Impeded Alveolar-Capillary Gas Transfer With Saline Infusion in Heart Failure

Abstract

Abstract-The microvascular pulmonary endothelium barrier is critical in preventing interstitial fluid overflow and deterioration in gas diffusion. The role of endothelium in transporting small solutes in pathological conditions, such as congestive heart failure (CHF), has not been studied. Monitoring of pulmonary gas transfer during saline infusion in CHF was used to probe this issue. Carbon monoxide diffusion (DL CO ), its membrane diffusion (D M ) and capillary blood volume (V C ) subcomponents, and mean right atrial (rap) and mean pulmonary wedge (wpp) pressures after saline or 5% .01 versus 750 mL of saline) and decreased V C (Ϫ9, PϽ0.01 versus 750 mL of saline); aldosterone (Ϫ40%), renin (Ϫ41%), hematocrit (Ϫ3%), rap, and wpp behaved as they did after saline infusion. In controls, responses to both saline amounts were similar to responses in CHF patients regarding aldosterone, renin, hematocrit, rap, and wpp, whereas DL CO , D M , and V C values tended to rise. Hindrance to gas transfer (reduced DL CO and D M ) with salt infusion in CHF, despite an increase in V C and no variations in pulmonary hydrostatic forces, indicates an upregulation in sodium transport from blood to interstitium with interstitial edema. Redistribution of blood from the lungs, facilitating interstitial fluid reabsorption, or sodium uptake from the alveolar lumen by the sodium-glucose cotransport system might underlie the improved alveolar-capillary conductance with glucose. (Hypertension. 1999;34:1202-1207.)Key Words: capillaries Ⅲ epithelium Ⅲ glucose Ⅲ heart failure Ⅲ sodium F or the lung parenchyma to allow gas exchange between blood and gas in the alveoli, a continuous clearance is required of the excess of fluid into the interstitial space and the alveolar lumen. Excessive water accumulation in these compartments is called pulmonary and alveolar edema, respectively. The pulmonary microvascular endothelium and the alveolar epithelium constitute a barrier that is critical for gas exchange and modulation of fluid and solute passage between blood, the interstitial compartment, and alveoli. 1 Despite the substantial progress that has been made in understanding the physiology of the endothelial and epithelial layers in regulating lung fluid balance, further study regarding the local and systemic regulatory factors under pathological conditions is necessary. 1 An imbalance in hydrostatic forces is interpreted as the basic mechanism for volume overload and cardiogenic pulmonary edema. 2 In congestive heart failure (CHF), pulmonary edema may be absent despite elevation of the hydrostatic pressures 3 or may be present even if pressures are normal. 4 Whether altered hemodynamics are the exclusive mechanisms for pulmonary edema in CHF and whether alterations in the capillary endothelium and/or in the alveolar epithelium barrier contribute to changes in salt, water, and gas transfer have been the subjects of only limited research. 3 Cardiogenic anatomic injuries of the alveolar-capillary membrane have been reported in animals and humans. 5,6 ...

Endothelial Dysfunction and Lung Capillary Injury in Cardiovascular Diseases

“…In a study performed in post-MI patients with normal LV systolic function, an infusion of ~800 mL of saline reduced Dm by 13% 49 . In patients with mild to severe HF, a 150 ml infusion of saline produced a significant Dm reduction equivalent to 750 ml saline, whereas a 750 mL infusion of isotonic glucose solution did not decrease DLco and Dm 50 . None of these infusions caused changes in right atrial or pulmonary wedge pressures.…”

Exertional dyspnoea in chronic heart failure: the role of the lung and respiratory mechanical factors

“…Indeed, in heart failure patients, a low SaO 2 at rest or after alveolar-capillary membrane challenge such as fluid overload or exercise is an unusual event [71][72][73]. In healthy subjects, rapid infusion of saline is associated to a slight reduction of spirometric parameters but an unchanged DLCO and SaO 2 [74,75].…”

“…The DLCO reduction is greater when a β1-β2 blocker (carvedilol) is used compared with a β1 selective blocker (bisoprolol) (figure 5) [74]. In contrast, heart failure patients show a decrease in DLCO with even a small amount of saline infusion or physical exercise [71][72][73], suggesting that the lung fluid balance is in a critical condition. Indeed, in heart failure the alveolar-capillary membrane undergoes an extensive remodelling process.…”

Patterns of alveolar fluid clearance in heart failure

“…Notably, Guazzi et al also showed that impediment of gas transfer with salt infusion in CHF, despite an increase in capillary blood volume and no variations in pulmonary hydrostatic forces, indicates an upregulation in sodium transport from blood to interstitium with interstitial edema. Redistribution of blood from the lungs, facilitating interstitial fluid reabsorption, or sodium uptake from the alveolar lumen by the sodium-glucose cotransport system might underlie the improved alveolar-capillary conductance with glucose [11,12]. In patients with chronic CHF, there is an increase in the number of alveolar type II cells [13].…”