Manual hyperinflation causes norepinephrine release

Objective sure hemodynamics and plasma catecholamines during manual hyperinflation (MHI) in ventilated patients. s s performed with a Mapleson “C” circuit, 2l-reservoir bag; peak inspiratory pressure was standardized to 35 mL water; and positive expiratory-end pressure of 5 mL water was administered to seven mechanically ventilated patients with septic (6) and cardiogenic (1) shock (67.2 ± 5.2 years, Acute Physiology Assessment and Chronic Health Evaluation II score 22.1 ± 3.1). Diastolic (DAP) and mean arterial pressure (MAP), continuous cardiac index, pulmonary artery occlusion pressure, dynamic compliance, plasma norepinephrine and epinephrine, and arterial blood gases were recorded, and systemic vascular resistance index (SVRI) and oxygenation ratio were calculated. s were no significant changes in pulmonary artery occlusion pressure, mean arterial pressure, or Pao2/Fio2. There were significant increases in SVRI (P < .001), DAP (P < .001), dynamic compliance (P < .01), and plasma norepinephrine (P < .001) and a decrease in cardiac index (P < .05) after MHI. sions creases in DAP, SVRI, and plasma norepinephrine suggest a sympathetic vasoconstrictive response during the application of MHI.