Hypertensive Crises: Diagnosis and Management in the Emergency Room
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European Review for Medical and Pharmacological Sciences 2004; 8: 143-152 Hypertensive crises: diagnosis and management in the emergency room A. MIGNECO, V. OJETTI, A. DE LORENZO**, N. GENTILONI SILVERI, L. SAVI* Dept. of Emergency Medicine, Catholic University - Rome (Italy) *Dept. of Internal Medicine, Catholic University - Rome (Italy) **Human Nutrition Unit, University of Tor Vergata - Rome (Italy) Abstract. – Hypertensive crises are com- by the absolute BP levels, but also by the monly observed in an emergency room. magnitude and the rate of the pressure in- Regardless blood pressure values, hyperten- crease and by the underlying conditions3,4. sive crises are classified in emergencies, char- acterized by life-threatening acute organ dam- For instance, blood pressure levels in eclamp- age, and urgencies, with no evidence of acute sia may be only slightly elevated; neverthe- or progressive organ injury. In an hypertensive less, immediate treatment of hypertension in emergency an appropriate and immediate man- this setting is mandatory. agement with parenteral drugs is mandatory, Hypertensive crises are traditionally subdi- while in an hypertensive urgency blood pres- vided in hypertensive emergencies and ur- sure should be decreased within 24-48 h with 5-7 orally active agents. gencies . This article reviews the spectrum of clinical The presence of acute or progressive life syndromes that comprise hypertensive emer- threatening organ damage such as acute coro- gencies, focusing on specific drugs and thera- nary syndrome, acute left ventricular failure peutic strategies available in the emergency with pulmonary oedema, eclampsia, aortic department, based on current literature. dissection, acute renal failure, hypertensive Since no randomized prospective trials are encephalopathy and haemorragic/ischaemic available, an evidence-based approach recom- mending an optimal therapeutical management stroke constitutes an hypertensive emer- 5-7 is not possible. Much of the therapy is there- gency . Many authors consider also accelerat- fore entirely empirical and based on the under- ed-malignant hypertension an emergency, be- lying pathophysiologic and clinical findings. cause sudden occurrence of complications such Further studies are needed to clarify patho- as stroke, acute renal failure or acute coronary physiologic mechanisms in order to optimize syndrome in this setting is possible8-10. therapeutic approach. In most hypertensive emergencies, BP Key Words: should be lowered within minutes using Hypertension, Hypertensive emergency, Hypertensive parental drugs1,5,6. urgency, Hypertensive crises, Hypertensive complication, An hypertensive urgency is an hyperten- Treatment. sive crises without acute or progressive organ damage, and BP should be lowered in 24-48 hours to prevent development of acute organ damage1,5,7. According to the JNC VII, hyper- tensive urgencies include upper levels of Introduction stage II hypertension with symptoms like headache, dizziness, severe anxiety, epistaxis Definition and shortness of breath. Some authors in- Hypertensive crisis is defined as a critical clude in the definition also hypertensive elevation of blood pressure in which diastolic crises in patients without evidence of acute or blood pressure (BP) generally exceeds 120 progressive organ damage but at high risk for mmHg1,2. This threshold value is, however, developing new injury (patients with known not univocally established, since the severity target organ diseases such as chronic is- of the clinical picture is not only determined chaemic heart disease or previous stroke)11. 143 A. Migneco, V. Ojetti, A. De Lorenzo, N. Gentiloni Silveri, L. Savi Casual detection of asymptomatic high BP initiated. Proinflammatory and adhesion mol- levels without any sign of acute or progres- ecules are released from the impaired en- sive organ involvement may be defined as dothelial cell layer, promoting local perme- simple blood pressure rise11. Simple blood ability, inflammation and vasoconstriction15. pressure rise may further be classified as The clinical picture of an hypertensive transient hypertension (generally a cardiovas- crises may range from an asymptomatic pre- cular response to pain or anxiety) or stable sentation to specific symptoms characterizing uncomplicated hypertension12. an acute organ damage (dyspnea, chest pain, neurological disorders). In the absence of or- Ethiology, Pathogenesis, Clinical Picture gan manifestations the patient may complain and Diagnosis about non-specific symptoms such as palpita- Any disorder that causes hypertension can tions, headache, dizziness. give rise to a hypertensive emergency (Table By documenting the medical history, the I). The