Ventricular fibrillation defibrillation

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. 

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

Implantable cardioverter-defibrillator (ICD) A device implanted into the heart transvenously with a generator implanted subcutaneously in the pectoral area that provides internal electrical cardioversion of ventricular tachycardia or defibriUation of ventricular fibrillation. 

Following resuscitation from ventricular fibrillation (VF) or pulseless VT, ICD implantation is a proven strategy for the prevention of recurrent SCD. Three prospective, randomized, controlled trials, the Antiarrhythmics Versus Implantable Defibrillators (AVID) study, the Canadian Implantable Defibrillator Study (CIDS), and the Cardiac Arrest Study Hamburg (CASH), support this strategy [27-29]. 

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. 

Raitt, M. H., Connor, W. E., Morris, C., Kron, J., Halperin, B., Chugh, S. S., McClelland, J., Cook, J., and MacMurdy, K. (2005). Fish oil supplementation and risk of ventricular tachycardia and ventricular fibrillation in patients with implantable defibrillators A randomized controlled trial. JAMA 293, 2884-2891. 

Some of the beneficial effects of fish oils after acute myocardial infarction have been attributed to an antidysr-hythmic effect on the heart (5). However, the results of a randomized trial in 200 patients with implantable cardioverter defibrillators are at variance with this the rate of cardioversion was higher in those taking fish oils 1.8 g/day than in a control group who took olive oil (6). The lack of benefit and the suggestion that fish oil supplementation may increase the risk of ventricular tachycardia or ventricular fibrillation in some patients with implantable cardioverter defibrillators can reasonably be interpreted as evidence that the routine use of fish oil supplementation in patients with implantable cardioverter defibrillators and recurrent ventricular dysrhythmias should be avoided. 

Exner, D., Reiffel, J., Epstein, A., Ledingham, R., Reiter, M., Yao, Q., Duff, H., Follmann, D., Schron, E., Greene, H., Carlson, M., Brodsky, M., Akiyama, T., Baessler, C., and Anderson, J., Beta-blocker use and survival in patients with ventricular fibrillation or symptomatic ventricular tachycardia The Antiarrhythmics Versus Implantable Defibrillators (AVID) trial, Journal of American College of Cardiology, Vol. 34, No. 2, 1999, pp. 325-333. 

A 34-year-old alcoholic man with acute pancreatitis was given continuous intravenous infusion of haloperidol (2 mg/hour) for agitation after 7 hours he received a bolus dose of haloperidol 10 mg for worsening agitation and 20 minutes later, QT interval was 560 ms (420 ms before treatment) (131). He developed torsade de pointes and ventricular fibrillation, which resolved with electric defibrillation. He was a smoker and was also taking tiapride and alprazolam for depression, in addition to pantoprazole, piperazilline + tazobactam, paracetamol, and vitamins Bi, B6, and B 12-... 

Bupivacaine can cause ventricular extra beats (8). Ventricular dysrhythmias and seizures were reported in a patient who received 0.5% bupivacaine 30 ml with adrenaline 5 micrograms/ml for lumbar plexus block, after a negative aspiration test (9). The patient developed ventricular fibrillation and required advanced cardiac life support for 1 hour, including 15 defibrillations, and adrenaline 40 mg before sinus rhythm could be restored. There were no neurological sequelae. 

Four prisoners drank a decoction of yew needles (T. baccata) (12). Two died in prison with cardiac arrest. One went into deep coma, and had several episodes of ventricular fibrillation, controlled by defibrillation after return of consciousness his general condition deteriorated suddenly, he lost consciousness again, his circulation stopped, and he died on the fourth day. The other patient drank a much smaller amount of the decoction he was conscious, had bradycardia requiring transient pacemaking, and had a mild ventricular dysrhythmia he recovered after 10 days. In both cases there was excessive diuresis and severe hypokalemia and atropine was effective for a short time in the control of bradycardia. 

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. 

White, R.D. Asplin, B.R. Bugliosi, T.F. Hankins, D.G. High discharge survival rate after out-of-hospital ventricular fibrillation with rapid defibrillation by police and paramedics. Ann. Emerg. Med. 1996, 28, 480-485. 

