Cardiogenic and noncardiogenic pulmonary edema each result in increased extravascular lung water, and each may may result in respiratory failure. Given the differences in pathophysiology, it is not surprising that the clinical manifestations are very different within the two syndromes.
Elevated Transmural Stress Pulmonary Edema (Cardiogenic Pulmonary Edema):
Early rises in pulmonary venous stress may be asymptomatic. The affected individual might notice only mild exertional dyspnea or a nonproductive cough stimulated by activation of irritant receptors coupled with C fibers.
Orthopnea and paroxysmal nocturnal dyspnea occur when recumbency causes redistribution of blood or edema fluid, usually pooled in the lower extremities, into the venous circulation, theby increasing thoracic blood volume and pulmonary venous pressures. Clinical signs start using the accumulation of interstitial fluid. Physical examination may reveal a third heart sound, but there's a paucity of lung finds in purely interstitial edema.
The earliest sign is frequently a radi radiographic showing an improvement in the caliber of the upper lobe vessels ("pulmonary vascular redistribution") and fluid accumulating within the perivascular and peribranchial spaces ("cuffing"). It may also show Kerley B lines, which represent fluid within the interlobular septa.
Pulmonary compliance falls, and also the patient starts to breathe more quickly and gradually to minimize the elevated elastic function of breathing. As alveolar flooding begins, there are further decreases in lung volume and pulmonary compliance. With some alveoli filled with fluid, there's an improved within the fraction of the lung that's perfused but poorly ventilated. This shift toward reduced / ratios brings about an improvement in Aa PO2, if not frank hypoxemia.
Supplemental oxygen corrects the hypoxemia. The PaCO2 is normal or reduced, reflecting the increased drive to breathe. The patient may turn out to be sweaty and cyanotic. The sputum may display edema fluid that is pink from capillary hemorrhage and frothy from protein. Auscultation reveals inspiratory crackles chiefly at the bases, exactly where the hydrostatic pressure is greatest, but potentially all through both lungs. Rhonchi and wheezing ("cardiac asthma") may occur. The radiograph shows areas of alveolar flooding.
Increased Permeability Pulmonary Edema (Noncardiogenic Pulmonary Edema):
Probably the most common form of increased-permeability pulmonary edema is ARDS. ARDS is the final typical pathway of a quantity of various serious medical conditions, all of which lead to elevated pulmonary capillary leak.
The range of clinical presentations includes all the diagnoses in the adult ICU, such as sepsis, aspiration of gastric contents, pneumonia, and pancreatitis. Neverheless, there are scientific observations that mirror the pathophysiology. After the initial insult (eg, an episode of high-grade bacteremia), there is usually a period of stability, reflecting the time it takes for numerous immunologic mediators to harm the pulmonary capillary integrity.
Surfactant is inactivated, primary to a significant increase in surface forces and markedly reduced pulmonary compliance. For that first 24-48 hours after the insult, the affected individual might experience elevated function of breathing, identified by dyspnea and tachypnea but without abnormalities in the chest radiograph. At this early stage, the elevated Aa PO2 reflects alveolar edema and / mismatching and is corrected by increased FiO2 and increased minute air flow.
Pathologically, there's alveolar edema, hemorrhage, and atlectasis. The clinical picture may enhance, or there might be a further fall in compliance and disruption of pulmonary capillaries, leading to areas of true shaking and refractory hypoxemia. The combination of increased function of breathing and progressive hypoxemia generally requires mechanical ventilation.
Alveolar filling with inflammatory fluid leads to reduced efficiency of surfactant and elevated atelectasis. This procedure, which leads to reduced lung compliance (ie, stiffer lungs), is heterogeneous and may increase ventilation / perfusion imbalance. The higher pressures required to ventilate these sufferers may overdistend normal alveoli and decrease blood flow to areas of sufficient air flow.
Hypoxemia can be profound, and hypercapnia due to growing dead space ventilation might ensue. Radiographically, there may be diffuse alveolar infiltrates or "whiteout" of the lungs, representing diffuse confluent alveolar filling. Pathologically, diffuse alveolar harm (DAD) is observed, characterized by inflammatory cells and also the formation of hyaline membranes.
The mortality rate is 30-40%. Most patients die from some complication of their presenting illness, not from refractory hypoxemia. Of those who survive, most will recover near-normal lung function, but their recovery may be prolonged to 6 or even 12 months. A significant number will develop new reactive airway illness or pulmonary fibrosis.