Causes of hypercarbia with oxygen therapy in patients with chronic obstructive pulmonary disease

Hanson, C. William; Marshall, Bryan E.; Frasch, H. Frederick; Marshall, Carol Lynn

doi:10.1097/00003246-199601000-00007

Cited by 79 publications

(30 citation statements)

References 10 publications

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“…[10][11][12][13] The Haldane effect refers to decreased carriage of CO 2 by oxyhemoglobin, and to increased CO 2 release in the presence of oxygen. 11 Hypoxic pulmonary vasoconstriction optimizes the distribution of ventilation/perfusion ratios, and minimizes the physiologic deadspace, improving the efficiency of CO 2 exchange at low FIO 2 .…”

Section: A B Cmentioning

confidence: 99%

Non-invasive ventilation corrects alveolar hypoventilation during spinal anesthesia

Ferrandière¹,

Hazouard²,

Ayoub³

et al. 2006

Can J Anesth/J Can Anesth

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Purpose: To document and explain the beneficial effects of non-invasive ventilation in correcting hypoxemia and hypoventilation in severe chronic obstructive pulmonary disease, during spinal anesthesia in the lithotomy position. Clinical features:A morbidly obese patient with severe chronic obstructive pulmonary disease underwent prostate surgery in the lithotomy position under spinal anesthesia. Hypoxemia was encountered during surgery, and a profound decrease of forced vital capacity associated with alveolar hypoventilation and ventilation/perfusion mismatching were observed. In the operating room, an M-mode sonographic study of the right diaphragm was performed, which confirmed that after spinal anesthesia and assuming the lithotomy position, there was a large decrease (-30%) in diaphragmatic excursion. Hypoxemia and alveolar hypoventilation were successfully treated with non-invasive positive pressure ventilation. Conclusions:Intraoperative application of non-invasive positive pressure ventilation improved diaphragmatic excursion and overall respiratory function, and reduced clinical discomfort in this patient. A N obese patient suffering from severe chronic obstructive pulmonary disease (COPD) utilizing his "hypoxic drive", underwent surgery in the lithotomy position (LP) under spinal anesthesia (SA). The respiratory consequences of both the anesthetic technique and patient positioning were studied. Impending hypoxemic respiratory failure, potentially requiring endotracheal intubation and controlled ventilation, was successfully treated with non-invasive positive-pressure ventilation (NiPPV). In accordance with the Institutional Review Board, all details of this procedure were discussed with the patient, and his written informed consent was obtained for the procedure and the publication of his personal health information. Objectif Case reportA 58-yr-old obese man (105 kg, body mass index 34 kg·m -2 ) with severe COPD was scheduled for transurethral resection of the prostate under SA. He was a heavy smoker with a 40-pack-yr history of cigarette usage and consequent severe respiratory disability. During four previous surgeries, supplemental oxygen administration had produced a hypoventilatory

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Section: A B Cmentioning

confidence: 99%

Non-invasive ventilation corrects alveolar hypoventilation during spinal anesthesia

Ferrandière¹,

Hazouard²,

Ayoub³

et al. 2006

Can J Anesth/J Can Anesth

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“…A second potential explanation for the arterial hypercapnia associated with supplemental oxygen administration in this patient group is worsening V /Q mismatch resulting in a significant increase in the dead space-to-Vt ratio. 86,87 V /Q mismatch occurring under these circumstances may be explained as follows. Before supplemental oxygen use, areas of local alveolar hypoxia produce pulmonary hypoxic vasoconstriction, thereby diverting the flow of CO 2 -rich blood from poorly ventilated to better ventilated lung segments.…”