On the other hand, the medical condition where the heart beats too fast is known as tachycardia. If untreated, tliis condition may lead to ventricular fibrillation, that is, a condition in which the heart stops beating and shakes uncontrollably and is usually fatal. In 1980, a special device was developed and implanted in patients. It could sense the condition and provide a shock that would stop the fibrillation and restore the normal sinus rhythm via an electrode sutured onto the heart. The device was first powered by a lithium/vanadium pentoxide system later it was replaced by a system using a cathode material of silver vanadium oxide (SVO or Ag2V40ii). This is the actual system used in modem ICDs (implantable cardioverter/defibrillator). Another material used is the lithium/manganese dioxide system. Also, a new system using a sandwich cathode design with an inner cathode material of carbon monofluoride and an external cathode layer of silver vanadium oxide is in wide use. 

For patients in ventricular fibrillation/pulseless ventricular tachycardia (VF/PVT), rapid defibrillation is the single most important intervention that affects survival. 

Cobb LA, Fahrenbruch CE, Walsh TR, et al. Influence of cardiopulmonary resuscitation prior to defibrillation in patients with out-of-hospital ventricular fibrillation. JAMA 1999 281 1182-1188. 

Wik L, Hansen TB, FylUng F, et al. Delaying defibrillation to give basic cardiopulmonary resuscitation to patients with out-of-hosptial ventricular fibrillation A randomized trial. JAMA 2003 289 1389-1395. 

Patients with hemodynamically significant ventricular tachycardia or ventricular fibrillation not associated with an acute Ml who are resuscitated successfully (electrical cardioversion, pressors, amiodarone) are at high risk for death and should receive implantation of an internal cardioverter-defibrillator. 

LQTS = long-QT syndrome SD = sudden death TdP = torsade de pointes PMVT = polymorphic ventricular tachycardia VF = ventricular fibrillation BB = j6-blocker ICD = internal cardioverter-defibrillator. 

FIGURE 17-16. Example of an approach to the management of survivors of cardiac arrest (resuscitated VT/VF). Reversible causes of cardiac arrest (e.g., electrolyte abnormalities, acute phase of Ml) should be treated with specific therapy. AADs = antiarrhythmic drugs BBs = /i-blockers EPS = invasive electrophysio-logic studies ICD = implantable cardioverter-defibrillator VT/VF = ventricular tachycardia/ventricular fibrillation Ml = myocardial infarction. 

Administration of atropine should be withheld until a cardiac monitor and a defibrillator arc in place and (he patient s airway is secured. Atropine can precipitate ventricular fibrillation in hypoxic patients. Continuous cardiac monitoring and an ECG are oeces.sary. Electrical pacing is the treatment... 

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

Defibrillation is the treatment of choice for a client in ventricular fibrillation. 

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 64-year-old woman was treated for hypertrophic cardiomyopathy with amiodarone 1.2 g daily and atenolol 50 mg daily. Five days later the atenolol was replaced by metoprolol 100 mg daily. Within 3 hours she complained of dizziness, weakness and blurred vision. On examination she was found to be pale and sweating with a pulse rate of 20 bpm. Her systolic blood pressure was 60 mmHg. Atropine 2 mg did not produce chronotropic or haemodynamic improvement. She responded to isoprena-line (isoproterenol). Severe hypotension has been reported in another patient taking sotalol when intravenous amiodarone (total dose 250 mg) was given. Another report describes cardiac arrest in one patient on amiodarone, and severe bradycardia and ventricular fibrillation (requiring defibrillation) in another, within 1.5 and 2 hours of starting to take propranolol. ... 

Cardiac defibrillators are electronic devices that have been used for decades to provide a strong electrical shock to a patient in an attempt to convert a very rapid (and often chaotic), ineffective heart rhythm to a slower, coordinated, and more effective rhythm. When used to treat ventricular fibrillation (VF) or very rapid ventricular tachycardia the shock may be lifesaving because the heart output is nil or is too low to sustain life. Occurrence of VF is a medical emergency and rapid treatment (within seconds to minutes) is essential for survival. 

An AED is an electronic device designed to deliver an electric shock to a victim of sudden cardiac arrest. Ventricular fibrillation may be restored to normal rhythm up to 60 percent of the time if treated promptly with an AED, a procedure called defibril-lation. The American Heart Association (AHA) estimates that approximately 890 deaths from coronary heart disease occur outside of the hospital or emergency room every day. According to the Occupational Safety and Health Administration (OSHA) in 2001 and 2002, there were reported 6628 workplace fatalities 1216 from heart attack, 354 from electric shock, and 267 from asphyxia. The AHA and OSHA have estimated that up to 60 percent of these victims might have been saved if automated external defibrillators (AEDs) were immediately available. Chances of survival from sudden cardiac death diminish by 7 to 10 percent for each minute without immediate CPR or defibrillation. After 10 minutes, resuscitation rarely succeeds. See Figure A.7 for an AED provided in a wall-mounted case. 

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