pursed lip breathing for COPD


The history, examination, and laboratory findings are most consistent with dyspnea due to dynamic hyperinflation related to his emotional distress and consequent tachypnea and increase in ventilation in the setting of severe COPD and flow limitation (choice C is correct). 

The patient has a baseline of severe COPD secondary to his long-standing smoking history. His history does not suggest that he is in the "frequent exacerbator" phenotype, and there is no evidence of an acute infection at this time with respect to change in cough or sputum. The very acute onset of his symptom also argues against an infectious cause (choice B is incorrect). The chest radiograph shows hyperinflation with expansion to 12 ribs and flat diaphragms. The heart size is normal, and there may be a bulla at the right base (Figure 2); the paucity of lung markings may raise the question of a pneumothorax, but one cannot see a definite line indicating the separation of the lung from the chest wall with air in the pleural space, and there is no shift of the mediastinum or deep sulcus sign.

In the use of steroids for COPD exacerbations, IV methylprednisolone is a common choice, although there is no demonstrated benefit relative to prednisone, which has good bioavailability (choice A is incorrect). The patient's Spo2 is adequate with supplemental oxygen via nasal cannula; there is no benefit to higher doses of oxygen in this situation and some evidence that treating patients in the ICU with high Spo2 levels may be harmful (choice D is incorrect). In addition, supplemental oxygen may worsen hypercapnia in patients with COPD primarily by worsening ventilation-perfusion mismatch owing to relief of hypoxic pulmonary vasoconstriction in poorly ventilated lung units (the Haldane effect and a small decrease in ventilatory drive also play small roles in the rise in PaCO2 with supplemental oxygen administration).

With severe COPD and flow limitation, increases in respiratory rate and tidal volume, as occur with exercise and emotional distress, will lead to dynamic hyperinflation. The increase in end-expiratory lung volume ultimately diminishes inspiratory capacity, leading to a sensation of "not being able to get a deep breath" as end-inspiratory volume approaches total lung capacity. The solution to this problem is to coach the patient to slow the respiratory rate and prolong expiratory time. Pursed lip breathing can reduce dyspnea, although the mechanism by which this occurs is not entirely known but may consist of one or more of the following: (1) prolongation of expiratory time with reduced hyperinflation; (2) stimulation of flow receptors in the mouth to give patients the sense of getting more air than they are; and (3) reduction of the negative transmural pressure of the downstream segment of the airways (toward the mouth from the equal pressure point), which may stimulate mechanoreceptors in the walls of the airways that may contribute to dyspnea. 1

Footnotes

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