Hypercapnic acidosis and mortality in acute lung injury*

Kregenow, David A.; Rubenfeld, Gordon D.; Hudson, Leonard D.; Swenson, Erik R.

doi:10.1097/01.ccm.0000194533.75481.03

Cited by 202 publications

(97 citation statements)

References 34 publications

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“…48 This effect was not observed in subjects who were ventilated at V T of 6 mL/kg of predicted body weight. The investigators theorized that ventilator-induced lung injury occurred to a greater extent in subjects receiving V T of 12 mL/kg of predicted body weight and that these harmful effects were mitigated by hypercapnic acidosis.…”

Section: Hypercapnia In Ardsmentioning

confidence: 90%

Carbon Dioxide in the Critically Ill: Too Much or Too Little of a Good Thing?

Marhong

Fan

2014

Respir Care

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Hypercapnia and hypocapnia commonly complicate conditions that are present in critically ill patients. Both conditions have important physiologic effects that may impact the clinical management of these patients. For instance, hypercapnia results in bronchodilation and enhanced hypoxic vasoconstriction, leading to improved ventilation/perfusion matching. Hypocapnia reduces cerebral blood volume through arterial vasoconstriction. These effects have also been exploited for therapeutic aims. In patients with traumatic brain injury (TBI), hypocapnia is often utilized to control intracranial pressure. However, this effect is not sustained, and prolonged hypocapnia increases the risk of mortality and severe disability in patients with TBI. Hypercapnia and hypercapnic acidosis are common consequences of lung-protective ventilation in ARDS. Hypercapnic acidosis reduces ischemic lung injury and preserves lung compliance, but concern has arisen over hypercapniainduced immunosuppression and the potential for bacterial proliferation in sepsis. Experimental studies suggest that buffering hypercapnic acidosis attenuates these effects, whereas hypocapnia appears to potentiate lung injury through increased capillary permeability and decreased lung compliance. Several areas of uncertainty surround the role of hypercapnia/hypocapnia in treating TBI and ARDS. Current data support recommendations to avoid hypocapnia in treating TBI, with the exception of emergent treatment of elevated intracranial pressure, while awaiting definitive management. Permissive hypercapnia is commonly accepted as a consequence of lung-protective ventilation in ARDS, but there is insufficient evidence to support the induction of hypercapnic acidosis in clinical practice. Buffering hypercapnic acidosis should be considered only for a specific clinical indication (eg, hemodynamic instability). For clinicians choosing to buffer hypercapnic acidosis, tris-hydroxymethyl aminomethane is recommended over sodium bicarbonate, as it is more effective in correcting pH and is not associated with increased carbon dioxide production. Future studies should aim to address these areas of uncertainty to help guide clinicians in the therapeutic use and management of hypercapnia/hypocapnia in critically ill patients.

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Section: Hypercapnia In Ardsmentioning

confidence: 90%

Carbon Dioxide in the Critically Ill: Too Much or Too Little of a Good Thing?

Marhong

Fan

2014

Respir Care

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“…In the absence of further large clinical trials, the debate over management of the attendant hypercapnic acidosis will therefore remain. There is strong animal data suggesting the many potential benefits of hypercapnic acidosis (3,11,22,24), recently augmented by secondary analysis of the ARDSNet data (12). On the other hand, skepticism persists among some, with experimental and clinical data touting drawbacks to hypercapnic acidosis (16) and benefits of various buffering strategies (17,23,28), with some compelling clinical arguments for the use of THAM.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, hypocapnia may have deleterious effects (14,15), whereas bicarbonate buffering of hypercapnic acidosis has been shown to worsen lung barrier function in animal models of ischemia-reperfusion lung injury (13,18), augment intracellular oxidative stress (4), and blunt hypercapnia-enhanced organ blood flow (3). Supporting data have also come from clinical studies, where a recent secondary analysis of ARDSNet data showed protective effects of hypercapnia on mortality in those patients ventilated with high tidal volumes, findings potentially at odds with mechanistic hypotheses put forth by the authors of the original ARDS low tidal volume trial (12).…”

mentioning

confidence: 86%

Impact of buffering hypercapnic acidosis on cell wounding in ventilator-injured rat lungs

Caples¹,

Rasmussen²,

Lee³

et al. 2009

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…It has been suggested, primarily from experimental models, that permissive hypercapnia may be protective. 18 Kregenow et al 19 evaluated the effect of hypercapnic acidosis in a secondary analysis of the ARDS Network database. They found that hypercapnic acidosis was associated with reduced 28-day mortality in the 12 mL/kg IBW V T group, after controlling for comorbidities and severity of lung injury.…”

Section: Volume or Pressure Limitation?mentioning

confidence: 99%

Approaches to Conventional Mechanical Ventilation of the Patient With Acute Respiratory Distress Syndrome

Hess

2011

Respir Care

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To minimize ventilator-induced lung injury, attention should be directed toward avoidance of alveolar over-distention and cyclical opening and closure of alveoli. The most impressive study of mechanical ventilation to date is the Acute Respiratory Distress Syndrome (ARDS) Network study of higher versus lower tidal volume (V T ), which reported a reduction in mortality from 39.8% to 31.0% with 6 mL/kg ideal body weight rather than 12 mL/kg ideal body weight (number-neededto-treat of 12 patients). To achieve optimal lung protection, the lowest plateau pressure and V T possible should be selected. What is most important is limitation of V T and alveolar distending pressure, regardless of the mode set on the ventilator. Accumulating observational evidence suggests that V T should be limited in all mechanically ventilated patients-even those who do not have ALI/ARDS. Evidence does not support the use of pressure controlled inverse-ratio ventilation. Although zero PEEP is probably injurious, an area of considerable controversy is the optimal setting of PEEP. Available evidence does not support the use of higher PEEP, compared to lower PEEP, in unselected patients with acute lung injury (ALI)/ARDS. However, results of a metaanalysis using individual patients from 3 randomized controlled trials suggest that higher PEEP should be used for ARDS, whereas lower PEEP may be more appropriate in patients with ALI. PEEP should be set to maximize alveolar recruitment while avoiding over-distention. Many approaches for setting PEEP have been described, but evidence is lacking that any one approach is superior to any other. In most, if not all, cases of ALI/ARDS, conventional ventilation strategies can be used effectively to provide lung-protective ventilation strategies.

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Hypercapnic acidosis and mortality in acute lung injury*

Cited by 202 publications

References 34 publications

Carbon Dioxide in the Critically Ill: Too Much or Too Little of a Good Thing?

Carbon Dioxide in the Critically Ill: Too Much or Too Little of a Good Thing?

Impact of buffering hypercapnic acidosis on cell wounding in ventilator-injured rat lungs

Approaches to Conventional Mechanical Ventilation of the Patient With Acute Respiratory Distress Syndrome

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