Continuous Infusion Of Nicardipine Research Articles

A randomized controlled trial: Comparing blood pressure reduction in hyperacute phase of spontaneous intracerebral hemorrhage by continuous nicardipine infusion with or without a preceding nicardipine bolus dose

ObjectivesTo determine whether addition of an intravenous bolus dose before continuous nicardipine infusion would improve blood pressure reduction in the hyperacute phase in patients with spontaneous intracerebral hemorrhage (ICH). DesignDouble-blind randomized controlled trial. SettingOne academic emergency department (ED) in Bangkok, Thailand. ParticipantsAdult patients with spontaneous ICH presented to the ED between June 30, 2022, and July 15, 2023. InterventionsThe bolus group (n = 31) received an intravenous bolus dose of nicardipine before nicardipine continuous infusion, whereas the non-bolus group (n = 31) was given a placebo and nicardipine continuous infusion. Main outcomesSystolic blood pressure (SBP) within the first hour (being measured every 5 min), neurological deterioration, and infusion dosage at 60 min were assessed. ResultsBasic characteristic features including the mean baseline SBP were not significantly different between the two groups. At 10 min after treatment initiation, the bolus group had a significant decrease in SBP (32.1 ± 13.6 vs 22.3 ± 18.5 mmHg; p-value = 0.020). Moreover, the target SBP of 180 mmHg could be achieved within 10 min in the bolus group compared with 15 min in the non-bolus group. However, the overall mean SBPs were not significantly different, with 152 ± 12 mmHg in the bolus group compared with 150 ± 15 mmHg in the non-bolus group (p-value = 0.564). None of the patients in both groups had neurological deterioration over the first hour of the treatment. The infusion dosages of nicardipine at 1 h were 6.2 mg/h (5.9, 7.7 mg/h) and 6.8 mg/h (5.9, 8.4 mg/h) in the bolus and non-bolus groups, respectively (p-value = 0.618). ConclusionsAdministering a 1-mg bolus dose of nicardipine before continuous nicardipine infusion notably reduces SBP at 10 min. However, the overall SBP does not exhibit a significant decline during the hyperacute phase of spontaneous intracerebral hemorrhage.

Use of continuous infusion of nicardipine to control persistent postpartum hypertension: A retrospective study

To evaluate the effect of continuous infusion of nicardipine on the management of uncontrolled blood pressure (BP) during postpartum period. This retrospective study included 209 women diagnosed in hospital with hypertensive disorders during pregnancy and had uncontrolled BP after delivery between January 2018 to December 2020 Uncontrolled BP was defined as persistent elevation of systolic BP ≥ 160 mm Hg or diastolic BP ≥ 110 mm Hg. Patients were divided into 2 groups: nicardipine (N = 53; continuous nicardipine infusion and additional bolus of labetalol or hydralazine) and control (N = 156; consecutive bolus of labetalol or hydralazine). BP data were analyzed using the Mann-Whitney U and χ2 tests by dividing the time interval of 4 hours by the delivery time. The highest BP trends showed that the mean values of both systolic and diastolic BP immediately before delivery were higher in the nicardipine group than in the control. After 8 to 12 hours following delivery, both systolic and diastolic BP were lower in the nicardipine group than in the control. Subsequently, 16 to 20 hours after delivery, both systolic and diastolic BP were significantly lower in the nicardipine group than in the control (137/80 vs 141/84 mm Hg). Initially, the proportions of uncontrolled BP in the nicardipine group were higher than those in the control; however, it then became lower at all time intervals 8 hours after delivery. The proportions of patients who received additional antihypertensive agents and the median cumulative dosages were lower in the nicardipine group than in the control. Continuous infusion of nicardipine can help manage uncontrolled BP during the postpartum period.

Effect of nicardipine on renal function following robot-assisted laparoscopic radical prostatectomy in patients with pre-existing renal insufficiency

To investigate the renoprotective effect of nicardipine in patients with pre-existing renal insufficiency undergoing robot-assisted laparoscopic radical prostatectomy (RALRP). Men with preoperative renal insufficiency (estimated glomerular filtration rate [eGFR] <60 ml/min per 1.73 m(2)) were enrolled and randomized to receive either 0.5 µg/kg per min nicardipine continuous infusion (nicardipine group) or normal saline (control group) during RALRP. Renal function was determined by eGFR and serum creatinine concentration. Serum creatinine levels on postoperative days (POD) 1 and 3 were significantly lower than baseline values in the nicardipine group (n = 50). In the control group (n = 50), eGFR was significantly higher on POD 3 than baseline, and was significantly higher than baseline on POD 1 and 3 in the nicardipine group. The change in eGFR from baseline to POD 1 was significantly higher in the nicardipine group than the control group. Continuous infusion of nicardipine during RALRP improved postoperative renal function on POD 1 in patients with pre-existing renal insufficiency.

