K

Pulmonary Edema: Cardiogenic vs Noncardiogenic, Radiology, Lab Markers, and Management

Pulmonary Edema: Key Concepts and Case-based Management

Radiographic patterns and terminology

  • Bat's wing / butterfly pattern
    • Description: bilateral, central/perihilar predominant shadowing with relatively clearer outer lungs. Common in congestive heart failure (CHF) with pulmonary edema; often bilateral but not perfectly symmetric.
    • Figure reference: Fig. 20.4 depicts a bat's wing pattern due to pulmonary edema.
  • Noncardiogenic pulmonary edema radiographic features
    • Typically fluffy densities that are denser near the hilum.
    • Infiltrates may be unilateral or bilateral.
    • Pleural effusion usually not present.
    • Cardiac silhouette is not enlarged.
  • Cardiogenic pulmonary edema radiographic features
    • Left-sided heart failure pattern: cardiomegaly, engorged pulmonary arteries, Kerley A and B lines.
    • Dense, fluffy opacities spreading outward from the hila toward the lung bases.
    • Kerley lines (see below) and pleural effusions may be present.
    • Chest radiographs can show signs of advanced edema (dense alveolar clouds) with a possible bat's wing pattern when central edema is prominent.
  • Kerley lines
    • Kerley A lines: lines radiating from the hila into the central lung; indicate deep interstitial edema.
    • Kerley B lines: short, horizontal, <1 cm lines at the lung periphery, parallel to the pleural surface; commonly at the bases.
  • Venous congestion indicators
    • Dilated pulmonary arteries
    • Left ventricular hypertrophy (cardiomegaly)
  • Lateral/portions of the lung affected
    • In CHF-related edema, central (perihilar) predominant involvement with relatively clearer peripheral lungs; in noncardiogenic edema, peripheral predominance can occur depending on cause.

Pathophysiology and clinical manifestations associated with edema

  • Causes summarized
    • Cardiogenic edema: due to elevated hydrostatic pressure from left heart failure or volume overload; impaired cardiac output increases venous pressures.
    • Noncardiogenic edema: due to alveolar-capillary permeability disturbance (e.g., toxins, sepsis, high altitude) leading to capillary leak.
  • Common clinical data at the bedside (examples from case)
    • Tachypnea, tachycardia, hypoxemia, and sometimes hypotension.
    • Cyanosis, discolored extremities, jugular venous distension.
    • Coarse crackles on auscultation; pink frothy sputum may be present.
    • Findings reflect increased alveolar-capillary membrane thickness and interstitial edema.
  • Common symptoms and signs related to pathophysiology
    • Paroxysmal nocturnal dyspnea (PND) and orthopnea: due to increased venous return when lying down, promoting pulmonary edema.
    • Cheyne-Stokes respiration: may occur in severe left-sided heart failure due to altered circulation time and central control.
    • Increased work of breathing and reduced lung compliance contribute to tachypnea and distress.
    • Posture-related symptoms: orthopnea worsens when recumbent; patient may improve with upright positioning.

BNP and laboratory findings in CHF/pulmonary edema

  • BNP (brain natriuretic peptide) levels and status
    • BNP < 100 pg/mL: no heart failure.
    • BNP 100–300 pg/mL: heart failure may be present.
    • BNP > 300 pg/mL: mild heart failure.
    • BNP > 600 pg/mL: moderate heart failure.
    • BNP > 900 pg/mL: severe heart failure.
  • Common electrolyte patterns in left-sided heart failure treated with diuretics
    • Hypokalemia, hyponatremia, hypochloremia can occur due to diuretic therapy or fluid shifts.
  • Radiologic findings associated with CHF on chest radiographs
    • Bilateral fluffy opacities with central predominance.
    • Dilated pulmonary arteries.
    • Cardiomegaly (left ventricular hypertrophy).
    • Kerley A and B lines.
    • Bat's wing pattern in severe edema.
    • Pleural effusions may be present.

Pathophysiology details linked to imaging and physiology

  • Increased alveolar-capillary membrane thickness contributes to impaired gas exchange and diffusion limitation.
  • Diffusion blockade and intrapulmonary shunting are common in acute edema, contributing to hypoxemia.
  • Reduced lung compliance is a hallmark of acute pulmonary edema, contributing to tachycardia and tachypnea.
  • Alveolar flooding and interstitial edema lead to potential atelectasis, which further impairs oxygenation and gas exchange.

General management principles for pulmonary edema

  • Overall goal: treat the underlying cause (cardiogenic vs noncardiogenic) and manage severity to optimize ventilation and perfusion.
  • Noncardiogenic pulmonary edema
    • Largely supportive care: ensure adequate ventilation and oxygenation.
    • No universal specific antidote for permeability trigger; address trigger when identifiable (e.g., antibiotics for sepsis, returning from high altitude, etc.).
    • May require mechanical ventilation if respiratory failure progresses.
  • Cardiogenic pulmonary edema
    • Early priorities: oxygen, diuresis, preload/afterload management, inotropic support if needed.
    • Digitalis is occasionally used if indicated; oxygen therapy and ventilation support as needed.
    • Diuretics for volume overload (e.g., loop diuretics such as furosemide).
    • Afterload reduction and preload reduction are central strategies to improve forward flow and reduce pulmonary congestion.
    • Inotropic support considered for hypotension or signs of organ hypoperfusion.
    • Mechanical ventilation may be necessary if acute ventilatory failure occurs; CPAP can be effective and may avoid intubation in many cases.

