Circulatory collapse and obtundation occurr in a 37-year-old woman following an iatrogenic overdose of labetalol.

Circulatory collapse and obtundation occurr in a 37-year-old woman following an iatrogenic overdose of labetalol. Conventional therapy with glucagon and alpha-adrenergic receptor-stimulating agents was ineffective in raising the patient's cardiac output or improving her mental status despite increasing the arterial hurry The administration of amrinone was temporally associated with significant increases in the cardiac output accompanied by way of improved mental status. This case give an inkling ofs that amrinone may be effective adjunctive therapy or beta-adrenergic receptor blocker overdoses on reversing their negative inotropic effects

We existing a patient who developed circulatory collapse and obtundation following the administration of labetalol. The addition of amrinone to more conventional therapies was associated with significant improvement in the patient's cardiac performance and was accompanied according to improvement in her mental status.

CASE REPORT

A 37-year-old black woman at handed to the emergency room with a 3-day history of dyspnea forward exertion. Her past medical history was remarkable for long-standing hypertension that had necessitated sum of two units previous hospitalizations for hypertensive crises. Her prescribed medications included furosemide, clonidine, labetalol (400 mg twice daily), and nifedipine. The past medical history was notable for a cerebral aneurysm that had been surgically clipped 8 years earlier. The patient's medical records and reports from her family members recommended non-compliance with her antihypertensive regimen.

In the necessity room, the systolic blood compressing was 300 mm Hg with a diastolic influence of 180 mm Hg. The patient was pressingly transferred to the intensive care unit, where a nitroprusside infusion was begun and a radial artery catheter was placed for offspring pressure monitoring. A chest radiograph demonstrated marked cardiomegaly. The electrocardiogram showed left ventricular hypertrophy with a sinus rhyme at 111 beats per minute. The life-current pressure was brought down to 210/125 mm Hg with the intravenous nitroprusside infusion. An echocardiogram demonstrated marked left ventricular hypertrophy with more [i]or[/i] less decrease in left ventricular function.

The day following hospital admission labetalol, 800 mg was given according to mouth. Over the nearest 2 h the blood crushing and heart rate progressively decreased despite discontinuation of the nitroprusside infusion. This was associated with progressive deterioration in the patient's mental status followed by way of a brief tonic-clonic seizure requiring tracheal intubation for airway protection. The life-blood pressure reached a nadir of 97/62 mm Hg with the lowest heart rate being 56 beats for minute. Repeated intravenous boluses of normal saline solution were administered along with infusions of dopamine, phenylephrine, and glucagon. Ten hours following the administration of labetalol the kin pressure was 161/105 mm Hg with a heart rate of 61 beats by minute associated with continued obtundation. A pulmonary artery catheter was inserted at this time.

The initial pulmonary artery catheter readings give an inkling ofed depression of left ventricular function as manifested by dint of a low cardiac index and elevated pulmonary capillary wedge compressing (Table 1). An infusion of amrinone was begun, which was associated with dose-related increments in the cardiac index corresponding with decreases in the pulmonary capillary wedge press despite the continued administration of intravenous fluids. These hemodynamic changes were temporally associated with significant improvements in the patient's mental status, which allowed her to be safely extubated 10 h after the beginning of the amrinone infusion. The remainder of the hospitalization was unremarkable, and the patient was left without just discovered neurologic deficits.

DISCUSSION

Labetalol is a lipid soluble medicine with combined alpha- and beta-adrenergic receptor blocking properties, which is used for the oral and intravenous treatment of hypertension.[1] It has an elimination half-life of approximately 6 h and the ratio of beta to alpha antagonism is 3:1 after oral administration and 69:1 after intravenous administration.[1] Documented overdoses with labetalol appear to be uncommon[2-5] A fresh study using transesophageal echocardiography in patients with postoperative hypertension insinuates that the antihypertensive effects of labetalol are primarily appropriate to its negative inotropic properties.[6] In that inquiry decreases in blood pressure were associated with significant decreases in heart rate, cardiac index, and mixed venous oxygen saturation and a significant increase in the end-diastolic area of the left ventricle.

The hemodynamic derangements that occurr in this patient were meditation to result from the iatrogenic overdose of labetalol. The temporal association between the administration of labetalol and the hypotension glance ats a causal relationship. The mien of marked left ventricular hypertrophy may have predisposed to the exhibition of toxicity from the negative inotropic validitys of labetalol. The observ hemodynamic rejoinder (Table 1) in this case moves that both the beta- and alpha-adrenergic receptor blocking properties of labetalol are important in mediating its hemodynamic tenors following an overdose. Our patient's hypotension be agreeable toed to the administration of alpha-adrenergic receptor agonists and glucagon. Improvement in cardiac function and mental status was temporally associated with the administration of amrinone, although the dose of phenylephrine was also decreased during this time period.

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