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Weaning Patients from Mechanical Ventilation Using Gastric pH
- Z. Mohsenifar, MD;
- Spencer K. Koerner, MD; and
- Michael I. Lewis, MD
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IN RESPONSE:
Dr. Rochester raises several interesting questions and makes many insightful comments. Gastric PCO2 is the main determinant of gastric intramural pH. As we stated [1], a rising gastric PCO2 would have predicted 9 of 11 weaning failures and an elevated baseline gastric PCO2 would have predicted the remaining 2 failures. Independent of weaning, hypotension or low cardiac states would be expected to be detrimental to splanchnic blood flow, which would eventually result in a rise in gastric CO2. Dead space in the nasogastric tube and bicarbonate flux are possible sources of error in measuring real-time gastric PCO2.
We believe that the blood flow demanded by the respiratory pump to support the excessive work of breathing during weaning trials was primarily responsible for the redistribution of blood flow from the splanchnic bed. Such diversion can occur in states other than hypotension or low cardiac output. In an animal model of oleic acid-induced pulmonary edema, Magder and colleagues [2] reported significantly increased respiratory muscle blood flow, coupled with a reduction in splanchnic blood flow without a significant decrease in blood pressure. In support of our hypothesis, three patients who failed weaning trials had restoration of gastric intramural pH to normal when assisted mechanical ventilation was resumed.
We will respond to Dr. Tobin's major points: We designed our study to investigate the utility of gastric intramural pH in predicting weaning success or failure and clearly stated that our protocol differed from Yang and Tobin's [3]. Of interest, Lee and colleagues [4] found the ratio of frequency/tidal volume not to be highly predictive using their protocol.
As stated [1], we used a 7200 A ventilator (Puritan-Bennett, Carlsbad, California), which measures BTPS-corrected tidal volume using an eight-breath running average. All patients received the same FIO2 as that was provided by assisted mechanical ventilation.
Nathan and colleagues [5] found an overcompensation of pressure support related to upper airway obstruction and increased work of breathing after extubation. The level of pressure support (7 to 8 cm H2O), calculated based on the product of airway resistance and peak spontaneous flow rate, has been reported to overcome the added respiratory work resulting from an endotracheal tube and circuit resistance [6].
Patients were managed in a standard way by physicians blinded to the results of gastric intramural pH and gastric PCO2 to prevent any bias. Of importance, however, they showed a high false-positive rate (even in Yang and Tobin's report), which unfortunately results in failed extubations.
Z. Mohsenifar, MD
Spencer K. Koerner, MD
Michael I. Lewis, MD
Cedars-Sinai Medical Center; Los Angeles, CA 90048
The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:
•Include no more than 300 words of text, three authors, and five references
•Type with double-spacing
•Send three copies of the letter, an authors' form signed by all authors, and a cover letter describing any conflicts of interest related to the contents of the letter.
Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned.
Annals welcomes electronically submitted letters.
- Copyright ©2004 by the American College of Physicians
