Delayed hyperemia causing intracranial hypertension after cardiopulmonary resuscitation

Objective To clarify whether early or delayed failure of cerebral perfusion after cardiopulmonary resuscitation (CPR) occurs in humans and contributes to secondary brain damage. Design Prospective, repeated-measures study. Setting Intensive care unit of Hiroshima University School of Medicine. Patients Eight comatose patients who had undergone successful resuscitation from cardiac arrest. Interventions All patients underwent transcranial Doppler sonography examination. The intracranial cerebral pressure (ICP) and jugular venous oxygen saturation (SO sub 2) also were continuously monitored in five patients and three patients, respectively. Measurements and Main Results In each patient, we measured the mean flow velocity of the middle cerebral artery transcranially and the mean flow velocity of the internal carotid artery, high in the neck, using transcranial Doppler sonography. The pulsatility index for each measurement was also calculated. The first examinations were performed within 4 to 12 hrs of CPR, and repeat examinations were performed approximately every 12 hrs. The initial mean flow velocities of the middle cerebral artery and the initial mean flow velocities of the internal carotid artery were relatively low, with relatively high pulsatility indices. The mean flow velocities of the middle cerebral artery began to increase at 12 to 24 hrs after CPR and peaked 24 to 120 hrs after CPR. A simultaneous increase in mean flow velocities of the internal carotid artery was observed during this period. The pulsatility index in both arteries dropped significantly during peak mean flow velocity of the middle cerebral artery. In six of seven patients with an abnormal increase (>100 cm/sec) in peak mean flow velocity of the middle cerebral artery, the ratio of mean flow velocity of the middle cerebral artery to mean flow velocity of the internal carotid artery was <3. This value tended to be lower in patients with poor outcomes. An increased mean flow velocity of the middle cerebral artery, with a ratio of <3 for mean flow velocity of the middle cerebral artery to mean flow velocity of the internal carotid artery, was defined as hyperemia. Although the mean flow velocity of the internal carotid artery was not measured, another patient with an abnormal increase in mean flow velocity of the middle cerebral artery revealed a high jugular venous SO2 value of 83.5%, also representing hyperemia. All ICP values were within the normal range 4 to 12 hrs after CPR and tended to increase before peak mean flow velocity of the middle cerebral artery. The two patients with the lowest ratios of mean flow velocity of the middle cerebral artery to mean flow velocity of the internal carotid artery showed significant increases in ICP after the peak mean flow velocity of the middle cerebral artery. These two patients subsequently developed brain death. Conclusions Delayed hyperemia occurs in humans after resuscitation from cardiac arrest. Our data suggest that this delayed hyperemia can lead to intracranial hypertension and occasionally acute brain swelling, contributing to a poor outcome. A high mean flow velocity of the middle cerebral artery with a low ratio of mean flow velocity of the middle cerebral artery to mean flow velocity of the internal carotid artery may be predictive of critical hyperemia. As an indirect method of measuring cerebral blood flow, transcranial Doppler sonography can be used to adjust treatment for failure of cerebral perfusion after resuscitation. (Crit Care Med 1997; 25:971-976)