Ischemic neurological injury accounts for much of the mortality and most of the morbidity among persons who are initially resuscitated from cardiac arrest. This chapter summarizes what is known about the determinants of cerebral blood flow during cardiopulmonary resuscitation (CPR) and the relationship of cerebral blood flow to neurological outcome.

Cerebral perfusion in the intact circulation has been characterized as a classical vascular waterfall. Arterial pressure is the upstream pressure, and cerebrospinal fluid pressure is the downstream pressure. Pressure in the venous sinuses is below the downstream pressure; that is, animal studies demonstrate a significant pressure gradient between the cortical veins and the sagittal sinus.

Determinants of cerebral blood flow

Halperin et al. reported a close correlation (r=0.89) between cerebral blood flow and the difference between carotid arterial pressure and pressure in the lateral ventricle during CPR in dogs. Accordingly, the determinants of carotid arterial pressure and intracranial cerebrospinal fluid pressure will be reviewed.

At the outset of CPR in laboratory animals, carotid artery pressure is usually equal to thoracic aortic pressure. As time goes by, however, carotid arterial pressure tends to fall, and cerebral blood flow declines in parallel. This phenomenon, termed carotid collapse, appears to be mediated by loss of vascular tone and physical collapse of the carotid artery at the thoracic inlet. α-Adrenergic agents and pressor doses of adrenalin reverse carotid collapse, in part by increasing the rigidity of the carotid artery and in part by raising peripheral resistance, thus limiting the runoff of blood to non-essential vascular beds. In animal studies, if CPR is begun immediately after the onset of cardiac arrest, carotid pressure remains as high as thoracic aortic pressure over periods of 1 hour or more as long as peripheral resistance is maximized.