rate of change in blood pressure de- medical status and by simple diagnostic proce- termines the likelihood that an acute hyper- dures (ECG, fundoscopy, laboratory exams, tensive syndrome will develop4. Pre-existing and when indicated, chest ray, cerebral or chest hypertension may lower the probability of an CT scan) the differential diagnosis between hypertensive emergency through adaptive emergency and urgency can generally be estab- vascular changes that protect end organs lished at the emergency site within a very short from acute changes in BP13. period of time. This approach may also give The pathophysiology of the hypertensive some clues to define the cause of the hyperten- crises is complex and incompletely under- sive crises (e.g., cocaine abuse, pheochromocy- stood: an initial abrupt rise in vascular resis- toma, poorly controlled or previously un- tance seems to be a necessary first step. This known stage II hypertension), guiding to a increased vasoreactivity may be precipitated more appropriate therapy. When an hyperten- by the release of vasodynamic substances such sive emergency is suspected, treatment should as norepinephrine and angiotensin II and can be started as soon as possible, even before the occur as a result of relative hypovolemia13,14. results of these exams are available. The compensatory endothelial vasodilatory responses are overwhelmed, leading to en- dothelial decompensation, which promotes further rises in BP13. Thus, a vicious circle, Management of with progressive increases on vascular resis- Hypertensive Emergencies tance and further endothelial dysfunction is Several parenteral agents are available for the treatment of hypertensive emergencies Table I. Causes of hypertensive emergencies. (Table II). Intravenous agents are generally preferred in this setting, since the effect of • Essential hypertension: poorly controlled blood the treatment is rapid and occurs within a cal- pressure, antihypertensive drugs withdrawal culable period of time13. Moreover, intra- • Renal parenchymal diseases: acute glomeru- venous treatment can be better regulated lonephritis, vasculitis, haemolytic uraemic syn- drome, thrombotic thrombocytopenic purpura than medication administered orally or by the • Renovascular diseases sublingual route . • Endocrine diseases: pheocromocytoma, Cushing’s Before administering the treatment, the syndrome, renin secreting tumors, mineralcorti- risk of worsening of the end-organ damage coid hypertension (rare) must be weighed against the risk of rapid • Drugs: cocaine, sympathomimetics, erythropoi- blood pressure lowering. Gradually decrease etin, cyclosporine, interactions with monoamine- of mean BP level while minimizing the risk of oxidase inhibitors (tyramine), amphetamines hypoperfusion is the most important thera- • Autonomic hyperactivity: Guillame-Barrè syn- peutic principle in this setting16. For instance, drome, acute intermittent porphyria patients with chronic hypertension have an • Central nervous system disorders: head injury, altered cerebral autoregulation curve17, and cerebral infarction/haemorrhage, brain tumors • Eclampsia acute normotension would lead to cerebral hypoperfusion. 144 Hypertensive crises: diagnosis and management in the emergency room Table II. Parenteral drugs for treatment of hypertensive emergencies: pharmacological properties. Drug Dose Onset of Duration Mechanism action of action of action Labetalol 20-80 mg iv boluses or 10 min 3-6 h α/β-adrenergic 0.5-2 mg/min by infusion blocker Esmolol 250-500 mg/kg/min 1-2 min 10-30 min β-adrenergic blocker iv bolus, then 50-100 µg /kg/min by infusion Phentolamine 5-15 mg iv boluses 1-2 min 10-30 min α-adrenergic antagonist Urapidil 25 mg iv boluses or 3-5 min 4-6 h α-adrenergic 5-40 mg/h by infusion antagonist Fenoldopam 0.1-0.3 mg/kg/min 5 min 30 min Dopamine 1 by infusion receptor agonist Nicardipine 5-15 mg/h by infusion 5-10 min 15-30 min Calcium-channel blocker Enalaprilat 1.25-5 mg boluses 15-30 min 6-12 h ACE inhibitor every 6h Sodium 0.25-10 mg/kg/min Immediate 1-2 min Nitric oxid Nitroprussiate by infusion compound direct venous and arterial vasodilator Nitroglicerine 5-100 mg/min 2-5 min 5–10 min Nitric oxid by infusion compound direct venous and arterial vasodilator (mainly venous) Hydralazine 10-20 mg iv 10–20 min 1-4 h Direct vasodilator boluses To avoid cerebral, coronary and renal is- the reliable effectiveness and on the con- chemia, mean BP levels should be reduced traindications of the drugs (Table 3). Other approximately by 25% within few minutes, selection criteria are duration of pressure reaching the goal of 160/100 mmHg within 2- elevation and underlying conditions (e.g., 6 hours5,18. BP should then be normalized in prior cardiovascular, cerebrovascular or re- the following 24-48 h. Patients with aortic dis- nal disorders).