Abstract

BackgroundWhether during spontaneous breathing arterial pressure variations (APV) can detect a volume deficit is not established. We hypothesized that amplification of intra-thoracic pressure oscillations by breathing through resistors would enhance APV to allow identification of a reduced cardiac output (CO). This study tested that hypothesis in healthy volunteers exposed to central hypovolemia by head-up tilt.MethodsThirteen healthy volunteers were exposed to central hypovolemia by 45° head-up tilt while breathing through a facemask with 7.5 cmH2O inspiratory and/or expiratory resistors. A brachial arterial catheter was used to measure blood pressure and thus systolic pressure variation (SPV), pulse pressure variation and stroke volume variation . Pulse contour analysis determined stroke volume (SV) and CO and we evaluated whether APV could detect a 10 % decrease in CO.ResultsDuring head-up tilt SV decreased form 91 (±46) to 55 (±24) mL (mean ± SD) and CO from 5.8 (±2.9) to 4.0 (±1.8) L/min (p < 0.05), while heart rate increased (65 (±11) to 75 (±13) bpm; P < 0.05). Systolic pressure decreased from 127 (±14) to 121 (±13) mmHg during head-up tilt, while SPV tended to increase (from 21 (±15)% to 30 (±13)%). Yet during head-up tilt, a SPV ≥ 37 % predicted a decrease in CO ≥ 10 % with a sensitivity and specificity of 78 % and 100 %, respectively.ConclusionIn spontaneously breathing healthy volunteers combined inspiratory and expiratory resistors enhance SPV during head-up tilted induced central hypovolemia and allow identifying a 10 % reduction in CO. Applying inspiratory and expiratory resistors might detect a fluid deficit in spontaneously breathing patients.Trial registrationClinicalTrials.gov number NCT02549482 Registered September 10th 2015.

Highlights

  • Whether during spontaneous breathing arterial pressure variations (APV) can detect a volume deficit is not established

  • Combined inspiratory and expiratory resistors might help detecting a fluid deficit in spontaneously breathing patients

  • Dahl et al BMC Anesthesiology (2016) 16:58 variation (APV) predicts volume responsiveness defined as an increase in stroke volume (SV) or cardiac output (CO) when the patient is exposed to an intravascular volume load [8,9,10,11,12,13,14]

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Summary

Introduction

Whether during spontaneous breathing arterial pressure variations (APV) can detect a volume deficit is not established. In mechanically ventilated patients without cardiac arrhythmias exposed to a tidal volume larger than 8 mL/kg lean body weight, arterial pressure. In spontaneously breathing patients APV is insufficient to guide volume therapy [15,16,17] and volume therapy is guided by recording of SV and/or CO response or change in end-tidal CO2 tension , e.g. when the patient is exposed to passive raising the legs [16, 18,19,20] or Trendelenburg’s position [21]. Zaniboni et al [22] found a correlation for APV between mechanically ventilated patients and patients ventilated by spontaneous flow triggered synchronized intermittent mechanical ventilation

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