Systemic and myocardial oxygen transport responses to brain death in pigs

Brain death is associated with profound disturbances of systemic and myocardial oxygen transport, but little is known regarding the acute response of systemic oxygen consumption (VO(2)).

Brain death was induced in 6 pigs (30.6 +/- 3.0 kg) by balloon inflation into the cranial cavity. VO(2) was continuously measured by respiratory mass spectrometry. Blood pressures and gases were measured from the aorta, superior vena cava, and coronary sinus, with arterial epinephrine and norepinephrine, prior to brain death, at 1, 10, and 90 minutes after brain death. Cardiac output (CO), systemic vascular resistance (SVR), oxygen delivery (DO(2)), oxygen extraction (EO(2)), and myocardial oxygen (mEO(2)) and lactate extractions (mE(1ac)) were calculated. Left ventricular contractility was assessed by micromanometer tipped catheters.

VO(2) increased from 4.8 +/- 0.9 to 6.3 +/- 0.9 mL/min/kg 1 minute after brain death (P < .001), and subsequently decreased to below baseline at 90 minutes (P < .001). Left ventricular contractility, CO, and DO(2) increased 1 minute after brain death (P < .001), followed by a rapid decrease to baseline within 10 minutes (P < .001). SVR and EO(2) decreased after brain death (P < .01) and remained low. Lactate remained unchanged. mE(1ac) decreased after brain death despite a decrease in mEO(2) (P < .01), and returned to baseline at 90 minutes.

The initial surge in VO(2) after brain death is offset by the greater increase in DO(2), thus tissue perfusion remains adequate. The lower than baseline VO(2) and SVR at the end of the study period may indicate general metabolic and hemodynamic compromise. The information regarding the profound metabolic alterations imposed by brain death may have implications for management of brain death donors.