Pathophysiology
Summary
Pulmonary edema is chiefly caused by elevated capillary hydrostatic pressure or direct injury to pulmonary capillaries. Increased hydrostatic pressure can be secondary to conditions like left-sided heart failure, mitral stenosis, acute mitral regurgitation, or volume overload in cases of CHF exacerbation and renal failure. This accumulation typically consists of transudate, a fluid low in cells and proteins, resulting from increased hydrostatic pressure.
Acute respiratory distress syndrome (ARDS) is caused by diffuse alveolar injury, resulting in pulmonary capillary damage and leakage of cell and protein rich serum known as exudate. ARDS can arise in cases of sepsis, pneumonia, aspiration of gastric contents, severe trauma like lung contusion and fat emboli, pancreatitis, and transfusion-related acute lung injury (TRALI).
Acute respiratory distress syndrome (ARDS) manifests as bilateral pulmonary edema and hypoxia, usually developing within 6 to 72 hours after inciting factors such as sepsis, severe trauma, or aspiration. The condition progresses through distinct stages, beginning with an exudative phase characterized by the release of cytokines by macrophages and the subsequent damage caused by neutrophils to both the alveolar epithelium and capillary endothelium. This results in decreased surfactant and alveolar collapse, as well as a bloody, cellular, protein-rich exudate filling the alveoli. Hyaline membranes may form, lining the small airways.
The ARDS proliferative phase is marked by proliferation of type II pneumocytes, resynthesis of surfactant, and differentiation into type I pneumocytes. This aids in the resolution of pulmonary edema and the restoration of the alveolar epithelium. Long-term complications may include chronic pulmonary fibrosis, induced by myofibroblasts depositing collagen throughout the lung.
Differentiating ARDS from congestive heart failure (CHF) can be accomplished through clinical markers and tests such as serum BNP, S3/S4 gallops, JVD, and rarely, elevated pulmonary wedge pressure, all of which are present in CHF. Clinical manifestations of ARDS also include bilateral diffuse crackles, dyspnea & tachypnea with accessory muscle use, and hypoxemia with increased A-a gradient that is not easily corrected with oxygen supplementation, often visible on CXR as bilateral opacities leading to a ‘white-out' appearance.
Lesson Outline
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FAQs
Acute respiratory distress syndrome (ARDS) is a severe, life-threatening condition characterized by bilateral pulmonary edema and hypoxia, leading to respiratory failure. It is caused by diffuse alveolar injury which may result from a range of conditions such as sepsis (the most common cause), pneumonia, severe trauma (like lung contusion or fat emboli), aspiration of gastric contents, pancreatitis, and transfusion-related acute lung injury (TRALI).
In ARDS, damage to pulmonary capillaries leads to the leakage of a cell and protein-rich fluid called exudate into the alveoli. This is a hallmark of the exudative phase of ARDS. During this phase, macrophages release cytokines, and neutrophils release reactive oxygen species and proteases, causing direct injury to both the alveolar epithelium and the alveolar capillary endothelium. This damage leads to decreased surfactant production and the formation of hyaline membranes in the small airways.
ARDS progresses through two primary stages: the exudative and the proliferative phases. The exudative phase is the initial stage following alveolar injury, marked by cytokine release and direct cellular damage that leads to pulmonary edema. The proliferative phase follows, characterized by the resolution of the edema and the regeneration of alveolar epithelium through the replication of type II pneumocytes. These cells differentiate into type I pneumocytes and resynthesize surfactant. If not properly managed, ARDS can progress to chronic pulmonary fibrosis due to collagen deposition by myofibroblasts.
Increased hydrostatic pressure in conditions such as left-sided heart failure, acute mitral regurgitation, or mitral stenosis leads to fluid leakage through the pulmonary capillaries, resulting in pulmonary edema. This elevated pressure is transmitted to the pulmonary venous system, subsequently increasing pulmonary capillary hydrostatic pressure. The fluid that accumulates, known as transudate, is generally low in cells and proteins.
Congestive heart failure (CHF) and ARDS have similar presentations but can be distinguished using certain clinical features and investigations. Common indications of heart failure include elevated JVD, S3/S4 gallops, and increased serum BNP. In addition, a pulmonary wedge pressure of ≥18 mmHg is observed in cases of heart failure. On the other hand, ARDS is characterized by hypoxemia with an increased A-a gradient, which does not easily correct with oxygen supplementation. It also presents with dyspnea, tachypnea, accessory muscle use, and bilateral diffuse crackles. On a chest X-ray, ARDS shows bilateral opacities leading to a 'white out' appearance.
