The first dose of OKT3 induced a significant rise in temperature that began within one hour of administration and peaked at three hours (mean temperature, 37.9°C vs 36.8°C before the dose). This increased temperature was still apparent at nine hours after the dose.
The cardiovascular response was notable for an early and persistent tachycardia. The heart rate rose 20 percent from 92.8 ±5.1 beats per minute to a maximum of 111.3 ±6.1 beats per minute within the first hour after the dose. Heart rate returned to baseline levels by nine hours.
Concomitant with this early peak heart rate was a 31 percent rise in mean cardiac output from 5.1 U min to 6.7 L/min. This rise was transient, with a return to baseline levels by three hours. Also temporally associated with this hyperdynamic interval was a 15 percent increase in blood pressure (mean arterial pressure from 85.5 to 98.8 mm Hg) and CVP (13.3 to 17.9 mm Hg). Despite the associated rise in oxygen transport (with stable hemoglobin level and Sa02), Sv02 fell (66.2 percent to 53.9 percent), with a simultaneous rise in extraction ratio from 32.7 percent to 38.9 percent, both with p<0.05. Thus, oxygen consumption was increased. Reading here
This early hyperdynamic hypertensive response dissipated by three to five hours after the first dose of OKT3. By five hours a new pattern appeared, characterized by relative hypotension, hypoxemia, and altered vasomotor tone as reflected by SVRI and PVRI.
Mean arterial pressure reached its nadir at 70 mm Hg at five hours after the dose. Associated with this decrease in blood pressure was a significant fall in the SVRI by 15 percent to 1728.2 dynes*s*cm”7m2. In 15 of the 23 patients, this hemodynamic instability required additional vasopressor or inotropic support (or both), resulting in an increased mean arterial pressure and Sv02 by nine hours after the dose.