For ventricular fibrillation

Subcutaneous administration of -hexanc at 143 mg/kg/day for 30 days has been reported to decrease the threshold for ventricular fibrillation in perfused hearts from male Wistar rats (Khedun et al. 1996). Myocardial magnesium and potassium levels were reduced in treated rats. When these levels were corrected by supplementation, the ventricular fibrillation potential was still reduced. Histological alterations (disordered myocardial Z-bands) were also observed in exposed rats. 

The cornerstone of therapy for ventricular fibrillation is electrical deflbrillation. In the acute setting, defibrination is first-line therapy. Intravenous bretylium can occasionally contribute to conversion, but this is infrequent. In the management of out-of-hospital cardiac arrest, high-dose epinephrine (5 mg intravenously) improves the rate of successful resuscitation in patients with asystole, but not in those with ventricular fibrillation, when compared with the standard dose of 1 mg. Vasopressin (40 U intravenously) may more effective than 1 mg intravenous epinephrine in out-of-hospital patients with ventricular fibrillation that is resistant to electrical defibrillation. The OPTIC smdy (see Connolly et al., 2006) showed that amiodarone plus jS-blocker is superior than sotalol or jS-blocker alone for reducing ICD shocks in patients with reduced left ventricular function and history of sustained VT, VF, or cardiac arrest. 

Digitalis-induced arrhythmias are frequently made worse by cardioversion this therapy should be reserved for ventricular fibrillation if the arrhythmia is glycoside-induced. 

Lowered threshold for ventricular fibrillation, even at carboxyhemo-globin levels <10% A... 

Yes, in cases of recurring ventricular tachycardia or as emergency therapy for ventricular fibrillation. 

Although the effect is smaller than that observed in the atrium, ACh produces a negative inotropic effect in the ventricle. This inhibition is most apparent when there is concomitant adrenergic stimulation or underlying sympathetic tone. ACh suppresses automaticity of Purkinje fibers and increases the threshold for ventricular fibrillation. To the extent that the ventricle receives cholinergic innervation, sympathetic and vagal nerve terminals lie in close proximity, and muscarinic receptors are believed to exist at presynaptic as well as postsynaptic sites. 

Ventricular tachycardia,with electric defibrillation as last resort for ventricular fibrillation. 

For ventricular fibrillation, immediately apply direct-current countershock at 3-5 J/kg. Repeat twice if no response. Continue CPR if the patient is still without a pulse, and administer epinephrine, repeated countershocks, amiodarone, and/or lidocaine as recommended in advanced cardiac life support (ACLS) guidelines. 

For patients in cardiac arrest, usual antiarrhythmic agents and direct-current countershock are frequently ineffective until the core temperature is above 32-35°C (90-95°F). Provide gastric or peritoneal lavage with warmed fluids and perfonn CPR. For ventricular fibrillation, bretylium, 5-10 mg/kg IV (see p 421), may be effective. 

I. Pharmacology. Bretylium is a quaternary ammonium compound that is an effective type III antifibrillatory dmg and also suppresses ventricular ectopic activity. It increases the threshold for ventricular fibrillation and reduces the disparity in action potential duration between nonnal and ischemic tissue, which is believed to abolish boundary currents responsible for reentrant arrhythmias. Its pharmacologic actions are complex. Initially, norepinephrine is released from sympathetic neurons this is followed by a block of further norepinephrine release. In addition, norepinephrine uptake is inhibited at adrenergic neurons. The result is a transient increase in heart rate, blood pressure, and cardiac output that may last from a few minutes to 1 hour. Subsequent adrenergic blockade produces vasodilation, which may result in hypotension. 

A. For ventricular fibrillation, give 5 mg/kg iV over 1 minute (in addition to cardiopulmonary resuscitation and defibrillation). If not effective, administration may be repeated with 10 mg/kg. 

A. Do not use isoproterenol for ventricular fibrillation or ventricular tachycardia (other than torsade de pointes). 

Behind-body-armor standards use the depth of the cavity created in clay after a bullet is stopped by the vest. The roots of this approach involve military research. However, the clay may not adequately simulate the human viscoelastic properties and biomechanical responses. Recent research has defined the blunt ballistic characteristics of the chest and the mechanisms for ventricular fibrillation [Bir and Viano, 1999 Bir et al, 2004]. 

