Effects of rapid permissive hypercapnia on hemodynamics, gas exchange, and oxygen transport and consumption during mechanical ventilation for the acute respiratory distress syndrome.
Details
Serval ID
serval:BIB_8886D6F1F1A5
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Effects of rapid permissive hypercapnia on hemodynamics, gas exchange, and oxygen transport and consumption during mechanical ventilation for the acute respiratory distress syndrome.
Journal
Intensive Care Medicine
ISSN
0342-4642 (Print)
ISSN-L
0342-4642
Publication state
Published
Issued date
1996
Peer-reviewed
Oui
Volume
22
Number
3
Pages
182-191
Language
english
Notes
Publication types: Clinical Trial ; Journal ArticlePublication Status: ppublish
Abstract
OBJECTIVE: To measure the effects of rapid permissive hypercapnia on hemodynamics and gas exchange in patients with acute respiratory distress syndrome (ARDS).
DESIGN: Prospective study.
SETTING: 18-bed, medical intensive care unit, university hospital.
PATIENTS: 11 mechanically ventilated ARDS patients.
INTERVENTION: Patients were sedated and ventilated in the controlled mode. Hypercapnia was induced over a 30-60 min period by decreasing tidal volume until pH decreased to 7.2 and/or P50 increased by 7.5 mmHg. Settings were then maintained for 2 h.
RESULTS: Minute ventilation was reduced from 13.5 +/- 6.1 to 8.2 +/- 4.1 l/min (mean +/- SD), PaCO2 increased (40.3 +/- 6.6 to 59.3 +/- 7.2 mmHg), pH decreased (7.40 +/- 0.05 to 7.26 +/- 0.05), and P50 increased (26.3 +/- 2.02 to 31.1 +/- 2.2 mmHg) (p < 0.05). Systemic vascular resistance decreased (865 +/- 454 to 648 +/- 265 dyne.s.cm-5, and cardiac index (CI) increased (4 +/- 2.4 to 4.7 +/- 2.4 l/min/m2) (p < 0.05). Mean systemic arterial pressure was unchanged. Pulmonary vascular resistance was unmodified, and mean pulmonary artery pressure (MPAP) increased (29 +/- 5 to 32 +/- 6 mmHg, p < 0.05). PaO2 remained unchanged, while saturation decreased (93 +/- 3 to 90 +/- 3%, p < 0.05), requiring an increase in FIO2 from 0.56 to 0.64 in order to maintain an SaO2 > 90%. PvO2 increased (36.5 +/- 5.7 to 43.2 +/- 6.1 mmHg, p < 0.05), while saturation was unmodified. The arteriovenous O2 content difference was unaltered. Oxygen transport (DO2) increased (545 +/- 240 to 621 +/- 274 ml/min/m2, p < 0.05), while the O2 consumption and extraction ratio did not change significantly. Venous admixture (Qva/Qt) increased (26.3 +/- 12.3 to 32.8 +/- 13.2, p < 0.05).
CONCLUSIONS: These data indicate that acute hypercapnia increases DO2 and O2 off-loading capacity in ARDS patients with normal plasma lactate, without increasing O2 extraction. Whether this would be beneficial in patients with elevated lactate levels, indicating tissue hypoxia, remains to be determined. Furthermore, even though hypercapnia was well tolerated, the increase in Qva/Qt, CI, and MPAP should prompt caution in patients with severe hypoxemia, as well as in those with depressed cardiac function and/or severe pulmonary hypertension.
DESIGN: Prospective study.
SETTING: 18-bed, medical intensive care unit, university hospital.
PATIENTS: 11 mechanically ventilated ARDS patients.
INTERVENTION: Patients were sedated and ventilated in the controlled mode. Hypercapnia was induced over a 30-60 min period by decreasing tidal volume until pH decreased to 7.2 and/or P50 increased by 7.5 mmHg. Settings were then maintained for 2 h.
RESULTS: Minute ventilation was reduced from 13.5 +/- 6.1 to 8.2 +/- 4.1 l/min (mean +/- SD), PaCO2 increased (40.3 +/- 6.6 to 59.3 +/- 7.2 mmHg), pH decreased (7.40 +/- 0.05 to 7.26 +/- 0.05), and P50 increased (26.3 +/- 2.02 to 31.1 +/- 2.2 mmHg) (p < 0.05). Systemic vascular resistance decreased (865 +/- 454 to 648 +/- 265 dyne.s.cm-5, and cardiac index (CI) increased (4 +/- 2.4 to 4.7 +/- 2.4 l/min/m2) (p < 0.05). Mean systemic arterial pressure was unchanged. Pulmonary vascular resistance was unmodified, and mean pulmonary artery pressure (MPAP) increased (29 +/- 5 to 32 +/- 6 mmHg, p < 0.05). PaO2 remained unchanged, while saturation decreased (93 +/- 3 to 90 +/- 3%, p < 0.05), requiring an increase in FIO2 from 0.56 to 0.64 in order to maintain an SaO2 > 90%. PvO2 increased (36.5 +/- 5.7 to 43.2 +/- 6.1 mmHg, p < 0.05), while saturation was unmodified. The arteriovenous O2 content difference was unaltered. Oxygen transport (DO2) increased (545 +/- 240 to 621 +/- 274 ml/min/m2, p < 0.05), while the O2 consumption and extraction ratio did not change significantly. Venous admixture (Qva/Qt) increased (26.3 +/- 12.3 to 32.8 +/- 13.2, p < 0.05).
CONCLUSIONS: These data indicate that acute hypercapnia increases DO2 and O2 off-loading capacity in ARDS patients with normal plasma lactate, without increasing O2 extraction. Whether this would be beneficial in patients with elevated lactate levels, indicating tissue hypoxia, remains to be determined. Furthermore, even though hypercapnia was well tolerated, the increase in Qva/Qt, CI, and MPAP should prompt caution in patients with severe hypoxemia, as well as in those with depressed cardiac function and/or severe pulmonary hypertension.
Keywords
Adult, Aged, Aged, 80 and over, Blood Gas Analysis, Female, Hemodynamics, Humans, Hypercapnia/etiology, Hypercapnia/metabolism, Male, Middle Aged, Oxygen Consumption, Prospective Studies, Pulmonary Gas Exchange, Respiration, Artificial/adverse effects, Respiration, Artificial/methods, Respiratory Distress Syndrome, Adult/physiopathology, Respiratory Distress Syndrome, Adult/therapy
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Create date
01/07/2013 14:15
Last modification date
20/08/2019 14:47
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