Temporal Hemodynamic Effects of Permissive Hypercapnia Associated with Ideal PEEP in ARDS

Abstract

The associated use of permissive hypercapnia (PHY) and high PEEP levels (PEEP(IDEAL)) has been recently indicated as part of a lung-protective-approach (LPA) in acute respiratory distress syndrome (ARDS). However, the net hemodynamic effect produced by this association is not known. We analyzed the temporal hemodynamic effects of this combined strategy in 48 patients (mean age 34 +/- 13 yr) with ARDS, focusing on its immediate (after 1 h), early (first 36 h), and late (2nd-7th d) consequences. Twenty-five patients were submitted to LPA--with the combined use of permissive hypercapnia (PHY), VT < 6 ml/kg, distending pressures above PEEP < 20 cm H2O, and PEEP 2 cm H2O above the lower inflection point on the static inspiratory P-V curve (P(FLEX))- and 23 control patients were submitted to conventional mechanical ventilation. LPA was initiated at once, resulting in an immediate increase in heart rate (p = 0.0002), cardiac output (p = 0.0002), oxygen delivery (DO2l, p = 0.0003), and mixed venous Po2 (p = 0.0006), with a maintained systemic oxygen consumption (p = 0.52). The mean pulmonary arterial pressure markedly increased (mean increment 8.8 mm Hg; p < 0.0001), but the pulmonary vascular resistance did not change (p = 0.32). Cardiac filling pressures increased (p < 0.001) and the systemic vascular resistance fell (p = 0.003). All these alterations were progressively attenuated in the course of the first 36 h, despite persisting hypercapnia. Plasma lactate suffered a progressive decrement along the early period in LPA but not in control patients (p < 0.0001). No hemodynamic consequences of LPA were noticed in the late period and renal function was preserved. A multivariate analysis suggested that these acute hyperdynamic effects were related to respiratory acidosis, with no depressant effects ascribed to high PEEP levels. In contrast, high plateau pressures were associated with cardiovascular depression. Thus, as long as sufficiently low distending pressures are concomitantly applied, the sudden installation of PHY plus PEEP(IDEAL) induces a transitory hyperdynamic state and pulmonary hypertension without harmful consequences to this young ARDS population.

Effects of spontaneous breathing during airway pressure release ventilation on renal perfusion and function in patients with acute lung injury

“…Consistent with our findings, an increase of right ventricular end-diastolic volume, right ventricular ejection fraction and CI has been demonstrated recently during APRV with spontaneous breathing in patients with ALI [16]. A marked increase in HR and CI at unchanged SVI, ITBVI and CVP tm , found during APRV without spontaneous breathing at the same Paw limits when compared to APRV with spontaneous breathing, may be attributed to hypercapnia and respiratory acidosis [25,26,27,28,29]. Compatible with these investigations [25,26,27,28,29], an increase in CI during permissive hypercapnia was associated with decreased systemic vascular resistance, reflecting systemic vasodilation, which effected no change in MAP in our patients.…”

Body position does not influence the location of ventilator-induced lung injury

“…On the other hand, hypercapnia should be avoided if patients have intracranial hypertension. Although the adverse effects of hypercapnia on hemodynamics are reportedly transient [6], hypercapnia does increase pulmonary vascular resistance and worsens pulmonary hypertension in ARDS [7]. If the prone position is less traumatic for the lungs, the effects of hypercapnia will be less intense.…”

Thoracoscopic lung biopsy in a patient with pulmonary lymphangiomyomatosis

“…We did not apply high frequency jet ventilation to the dependent lung, because HFJV during IPPV sometimes increases PIP. We did not employ PEEP because high plateau airway pressures were associated with cardiovascular depression 6 and propofol decreases left ventricular afterload and myocardial contractility. 7 Volatile anesthetics, but P not propofol, inhibit hypoxic pulmonary vasoconstriction, 8 , 9 and propofol inhibits airway smooth muscle contraction.…”