Case 13 – A 70-year-old man with narcotic overdose

A 70-year-old man with a history of chronic obstructive pulmonary disease (COPD), congestive heart failure (CHF), myasthenia gravis, and chronic back pain is recovering after a motor vehicle accident. The patient fractured both tibiae and multiple ribs, but remains without serious internal organ injury. His problem during this hospitalization has been pain control. He has recently been transitioned to oral oxycodone, but morphine injections are still being used for breakthrough pain. At the 4 a.m. vital sign check, the night nurse notes the patient is unarousable. He has a respiratory rate of 5/min and an oxygen saturation of 80% by pulse oximetry. His heart rate is 80/min and blood pressure is 130/80 mm Hg. He has pinpoint pupils, a normal cardiac examination, and clear lung fields. Arterial blood gas analysis shows a pH of 7.02, partial pressure of carbon dioxide of 90 mm Hg, partial pressure of oxygen of 45 mm Hg, and bicarbonate of 15 mEq/L. Administration of 100% oxygen via a non-rebreather mask raises the oxygen saturation to 95%. Review of the medication logs shows that the patient accidentally got two morphine boluses in addition to his maximum oxycodone dosage.

What is the most likely diagnosis?

Acute hypercarbic respiratory failure secondary to narcotic overdose. Opiates depress the central drive to breathe, first causing hypercarbia and then hypoxia. Some of the other causes suggested by the patient’s history include COPD or asthma exacerbation, flash pulmonary edema secondary to CHF, or respiratory muscle weakness due to myasthenia gravis. However, the clinical picture of decreased mental status, depressed respiratory rate, and overmedication suggest narcotic overdose.

How is the diagnosis approached?

The first step should be an arterial blood gas analysis. This will differentiate between hypercarbic or hypoxemic respiratory failure. Pure inhaled oxygen should also be administered. If this improves oxygenation, the pathology is due to ventilation/perfusion (V/Q) mismatch. If oxygenation does not improve, a shunt physiology is suggested.

How is the A-a gradient calculated and what is its significance?

The A-a gradient is the difference between alveolar and arterial oxygenation. It is calculated as:

[(PATM ? 47) × FIO2] ? [(PAO2 ? PACO2 / 0.8)]

A normal A-a gradient is 5-10 mm Hg. An increased gradient indicates a problem getting alveolar oxygen into the bloodstream. Hypoventilation alone results in hypoxemia with a normal A-a gradient.

What other conditions should be included in the differential diagnosis?

The differential list for acute respiratory failure is very broad and can be divided into two categories: hypercarbic and hypoxemic. Hypercarbia is caused by decreased ventilation, due to loss of central drive (secondary to toxins or brain stem injury) or respiratory muscle failure (due to myasthenia gravis, Guillain-Barré syndrome, or botulism). Hypoxemia that corrects with oxygen therapy can be due to V/Q mismatch, often due to intrinsic lung disease such as COPD, asthma, interstitial lung disease, or a pulmonary embolus. Hypoxemia due to shunt physiology can be the result of a true vascular or intracardiac shunt; severe alveolar filling as seen in pneumonia, pulmonary edema, or hemothorax; or alveolar collapse as seen in COPD or asthma.

What is the most appropriate management for this patient?

The underlying disease process must be addressed; in this case, naloxone should be given to reverse the effects of the narcotics. Oxygenation can be improved by increasing FIO2 and adding positive end-expiratory pressure in a mechanically ventilated patient. Hypercarbia is controlled by changing minute ventilation (increasing respiratory rate and/or tidal volume).

By Melissa Rosenstein, MD, Resident in Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco Medical Center; in association with Le TT, Schabelman E, Shivaram A, and Klein J, eds: First Aid Cases for the USMLE Step 2 CK. New York: McGraw-Hill, 2007.