Abstract WP277: Aggressive Blood Pressure Management: A Perceived Contraindication to IV-tPA

Background: Our recent poll of US Primary Stroke Centers demonstrated that 23% of practitioners perceived the need for blood pressure (BP) management by means of a continuous dihydropyridine calcium channel blocker infusion (i.e. nicardipine) as a contraindication to IV-tPA. While the NINDS study originally excluded patients who required "aggressive" BP management, the Activase® label is silent on this criterion. In view of this persistent belief, we sought to examine the safety of IV tPA administered with nicardipine. Methods: A retrospective cohort study was performed over a period of 36 months examining consecutive patients treated with IV-tPA at our comprehensive stroke center who received nicardipine vs. intermittent IV labetalol or those requiring no BP medications. Patient demographics, past medical history, and stroke severity were compared. Safety was assessed by (1) symptomatic intracerebral hemorrhage (sICH) within 36 hours, defined as parenchymal hemorrhage in combination with ≥ 4 points increase in NIHSS, and (2) the presence of any hemorrhagic transformation (HT) on repeat CT or MRI. Results: A total of 212 patients were treated with IV-tPA, median age 68 (range 24-99), median pre-tPA bolus NIHSS 8 (range 0-32) with no differences between nicardipine treated (n=32, 15%) vs. others (n=180). Patients treated with nicardipine were more frequently female (63%; p=0.0337). Past medical history was similar except for CHF (nicardipine 0, other 15%, p=0.0087) and previous stroke (nicardipine 59%, other 36%, p=0.0132). Despite these imbalances, nicardipine patients vs. others had similar rates of sICH (0 vs. 3.3%; p=NS), or any HT (3.1% vs. 9.5%; p=NS). No telephone-assisted tPA drip-n-ship patients (n=96) received nicardipine prior to or during tPA infusion due to non-formulary status at transferring hospitals; sICH rate in this group was 4% vs. 2% (p=NS) in non-transfers with or without nicardipine. Conclusions: IV thrombolysis in patients requiring continuous nicardipine infusion is safe compared to those requiring less intensive BP management. The need for continuous nicardipine infusion should not be construed as rationale for withholding IV tPA in acute ischemic stroke patients.

Effect of Nicardipine on Renal Function After Robot-assisted Laparoscopic Radical Prostatectomy

To investigate the renoprotective effect of nicardipine in patients undergoing robot-assisted laparoscopic radical prostatectomy (RALRP) in a prospective trial. Superior visualization of the increasingly performed RALRP requires pneumoperitoneum and extreme head-down tilt, both of which are associated with a decrease in postoperative renal function. Nicardipine causes preferential dilation of the renal arterioles and attenuates renal dysfunction after cardiac surgery. After we obtained institutional review board approval, we randomly treated 100 patients undergoing RALRP with a continuous infusion of nicardipine at a rate of 0.5 microg/kg/min (nicardipine group, n = 50) or with normal saline (control group, n = 50) during surgery. We measured the serum creatinine (Cr) level and estimated glomerular filtration rate (eGFR) 1 day before surgery and the first and third postoperative days (POD 1 and 3, respectively). Patients' characteristics and operative data were similar between groups. The serum Cr was significantly higher and the eGFR was significantly lower in the control group at POD 1. The number of patients having renal insufficiency (eGFR < 60 mL/min/1.73 m(2)) and abnormal serum creatinine level (>1.4 mg/dL) was significantly greater in the control group (9 vs 1, and 4 vs none, respectively) at POD 1. Continuous infusion of low-dose nicardipine during RALRP seems to offset the deleterious effects of inevitable pneumoperitoneum and extreme head-down tilt on renal function in preserving the eGFR and attenuating the development of renal insufficiency in the immediate postoperative period.

