Hemodynamic Responses to Mechanical Ventilation with PEEP

Qvist, J; Pontoppidan, Henning; Wilson, Roger S.; Lowenstein, Edward; Laver, Myron B.

doi:10.1097/00000542-197501000-00009

Cited by 397 publications

(81 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The increase in intrathoracic pressure has been shown to correlate with a decrease in renal plasma flow, glomerular filtration rate (GFR) and urine output during PPV (9). This aspect of renal hemodynamics has in part been validated by the canine work performed by Qvist et al, who showed that a stable cardiac output in the setting of PPV is not associated with a decrease in GFR or urine output (13). There are other, clinically occult adverse hemodynamic effects of PPV in the pulmonary, systemic, and renal circulations.…”

Section: Hemodynamic Effects Of Ppvmentioning

confidence: 93%

Mechanical Ventilation and Lung–Kidney Interactions

Koyner

Murray

2008

Clinical Journal of the American Society of Nephrology

View full text Add to dashboard Cite

Section: Hemodynamic Effects Of Ppvmentioning

confidence: 93%

Mechanical Ventilation and Lung–Kidney Interactions

Koyner

Murray

2008

Clinical Journal of the American Society of Nephrology

View full text Add to dashboard Cite

“…Of note, MV also is associated with a threefold increase in the risk of AKI (36). Renal consequences of MV have been known for several decades, and hemodynamic alterations and neurohormonal activation were implicated, as mechanisms leading to reduced renal function (9,27,28). Recently, inflammatory crosstalk from lungs to kidneys via systemic cytokines generated by ventilator-induced lung injury (VILI), due to high tidal volume MV, has been suggested to contribute to AKI in preclinical and clinical studies (16 -18, 31).…”

mentioning

confidence: 99%

Ventilator-induced lung injury increases expression of endothelial inflammatory mediators in the kidney

Hepokoski

Englert

Baron

et al. 2017

American Journal of Physiology-Renal Physiology

View full text Add to dashboard Cite

In critical illness, such as sepsis or the acute respiratory distress syndrome, acute kidney injury (AKI) is common and associated with increased morbidity and mortality. Mechanical ventilation in critical illnesses is also a risk factor for AKI, but it is potentially modifiable. Injurious ventilation strategies may lead to the systemic release of inflammatory mediators from the lung due to ventilator induced lung injury (VILI). The systemic consequences of VILI are difficult to differentiate clinically from other systemic inflammatory syndromes, such as sepsis. The purpose of this study was to identify unique changes in the expression of inflammatory mediators in kidney tissue in response to VILI compared with systemic sepsis to gain insight into direct effects of VILI on the kidney. Four groups of mice were compared—mice with sepsis from cecal ligation and puncture (CLP), mice subjected to injurious mechanical ventilation with high tidal volumes (VILI), mice exposed to CLP followed by VILI (CLP+VILI), and sham controls. Protein expression of common inflammatory mediators in kidneys was analyzed using a proteome array and confirmed by Western blot analysis or ELISA. VEGF and VCAM-1 were found to be significantly elevated in kidneys from VILI mice compared with sham and CLP. Angiopoietin-2 was significantly increased in CLP+VILI compared with CLP alone and was also correlated with higher levels of AKI biomarker, neutrophil gelatinase-associated lipocalin. These results suggest that VILI alters the renal expression of VEGF, VCAM-1, and angiopoietin-2, and these proteins warrant further investigation as potential biomarkers and therapeutic targets.

show abstract

“…PEEP should be maintained since discontinuing PEEP may cause severe hypoxaemia, increase intrapulmonary shunt and induce a different haemodynamic situation created by a sudden decrease in mean intrathoracic pressure and a rebound hypervolemia in central vessels. 29 In the presence of important respiratory fluctuations, the readings of pulmonary vascular pressures can be inaccurate especially when they are taken from a digital panel meter printout as there is usually a time delay in the digital printout. Also, the digital printout value is an average over time.…”

Section: Mode Of Ventilation and Peepmentioning

confidence: 99%