Cardiogenic Pulmonary Edema
Definition
Cardiogenic pulmonary edema(CPE) is the accumulation of fluid in the pulmonary interstitium and alveoli due to elevated hydrostatic pressure in pulmonary capillaries, secondary to left heart dysfunction.
—It represents acute decompensated heart failure (ADHF) with pulmonary congestion.
Pathophysiology
Normal Starling Forces
Fluid movement across pulmonary capillaries is governed by:
- Capillary hydrostatic pressure
- Plasma oncotic pressure
- Capillary permeability
- Lymphatic drainage
In CPE
- Pulmonary capillary wedge pressure (PCWP) > 18 mmHg
- Increased left atrial pressure → pulmonary venous hypertension
- Transudation of low-protein fluid into:
- Interstitium → alveoli
💡 Key point:
CPE is due to pressure overload, not increased permeability (unlike ARDS).
Etiology
1. Left Ventricular Systolic Dysfunction
- Acute MI (most common)
- Dilated cardiomyopathy
- Myocarditis
- Severe ischemia
2. Left Ventricular Diastolic Dysfunction
- Hypertensive crisis
- HFpEF
- Aortic stenosis
- Hypertrophic cardiomyopathy
3. Valvular Heart Disease
- Acute MR (papillary muscle rupture)
- Severe MS
- Acute AR
- Prosthetic valve dysfunction
4. Arrhythmias
- Rapid AF
- VT/VF
- Severe bradycardia / AV block
5. Mechanical / Structural Causes
- Ventricular septal rupture (post-MI)
- Acute LV aneurysm
6. Volume Overload
- Renal failure
- Excess IV fluids
- Blood transfusion (TACO)
Pathophysiological Sequence (Stepwise)
- LV failure → ↑ LVEDP
- ↑ Left atrial pressure
- ↑ Pulmonary venous pressure
- Interstitial edema (Kerley B lines)
- Alveolar flooding
- ↓ Lung compliance
- V/Q mismatch → hypoxemia
- Dyspnea, orthopnea, respiratory failure
Clinical Presentation
Symptoms
- Acute dyspnea
- Orthopnea
- Paroxysmal nocturnal dyspnea
- Cough with pink frothy sputum
- Chest pain (if ischemic)
Signs
- Tachypnea, tachycardia
- Hypoxia
- Bibasal crackles → diffuse crepitations
- Wheeze (“cardiac asthma”)
- S3 gallop
- Raised JVP
- Peripheral edema (may be absent in acute cases)
Investigations
1. Arterial Blood Gas
- Hypoxemia
- Respiratory alkalosis (early)
- Respiratory acidosis (late/fatigue)
2. Chest X-ray (Classic Progression)
|
Stage |
Radiological Feature |
|
Early |
Upper lobe diversion |
|
Interstitial edema |
Kerley B lines |
|
Alveolar edema |
Bat-wing / butterfly pattern |
|
Pleural effusion |
Blunting of costophrenic angle |
|
Cardiomegaly |
Usually present |
Cardiomegaly helps differentiate CPE from ARDS.
3. ECG
- MI / ischemia
- Arrhythmias
- LVH
4. Echocardiography (Key Investigation)
- LV systolic function (EF)
- Diastolic dysfunction
- Valvular lesions
- Regional wall motion abnormalities
- Acute mechanical complications
5. Biomarkers
- BNP / NT-proBNP ↑ (supports cardiogenic origin)
- Troponin (MI)
- Renal function, electrolytes
6. Hemodynamics (if monitored)
|
Parameter |
Cardiogenic Pulmonary Edema |
|
PCWP |
↑ (>18 mmHg) |
|
Cardiac output |
↓ |
|
SVR |
↑ |
|
ScvO₂ |
↓ |
|
Lactate |
May be ↑ |
Differential Diagnosis
|
Feature |
Cardiogenic PE |
ARDS |
|
PCWP |
↑ |
Normal/low |
|
Protein content |
Low |
High |
|
Cardiomegaly |
Common |
Rare |
|
BNP |
High |
Normal/mild ↑ |
|
Cause |
Cardiac |
Inflammatory |
|
Response to diuretics |
Good |
Poor |
Management (ICU-Focused, Guideline-Based)
1. Oxygenation & Ventilatory Support
Supplemental Oxygen
- Target SpO₂ > 92%
Non-Invasive Ventilation (First Line)
- CPAP / BiPAP
- Benefits(reason see below):
- ↓ preload
- ↓ afterload
- ↓ work of breathing
- ↓ need for intubation
—Strong evidence supports early NIV in acute cardiogenic pulmonary edema.
