User:Jrb2022/Cardiac asthma

Pathophysiology
The underlying causes for cardiac asthma stem from the eventual back up of fluid into the pulmonary vasculature as a result of the heart's, particularly left sided, inability to effectively and efficiently pump blood.(Buckner) The accumulation of fluid in the heart creates a higher than normal pressure system that places increasing pressure demands on the pulmonary venous system in order for appropriate oxygenation of blood to occur. (Tanabe) This results in what is called pulmonary venous hypertension (PVH), and results in distention and recruitment of pulmonary capillaries to help distribute the increased pressure gradient. (Buckner, Tanabe) At the capillary, there is a microvascular barrier that helps regulate fluid status via molecular pressure forces such as forces that push outward from vessels (hydrostatic) and pressures that pull or attract into vessels (oncotic). (Buckner) With increasing PVH, pressure outward overcomes pressure inward, and fluid is distributed to the (lung interstitum), preserving oxygen exchange at the capillary. (Buckner) Fluid is transported to the (hilum) and (pleural space), and removed via the (lymphatic system). (Buck) At first, the body is capable of handling excess water. However, over time the capillary vasculature is overwhelmed by increased pressure and fluid backs up into the alveolar sac, resulting in pulmonary edema and decreased oxygenation capability. (Buck) Additionally, increased pressure demands on capillary vasculature result in increases in vascular tone to include remodeling of pre-capillary vessels such as (medial wall hypertrophic changes). (Buck) Overtime, the remodeling efforts of the vessels can progress to hyperplastic changes of the vessels' wall construction, and results in increased pulmonary vascular resistance. (Buck)

There also is ongoing interest into establishing connections of cardiac asthma to abnormalities in bronchiole anatomy. (Litz, Tanabe) Current evaluation has proposed multiple mechanisms for increased airway resistance, and focus is on four (4) alternate explanations:


 * Bronchoconstriction as a result of pulmonary edema. (Buck, Tanabe)
 * Intrathoracic space competition from heart enlargement and pulmonary edema (complications of CHF) that compress airway construction and bronchioles. (Litz)
 * Bronchial obstruction secondary to intraluminal edema. (Buck, Litz)
 * Bronchial mucosa edema. (Buck)