Ventricular fibrillation causes

Cardiovascular Cardiac toxicity due to chronic chloroquine use includes conduction disorders, congestive heart failure, prolongation of the QT interval, myocardial hypertrophy, and restrictive cardiomyopathy. Third degree atrioventricular block and sudden cardiac arrest due to ventricular fibrillation caused by chloroquine, unusual reactions, have been reported [6" ]. 

There is a close correlation between myocardial infarctions and tachyarrhythmias, illustrated by the presence of complex ventricular arrhythmias among heart attack victims which are estimated to affect one-third of the survivors each year. Frequendy, the immediate cause of sudden death is ventricular fibrillation, an extreme arrhythmia that is difficult to detect or treat. In the majority of cases, victims have no prior indication of coronary heart disease. 

Barium metal and most barium compounds are highly poisonous. A notable exception is barium sulfate which is nontoxic because of its extreme iasolubihty ia water. Barium ion acts as a muscle stimulant and can cause death through ventricular fibrillation of the heart. Therefore, care must be taken to avoid contact with open areas of the skin. Workers must wear respirators (of type approved for toxic airborne particles), goggles, gloves, and protective clothing at all times. The toxic barium aluminate residue obtained from barium production is detoxified by reaction with a solution of ferrous sulfate and converted iato nontoxic barium sulfate. According to OSHA standards, the TWA value for Ba and Ba compounds ia air is 0.5 mg/m. ... 

Cardiac arrhythmias are an important cause of morbidity and mortality approximately 400,000 people per year die from myocardial infarctions (MI) in the United States alone. Individuals with MI exhibit some form of dysrhythmia within 48 h. Post-mortem examinations of MI victims indicate that many die in spite of the fact that the mass of ventricular muscle deprived of its blood supply is often quite small. These data suggest that the cause of death is ventricular fibrillation and that the immediate availability of a safe and efficacious antiarrhythmic agent could have prolonged a number of Hves. The goals of antiarrhythmic therapy are to reduce the incidence of sudden death and to alleviate the symptoms of arrhythmias, such as palpitations and syncope. Several excellent reviews of the mechanisms of arrhythmias and the pharmacology of antiarrhythmic agents have been pubflshed (1,2). 

The answer is g. (Hardman, p 870. Katzung, pp 230-231) Quini-dine causes prolongation of the QT interval at therapeutic doses, possibly because of its anti muscarinic actions In some patients, this is associated with recurrent lightheaded ness and fainting (known as qmmdine syncope). The symptoms result from torsades de pointes. They typically terminate but may become fatal by degeneration into ventricular fibrillation. 

Proarrhythmia refers to development of a significant new arrhythmia (such as VT, ventricular fibrillation [VF], or TdP) or worsening of an existing arrhythmia. Proarrhythmia results from the same mechanisms that cause other arrhythmias or from an alteration in the underlying substrate due to the antiarrhythmic agent. TdP is a rapid form of polymorphic VT associated with evidence of delayed ventricular repolarization due to blockade of potassium conductance. TdP may be hereditary or acquired. Acquired forms are associated with many clinical conditions and drugs, especially type la and type III IKr blockers. 

Use extreme caution in a hypoxic patient. Giving Atropine to a hypoxic heart can cause ventricular fibrillation. 

First, drug-induced lengthening of the QT interval has been associated with the occurrence of ventricular tachyarrhythmias, namely TdP, a polymorphous ventricular arrhythmia that may cause syncope and degenerate into ventricular fibrillation and sudden death although the incidence of TdP is a rare event (usually, less than 1 in 100 000) [32], even a low risk is not justified for drugs with uncertain benefits or drugs providing only symptomatic improvement of a mild disease. 

Many of bariums compounds are toxic, especially barium chloride, which affects the functioning of the heart, causing ventricular fibrillation, an erratic heartbeat that can lead to death. 

Halothane exerts a pronounced hypotensive effect, to which a negative inotropic effect contributes. Enflurane and isoflurane cause less circulatory depression. Halothane sensitizes the myocardium to catecholamines (caution serious tachyarrhythmias or ventricular fibrillation may accompany use of catecholamines as antihypotensives or toco-lytics). This effect is much less pronounced with enflurane and isoflurane. Unlike halothane, enflurane and isoflurane have a muscle-relaxant effect that is additive with that of nondepolarizing neuromuscular blockers. 

Barium ion is a muscle poison causing stimulation and then paralysis. Initial symptoms are gastrointestinal, including nausea, vomiting, colic, and diarrhea, followed by myocardial and general muscular stimulation with tingling in the extremities. Severe cases continue to loss of tendon reflexes, general muscular paralysis, and death from respiratory arrest or ventricular fibrillation. Threshold of a toxic dose in humans is reported to be about 0.2-0.5 g Ba absorbed from the gut the lethal dose is 3 g Ba. 

Toxieology. Sodium fluoroacetate is highly toxic and causes convulsions and ventricular fibrillation. 

Cardiac arrhythmias have been provoked in a number of species. Inhalation of 3 5 00-6100 ppm by dogs for 5 minutes caused ventricular fibrillation and cardiac arrest after injection of epinephrine. The minimal concentration that elicited cardiac arrhythmias in the anesthetized monkey was 50,000ppm. ... 

Pharmacology Therapeutic concentrations of lidocaine attenuate phase 4 diastolic depolarization, decrease automaticity and cause a decrease or no change in excitability and membrane responsiveness. Action potential duration and effective refractory period (ERP) of Purkinje fibers and ventricular muscle are decreased, while the ratio of ERP to action potential duration is increased. Lidocaine raises ventricular fibrillation threshold. AV nodal conduction time is unchanged or shortened. Lidocaine increases the electrical stimulation threshold of the ventricle during diastole. 

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. 

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... 

All barium salts, especially the water and acid-soluble compounds, are highly toxic. Barium ion can cause death through ventricular fibrillation of the heart. It is a stimulant to the heart muscle. Intake of a few grams of barium salt can be lethal to humans. The insoluble salts such as barium sulfate, however, have little toxic action. 

The greatest hazards of accidental overdosage with epinephrine and norepinephrine are cardiac arrhythmias, excessive hypertension, and acute pulmonary edema. Large doses of isoproterenol can produce such excessive cardiac stimulation, combined with a decrease in diastolic blood pressure, that coronary insufficiency may result. It also may cause arrhythmias and ventricular fibrillation. Tissue sloughing and necrosis due to severe local ischemia may follow extravasation of norepinephrine at its injection site. 

Trichloroethylene Cleaning, degreasers, waxes, resins, mb-bers, paints, extractants, feedstock Inebriation at moderate exposure Heavy exposure can cause ventricular fibrillation, death 100 4.92 mL/kg... 

Sudden death is a rare phenomenon with the antipsychotics. An accurate assessment as to whether these drugs are causally or coincidentally involved cannot be made, because sudden death can occur in young, apparently healthy persons on no medication. For example, every year in the United States, some 600,000 people die suddenly. Although the most commonly postulated cause of sudden death is ventricular fibrillation, it can also result from ... 

Regional ischemia in the course of atherosclerotic coronary artery disease is one of the most important causes of arrhythmia in the Western industrial world. These arrhythmias start with or often degenerate into ventricular fibrillation and are the main cause of sudden cardiac death in these countries. However, in the course of ischemia and infarction the mechanisms by which arrhythmia is induced vary with the duration of ischemia. In the acute phase of ischemia, i.e. within the first 2 1 h ventricular arrhythmias often occur. 

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