Lung Edema Clearance: Relevance to Patients with Lung Injury.

Zaher S Azzam,Jacob I Sznajder

doi:10.5041/rmmj.10210

Abstract

Pulmonary edema clearance is necessary for patients with lung injury to recover and survive. The mechanisms regulating edema clearance from the lungs are distinct from the factors contributing edema formation during injury. Edema clearance is effected via vectorial transport of Na+ out of the airspaces which generates an osmotic gradient causing water to follow the gradient out of the cells. This Na+ transport across the alveolar epithelium is mostly effected via apical Na+ and chloride channels and basolateral Na,K-ATPase. The Na,K-ATPase pumps Na+ out of the cell and K+ into the cell against their respective gradients in an ATP-consuming reaction. Two mechanisms contribute to the regulation of the Na,K-ATPase activity:recruitment of its subunits from intracellular compartments into the basolateral membrane, and transcriptional/translational regulation. Na,K-ATPase activity and edema clearance are increased by catecholamines, aldosterone, vasopressin, overexpression of the pump genes, and others. During lung injury, mechanisms regulating edema clearance are inhibited by yet unclear pathways. Better understanding of the mechanisms that regulate pulmonary edema clearance may lead to therapeutic interventions that counterbalance the inhibition of edema clearance during lung injury and improve the lungs’ ability to clear fluid, which is crucial for patient survival.

Highlights

Pulmonary edema is a life-threatening condition of fluid excess in the lungs that causes impaired gas exchange with consequent symptoms that range from mild shortness of breath to acute respiratory failure
56% of intensive care unit patients suffer from acute respiratory failure (ARF), with one-third of those subsequently dying.[1]
More recently it has been demonstrated that the alveolar epithelium has an active role in clearing edema out of the alveoli, a process called alveolar fluid clearance (AFC)

Summary

INTRODUCTION

Pulmonary edema is a life-threatening condition of fluid excess in the lungs that causes impaired gas exchange with consequent symptoms that range from mild shortness of breath to acute respiratory failure. 56% of intensive care unit patients suffer from acute respiratory failure (ARF), with one-third of those subsequently dying.[1] The pathogenesis of ARF can be classified to cardiogenic and non-cardiogenic pulmonary edema. Acute heart failure is the most common cause of increased hydrostatic pressure and is very prevalent, with almost 658,000 emergency department visits in the United States per year. The mortality rate from acute cardiogenic pulmonary edema ranges from 12% to 15%.2. Acute lung injury (ALI) that is due to increased permeability pulmonary edema is common, with an incidence of 86 per 100,000 person-years, and equates to over 190,000 cases and 74,500 fatalities annually in the United States. It was believed that fluid accumulation in the lung depends only on the abrogation of balanced Starling forces—the hydrostatic pressure and oncotic pressures.[4,5] more recently it has been demonstrated that the alveolar epithelium has an active role in clearing edema out of the alveoli, a process called alveolar fluid clearance (AFC)

LUNG STRUCTURE

HISTORIC PERSPECTIVE

ALVEOLAR ACTIVE SODIUM TRANSPORT MECHANISM

Findings

CONCLUSIONS