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Revisiting Alveolar Hypoventilation: Effect of Methadone on Ventilation in a Patient With Chronic Obstructive Pulmonary Disease FREE TO VIEW

Benjamin Wu, MD; Shawn Cohen, BA; Natoushka Trenard, MD; Gregory Mints, MD; Roberta Goldring, MD; Kenneth Berger, MD
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New York University Medical Center, New York City, NY

Chest. 2014;146(4_MeetingAbstracts):329A. doi:10.1378/chest.1991935
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SESSION TITLE: Miscellaneous Case Report Posters I

SESSION TYPE: Affiliate Case Report Poster

PRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PM

INTRODUCTION: A case report of a patient with severe lung disease on methadone with chronic hypercapnia. Specific mechanism for chronic hypercapnia is explored with spirometry, ventilation awake and asleep, and CO2 response.

CASE PRESENTATION: A 68 year old man with a history of hypertension, tobacco use, methadone maintenance, presented with chronic hypercapnia (pH 7.43, PCO2 55mmHg, CO2 30 mmol/L). He had acute dyspnea, cough and wheezing. Chest radiograph was compatible with emphysema. Spirometry confirmed obstructive dysfunction with FEV1 = 0.63 liter (32% predicted) and FEV1/FVC = 32%. Resting ventilation was elevated at 11.7 liter/minute with an elevated dead space fraction (VD/VT = 56%). Sleep evaluation revealed multiple central apneic events. He was treated with albuterol and prednisone, and his methadone was discontinued. Thirty-six hours after methadone discontinuation the hypercapnia resolved (pH 7.41, PaCO2 37 mmHg, CO2 23 mmol/L). Repeat evaluation revealed improved FEV1 = 1.33 liter with severe persistent obstruction (FEV1/FVC = 45%) and unchanged dead space fraction (VD/VT = 53%). A repeat sleep study showed reversal of his central sleep apnea. CO2 response test revealed a normal ventilation slope. Based on these data, patient was transitioned to Suboxone, a partial opioid μ-receptor agonist with potential for less respiratory suppression. Repeat blood gas remained normal (pH 7.42, PaCO2 36, CO2 23).

DISCUSSION: This case describes the evaluation of a patient with chronic hypercapnia from multiple potential etiologies. Testing revealed obstructive lung disease with increased dead space consistent with COPD. Despite minimal improvement in FEV1 after therapy, there was no change in the physiologic dead space. Although minute ventilation was elevated during wakefulness, sleep study revealed central apnea compatible with ventilatory depression. Despite the persistence of severe lung disease, the patient was able to achieve eucapnia and remained eucapnic when Suboxone was substituted for Methadone.

CONCLUSIONS: Assessment of ventilation both during wakefulness and during sleep uncovered mechanisms for hypoventilation related to methadone use that provided the basis for therapy in a patient with severe lung disease. Understanding the pathophysiology of hypercapnia is required to determine appropriate therapy. Suboxone may be an alternative therapy in patients with chronic hypercapnia.

Reference #1: Marks CE, Jr., Goldring RM. Chronic hypercapnia during methadone maintenance. Am Rev Respir Dis. 1973;108(5):1088-1093.

DISCLOSURE: The following authors have nothing to disclose: Benjamin Wu, Shawn Cohen, Natoushka Trenard, Gregory Mints, Roberta Goldring, Kenneth Berger

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