An adult patient is admitted for an asthma attack. Which assessment obtained by the nurse would support that beta2 adrenergic agonist albuterol was effective?

Choice A reason: Hyperplasia and deformation of bronchial cartilage are not the causes of airway obstruction in COPD type B. Bronchial cartilage is the rigid structure that supports the bronchi, the large airways that branch from the trachea. Hyperplasia is an increase in the number of cells, and deformation is a change in the shape or structure of the cells. These processes can affect the bronchial cartilage, but they do not directly obstruct the airway.

Choice B reason: Loss of alveolar elastin is not the cause of airway obstruction in COPD type B. Alveolar elastin is the elastic fiber that allows the alveoli, the tiny air sacs at the end of the bronchioles, to expand and recoil during breathing. Loss of alveolar elastin is a characteristic of COPD type A (emphysema), which causes the alveoli to lose their shape and collapse. This reduces the surface area for gas exchange, but it does not obstruct the airway.

Choice C reason: Pulmonary edema is not the cause of airway obstruction in COPD type B. Pulmonary edema is the accumulation of fluid in the lungs, usually due to heart failure or lung injury. It causes shortness of breath, coughing, and crackles in the lungs. It can impair gas exchange and oxygenation, but it does not obstruct the airway.

Choice D reason: Thick mucus, fibrosis, and smooth muscle hypertrophy are the causes of airway obstruction in COPD type B. Thick mucus is the result of chronic inflammation and infection of the bronchi, which stimulates the mucus glands to produce more and thicker mucus. Fibrosis is the formation of scar tissue in the bronchial walls, which narrows the airway and reduces its elasticity. Smooth muscle hypertrophy is the enlargement of the smooth muscle cells that surround the bronchi, which increases the airway resistance and causes bronchospasm. These processes combine to obstruct the airway and cause chronic cough, wheezing, and dyspnea.

Choice A reason: Cardiac output has not fallen below normal levels. Cardiac output is the amount of blood pumped by the heart per minute. It is affected by the heart rate and the stroke volume. Angina pectoris does not directly affect the cardiac output, but it can reduce the stroke volume due to impaired ventricular filling.

Choice B reason: The vagus nerve is not stimulated. The vagus nerve is a cranial nerve that innervates the heart and other organs. It is part of the parasympathetic nervous system, which slows down the heart rate and lowers the blood pressure. Angina pectoris does not activate the vagus nerve, but it can trigger the sympathetic nervous system, which increases the heart rate and blood pressure.

Choice C reason: Myocardial stretch has not exceeded the upper limits. Myocardial stretch is the degree of tension or load on the cardiac muscle fibers. It is determined by the end-diastolic volume, which is the amount of blood in the ventricle at the end of relaxation. Angina pectoris does not cause excessive myocardial stretch, but it can impair the myocardial contractility due to ischemia.

Choice D reason: The myocardial oxygen supply has fallen below demand. This is the main cause of angina pectoris. It occurs when the coronary arteries, which supply blood and oxygen to the heart muscle, are narrowed or blocked by atherosclerosis or spasm. This creates an imbalance between the oxygen demand of the heart, which increases during exertion, and the oxygen supply, which is reduced by the obstruction.