of normal saline loading correlated well with initial stroke volume index and changes in stroke volume index, respectively. The relationship between left ventricular end-diastolic volume index and stroke volume index was confirmed in group 2 subjects using mathematically independent techniques to measure these variables. In addition, initial central venous pressure, right ventricular end-diastolic volume index, pulmonary artery occlusion pressure, and left ventricular end-diastolic volume index failed to correlate significantly with changes in cardiac performance in response to saline infusion in group 1 subjects. Conclusions: Normal healthy volunteers demonstrate a lack of correlation between initial central venous pressure/pulmonary artery occlusion pressure and both end-diastolic ventricular volume indexes and stroke volume index. Similar results are found with respect to changes in these variables following volume infusion. In contrast, initial enddiastolic ventricular volume indexes and changes in end-diastolic ventricular volume indexes in response to saline loading correlate strongly with initial and postsaline loading changes in cardiac performance as measured by stroke volume index. These data suggest that the lack of correlation of these variables in specific patient groups described in other studies represents a more universal phenomenon that includes normal subjects. Neither central venous pressure nor pulmonary artery occlusion pressure appears to be a useful predictor of ventricular preload with respect to optimizing cardiac performance. (Crit Care Med 2004; 32:691‐699)

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Pulmonary artery occlusion pressure and central venous pressure fail to predict ventricular filling volume, cardiac performance, or the response to volume infusion in normal subjects.

We repeatedly assessed pulmonary and systemic hemodynamics in 30 patients undergoing therapy for severe acute respiratory failure of diverse causes. Pulmonary-artery hypertension and elevated pulmonar vascular resistance were observed in all patients after correction of systemic hypoxemia. Increasing pulmonary blood flow by isoproterenol infusion or decreasing pulmonary blood flow by partial bypass of the right side of the heart minimally altered pulmonary-artery pressure. Although neither elevated pulmonary vascular resistance nor low cardiac index reliably predicted death, survivors had preogressive decreases of pulmonary vascular resistance with time, whereas nonsurvivors tended to maintain or increase pulmonary vascular resistance. Right ventricular stroke-work index was markedly elevated in all patients. The work load imposed upon the right ventricle by elevation of pulmonary vascular resistance may be a factor limiting survival in severe acute respiratory failure.

https://www.nejm.org/doi/pdf/10.1056/NEJM197703032960903?listPDF=true

Pulmonary Hypertension in Severe Acute Respiratory Failure

Although left ventricular dysfunction is common during ventilatory support with positive end-expiratory pressure (PEEP), the mechanism of this disorder remains unclear. In 10 patients with the adult respiratory-distress syndrome we studied the effects of a stepwise increase in PEEP from 0.to 30 cm H2O on left ventricular output, intracardiac transmural pressures, and two-dimensional echocardiographic measurements of left ventricular cross-sectional area at end-systole and at end-diastole. Increasing PEEP was associated with progressive declines in cardiac output, mean blood pressure, and left ventricular dimensions and with equalization of right and left ventricular filling pressures. The radius of septal curvature decreased at both end-diastole and end-systole, implying a leftward shift of the interventricular septum. At the highest PEEP, blood-volume expansion did not restore cardiac output, although left ventricular transmural filling pressures had returned to base-line values. We conclude that decreased cardiac output during PEEP is mediated by a leftward displacement of the interventricular septum, which restricts left ventricular filling.

https://www.nejm.org/doi/pdf/10.1056/NEJM198102123040703?listPDF=true

Influence of positive end expiratory pressure on left ventricular performance

Objective
In mechanically ventilated patients the indices which assess preload are used with increasing frequency to predict the hemodynamic response to volume expansion. We discuss the clinical utility and accuracy of some indices which were tested as bedside indicators of preload reserve and fluid responsiveness in hypotensive patients under positive pressure ventilation.

/pdf/fluid-responsiveness-in-mechanically-ventilated-patients-a-fl1wmkixlf.pdf

Fluid responsiveness in mechanically ventilated patients: a review of indices used in intensive care

Misled by the Wedge? : The Swan-Ganz Catheter and Left Ventricular Preload

A prospective study of five patients was performed utilizing both left atrial and wedge catheters. As positive end expiratory pressure (PEEP) was altered, left atrial pressure, cardiac index, net left atrial pressure, pulmonary vascular resistance, and stroke work were determined. At low levels of PEEP, wedge and left atrial pressure correlated significantly ( r =.83). As PEEP increased, cardiac index was frequently compromised. Measurements of net left atrial pressure and stroke work indicated that high levels of PEEP resulted in left ventricular failure. This may have been due to reduced coronary flow secondary to an elevated myocardial interstitial pressure with high levels of PEEP.

https://jamanetwork.com/journals/SURG/articlepdf/579344/archsurg_109_2_025.pdf

David Marco

Papers

Correlation of pulmonary wedge and left atrial pressures. A study in the patient receiving positive end expiratory pressure ventilation.