Ventricular arrhythmias asystole

Adverse effects With chronic use, procainamide causes a high incidence of side effects, including a reversible lupus erythe-matosus-like syndrome that develops in 25 to 30% of patients. Toxic concentrations of procainamide may cause asystole or induction of ventricular arrhythmias. Central nervious system (CNS) side effects include depression, hallucination and psychosis. With this drug, gastrointestinal intolerance is less frequent than with quinidine. 

The primary clinical effects observed in beta blocker toxicity are cardiovascular in nature. Direct cardiac effects include bradycardia (sinus, atrioventricular node, and ventricular), all degrees of atrioventricular block, bundle branch blocks, and asystole. Ventricular arrhythmias may occur secondary to bradycardia. Torsades de pointes has been associated with chronic toxicity from sotalol. Hypotension occurs and is due to decreased cardiac output and/or vasodilation. Central nervous system effects of these drugs including lethargy, coma, and seizures are secondary to the cardiovascular toxicities. Seizures and coma may be secondary to hypoglycemia. Bronchospasm can occur secondary to beta-2 blockade. Hypoglycemia and hyperkalemia can occur. 

Early signs of tricyclic antidepressant toxicity are due to anticholinergic effects and include tachycardia, mydriasis, dry mouth, low-grade fever, diminished bowel sounds, CNS excitation, and delirium. More serious toxicity is manifested by coma, respiratory depression, seizures, and cardiovascular toxicity including conduction disturbances, hypotension, ventricular arrhythmias, and asystole. Seizures cause hyperthermia, rhabdomyolysis, and metabolic acidosis. Clinical deterioration can be rapid and catastrophic in patients with tricyclic antidepressant overdose. Death most often occurs due to dysrhythmia and circulatory collapse. The typical therapeutic dose of a tricyclic antidepressant is 2-4 mg kg day Doses of 15-20 mg kg are potentially lethal. Therapeutic drug levels for most tricyclic antidepressants range from 100 to... 

In addition to drugs in these classes, others may be used for certain arrhythmias. Digoxin may be used for treatment of atrial fibrillation, adrenaline for asystolic cardiac arrest, atropine for sinus bradycardia, methacholine (rarely) for supraventricular tachycardia, magnesium salts for ventricular arrhythmias, and calcium salts for ventricular arrhythmia due to hyperkalaemia. 

Heart disease is the leading cause of death in the United States and is responsible for approximately 870,000 deaths per year (1). Sudden cardiac death (SCD) is responsible for almost half of these deaths, claiming 350,000 to 400,000 lives per year (2). SCD is defined by the World Health Organization as death due to any cardiac disease that occurs out of hospital, in an emergency room, or a patient who is dead on arrival to a care facility. Of note, the death must occur within one hour after the onset of symptoms. The majority of SCD is likely arrhythmic in etiology. In women, up to 88% of sudden cardiac arrests may be due to arrhythmic causes (3). Of SCD due to cardiac arrhythmias, greater than 80% of events are due to ventricular tachycardia (VT) and ventricular fibrillation (VF), with the remainder due to bradyarrhythmias and asystole (4). Coronary artery disease (CAD), manifesting acutely as ischemic ventricular arrhythmias or chronically as scar-mediated... 

Overdose causes hypotension, bradycardia, AV block, and asystole. The QRS and QT intervals are prolonged, and ventricular arrhythmias may occur. 

Sudden death caused by cardiac arrest due to ventricular tachycardia or ventricular fibrillation remains a serious health problem worldwide. In the United States alone, cardiovascular disease accounts for over 900,000 deaths annually (1). Of these deaths, 350,000 are due to out-of-hospital cardiac arrest (2), two-thirds of which occur without prior recognition of cardiac disease (1). In the United States, 15-20% of all fatalities and 50% of all cardiac fatalities are sudden. Although sudden death caused by asystole or pulseless electrical activity is not preventable, sudden death caused by a ventricular arrhythmia can be. Prompt treatment to stop the ventricular arrhythmia before it causes death is possible. 

RED FLAG If vagal maneuvers are used, keep resuscitative equipment readily available because vagal stimulation can cause bradycardia, ventricular arrhythmias, and asystole. 

Digitalis intoxication Exercise caution in the use of procainamide in arrhythmias associated with digitalis intoxication. Procainamide can suppress digitalis-induced arrhythmias however, if there is concomitant marked disturbance of AV conduction, additional depression of conduction and ventricular asystole or fibrillation may result. Consider use of procainamide only if discontinuation of digitalis, and therapy with potassium, lidocaine, or phenytoin are ineffective. 

Deflbrillation is one of the few interventions that has been shown to improve outcome from cardiac arrest. The cardiac arrhythmias commonly associated with sudden collapse are (1) asystole and (2) rapid and ineffective depolarization due to ventricular flbrillation (VF), pulseless ventricular tachycardia (VT), or supraventricular tachycardia with 1 1 ventricular response (as can occur with pre-excitation syndromes). The best strategy is to treat collapsed patients who have a broad-complex tachycardia at once by external Direct Current (DC) defibrillation. 

Adverse effects include SA block or arrest, high grade AV block, ventricular tachycardia, arrhythmia or ventricular asystole, polymorphic ventricular tachyarrhythmia, hypotension (particularly when given IV), cinchonism, tinnitus, loss of hearing, gastrointestinal upset, severe headache, diplopia, photophobia, etc. 

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. 

Cardiovascular System. Atropine is sometimes used to block the effects of the vagus nerve (cranial nerve X) on the myocardium. Release of acetylcholine from vagal efferent fibers slows heart rate and the conduction of the cardiac action potential throughout the myocardium. Atropine reverses the effects of excessive vagal discharge and is used to treat the symptomatic bradycardia that may accompany myocardial infarction.4 Atropine may also be useful in treating other cardiac arrhythmias such as atrioventricular nodal block and ventricular asystole. 

The effects of berbamine of the isolated and perfused working heart of the guinea pig was studied. The alkaloid was observed to depress the function of the isolated working heart in a dose-dependent manner. The alkaloid (3 mol/l) decreased the left ventricular pressure, aortic pressure -dP/dtmax, aortic blood flow and coronary blood flow, and increased left ventricular end-diastolic pressure. At a concentration of 100 mol/l, ventricular asystole was produced, but there was no influence on atrial contraction. Berbamine was also observed to antagonize epinephrine-induced arrhythmias [202]. 

Death may result from ventricular fibrillation, heart block or asystole (see below under arrhythmias). 

Unless the patient is in cardiac arrest (asystole or ventricular fibrillation), rewamn slowly (using blankets, wamn intravenous fluids, and warmed-mist inhalation) to prevent rewarming arrhythmias. 

Is a reperfusion arrhythmia commonly seen after a Myocardial Infarction (MI). Idioventricular rhythm acts as a ventricular escape rhythm, with the dominant pacemaker originating from the ventricles. This rhythm protects the heart from asystole. It can be identified on the ECG by the wide strangely shaped QRS complexes with the absence of P waves (Fig. 6.38). The rate in Idioventricular rhythm is usually between 20 and 40 BPM. Idioventricular rhythm with a rate above this is termed accelerated Idioventricular rhythm. 

Intravenous phenytoin is effective for the treatment of cardiac arrhythmias, but fatal ventricular asystole secondary to i.v. phenytoin has been reported (60 ). Massive overdose from oral Garoin (phenytoin plus phenobarbitone) has produced right bundle branch block (19 ). It has been suggested that the stopping of diphenylhydantoin before anaesthesia for surgery may precipitate atrioventricular or intraventricular conduction defects during the anaesthesia (30 ). 

---