Pulmonary Vascular Dysfunction Induced by High Tidal Volume Mechanical Ventilation*

Menéndez, Carmen; Martínez-Caro, Leticia; Moreno, Laura; Nin, Nicolás; Moral-Sanz, Javier; Morales, Daniel; Cogolludo, Ángel; Esteban, Andrés; Lorente, José A.; Pérez‐Vizcaíno, Francisco

doi:10.1097/ccm.0b013e318287ef4a

Cited by 26 publications

(22 citation statements)

References 34 publications

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“…Earlier studies reported an incidence of PH and right ventricular dysfunction of up to 70% 6. In line with this, it has been shown that injurious mechanical ventilation is an important cause of pulmonary vascular injury in patients and in animal models of ALI/ARDS 7. However, in the setting of mechanical ventilation with lung protective strategies, pulmonary vascular dysfunction is still a prominent feature, with a prevalence of 20–25%, and is independently associated with poor outcomes in patients with ARDS 8 9.…”

Section: Introductionmentioning

confidence: 87%

Role of acid sphingomyelinase and IL-6 as mediators of endotoxin-induced pulmonary vascular dysfunction

Pandolfi

Barreira

Moreno

et al. 2016

Thorax

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Section: Introductionmentioning

confidence: 87%

Role of acid sphingomyelinase and IL-6 as mediators of endotoxin-induced pulmonary vascular dysfunction

Pandolfi

Barreira

Moreno

et al. 2016

Thorax

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“…Animal studies have shown that high V T ventilation increases levels of pro-inflammatory mediators, leads to pulmonary edema, and causes increased alveolar-capillary permeability and structural abnormalities. [2][3][4][5][6][7][8] With the emergence of these animal data, clinicians began to question the traditional use of V T values in the range of 10 -15 mL/kg PBW in humans. Several small human studies were reported in the mid-to late 1990s that produced conflicting results.…”

Section: Early Studiesmentioning

confidence: 99%

Should A Tidal Volume of 6 mL/kg Be Used in All Patients?

2016

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It has been shown that mechanical ventilation by itself can cause lung injury and affect outcomes. Ventilator-induced lung injury is associated with high tidal volumes in lungs afflicted with ARDS. However, the question is: Do high tidal volumes have this same effect in normal lungs or lungs that have respiratory compromise stemming from something other than ARDS? Many clinicians believe that a tidal volume strategy of 6 mL/kg predicted body weight should be standard practice in all patients receiving mechanical ventilation. There is a growing body of evidence related to this issue, and this is the debate that will be tackled in this paper from both pro and con perspectives. Key words: tidal volume; predicted body weight; mechanical ventilation; lung-protective ventilation; time constant; ARDS; stress; strain; hypercapnia. [Respir Care 2016;61(6):774 -790 . © 2016 Daedalus Enterprises] IntroductionIt is well known that the use of mechanical ventilation has the potential to aggravate pulmonary injury, but emerging evidence indicates that it may also precipitate lung injury in patients with no previous injury. Lung-protective ventilation has evolved over the past couple of decades to the point that it has become standard of care for patients with ARDS. The use of lower tidal volume (V T ) 4 -8 mL/kg predicted body weight (PBW) is part of this lung-protective strategy for mechanical ventilation (mechanical ventilation) along with limiting the plateau pressure to a maximum of 30 cm H 2 O and prudent use of PEEP to prevent atelectasis. Since we now know that the use of lower V T strategies (more specifically 6 mL/kg PBW) helps to limit the pulmonary damage during ARDS, the question now is: Should we be using this strategy in all mechanically ventilated patients? Anatomically speaking, it makes sense to, since the normal physiologic V T for humans is approximately 6 mL/kg PBW. 1 There is a growing body of evidence that points toward the use of lower V T values leading to improved outcomes in patients suffering from other forms and degrees of respiratory failure. The aim of this paper is to examine the evidence relating to the use of lower V T values in conditions other than ARDS in which mechanical ventilation is required. This will be done with viewpoints from both the pro and con positions. Early StudiesThere is a plethora of preclinical evidence from animal studies supporting the fact that the use of high V T values can directly cause injury to normal lungs. Animal studies have shown that high V T ventilation increases levels of pro-inflammatory mediators, leads to pulmonary edema, and causes increased alveolar-capillary permeability and structural abnormalities. [2][3][4][5][6][7][8] With the emergence of these animal data, clinicians began to question the traditional use of V T values in the range of 10 -15 mL/kg PBW in humans. Several small human studies were reported in the mid-to late 1990s that produced conflicting results. 9-11 These studies were hampered by several factors, including higher than predicte...

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“…PE (10 -6 mol/L) was used to precontract the main pulmonary artery rings, but in the whole pulmonary circulation, PE could not contract the lung vascular bed adequately. Following the protocols of several previous studies (Menendez et al, 2013;Xia et al, 2013), we used serotonin (10 -6 mol/L) to precontract the lung vascular bed. To study TRPV4 channels in the function of pulmonary circulation, GSK1016790A was used to directly contract perfused lung without serotonin ( Figure 6A), GSK1016790A retains normal potency towards its target across a variety of species making it an attractive for investigating TRPV4 channel pharmacology and physiology (Robert et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Opposing actions of TRPV4 channel activation in the lung vasculature

Chen

Duan

et al. 2015

Respiratory Physiology & Neurobiology

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Pulmonary Vascular Dysfunction Induced by High Tidal Volume Mechanical Ventilation*

Abstract: High tidal volume ventilation-induced pulmonary vascular dysfunction was characterized by reduced alpha-adrenergic-induced vasoconstriction, reduced endothelium-dependent vasodilatation, and enhanced hypoxic pulmonary vasoconstriction.

Cited by 26 publications

References 34 publications

Role of acid sphingomyelinase and IL-6 as mediators of endotoxin-induced pulmonary vascular dysfunction

Role of acid sphingomyelinase and IL-6 as mediators of endotoxin-induced pulmonary vascular dysfunction

Should A Tidal Volume of 6 mL/kg Be Used in All Patients?

Opposing actions of TRPV4 channel activation in the lung vasculature

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