Pico: Hypoxia

Tamara Waner

Systematic Review Assignment

I located this article via EBSCO host research database with supporting articles via CINAL.

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

PICO format

         The population involved in this study was patients with COPD who were in acute of chronic respiratory failure. The goal was to identify if higher delivery of oxygen caused a decrease in respiratory drive and increased hypercarbia, a condition of abnormally elevated carbon dioxide levels. They compared COPD patients who required additional ventilation for both a loss of respiratory drive and hypercarbia. The results indicated that neither a decrease in respiratory drive or hypercarbia occurred, but rather providing high oxygen levels provided a beneficial rest period, improved muscle fatigue and improved outcomes (Teixeira, Savi & Tonietto, 2014).

Introduce, analyze and discuss all relevant aspects

Patients with COPD work at a mechanical disadvantage compared to patients without the disease. Chronic inflammatory changes lead to destructive changes in the airways and pulmonary vasculature. The thickening of smooth muscle and connective tissues of the airways leads to scaring a fibrosis which effect gas exchange and progressively limit airflow (Calverley, 2005) . The loss of lung elasticity contributes to hyperinflation and displaces the diaphragm into a flattened position expanding the chest into the stereotypical barrel shape. Exhalation is active, contributing to the high work load of breathing. Eventually the effort to maintain carbon dioxide levels within normal limits fails and the patient retains carbon dioxide. Kidney compensation occurs by retaining bicarbonate to normalize PH (Calverley, 2005)  .

        Previously, the belief was that the chronically elevated levels of carbon dioxide blunted the normal response of chemoreceptors, resulting in the drive to breathe becoming reliant on oxygen chemoreceptors to respond to low oxygen levels, a mechanism called hypoxic drive (Calverley, 2005). The assumption was that the high delivery of oxygen obliterated the drive to breathe in patients with COPD. Hypoxic drive is a real phenomenon; however it is responsible for only about 10% of the total drive to breathe (Reade, 2007).  

        In patients with COPD, the provision of oxygen may lead to an increase in carbon dioxide levels, apnea and other adverse outcomes. However, the elevation of carbon dioxide in not primarily due to hypoxic drive, three other mechanisms also play a role. These are the Haldane effect, hypoxic vasoconstriction and a decrease in minute ventilation (Calverley, 2005).

        The physiological mechanism associated with the ability of hemoglobin to carry oxygen and carbon dioxide in known as the Haldane effect (Calverley, 2005) . As hemoglobin becomes de-saturated the capacity to bond to carbon dioxide increases and so does its level in plasma. Patients with COPD cannot increase minute ventilation and blow off carbon dioxide. The result is respiratory acidosis.

        Hypoxic vasoconstriction is a normal response to a decrease in oxygen levels. It is designed to move blood flow from inadequate alveoli to those that are open. In COPD patients this does not occur when oxygen is administered.

        The third mechanism is a decrease in minute ventilation. COPD patients decrease their minute ventilation as a reaction to increased carbon dioxide levels and dead space, further limiting inspiratory reserve. Although does not occur in all COPD patients in acute respiratory failure, it does account for approximately a 20% decrease in minute ventilation and increase in carbon dioxide levels (Calverley, 2005).

        Hypoxemia in patients with COPD has many adverse effects. These include cor pulmonale, poor nutritional status, cardiac modulation and poor wound healing (Barbera,1997) . However, failure to administer oxygen to treat hypoxemia puts the patient at greater risk. Oxygen should be administered to increase oxygen saturation above 90% or a PaO2 of 60-70mm Hg.  This therapy improves survival by providing a reversal of respiratory muscle fatigue and improving oxygenation (Teixeira et al, 2014).  

The research design

         This was an experimental prospective study set in an 18-bed medical-ICU in a university teaching hospital involving CO2-retaining COPD patients recovering from acute respiratory failure (Teixeira et al, 2014). 

The subjects were 17 COPD subjects admitted to the medical-ICU in a primary who required non-invasive ventilation during treatment of acute respiratory failure. These subjects were all chronic CO2-retaining COPD patients, as defined by a resting PaCO2 of ≥45mmHg, and had a previous hospitalization due to COPD.  The diagnosis of COPD was based on history, physical examination, chest radiograph, and previous pulmonary function tests. The subjects had all received a period of ventilator support with bilevel pressure ventilator (BiPAP) delivered by a full face mask during at least 24 hours, until stabilization (Teixeira et al, 2014). 

The study was conducted only after stabilization, and they were judged to be of no risk for intubation. Before start the experiment, the noninvasive ventilator was calibrated using specific equipment, leakage of ventilator circuit was tested to calibrate the exhalation port and the full face mask was positioned to permit no  leak up to 20L/min. Bilevel pressure ventilators were set in the spontaneous/timed mode, with a positive end-expiratory pressure (PEEP) ≥5 cm H2O, and peak inspiratory pressure(PIP) ≥10cmH2O, targeting and guarantying a tidal volume of ≥8mL/kg. The FIO2was adjusted to maintain SpO2 ≥90%. Subjects were excluded if they or their family refused to give consent, if they were uncooperative, needed of intubation or requiring mechanical ventilation (Teixeira et al, 2014).

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