Respiratory

ARDS vs Cardiogenic Pulmonary Edema

Injured barrier vs elevated pressures

ARDS vs Cardiogenic Pulmonary Edema
Feature	ARDS	Cardiogenic edema
Mechanism
Mechanism	Alveolar-capillary barrier injury → protein-rich, non-cardiogenic edema (diffuse alveolar damage)	Elevated LV filling pressures → hydrostatic transudative edema
Assessment
History / context	Pneumonia, aspiration, sepsis, pancreatitis, trauma/transfusion; onset over hours–days; no JVD	HF, ischemia, arrhythmia, hypertensive crisis, fluid overload; JVD, S3, orthopnea
CXR	Bilateral opacities; normal heart size; air bronchograms; effusions atypical	Congestion ± cardiomegaly, Kerley lines, pleural effusions
POCUS	B-lines with spared areas, pleural-line irregularity, consolidations	Diffuse homogeneous B-lines, effusions, plethoric IVC
Echo	Normal LV function (unless concurrent septic cardiomyopathy)	Reduced EF and/or diastolic dysfunction, valvular lesion
Traps & pitfalls
BNP limitations	BNP/NT-proBNP rises in sepsis and ARDS too — an elevated value does NOT prove cardiogenic	A low value argues strongly against cardiogenic edema; interpret with context, never alone
Assessment
Hemodynamics	Normal filling pressures (if measured)	Elevated filling pressures
Management
Response to PEEP	Recruits alveoli; oxygenation improves — PEEP is therapy within a lung-protective framework	Oxygenation improves by redistributing edema — definitive therapy is pressure/volume offload
Treatment priorities	Treat the trigger; 4–6 mL/kg PBW, Pplat ≤30; prone if severe; avoid fluid overload while supporting perfusion	Oxygenation/NIV support, afterload/preload reduction, diuresis; treat the cardiac cause (ischemia, rate, valve)

Comparing: ARDS

Mechanism · Mechanism

Alveolar-capillary barrier injury → protein-rich, non-cardiogenic edema (diffuse alveolar damage)

Assessment · History / context

Pneumonia, aspiration, sepsis, pancreatitis, trauma/transfusion; onset over hours–days; no JVD

Assessment · CXR

Bilateral opacities; normal heart size; air bronchograms; effusions atypical

Assessment · POCUS

B-lines with spared areas, pleural-line irregularity, consolidations

Assessment · Echo

Normal LV function (unless concurrent septic cardiomyopathy)

Traps & pitfalls · BNP limitations

BNP/NT-proBNP rises in sepsis and ARDS too — an elevated value does NOT prove cardiogenic

Assessment · Hemodynamics

Normal filling pressures (if measured)

Management · Response to PEEP

Recruits alveoli; oxygenation improves — PEEP is therapy within a lung-protective framework

Management · Treatment priorities

Treat the trigger; 4–6 mL/kg PBW, Pplat ≤30; prone if severe; avoid fluid overload while supporting perfusion

For healthcare-professional education. Clinical decisions require patient-specific assessment and local protocols.

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