Specific therapeutic interventions by mechanism

  • Preload reducers (reduce left-sided filling pressures and pulmonary capillary hydrostatic pressure)
    • Nitroglycerin (Nitro-Bid, Minitran, Nitrostat): rapid-acting preload reducer.
    • Loop diuretics (e.g., furosemide): decrease preload via diuresis and vasodilatory effects.
    • Morphine sulfate: may be used to reduce preload in some cases, though adverse effects (nausea, respiratory depression) may offset benefits; nitroglycerin is often preferred.
  • Afterload reducers (lower systemic vascular resistance to improve cardiac output and renal perfusion)
    • Captopril: ACE inhibitor; reduces angiotensin II levels; afterload improvement typically within 10–15 minutes.
    • Enalapril (Vasotec): ACE inhibitor; reduces angiotensin II.
    • Nitroprusside (Nitropress): potent direct vasodilator; primarily reduces afterload and may modestly reduce preload.
  • Positive inotropic agents (increase contractility and/or support perfusion; may accompany vasodilation in some regimens)
    • Dobutamine: beta-adrenergic activity; used for mild hypotension and inotropy.
    • Dopamine: dose-dependent effects; low dose favors renal/visceral vasodilation and diuresis; higher doses increase contractility and heart rate; very high dose increases afterload; use with caution in normotensive patients.
    • Norepinephrine: potent alpha-adrenergic vasoconstriction with beta activity; increases afterload and BP; used in severe hypotension.
    • Milrinone: phosphodiesterase-3 inhibitor; inotropic effect with vasodilation; lowers preload and afterload while increasing cardiac output.

Oxygen therapy and lung expansion strategies

  • Oxygen Therapy Protocol
    • Purpose: treat hypoxemia, reduce work of breathing, and decrease myocardial work.
    • Hypoxemia in edema arises from interstitial/alveolar fluid, atelectasis, and capillary shunting; shunting-related hypoxemia may be partially refractory to oxygen alone.
    • Adjust oxygen to improve oxygenation while monitoring ABG and clinical status.
  • Lung Expansion Therapy Protocol
    • High-flow mask CPAP is effective for rapidly improving oxygenation and ventilation in pulmonary edema.
    • CPAP benefits: improves lung compliance, reduces work of breathing, enhances gas exchange, reduces vascular congestion.
    • CPAP trial is often used when ABG suggests impending ventilatory failure to avoid intubation.
  • Mechanical Ventilation Protocol
    • Indicated when acute ventilatory failure is present or anticipated and reversible.
    • CPAP or full mechanical ventilation may be employed depending on severity and reversibility.

Case Study: Pulmonary edema due to congestive heart failure (CHF)

  • Admitting history and presentation
    • 76-year-old man with chest pain, severe dyspnea, respiratory distress in ED.
    • History: longstanding heart disease; poor adherence to medications for several days.
    • Exam: disorientation, cyanosis, neck vein distention, mottled skin, coarse crackles in lungs, pink frothy sputum.
    • Vitals: BP 105/50, HR 124, RR 28; afebrile.
    • ECG: old MI, sinus tachycardia, occasional PVCs.
    • Chest X-ray (sitting): bilateral fluffy infiltrates, enlarged heart.
    • ABG on FiO2 0.30: pH 7.11, PaCO2 72 mmHg, HCO3− 22 mEq/L (metabolic data not severely deranged at that moment).
  • Initial management and monitoring at admission
    • Cardiology service; continuous ECG and oximetry monitoring; Foley catheter placed.
    • Treatments: intravenous furosemide, dopamine, nitroprusside, mask CPAP at 25 cm H2O with FiO2 0.60.
    • ABG and vitals reassessment after 2 hours: substantial clinical improvement; BP 126/70, HR 96, RR 18; lungs clearer; no ectopy; LVEF 47%.
    • Repeat ABG with FiO2 0.60 and CPAP 25 cm H2O: pH 7.35, PaCO2 46 mmHg, PaO2 120 mmHg, SaO2 97%.
    • Outcome: urine output > 600 mL/h; patient stable, less dyspnea, no chest pain; discharged after 48 hours with instructions to continue cardiac medications and diuretics and follow up in 3 days.
  • Respiratory therapy SOAP notes (summarized)
    • SOAP: patient reports less shortness of breath; ABG improved; CPAP tolerated; lung edema resolving; continue oxygen therapy adjustments to 2 L/min nasal cannula; discontinue CPAP eventually.
    • LVEF reported at 47%; oxygenation achieved with CPAP and FiO2 0.60; no evidence of acute myocardial infarction.

