A 55-year-old man with a 10-year history of COPD presents to the emergency department with acute-onset wheezing, dyspnea, and chest tightness. Vital signs are BP 210/130 mmHg, HR 138 bpm, RR 26/min, and SpO2 79%. On examination, he has diffuse bilateral wheezing and appears diaphoretic and anxious. The medical team administers intravenous epinephrine for presumed bronchospasm. Within 10 minutes, his blood pressure rises to 280/160 mmHg, he develops severe substernal chest pain radiating to the left arm, and his electrocardiogram shows ST-segment depression in the precordial leads. His troponin I is elevated at 0.08 ng/mL. Laboratory studies reveal plasma free metanephrines of 4.8 nmol/L (normal <0.9 nmol/L). Which of the following best explains the acute clinical deterioration following epinephrine administration?
- A)Unopposed alpha-adrenergic vasoconstriction in a patient with undiagnosed pheochromocytomaGABARITO
- B)Beta-2 adrenergic receptor desensitization from chronic bronchodilator use in COPD
- C)Direct myocardial depression from excessive catecholamine exposure
- D)Activation of muscarinic receptors causing coronary artery vasospasm
- E)Inhibition of phosphodiesterase leading to excessive cAMP accumulation
Explicação
The markedly elevated plasma metanephrines indicate autonomous catecholamine production from pheochromocytoma. When exogenous epinephrine (which has both alpha and beta agonist effects) is administered to a patient with pheochromocytoma, the additional catecho... Ver explicação completa e trilha adaptativa →