The Effects of Continuous Nicardipine Infusion on Blood Pressure and Heart Rate during Endotracheal Intubation

Background: Laryngoscopy and tracheal intubation often induced an undesirable increase in blood pressure and heart rate. We evaluated the preventing effect of nicardipine infusion on the increase of the blood pressure (BP) and heart rate (HR) following a direct laryngoscopy and tracheal intubation. Methods: Sixty, ASA physical status 1-2, adult patients were selected with informed consent, and randomly allocated into two groups; control group (n = 30) and nicardipine group (n = 30). In the control group, 1.8 ml/kg/h of normal saline was infused, and in the nicardipine group, 5μg/kg/min of nicardipine was infused continuously from 2 minutes before intubation to 3 minutes after intubation. BP and HR were measured by non-invasive method after arrival at the operating room, before tracheal intubation, shortly after tracheal intubation, and 1, 3, 5, and 10 minutes following intubation. Data were analyzed by repeated measure of ANOVA and t-test. Results: Systolic and diastolic BP were significantly lower in the nicardipine group than in the control group (P ＜ 0.05). HR showed significantly higher value in the nicardipine group (P ＜ 0.05). Conclusions: The continuous infusion of nicardipine (5μg/kg/min) was effectively attenuating an increase of BP during tracheal intubation. But the increase in HR is not blunted by nicardipine infusion and there is a significant increase in HR. Although rate-pressure product (RPP) does not increase, the use of nicardipine for blunting hemodynamic responses should be considered carefully in patients with ischemic heart disease.

Effects of nicardipine-, nitroglycerin-, and prostaglandin E1-induced hypotension on human cerebrovascular carbon dioxide reactivity during propofol-fentanyl anesthesia

Study Objective: To investigate the effects of nicardipine-, nitroglycerin-, and prostaglandine E1-induced hypotension on cerebrovascular carbon dioxide (CO2) reactivity over a wide range of arterial CO2 tension (PaCO2) (PaCO2; range 25 to 50 mmHg).Design: Prospective, randomized study.Setting: Operating room of a university-affiliated hospital.Patients: 36 ASA physical status I and II patients without cerebrovascular disease, hypertension, or diabetes mellitus, undergoing an elective abdominal surgery.Interventions: Patients were randomly allocated to one of three groups (nicardipine-, nitroglycerin-, or prostaglandin E1-induced hypotension group; 12 in each group). Anesthesia was induced and maintained with a bolus dose, followed by a continuous infusion of propofol (6.7 ± 1.5 mg/kg/hr) and fentanyl (1.68 ± 0.4 μg/kg/hr). Deliberate hypotension of mean arterial pressure 55 to 60 mmHg was induced and maintained with a bolus dose, followed by a continuous infusion of nicardipine (6.80 ± 0.75 μg/kg/min), nitroglycerin (3.20 ± 1.10 μg/kg/min), or prostaglandin E1 (0.103 ± 0.052 μg/kg/min).Measurements and Main Results: Time-averaged mean red blood cell velocity in the right middle cerebral artery (Vmca) at PaCO2 ranging from 25 to 50 mmHg was measured with transcranial Doppler ultrasonography. A minimum of six simultaneous measurements of Vmca and PaCO2 were obtained during baseline and deliberate hypotension in each patient. Absolute slope between Vmca and PaCO2 during baseline and deliberate hypotension was determined individually by linear regression analysis. Absolute slope was treated as the variable, because it yielded a significant close correlation coefficient (r > 0.95; p < 0.05). Comparisons between baseline and deliberate hypotension were made by analysis of variance for repeated measures. Mean absolute slope was significantly reduced from 1.88 ± 0.57 cm/sec/mmHg (mean ± SD) to 1.21 ± 0.46 in the nicardipine group (p < 0.05), from 1.75 ± 0.69 to 1.35 ± 0.47 in the nitroglycerin group (p < 0.05), and from 1.95 ± 0.89 to 1.33 ± 0.70 (p < 0.05) in the prostaglandin E1 group, respectively.Conclusion: Nicardipine-, nitroglycerin-, and prostaglandin E1-induced hypotension attenuate the human cerebrovascular CO2 reactivity during propofol-fentanyl anesthesia.

RETRACTED: Post-tetanic count and train-of-four responses during neuromuscular block produced by vecuronium and infusion of nicardipine

We have examined onset and recovery of neuromuscular block produced by vecuronium using either post-tetanic count (PTC), or the first twitch of the train-of-four (TOF) (T1/T0) and TOF ratio (T4/T1) during continuous infusion of nicardipine. Sixty adult patients were allocated to one of four groups of 15 patients each: nicardipine-PTC, nicardipine-TOF, control-PTC and control-TOF. In the nicardipine-PTC and nicardipine-TOF groups, nicardipine 0.03 mg kg-1 was given before vecuronium 0.1 mg kg-1 and a continuous infusion of nicardipine was started immediately at a rate of 2 micrograms kg-1 min-1. Mean time from administration of vecuronium to onset of neuromuscular block in the nicardipine-PTC and nicardipine-TOF groups was significantly shorter than in the control-PTC and control-TOF groups (166 (SD 39) vs 220 (28) s; P < 0.05). There was no significant difference in recovery of PTC between the nicardipine-PTC and control-PTC groups or in recovery of TOF ratio in the nicardipine-TOF and control-TOF groups. However, during recovery, T1/T0 in the nicardipine-TOF group was significantly less than that in the control-TOF group, 60-100 min after administration of vecuronium.

