Midazolam maleate induction in patients with ischaemic heart disease: haemodynamic observations.

Abstract

Midazolam maleate is a new water soluble benzodiazepine used for induction of anaesthesia. Ten patients with symptomatic ischaemic heart disease were premedicated intramuscularly with morphine 0.l mg · kg-1 and scopolamine 6–8 µg · kg-1, 60–90 minutes before induction. The heart rate, systolic/diastolic blood pressure, mean systolic blood pressure, mean pulmonary artery blood pressure, pulmonary artery occluded pressure, mean right atrial pressure, cardiac output (duplicate thermodilution) and arterial blood gas tensions were measured at four time periods: (1) after instrumentation while breathing room air, (2) after transfer to the operating room while breathing 100 percent oxygen by mask, (3) one to two minutes after intravenous midazolam maleate 0.2 mg · kg-1 and (4) four to five minutes after midazolam maleate. The cardiac index, stroke index, heart ratesystolic blood pressure product, systemic vascular resistance index, pulmonary vascular resistance index, left ventricular stroke work index and right ventricular stroke work index were calculated for each of the study time-periods from the measured parameters. Midazolam maleate anaesthetized all patients and times for induction ranged from 30 to 90 seconds (mean 44). Apnoea occurred in 75 per cent of patients and ventilation was assisted in those instances. The $$Pa_{o_2 } $$ was unchanged by midazolam maleate, but the $$Pa_{co_2 } $$ rose significantly (p < 0.02) from 5.32 ± 0.19 to 5.85 ± 0.17kPa(40 ± 1.4 to 44 ± 1.3 mm Hg) (1–2 min) and 6.1 ± 0.17 kPa (46 ± 1.3 mm Hg) (4–5 minutes after midazolam maleate). Haemodynamic effects of midazolam maleate were minor and in most cases less than those associated with transfer of the patients to the operating room when the systemic systolic/diastolic blood pressure, mean systemic blood pressure, mean right atrial pressure, pulmonary artery occluded pressure and systemic vascular resistance index alt significantly increased (p < 0.01). Midazolam maleate significantly reduced systemic systolic/diastolic pressure, mean systemic blood pressure, stroke volume, left and right ventricular stroke work index and systemic vascular resistance index toward the original resting control. The heart rate rose from 55 ± 6.6 to 66 ± 5.3 beats per minute (p < 0.01) one to two minutes after midazolam maleate, and the mean right atrial pressure, mean pulmonary artery pressure, pulmonary artery occluded pressure, cardiac index, stroke index, pulmonary vascular resistance index and heart rate-systolic blood pressure product remained unchanged. There were no further significant changes four to five minutes after midazolam maleate, except in systemic systolic/diastolic pressure which continued to decline to the level of the resting control (125/61). It is concluded that the rapid action of midazolam maleate and its modest effects on haemodynamic parameters, make it a safe and efficacious induction agent in patients with ischaemic heart disease.