Jan 1, 1976

The effects of sodiumnitroprusside and trimethaphan induced hypotension on haemodynamics and myocardial oxygen consumption (author's transl)

Der Anaesthesist
W HessJ B Brückner

Abstract

The influence of controlled hypotension (mean arterial pressure 60 mmHg) induced by sodium nitroprusside and trimethaphan on systemic circulation and myocardial oxygen consumption was studied in 7 anaesthetized closed chest dogs. The hypotensive effect of both drugs was primarily mediated by a reduction in total peripheral resistance. No change in cardiac output was observed. Stroke volume decreased in the presence of tachycardia. Left ventricular max dp/dt remained unaffected during sodium nitroprusside hypotension and was reduced by trimethaphan. Max dp/dt, load data and heart rate indicated that trimetaphan possesses negative inotropic properties. Sodium nitroprusside induced a hyperperfusion of the heart with a marked decrease in myocardial arteriovenous difference in oxygen. Myocardial oxygen consumption remained unchanged. Trimethaphan, on the other hand, induced only small increments in coronary blood flow and a rise in the arteriovenous difference in oxygen of the heart. This resulted in a higher myocardial oxygen consumption (+16%). Cardiac efficiency was lessened by trimethaphan and remained unaffected in the presence of sodium nitroprusside. As sodium nitroprusside neither affects myocardial oxygen consumption nor al...Continue Reading

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Mentioned in this Paper

Arterial Pulse Pressure
Myocardial Contraction
Sodium Nitroprusside
Total Peripheral Resistance
Thyroid Crisis
Left Ventricular Structure
Diastolic Blood Pressure
Hypertensive Crisis
Myocardium
Blood Flow

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