Spontaneous gasping increases cerebral blood flow during untreated fatal hemorrhagic shock

Gasping has been found to be associated with improved ventilation, stroke volume, and cerebral blood flow (CBF) during untreated ventricular fibrillation. However, its effects have not been thoroughly assessed during fatal hemorrhagic shock. In this study, we hypothesized that gasping increases CBF during fatal hemorrhagic shock.

Ten male Wistar rats (body weight: 195-225g) were intraperitoneally anesthetized with sodium pentobarbital (50mg/kg). Arterial pressure was recorded in the left femoral artery. Respiratory thoracic movements were recorded with a pressure sensor placed under the animal's back. The left carotid artery was cannulated to continuously withdraw blood (0.1ml/min) as a means of inducing hemorrhagic shock. CBF was measured with a laser flow meter.

The arterial pulse wave was lost after withdrawing 7.3+/-0.9ml of blood and at that point, spontaneous gasping developed in all of the animals. CBF averaged 48.8+/-8.8ml/(min100g-brain) under control conditions before the start of blood withdrawal, and it decreased significantly to 4.4% of baseline during the pulseless state (P<0.01). The gasping, observed during in the pulseless state increased CBF to an average of 54.2% of baseline (P<0.01).

Gasping was observed during fatal hemorrhagic shock and generated large increases in CBF. The forceful contraction of the inspiratory muscles during gasping may increase CBF by decreasing intrathoracic pressure, which increases venous return to the heart.