Title Variations in the pre-ejection period induced by deep breathing do not predict the hemodynamic response to early haemorrhage in healthy volunteers.
Author Vistisen, Simon Tilma; Juhl-Olsen, Peter; Frederiksen, Christian Alcaraz; Kirkegaard, Hans
Journal J Clin Monit Comput Publication Year/Month 2014-Jun
PMID 24165897 PMCID -N/A-
Affiliation 1.Research Centre for Emergency Medicine, Institute of Clinical Medicine, Aarhus University, Trojborgvej 72-74, Building 30, 1st Floor, 8200, Arhus N, Denmark, vistisen@ki.au.dk.

Monitoring that can predict fluid responsiveness is an unsettled matter for spontaneously breathing patients. Mechanical ventilation induces cyclic variations in blood pressure, e.g. pulse pressure variation, whose magnitude predicts fluid responsiveness in mechanically ventilated patients. In this study, we hypothesised that a deep breathing manoeuvre with its effect on heart rate variability (HRV) could induce similar cyclic variations in blood pressure in spontaneously breathing healthy subjects and that the magnitude of these variations could predict the hemodynamic response to controlled haemorrhage. 37 blood donors were instructed to perform two simple deep breathing manoeuvres prior to blood donation; one manoeuvre with a respiratory cycle every 10 s (0.1 Hz) and one every 6 s (0.167 Hz). The variation in the pre-ejection period (鈭哖EP) was captured with the electrocardiographic and plethysmographic curves, while the hemodynamic response to haemorrhage was estimated with the cardiac output change assessed with ultrasonography. Respiratory HRV was estimated with root mean square of successive differences (RMSSD). Deep breathing induced cyclic changes in 鈭哖EP magnitude was significantly correlated to RMSSD (p < 0.005). 鈭哖EP indexed to RMSSD increased significantly following haemorrhage at the 0.167 Hz respiratory frequency (p = 0.01). At none of the respiratory manoeuvres was 鈭哖EP nor 鈭哖EP/RMSSD prior to haemorrhage correlated to changes in cardiac output following haemorrhage. Deep breathing induces cyclic changes in blood pressure that are strongly dependent on HRV. These blood pressure variations do, however, not predict the cardiac output response to controlled haemorrhage.

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