Does the bronchial circulation contribute to congestion in heart failure?

Abstract

Pulmonary congestion is a hallmark feature of heart failure and is a major reason for hospital admissions in this patient population. Heart failure patients often demonstrate restrictive and obstructive pulmonary function abnormalities; however, the mechanisms of these changes remain controversial. It has been suggested that the bronchial circulation may play an important role in the development of these pulmonary abnormalities and in the symptoms associated with pulmonary congestion. Congestion may occur in the bronchial circulation from either a marked increase in flow or an increase in blood volume but with a reduction in flow due to high cardiac filling pressures and high pulmonary vascular pressures (a stasis like condition). Either may lead to thickened bronchial mucosal and submucosal tissues and reduced airway compliance resulting in airway obstruction and restriction and a lack of airway distensibility. These structural changes may contribute to "cardiac asthma" and dyspnea, characteristic features common in HF patients. Thus the bronchial circulation may be a potential target for therapeutic interventions. The aim of this paper is to review factors governing the control of the bronchial circulation, how bronchial vascular conductance may change with HF and to pose arguments, both supporting and in opposition to the bronchial circulation contributing to congestion and altered pulmonary function in HF. We ultimately hypothesize that the engorgement of the bronchial circulatory bed may play a role in pulmonary function abnormalities that occur in HF patients and contribute to symptoms such as orthopnea and exertional dyspnea.

Figure 1. Central role of the Bronchial Circulation in the Pulmonary Abnormalities of Heart Failure

The various respiratory control, neurohumoral, inflammation, and hemodynamic changes induced by the heart failure pathology are thought to affect the bronchial circulation and in turn contribute pulmonary congestion and increased work of breathing. Increased circulating neurohumoral (e.g. ANP, BNP, bradykinin, angiotensin-II, etc.) and inflammatory (e.g. TNF-α, IL family cytokines, ET-1, etc.) mediators serve to disrupt the balance between efferent vasoconstrictor and local vasodilatory mechanisms of the bronchovasculature. Additionally, mechanical stretch of the myocardium in a failing heart and the increase in pulmonary vascular pressures activate reflexes (cardiac and spinal afferent) normally quiet in healthy individuals. These alterations are thought to reduce bronchovascular constrictor tone and increase reflex brochovascular dilation. Altered vascular tone coupled with the impedance to forward flow caused by the increase in pulmonary capillary pressure in the bronchial circulation ultimately increase bronchial blood flow conductance and the overall volume of blood in the bronchial wall. Engorgement of this circulation stiffens the airways and may cause tissue impingement upon the lumen space translating to both restrictive and obstructive pulmonary function abnormalities. The combined effect of these alterations is hypothesized to contribute to the condition of pulmonary congestion that is further exacerbated by exercise, the supine position, and may be influenced by individual genetic variation.

Figure 2. Proposed Alterations in Airway Structure in Heart Failure

It is proposed that lung function may be altered in heart failure either through (A) vascular engorgement in the mucosal plexus of the bronchial circulation, or through (B) expansion of the pulmonary circulation, interstitial pulmonary edema , and/or other sources competing for intrathoracic space displacing airspace by compressing the entire airway structure, including the bronchiole wall. In the latter example, wall thickness remains relatively unchanged. Also possible, but not shown, is the potential impact of smooth muscle proliferation.