Cardiogenic Pulmonary Edema.



    Increased hydrostatic pressure in the pulmonary capillaries results in increased transvascular fluid filtration and is most often caused by volume overload or impaired left ventricular function resulting in elevated pulmonary vascular pressures.


    Elevations of Pulmonary capillary wedge pressure (PCWP) 18-25 mm Hg cause edema formation in the perimicrovascular and peribronchovascular interstitial space. PCWP > 25 mm Hg: fluid overwhelms the lung epithelial barrier.

 CAUSES:

  • Acute exacerbation of heart failure
  • Acute valve dysfunction (e.g., mitral valve chordae tendineae rupture)
  • Arrhythmia/Myocardial infarction
  • Hypertensive crisis
  • Fluid overload following aggressive volume resuscitation (e.g., postoperative)
  • Ventricular septal rupture
  • Pericardial tamponade


 CLINICAL FINDINGS:

  • Orthopnea
  • Distended neck veins
  • S3 heart sound
  • Dependent edema
  • Elevated blood pressure
  • Cool extremities

 LABORATORY FINDINGS:

  • B-type natriuretic peptide (brain natriuretic peptide: BNP)  > 1200 pg/mL
  • Elevated Creatinine (in case of volume overload)
  • Elevated Troponin
IMAGING:

CXR: Pleural effusions, Kerley B lines (see picture):



TEE: ↓LVEF, Diastolic filling defect, Severe mitral or aortic valvular disease, Pericardial effusion with tamponade, VSD.
Pulmonary Artery Catheter: PCWP > 18 mm Hg, CVP > 12 mm Hg.

MANAGEMENT OF CARDIOGENIC PULMONARY EDEMA.

RESPIRATORY MAINTENANCE: 
Adequate oxygenation, increased FiO2,  administration of positive end expiratory pressure ( 5-15 cm H2O). early using of noninvasive positive pressure ventilation

DECREASING PRELOAD:

• Diuretics (e.g., furosemide): decrease systemic venous tone and extracellular volume/volume overload.
• Opiates (e.g., morphine sulfate): reduces sympathetic tone.
• Nitrates (e.g., nitroglycerin): venous and arterial vasodilator, reduces myocardial oxygen demand.
• Nesiritide: recombinant BNP that results in vasodilation and diuresis.
• Ultrafiltration (volume removal).

DECREASING AFTERLOAD:

• ACE inhibitor/ARB: reduce preload and afterload.
• Nitroprusside (decreases venous return and afterload).
• Intraaortic balloon pump.

INOTROPIC SUPPORT:

• Dobutamine
• Dopamine
• Phosphodiesterase inhibitors (e.g., milrinone)

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