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{{WBRQuestion | {{WBRQuestion | ||
|QuestionAuthor=Chetan Lokhande | |QuestionAuthor=Chetan Lokhande | ||
|ExamType=USMLE Step 2 CK | |ExamType=USMLE Step 2 CK |
Latest revision as of 02:33, 28 October 2020
Author | PageAuthor::Chetan Lokhande |
---|---|
Exam Type | ExamType::USMLE Step 2 CK |
Main Category | MainCategory::Internal medicine |
Sub Category | SubCategory::Respiratory |
Prompt | [[Prompt::A 65-year-old male who smokes 1 pack per day for 35 years was brought to the emergency oepartment for acute shortness of breath. The emergency room physician administers 5L of Oxygen, orders an arterial blood gas, CXR, start inhaled albuterol plus ipratropium bromide and a steroid bolus. Initially he responds well, but after 15 min he complains of increasing difficulty breathing . A repeat steroid bolus and inhaled albuterol fails to relieve the shortness of breath. Which of these is the most probable cause of his increasing breathing difficulty?]] |
Answer A | AnswerA::CO2 retention |
Answer A Explanation | AnswerAExp::A failure to improve even after a repeat steroid and albuterol is typical for decreased hypoxic drive. A quick initial improvement followed by worsening of the dyspnea is specific for decreased hypoxic drive. |
Answer B | AnswerB::Respiratory acidosis |
Answer B Explanation | [[AnswerBExp::Acute respiratory acidosis occurs when an abrupt failure of ventilation occurs. This failure in ventilation may be caused by depression of the central respiratory center by cerebral disease or drugs, inability to ventilate adequately due to neuromuscular disease (e.g., myasthenia gravis, amyotrophic lateral sclerosis, Guillain-Barré syndrome, muscular dystrophy), or airway obstruction related to asthma or chronic obstructive pulmonary disease (COPD) exacerbation.Chronic respiratory acidosis may be secondary to many disorders, including COPD. Hypoventilation in COPD involves multiple mechanisms, including decreased responsiveness to hypoxia and hypercapnia, increased ventilation-perfusion mismatch leading to increased dead space ventilation, and decreased diaphragm function secondary to fatigue and hyperinflation.
Chronic respiratory acidosis also may be secondary to obesity hypoventilation syndrome (i.e., Pickwickian syndrome), neuromuscular disorders such as amyotrophic lateral sclerosis, and severe restrictive ventilatory defects as observed in interstitial fibrosis and thoracic deformities. Lung diseases that primarily cause abnormality in alveolar gas exchange usually do not cause hypoventilation but tend to cause stimulation of ventilation and hypocapnia secondary to hypoxia. Hypercapnia only occurs if severe disease or respiratory muscle fatigue occu]] |
Answer C | AnswerC::No response to treatment. |
Answer C Explanation | AnswerCExp::This is the wrong answer as the quick initial improvement followed by worsening of the dyspnea is specific for decreased hypoxic drive. |
Answer D | AnswerD::Decreased hypoxic drive |
Answer D Explanation | [[AnswerDExp::The hypoxic drive is a form of respiratory drive in which the body uses oxygen chemoreceptors instead of carbon dioxide receptors to regulate the respiratory cycle.
Normal respiration is driven mostly by the levels of carbon dioxide in the arteries, which are detected by peripheral chemoreceptors, and very little by the oxygen levels. An increase in carbon dioxide will cause chemoreceptor reflexes to trigger an increase in respirations. Hypoxic drive accounts normally for 10% of the total drive to breathe. This increases as the PaO2 goes to 70 torr and below, while hypoxic drive is no longer active when PaO2 exceeds 170 torr. The hypoxic drive is so weak that unconsciousness will develop before respiratory distress is noted and is therefore a risk for pilots flying at high altitudes. For this reason, supplemental oxygen is required by Federal Aviation Regulations[1] for pilots flying above about 12,500 feet altitude in unpressurized airplanes. In the past, it was believed that in cases where there are chronically high carbon dioxide levels in the blood such as in COPD patients, the body will begin to rely more on the oxygen receptors and less on the carbon dioxide receptors. And that in this case, when there is an increase in oxygen levels the body will decrease the rate of respiration. Recent studies have proven that COPD patients who have chronically compensated elevated CO2 levels (known as "CO2 Retainers") are not in fact dependent on hypoxic drive to breathe. However, when in respiratory failure and put on high inspired oxygen, the CO2 in their blood may increase via three mechanisms, namely the Haldane Effect, the Ventilation/Perfusion mismatch (where the regional pulmonary hypoxic vasoconstriction is released) and by the removal or reduction of the hypoxic drive itself.]] |
Answer E | AnswerE::Fatigue |
Answer E Explanation | AnswerEExp::Fatigue will not cause an initial improvement and then worsening |
Right Answer | RightAnswer::D |
Explanation | [[Explanation::The hypoxic drive is a form of respiratory drive in which the body uses oxygen chemoreceptors instead of carbon dioxide receptors to regulate the respiratory cycle.
Normal respiration is driven mostly by the levels of carbon dioxide in the arteries, which are detected by peripheral chemoreceptors, and very little by the oxygen levels. An increase in carbon dioxide will cause chemoreceptor reflexes to trigger an increase in respirations. Hypoxic drive accounts normally for 10% of the total drive to breathe. This increases as the PaO2 goes to 70 torr and below, while hypoxic drive is no longer active when PaO2 exceeds 170 torr. The hypoxic drive is so weak that unconsciousness will develop before respiratory distress is noted and is therefore a risk for pilots flying at high altitudes. For this reason, supplemental oxygen is required by Federal Aviation Regulations[1] for pilots flying above about 12,500 feet altitude in unpressurized airplanes. In the past, it was believed that in cases where there are chronically high carbon dioxide levels in the blood such as in COPD patients, the body will begin to rely more on the oxygen receptors and less on the carbon dioxide receptors. And that in this case, when there is an increase in oxygen levels the body will decrease the rate of respiration. Recent studies have proven that COPD patients who have chronically compensated elevated CO2 levels (known as "CO2 Retainers") are not in fact dependent on hypoxic drive to breathe. However, when in respiratory failure and put on high inspired oxygen, the CO2 in their blood may increase via three mechanisms, namely the Haldane Effect, the Ventilation/Perfusion mismatch (where the regional pulmonary hypoxic vasoconstriction is released) and by the removal or reduction of the hypoxic drive itself. |
Approved | Approved::Yes |
Keyword | WBRKeyword::Hypoxic drive, WBRKeyword::COPD, WBRKeyword::C02 retention |
Linked Question | Linked:: |
Order in Linked Questions | LinkedOrder:: |