Brain Injury From Cerebral Hypoperfusion

Introduction

There is a spectrum of brain injury from cerebral hypoperfusion ranging from transient loss of consciousness to devastating anoxic neuronal damage. At the root of this injury is the fact that with limited stores of high-energy phosphate compounds and a high metabolic demand, the brain is critically dependent on cerebral blood flow (CBF) to continuously supply oxygen and glucose. CBF in turn is governed by the Hagen–Poiseuille equation, correlating directly with cerebral perfusion pressure (CPP) (which is the difference between mean arterial pressure and intracranial pressure) and vessel radius and inversely with blood viscosity and vessel length. Blood pressure is the product of cardiac output and systemic vascular resistance. Cardiac output also correlates directly with CBF, independent of blood pressure. A decrease in blood pressure and/or cardiac output results in cerebral hypoperfusion.

When mild, cerebral hypoperfusion can lead to syncope, a temporary loss of consciousness and motor control characterized by a relatively rapid onset, brief duration, and spontaneous and full recovery. More prolonged hypoperfusion, together with extracranial vascular disease, can cause selective damage to vulnerable areas of the cerebral cortex that lie in between vascular territories and lead to the so-called watershed territory infarcts. In cardiac arrest, it is a sudden ventricular arrhythmia or asystole that leads to the immediate loss of cardiac output. This is accompanied by respiratory failure and reduced partial pressure of oxygen (hypoxemia). The combination of the two conditions culminates in the dual nature of hypoxic-ischemic brain injury.