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For US Healthcare Professionals Only

Ready-to-use CARDENE® I.V. (nicardipine hydrochloride) for blood pressure reduction in the emergency setting

Key considerations for choosing an antihypertensive agent in hypertensive emergencies

Key considerations for choosing an antihypertensive agent in hypertensive emergencies
Desired Characteristics Ready-to-use CARDENE® I.V. (nicardipine hydrochloride)
Rapid onset of action2
  • BP begins to fall within minutes1
Rapid offset of action2
  • 50% offset of action in about 30 minutes1
  • Plasma concentrations decline triexponentially, with a rapid early distribution phase (α-half-life of 2.7 minutes)1
Minimal preparation required2
  • Premixed and ready to use1
Predictable dose repsonse requiring few dose adjustments2
  • Formulation allows for rapid or gradual titration1
  • Effect on BP significantly correlated with plasma concentrations1
Well tolerated and little potential for adverse effects3
  • FDA approved since 2008 [CARDENE® I.V. (nicardipine hydrochloride) Premixed Injection]4
  • No soy or egg allergens
  • The most common adverse reactions (>3%) are headache, nausea/vomiting, hypotension, and tachycardia1
No invasive BP monitoring required3
  • Close monitoring of BP and heart rate by means appropriate to the clinical setting is necessary1

CARDENE I.V. for hypertensive emergencies5

Beginning of study (N=110)

End of study

Patients Achieved Relevant SBP Reductions Over Time5

In a randomized study, 92% of patients experiencing a hypertensive emergency reached target systolic blood pressure range within 30 minutes.In a randomized study, 92% of patients experiencing a hypertensive emergency reached target systolic blood pressure range within 30 minutes.


Adapted from Peacock, 2011.
*Median.
Mean.

A multicenter, randomized study of patients who presented to the ED with an SBP reading of ≥180 mm Hg on 2 consecutive readings (10 minutes apart). CARDENE® I.V. (nicardipine hydrochloride) was administered at 5 mg/hr and increased every 5 minutes by 2.5 mg/hr until target SBP range was reached or a maximum of 15 mg/hr was achieved. Before randomization, the physician specified a target SBP ± 20 mm Hg. Vital signs (BP and HR) were taken every 5 minutes for the first 30 minutes.5

Hypertensive crises: emergency vs urgency6,7

Hypertensive emergency:

  • Patients with SBP >180 mm Hg or DBP >120 mm Hg plus evidence of impending or progressive target-organ damage

What is it?

  • Presence of acute target-organ damage manifest by clinical sequelae or diagnostic test abnormalities

What are the implications?

  • Requires immediate intervention with parenteral therapy
  • Admission to a monitored setting

Hypertensive urgency:

  • Patients with SBP >180 mm Hg or DBP >120 mm Hg

What is it?

  • Presence of chronic target-organ damage without evidence of acute deterioration

What are the implications?

  • Requires reinitiation or uptitration of oral antihypertensive therapy
  • Acute BP reduction with parenteral or rapid-acting oral agents should be avoided
  • May necessitate serial testing in an observation setting

Either scenario should also prompt a search for potential medications that may increase BP including nonsteroidal anti-inflammatory drugs, steroids, decongestants, appetite suppressants, over-the-counter stimulants, oral contraceptives, and tricyclic antidepressants.

Did you know?

In a one-year study of 14,209 ED patients:

  • 11.5% of all ED visits were medical urgencies/emergencies (n=1634)8
  • 27.5% of all medical urgencies/emergencies were a hypertensive crisis (n=449)8

Of the hypertensive crises:

  • 24% were hypertensive emergencies (n=108)8
  • 76% were hypertensive urgencies (n=341)8

Pathophysiology of hypertensive emergency9-11

A closer look

A hypertensive emergency typically results from a failure of the body’s autoregulation system. Autoregulation refers to the inherent ability of arteries to dilate and contract in response to changing perfusion pressures in order to maintain a relatively constant blood flow. Failure of autoregulation results in an increase in vascular resistance, both regionally and systemically.

Pathophysiology of hypertensive emergency

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