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We thank Dr. Axler (1) for his interest in our study (2) of central venous pressure (CVP) and mean airway pressure (Pmean). We believe that CVP is as true a physiologic variable as the heart rate and blood pressure; it has intrinsic meaning in that it is the lowest pressure within the circulatory system because it approaches the right atrium, and it reflects the right atrial pressure. As the pulmonary arterial wedge pressure serves as a variable reflecting left ventricular function, CVP may serve as a variable reflecting right ventricular function. Guyton et al (3) found that the mean atrial pressure rose by an imperceptible amount while the right ventricle was increasing its force of contraction during a progressive pulmonary artery occlusion test in mongrel dogs. However, as soon as the ventricle reached its maximal force and then began to fail, the right atrial pressure immediately began to rise. Thus, an elevation of CVP indicates right ventricular dysfunction, and CVP serves as a more effective variable reflecting right ventricular function than the volume status or volume responsiveness, which have caused much controversy (4). An elevated airway pressure, fluid overload, and hypoxia are possible causes of right ventricular dysfunction and CVP elevation while patients are undergoing mechanical ventilation.
We believe that patients’ outcomes are determined not only by alveolar stretching but also, and more importantly, the heart-lung interaction on the first day of mechanical ventilation. As you mentioned, the Pmean differs from the plateau pressure (Pplat) and driving pressure (DP); the Pmean is much more hemodynamically accurate because it reflects the whole respiratory cycle; the latter variables reflect alveolar stretching, which only occurs during the inspiratory phase. Our study revealed that an elevated Pmean (odds ratio, 1.125; 95% CI, 1.069–1.184; p < 0.001) was independently associated with 28-day mortality instead of Pplat and DP. We provided evidence and discussed why Pmean was employed in our study (2).
We agree that our study had limitations because of its retrospective and single-center design. However, both CVP and Pmean are easy to measure consecutively at the bedside and have a greater possibility to be generalized. As mentioned above, CVP and Pmean may be variables that serve as a bridge between right heart function and the respiratory system, reflecting the cardiopulmonary interaction in critically ill patients undergoing mechanical ventilation. Certainly, elucidation of the exact effect of Pmean and CVP on right ventricular function requires the use of specific right ventricular function variables by echocardiography or Swan-Ganz catheterization to reveal the mechanism.
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