THE HAeMODYNAMIC EFFECTS OF SODIUM AMOBARBITAL IN HYPERTENSION

Abstract

It has long been accepted that barbiturates tend to lower the systemic arterial pressure in patients with hypertension, and this effect has been used in various diagnostic sedation tests. However, because ofthe inadequate description of the drugs' effect on the cardiac output in hypertension, the hmemodynamic mechanism responsible for the hypotensive action is not clear. As barbiturates are often administered at the same time as powerful hypotensive agents either for sedation or anmsthesia, it is important to know the mode of action of the drug on the cardiovascular system.The purpose of this paper is to describe the acute effects of sodium amobarbital on the cardiac output, stroke output, blood pressure, and peripheral resistance in a series of patients with hypertension. SUBJECTS AND METHODSThe subjects of this study were 13 patients with hypertension admitted to the medical wards for diagnosis and treatment: 7 were women and 6 were men, and their average age was 52 years, varying between 29 and 71 years. The diagnoses at the time of discharge are listed in the Table. The average of the control mean arterial pressures was 157 mm. Hg; one of the patients (M. M.) had a normal blood pressure (145/90 mm. Hg) at the time of study although she had had hypertension at the time of admission. None of the patients was acutely ill, had fundoscopic evidence of malignant hypertension (Keith-Wagner grades III and IV), or had signs of peripheral or pulmonary cedema. With the exception of patient M. M., all had electrocardiographic and radiological evidence of minimal to moderate left ventricular hypertrophy. None, except patient E. M., had received drugs during the several weeks before study; E. M. was on daily maintenance digitalis and received three daily oral doses of 60 mg. of guanethidine and one 500 mg. dose of chlorothiazide during the three days preceding investigation.Patients received no premedication and the investigations were begun two hours after a light lunch. Cardiac outputs were measured by the indicator dilution method from dye curves recorded with a photoelectric earpiecet, chopper amplifiert, and direct writer: recording system (Gabe, Tuckman, and Shillingford, 1962). A catheter was passed to the right atrium and then the earpiece fastened to an ear pinna previously treated with vasodilating ointment §. When the catheter and earpiece were in place the patient was allowed to rest quietly for about 30 minutes, after which at least three control measurements of cardiac outputs and right atrial pressures were made; measurements of arterial pressures (by auscultation) and heart rates were obtained more frequently. Sodium amobarbital, 2-5 per cent, was then given slowly into an antecubital vein. The total dosages varied between patients and were decided from observations of arterial pressure