What Do You Know About Respiratory Failure? Trivia Questions

Explanation
The causes of acute hypoxemic respiratory failure are a low inspired concentration of oxygen, alveolar hypoventilation, ventilation-perfusion mismatch, intrapulmonary shunting, a low mixed venous oxygen content, and, rarely, diffusion impairment. Low inspired concentration of oxygen is an uncommon cause of acute hypoxemic respiratory failure. This can occur at high altitudes or when toxic gases are inhaled (e.g., smoke inhalation). Diffusion impairment is a relatively uncommon cause of acute hypoxemic respiratory failure but may occur with severe interstitial lung disease. In patients with acute respiratory distress syndrome, diffusion impairment can contribute to hypoxemia, but shunting is the more important physiologic derangement in this disorder. Pure alveolar hypoventilation is a relatively rare form of acute hypoxemic respiratory failure that is caused by neuromuscular or central nervous system dysfunction (e.g., opiate overdose). Ventilation-perfusion mismatching is the most common pathophysiologic cause of acute hypoxemia. It develops when there is a decrease in ventilation to normally perfused regions of the lung, a decrease in perfusion to normally ventilated regions of the lung, or some combination of a decrease in both ventilation and perfusion. A low mixed venous oxygenation saturation can also contribute to hypoxemia. However, it is uncommon for this to be the only factor contributing to acute hypoxemic respiratory failure.

Explanation
Acute hypercapnic respiratory failure is defined as an arterial carbon dioxide tension (PaCO2) greater than 45 to 50 mm Hg, in association with respiratory acidosis. Chronic failure is also marked by an elevation in arterial carbon dioxide tension (PaCO2), but in patients with chronic respiratory failure, renal compensation tends to normalize the pH. The distinction between acute and chronic hypercapnic respiratory failure is important because the two have different prognoses and therapeutic implications. Signs and symptoms of hypercapnia depend not only on the absolute level of PaCO2 but also on the rate at which the level increases. A PaCO2 higher than 100 mm Hg may be well tolerated if the hypercapnia develops slowly and acidemia is minimized by renal compensatory changes. However, acute increases in PaCO2 levels may produce many neurologic symptoms and signs, including confusion, headaches, seizures, and coma. Nasal cannulas allow patients to eat, drink, and speak during oxygen administration. The disadvantage is that the exact fraction of inspired oxygen (FIO2) that is delivered is not known, because FIO2 is influenced by peak inspiratory flow demand. Noninvasive positive pressure ventilation is not indicated for patients with cardiac or respiratory arrest; nonrespiratory organ failure; impaired consciousness; unstable cardiac rhythms; hemodynamic instability; severe upper gastrointestinal bleeding; inability to protect the upper airway or clear secretions; or facial surgery, trauma or deformity. When adequate oxygenation cannot be obtained by noninvasive means or if progressive hypoventilation and hypercapnia with respiratory acidosis occur, endotracheal intubation and mechanical ventilatory support should be initiated.

Explanation
Guillain-Barre syndrome: Guillain-Barre syndrome is a peripheral nervous system disorder that affects nerve function and can lead to muscle weakness or paralysis. While respiratory muscle weakness can occur in Guillain-Barre syndrome, it is not typically associated with acute hypercapnic respiratory failure unless severe respiratory muscle involvement leads to respiratory failure.
Acute respiratory distress syndrome (ARDS): ARDS is a severe lung condition characterized by inflammation and injury to the lungs, leading to impaired gas exchange and severe hypoxemia. While ARDS can lead to respiratory failure, it typically presents with hypoxemic respiratory failure rather than hypercapnic respiratory failure.
Large pulmonary embolism: A large pulmonary embolism can cause acute respiratory distress and hypoxemia due to obstruction of pulmonary blood flow. However, it is not typically associated with acute hypercapnic respiratory failure unless there are significant underlying lung disease or comorbidities contributing to hypoventilation.
Pulmonary edema: Pulmonary edema is the accumulation of fluid in the lungs, often due to heart failure or acute respiratory distress. While severe pulmonary edema can cause respiratory distress and hypoxemia, it is not typically associated with acute hypercapnic respiratory failure unless there are underlying lung disease or comorbidities contributing to hypoventilation.
Given the patient's history of stage IV breast cancer with widespread bony metastases and long-acting morphine use for pain control, the most likely condition placing her at risk for acute hypercapnic respiratory failure is Guillain-Barre syndrome.

Explanation
Respiratory failure is defined as the inability of the respiratory system to provide an adequate gas exchange to meet the requirements of the individual patient. This can take the form of inadequate oxygenation of the arterial blood, the inability to remove sufficient CO2 from the blood (impaired ventilation), or a combination of both processes. Acute respiratory failure can result from lesions affecting several parts of the respiratory pump. Understanding the respiratory pump allows the clinician to classify any perturbation in the system on the basis of pathophysiology and helps the clinician narrow the differential diagnosis and decide on appropriate clinical management. Hypoxemic respiratory failure is a consequence of gas exchange failure and is recognized by hypoxemia (PaO2 < 60 mm Hg) with or without an increase in the alveolar-arterial O2 gradient. Hypercapnic respiratory failure is a consequence of ventilatory failure and is recognized by an elevation in PaCO2 (> 45 mm Hg at sea level).

Explanation
A clinical approach to hypoxemic respiratory failure requires the differentiation of potential causes on the basis of the alveolar gas equation and the A-aDO2. The value is influenced by age; it increases by 3 mm Hg every decade after 30 years of age. Hypoxemic respiratory failure with a normal A-aDO2 is caused by a low inspired oxygen concentration or alveolar hypoventilation. V/Q mismatching, shunt pathophysiology, or a diffusion abnormality will result in an increase in A-aDO2.