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At least 19 recordsLinked to original sources
PubMed1964

TREATMENT OF CARDIAC ARRHYTHMIAS WITH SYNCHRONIZED ELECTRICAL COUNTERSHOCK.

Synchronized electrical countershock is an intriguing new method for the treatment of ectopic tachycardias. The authors applied this treatment to 20 patients with chronic atrial fibrillation and, in 17 patients, sinus rhythm was restored immediately. An additional four patients with atrial flutter were successfully converted to sinus rhythm. One patient developed a hemiplegia two weeks after cardioversion. No other untoward side effects were observed. In two patients with ventricular fibrillation electrical countershock terminated the arrhythmia. After successful cardioversion of atrial fibrillation, a maintenance dose of quinidine is given to help maintain sinus rhythm. In spite of this precaution, one-half of the patients reverted to atrial fibrillation within a month. The quinidine was administered for two to three days in advance of cardioversion; on this regimen, 10 of 34 patients reverted to sinus rhythm on quinidine alone and did not require countershock. The exact place of this treatment of cardiac arrhythmias has not yet been clearly defined.

Arrhythmias, Cardiac↗
PubMed1976

Effects of electrical countershock on serum creatine phosphokinase (CPK) isoenzyme activity.

Total and MB serum creatine phosphokinase (CPK) activity levels were measured serially in 30 patients treated with direct current electrical countershock, 17 patients with acute myocardial infarction and 25 normal subjects. In addition, serial determinations of total and MB CPK in serum were performed in 11 closed chest anesthetized dogs subjected to 10 repetitive countershocks at 15 second intervals with a delivered energy of 240 joules per countershock. Less than 4 milli-international units (mlU)/ml of MB CPK was found in the serum of normal subjects. Patients with myocardial infarction whose elevated total CPK levels were comparable with those of patients treated with cardioversion had a usbstantial rise in MB CPK activity, with peak values averaging 39 +/- 6 mlU/ml (mean +/- standard error). Fifteen of the 30 patients treated with countershock had elevated total CPK activity that peaked within 4 hours. In this group, MM CPK elevations accounted for the overall rise in CPK activity. In two patients, modest elevations of MB CPK (11 and 13 mlU/ml, respectively) were observed after cardioversion. In all 11 dogs total CPK increased after countershock, peaking to 1,888 +/- 410 MLU/ml within 6 hours. Six dogs had increased MB CPK activity (52+/- 6 mlU/ml) and myocardial necrosis demonstrable histologically 4 days later. The results indicate that (1) myocardial damage in dogs produced by intense, repetitive countershock is associated with increased serum MB CPK; and (2) countershock as conventionally used in patients does not generally produce myocardial damage and serum MB CPK elevation. Although release of MB CPK into serum occasionally occurs after countershock, perhaps reflecting myocardial damage, the elevations appear to be modest. Thus, electrical countershock does not obscure the diagnosis of myocardial infarction or impair quantitative assessment of the extent of myocardial damage based on analysis of serum MB CPK activity.

Adult↗
PubMed1985

Treatment of presumed asystole during pre-hospital cardiac arrest: superiority of electrical countershock.

Standard drug therapy for asystole during cardiac arrest includes epinephrine, atropine, and calcium chloride (CaCl). Recent studies have shown that ventricular fibrillation (VF) can appear to be asystole when recorded from the chest surface. To determine the efficacy of these drugs and electrical countershock for asystole, a group of 83 adult nontraumatic cardiac arrest victims (55 men, 28 women, mean age of 64 +/- 14 years) were studied. Asystole appeared at some time during arrest in 44 patients (53%) and was the initial rhythm in 24 (29%). The rate of survival to hospital discharge was significantly higher in patients whose initial rhythm was VF (46%) than in patients whose initial rhythm was asystole (0%). Epinephrine, CaCl and atropine infrequently changed the rhythm from asystole. Electrical countershock infrequently altered the rhythm from asystole when it appeared as the initial rhythm. However, countershock was significantly more effective than epinephrine (P less than 0.003), atropine (P less than 0.04), or CaCl (P less than 0.03) in altering the rhythm from asystole, which appeared later in resuscitation. Ventricular fibrillation was the most common rhythm appearing after countershock for asystole. Countershock appears to be superior to epinephrine, CaCl, and atropine for treating asystole during the course of resuscitation, suggesting that the rhythm diagnosed as asystole may actually be VF in many cases.

Aged↗
PubMed1974

Effects of DC electric countershock on ventricular function, cation balance and endogenous norepinephrine in the dog heart.

Effects of DC electric countershock on cardiac function in thoracotomized dogs were evaluated from recordings of ECG, aortic pressure, left ventircular pressure and its first derivative, and coronary sinus flow. Samples of arterial and coronary venous plasma and left ventricular myocardium obtained before and after countershock at times corresponding to post-shock arrhythmias and recovery were analyzed for Mg++, K+ and Ca++, and norepinephrine. At 1 min after countershock, ECG changes included transient cardiac arrhythmias and ST segment alterations, accompanied by depressed ventricular function and decreased myocardial Ca++ concentration. At 5 min postshock, coronary venous Mg++ and K+ concentrations had risen and ventricular function was still depressed. Function recovered within 10-20 min. There was no evidence of consistent loss of endogenous myocardial norepinephrine.

Animals↗
PubMed1988

Effects of electrophysiologic studies resulting in electrical countershock or burst pacing on left ventricular systolic and diastolic function.

To determine the acute effects of electrophysiologic study on left ventricular systolic and diastolic function in patients requiring termination of induced tachyarrhythmias by either electrical countershock or burst pacing, we examined 16 patients (11 men and five women), aged 43 to 78 years (mean 58 +/- 13), undergoing programmed electrical stimulation. Indices of systolic and diastolic left ventricular function were measured by M-mode echocardiography before and within 1 minute after termination of 22 episodes of induced tachyarrhythmias by defibrillation (n = 16) and burst pacing (n = 6). The left ventricular septal and posterior endocardial surfaces were digitized immediately below the mitral valve leaflets, and indices of systolic and diastolic function were calculated. The results showed a significant impairment in both systolic and diastolic function after termination of tachyarrhythmias by defibrillation, as seen by a decrease in the shortening fraction (23.7 +/- 7.6% to 19.8 +/- 7.8%; p less than 0.005) and a decline in the peak rate of increase in left ventricular diameter during diastole called dD/dtmax (87.4 +/- 36.1 mm/sec to 71.5 +/- 28.9 mm/sec; p less than 0.01), respectively. In addition, indices of systolic and diastolic function measured at baseline were predictive of impairment in diastolic function, as seen by modest but highly significant correlations between the absolute change in dD/dtmax after defibrillation versus the peak velocity of fiber shortening (r = -0.69; p less than 0.005) and dD/dtmax (r = -0.60; p less than 0.02) measured at baseline. Left ventricular function after termination of tachyarrhythmias by burst pacing was not significantly altered.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