Airway Obstruction and Bronchial Hyperresponsiveness in Left Ventricular Failure and Mitral Stenosis

Abstract

Small and large airways narrow in LVF and the term cardiac asthma is often used. However, current usage of this term is inconsistent and its meaning is therefore ambiguous. The term is better avoided despite several emerging similarities with bronchial asthma. Airway narrowing may be precipitated by acute elevation of pulmonary or bronchial vascular pressures. This appears to be mainly due to reflex bronchoconstriction. The afferents of this reflex are C-fibers with their endings in the lung parenchyma, bronchi, and pulmonary blood vessels and RAR in the larger airways, and they run in the vagus nerves, as do the efferent bronchoconstrictor fibers. Chronic elevation of pulmonary vascular pressures, as in mitral stenosis, are also associated with airway narrowing. Pulmonary edema (in the absence of vascular hypertension) also causes reflex bronchoconstriction. Bronchial responsiveness to bronchoconstrictor drugs is increased in LVF, partly, at least, due to reflex mechanisms. Bronchial mucosal swelling may also contribute. Narrowing by nonreflex mechanisms definitely occurs and there is direct evidence that decreased lung volume caused by pulmonary edema may cause this. There is little evidence for bronchial narrowing due to the mechanical effect of peribronchial edema, or by swelling of the bronchial mucosa. However, edema foam may terminally cause grave obstruction. Patients with LVF are commonly treated with bronchodilator drugs, but the basis for this approach needs further clarification.

Hemodynamic Determinants of Dyspnea Improvement in Acute Decompensated Heart Failure

“…31,32 It has also been postulated that vascular distension and interstitial edema may directly stimulate pulmonary vascular nerve endings and result in dyspnea. 29,33 …”

Interactions between pulmonary hemodynamics and lung mechanics

“…pressures have no consistent consequences on the central airway resistance [56,57], where the edema affects primarily the pulmonary vasculature and is not severe enough to be manifested in the appearance of extravascular edema fluid around the bronchial wall [54]. Reports of impairments in the lung mechanical parameters mentioned the presence of severe interstitial and peribronchial edema [58,59] which was not the case in the present study.…”

Using the Lower Limit of Normal Instead of the Conventional Cutoff Values to Define Predictors of Pulmonary Function Impairment in Subjects With Chronic Heart Failure

“…[8][9][10][11][12] Several factors have been implied to play a role in the etiology of pulmonary function impairment in patients with heart failure, including the effects of heart failure itself on pulmo-nary function in addition to (previously undiagnosed) underlying pulmonary disease and confounding influences, such as smoking, coronary artery bypass grafting, and obesity. [4][5][6][7]13 However, results are not consistent among the studies. For example, although smoking and a history of coronary artery bypass grafting were associated with more impaired pulmonary function in the study of Johnson et al, 13 with also weak associations between left ventricular function and both lung volumes as well as diffusing capacity, none of the described pulmonary function abnormalities were found to be related to either smoking status, use of cardiac drugs, chest radiographic changes, hemodynamic findings, or clinical features, including the duration of heart failure in the study of Wright et al 14 Misdiagnosis of pulmonary function abnormalities may have interfered with the interpretation of prior research aiming to investigate the impact of heart failure and several clinical variables on pulmonary function in this group of patients.…”

“…Several factors have been implied to play a role in the etiology of pulmonary function impairment in patients with heart failure, including the effects of heart failure itself on pulmonary function in addition to (previously undiagnosed) underlying pulmonary disease and confounding influences, such as smoking, coronary artery bypass grafting, and obesity. [4][5][6][7]13 Diffusion impairment has been thought to be related to the thickening of the alveolar-capillary membrane due to hydrostatic mechanical injury, interstitial edema, remodeling, and fibrosis. 1,2,[4][5][6]27 Because heart transplantation does not affect or may even worsen pulmonary diffusing capacity despite an improvement in hemodynamic status and lung volumes, 28 it has been suggested that reduced diffusing capacity in chronic heart failure may be related to permanent damage to the alveolar-capillary membrane.…”

“…Isolated or combined pulmonary function abnormalities, such as restriction, diffusion impairment, and to a lesser extent airway obstruction are common in patients with chronic heart failure [1][2][3][4][5][6][7] and can contribute to the perception of dyspnea 8 and exercise intolerance. [8][9][10][11][12] Several factors have been implied to play a role in the etiology of pulmonary function impairment in patients with heart failure, including the effects of heart failure itself on pulmo-nary function in addition to (previously undiagnosed) underlying pulmonary disease and confounding influences, such as smoking, coronary artery bypass grafting, and obesity.…”