e52 www.ccmjournal.org February 2015 • Volume 43 • Number 2 pressure of the SVC (PtmSVC), the authors report a significant decrease during tidal ventilation. If we calculate, using the data provided in Table 2 in (1), mean changes in PtmSVC during tidal ventilation at 8 mL/kg at two different parts of the SVC, one just at the entry into the right atrium (where the surrounding pressure is the pericardial pressure) and the other above (where the surrounding pressure is actually the pleural pressure), they found a mean decrease of 2.2 mm Hg for the latter and a 0.5 mm Hg increase for the former, just reflecting that the SVC actually acts as a Starling resistor and may collapse at the junction between the pleural and pericardial pressure (3). Second, we are puzzled by the absence of change in the transmural right atrial pressure (PtmRA) during tidal ventilation. The reason for this is not so obvious. As noted by the authors, it could reflect the absence of change in the pressure gradient for systemic venous return (SVR), as previously suggested by Fessler et al (4), although we do not have the mean systemic pressure, that is, the inflow pressure for SVR, and the outflow pressure for SVR is not the PtmRA but the intravascular right atrial pressure. However, it could also reflect the fact that the afterload effect of mechanical ventilation on the right ventricle plays a large role in some patients. Presentation of the data in two groups of patients according to the change (increase or decrease) in PtmRA would help us to analyze the results. Unfortunately, the authors did the analysis according to pulse pressure variation (PPV, low or high), which, to our knowledge, are not relevant since the afterload effect of mechanical ventilation has also been reported to induce significant PPV. Finally, we disagree somewhat with the authors’ interpretation that a decrease in chest wall compliance may increase the transmission of pressure from the airways to the pleural space. This is an “unsuitable” wording. In fact, it just reflects the fact that since chest wall compliance (C CW ) is decreased, the pleural pressure (P pl ) is increased for the same delivered tidal volume (TV), as indicated by the equation C CW = TV changes/P pl changes. The authors have disclosed that they do not have any potential conflicts of interest.
[1]
L. Lorente.
Does chlorhexidine-impregnated dressing reduce the risk of catheter-related bloodstream infection in all vascular access?
,
2015,
Critical care medicine.
[2]
M. V. van Putten,et al.
Mechanical Ventilation–Induced Intrathoracic Pressure Distribution and Heart-Lung Interactions*
,
2014,
Critical care medicine.
[3]
Y. Mahjoub,et al.
Chlorhexidine-impregnated dressing: an efficient weapon against catheter-related bloodstream infection?*.
,
2014,
Critical care medicine.
[4]
L. Lorente,et al.
Arterial catheter-related infection of 2,949 catheters
,
2006,
Critical care.
[5]
F. Jardin,et al.
Ultrasonographic examination of the venae cavae
,
2006,
Intensive Care Medicine.
[6]
K. Chergui,et al.
Superior vena caval collapsibility as a gauge of volume status in ventilated septic patients
,
2004,
Intensive Care Medicine.
[7]
D. Maki,et al.
The pathogenesis of catheter-related bloodstream infection with noncuffed short-term central venous catheters
,
2004,
Intensive Care Medicine.
[8]
H. Fessler,et al.
Effects of positive end-expiratory pressure on the gradient for venous return.
,
1991,
The American review of respiratory disease.