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Keywords: Hypertension, Hypertensive emergency, Hypertensive urgency, End-organ damage, Treatment
How to cite this article:
Tepel M, van der Giet M, Zidek W. Therapy of Hypertensive Emergencies. Saudi J Kidney Dis Transpl 1999;10:279-82 |
 Characteristics of Hypertensive Emergencies and Urgencies | |  |
The severe elevation of blood pressure, e.g. a diastolic blood pressure elevated above 120 mmHg, is a potentially life-threatening event. [1],[2],[3],[4],[5],[6],[7],[8],[9],[10],[11] Hypertensive emergencies are characterized by the presence of end-organ damage, whereas hypertensive urgencies are characterized by the absence of end-organ damage. Intracerebral hemorrhage, cerebral infarction, hypertensive retinopathy including hemorrhage and papilledema, myocardial infarction, pulmonary edema, aortic dissecttion or microangiopathic hemolytic anemia are well-known features of a hypertensive emergency. It should be noted that in patients with chronic hypertension an elevated diastolic blood pressure in the range between 120 mmHg to 140 mmHg might not show end-organ damage, probably due to adaptive vascular changes. On the other hand, in patients who develop acute severe hypertension due to acute glomerulonephritis, preeclampsia or pheochromocytoma, a hypertensive emergency might occur even at "moderate" diastolic blood pressures of 100 mmHg or 110 mmHg.
| Etiology of Hypertensive Emergencies | | |
The underlying causes of hypertensive emergencies are essential hypertension, renovascular hypertension, preeclampsia, acute glomerulonephritis, acute vasculitis, pheochromocytoma, sympathomimetic drugs (amphetamines, antidepressants), increased intracerebral pressure (head injury, cerebral infarction, hemorrhage, brain tumors) and autonomic hyperactivity (acute intermittent porphyria, Guillain Barre Syndrome). In addition, tyramine ingestion in the presence of monoamine oxidase inhibitors, intoxication with nasal decongestants and cough medications, [12] lead intoxication, tobacco smoking, [13] and abrunt withdrawal of clonidine or β-blockers can be causes of hypertensive emergencies. Primary aldosteronism, rennin-secreting tumors or coarctation of the aorta are rare causes of hypertensive crisis. An increase in the vascular resistance due to an elevated release of angiotensin II, norepi-nephrine or endothelin may produce the hypertensive crisis.
Damage of the endothelium will cause fibrinoid necrosis that primarily involves the arterioles and capillaries, leading to disturbances of regulation of organ perfusion and coagulation. These changes are seen in the retina as hemorrhages, exudates or papill-edema; and in the kidney as active urine sediment with red cells and casts. The clinical picture of severe hypertension with damage of the vascular endothelium may result in microangiopathic hemolytic anemia.
| Diagnostic Approach | | |
Repeated standardized measurements of blood pressure are necessary for the diagnosis of hypertensive emergency or urgency. If hypertensive encephalopathy is present, restlessness, headache, nausea, vomiting, or confusion may be seen. Aortic dissection may occur and manifests itself as chest pain, dyspnea, or abdominal pain. Physical examination may show hypertensive retinopathy or signs of pulmonary edema. An abdominal bruit may point to renal artery stenosis. Bilateral palpable abdominal tumors may point to polycystic kidney disease. For complete diagnosis an electrocardiogram, a chest x-ray, an abdominal ultrasound examination, urinalysis, complete blood count and measurements of serum creatinine, blood urea nitrogen, serum potassium, serum sodium, and serum calcium are needed
| Therapeutic Approach | | |
Hypertensive emergencies should be treated carefully and immediately to avoid further damage to target organs. The goal of the therapy is to reduce the diastolic blood pressure to about 100 to 105 mmHg rather than to achieve normotensive values. In fact, too intensive lowering of blood pressure may be harmful by reduction of the perfusion of vital organs, such as heart brain and kidneys, which results in their failure.[3],[7]
