Ventricular fibrillation caused

Disturbances of cardiac rhythm (e.g., tachycardia, atrial fibrillation, ventricular flutter, and A-V or intraventricular block) are the most frequent causes of death. Thus, management of cardiac function is critical. If the patient survives the early phase, recovery without sequelae is probable, and vigorous resuscitative measures are important. A major clinical problem is determining when a patient is no longer in danger. Many patients with mild overdose have been hospitalized... 

One of the more serious complications of magnesium deficiency is cardiac arrhythmias. Premature atrial complexes, atrial tachycardia and fibrillation, ventricular premature complexes, ventricular tachycardia, and ventricular fibrillation may be associated with magnesium deficiency. These effects maybe partly caused by the hypokalemia, renal wasting, and intracellular depletion of potassium caused by hypomagnesemia. 

Cardiovascular System Following systemic absorption, local anesthetics decrease electrical excitabdity, conduction rate, and force of contraction. Most local anesthetics also cause arteriolar dilation. Untoward cardiovascular effects usually are seen only after high systemic concentrations are attained and effects on the CNS are produced. However, on rare occasions, lower doses of some local anesthetics wUl cause cardiovascular collapse and death, probably due to either an action on the pacemaker or the sudden onset of ventricular fibrillation. Ventricular tachycardia and fibrillation are relatively uncommon consequences of local anesthetics other than bupivacaine. The use of local anesthetics as antiarrhythmic drugs is discussed in Chapter 34. Untoward cardiovascular effects of local anesthetic agents may result from their inadvertent intravascular administration, especially if epinephrine also is present. 

Experimental studies117,159 have shown that when animals are poisoned with ChE inhibitors and then allowed to become cyanotic, rapid intravenous administration of atropine will cause ventricular fibrillation. Ventricular fibrillation after rapid intravenous administration of atropine has not been reported in humans. 

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. 

Implantable tachyrhythmia devices, available for some years, address far less dangerous atrial tachyarrhythmias and fibrillation. The technical barriers to counteracting ventricular tachyarrhythmias and fibrillation using massive shocks have been formidable and are compounded by the possibiUty of causing the very problem the shock is designed to overcome. Newer tachyrhythmia devices are being readied that can safely regulate arrhythmias across the hiU spectmm. 

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). 

Atrial fibrillation Irregular and rapid atrial contraction, resulting in a quivering of the atria and causing an irregular and inefficient ventricular contraction... 

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. 

Serum CK is consistently increased in all forms of AMD. Forearm ischemic exercise causes a normal rise of venous lactate concentration in patients with childhood or adult AMD. The electrocardiogram (ECG) is altered in Pompe s disease, with a short P-R interval, giant QRS complexes and left ventricular or biventricular hypertrophy, but is usually normal in the later-onset forms. The EMG shows myopathic features and fibrillation potentials, bizarre high-frequency discharges and myotonic discharges. 

There is no glycemic response to glucagon or epinephrine (Fig. 42-1), whereas a galactose load causes a normal glycemic response. Forearm ischemic exercise produces a blunted venous lactate rise or no response. Serum CK activity is variably, often markedly, increased. The ECG shows left ventricular or biventricular hypertrophy in most patients, and the EMG may show myopathic features alone or associated with fibrillations, positive sharp waves and myotonic discharges. This mixed EMG pattern in patients with weakness and distal wasting often reinforces... 

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. ... 

Atrial fibrillation Peak digoxin body stores larger than the 8 to 12 mcg/kg required for most patients with heart failure and normal sinus rhythm have been used for control of ventricular rate in patients with atrial fibrillation. Titrate doses of digoxin used for the treatment of chronic atrial fibrillation to the minimum dose that achieves the desired ventricular rate control without causing undesirable side effects. Data are not available to establish the appropriate resting or exercise target rates that should be achieved. 

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. 

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