Hypertensive Crises: Recognition and Management

Joseph Varon, M.D., F.A.C.P.

Assistant Professor, Anesthesiology, Critical Care & Medicine

Assistant Director, Surgical Intensive Care Unit and

Post Anesthesia Care Unit

Department of Anesthesiology and Critical Care

The University of Texas M.D. Anderson Cancer Center

Houston, Texas

Maura Polansky, M.S., P.A.-C.

Physician Assistant, Surgical Intensive Care Unit and

Post Anesthesia Care Unit

Department of Anesthesiology and Critical Care

The University of Texas M.D. Anderson Cancer Center

Houston, Texas

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Epidemiology, Etiology, and Pathogenesis

Clinical Manifestations

Pharmacological Management





Hypertension is a common medical problem in the United States and clinicians of many specialities are likely to encounter patients with hypertensive crises. Although various terms have been applied to this condition, it is characterized by acute elevations in blood pressure and evidence of end-organ injury. Prompt, but carefully considered therapy is necessary to limit morbidity and mortality. A wide range of pharmacologic alternatives is available to the practitioner to control blood pressure and reduce the risk of complications in these patients.


Hypertension is a common medical problem in the United States. A number of different clinical situations accompany hypertensive crises and acute elevations of BP are not uncommon.1 Thus, health care providers of all specialties will undoubtedly be exposed to patients with hypertension and similarly hypertensive crises will be seen by many types of health care professionals.

Rapid control of blood pressure (BP) is sometimes needed in the emergency department (ED), operating room (OR) and intensive care unit (ICU). Hypertensive crises are acute elevations in BP associated with end-organ damage which can potentially be life-threatening.2-4 If these crises are not treated, the incidence of morbidity, including stroke, coronary events, congestive heart failure, and renal failure, as well as mortality increases.

Various clinical factors influence the therapeutic approach of the practitioner when managing BP. Due to the prevalence and gravity hypertensive crises as well as the variety of therapeutic options available, practitioners of anesthesiology, emergency medicine, surgery, and critical care medicine must master the management of hypertensive crises.


Unfortunately, a number of different terms have been applied to acute elevations of BP associated with end-organ dysfunction. Calhoun and Oparil described hypertensive crises simply as elevations of BP.2 Other authors have defined hypertensive crises as a sudden increase in systolic and diastolic BP that causes end-organ damage including ischemia to the central nervous system, the heart, or the kidneys.5,6 Another frequently encountered term, "malignant hypertension" is defined as a syndrome characterized by elevated blood pressure accompanied by encephalopathy or nephropathy.4,7

The term hypertensive urgency has been used by some authors to refer to clinical situations in which blood pressure control should be achieved within a few hours.4 The same authors reserve the term hypertensive emergencies for those elevations of blood pressure requiring specific reductions within one hour in order to avoid serious morbidity or death.

Postoperative hypertension has arbitrarily been defined as systolic BP 190 mm Hg and/or diastolic BP 100 mm Hg on two consecutive readings following surgery.8,9 It is important to keep in mind that different investigators use these terms to represent various degrees of hypertension.


Hypertension is very prevalent in the American population. Sixty million United States inhabitants suffer from hypertension.7 The vast majority of these patients have essential hypertension. Less than 1% of these patients will develop one or multiple episodes of hypertensive crises. The incidence of hypertensive crises is higher among blacks and the elderly. The majority of patients presenting with hypertensive crises have previously been diagnosed as hypertensive, and many have been prescribed antihypertensive therapy with inadequate BP control.10,11

The incidence of postoperative hypertensive crises varies depending on the population examined. Postoperative hypertension has been reported to occur in 4 - 35% of patients shortly after the surgical procedure.12-14 Like other forms of hypertensive emergencies a prior history of hypertensive is quite common.

Table 1 depicts many of the contributing factors and causes in hypertension crises. As noted above, hypertensive crises occur more commonly in patients who have a previous history of hypertension and frequently accompany discontinuation of antihypertensive medications.

