Gas Exchange Consequences of Left Heart Failure

Abstract

This review explores the pathophysiology of gas exchange abnormalities arising consequent to either acute or chronic elevation of pulmonary venous pressures. The initial experimental studies of acute pulmonary edema outlined the sequence of events from lymphatic congestion with edema fluid to frank alveolar flooding and its resultant hypoxemia. Clinical studies of acute heart failure (HF) suggested that hypoxemia was associated only with the final stage of alveolar flooding. However, in patients with chronic heart failure and normal oxygenation, hypoxemia could be produced by the administration of potent pulmonary vasodilators, suggesting that hypoxic pulmonary vasoconstriction is an important reflex for these patients. Patients with chronic left HF commonly manifest a reduced diffusing capacity, an abnormality that appears to be a consequence of chronic elevation of left atrial pressure. That reduction in diffusing capacity does not appear to be primarily attributable to increases in lung water but is improved by any sustained treatment that improves overall cardiac function. Patients with heart failure may also manifest an abnormally elevated VE/VCO2 during exercise, and that exercise ventilation abnormality arises as a consequence of both alveolar hyperventilation and elevated physiologic dead space. That elevated exercise VE/VCO2 in an HF patient has proven to be a powerful predictor of an adverse outcome and hence it has received sustained attention in the HF literature. At least three of the classes of drugs used to treat HF will normalize the exercise VE/VCO2, suggesting that the excessive ventilation response may be linked to elevated sympathetic activity.

Dead space: the physiology of wasted ventilation

“…As the solubility of CO 2 remains unchanged, the exercise associated V′A/Q′ shift leads to an increased physiological dead space measurement for CO 2 . Hence a consistent explanation for the elevated dead space measurements seen during exercise in the most impaired heart failure patients is the abnormally elevated overall V′A/Q′ ratio and its interaction with V′A/Q′ heterogeneity [49,50].…”

Resting arterial hypoxaemia in subjects with chronic heart failure, pulmonary hypertension and patent foramen ovale

“…Previous work investigating pulmonary gas exchange at rest in subjects with stable left heart failure has found that blood gases and data obtained from studies using the multiple inert gas elimination technique are typically within the normal range expected (Robertson, 2011). Additionally, these studies suggest that the primary cause for any abnormalities in pulmonary gas exchange efficiency is diffusion limitation caused by pulmonary oedema.…”

“…As a group, subjects with CHF typically have normal arterial oxygenation at rest and even during exercise (Clark & Coats, 1994;Robertson, 2011). Nevertheless, when present, the worsening of pulmonary gas exchange efficiency and arterial hypoxaemia observed in some subjects with CHF is typically attributed to diffusion limitation and pulmonary oedema (Robertson, 2011).…”

“…There are well-known consequences of chronic heart failure (CHF) and associated pulmonary hypertension on pulmonary gas exchange and arterial hypoxaemia (Robertson, 2011). As a group, subjects with CHF typically have normal arterial oxygenation at rest and even during exercise (Clark & Coats, 1994;Robertson, 2011).…”

“…As a group, subjects with CHF typically have normal arterial oxygenation at rest and even during exercise (Clark & Coats, 1994;Robertson, 2011). Nevertheless, when present, the worsening of pulmonary gas exchange efficiency and arterial hypoxaemia observed in some subjects with CHF is typically attributed to diffusion limitation and pulmonary oedema (Robertson, 2011). However, there are other potential causes for individual variability in arterial oxygenation in subjects with CHF, and it has been suggested that one potential cause of resting arterial hypoxaemia could be right-to-left shunt (Clark & Coats, 1994).…”