Case-specific respiratory assessment framework and plan

  • Initial bedside assessment indicators
    • Respiratory distress, cyanosis, hypoxemia, tachycardia, tachypnea, hypotension or borderline BP, JVD, crackles, pink frothy sputum, enlarged heart on CXR.
  • Management decisions informed by hemodynamics and oxygenation status
    • Use CPAP and diuresis to reduce preload and improve oxygenation when feasible.
    • Escalate to vasodilators or inotropes according to blood pressure and perfusion status.
    • Monitor ABG, electrolytes, renal function, and urine output closely during therapy.

Abnormal laboratory and physiologic references (contextual)

  • Typical electrolyte disturbances in CHF with diuretic use
    • Hypokalemia, hyponatremia, hypochloremia.
  • BNP and heart failure status (summarized)
    • BNP is elevated in heart failure and helps establish CHF diagnosis and severity.
  • ABG and gas exchange implications in acute edema
    • Initial ABG may show acidemia and hypercapnia with hypoxemia if ventilation is impaired; rapid improvement can occur with CPAP and diuresis.

Self-assessment questions (from the source material)

  • 1. Which of the following is an afterload reducer?
    • a. Procainamide
    • b. Dopamine
    • c. Furosemide
    • d. Nitroprusside
  • 2. What is the normal hydrostatic pressure in the pulmonary capillaries?
    • a. 5 to 10 mm Hg
    • b. 10 to 15 mm Hg
    • c. 15 to 20 mm Hg
    • d. 20 to 25 mm Hg
  • 3. What is the normal oncotic pressure of the blood?
    • a. 10 to 15 mm Hg
    • b. 15 to 20 mm Hg
    • c. 20 to 25 mm Hg
    • d. 25 to 30 mm Hg
  • 4. Which of the following are causes of cardiogenic pulmonary edema?
    • 1. Excessive fluid administration
    • 2. Right ventricular failure
    • 3. Mitral valve disease
    • 4. Pulmonary embolus
    • a. 1 and 2 only
    • b. 1, 2, and 3 only
    • c. 2, 3, and 4 only
    • d. 1, 3, and 4 only
  • 5. As a result of pulmonary edema, the patient's:
    • 1. RV is decreased
    • 2. FRC is increased
    • 3. VC is increased
    • 4. TLC is increased
    • a. 1 only
    • b. 1 and 4 only
    • c. 2 and 3 only
    • d. 3 and 4 only
  • 6. The left ventricular ejection fraction:
    • 1. Normally is greater than 75%
    • 2. Is a good measure of alveolar ventilation
    • 3. Correlates well with the brain natriuretic peptide values
    • 4. Provides a noninvasive measurement of cardiac contractility
    • a. 1 and 2 only
    • b. 2 and 4 only
    • c. 3 and 4 only
    • d. 2, 3, and 4 only

Radiology-focused recap and clinical relevance

  • In CHF with edema, chest radiographs commonly show cardiomegaly, Kerley lines, and central predominance of edema with possible pleural effusions.
  • The bat’s wing pattern is a hallmark of central edema with relative peripheral sparing in many cases.
  • BNP elevation supports the diagnosis of heart failure and helps guide management intensity, while renal and electrolyte status influence diuretic therapy.

Quick clinical correlations for exams

  • If imaging shows central dense edema with an enlarged heart and Kerley lines, consider cardiogenic edema due to left heart failure.
  • If imaging shows fluffy, peripheral-predominant edema without cardiomegaly, consider noncardiogenic etiologies; verify with clinical context and labs.
  • For cardiogenic edema, initial therapy often includes preload reduction (e.g., nitroglycerin, diuretics), afterload reduction (e.g., nitroprusside, ACE inhibitors), and augmentation of cardiac output if needed (e.g., dobutamine, milrinone).
  • CPAP can be highly effective in improving oxygenation and reducing the need for invasive ventilation in acute pulmonary edema when used early and titrated carefully.

Key numerical references (for quick recall)

  • Normal pulmonary capillary hydrostatic pressure: P_{HP} ext{ (pulmonary capillary hydrostatic pressure)}
    ightarrow 10 ext{ to } 15 ext{ mmHg}.
  • Normal oncotic pressure: ext{oncotic pressure}
    ightarrow 20 ext{ to } 25 ext{ mmHg}.
  • BNP thresholds in the provided framework:
    • < 100 pg/mL: no heart failure
    • 100–300 pg/mL: heart failure may be present
    • > 300 pg/mL: mild heart failure
    • > 600 pg/mL: moderate heart failure
    • > 900 pg/mL: severe heart failure
  • Patient case (example values):
    • On admission: ABG (FiO2 0.30): pH = 7.11, \, PaCO2 = 72 \, ext{mmHg}, \, HCO3^- = 22 \, \text{mEq/L}.
    • After CPAP and therapy (FiO2 0.60, CPAP 25 cm H2O): pH = 7.35, \, PaCO2 = 46 \, \text{mmHg}, \, PaO2 = 120 \, \text{mmHg}, \, SaO_2 = 97\%.
  • LVEF in the case: \text{LVEF} = 47\%.