Table 1. Common Causes of Hypertensive Crises

Antihypertensive drug withdrawal (e.g., clonidine)

Autonomic hyperactivity

Collagen-vascular diseases

Drugs (e.g., cocaine, amphetamines)

Glomerulonephritis (acute)

Head trauma

Neoplasias (e.g., pheochromocytoma)

Preeclampsia & eclampsia

Renovascular hypertension

The pathophysiology of hypertensive crises is thought to be due to abrupt increases in systemic vascular resistance likely related to humoral vasoconstrictors.15 With severe elevations of blood pressure endothelial injury occurs and fibrinoid necrosis of the arterioles ensues. This vascular injury leads to deposition of platelets and fibrin, and a breakdown of the normal autoregulatory function. The resulting ischemia prompts further release of vasoactive substances completing a vicious cycle.16


The manifestations of hypertensive crises are those of end-organ dysfunction (See Table 2). Organ dysfunction is uncommon with diastolic blood pressures less than 130 mm Hg, although it may occur.17,18

Table 2. Manifestations of end-organ dysfunction


  Hypertensive encephalopathy

 Acute aortic dissection

 Acute myocardial infarction

 Acute cerebral vascular accident

 Acute hypertensive renal injury

 Acute congestive heart failure

It is important to recognize that the absolute level of BP may not be as important as the rate of increase.19 For example, patients with longstanding hypertension may tolerate systolic BPs of 200 mm Hg or diastolic BPs of up to 150 mm Hg without developing hypertensive encephalopathy, while children or pregnant women may develop encephalopathy with diastolic BPs 100 mm Hg.20

Headache, altered level of consciousness and less severe degrees of central nervous system dysfunction are the classic manifestations of hypertensive encephalopathy. Acute cerebral vascular accidents with intraventricular bleeding or ischemic infarction may result in focal neurological abnormalities. Advanced retinopathy with arteriolar changes, hemorrhages and exudates as well as papilledema is commonly seen on examination of fundi in patients with hypertensive encephalopathy.

Cardiovascular manifestations of hypertensive crises may include angina or acute myocardial infarction. Cardiac decompensation may lead to symptoms of dyspnea, orthopnea, cough, fatigue or frank pulmonary edema. Severe injury to the kidney may lead to renal failure with oliguria and/or hematuria.

One syndrome warranting special consideration is aortic dissection. Propagation of the dissection is dependent not only on the elevation of the blood pressure itself, but also on the velocity of left ventricular ejection. For this reason, specific therapy aimed at both targets (blood pressure and rate of pressure rise) is utilized for these cases.21


The key to successful management of a patient with hypertensive crisis is the prompt recognition and initiation of treatment.22,23 The diagnosis is accomplished by medical history and physical examination supported by appropriate laboratory evaluation. Certain critical information should be ascertained, if possible, such as what was the patient's blood pressure prior to presentation, does the patient have any prior or current complaints, and what medications, prescription and nonprescription, has the patient taken.

Once these basic questions have been answered, the next issue is to determine whether or not the medical problem is a hypertensive emergency or urgency.1,2,4,24 The BP should be determined in both arms by the clinician. In addition, palpation of pulses in all extremities is necessary. A funduscopic examination is mandatory in these cases as well.

A complete blood count, electrolytes, blood urea nitrogen (BUN), creatinine and urinalysis should be obtained.25 In addition, a chest x-ray, electrocardiogram and head computed tomography are useful in patients with evidence of shortness of breath, chest pain, or neurological changes, respectively.22 In many instances, these tests are performed simultaneously with the initiation of antihypertensive therapy.


A growing number of agents are available for management of hypertensive crises. The appropriate therapeutic approach will depend on the form of presentation and cause of hypertensive crises. A variety of routes of administration are currently used to treat patients with severe hypertension in whom it is felt necessary to lower BP over a short period of time. The following discussion is limited to hypertensive crises with cardiovascular etiopathogenesis.

As previously mentioned, in patients with hypertensive crises, the systolic and diastolic BP should be promptly reduced. However, the goal of therapy is to halt the vascular damage and reverse the pathological process, not to normalize the BP. Many authorities recommend that the mean arterial pressure (MAP) is reduced by approximately 15% during the first hour and a total reduction of 25% over the first six hours. In addition, in patients with severe pre-existing hypertension, diastolic BP should only be reduced to 100 or 110 mm Hg.26 Reductions in BP may result in ischemia and, thus, these patients must be carefully followed.27-29 Parenteral therapy with short acting agents is initially recommended (Table 3). In our practice, most patients receiving parenteral therapy should have continuous arterial BP monitoring.26

Table 3. Common Antihypertensive Agents for Use in Hypertensive Crises

Nitroprusside 0.5-10 mcg/Kg/min

Labetalol 20 mg bolus, 2 mg/min (max. 300 g/day)

