Hypoxia in a Patient With Chronic Obstructive Pulmonary Disease (COPD)

Case Study

The bedside nurse initiated a rapid response event after the patient was found to be in significant respiratory distress and with oxygen saturation in the 80 s. On prompt arrival of the rapid response team, the patient was found to be a 65-year-old male with an extensive history of smoking, oxygen-dependent chronic obstructive pulmonary disease (COPD), hypertension, and heart failure with a preserved ejection fraction. The patient used 2 L/min (LPM) oxygen (O ₂ ) at baseline. He reported progressive shortness of breath and increasing sputum production in the few days before admission and had been using 4 LPM O ₂ through a nasal cannula at home. He was admitted earlier in the day after a friend found him confused at home. He was briefly trialed on bilevel positive airway pressure (BiPAP) in the emergency department (ED), which led to improved mental status, and the patient was admitted.

Vital Signs

Temperature: 100.4 °F, axillary
Blood Pressure: 155/97 mmHg
Pulse: 101 beats per min (bpm) – regular rhythm.
Respiratory Rate: 30 breaths per min
Pulse Oximetry: 83% on 6 LPM O ₂through nasal canula

Focused Physical Examination

A quick exam showed a frail, middle-aged male in respiratory distress. The patient was using accessory muscles of respiration and could not complete a sentence. The lung exam was significant for minimal breath sounds and absence of wheezing. His heart sounds were distant but unremarkable. The patient became increasingly somnolent and difficult to arouse during the evaluation. The rest of his exam was unremarkable.

Interventions

A cardiac monitor and pads were attached to the patient. Then, 15 LPM of O ₂ was administered through a non-rebreather mask which improved oxygen saturation to 96%. Stat arterial blood gas was ordered, which showed a pH of 7.28, pO ₂ of 50 mmHg on 15 LPM non-rebreather, pCO ₂ of 135 mmHg, lactate of 4.9 mmol/L, and oxygen saturation of 85%. A basic metabolic panel (BMP) drawn simultaneously showed a bicarbonate level of 26 meq/L. The patient was started on BiPAP at inspiratory pressure of 12 cm H ₂ O, expiratory pressure of 6 cm H ₂ O, and 100% FiO ₂ . A stat chest X-ray was obtained, which was negative for any acute pulmonary infiltrates ( Fig. 23.1 ). The patient was ordered nebulizer treatment with ipratropium and albuterol. No glucocorticoids were administered as the patient had already received intravenous (IV) 125 mg methylprednisolone in the ED a few hours earlier. One dose of IV azithromycin was administered, and the patient was transferred to the intensive care unit (ICU) for further care.

Final Diagnosis

Acute on chronic hypoxic and hypercapnic respiratory failure secondary to COPD exacerbation.

COPD Exacerbation and CO ₂Narcosis

COPD is a combination of two pulmonary pathologies: emphysema caused by the destruction of pulmonary parenchyma resulting in reduced surface area for gas exchange, and chronic bronchitis caused by chronic inflammation of the airways causing airflow obstruction. An exacerbation is an event characterized by an acute worsening of a patient’s symptoms beyond the variation seen on a day-to-day basis. This change should be sufficient to warrant a change in management. Among patients with COPD, the frequency of exacerbation varies with the severity of the disease. Some patients have more frequent exacerbations than others, independent of other measures of disease severity. Table 23.1 outlines some symptoms, risk factors, and diagnostic criteria for COPD exacerbation.

Table 23.1

Symptoms, diagnosis, and risk factors for chronic obstructive pulmonary disease (COPD) exacerbation

Symptoms of exacerbation	Risk factors for exacerbation
The presence of two out of three of the following is required for diagnosis: • Increased cough • Increased sputum production • Increased sputum purulence Other symptoms: • Increased shortness of breath	Advanced age Productive cough Longer duration of COPD History of antibiotic therapy COPD related hospitalization within the previous year Chronic mucous hypersecretion Peripheral blood eosinophil count >0.3 × 10 ⁹ Presence of comorbidities

Symptoms of exacerbation

Risk factors for exacerbation

The presence of two out of three of the following is required for diagnosis:

•

Increased cough
•

Increased sputum production
•

Increased sputum purulence

Other symptoms:

•

Increased shortness of breath

Advanced age
Productive cough
Longer duration of COPD
History of antibiotic therapy
COPD related hospitalization within the previous year
Chronic mucous hypersecretion
Peripheral blood eosinophil count >0.3 × 10 ⁹
Presence of comorbidities

An increase in airway inflammation is considered an important mechanism in the pathophysiology of exacerbation. Increased inflammation leads to increased bronchial tone, increased edema of the bronchial wall, and increased mucous production. These mechanisms lead to a ventilation-perfusion mismatch and reduced expiratory flow.

Hypercapnia is a classic feature of respiratory failure in COPD exacerbation and is produced by decreased minute ventilation and increased dead space ventilation in the setting of the poor pulmonary reserve. Classically called type-II respiratory failure, hypercapnic respiratory failure is associated with paCO ₂ greater than 50 mmHg. Mild to moderate cases present with daytime sluggishness, headaches, or increased somnolence ( Table 23.2 ). Severe cases are associated with confusion and decreased arousal, which can eventually progress to coma. Other comorbid illnesses and differentials of a simple COPD exacerbation should be ruled out appropriately ( Table 23.3 ).

Table 23.2

Various physiological changes seen with increased carbon dioxide tension in the blood

Physiological effects of hypercapnia
Cerebral effects	• An initial increase in respiratory drive followed by decreased level of arousal and then decreased respiratory drive • Increased cerebral blood flow and increased intracranial pressure which can lead to seizures
Cardiorespiratory effects	• An initial feeling of dyspnea as a compensatory mechanism • Myocardial and diaphragmatic suppression leading to arrhythmia and arrest
Hematological effects	• Increased release of oxygen from hemoglobin in acute cases • Polycythemia in chronic cases
Metabolic effects	• Acute cases associated with acidosis, hyperkalemia, and increased ionized serum calcium. Bicarbonate does not change significantly • Chronic cases associated with increased renal retention of bicarbonate