Choice A rationale:
Incorrect. Deep-breathing exercises could potentially worsen stridor. Stridor is a high-pitched, wheezing sound caused by a partial obstruction of the upper airway. Deep breathing can increase airflow through the narrowed airway, making the stridor more pronounced and potentially worsening the obstruction. In severe cases, it could lead to complete airway obstruction and respiratory distress.
Risk of aggravation: Deep-breathing exercises could aggravate the underlying cause of stridor, such as laryngeal edema or vocal cord dysfunction, by increasing inflammation or muscle tension in the airway.
Delay in definitive treatment: Focusing on deep-breathing exercises might delay more definitive interventions, such as intubation, which might be necessary to secure the airway and prevent respiratory failure.
Choice B rationale:
Incorrect. While albuterol nebulizer therapy can be helpful for bronchospasm, it is not the first-line treatment for stridor. Stridor is typically caused by an upper airway obstruction, and albuterol primarily targets the lower airways (bronchioles).
Limited effectiveness: Albuterol might not be effective in reducing stridor caused by upper airway obstruction, as it does not directly address the narrowing of the airway.
Potential for adverse effects: Albuterol can cause tachycardia, tremors, and anxiety, which could further complicate the patient's condition.
Choice C rationale:
Not the most immediate action. While calling a Rapid Response might be necessary if the patient's condition deteriorates, the first priority is to secure the airway and ensure adequate ventilation.
Time-consuming: Activating a Rapid Response team can take several minutes, and the patient's condition might not allow for that delay.
Choice D rationale:
Prioritizes airway management: Intubation is the most effective way to secure the airway and ensure adequate ventilation in a patient with stridor. It bypasses the obstruction and allows for controlled delivery of oxygen and ventilation.
Addresses potential for deterioration: Stridor can rapidly progress to complete airway obstruction, so prompt preparation for intubation is crucial to prevent respiratory failure.
Involves the primary healthcare provider: Consulting the primary health care provider ensures timely decision-making, appropriate medication administration (such as sedatives or paralytics for intubation), and coordination of care.

Choice A rationale:
Hyperventilation is a condition characterized by rapid and deep breathing, leading to excessive removal of carbon dioxide (CO2) from the body. This decrease in CO2 levels actually causes respiratory alkalosis, not respiratory acidosis.
CO2 is a weak acid, and its removal from the blood raises the blood pH, making it more alkaline. Key mechanisms involved in hyperventilation-induced respiratory alkalosis:
Increased alveolar ventilation: Hyperventilation increases the rate at which CO2 is expelled from the lungs, reducing its concentration in the blood.
Shift in the equilibrium of the carbonic acid-bicarbonate buffer system: The reduction in CO2 levels drives the equilibrium towards the formation of bicarbonate ions, further reducing the concentration of hydrogen ions and increasing pH.
Renal compensation: The kidneys respond to respiratory alkalosis by excreting more bicarbonate ions, which helps to normalize the blood pH.
Choice B rationale:
Asthma is a chronic respiratory disease characterized by inflammation and narrowing of the airways. This can lead to impaired ventilation and retention of CO2, which can contribute to respiratory acidosis.
Mechanisms by which asthma can cause respiratory acidosis:
Bronchoconstriction: Narrowed airways impede airflow, making it difficult to expel CO2 from the lungs.
Air trapping: Inflammation and mucus production can lead to air becoming trapped in the lungs, further increasing CO2 levels.
Hypoventilation: Severe asthma attacks can cause respiratory muscle fatigue, leading to a decrease in breathing rate and inadequate CO2 removal.
Choice C rationale:
Chronic obstructive pulmonary disease (COPD) is a group of lung diseases characterized by chronic obstruction of airflow. This obstruction can lead to impaired ventilation and retention of CO2, which can contribute to respiratory acidosis.
Mechanisms by which COPD can cause respiratory acidosis:
Emphysema: Destruction of lung tissue reduces the surface area available for gas exchange, making it difficult to expel CO2. Chronic bronchitis: Inflammation and mucus production in the airways can obstruct airflow and trap CO2 in the lungs.
Hypoventilation: COPD can lead to respiratory muscle fatigue and a decrease in breathing rate, further impairing CO2 removal.
Choice D rationale:
Pulmonary embolism (PE) is a blockage of an artery in the lungs, usually by a blood clot. This can lead to impaired gas exchange and a decrease in oxygen levels in the blood. In severe cases, PE can also cause respiratory acidosis due to inadequate CO2 removal.
Mechanisms by which PE can cause respiratory acidosis:
Ventilation-perfusion mismatch: PE obstructs blood flow to a portion of the lungs, reducing the amount of CO2 that can be removed from those areas.
Hypoxemia: Low oxygen levels in the blood can stimulate the respiratory drive, leading to hyperventilation and CO2 retention.
Right heart failure: PE can strain the right side of the heart, leading to decreased pulmonary blood flow and impaired CO2 removal.