oxygenation capability. 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. Over time, the remodeling efforts of the vessels can progress to hyperplastic changes of the vessels' wall construction, and results in increased pulmonary vascular resistance. There is ongoing interest into establishing connections of cardiac asthma to abnormalities in bronchiole anatomy. Current evaluation has proposed multiple mechanisms for increased airway resistance, and focus is on four alternate explanations: Bronchoconstriction as a result of pulmonary edema. Intrathoracic space competition from heart enlargement and pulmonary edema (complications of CHF) that compress airway construction and bronchioles. Bronchial obstruction secondary to intraluminal edema. Bronchial mucosa edema. Diagnosis The diagnosis of cardiac asthma is accomplished through workup of congestive heart failure, complete with: Evaluation of current symptoms with specific consideration of chronological progression or worsening. Past Medical History screen with consideration for conditions that predispose to heart failure, such as prior heart attack, history of coronary revascularization, high blood pressure, or diabetes (heart). Physical Exam with emphasis on listening for abnormalities of heart sound, abnormalities of lung sound, or presence of increased fluid retention in neck or in extremities. Laboratory Evaluation with specific interest in B-type natriuretic peptide levels. Electrocardiography to evaluate for irregularities in heart rhythm. Chest Radiograph to evaluate for presence of lung congestion or increased heart size. Echocardiography to evaluate heart function. Echocardiography is the preferred choice for diagnosis of heart failure in patients. As well as evaluation of lung function via: Pulmonary function testing (PFT) complete with bronchoprovocation testing. PFTs represent the preferred method for evaluating for bronchial asthma. Management Treatment of asthma symptoms in CHF patients is directed towards optimizing the patient's cardiovascular status and correcting potential oxygen deficit. Current recommendations in acute asthma symptoms are utilization of diuretics such as furosemide, venodilators such as nitroglycerin, and morphine. The initial strategy should focus on decreasing patient fluid retention with diuretic therapy, thereby decreasing cardiac preload and overall fluid load in pulmonary circuit (pulmonary congestion). Next, if aggressive diuresis is not adequately correcting symptoms, venodilators can be used to distribute blood and fluid to the venous system, thereby decreasing cardiac preload and left heart pressures contributing to pulmonary congestion. Lastly, morphine can be utilized for assistance in improving ease of breathing through a presumed mechanism similar to venodilation, as well as reducing patient anxiety. Additionally,