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| Acute Hypertension |
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Disease State
Hypertension affects greater than 73 million people—nearly 1 in 3 adults—in the United States and can directly increase a patient’s risk of coronary heart disease, which may lead to stroke or heart attack.1 Chronic hypertension can usually be managed with oral therapy, but if an acute episode of high blood pressure (BP) needs to be controlled rapidly, then an IV antihypertensive is required. IV treatment is also necessary when oral therapy is not feasible (eg, in patients who are awaiting surgery or who are intubated).
Hypertensive Crises: Emergencies and Urgencies
Patients with a systolic BP (SBP) >179 mm Hg or a diastolic BP (DBP) >109 mm Hg are usually considered to be having a “hypertensive crisis,” which requires BP reduction. Hypertensive crises may be further classified as emergencies, when there is acute end-organ damage, and urgencies, when there is no end-organ involvement. Although the distinction between the two is not based on a specific BP level, organ dysfunction is uncommon with DBP <130 mm Hg (except in children and pregnancy). In addition, the absolute BP level may not be as important as the rate of increase.2
Distinguishing between the 2 types of crisis is important to the development of an appropriate treatment plan. Patients with hypertensive emergency should have their BP lowered immediately, although not to “normal” levels (See Goals of Therapy in Hypertensive Crises). Patients with hypertensive urgency should have their BP lowered within 24 to 48 hours, usually with an oral antihypertensive.2
It is estimated that less than 1% to 2% of patients with hypertension will experience a hypertensive emergency.2,3 Because of the high prevalence of hypertension in the United States, however, about 500,000 patients experience a hypertensive emergency annually.3
End-Organ Damage in Hypertensive Emergencies
Examples of end-organ damage that may be observed in a hypertensive emergency are shown below.
Pathophysiology of Hypertensive Emergency
Regardless of the underlying cause of the hypertensive emergency, it is hypothesized that the final common pathway is a sudden increase in systemic vascular resistance (SVR) and, consequently, an increase in BP due to the action of circulating vasoconstrictors, such as catecholamines and angiotensin, on arterioles.5-8
The resulting increase in BP damages the endothelium, leading to the release of local vasoconstrictors, such as endothelin, which cause further vasoconstriction, often with intravascular hypovolemia.5-8
Damage to the endothelium impairs autoregulatory function. Autoregulation refers to the inherent ability of arteries to dilate or constrict in response to changing perfusion pressures in order to maintain a relatively constant blood flow.6 Further release of humoral vasoconstrictors perpetuates the “vicious circle.” 5,6,8
It is important to note that, in this setting, hypovolemia is often due to 2 factors2,6:
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An initial pressure natriuresis and diuresis accompany the onset of the hypertensive episode
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Fluid intake usually decreases as the episode and symptoms progress
The resultant hypovolemia contributes to end-organ damage.2
Goals of Therapy in Hypertensive Crises
Hypertensive urgencies
The majority of patients experiencing a hypertensive crisis will not have evidence of end-organ damage. Therefore, they will have a hypertensive urgency. In these patients, the goal of therapy is to lower BP gradually over 24 to 48 hours. This is usually accomplished with oral medications. Rapid reduction of BP in these patients may cause BP to fall below the autoregulatory range and may be associated with significant morbidity.2
Hypertensive emergencies
The goal in treating a hypertensive emergency is to lower BP immediately but in a controlled manner, so as not to fall off the autoregulatory curve and risk ischemia and additional end-organ damage.2 Rapid and uncontrolled reduction of BP may result in cerebral, myocardial, and renal ischemia/infarction.5
In patients experiencing a hypertensive emergency, it is recommended that resting mean arterial pressure (MAP) not be reduced >25%.3
It is recommended that DBP initially be decreased by 10% to 15%, or to approximately 110 mm Hg over 30 to 60 minutes. In patients with aortic dissection, the BP should be reduced rapidly (within 5 to 10 minutes), targeting a SBP of <120 mm Hg and MAP <80 mm Hg.2
Patients experiencing a hypertensive emergency are best managed with a continuous infusion of a short-acting, titratable antihypertensive agent.2 Ready-to-Use CARDENE I.V. is such an agent (see Dosing and Administration in Product Overview).
Important Safety Information
Close monitoring of the blood pressure is required during therapy. CARDENE I.V. is contraindicated in patients with known hypersensitivity to the drug and in patients with advanced aortic stenosis. Reduction of diastolic pressure and reduced afterload may worsen rather than improve myocardial oxygen balance. Caution is advised when administering CARDENE I.V. to patients with impaired renal or hepatic function, in combination with a beta-blocker in patients with congestive heart failure, or portal hypertension. Observe caution in patients with significant left ventricular dysfunction due to possible negative inotropic effect. CARDENE I.V. gives no protection against the dangers of abrupt beta-blocker withdrawal; beta-blocker dosage should be gradually reduced. Levels of cyclosporine should be closely monitored during therapy. The most common side effects of CARDENE I.V. are headache (14.6%), hypotension (5.6%), nausea/vomiting (4.9%), and tachycardia (3.5%). Less frequent adverse effects, in each case occurring at 1.4%, include ECG abnormalities, postural hypotension, ventricular extrasystoles, injection-site reaction, dizziness, sweating and polyuria.
References: 1. American Heart Association. Heart Disease and Stroke Statistics, 2009 update.: http://americanheart.org/presenter.jhtml?identifier=3000090. Accessed July 28, 2009. 2. Marik, PE, Varon J. Hypertensive crises: challenges and management. Chest. 2007;131(6):1949-1962. 3. Mansoor GA, Frishman WH. Comprehensive management of hypertensive emergencies and urgencies. Heart Dis. 2002;4:358-371. 4. Rynn KO, Hughes FL, Faley B. An emergency department approach to drug treatment of hypertensive urgency and emergency. J Pharm Prac. 2005;18(5):363-376. 5. Varon J, Marik PE. The diagnosis and management of hypertensive crises. Chest. 2000;118(1):214-227. 6. Ault NJ, Ellrodt AG. Pathophysiological events leading to the end-organ effects of acute hypertension. Am J Emerg Med. 1985;3(suppl 6):10-15. 7. Wallach R, Karp RB, Reves JG, et al. Pathogenesis of paroxysmal hypertension developing during and after coronary bypass surgery: a study of hemodynamic and humoral factors. Am J Cardiol. 1980;46:559-565. 8. Kincaid-Smith P. Malignant hypertension. J Hypertens. 1991;9(10):893-899.
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