Hypoxia in a Morbidly Obese Patient

Case Study

The bedside nurse initiated a rapid response event for a patient who went to sleep earlier in the evening and was unable to be aroused by verbal commands. The nurse noted his oxygen saturation drop as low as 78% and prolonged episodes of apnea lasting up to 20 s. On prompt arrival of the rapid response team, the patient was given a sternal rub, to which he responded by briefly opening his eyes but promptly went back to sleep. He was a 40-year-old obese male with a known history of heart failure with a preserved ejection fraction, hypertension, coronary artery disease. He was admitted earlier for altered mental status. On admission, it was noted that the patient’s arterial blood gas (ABG) showed a pH of 7.28, PCO 2 of 69 mmHg, PO 2 of 72 mmHg, and bicarbonate level of 35 meq/L. He was not on any diuretics.

Vital signs

  • Temperature: 98.2 °F, axillaryBlood Pressure: 155/97 mmHg Heart Rate: 75 beats per min (bpm) – regular rhythm

  • Respiratory Rate: 12 breaths per min

  • Pulse Oximetry: 78% on room air, placed on a 15 L/min non-rebreather up to 94%.

Focused physical examination

A quick exam showed a morbidly obese male with a thick neck who was extremely somnolent. Pertinent findings on the exam included intermittent loud snoring, choking during sleep, apneic episodes, fatigue, and impaired concentration. His heart sounds were normal, and lungs were clear to auscultation with diminished breath sounds bilaterally. His abdomen was distended but had no rigidity or guarding, bowel sounds heard. Of note, his pupils were equal round and reactive.


A cardiac monitor and pads were attached to the patient. 15 L of oxygen was administered through a non-rebreather mask which improved oxygen saturation to 96%. Stat ABG was ordered, which showed pH 7.18, pO 2 85 mmHg, pCO 2 90 mmHg, lactate 2.9, SpO 2 96% on 15 L non-rebreather. A BMP drawn at the same time showed a bicarbonate level of 26. The patient started to wake up slightly and was protecting his airway appropriately; thus, a decision was made to try non-invasive bi-level positive airway pressure (BiPAP) ventilation for him. BiPAP was started at 16 cm H 2 O IPAP, 6 cm H 2 O EPAP, and 100% FiO 2 to manage the acute on chronic respiratory acidosis, with a goal to be transitioned to continuous positive airway pressure (CPAP) overnight. Stat chest X-ray was obtained, which was negative for any acute pulmonary pathologic condition. A pulmonary consult was requested to evaluate the patient for formal sleep testing and further management. The patient was transferred to the intensive care unit (ICU) for closer monitoring and escalation of airway management if needed.

Final Diagnosis

Obesity hypoventilation syndrome with acute decompensation.

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