The Controller: Directing the Orchestra

Ventilatory Control in Acute on Chronic Respiratory Failure

One definition of respiratory failure is the inability to breathe in a manner that supports the basic metabolic needs of the body. If alveolar ventilation is not adequate for the carbon dioxide production of the body, the individual will have an elevated P_aCO₂. If the condition that leads to respiratory failure is chronic and irreversible, then the patient may experience chronic hypercapnia. Acutely, hypercapnia leads to an increase in ventilation as a result of the stimulation of the chemoreceptors, primarily the central chemoreceptor. Within a few days, however, the pH of the blood and the fluid bathing the brain approaches normal levels, and the ventilation comes back down. Because of the increased levels of buffers now present in the blood and brain, further increases in P_aCO₂ have an attenuated effect on ventilation.

Patients with chronic respiratory failure often have problems with hypoxemia as well, with a P_aO₂ that may be near 60 mm Hg. In the clinical setting in which the P_aO₂ decreases acutely (and the P_aCO₂ may increase above the baseline chronic levels) because of a respiratory infection or some other cardiopulmonary process, we describe the situation as acute on chronic respiratory failure. The classic teaching about such patients (and you will likely encounter physicians who will tell you this is true) is that because of the chronic hypercapnia and the resulting buffering of the blood and brain, these patients depend on their “hypoxic drive to breathe.” The classic teaching also suggests that if you give such a patient supplemental oxygen during an acute problem such as bronchitis or pneumonia, “they will stop breathing” because the stimulation of the peripheral chemoreceptors resulting from hypoxemia will have been relieved. Unfortunately, this teaching, which developed as an explanation for the increase in P_aCO₂ observed with the administration of supplemental oxygen in these patients, is wrong. As you now realize, the controller is more complicated than merely responding to hypoxemia or hypercapnia.

Michel Aubier, in a very informative study performed in 1980, examined patients with chronic respiratory failure and chronic hypercapnia who presented with an acute respiratory illness and acute hypoxia (M. Aubier et al., American Review of Respiratory Disease, 1980;122:747). Dr. Aubier and his colleagues asked these patients to inhale gas with an FIO₂ of 1.0, or 100% oxygen. On average, the P_aCO₂ increased by approximately 20 mm Hg with the supplemental oxygen, but these patients did not stop breathing! Why did the P_aCO₂ increase this much?

In this and subsequent studies, the data showed that the increase in P_aCO₂ with supplemental oxygen could be attributed to three factors. First, there is a small decrease in ventilation as the hypoxemia is relieved. After 15 minutes on the supplemental oxygen, the ventilation was approximately 7% lower than before the administration of oxygen. Second, ventilation/perfusion mismatch is worsened by the administration of oxygen. Recall that poorly ventilated alveoli have a low P_aO₂, which leads to hypoxic pulmonary vasoconstriction of the pulmonary arterioles leading to those alveoli. Blood is sent to better-ventilated alveoli. With the administration of supplemental oxygen, however, oxygen diffuses into the poorly ventilated alveoli, P_AO₂ increases, and the hypoxic pulmonary vasoconstriction is reversed. More blood now goes to what are still poorly ventilated alveoli, and P_aCO₂ increases. This factor accounts for approximately 40% of the acute elevation in P_aCO₂ seen in these patients. The third factor responsible for the increase in P_aCO₂ in these patients is the Haldane effect (see Fig. 5-7). With the administration of oxygen and the increase in P_aO₂, carbon dioxide is displaced from hemoglobin and enters the liquid portion of the blood, resulting in a higher P_aCO₂ (Quick Check 6-1).

A 20-mm Hg increase in the P_aCO₂ is not good for the patient because it leads to acute acidosis and, depending on the original P_aCO₂, may bring the level of hypercapnia near the point where it will have an anesthetic effect on the brain. However, acute hypoxemia can be a life-threatening problem and must be treated with supplemental oxygen. Use the lowest amount of oxygen that is necessary to raise the P_aO₂ to approximately 60 mm Hg (oxygen saturation of 90%), and remember that it will not cause the patient to stop breathing.