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Aspirin overdose
61%
55/90
COPD
9%
8/90
Diabetic ketoacidosis
12%
11/90
Ethylene glycol intoxication
6%
5/90
Heroin overdose
11%
10/90
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This patient is presenting with an acute respiratory acidosis without metabolic compensation suggesting a diagnosis of a heroin overdose. Blood gas analysis provides insight into the etiology of a suspected acid-base pathology. Common causes of respiratory alkalosis include sepsis, pulmonary embolism, pain, anxiety, pregnancy, and salicylate intoxication (early in the course). Common causes of respiratory acidosis include exacerbations of COPD, severe exacerbation of asthma, and narcotic overdose. Importantly, with an acute asthma attack, there can be an evolution from a decreased PaCO2 in the initial presentation (hypoxemia-driven hyperventilation) followed by an increase in PaCO2 as the patient tires out, the obstructive nature of the disease takes over, and the condition worsens. In opioid overdose, patients acutely hypoventilate leading to a respiratory acidosis. However, because this is an acute/sudden change, the kidney does not have time to respond thus there is a respiratory acidosis without metabolic compensation. The best initial step in management in these patients is first naloxone. If this fails, intubation is needed. Incorrect Answers: Answer 1: Aspirin overdose presents initially with a respiratory alkalosis due to hyperstimulation of the medullary respiratory centers. Subsequently, an overwhelming metabolic acidosis ensues. Answer 2: COPD exacerbations presents with an acute on chronic respiratory acidosis; however, this is a chronic condition thus the patient's bicarbonate should be elevated given the kidney has had time to respond to the underlying lung pathology. Answer 3: Diabetic ketoacidosis presents with an anion gap acidosis with compensatory hyperventilation (a low CO2). Answer 4: Ethylene glycol intoxication presents with an anion gap acidosis with compensatory hyperventilation. Bullet Summary: Opioid overdose can lead to an acute respiratory acidosis from hypoventilation without metabolic compensation.
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