A 68-year-old male with a history of coronary artery disease/myocardial infarction treated with a drug-eluting stent and controlled hypertension develops microscopic hematuria and is scheduled for cystoscopy. His medication list includes metoprolol XL 100 mg daily, losartan 50 mg daily, atorvastatin 80 mg daily, and aspirin 81 mg. His preoperative examination is unremarkable, and patient reports exercise capacity >4 METs. Per his instructions from his surgeon, he has continued taking all his medications except for holding his lisinopril and metformin the night before. After an uneventful induction and intubation, the patient’s blood pressure drops from 132/68 to 70/42 mm Hg, with pulse continuing at 66 beats/min. The patient’s five-lead electrocardiogram demonstrates sinus rhythm but with new 1 mm ST depressions in his precordial leads. End-tidal CO2 and pulse oximetry are unchanged. The blood pressure does not improve with repeated boluses of phenylephrine and ephedrine, or with a fluid bolus of 500 mL, necessitating vasopressin and epinephrine boluses. Bedside transthoracic echocardiogram demonstrates a hyperdynamic and collapsed LV, no wall motion abnormalities, no valvular lesions, and no pericardial effusion. Decision is made to postpone the patient’s elective surgery and awaken him. Upon emergence, the patient’s blood pressure recovers to 124/62 mm Hg and pulse 60 beats/min. The patient is extubated successfully with no neurological sequelae.
Which of the following is the most likely etiology of the patient’s hypotension?
A. HypovolemiaCorrect Answer: B
Losartan is a highly selective angiotensin (AT1) receptor blocker (ARB), and like other ARBs and ACE inhibitors, is used for treatment of hypertension, heart failure, and prevention of cardiac remodeling after myocardial infarction. By displacing angiotensin II from the AT1 receptor, ARBs antagonize AT1-receptor–induced vasoconstriction, aldosterone, catecholamine and arginine-vasopressin release, water intake, and hypertrophic responses. During general anesthesia, maintenance of blood pressure is dependent on the RAAS and AT1 activation. By blocking AT1, losartan may precipitate severe hypotension under general anesthesia. Chronic AT1-blockade can also reduce the vasoconstrictor response to alpha1 receptors activated by norepinephrine, causing resistance to direct and indirect pharmacologic intervention, as seen in this patient. Clinical studies have shown that vasopressin can restore the sympathetic response and is useful in cases of refractory hypotension in patients with chronic RAAS inhibition undergoing general anesthesia. Norepinephrine, with much more potent alpha1 activation than phenylephrine, is also recommended as it may have a more favorable effect on splanchnic perfusion and oxygen.
While the patient’s NPO status may result in hypovolemia, the lack of response to a fluid bolus makes hypovolemia alone a less likely cause of this patient’s hypotension during general anesthesia. The patient reported great exercise capacity, no symptoms of heart failure, no signs of acute infarction on ECG, and return to normal blood pressure after discontinuation of general anesthesia, making an acute myocardial infarction or pulmonary embolism unlikely.
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