Pulmonary edema is most commonly due to heart failure from left ventricular or biventricular dysfunction. Pulmonary hypertension and associated cor pulmonale (rightventricular dysfunction) do not usually cause pulmonaryedema as the increased vascular resistance is proximal tothe capillary bed. Increased capillary permeability, seen indisease states such as sepsis and acute respiratory distresssyndrome, can lead to pulmonary edema. Pulmonary edemamay also occur with excessive swings in intrathoracic pressure, as seen after tracheal foreign body aspiration or severeobstruction from hypertrophied tonsils and adenoids (postobstructive pulmonary edema). Pulmonary edema mayalso be present in conditions with decreased serum oncotic pressure (hypoalbuminemia); after administration of largevolumes of intravenous (IV) fluids, especially if there iscapillary injury; with ascent to high altitude (high altitude pulmonary edema); and after central nervous system injury (neurogenic pulmonary edema).
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Chapter 136 u Lower Airway, Parenchymal, and Pulmonary Vascular Diseases 473
The clinical manifestations of pulmonary edema are dyspnea, tachypnea, and cough (often with frothy, pink-tinged sputum). As the edema worsens, there is increased work of breathing and hypoxemia; diffuse inspiratory crackles can be heard on auscultation.
Chest radiographs may reveal diffuse hazy infiltrates, classically in a perihilar pattern, but these findings may be obscured by underlying lung disease. Interstitial edema (Kerley B lines)may be seen, especially at the lung bases.
Treatment and prognosis depend on the cause of the pulmonary edema and response to therapy. Patients should be positioned in an upright posture and given supplemental O2. Diuretic therapy and rapidly acting IV inotropic agents may be helpful in cardiogenic pulmonary edema. Continuous positive airway pressure (CPAP) or intubation with positive pressure ventilation using high positive end-expiratory pressures (PEEP) may be required.
SEE CHAPTER 39.
Pulmonary hypertension (PH) is classified in five groups basedon mechanism. Group 1 is pulmonary arterial hypertension(PAH) due to diseases within veins and small pulmonary muscular arteries such as persistent pulmonary hypertension of thenewborn, congenital heart disease (including those with excessive pulmonary blood flow due to left-to-right cardiac shunting), exposure to various drugs (e.g., cocaine, amphetamines),and idiopathic pulmonary arterial hypertension (previouslycalled primary pulmonary hypertension). Hereditary IPAH isalso in this group and has been linked with the bone morphogenetic receptor-2 (BMPR2) gene. Group 2 is caused by dysfunction of the left heart such as valvular disease. Group 3 issecondary to lung disease or chronic hypoxia, including upperairway obstruction resulting in obstructive sleep apnea and hypoxemia. In Group 4, PH is secondary to chronic pulmonarythromboembolism. Group 5 includes PH of unclear but multifactorial diseases, including some autoimmune diseases andmetabolic diseases. With prolonged PAH, irreversible changesmay occur in the intima and media of the pulmonary arterioles.