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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 (∆PEP) 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 ∆PEP magnitude was significantly correlated to RMSSD (p < 0.005). ∆PEP indexed to RMSSD increased significantly following haemorrhage at the 0.167 Hz respiratory frequency (p = 0.01). At none of the respiratory manoeuvres was ∆PEP nor ∆PEP/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.

Background: Ultrasonographic evaluation of the inferior vena cava (IVC) provides information on central hemodynamics and predicts fluid responsiveness during positive pressure ventilation. In spontaneously breathing patients, the correlations between IVC dynamics and the hemodynamic response to volume shifts remain to be described., Objectives: We aimed to describe the correlation between IVC dynamics and the changes in cardiac output (CO) caused by controlled hemorrhage., Methods: Healthy donors from the blood bank were eligible for inclusion. Measurements of the IVC and CO were performed before and immediately after blood donation using ultrasound methods. A control group served to evaluate the effect of resting., Results: Thirty-seven participants completed the study. IVC collapsibility index (IVC-CI) and IVC end expiratory diameter (IVCe) both changed significantly after blood donation (p < 0.001). The baseline IVC-CI and IVCe did not correlate with the change in CO (p-values ≥ 0.40). The alterations in IVC-CI and IVCe induced by blood donation also did not correlate with the change in CO (p ≥ 0.71). The sensitivities of IVC-CI or IVCe, defined as an increase in IVC-CI and a decrease in IVCe, for picking up any decrease in CO were 81.3% and 84.4%, respectively. In the control group, no effect was seen between measurements., Conclusion: IVC-CI and IVCe did not correlate with the magnitude of hemodynamic response to early hemorrhage. The sensitivity of serial IVC measurements was approximately 80% for detecting early blood loss., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Aims Left ventricular filling pressure (preload) can be assessed by pulmonary capillary wedge pressure (PCWP) during pulmonary arterial catheterization (PAC). An emerging method [pulse indexed contour cardiac output (PICCO)] can estimate preload by global end-diastolic volume (GEDV) and congestion as extravascular lung water (EVLW) content. However, no reliable quantitative non-invasive methods are available. Hence, in a porcine model of pulmonary congestion, we evaluated EVLW and GEDV by positron emission tomography (PET). The method was applied in 35 heart failure (HF) patients and 9 healthy volunteers. Methods and results Eight pigs were studied. Pulmonary congestion was induced by a combination of beta-blockers, angiotensin-2 agonist and saline infusion. PAC, PICCO, computerized tomography, and 15O-H2O-PET were performed. EVLW increased from 521 ± 76 to 973 ± 325 mL (P  < 0.001) and GEDV from 1068 ± 170 to 1254 ± 85 mL (P  < 0.001). 15O-H2O-PET measures of EVLW increased from 566 ± 151 to 797 ± 231 mL (P  < 0.001) and GEDV from 364 ± 60 to 524 ± 92 mL (P  < 0.001). Both EVLW and GEDV measured with PICCO and 15O-H2O-PET correlated (r 2 = 0.40, P  < 0.001; r 2 = 0.40, P  < 0.001, respectively). EVLW correlated with Hounsfield units (HU; PICCO: r 2 = 0.36, P  < 0.001, PET: r 2 = 0.46, P  < 0.001) and GEDV with PCWP (PICCO: r 2 = 0.20, P  = 0.01, PET: r 2 = 0.29, P  = 0.002). In human subjects, measurements were indexed (I) for body surface area. Neither EVLWI nor HU differed between chronic stable HF patients and healthy volunteers (P  = 0.11, P  = 0.29) whereas GEDVI was increased in HF patients (336 ± 66 mL/m2 vs. 276 ± 44 mL/m2, P  = 0.01). Conclusion The present study demonstrates that 15O-H2O-PET can assess pulmonary congestion and preload quantitatively. Hence, prognostic information from 15O-H2O-PET examinations should be evaluated in clinical trials. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article "Hemodynamic changes during a deep inspiration maneuver predict fluid responsiveness in spontaneously breathing patients" by S. Preau et al which was published in the previous issue of the periodical.