Studies of the Central and Peripheral Hemodynamic Effects of Amyl Nitrite in Patients with Aortic Insufficiency

Abstract

SUMMARYThe cardiovascular reaction induced by amyl nitrite was studied in a main group of 11 patients with pronounced and isolated aortic insufficiency, and in an additional and more heterogeneous group of seven patients with moderate aortic insufficiency combined with other lesions, by measuring left ventricular end-diastolic pressure, systemic and peripheral arterial pressures, cardiac output, peripheral blood flow, and venous tone.Total peripheral resistance decreased, but local vascular resistance differed significantly between the upper and the lower extremities. In most cases arterial dilatation in the forearm (mainly muscle) was found. Simultaneously, there was uniform vasoconstriction in the calf (mainly muscle) which was interpreted to be secondary (baroreceptor reflex). This regional difference in circulatory reaction was also manifested in a pronounced change of the contour of the brachial arterial pulse, while the femoral arterial pulse was practically unchanged. The hand blood flow (skin) decreased while the foot blood flow did not change significantly.A marked fall in systemic arterial pressure and in left ventricular end-diastolic pressure was clearly demonstrated, and secondarily there was a rise in heart rate as well as a pronounced venoconstriction in both the upper and lower extremities, also interpreted to be secondary (a baroreceptor reflex). There was good correlation between maximal increase in heart rate and maximal increase in venous tone and also between the augmentation in heart rate and cardiac output. An A complete hemodynamic study was obtained in all patients by means of a routine cardiac catheterization including right heart catheterization, transseptal left heart catheterization, and angiocardiography. Approximately 1 hour before the catheterization was started in the morning, the patients, who were fasting, were given a small dose of a barbiturate (amobarbital, 0.1 g). The patients were studied in the supine position throughout the whole procedure. A polyethylene catheter (PE 160) 75 cm long was introduced percutaneously via the brachial artery to the arch of the aorta. Right heart catheterization was performed in the usual manner via an exposed superficial cubital vein, followed by transseptal left heart catheterization. The transseptal catheter, a radiopaque Teflon catheter, was introduced into the right femoral vein by the percutaneous technic of Seldinger.14 For the interatrial septal puncture we used the modified instrument of Bevegard's group.15 The tip of the right heart catheter was placed in the pulmonary artery, and the transseptal catheter was in the left ventricle. Pressure measurements were made with pressure transducers EMT 34 or 35 and electromanometer EMT 31.* The pressure curves and ECG were recorded on a direct-writing sixchannel ECG apparatus (Mingograf 81*).Owing to the short duration of the effects of amyl nitrite, the dye-dilution method was used for determination of cardiac output: 5 mg of indocyanine green (Cardio-Green) was injected into the pulmonary ...

Changes in phasic femoral artery flow induced by various stimuli: a study with percutaneous pulsed Doppler ultrasound

“…2). The responses to amyl nitrite in mean Q are inconsistent, but correspond in the average to the decreasing flow values shown in earlier plethysmographic measurements (Delius and Enghoff, 1970).…”

“…Therefore, this compound induces a marked increase in mean Q, although heart rate is less accelerated than after amyl nitrite. The divergent responses in mean Q to amyl nitrite and xanthinol nicotinate, both of them being vasodilators, may be related to a regionally different action of these 2 drugs on the arterial resistance (Delius and Enghoff, 1970). While xanthino1 nicotinate may mainly dilate the arteries of the extremities, the main action of amyl nitrite may be restricted to vessels of areas other than the lower limbs.…”

Long-term vasodilator therapy of chronic aortic insufficiency. A randomized double-blinded, placebo-controlled clinical trial.

“…Left ventricular dilatation develops in response to chronic regurgitant flow, and in general, it reflects the severity and duration of the valve lesion. 1 it is reasonable to speculate that a treatment producing sustained reductions in LVEDVI might also alter the natural history of the disease and delay the need for valve replacement. LVESVI, another important prognostic factor,24-29 and EF were also followed as end points in the trial.…”

“…(Circulation 1988;78:92-103) P revious studies have shown that vasodilator drugs acutely reduce the regurgitant volume and improve cardiac performance in aortic insufficiency. [1][2][3][4][5][6][7] Consequently, vasodilator therapy has emerged as an important modality for the shortterm management of patients with this lesion. These findings also raise the possibility that long-term therapy may chronically reduce the volume overload to the left ventricle.…”

Vasodilator treatment for acute and chronic heart failure.

“…Indeed, the administration of amyl nitrite results in a decrease in arterial pressure and left ventricular end diastolic pressure, together with an increase in effective stroke volume (Delius and Enghoff, 1970). Similar beneficial haemodynamic effects of sodium nitroprusside are seen particularly in those patients with a raised left ventricular end diastolic pressure and reduced ejection fraction.…”