Nicardipine for acute stroke: Playing the Cards Right with Nicardipine
Since starting my residency, nicardipine has become one of the drugs that I have grown to love…maybe even becoming one of my favorite drugs to use for blood pressure control, especially in neurological emergencies such as acute ischemic stroke and subarachnoid hemorrhage. Time and time again, it has never failed me in these settings. It’s like a best friend who shows up at the right place and at the right time who knows exactly what to do in a difficult situation and does it right.
Nicardipine is a dihydropyridine calcium channel blocker that exerts its physiological effect by relaxing the vascular smooth muscle, leading to vasodilation and reduced systemic blood pressure. The great thing about it in the setting of neurological emergencies is that it has the added benefit of crossing the blood-brain barrier, allowing for relaxation of the smooth muscle within the cerebral vasculature. Its onset of action is anywhere from 5 to 15 minutes, and it has a predictable dose-response relationship. The other property that nicardipine has that makes it an ideal parenteral antihypertensive agent to use is its ease of dose titration, which is illustrated below:
- Starting dose: 5 mg/hr
- Titrate upward by 2.5 mg/hr every 5 to 15 minutes based on observed blood pressure response
- Maximum dose: 15 mg/hr
- Decrease rate by 2.5 mg/hr increments every 15 minutes if blood pressure is overcorrected until target blood pressure is reached
In my own personal experience, however, for some reason, EM attending physicians and EM residents resort to other parenteral antihypertensive medications first. As long as the pulse of the patient can tolerate it, the agent that is chosen first by most of the physicians that I work with is typically labetalol, which in many cases ends up not sufficiently reducing the blood pressure to our target. We usually end up switching to a nicardipine drip anyway. As this study demonstrated for a variety of hypertensive crises, many clinicians ultimately use nicardipine when labetalol fails due to the fact that nicardipine provides more dependable control of blood pressure. Speaking to some of the clinicians at my own institution, they tend to favor nicardipine as well due to the fact that there is a lesser incidence of bradycardia and hypotension compared to labetalol. The one thing that tends to be cumbersome for them with nicardipine is the fact that if a peripheral IV is used to infuse the drug, the line must be changed every 12 hours as long as the infusion is running to minimize irritation of the peripheral veins.
Granted, it may take some time for the nicardipine drip to be made and to program the infusion pump to deliver the medication, but this should not be a limiting factor in not using the medication at all. In fact, it does come in a premixed bag ready for use, so this can certainly reduce some time associated with preparing the product; in addition, the premixed formulation of nicardipine demonstrated greater benefit in controlling blood pressure for patients in the emergency department in comparison to labetalol in the CLUE study.
For neurological emergencies, I recommend the use of nicardipine over labetalol. It is important to remember that in this setting, the blood pressure should not be overcorrected too rapidly; this can be achieved by maintaining the systolic blood pressure between 140 and 160 mmHg. With this kind of control, the cards are indeed played right with nicardipine.
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