Diazoxide 25-150 mg IV over 5 min or infusion of 30 mg/min to effect

Nicardipine 5 mg/h, titrate to effect by increasing 2.5 mg/h every 5 min (max. 15 mg/h)

Trimethaphan l mg-15 mg/min

Nitroglycerin 5 mcg/min increase by 5 mcg- 10 mcg every 3-5 min as needed)

Sodium Nitroprusside

Sodium nitroprusside is a combined arterial and venous vasodilator that decreases both the afterload and preload. The mechanism of action of this drug is by reacting with cysteine to form nitrocysteine. The later activates guanylate cyclase which, in turn, stimulates the formation of cyclic GMP (cGMP) that relaxes the smooth muscle.30 When using this agent, cerebral blood flow may decrease in a dose-dependent manner.28 It is a very potent agent. The onset of action of this drug is within seconds, with a duration of action of one-to-two minutes and a plasma half-life of three to four minutes. Therefore, continuous BP measurement is recommended.26 If the infusion is stopped, the BP begins to rise immediately and returns to the pre-treatment level within one to ten minutes.

Sodium nitroprusside is metabolized into cyanogen, which is converted into thiocyanate by the enzyme thiosulfate sulfurtransferase.30 Therefore, cyanide poisoning may occur with prolonged intravenous administration of sodium nitroprusside. Consider this diagnosis in patients who develop central nervous system depression, seizures, lactic acidosis and/or cardiovascular instability.26 The toxicity of sodium nitroprusside usually occurs after several days of infusion however, it may occur within the first 24 hours with high dose administration. In addition, cyanide poisoning may occur with infusion rates greater than 2 mcg/Kg/min. For that reason, infusion rates of greater than 10 mcg/Kg/min should not be continued for prolonged periods of time.26

Calcium Channel Blockers

Oral therapy with nifedipine 10 mg q 5 min x 2, has been suggested by some authors as an acceptable form of therapy in patients with hypertensive crises.31-35 Nifedipine is not absorbed through the buccal mucosa, and the common order for administration sublingually should be changed to bite and swallow.36,37 Nifedipine causes direct vasodilatation of arterioles reducing peripheral vascular resistance promptly. The onset of action begins within 15 minutes of oral administration and peaks at 30 minutes. The duration of action may be four to six hours. This form of therapy however, is not without drawbacks.38 Sudden reductions in BP accompanying administration of nifedipine may precipitate ischemic events.27-29 Nifedipine also produces reflex tachycardia, which in turn, in patients with preexisting coronary artery disease may induce myocardial ischemia. The authors do not encourage the use of this medication for patients with hypertensive crises.

Recently, an intravenous form of nicardipine has been approved by the Food and Drug Administration (FDA) for the treatment of severe hypertension. Nicardipine is a dihydropirydine derivative calcium channel blocker.39 It differs from nifedipine by the addition of a tertiary amine structure in the ester side chain from position three of the hydropyridine ring and the movement of the nitro group to the meta position of the phenyl ring. These differences make nicardipine one hundred times more water soluble than nifedipine and, therefore, it can be administered intravenously making nicardipine a titratable intravenous calcium channel blocker.40

Several studies have examined the acute effects of nicardipine when administered to patients with severe hypertension.41-45 There have also been several published studies comparing the effects of nicardipine with sodium nitroprusside. Halpern and coauthors, conducted a multi center, prospective, randomized study comparing the effects of this agent in patients with severe postoperative hypertension.44 They found nicardipine to be as effective as sodium nitroprusside.

Intravenous nicardipine offers some advantages in the emergency treatment of hypertensive crises. This drug has been shown to reduce both cardiac and cerebral ischemia.46,47 Its dosage is independent of the patient's weight. The current recommended dosage for rapid BP control is 5 mg/hr increasing the infusion rate by 2.5 mg/hr every 5 minutes (to a maximum of 15 mg/hr) until the desired BP reduction is achieved.

Adrenergic-Blocking Agents


Labetalol is a combined blocker of the alpha and beta adrenergic receptors. When given intravenously, labetalol produces a prompt and controlled reduction in BP in patients with hypertensive crises.48 The effects of this drug begin five minutes after administration, and may last for at least four to six hours. The rapid fall in BP results from a decrease in peripheral vascular resistance and a slight fall in cardiac output. One of the advantages of this drug is that it is also effective as an oral antihypertensive agent and once the initial parenteral treatment has been established, it can be followed with oral administration. A reasonable administration protocol is to give an initial intravenous bolus of 0.25 mg/Kg, followed by larger boluses (0.5 mg/Kg) every 15 minutes until the BP is controlled or a total dose 3.25 mg/Kg has been given.


