Pico: Hypoxia

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Demographic and background information included age, gender, weight,

Primary disease process, predicted risks of death and baseline respiratory function were obtained. The study involved increasing the baseline FIO2 up to 100% oxygen. No other parameters were altered. Following 40 minutes at an FIO2 of 1.0, the VT, RR, VE, ABG and SaO2 were again recorded, as well changes in mental status. The subjects were then returned to their baseline FIO2(Teixeira et al, 2014). .

All data was expressed as mean ± standard deviation for continuous variables. Differences between the baseline and FIO2 of 1.0 were analyzed with the use of paired t-test, except for Glasgow coma scale results which were analyzed with Wilcoxon signed rank test. All statistical analysis was performed by a statistician using the commercially available software SPSS 16.0. Statistical significance was set at p

In these 17 CO2-retaining COPD subjects, an increase in FIO2 from baseline to

1.0 caused a statistically significant increase in the subject's PaO2 (101.4 ± 21.7mmHg

vs. 290.5 ± 35.7mmHg; p

They considered that an increase in PaCO2 of 5 mmHg would indicate a clinically significant degree of CO2 retention when the FIO2 was increased from baseline to 1.0. The SD of the difference between the PaCO2 recordings at the two different FIO2 levels was 4mmHg. For a paired sample of 17 patients, this study has a power of 99% (Teixeira et al, 2014). .

The results support the hypothesis that increase in the FIO2 in CO2-retaining COPD subjects ventilated with non-invasive ventilation do not cause any clinically significant degree of CO2 retention.

Resources

The article lists 28 references all of which relate to the subject matter. Although some date back to 1978 they still have relevance to COPD treatments or address the pathophysiology of COPD. In text only several studies were referenced. One concluded that COPD patients following a period of mechanical ventilation can receive oxygen supplementation with retaining carbon dioxide or suffering a depression of the respiratory drive (Crossley et al,2012). There other studies were grouped and referenced as a collective group which involved authors who studied the behavior of PaCo2 levels in COPD patients ventilating spontaneously. They did state that no prior study of COPD patients involved non-invasive ventilation. There was no formal literature review included with this study.

Conclusion

The assumption has always been that in patients with COPD that oxygen therapy can and does eliminate the hypoxic drive resulting in serious complications such as hypercarbia, acidosis and death. It is true that carbon dioxide levels increase with the administration of oxygen but that increase is not due to the elimination of the hypoxic drive. Three mechanisms are responsible and were previously discussed. The results of this study support the hypothesis that increase in the FIO2 in CO2 retaining COPD subjects ventilated with NIV do not cause any clinically significant degree of CO2 retention.

Administration of controlled oxygen therapy is the single most useful treatment in COPD induced acute respiratory failure, and supplemental oxygen therapy should be administered to all hypoxemic patients who present with an acute exacerbation. The use of supplemental oxygen leads to a decrease in anaerobic metabolism and lactic acid production, an improvement in brain function, a decrease in cardiac arrhythmias and ischemia, a decrease in pulmonary hypertension and an improvement in survival. Withholding of oxygen therapy can be dangerous and lead organ failure. It is in the understanding of such evidence and carefully application such evidence in clinical practice that can improve the well-being of patients and extend life expectancies.

Although in reviewing the literature associated with this study there is ample evidence to support the use of aggressive oxygen therapy in COPD patients, it remains a reality that many still believe that hypoxic drive is the main driving factor behind respiratory failure and death such patients. It is common knowledge in nursing that you do not aggressively supplement oxygen in COPD patients for fear of respiratory arrest. Only through the education of nursing and medical professionals that such misinformation can be corrected and this type of evidence used in clinical practice to benefit patients with COPD.

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References

Crossley, D., Mcguire, G., Barrow, P., & Houston, P. (1997). Influence of inspired oxygen concentration on deadspace, respiratory drive, and PaCO sub 2 in intubated patients with chronic obstructive pulmonary disease. Critical Care Medicine, 25(9), 1522-1526. doi:10.1097/00003246-199709000-00019

Pankow, W., Lies, A., & Becker, H. (2010). Patient–ventilator interaction during noninvasive pressure-supported spontaneous respiration in patients with hypercapnic Chronic Obstructive Pulmonary Disease. Noninvasive Mechanical Ventilation, 67-71. doi:10.1007/978-3-642-11365-9_10

Makic, M., Martin, S., Burns, S., Philbrick, D., & Rauen, C. (2013). Putting evidence into nursing practice: Four traditional practices not supported by the evidence. Critical Care Nurse, 33(2), 28-42. doi:10.4037/ccn2013787

Teixeira, C., Savi, A., & Tonietto, T. (2014). Influence of FIO2 on PaCO2 during noninvasive ventilation in patients with COPD: What will be constant over time? Influence of FIO2 on PaCO2 in COPD patients with chronic CO2 retention. Respiratory Care, 59(7). doi:10.4187/respcare.03481

Calverley, P., (2005) Chronic Obstructive Pulmonary Disease, in Textbook of

Critical Care, M.P. Fink, Editor. Elsevier Sauders.

Reade, M. (2007), High inspired oxygen in hypercapnic respiratory failure. British Journal

Of Hospital Medicine (Lond). 68(7): p. 393.

Barbera, J.,(1997) Mechanisms of worsening gas exchange during acute

exacerbations of chronic obstructive pulmonary disease. European Respiratory Journal.

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