Anning Luke, Paratz Jennifer, Wong Wai Pong, Wilson Kathleen
Department of Physiotherapy, University of Queensland, Australia.
Physiother Res Int. 2003;8(3):155-63. doi: 10.1002/pri.283.
Manual hyperinflation is a physiotherapy technique that improves static compliance and mobilizes secretions, but has the potential to alter haemodynamic function. The aim of the present study was to investigate the effects of manual hyperinflation on haemodynamic function in a healthy animal model, without the usual confounding effects inherent in an heterogeneous intensive care population.
The study used a within-subjects design, in an animal research theatre. Nine healthy sheep (eight Border Leicester, one Merino, mean weight 39.5 kg, standard deviation (SD) 1.6 kg) completed the study. The sheep were induced (thiopentane 15-20 ml), intubated, ventilated and surgically instrumented for an arterial line and pulmonary artery catheter. Anaesthesia was maintained by 1.5% halothane/oxygen. Manual hyperinflation was delivered for two minutes with a Mapleson C circuit, using a peak inspiratory pressure of 35 cmH2O and an inspiratory:expiratory ratio of 2:1.
Mean tidal volume during manual hyperinflation was 294% (SD 22%) of the ventilator tidal volume. A paired Student's t-test demonstrated that cardiac output (thermodilution method) decreased significantly (p < 0.05) and systemic vascular resistance increased significantly (p < 0.01) after manual hyperinflation. A repeated-measures analysis of variance (ANOVA) and a least-significant difference pairwise comparison revealed that mean arterial pressure and pulse pressure decreased significantly during (p < 0.01) and increased significantly (mean arterial pressure, p < 0.05 and mean pulse pressure p < 0.001) after the technique. Pulmonary artery pressure also increased significantly during manual hyperinflation (p < 0.01). There were no significant effects on right atrial pressure, pulmonary artery occlusion pressure or heart rate.
Significant haemodynamic changes occurred in this animal model. The increased intrathoracic pressure, applied for an increased period during inspiration, decreased cardiac output with compensatory vasoconstriction evident by the increased systemic vascular resistance and mean arterial pressure. The results suggest that there may be a decrease in cardiac output after increased positive pressure in subjects with normal cardiac and respiratory function.
