A client who has asthma has had peak flow readings in the yellow zone "since last night" & goes to urgent care. The nurse identifies which values as respiratory acidosis with partial compensation.

Please refer to arterial blood gas (ABG) tab for reference ranges

ABG

pH 7.35-7.45

p02 80-100 mmHg

pCO2 35-45 mmHg

PHCO3 22-26 mEq/L

A. Pulmonary edema: Pulmonary edema is a condition where fluid accumulates in the lungs, typically due to heart failure or other conditions that increase pressure in the blood vessels of the lungs. While pulmonary edema may occur in ARDS, the primary issue in ARDS related to surfactant damage is not fluid accumulation in the lungs but the inability of the lungs to properly expand and maintain gas exchange.

B. Atelectasis: In ARDS, damage to the lung cells that produce surfactant impairs the lungs' ability to maintain surface tension in the alveoli. Surfactant is a substance that helps keep the alveoli open by reducing surface tension. Without sufficient surfactant, the alveoli can collapse, leading to atelectasis (collapse of the alveoli), which further impairs oxygen exchange and contributes to hypoxemia in ARDS.

C. Bronchoconstriction: Bronchoconstriction refers to the narrowing of the airways due to muscle contraction, often seen in conditions like asthma. While bronchoconstriction may occur in other respiratory conditions, it is not the primary pathologic process in ARDS. ARDS is primarily characterized by damage to the alveolar-capillary membrane and impaired surfactant production, leading to atelectasis and impaired gas exchange.

D. Upper airway blockage: Upper airway blockage refers to an obstruction in the airway above the level of the trachea, often due to foreign objects, swelling, or other causes. This is not the primary concern in ARDS, which is a lower respiratory issue affecting the alveoli and gas exchange in the lungs.

A. Decrease in blood pressure: Nitroglycerin can cause vasodilation, leading to a decrease in blood pressure. However, the goal of administering nitroglycerin during an acute myocardial infarction (MI) is not primarily to lower blood pressure, but to improve oxygen supply to the heart and relieve pain. A decrease in blood pressure may occur as a side effect but is not the primary indication for its use.

B. Decrease in cardiac dysrhythmias: While nitroglycerin may help reduce myocardial oxygen demand, it is not specifically aimed at treating or preventing cardiac dysrhythmias. The primary action of nitroglycerin is to relieve chest pain by vasodilation and improving blood flow to the heart muscle.

C. Relief of chest pain: The primary effect of nitroglycerin in the setting of an acute MI is to relieve chest pain (angina). It works by dilating coronary arteries and improving blood flow to the heart muscle, thus reducing ischemia and relieving pain.

D. Decrease in heart rate: Nitroglycerin may have a secondary effect of reducing heart rate due to a reduction in preload and afterload, but this is not the primary objective. Nitroglycerin’s main goal is to relieve chest pain by improving oxygen supply to the heart muscle.