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Labetalol
See also Beta-adrenoceptor antagonists
General information
Labetalol is a non-selective alpha- and beta-adrenoceptor antagonist; these actions reside in four different enantiomers.
Labetalol is less likely to increase airways resistance in patients with bronchial asthma or to reduce peripheral blood flow. However, it can produce postural hypotension [ ], and paresthesia of the scalp [ ] and perioral numbness [ ] have been described.
Organs and systems
Cardiovascular
Labetalol is generally used effectively as an antihypertensive drug without reports of high vascular resistance, even in patients with pheochromocytoma. However, pheochromocytoma with increased systemic vascular resistance and reduced cardiac index has been described [ ].
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A 36-year-old man with a pheochromocytoma underwent adrenalectomy. After induction of anesthesia he was given intravenous labetalol 30 mg, and after intubation his blood pressure rose from 147/85 to 247/150 mmHg, his systemic vascular resistance index rose from 1958 to 3458 dyn sec − 1 m 2 cm 5 , and his cardiac index fell to 3.6 l min − 1 m 2 . During tumor resection, he was given sodium nitroprusside to reduce his blood pressure. After tumor resection, his blood pressure fell to 77/52 mmHg and his systemic vascular resistance index to 1635 dyn sec − 1 m 2 cm 5 . His blood pressure was effectively controlled with dobutamine.
This case affords a reminder that intravenous labetalol can increase the systemic vascular resistance and cause a hypertensive crisis. In these cases, labetalol should be replaced with a pure alpha-blocker or another vasodilator, to prevent the possibility of cardiovascular complications.
Neonatal cardiac arrest was precipitated in one case by labetalol [ ].
Electrolyte balance
Three cases of severe hyperkalemia have been reported in renal transplant recipients taking labetalol for acute hypertension [ ] and life-threatening hyperkalemia has been reported after intravenous labetalol [ ].
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A 28-year-old man with severe hypertension and end-stage renal disease was given two intravenous doses of labetalol 20 mg 1 hour apart for malignant hypertension. The serum potassium concentration before treatment was 6.2 mmol/l, but 8 hours after labetalol it rose to 9.9 mmol/l and he developed left bundle branch block, ventricular tachycardia, and hypotension. He was given intravenous calcium gluconate, sodium bicarbonate, and lidocaine and reverted to sinus rhythm. The potassium concentration after 2 hours was 8.0 mmol/l. After hemodialysis the potassium concentration fell to 6.1 mmol/l.
In a retrospective chart review in 103 transplanted patients from January to November 1994, hypertension requiring perioperative treatment was observed in 51 cases [ ]. Treatment for hyperkalemia was necessary in 13 of the 38 patients who were treated with labetalol, compared with 11 of the 65 who were treated with another antihypertensive treatment.
Patients with end-stage renal disease on dialysis can have an enhanced hyperkalemic response to labetalol, which is partly attributable to electrochemical disturbances in the cells, characterized by an increase in intracellular sodium and chloride and a fall in intracellular potassium.
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