Ventricular fibrillation epinephrine

M (7/12 ventricular fibrillation after epinephrine challenge, 1/12 cardiac arrest)... 

Report 957-77, E.I. du Pont de Nemours and Co., Newark, DE. Test species/Strain/Sex/Number male beagle dogs (1-2 per exposure group) Exposure route/Concentrations/Durations Inhalation 2,600, 5,200, 10,000, and 21,600 ppm for 10 min (the cardiac sensitization test is a 10-min test) epinephrine dose at 8 g/kg. The cardiac sensitization test is based on the observation that some halocarbons make the mammalian heart abnormally sensitive to epinephrine, resulting in ectopic beats and/or ventricular fibrillation, which may result in death. 

Chenoweth MB Ventricular fibrillation induced by hydrocarbons and epinephrine. J Ind Hyg Toxicol 28 151-158, 1946... 

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. ... 

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. 

Lindner KH, Dirks B, Strohmenger HU, Prengel AW, Lindner IM, Lurie KG. Randomised comparison of epinephrine and vasopressin in patients with out-of-hospital ventricular fibrillation. Lancet 1997 349 535-97. 

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. 

Patients treated with recommended dosages of epinephrine will complain of feeling nervous or anxious. Some will have tremor of the hand or upper extremity and many will complain of palpitations. Epinephrine is dangerous if recommended dosages are exceeded or if the drug is used in patients with coronary artery disease, arrhythmias, or hypertension. The inappropriate use of epinephrine has resulted in extreme hypertension and cerebrovascular accidents, pulmonary edema, angina, and ventricular arrhythmias, including ventricular fibrillation. 

VENTRICULAR FIBRILLATION (not responding to electrical defibrination) Lidocaine I. ... I Bretvlium Epinephrine... 

Weaver WD, Fahrenbruch CE, Johnson DD, Hallstrom AP, Cobb LA, Copass MK. Effect of epinephrine and lidocaine therapy on outcome after cardiac arrest due to ventricular fibrillation. Circulation 1990 82(6) 2027-34. 

HPI CS is a 5 -year-old man admitted for an anterior Ml. Three days after admission, the patient s nurse found him unresponsive. His vital signs included no detectable blood pressure or pulse. ECG showed VT that progressed to ventricular fibrillation (VF). Immediate electrical defibrillation was applied. Other treatments instituted include airway management, chest compression, and establishment of IV access. After three shocks, 1 mg epinephrine was given and patient was shocked again. However, he was still in VF and amiodarone was administered. 

R-8I8 (17) prevented chloroform-induced ventricular fibrillation in mice as well as arrhythmias caused by hydrocarbon-epinephrine, ouabain, aconitine and coronary occlusion in dogs.5° The activity of numerous analogs in the mouse chloroform test has been described.57... 

Lindner KH, Ahnefeld FW, Grunert A. Epinephrine versus norepinephrine in prehospital ventricular fibrillation. Am J Cardiol 1991 67 427 28. 

Garb, S., and M.B. Chenoweth. 1948. Studies on hydrocarbon-epinephrine induced ventricular fibrillation. J. Pharmacol. Exp. Ther. 94 12-18. 

Cyclopropane increases the irritability of the heart by acting on its autonomic tissue and has a tendency to induce irregularities that may terminate in fatal fibrillation. The use of epinephrine is contraindicated in cyclopropane anesthesia because this drug tends to induce ventricular fibrillation (see Table 16). 

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. 

Vasopressin levels in patients with vasodilatory shock are inappropriately low, and such patients are extraordinarily sensitive to the pressor actions of vasopressin. The combination of vasopressin and norepinephrine is superior to NE alone in the management of catecholamine-resistant vasodilatory shock. Although the efficacy of vasopressin in the resuscitation of patients with ventricular fibrillation or pulseless electrical activity is similar to that of epinephrine, vasopressin followed by Epi appears to be more effective than Epi alone in the treatment of patients with asystole. 

Van Dongen and Sanchez (29) compared the antifibrillatory activity of hydroquinidine with a specially purified quinidine. They present the viewpoint that the activity of commercially prepared quinidine in auricular fibrillation is based entirely on its content of dihydroquinidine. They used the rabbit as a test animal and observed that dihydroquinidine produced an increase in the electrical stimulus thresholds required to provoke premature systoles, tachycardia, auricular fibrillation, and ventricular fibrillation. With dihydroquinidine there was also a decrease in the duration of fibrillation which occurs after the electrical stimulus is ended. Dihydroquinidine, they found, could prevent the heterotropic rhythms (largely ventricular arrhythmias) provoked by the intravenous injection of barium chloride or epinephrine. They also observed that hydroquinidine, at 8 mg./kg., prolonged the auricular conduction time by 50%, the AV conduction time by 30 %, and increased the refractory period by 15%. Pure quinidine was inactive at this dosage. 

Additional evidence for an antifibrillatory action for ajmaline was supplied by van Dongen (13). He found that in the decerebrate cat 0.5 mg./kg. ajmaline increased the amount of faradic current required to produce auricular fibrillation, ventricular fibrillation, and post-stimulus arrhythmias. This action differs from that of quinidine, which prolonged auricular conduction time and atrioventricular conduction times by 52-100 %, while ajmaline did not alter refractory periods or conduction times. Heterotropic cardiac rhythms were produced by a variety of means (barium chloride, epinephrine, and strophantin-ephedrine) which in all cases may be prevented by ajmaline. 

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. 

Treatment is nonspecific and should be directed to promote recovery from an anesthetic agent. In treating persons suffering toxic effects caused by exposure to halo-genated solvents, the use of epinephrine (adrenalin) and similar drugs must be avoided because they may produce cardiac arrhythmias, including ventricular fibrillation. 

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