The oral application of drugs may be sufficient as a first line therapy. Isosorbide dinitrate (10 mg sublingual), nifedipine (10 mg sublingual) or nitrendipine (5 mg sublingual) or captopril (12.5 mg orally) are widely used drugs. Isosorbide dinitrate may be the drug of choice since side effects such as hypotension and reflex tachycardia are less frequent compared with dihydropyridinetype calcium channel blockers or angiotensin converting enzyme inhibitors. Recently, the safe use of dihydropyridinetype calcium channel blockers such as nifedipine has been questioned because of their possible side effects, in particular myocardial ischemia.[14],[15] The administration of nifedipine in suspected acute myocardial infarction should be avoided since an excess mortality has been observed.[16]
In severe hypertension with severe endorgan damage the elevated blood pressure should be treated with intravenously (I.V.) administered antihypertensive medications, with continuous monitoring of the patient in an intensive care unit. Under these circumstances the use of urapidil (initial dose 10-50 mg I.V., slowly I.V. up to 250 mg per day) appears to be safe and efficacious. Concomitant therapy with cimetidine increases The serum concentration of urapidil. Diazoxide (50-100 mg boluses I.V. every 5-10 minutes up to 600 mg), sodium nitroprusside (0.2510µg/kg/min I.V.), dihydralazine (6.25-25 mg slowly I.V. up to 100 mg per day) or clonidine (75µg I.V.) can be given. Vasodilating drugs such as urapidil, diazoxide or dihydralazine may cause reflex tachycardia and volume retention. Diazoxide should be administered only into peripheral veins. However, the extravasation of diazoxide can be caustic since its PH is 11.6. The use of diazoxide is prohibited in patients with myocardial ischemia, intracerebral hemorrhage or aortic dissection. Under prolonged use the thiocyanate toxicity of sodium nitroprusside should be taken into consideration. Increased thiocyanate toxicity must be considered in renal and hepatic failure. Dihydralazine may cause fever, pain of muscles and joints or glomerulonephritis. Dihydralazine may exacerbate myocardial ischemia.
| Special Therapeutic Considerations | | |
Dissection of the aorta may complicate hypertensive emergency by increasing the shear stress. Under these circumstances, dihydralazine and diazoxide should be avoided. β-blockers, like metoprolol or propranolol, should be used instead together, with clonidine or sodium nitroprusside. [3]
Using isosorbide dinitrate, captopril, µ-blockers or furosemide is effective in the treatment of left ventricular failure during severe hypertension. Additional data from studies on the mortality in patients with heart failure have shown the beneficial effects of angiotensin converting enzyme inhibitors [17],[18] or β-blockers. [19],[20] On the other hand, dihydrtlazine and diazoxide should be avoided in patients with left ventricular failure since they increase cardiac work by stimulation of reflex tachycardia.
The clinical characteristics of pheochromocytoma are severe hypertension, headache, paleness, diaphoresis, nausea, vomiting, and abdominal pain. Severe hypertension due to pheochromocytoma is treated with alpha-blockers, e.g. phentolamine or doxazosin, together with urapidil or dihydralazine. β-blockers should be used only after alpha-adrenergic blockade.[21]
Severe hypertension in patients with advanced chronic renal failure due to fluid overload as judged by clinical and radiological signs should be treated with furosemide (500 mg) plus chlorothiazid (25 mg) or by hemodialysis.
In pregnant women, hypertension with blood pressure levels above 140/90 mmHg, proteinuria, and edema are characteristic of preclampsia. Severe hypertension and seizures are diagnostic of eclampsia. The HELLP syndrome is accompanied by hypertension elevated liver enzymes and low platelet count. Methyldopa and β1-selective β-blockers, e.g. metoprolol or atenolol, appear to be safe and efficacious in hypertensive pregnant women. Eclampsia can be treated by dihydralazine or magnesium sulfate (10-g i.m. loading dose and 5g-i.m.-maintenance dose). The latter has both antihypertensive and antiepileptic properties.[8],[22],[23]
Severe hypertension is often seen in patients with severe head injuries probably due to the activation of the sympathetic nervous system. A carefully monitored reduction of diastolic blood pressure to about 100 mmHg should be reached using β-blockers or urapidil. Centrally acting Drugs such as clonidine should be avoided.
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Correspondence Address:
Martin Tepel
Universitatsklinik Marienhospital, Medizinische Klinik I, Ruhr-Universitat Bochum, Holkeskampring 40, D-44625 Herne
Germany
 Source of Support: None, Conflict of Interest: None  | Check |
PMID: 18212437 
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