Invasive Ventilation (If Needed)
- Indications:
- NIV failure
- Shock
- Altered sensorium
- Use:
- Low tidal volume
- Moderate PEEP (improves LV afterload)
2. Diuretics (Cornerstone)
Loop Diuretics
- Furosemide IV
- Reduces:
- Intravascular volume
- Pulmonary congestion
- LV preload
Caution in:
- Hypotension
- RV failure
- Severe AS
3. Vasodilators (If BP Permits)
Nitrates
- Nitroglycerin IV
- First-line in hypertensive pulmonary edema
Effects:
- Venodilation → ↓ preload
- Arterial dilation → ↓ afterload
Avoid if:
- SBP < 100 mmHg
- Severe AS
- RV infarction
4. Inotropes (If Low Output / Shock)
- Dobutamine → ↑ CO
- Milrinone (esp. on beta-blockers)
Used only if:
- Hypotension
- Evidence of poor perfusion
5. Vasopressors (If Shock)
- Norepinephrine preferred
- Maintain MAP ≥ 65 mmHg
6. Treat the Underlying Cause
|
Cause |
Specific Treatment |
|
Acute MI |
Reperfusion (PCI) |
|
Hypertensive crisis |
IV nitrates |
|
AF with RVR |
Rate/rhythm control |
|
Acute MR |
IABP + surgery |
|
Renal failure |
Dialysis/ultrafiltration |
Special Situations
Flash Pulmonary Edema
- Sudden onset
- Often due to:
- Severe hypertension
- Bilateral renal artery stenosis
- Responds dramatically to nitrates + NIV
Cardiogenic Pulmonary Edema vs TACO
- TACO occurs post transfusion
- Elevated BNP, cardiomegaly
- Managed similarly (diuretics + NIV)
Prognosis
- Depends on:
- Underlying cardiac disease
- Speed of treatment
- Presence of cardiogenic shock
- Mortality increases if associated with:
- MI
- Mechanical complications
- Renal failure
High-Yield Exam Pearls
- PCWP > 18 mmHg → cardiogenic edema
- Bat-wing shadow + cardiomegaly → CPE
- NIV is first-line ventilatory support
- Diuretics + nitrates = mainstay
- ARDS ≠ CPE (permeability vs pressure)
- Pink frothy sputum = alveolar flooding
How NIV (CPAP/BiPAP) ↓ Preload and ↓ Afterload
Core Mechanism
NIV applies positive pressure to the thorax → ↑ intrathoracic pressure (ITP)
This single change explains both preload and afterload effects.
—>How NIV ↓ PRELOAD
Normal Physiology
Venous return depends on the pressure gradient:
Venous Return=Pmsf −PRA
Where:
- Pmsf = mean systemic filling pressure
- PRA = right atrial pressure
Effect of NIV
- NIV ↑ intrathoracic pressure
- ↑ Right atrial pressure (PRA)
- ↓ Gradient for venous return
—>↓ Venous return → ↓ RV preload → ↓ LV preload
Additional Preload-Reducing Effects
- Positive pressure compresses thoracic veins (IVC, SVC)
- Blood pools in peripheral capacitance vessels
- Venodilation effect similar to nitrates
—Net effect:
✔ Reduced pulmonary venous congestion
✔ Reduced LV end-diastolic volume & pressure
✔ ↓ PCWP
Exam Line (Preload)
NIV decreases preload by increasing intrathoracic pressure, which reduces venous return to the heart.
How NIV ↓ AFTERLOAD (THIS IS THE MOST IMPORTANT PART)
Key Concept
LV afterload is determined by transmural LV pressure, not just systemic BP.
LV transmural pressure=PLV −PITP
In Spontaneous Breathing (Negative Pressure)
- Inspiration → ↓ ITP
- LV must generate higher pressure to eject blood
- ↑ LV afterload
—Bad for failing LV
With NIV (Positive Pressure)
- NIV ↑ ITP
- External pressure on LV increases
- LV transmural pressure decreases
—> LV ejects blood against LOWER effective afterload
Analogy (Exam-Friendly)
Think of LV inside a pressurized box:
- Higher outside pressure → LV doesn’t need to generate as much pressure to eject blood
Result
✔ ↑ Stroke volume
✔ ↑ Cardiac output
✔ ↓ Pulmonary congestion
This is why NIV improves hemodynamics even before diuretics act
Exam Line (Afterload)
NIV reduces LV afterload by increasing intrathoracic pressure, thereby decreasing LV transmural pressure during systole.
Additional Beneficial Effects (Often Ignored)
↓ Work of Breathing
- Less O₂ consumption by respiratory muscles
- More oxygen available for myocardium
↓ Sympathetic Drive
- Relief of dyspnea → ↓ catecholamines
- ↓ SVR → further afterload reduction
Improved Oxygenation
- ↓ hypoxic pulmonary vasoconstriction
- ↓ RV afterload → better LV filling synchrony
CPAP vs BiPAP (Hemodynamic Perspective)
|
Mode |
Hemodynamic Effect |
|
CPAP |
Best for ↓ preload & ↓ afterload |
|
BiPAP |
CPAP effects + ↓ work of breathing |
|
PEEP |
Key determinant of preload reduction |
📌 CPAP alone is often sufficient in pure cardiogenic pulmonary edema
When NIV Can Be Harmful
- Hypovolemia
- RV infarction
- Severe aortic stenosis
- Obstructive shock
>>Excess preload reduction → hypotension