Section: Copdmentioning

confidence: 99%

The Control of Breathing in Clinical Practice

Caruana-Montaldo¹,

Gleeson

Zwillich

2000

Chest

128

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The control of breathing results from a complex interaction involving the respiratory centers, which feed signals to a central control mechanism that, in turn, provides output to the effector muscles. In this review, we describe the individual elements of this system, and what is known about their function in man. We outline clinically relevant aspects of the integration of human ventilatory control system, and describe altered function in response to special circumstances, disorders, and medications. We emphasize the clinical relevance of this topic by employing case presentations of active patients from our practice.(CHEST 2000; 117:205-225)Key words: carotid body; chemoreceptors; control of ventilation; pulmonary receptors Abbreviations: CPAP ϭ continuous positive airway pressure; CSF ϭ cerebrospinal fluid; CSR ϭ Cheyne-Stokes respiration; DRG ϭ dorsal respiratory group; [H ϩ ] ϭ hydrogen ion concentration; HCO 3 Ϫ ϭ bicarbonate; MVV ϭ maximal voluntary ventilation; OSA ϭ obstructive sleep apnea; pHa ϭ arterial pH; PIIA ϭ postinspiration inspiratory activity; PImax ϭ maximal inspiratory pressure; RAR ϭ rapidly adapting receptor; REM ϭ rapid eye movement; Sao 2 ϭ arterial oxygen saturation; SAR ϭ slowly adapting receptor; VC ϭ vital capacity; V e ϭ minute ventilation; V o 2 ϭ oxygen uptake; V /Q ϭ ventilation/perfusion; VRG ϭ ventral respiratory group; Vt ϭ tidal volume; WOB ϭ work of breathing

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“…In agreement, Hanson et al 24 and Dick et al 25 concluded that changes in physiologic dead space are sufficient to account for the hypercapnia.…”

Section: Discussionmentioning

confidence: 61%

Influence of F_IO₂on P_aCO₂During Noninvasive Ventilation in Patients With COPD

et al. 2013

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BACKGROUND:The administration of a high F IO 2 to COPD patients breathing spontaneously may result in hypercapnia, due to reversal of preexisting regional hypoxic pulmonary vasoconstriction, resulting in a greater dead space. Arterial blood gas trends have not been reported in these patients. In a 31-bed medical ICU in a teaching hospital we prospectively investigated the response of 17 CO 2 -retaining COPD patients, after acute respiratory crisis stabilization with noninvasive ventilation, to an F IO 2 of 1.0 for 40 min, after having been noninvasively ventilated with an F IO 2 of < 0.50 for 40 min. RESULTS: The mean ؎ SD baseline findings were: P aO 2 101.4 ؎ 21.7 mm Hg, P aCO 2 52.6 ؎ 10.4 mm Hg, breathing frequency 17.8 ؎ 3.7 breaths/min, tidal volume 601 ؎ 8 mL, and Glasgow coma score of 14.8 ؎ 0.3. P aO 2 significantly increased (P < .001) when F IO 2 was increased to 1.0, but there was no significant change in P aCO 2 , breathing frequency, tidal volume, or Glasgow coma score. CONCLUSIONS: During noninvasive ventilation with an F IO 2 sufficient to maintain a normal P aO 2 , a further increase in F IO 2 did not increase P aCO 2 in our CO 2 -retaining COPD patients.

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Causes of hypercarbia with oxygen therapy in patients with chronic obstructive pulmonary disease

Abstract: Changes in physiologic deadspace are sufficient to account for the hypercarbia developed by patients with acute exacerbations of COPD when treated with supplemental oxygen.

Cited by 79 publications

References 10 publications

Non-invasive ventilation corrects alveolar hypoventilation during spinal anesthesia

Non-invasive ventilation corrects alveolar hypoventilation during spinal anesthesia

The Control of Breathing in Clinical Practice

Influence of F_IO₂on P_aCO₂During Noninvasive Ventilation in Patients With COPD

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Causes of hypercarbia with oxygen therapy in patients with chronic obstructive pulmonary disease

Abstract: Changes in physiologic deadspace are sufficient to account for the hypercarbia developed by patients with acute exacerbations of COPD when treated with supplemental oxygen.

Cited by 79 publications

References 10 publications

Non-invasive ventilation corrects alveolar hypoventilation during spinal anesthesia

Non-invasive ventilation corrects alveolar hypoventilation during spinal anesthesia

The Control of Breathing in Clinical Practice

Influence of FIO2on PaCO2During Noninvasive Ventilation in Patients With COPD

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Product

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Influence of F_IO₂on P_aCO₂During Noninvasive Ventilation in Patients With COPD