Critical Care Medicine-Neurologic Disorders>>>>>Other Parenchymal Disease and pulmonary edema
Question 1#

A 79-year-old male with a history of hypertension, dyslipidemia, and type-2 diabetes mellitus presents to the emergency department complaining of increasing shortness of breath, over the past 4 hours. Arterial blood gas (ABG) analysis at room air shows:

• PaO₂ 54 mm Hg
• PaCO₂ 28 mm Hg
• pH 7.48
• HCO₃ − 22 mEq/L

Upon admission, the patient is administered oxygen via a face mask with oxygen reservoir at 15 L/min. The SpO₂ raises from 87% to 99%. Thirty minutes later, the patient is still dyspneic (respiratory rate: 32 breaths/min). Noninvasive blood pressure is 180/85 mm Hg, heart rate is 100 bpm. ABG now shows:

• PaO₂ 249 mm Hg
• PaCO₂ 27 mm Hg

Chest auscultation reveals mild bilateral crackles at the bases of the lungs and mild wheezing.

• Body temperature is 36.2°C
• WBC 6500/mL
• creatinine 1.8 mg/dL
• lactate 1.4 mmol/L

What is the MOST likely diagnosis?

A. Pulmonary embolism
B. Acute pulmonary edema
C. Bilateral pneumonia
D. Exacerbation of COPD

Correct Answer is B

Comment:

Correct Answer: B

Cardiogenic pulmonary edema triggers dyspnea through various mechanisms. In this scenario, acidosis and hypercapnia are absent. Here, the correction of hypoxia does not reduce the respiratory drive. No major alteration in respiratory mechanics is seen, except the increased respiratory rate. These observations indicate interstitial congestion as a potential trigger for the respiratory failure. The patient’s past medical history of various cardiovascular risk factors pointing to congestive heart failure as a potential etiology. Nonetheless, no options can be safely excluded without the execution of primary diagnostic tests (ECG and chest x-ray). Bilateral wheezing is a sign of bronchial constriction. It may be caused by the irritation due to an underlying infectious disease (pneumonia), particularly in a context of chronic self-triggering inflammation, like that associated with a chronic obstructive pulmonary disease (COPD). Bronchospasm may be associated to pulmonary vascular congestion as well. The absence of a raised white blood cell count makes pneumonia and COPD exacerbation unlikely. The absence of signs of impaired respiratory mechanics such as the use of abdominal wall muscles to counteract outflow obstruction does not support this hypothesis either. Pulmonary embolism fits with the described scenario in which minute ventilation cannot be reduced without sedating the patient. Wheezing, however, is uncommon and a depressed PO₂ /FiO₂ of less than 210 mm Hg in the setting of pulmonary embolism indicates a significant shunt and is usually accompanied by right heart failure and some degree of hemodynamic instability.

References:

1. Soldati G, Copetti R, Sher S. Sonographic interstitial syndrome: the sound of lung water. J Ultrasound Med. 2009;28(2):163-174.
2. Dyspnea. Mechanisms, assessment, and management: a consensus statement. American Thoracic Society. Am J Respir Crit Care Med. 1999;159(1):321-340.