Left ventricular performance can be significantly influenced by changes in intrathoracic pressure. In man, sustained increases in intrathoracic pressure unload the left ventricle, but since venous return decreases, increased intrathoracic pressure is associated with a decreased cardiac output. In a canine model of acute ventricular failure, it has been shown that phasic increases in intrathoracic pressure, which do not decrease venous return, improve steady-state cardiac output. We thus studied the cardiovascular effects of phasic high intrathoracic pressure support (PHIPS) in seven patients with shock in our intensive care unit whose condition was not responsive to conventional types of therapy. The PHIPS was generated by abdominal and chest wall binding during positive-pressure ventilation. As compared to the state before PHIPS, the PHIPS was associated with an increase in esophageal pressure (6.6 +/- 1.1 mm Hg; p less than 0.01) and in mean arterial pressure (43.0 +/- 6.1 to 51.0 +/- 7.7 mm Hg; p less than 0.01) while not changing arterial pressure relative to esophageal pressure. Cardiac output also increased from 3.6 +/- 0.5 to 4.2 +/- 0.6 L/min (p less than 0.05), while left ventricular filling pressures remained constant. In one subject a gated cardiac blood pool scan demonstrated a PHIPS-associated increase in ejection fraction and decreased end-diastolic volume. These results are consistent with the hypothesis that PHIPS, by increasing intrathoracic pressure, augments left ventricular performance by reducing left ventricular afterload. This appears to be a promising area for future research.