Hypertensive crisis in children.

Children presenting with hypertension should be considered for emergency treatment when there is evidence of end-organ toxicity. Complications of extreme hypertension may be very serious, even life threatening, with the potential for life-long sequelae. Of greatest significance is damage to the central nervous system. Treatment of hypertensive emergencies should be directed toward the lowering of blood pressure enough to reduce toxicity, but not at a rate likely to cause hypoperfusion of vital organs. This blood pressure reduction should, in general, be carefully controlled in an intensive care unit, with attention to central nervous system, cardiac, and renal function. Intravenous agents are preferable under these circumstances, due to greater ease in modulating blood pressure. In the absence of specific contraindications, a continuous infusion of nicardipine or sodium nitroprusside is preferable. Intravenous labetalol by bolus injection, followed by continuous infusion, also may be used. Oral agents should be reserved for circumstances in which symptoms of end-organ toxicity are mild or absent. Since general pediatricians have limited experience with the treatment of hypertensive emergencies, consultation with physicians experienced in treating hypertensive emergencies is suggested when possible.

Systemic vasomotor interaction between nicardipine and hypocapnic alkalosis in man.

The effects of hypocapnic alkalosis on the vasodilating action of nicardipine were studied in 6 patients after cerebral arterial aneurysm surgery. Each patient served as his/her own control during the 6 steps of the study. T0: baseline; T1: hypocapnic alkalosis alone (PaCO2: 3.5 kPa); T2: hypocapnic alkalosis and bolus injection of nicardipine (30 micrograms.kg-1 i.v.); T3: hypocapnic alkalosis and continuous 60 min infusion of nicardipine (0.5 microgram.kg-1.min-1), T4: determination of the infusion rate required to neutralize the effect of hypocapnic alkalosis; T5: same continuous dose of nicardipine as in T4 but reversal of hypocapnic alkalosis. Hypocapnic alkalosis alone caused a significant increase in the systemic vascular resistance index by 20% (T1). The bolus injection of nicardipine reversed this first effect (T2). The continuous infusion of nicardipine in T3 was insufficient to cancel the haemodynamic effect of hypocapnic alkalosis. During T4 the plasma levels required to neutralize completely the effect of hypocapnic alkalosis were twice those at T3. Normalization of the PaCO2 in step T5 induced a significant fall in the systemic vascular resistance index by 27.5% as compared with T0. In this study hypocapnic alkalosis modified the relationship between plasma levels of nicardipine and its expected vasoactive effects. This interaction was reversible.

The Use Of A Calcium‐Channel Blocker, Nicardipine, For Severely Asphyxiated Newborn Infants

A continuous infusion of nicardipine was given to four severely asphyxiated fullterm infants who were at high risk for adverse outcome and had abnormal cerebral Doppler haemodynamic studies. The heart rate increased in all four infants and mean arterial blood pressure (MAP) fell in three. Two infants had a sudden and marked fall in MAP, together with severe impairment of skin blood-flow and a concurrent fall in cerebral blood-flow velocity. The serum level of nicardipine was less than 40ng/mL in all cases. The use of nicardipine, and possibly other calcium-channel blockers, may be associated with marked hypotension, and if there is no cerebral autoregulation, may cause further cerebral hypoperfusion, so use of these drugs in asphyxiated newborn infants should only be attempted if blood pressure is carefully monitored.

Prevention of postischemic hypoperfusion after canine cardiac arrest by nicardipine.

We studied the effect of nicardipine (NC) on canine cerebral blood flow (CBF) after cerebral ischemia induced by cardiac arrest. Cerebral ischemia was produced by 10 min of electrically mediated ventricular fibrillation. An iv injection of NC (10 micrograms/kg) bolus was followed by continuous NC infusion (0.33 micrograms/kg X min) immediately after the circulation re-established itself. Local CBF was measured using the hydrogen-gas clearance method. The administration of NC maintained CBF at the pre-arrest level during postischemia, thus preventing the hypoperfusion observed in the control group with no NC. However, in the controls, CBF, reduced at 180 min after re-circulation, was not improved by NC infusion. Consequently, administering NC immediately after re-establishment of circulation may help maintain CBF during the postresuscitation period.