Esmolol is a beta-adrenergic blocking agent that has an extremely brief elimination half-life (<10 minutes). This agent is available for intravenous use both as a bolus and as an infusion. It is of particular value for some dysrhythmias and recently has been used in some patients with hypertensive crises. The recommended initial dosage is 0.5-1 mg/Kg followed by an infusion at 50-200 mcg/Kg/min.


Phentolamine is an alpha-adrenergic blocking agent which is frequently used for management of catecholamine-induced hypertensive crises. This medication is given intravenously in 5-10 mg boluses.3,26 The effect is immediate and may last up to 15 minutes. Continuous intravenous infusions have also been used with variable effects. This agent may cause tachydysrhythmias or angina. Once the initial BP is under control, oral phenoxybenzamine, a long acting alpha adrenergic blocking agent, may be given.

Trimethaphan Camsylate

This drug is a non-depolarizing ganglionic blocking agent. It blocks the transmission of impulses at the sympathetic and parasympathetic ganglia by competing with acetylcholine for cholinergic receptors. This accounts for both its efficacy and its numerous side effects. The reduction in BP observed with this agent is caused by the adrenergic blockade resulting in vasodilatation. The administration is by constant intravenous infusion (500 mg is mixed in 500cc of D5 water), and is given as initial dose of 0.5 to 1 mg/min.3,26 The dose is then titrated to achieve the desired BP. Tachyphylaxis are a common side effect with this medication. It usually occurs within the first two days of administration.


The mechanism of action of this drug is to relax the arteriolar smooth muscle and, thus reduce peripheral vascular resistance.22 When given intravenously, the onset of action is within one minute with a peak action at ten minutes, and a total duration of action ranging from three to eighteen hours.24 The dose of administration of diazoxide is a minibolus of 1-3 mg/kg to 150 mg (single dose) injected over ten to fifteen seconds. If the response is inadequate, repeated doses at 10-15 minute intervals may be given.24,26 Diazoxide also has significant side effects. Salt and water retention are commonly seen and hyperglycemia and hyperuricemia may also occur.


Clonidine (0.1 mg PO q 20 min.) has been used for the treatment of hypertensive crises, particularly in hypertensive urgencies.49-51 This medication has been widely studied. In a random, double blind study, comparing the effects of oral nifedipine versus oral clonidine in 51 patients, clonidine was found to produce a more gradual decrease in BP than nifedipine.52 Sedation was observed in those patients taking clonidine. In the authors' experience, this medication is an excellent choice for those patients in whom BP control within a few hours is desired.26

Angiotensin-Converting Enzyme Inhibitors

The use of angiotensin-converting enzyme inhibitors for the treatment of hypertensive crises has been studied over the last few years. 53-56 Captopril is the prototype of these agents. In a study by Ceyhan and coworkers, the effects of sublingual captopril were compared to the effects of nifedipine in patients with hypertensive crises.57 These authors found that sublingual captopril was very effective and that it was an excellent alternative to nifedipine in the urgent treatment of hypertensive crises. The hypertensive effects of sublingual captopril occurred at five minutes and persist for about 240 minutes. It is interesting to note that, whereas the heart rate increased in those patients who were treated with nifedipine, it decreased in those patients treated with captopril. No significant side-effects were seen in the captopril-treated group.

Furthermore, the intravenous angiotensin-converting enzyme inhibitor Enalaprilat is now gaining popularity for use in some hypertensive emergencies.

Other Agents

Nitroglycerin and hydralazine are sometimes used in the treatment of hypertensive crises and nitroglycerin may play a significant role in those patients with cardiac ischemic.3,48,58 Hydralazine and nitroglycerin are still widely used because compared to other agents, these drugs are inexpensive. However, these agents have disadvantages, including unpredictable antihypertensive effects, difficult BP titrations, and serious potential adverse effects, such as profound hypotension, reduction of myocardial and cerebral blood flow, and increased myocardial workload. Other regimens utilizing medications such as reserpine, methyldopa or guanethidine have largely been replaced by the agents described above.


Hypertensive crises are acute elevations in BP which require rapid control to prevent serious complications. Several antihypertensive agents are available such as sodium nitroprusside, labetalol and nicardipine. Clinicians likely to encounter patients with hypertensive crises should master the various therapeutic options available to manage this condition.


