Increasing positive end-expiratory pressure from 0 to 15 cm H2O significantly varied right ventricular end-diastolic volume for individuals (p < 0.05) independently of filling pressure changes.
Observational (n=12)
Does increasing positive end-expiratory pressure (PEEP) alter right ventricular function and volumes in patients after thoracotomy?
Increasing PEEP in post-thoracotomy patients alters RV volumes independently of filling pressures, likely due to RV shape changes dissociating EDV from wall stress.
Abstract The effect of positive end-expiratory pressure (PEEP) on right ventricular (RV) function in humans is complex. Previous studies have been limited in their interpretation by not defining either pericardial pressure (Ppc) or RV volumes. Accordingly, we measured RV volumes and pressures and Ppc as PEEP was increased from zero to 15 cm H2O in 12 patients after thoracotomy, using a pulmonary arterial catheter equipped with a rapid responding thermistor that allowed measurement of RV ejection fraction (ef), while Ppc was measured via a pericardial balloon catheter. RV end-diastolic volume (EDV) was estimated as the ratio of stroke volume (SV) to RVef, whereas RV end-systolic volume (ESV) was estimated as RV EDV-SV. Right atrial pressure (Pra) was defined as end-diastolic pressure, and pulmonary arterial pressures (Ppa), both peak and mean, were used as end-systolic pressures. PEEP increased Ppc, Pra, and lung compliance (CI). Cardiac output also decreased but not significantly. Neither mean nor peak systolic Ppa, nor RVef was significantly altered by PEEP. There was no relation between either RV filling pressure (Pra-Ppc) and EDV or the change in RV filling pressure and EDV, although EDV varied significantly as PEEP varied for individuals (p 0.05). Similarly, there was no relation between Ppa and ESV when either mean or peak Ppa values relative to Ppc were used. The relations between EDV and both SV and RVef were weak (r = 0.54 and 0.55, respectively). RVef varied inversely with ESV (r = −0.77), although it showed no relation to transmural peak Ppa (r = 0.28). Both absolute and relative changes in EDV corresponded closely with respective ESV values (r = 0.94). For individuals, decreases in RVef, SV, and RV filling pressure were associated with increases in CI (p 0.01). We conclude that EDV varies independently of changes in filling pressure, and that changes in ESV occur independently of changes in ejection pressure. These data can be explained by assuming that the RV shape changes can dissociate changes in RV EDV from changes in RV wall stress (preload). Thus, changes in RV EDV may or may not alter SV but should proportionately change ESV to a degree dependent on ejection pressure and contractility.
Pinsky et al. (Tue,) conducted a observational in Post-thoracotomy (n=12). Positive end-expiratory pressure (PEEP) vs. Baseline (PEEP of 0 cm H2O) was evaluated on Right ventricular volumes, pressures, and pericardial pressure. Increasing positive end-expiratory pressure from 0 to 15 cm H2O significantly varied right ventricular end-diastolic volume for individuals (p < 0.05) independently of filling pressure changes.
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