Pathophysiologic role of hypocarbia in post-traumatic pulmonary insufficiency

Trimble, Cleve; Smith, David Eugene; Rosenthal, Myer H.; Fosburg, Richard G.

doi:10.1016/0002-9610(71)90291-1

Cited by 26 publications

(7 citation statements)

References 22 publications

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“…Hypocapnic alkalosis has been implicated in pathogenesis of multiple clinically relevant respiratory entities (9), including asthma (44), ARDS (45), bronchopulmonary dysplasia (13), and high-altitude pulmonary edema (46). Experimentally induced hypocapnia may exert adverse pulmonary effects via several distinct mechanisms, including increases in airway resistance (47), increased microvascular permeability (23), and attenuation of hypoxic pulmonary vasoconstriction, which worsens intrapulmonary shunt and systemic oxygenation (48).…”

Section: Discussionmentioning

confidence: 99%

Carbon dioxide attenuates pulmonary impairment resulting from hyperventilation*

Laffey

Engelberts

Duggan

et al. 2003

Critical Care Medicine

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Section: Discussionmentioning

confidence: 99%

Carbon dioxide attenuates pulmonary impairment resulting from hyperventilation*

Laffey

Engelberts

Duggan

et al. 2003

Critical Care Medicine

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“…Edmunds and Holm demonstrated more than 30 years ago that alveolar hypocapnia produces hemorrhagic consolidation in the lung, and that attenuation of such adverse effects could be achieved by addition of inhaled CO 2 [48]. In the clinical context, Trimble and colleagues in 1971 demonstrated that hypocapnia increased airway resistance, increased work of breathing, worsened ventilation/perfusion matching, increased the alveolar-arterial O 2 gradient and decreased the partial pressure of O 2 in the blood in ARDS patients, and that administration of CO 2 (that is, therapeutic hypercapnia) improved systemic oxygenation and reduced the shunt fraction [58]. Both hyperventilation and hypocapnia have been identified as independent determinants of long-term pulmonary dysfunction in patients with bronchopulmonary dysplasia, as well as being implicated in the pathogenesis of asthma.…”

Section: Clinical Profile Of Hypocapnia In the Critically Ill Patientmentioning

confidence: 99%

Bench-to-bedside review: Carbon dioxide

2010

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Carbon dioxide is a waste product of aerobic cellular respiration in all aerobic life forms. PaCO2 represents the balance between the carbon dioxide produced and that eliminated. Hypocapnia remains a common - and generally underappreciated - component of many disease states, including early asthma, high-altitude pulmonary edema, and acute lung injury. Induction of hypocapnia remains a common, if controversial, practice in both adults and children with acute brain injury. In contrast, hypercapnia has traditionally been avoided in order to keep parameters normal. More recently, advances in our understanding of the role of excessive tidal volume has prompted clinicians to use ventilation strategies that result in hypercapnia. Consequently, hypercapnia has become increasingly prevalent in the critically ill patient. Hypercapnia may play a beneficial role in the pathogenesis of inflammation and tissue injury, but may hinder the host response to sepsis and reduce repair. In contrast, hypocapnia may be a pathogenic entity in the setting of critical illness. The present paper reviews the current clinical status of low and high PaCO2 in the critically ill patient, discusses the insights gained to date from studies of carbon dioxide, identifies key concerns regarding hypocapnia and hypercapnia, and considers the potential clinical implications for the management of patients with acute lung injury.

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“…41 Hypocapnia has long been recognized as the most common acidbase disturbance in critically ill patients, 9 and it is a consistent feature of both septic shock 10 and the systemic inflammatory response syndrome. 8 In fact, hypocapnia is a diagnostic criterion for the latter condition.…”

Section: Hypocapnia As a Common Component Of Diseasementioning

confidence: 99%

“…However, the concept that hypocapnia might have a pathogenic role in the acute respiratory distress syndrome was first proposed in 1971 by Trimble and colleagues. 41 They reported that, in a small study of patients with post-traumatic lung injury, hypocapnia was associated with worsened pulmonary function that was reversed by supplemental inspired carbon dioxide. 41…”

Section: Clinical Consequencesmentioning

confidence: 99%