Echocardiographic evaluation of hemodynamic effects of propofol (hemodynamic effects of propofol

Several studies evaluating the mechanisms of the propofol induced hypotension have shown conflicting results suggesting that the hypotensive action could be due to changes in peripheral resistances, to a direct action on cardiac contractility, or both. We evaluated the hemodynamic effects of intravenous administration of propofol (2.5 mg Kg-1) without premedication in twenty adults, free from cardiovascular pathology and undergoing elective otorhinolaryngologic surgery. End-systolic quotient (systolic pressure/end-systolic diameter), fractional shortening (end diastolic diameter-end systolic diameter/end diastolic diameter), obtained by means of a transthoracic echocardiography, were adopted as indices of ventricular function. After the induction of anesthesia, a significant decrease of arterial pressure, heart rate, end-systolic quotient were observed, while fractional shortening remained stable. End-systolic quotient is correlated with changes in contractility and afterload, (increased after-load and contractility correspond to increased end-systolic quotient, and vice versa). Fractional shortening is a confirmatory factor for changes in inotrophism and is dependent on after load with an inverse correlation (increased after-load corresponds to decreased fractional shortening values). The significant reduction in the end-systolic quotient and the stability of the fractional shortening both suggest a decrease in contractility and a reduction of peripheral resistances. Also, the non invasive setting avoids that the results are influenced by the increase in the pre-operative sympathetic tone.