karki et al. (2004) and also by Saadeh et al. (1997). Sixty-seven percent of the acute OP cases had QT prolongation, 24% experienced ST-segment elevation, and 17% had inverted T-waves. Nine percent had atrial tachycardia, 9% ventricular tachycardia, and 4% had ventricular fibrillation. Sinus tachycardia was observed in 35% of admissions while sinus bradycardia was noted in 28%. Noting that acidosis and electrolyte derangement play a major role in the development of cardiac events, they recommend atropine in adequate doses very early in the course of the illness as the strategy to be implemented. 

A 58-year-old man is hospitalized in cardiac intensive care following an acute myocardial infarction. He has had recurrent episodes of ventricular tachycardia that have not responded to lidocaine, and an intravenous infusion of procainamide will now be administered. The patient weighs 80 kg and expected values for his procainamide distribution volume and elimination half-life are 2.0 L/kg and 3 hours, respectively. 

Acute sinus bradycardia requires treatment if it is symptomatic e.g. where there is hypotension or escape rhythms extreme bradycardia may allow a ventricular focus to take over and lead to ventricular tachycardia. The foot of the bed should be raised to assist venous return and atropine should be given i.v. Chronic symptomatic bradycardia is an indication for the insertion of a permanent pacemaker. 

Morady F, Scheinman MM, Shen E, Shapiro W, Sung RJ, DiCarlo L. Intravenous amiodarone in the acute treatment of recurrent symptomatic ventricular tachycardia. Am J Cardiol 1983 51(l) 156-9. 

Kowey PR, Marinchak RA, Rials SJ, Bharucha DB. Intravenous antiarrhythmic therapy in the acute control of in-hospital destabilizing ventricular tachycardia and fibrillation. Am J Cardiol 1999 84(9A) R46-51. 

A much more serious complication of dobutamine therapy is ventricular dysrhythmias. Of 305 patients with acutely decompensated congestive heart failure, 58 were given dobutamine (although it is difficult to ascertain the dose), 44 were given other standard inotropic drugs such as milrinone, and 203 were treated with brain natriuretic peptide (nesiritide, 0.015 or 0.03 micrograms/kg/minute) (9). Of those given dobutamine 7% had sustained ventricular tachycardia, 17% had non-sustained ventricular tachycardia, and 5% had a cardiac arrest. In contrast. 

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. 

Quinidine gluconate Acute-onset atrial fibrillation ventricular tachycardia 2.2 mg/kg i.v. every 10 min 12 mg/kg total... 

Procainamide is available for i.v. and p.o. administration. It has been used for the treatment of acute-onset AF in horses (Marr Reef 1995a), although this requires further investigation. It is used primarily for the treatment of ventricular tachycardias in horses, where its main advantage is the absence of significant side-effects. 

Patients presenting with acute erythromycin overdose are usually asymptomatic or experiencing minor to moderate gastrointestinal side effects/ discomfort. Serious cardiac effects, including prolongation of the QT interval, arrhythmias (i.e., ventricular tachycardia. Torsades de Pointes, ventricular fibrillation, and heart block), may be observed after rapid intravenous administration and coincident with high, peak erythromycin plasma concentrations. The occurrences of these QT prolongation-associated arrhythmias are rare. 

Acute overdosage can result in both cardiovascular and neurologic effects. Ventricular dysrhythmias and hypotension are the most serious toxicities. Cardiac effects occur as a result of myocardial depression and depression of atrial, atrioventricular, and ventricular conduction. EKG changes will be evident. These EKG changes include a widening of the QT, PR, and QRS complexes ST depression and T inversion. Myocardial depression and vasodilation can cause hypotension to develop. Syncope can result from transient Torsade de Pointes (i.e., bursts of atypical ventricular tachycardia). Ventricular tachycardia and ventricular fibrillation may develop. Possible central nervous system (CNS) effects include lethargy, seizures, and coma. Other acute effects can include apnea. Signs of toxicity are expected to occur in... 

Figure 8.32 Final arrhythmias in case of sudden death in different clinical situations. (A) In the acute phase of an ischaemic heart disease (Adgey et at, 1982). In the majority of cases final arrhythmia was primary ventricular fibrillation and only in few cases it was sustained ventricular tachycardia, which developed in fibrillation. (B) In ambulatory patients the most frequent final arrhythmia was sustained VT leading to VF (Bayes de Luna, Coumel and Leclercq, 1989).

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