Fig. 20.2 Detection and therapy parameters for an ICD. Top Detection parameters. As programmed the ICD defines ventricular tachycardia (VT) as 12 beats greater than 150 bpm and ventricular fibrillation (VF) as 12 of 16 beats greater than 188 bpm. An optional fast ventricular tachycardia (FVT) zone has not been programmed on. Bottom Therapies for ventricular fibrillation are a first shock at 24 J and subsequent shocks at 35 J. Therapies for ventricular tachycardia are two pacing sequences followed by cardioversion attempts at 15,35,35, and 35 J. Pacing for bradycardia is set at 40 bpm.

Dalziel s Prediction Dalziel felt that the three major factors of concern for ventricular fibrillation are body weight, current magnitude, and shock duration. He used the results of animal studies, conducted by Ferris (1936) and Kouwenhoven (1959), to establish an equation for the minimum threshold of fibrillation. Dalziel developed the following equation for predicting the minimum threshold value of fibrillation for a body weight of 50 kg (110 lb) ... 

D Defibrillab on Assess for ventricular fibrillation or pulseless ventricular tachycardia defibril-late, if indicated. 

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. ... 

Ventricular fibrillation should be terminated by electrical defibrillation. Alternatively, lidocaine can be injected intravenously. In cases with lower frequency, ventricular tachyarrhythmia class I diugs such as aj marine, flecainide or propafenone are more effective as a result of the use-dependence of lidocaine. For prophylaxis treatment, amiodarone or sotalol may be helpful or the implantation of a cardioverter-defibrillator system. Acute amiodarone (i.v. in higher doses) can also terminate ventricular tachyarrhythmias. This action, however, seems to be mediated by its INa-blocking side effects and not (or less) by its class III like effects. 

Cardiac glycosides have a small ratio of toxic to therapeutic concentration. Possible adverse effects are nausea, vomiting, abdominal pain, diarrhoea, fatigue, headache, drowsiness, colour vision disturbances, sinus bradycardia, premature ventricular complexes, AV-block, bigeminy, atrial tachycardia with AV-Block, ventricular fibrillation. There are several mechanisms relevant for their toxic action (Table 2). 

Abnormal initiation of electrical impulses occurs as a result of abnormal automaticity. If the automaticity of the SA node increases, this results in an increased rate of generation of impulses and a rapid heart rate (sinus tachycardia). If other cardiac fibers become abnormally automatic, such that the rate of initiation of spontaneous impulses exceeds that of the SA node, other types of tachyarrhythmias may occur. Many cardiac fibers possess the capability for automaticity, including the atrial tissue, the AV node, the Purkinje fibers, and the ventricular tissue. In addition, fibers with the capability of initiating and conducting electrical impulses are present in the pulmonary veins. Abnormal atrial automaticity may result in premature atrial contractions or may precipitate atrial tachycardia or atrial fibrillation (AF) abnormal AV nodal automaticity may result in junctional tachycardia (the AV node is also sometimes referred to as the AV junction). Abnormal automaticity in the ventricles may result in ventricular premature depolarizations (VPDs) or may precipitate ventricular tachycardia (VT) or ventricular fibrillation (VF). In addition, abnormal automaticity originating from the pulmonary veins is a precipitant of AF. 

TABLE 6-5. Drugs for Ventricular Rate Control in Atrial Fibrillation... 

FIGURE 6-5. Decision algorithm for ventricular rate control using intravenous drug therapy for patients presenting with the first detected episode or an episode of persistent atrial fibrillation that is hemody-namically stable. 

Ventricular fibrillation is by definition hemodynamically unstable, due to the absence of pulse and blood pressure. Initial management includes provision of basic life support, including calling for help and initiation of cardiopulmonary I resuscitation (CPR).48 Oxygen should be administered as soon... 

TABLE 6-12. Drugs for Facilitation of Defibrillation in Patients with Ventricular Fibrillation... 

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