Master Acute Respiratory Distress Syndrome (ARDS) Assessment with Picmonic for Medicine

Damage to the alveolar–capillary membrane in acute respiratory distress syndrome (ARDS) leads to the release of inflammatory cytokines such as TNF-α, IL-1, and IL-6. These mediators increase capillary permeability, causing protein-rich fluid to leak into the alveoli and interstitial spaces. This noncardiogenic pulmonary edema results in diffuse alveolar damage, hyaline membrane formation, and severe impairment of gas exchange.

Early in ARDS, patients may appear restless, anxious, and diaphoretic due to hypoxemia. The sympathetic nervous system responds by increasing heart rate and respiratory rate in an attempt to compensate for low oxygen levels.

Damage to the alveoli and the resulting decrease in lung compliance cause dyspnea and tachypnea. The patient often develops respiratory alkalosis initially due to hyperventilation, followed later by respiratory acidosis as fatigue and worsening hypoxemia occur.

A hallmark of ARDS is hypoxemia that does not improve with supplemental oxygen. This is due to intrapulmonary shunting and ventilation–perfusion (V/Q) mismatch, as alveoli are filled with fluid or collapsed, preventing oxygen from entering the bloodstream despite adequate perfusion.

Despite high concentrations of inspired oxygen, arterial oxygen tension (PaO₂) remains low because of impaired diffusion and alveolar flooding. The PaO₂/FiO₂ ratio is used diagnostically, with a ratio less than 300 indicating ARDS severity.

Chest imaging reveals bilateral diffuse alveolar infiltrates, often described as “whiteout” or “white lung” on chest X-ray. This radiographic pattern reflects widespread alveolar consolidation and edema.

Injury to type II pneumocytes reduces surfactant production, promoting alveolar collapse. Together with fluid accumulation, this atelectasis further worsens hypoxemia and decreases lung compliance.

Chronic inflammation and hypoxic vasoconstriction increase pulmonary vascular resistance, leading to pulmonary hypertension and potential right heart strain as a late complication of ARDS.