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3. Gifford RW: Management of Hypertensive Crises. JAMA 1991;266:829-835.Back to text.

4. Ferguson RK, Vlasses PH: Hypertensive Emergencies and Urgencies. JAMA 1986;255:1607-1613. Back to text

5. Rahn KH: How Should We Treat a Hypertensive Emergency? Am J Cardiol 1989;63:48C-50C. Back to text.

6. Kaplan NM: Treatment of Hypertensive Emergencies and Urgencies. Heart Disease and Stroke 1992;1:373-378.Back to text.

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8. Van Aken H, Cottrell JE, Anger C, Puchstein C: Treatment of Intraoperative Hypertensive Emergencies in Patients with Intracranial Disease. Am J Cardiol 1989;63:43C-47C. Back to text.

9. Plets C: Arterial Hypertension in Neurosurgical Emergencies. Am J Cardiol 1989;63:40C-42C.Back to text.

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11. Bennett NM, Shea S: Hypertensive Emergency: Case Criteria, Sociodemographic Profile, and Previous Care of 100 Cases. AJPH 1988;78(6):636-640.Back to text

12. Halpern NA, Goldberg M, Neely C, et al: Postoperative Hypertension: A Multicenter, Prospective, Randomized Comparison Between Intravenous Nicardipine and Sodium Nitroprusside. Crit Care Med 1992;20:1637-43. Back to text

13. Gal TJ, Cooperman LH: Hypertension in the Immediate Postoperative Period. Br J Anesth 1975;47:70-4.Back to text

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16. Wallach R, Karp RB, Reves JG, et al: Pathogenesis of Paroxysmal Hypertension During and After Coronary Bypass Surgery: A Study of Hemodynamic and Humoral Factors. Am J Cardiol 1980:46:559-565.Back to text.

17. Hickler RB: Hypertensive Emergency: A Useful Diagnostic Category. AJPH 1988;78(6):623-624.Back to text.

18. Garcia JY, Vidt DG: Current Management of Hypertensive Emergencies. Drug 1987;34:263-278. Back to text.

19. Prisant LM, Carr AA, Hawkins DW: Treating Hypertensive Emergencies. Controlled Reduction of Blood Pressure and Protection of Target Organs. Postgrad Med 1993;93:92-6, 101-4, 108-10.Back to text.

20. Ziegler MG: Advances in Acute Therapy of Hypertension. Crit Care Med 1992;20:1630-1. Back to text.

21. Cohn LH: Aortic Dissection: New Aspects of Diagnosis and Treatment. Hosp Prac 1994;29:27-36.Back to text.

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23. Ram CVS: Management of Hypertensive Emergencies: Changing Therapeutic Options. Am Heart J 1991;122:356-63.Back to text.

24. Reuler JB, Magarian GJ: Hypertensive Emergencies and Urgencies. J Gen Int Med 1988;3:64-74.Back to text.

25. Vidt DG: Current Concepts in the Treatment of Hypertensive Emergencies. Am Heart J 1986;111:220-225. Back to text.

26. Fromm RE, Varon J: Cardiovascular Disorders in the ICU. In: Varon J (Ed.): Practical Guide to the Care of the Critically Ill Patient. St. Louis: Mosby-Year Book, Inc. 1994:64-94. Back to text.

27. Bannan LT, Beevers DG, Wright N: Emergency Reduction, Hypertension in Pregnancy, and Hypertension in the elderly. Brit Med J 1980;281:1120-1122.Back to text.

28. Bertel O, Marx BE, Conen D: Effects of Antihypertensive Treatment on Cerebral Perfusion. Am J Med 1987;82(3B):29-36. Back to text.

29. Reed WG, Anderson RJ: Effects of Rapid Blood Pressure Reduction on Cerebral Blood Flow. Am Heart J 1986;111:226-228.Back to text.

30. Sodium Nitroprusside. In: McEvoy GK (Ed): AHFS Drug Information. Bethesda: American Society of Hospital Pharmacists, 1993:1089-92. Back to text.

31. Schillinger D: Nifedipine in Hypertensive Emergencies: A Prospective Study. J Emer Med 1987;5:463-473.Back to text.

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34. Diker E, Erturk S, Akgun G: Is Sublingual Nifedipine Administration Superior to Oral Administration in the Active Treatment of Hypertension? Angiology 1992;43:477-481.Back to text.

