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Effects of DC electric countershock on ventricular function, cation balance and endogenous norepinephrine in the dog
Insights
DC electric countershock transiently impairs cardiac function and alters myocardial ion concentrations in dogs. Ventricular function and ion levels recover within 20 minutes post-shock, with no significant norepinephrine loss.
Area of Science:
- Cardiovascular Physiology
- Electrophysiology
- Cardiac Pharmacology
Background:
- DC electric countershock is used to treat cardiac arrhythmias.
- Its effects on myocardial function and biochemistry are not fully understood.
- Previous studies have not comprehensively assessed immediate post-shock cardiac status.
Purpose of the Study:
- To evaluate the immediate effects of DC electric countershock on cardiac function.
- To analyze changes in myocardial and plasma ion concentrations (Mg++, K+, Ca++) and norepinephrine.
- To determine the recovery time course of cardiac function post-countershock.
Main Methods:
- Measurements included ECG, aortic pressure, left ventricular pressure, and coronary sinus flow in thoracotomized dogs.
- Plasma and myocardial samples were analyzed for Mg++, K+, Ca++, and norepinephrine.
- Data collected pre- and post-countershock at specific time points.
Main Results:
- Transient cardiac arrhythmias and ST segment changes observed post-countershock.
- Ventricular function was depressed, with decreased myocardial Ca++ at 1 minute.
- Elevated coronary venous Mg++ and K+ noted at 5 minutes; function recovered in 10-20 minutes; no norepinephrine depletion.
Conclusions:
- DC electric countershock induces transient cardiac dysfunction and alters myocardial ion balance.
- Myocardial Ca++ decrease and subsequent Mg++/K+ increase correlate with functional depression.
- Cardiac function and ionic homeostasis recover relatively quickly post-countershock.
Abstract:
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.