Intrathoracic pressure regulation augments stroke volume and ventricular function in human hemorrhage

Obtaining intravenous (i.v.) access for fluid administration is a critical step in treating hemorrhage. However, expertise, supplies, and personnel to accomplish this task can be delayed or even absent in austere environments. An alternative approach that can "buy time" and improve circulation when i.v. fluids are absent is needed. Preclinical studies show that intrathoracic pressure regulation (ITPR) can increase perfusion in hypovolemia in the absence of i.v. fluid. We compared ITPR with placebo in humans undergoing a 15% hemorrhage under general anesthesia. Paired healthy volunteers (n = 7, aged 21 Y 35 years) received either ITPR or placebo on different study days. Institutional review board informed consent was obtained. Subjects were anesthetized using propofol, intubated, and mechanically ventilated and hemorrhaged (10 mL/kg). Twenty minutes after hemorrhage, ITPR (j12 cm H2O vacuum) or placebo (device but no vacuum) was administered for another 60 min. Intravenous fluid was administered when systolic blood pressure was less than 85 mmHg. Hemodynamics, cardiac function by echocardiography, and volumetric data were compared. Data were expressed in $mean T SEM before and after ITPR/placebo intervention. There were no differences in mean arterial pressure (ITPR, 2.1 T 3 mmHg; placebo, j0.7 T 3 mmHg) or fluid infused (ITPR, 17.4 T 4 mL/kg; placebo, 18.6 T 5 mL/kg). Urinary output and plasma volume also were not significantly different. Intrathoracic pressure regulation augmented stroke volume (ITPR, 22 T 5 mL, placebo, 6 T 4 mL; P G 0.05), ejection fraction (ITPR, 4% T 1%; placebo, 0% T 1%), and diastolic function ($E/e¶) (ITPR, j0.8 T 0.4 vs. placebo, +0.81 T 0.6; P G 0.05). Intrathoracic pressure regulation did not improve mean arterial pressure in healthy volunteers aged 21 to 35 years. However, ITPR augmented stroke volume, which could be caused by improved ventricular function.