Ventricular tachycardia causes

SOTALOL DIURETICS-CARBONIC ANHYDRASE INHIBITORS, LOOP DIURETICS, THIAZIDES t risk of ventricular arrhythmias, particularly torsades de pointes ventricular tachycardia, caused by sotalol Hypokalaemia, a side-effect of these diuretics, predisposes to arrhythmias during sotalol therapy Normalize potassium levels before starting sotalol in patients already taking these diuretics. When starting these diuretics in patients already taking sotalol, monitor potassium levels eveiy 4-6 weeks until stable... 

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). 

Propranolol has been studied most carefully in experiments and in clinics. It is used for ventricular tachycardia, arrhythmia caused by digitalis drug overdose, or as a result of thy-rotoxosis or excess catecholamine activity. Despite the fact that there are a number of )8-adrenoblockers, propranolol is considered the first choice of drugs although other blockers of calcium blockers can be just as effective. 

Proarrhythmic effects Propafenone may cause new or worsened arrhythmias. Such proarrhythmic effects range from an increase in frequency of PVCs to the development of more severe ventricular tachycardia, ventricular fibrillation or torsade de pointes, which may lead to fatal consequences. It is essential that each patient be evaluated electrocardiographically and clinically prior to, and during therapy to determine whether response to propafenone supports continued use. Non-life-threatening arrhythmias Use of propafenone is not recommended in patients with less severe ventricular arrhythmias, even if the patients are symptomatic. 

Proarrhythmic effects Flecainide can cause new or worsened arrhythmias. Such proarrhythmic effects range from an increase in frequency of PVCs to the development of more severe ventricular tachycardia. 

Pharmacology Bretylium tosylate inhibits norepinephrine release by depressing adrenergic nerve terminal excitability, inducing a chemical sympathectomy-like state. Bretylium blocks the release of norepinephrine in response to neuron stimulation. Peripheral adrenergic blockade causes orthostatic hypotension but has less effect on supine blood pressure. It has a positive inotropic effect on the myocardium. Pharmacokinetics Peak plasma concentration and peak hypotensive effects are seen within 1 hour of IM administration. However, suppression of premature ventricular beats is not maximal until 6 to 9 hours after dosing, when mean plasma concentration declines to less than 50% of peak level. Antifibrillatory effects occur within minutes of an IV injection. Suppression of ventricular tachycardia and other ventricular arrhythmias develops more slowly, usually 20 minutes to 2 hours after parenteral administration. 

Bepridil has Class I antiarrhythmic properties and, like other such drugs, can induce new arrhythmias, including ventricular tachycardia/ventricular fibrillation (VTA/F). In addition, because of its ability to prolong the QT interval, bepridil can cause torsades de pointes type VT. Because of these properties, reserve bepridil for patients in whom other antianginal agents do not offer a satisfactory effect (see Warnings). P.285... 

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. 

Overdose with TCAs causes tachycardia, hypotension, prolonged EKG intervals, and fatal arrhythmias, including ventricular tachycardias and bundle branch blocks (lack of conduction of the cardiac impulse). Conduction deficits alone and in combination with hypotension account for most of the morbidity and mortality associated with TCA overdose (Baldessarini, 1996). 

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. 

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. 

Digitoxin causes inhibition of the Na+/K+ ATPase, this reduces the sodium gradient and leads to increased intracellular calcium. This causes the adverse effects, including vomiting, diarrhea, visual disturbances, hypotension, and ventricular tachycardia, leading to fibrillation. 

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. 

Adverse effects Flecainide can cause dizziness, blurred vision, headache, and nausea. Like other Class IC drugs, flecainide can aggravate preexisting arrhythmias or induce life-threatening ventricular tachycardia that is resistant to treatment (see p. 166). 

Digoxin (see p. 158) shortens the refractory period in atrial and ventricular myocardial cells while prolonging the effective refractory period and diminishing conduction velocity in Purkinje fibers. Digoxin is used to control the ventricular response rate in atrial fibrillation and flutter. At toxic concentrations, digoxin causes ectopic ventricular beats that may result in ventricular tachycardia and fibrillation. [Note This arrhythmia is usually treated with lidocaine or phenytoin.]... 

Trazodone is less cardiotoxic than tricyclic antidepressants, although it has rarely been reported to cause ventricular tachycardia. QT interval prolongation has been reported in overdose (34). 

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