Faculty Bibliography

The hemodynamic response to nafcillin administration was studied in 45 patients with good left ventricular function and no known history of hypersensitivity to penicillin during coronary artery bypass grafting (CABG). Group I (15 patients) received 1 gram of nafcillin in 10 mL of saline as an intravenous (IV) bolus, group II (15 patients) received 1 gram of nafcillin in 50 mL of saline as a slow IV infusion over 15 minutes, and group III (15 patients) did not receive nafcillin. Hemodynamic variables and plasma histamine and catecholamine levels were measured before and after nafcillin administration, after 500 mg of CaCl2, and after 0.1 mg of phenylephrine. Bolus nafcillin administration produced profound hypotension secondary to vasodilatation with significant increases in cardiac index and decreases in systemic and pulmonary vascular resistances. Cardiac index increased from 3.15 +/- 0.3 L/min/m2 to 5.75 +/- 0.25 L/min/m2 (P less than 0.005) one minute after nafcillin administration, and remained at 5.1 +/- 0.35 L/min/m2 after administration of CaCl2 (P less than 0.005). All hemodynamic parameters returned toward control values after administration of 0.1 mg of phenylephrine, IV. Plasma epinephrine, norepinephrine, and histamine levels increased more than 100%. In group II, cardiac index increased, while systemic and pulmonary vascular resistances and mean arterial pressure decreased. However, these changes were less significant than those found in group I.(ABSTRACT TRUNCATED AT 250 WORDS)

Pulmonary shunt (Qs/Qt) was calculated in 49 mongrel dogs weighing 18-20 kg during mechanical ventilation, before and during deliberate hypotension with either nifedipine (group N), diltiazem (group D), labetalol (group L), or ethyl alcohol and polyethylene glycol (group E). A 30 per cent decrease in mean arterial blood pressure occurred after two minutes of nifedipine infusion, two minutes after diltiazem, and three minutes after labetalol; these effects lasted two hours after nifedipine administration, 90 minutes after diltiazem and three hours after labetalol. There was an accompanying significant decrease in systemic and pulmonary vascular resistance. Qs/Qt and cardiac output increased significantly after nifedipine infusion. Shunt increased (mean +/- S.E.) from 9.7 +/- 0.8 to 18.25 +/- 1.05 per cent at two minutes (p less than 0.0005); 19.05 +/- 1.2 per cent at 30 minutes (p less than 0.005); 17.5 +/- 1.6 per cent at two hours (p less than 0.01); and 12 +/- 1.1 per cent at three hours (p less than 0.025). No increase in shunt occurred after the administration of diltiazem, labetalol or polyethylene glycol and ethyl alcohol. Arterial oxygen tension (PaO2) decreased significantly after nifedipine infusion from 146 +/- 11.5 to 105 +/- 3.5 mmHg two minutes after infusion; to 89.5 +/- 3 mmHg 30 minutes after; 115 +/- 4.75 mmHg two hours after; and 130 +/- 10.75 mmHg three hours later. PaO2 was not significantly different after diltiazem, labetalol, or polyethylene glycol and ethyl alcohol administration. With nifedipine cardiac output increased from 2.25 +/- 0.3 to 3.95 +/- 0.25 after two minutes (p less than 0.005) to 3.85 +/- 0.35 after 30 minutes (p less than 0.005), 3.7 +/- 3 after two hours (p less than 0.01) to 2.9 +/- 1.1 after three hours. No significant increase in cardiac output occurred in groups D or L. These results suggest that only nifedipine infusion significantly alters oxygenation in dogs and therefore its use warrants caution in the presence of a preexisting abnormal Qs/Qt.