A 38-year-old man comes to the emergency department with high-grade fever, shaking chills, productive cough, and shortness of breath. He has had 2 hospital admissions for alcohol-withdrawal seizures in the past year but continues to drink alcohol every day. The patient has no other medical problems and takes no medications. Temperature is 39.7 C (103.5 F), blood pressure is 100/70 mm Hg, pulse is 110/min, and respirations are 20/min. Skin and mucous membranes are dry. Physical examination reveals crackles and bronchial breath sounds in the right lower lung field. Cardiac examination is unremarkable. Chest x-ray reveals right lower lobe consolidation. The patient is prescribed intravenous antibiotics. Twelve hours later, he develops significant shortness of breath. Respirations are 38/min. Oxygen saturation is 80% on a nonrebreather mask. A repeat chest x-ray is shown in the image below.
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The patient is intubated immediately. Which of the following is most likely to be present in this patient just prior to intubation?
Acute respiratory distress syndrome: pathogenesis & diagnosis | |
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Pathophysiology |
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| PHTN = pulmonary hypertension; RV = right ventricular; V/Q = ventilation/perfusion. | |
This patient most likely has acute respiratory distress syndrome (ARDS) due to infectious pneumonia and sepsis (fever, purulent sputum, chills). ARDS develops in the setting of direct (eg, aspiration, pneumonia, toxic inhalation) or indirect (eg, trauma, sepsis, pancreatitis) lung injury. The lung injury causes the release of proteins, inflammatory cytokines, and neutrophils into the alveolar space, leading to leakage of fibrinous proteinaceous fluid into the airspaces and alveolar collapse due to loss of surfactant. These changes result in the following:
Clinical findings of ARDS include respiratory distress, diffuse crackles, severe hypoxemia, and bilateral alveolar infiltrates within 1 week of a clinical insult. PaO2 decreases and requires a higher FiO2 to maintain oxygenation. As a result, PaO2/FiO2 is decreased (≤300). Lower ratios indicate more severe degrees of ARDS (Choice C).
(Choice B) Left ventricular end-diastolic pressure (LVEDP) is increased in decompensated left-sided heart failure, characterized by pulmonary venous congestion resulting in hydrostatic pulmonary edema. In contrast, ARDS causes noncardiogenic pulmonary edema. The pulmonary capillary wedge pressure, a measure of venous back pressure in the lungs (transmitted from the left atrium) serving as a surrogate for LVEDP, is normal in ARDS. This patient's normal cardiac examination (no jugular venous distension, no S3 gallop) makes decompensated heart failure unlikely. Euvolemic pulmonary edema developing rapidly in the setting of sepsis is more consistent with ARDS.
(Choice D) ARDS causes intrapulmonary shunting and V/Q mismatch with an increased alveolar-arterial (A-a) oxygen gradient. In contrast, a normal A-a gradient is seen with hypoventilation (eg, opioid intoxication, neuromuscular weakness) and reduced partial pressure of inspired oxygen (eg, high altitude).
Educational objective:
Acute respiratory distress syndrome involves acute pulmonary edema and is diagnosed by hypoxemia and bilateral alveolar infiltrates that are not explained by cardiac dysfunction. The pulmonary edema causes impaired gas exchange (due to intrapulmonary shunting and ventilation-perfusion mismatch) and decreased lung compliance. Increased hypoxic vasoconstriction leads to acute pulmonary hypertension.