Effects of rapid permissive hypercapnia on hemodynamics, gas exchange, and oxygen transport and consumption during mechanical ventilation for the acute respiratory distress syndrome

Thorens, Jean-Benoît; Jolliet, Philippe; Ritz, M; Chevrolet, Jean-Claude

doi:10.1007/bf01712235

Cited by 118 publications

(58 citation statements)

References 36 publications

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“…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.…”

Section: Discussionsupporting

confidence: 78%

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

et al. 2002

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Section: Discussionsupporting

confidence: 78%

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

et al. 2002

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“…In both animal models and human studies, modest hypercapnia has been shown to have reproducible hemodynamic effects that are well tolerated and reversible [88] . In both canine and human studies, these effects have included a decrease in systemic vascular resistance (systemic vasodilation), and increased cardiac output despite a decrease in cardiac contractility [89][90][91] , although these findings are not consistent in all studies [92] . One human study evaluated the effects of buffer therapy on hypercapnic acidosis.…”

Section: Clinical Effects Of Permissive Hypercapniamentioning

confidence: 79%

Mechanical Ventilation and the Kidney

2009

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Acute lung injury (ALI) and acute kidney injury (AKI) are complications often encountered in the setting of critical illness. Both forms of end-organ injury commonly occur in similar settings of systemic inflammatory response syndrome, shock, and evolving multiple organ dysfunction. Recent elucidation of the pathobiology of critical illness has led to a more basic mechanistic understanding of the complex interplay between injured organs in patients with multiple organ dysfunction syndrome; this has been aptly called ‘the slippery slope of critical illness’ [Kidney Int Suppl 1998;66:S25–S33]. Distant organ effects of apparently isolated injuries to the lungs, gut, and kidneys have all been discovered in recent years. In this article, we will review the harmful bidirectional interaction between ALI and AKI, which appears to be a common clinical syndrome with routine clinical implications. We will review the current understanding of lung-kidney interactions from both perspectives, including the renal effects of ALI and mechanical ventilation, and the pulmonary sequelae of AKI. In this review of the emerging evidence of deleterious bidirectional organ cross talk between lung and kidney, we will focus on the role of ventilator-induced kidney injury in the pathogenesis of AKI in patients with ALI.

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“…Nevertheless, the arterial CO 2 tension in the low rate, high PEEP group was systematically greater than the arterial CO 2 tension in the high rate, low PEEP group. Increased arterial CO 2 levels, however, are associated with increased cardiac output, a result of catecholamine release and systemic vasodilation (51,55,67). If any effect would be expected from the difference in Pa CO 2 between the two strategies, it would be to increase the cardiac output in the low rate, high PEEP group.…”

Section: Discussionmentioning

confidence: 99%

Maintenance of end-expiratory recruitment with increased respiratory rate after saline-lavage lung injury

Syring

Otto²,

Spivack³

et al. 2007

Journal of Applied Physiology

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Cyclical recruitment of atelectasis with each breath is thought to contribute to ventilator-associated lung injury. Extrinsic positive end-expiratory pressure (PEEPe) can maintain alveolar recruitment at end exhalation, but PEEPe depresses cardiac output and increases overdistension. Short exhalation times can also maintain end-expiratory recruitment, but if the mechanism of this recruitment is generation of intrinsic PEEP (PEEPi), there would be little advantage compared with PEEPe. In seven New Zealand White rabbits, we compared recruitment from increased respiratory rate (RR) to recruitment from increased PEEPe after saline lavage. Rabbits were ventilated in pressure control mode with a fraction of inspired O(2) (Fi(O(2))) of 1.0, inspiratory-to-expiratory ratio of 2:1, and plateau pressure of 28 cmH(2)O, and either 1) high RR (24) and low PEEPe (3.5) or 2) low RR (7) and high PEEPe (14). We assessed cyclical lung recruitment with a fast arterial Po(2) probe, and we assessed average recruitment with blood gas data. We measured PEEPi, cardiac output, and mixed venous saturation at each ventilator setting. Recruitment achieved by increased RR and short exhalation time was nearly equivalent to recruitment achieved by increased PEEPe. The short exhalation time at increased RR, however, did not generate PEEPi. Cardiac output was increased on average 13% in the high RR group compared with the high PEEPe group (P < 0.001), and mixed venous saturation was consistently greater in the high RR group (P < 0.001). Prevention of end-expiratory derecruitment without increased end-expiratory pressure suggests that another mechanism, distinct from intrinsic PEEP, plays a role in the dynamic behavior of atelectasis.

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Effects of rapid permissive hypercapnia on hemodynamics, gas exchange, and oxygen transport and consumption during mechanical ventilation for the acute respiratory distress syndrome

Cited by 118 publications

References 36 publications

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

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

Mechanical Ventilation and the Kidney

Maintenance of end-expiratory recruitment with increased respiratory rate after saline-lavage lung injury

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