35. Komsuoglu SS, Komsuoglu B, Ozmenoglu M, et al: Oral nifedipine in the Treatment of Hypertensive Crises in Patients with Hypertensive Encephalopathy. Int J Cardiol 1992;34:277-282.Back to text.

36. Haft JI, Litterer WE: Chewing Nifedipine to Rapidly Treat Hypertension. Arch Intern Med 1984;144:2357-2359.Back to text.

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38. Woodmaney P, Channer KS: Nifedipine and Hypotension. Lancet 1991;ii:763-764.Back to text.

39. Turlapaty P, Vary R, Kaplan JA: Nicardipine, a New Intravenous Calcium Antagonist: A Review of its Pharmacology, Pharmacokinetics, and Perioperative Applications. J Cardiothorac Anesth 1989;3:344-55. Back to text.

40. IV Nicardipine Study Group: Efficacy and Safety of Intravenous Nicardipine in the Control of Postoperative Hypertension. Chest 1991;99:393-398. Back to text.

41. Wallin JD: Intravenous Nicardipine Hydrochloride: Treatment of Patients With Severe Hypertension. Am Heart J 1990;119:434-437.Back to text.

42. Goldberg ME, Clark S, Joseph J, et al: Nicardipine Versus Placebo for the Treatment of Postoperative Hypertension. Am Heart J 1990;119:446-450.Back to text.

43. Halpern NA, Sladen RN, Goldberg JS, et al: Nicardipine Infusion for Postoperative Hypertension After Surgery of the Head and Neck. Crit Care Med 1990;18:950-5.Back to text.

44. Halpern NA, Alicea M, Krakoff LR, Greenstein R: Postoperative Hypertension: A Prospective, Placebo-Controlled, Randomized, Double Blind Trial, with Intravenous Nicardipine Hydrochloride. Angiology 1990;41:992-1004. Back to text.

45. Clifton GG, Cook ME, Bienvenu GS, Wallin JD: Intravenous Nicardipine in Severe Systemic Hypertension. Am J Cardiol 1989;64:16H-18H.Back to text.

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47. Cheung DG, Gasster JL, Neutel JM, Weber MA: Acute Pharmacokinetic and Hemodynamic Effects of Intravenous Bolus Dosing of Nicardipine. Am Heart J 1990;119:438-442.Back to text.

48. Stumpf JL: Drug Therapy for Hypertensive Crises. Clin Pharm 1988;7:582-91. Back to text.

49. Houston MC: The Comparative Effects of Clonidine Hydrochloride and Nifedipine in the Treatment of Hypertensive Crises: Am Heart J 1988;115:152-154.Back to text.

50. Greene CS, Gretler DD, Cervenka K, et al: Cerebral Blood Flow During the Acute Therapy of Severe Hypertension with Oral Clonidine. Am J Emerg Med 1990;8:293-296. Back to text.

51. Houston MC: Treatment of Hypertensive Emergencies and Urgencies with Oral Clonidine Loading and Titration. Arch Intern Med 1986;146:586-589.Back to text.

52. Jaker M, Atkin S, Soto M, et al: Oral Nifedipine vs Oral Clonidine in the Treatment of Urgent Hypertension. Arch Intern Med 1989;149:260-265.Back to text.

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54. Komsuoglu B, Sengun B, Bayram A, et al: Treatment of Hypertensive Urgencies with Oral Nifedipine, Nicardipine, and Captopril. Angiology 1991;42:447-454. Back to text.

55. DiPette DJ, Ferraro JC, Evans RR, et al: Enalaprilat, an Intravenous Angiotensin- Converting Enzyme Inhibitor, in Hypertensive Crises. Clin Pharmacol Ther 1985;38:199-204.Back to text.

56. Angeli P, Chiesa M, Caregaro L, et al : Comparison of Sublingual Captopril and Nifedipine in Immediate Treatment of Hypertensive Emergencies. A Randomized, Single-Blind Clinical Trial. Arch Intern Med 1991;151:678-682. Back to text.

57. Ceyhan B, Karaaslan Y, Caymaz O, et al: Comparison of Sublingual Captopril and Sublingual Nifedipine in Hypertensive Emergencies. Jpn J Pharmacol 1990;52:189-193.Back to text.

58. Bussmann WD, Kenedi P, von Mengden HJ, et al: Comparison of Nitroglycerin With Nifedipine in Patients With Hypertensive Crisis or Severe Hypertension. Clin Investig 1992;70:1085-1088.Back to text.

© Internet Scientific Publications, L.L.C., 1996, 1997.

First Published: October 1996

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