ACUTE CARDIOGENIC PULMONARY EDEMA

Definition

Cardiogenic pulmonary edema (CPE) is defined as development of pulmonary edema as a consequence of increased capillary hydrostatic pressure secondary to elevated pulmonary venous pressure.

Pathophysiology CPE

(1) increased capillary hydrostatic pressure

(2) increased capillary permeability

(3) decreased plasma oncotic pressure

(4) lymphatic obstruction

Starling equation

Q = K(P.cap – P.is) - l(P.cap- P.is)

Q is net fluid filtration.

K is a constant called the filtration coefficient.

Pcap is capillary hydrostatic pressure

Pis is hydrostatic pressure in the interstitial fluid.

l is the reflection coefficient, which indicates the effectiveness of the capillary wall in preventing protein filtration.

Pcap is the colloid osmotic pressure of plasma

Pis is the colloid osmotic pressure in the interstitial fluid

When the pulmonary capillary hydrostatic pressure exceeds pulmonary interstitial pressure, transudation of fluid in the pulmonary interstitium and alveoli occurs.

Normal value

Pulmonary capillary pressure is 8-12 mm Hg

Colloid osmotic pressure is 28 mm Hg.

High pulmonary capillary wedge pressure (PCWP) may not always be evident in established CPE because the capillary pressure may have returned to normal at the time the measurement is performed.

Stages

Stage I: Fluid and colloid shift into the lung interstitium from pulmonary capillaries, but an increase in lymphatic outflow efficiently removes the fluid.

Stage II: The continuing filtration of liquid and solutes overpowers the pumping capacity of the lymphatics. The fluid initially collects in the more compliant interstitial compartment, which generally surrounds bronchioles, arterioles, and venules in the dependent zones.

Stage III: As fluid filtration continues to increase and the filling of loose interstitial space occurs, fluid accumulation in the less compliant interstitial space takes place. The interstitial space can contain up to 500 mL of fluid; with further accumulations, the fluid crosses the alveolar epithelium in to the alveoli, leading to alveolar flooding

Etiology

Acute exacerbation of chronic LV failure

Nonischemic acute mitral regurgitation (ruptured chordae tendineae)

Dysrhythmias: New-onset rapid atrial fibrillation and ventricular tachycardia

Acute left-sided valvular heart disorders

Fluid overload in patients with renal failure

Acute myocardial infarction , at least 25% of the left ventricle can produce de novo CPE (Killip class III and IV).

Other possible etiologies and contributing factors include the following:

Mitral stenosis

Peripartum cardiomyopathy

Severe diastolic dysfunction

Restrictive cardiomyopathy

Constrictive pericarditis

Pericardial tamponade

Severe myocardial contusion

Physical Finding

Tachypnea , tachycardia, agitated, very anxious and diaphoretic.

Skin pallor or mottling resulting from peripheral vasoconstriction and shunting of blood to the central circulation in patients with very poor LV function.

Hypertension à hyperadrenergic state Hypotension à LV systolic dysfunction

concurrent right ventricular failure à present with hepatomegaly, hepatojugular reflux, and peripheral edema.

Auscultation

- lungs à rales,wheezes also may be present.

- cardiovascular à usually is notable for S3 ..

- acute aortic regurgitation à short soft diastolic murmur.

Acute mitral regurgitation à loud systolic murmur heard best at the apex or lower sternal border. (Part 1)