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.

Interventions

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.

Obesity Hypoventilation Syndrome

Obesity Hypoventilation Syndrome (OHS) is defined as the presence of daytime alveolar hypoventilation with arterial paCO ₂ >45 mmHg and paO ₂ <70 mmHg in an obese individual with body mass index (BMI) >30 kg/m ² , which cannot be attributed to any other mechanical, neuromuscular, or metabolic conditions associated with alveolar hypoventilation. OHS is associated with increased cardiovascular morbidity and mortality, which might be secondary to changes in respiratory dynamics and the contribution of obesity to other systemic illnesses. Consequently, early detection and treatment are crucial to minimizing these adverse effects.

Pathophysiology

Patients with increased body weight (especially with BMI >30 kg/m ² ) experience increased demands on the respiratory system to maintain adequate ventilation. When considering respiratory dynamics, specific ventilation challenges associated with obese patients include a decrease in total lung capacity (TLC), functional residual capacity (FRC), and vital capacity (VC), as well as increases in pleural pressure and upper and lower airway resistance. There are compensatory mechanisms triggered to maintain adequate ventilation in obesity, but with rising BMI, these mechanisms can fail and give way to OHS. Although 90% of all patients with OHS have some degree of obstructive sleep apnea (OSA), at least 10% of OHS patients have no obstructive symptoms and have pure sleep hypoventilation syndrome.

Although the complete pathophysiology of OHS is not known, several factors are known to produce the symptoms of this disease; some of these are mentioned below:

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Sleep-disordered breathing, including apneic/hypopniec episodes, altered respiratory mechanics, and impaired ventilator control.
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Reduced clearance of carbon dioxide during sleep.
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Hypoxemia during sleep.
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Impaired pulmonary mechanics, including ventilation/perfusion mismatching, especially in lower lobes and decreased respiratory muscle strength.
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Impaired ventilatory control because of reduced neural drive, reduced ventilatory responsiveness, carbon dioxide overproduction, and leptin resistance.

Some risk factors that contribute to the development of OHS are:

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Significant increase in body weight in a small span of time
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Considerable increase in waist to hip ratio (leading to central obesity)
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Reduced lung function because of obesity
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Reduced respiratory muscles strength
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Presence of OSA

Clinical manifestations of OHS are similar to signs and symptoms of OSA, as 90% of patients with OHS have OSA. Clinical manifestations of OSA are given in Table 30.1 . Some patients with OHS might present with acute on chronic respiratory failure, which might be triggered by other systemic illnesses leading to excess burden of disease on the body and failure of some compensatory mechanisms which were previously maintaining adequate ventilation.

Table 30.1

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