1. Description of the problem
What every clinician needs to know
Severe hypertension is a common scenario encountered in intensive care patients. The role of the clinician is to establish the etiology and to determine whether blood pressure reduction may be detrimental or desirable.
Table I. Classification of hypertension
Two terms describe conditions associated with acute severe elevations in systemic arterial pressure when rapid reduction in blood pressure is required.
A hypertensive emergency is defined by the onset or progression of end-organ damage pertaining to the cerebrovascular, cardiovascular or renovascular system. Expeditious control of blood pressure is necessary to prevent catastrophic organ damage and should be carried out over a period of minutes to hours but not necessarily aiming for normal values.
Hypertensive urgencies are distinguished by the lack of end-organ damage; however, gradual blood pressure reduction over hours or days is indicated. Untreated hypertensive urgencies may evolve as sustained high blood pressure can lead to end-organ damage.
Accelerated hypertension and malignant hypertension also denote end-organ damage; however, they are characterized by pathognomonic changes. Accelerated hypertension is defined by retinal damage, including hemorrhages, exudates and arteriolar narrowing. The additional presence of papilloedema constitutes malignant hypertension, which is usually associated with diastolic blood pressure greater than 140 mmHg.
Table I summarizes the classification of high blood pressure. Hypertensive emergencies would usually be associated with values in the grade 3 range; however, there is no set blood pressure above which a hypertensive emergency is inevitable. Wide inter-person variability means that some people may tolerate high pressures unharmed in the short term.
In the long-term management of hypertension, if a person’s systolic and diastolic blood pressures fall into different categories, then the higher value should be used to quantify risk and guide treatment. There are no data in this respect for hypertensive emergencies, but intuitively the same principle should apply.
Table II. Hypertensive emergencies
It is important to carefully consider what the patient’s normal blood pressure may be before appropriate diagnostic and management plans can be instigated. In patients without pre-existing hypertension, a crisis can occur at lower than expected values.
Excessive lowering of blood pressure below the organ’s autoregulatory threshold can exacerbate ischemia and worsen outcome.
Patients presenting with neurological syndromes can deteriorate rapidly and therefore need re-assessment on a regular basis.
In catecholamine excess states unopposed alpha-adrenergic stimulation (i.e. beta-blockade without alpha-blockade) can cause life-threatening vasoconstriction.
It is important to acknowledge that hypertension per se is asymptomatic, and therefore the symptoms and signs of a hypertensive emergency will relate to the organ systems involved.
Hypertensive encephalopathy most commonly presents with global phenomena of headache, nausea and vomiting, which progress to visual disturbances with or without retinal changes, focal neurological deficits, seizures that may be focal or generalized, coma and death.
Onset of symptoms is usually gradual and although blood pressure will be markedly elevated from the patient’s baseline, it may be lower than that associated with other target organ injury.
Hypertension is implicated in acute ischemic or hemorrhagic stroke and subarachnoid hemorrhage (SAH) causation. Onset of symptoms will be sudden and as with encephalopathy can range from headache (often very severe) to coma.
In addition to the original insult, further neurological deterioration can occur in all these patients due to evolving cerebral edema; ischemic strokes can be complicated by hemorrhagic transformation; and patients with SAH may rebleed or develop hydrocephalus or vasospasm, which may also cause ischemic infarcts.
This picture is complicated by the pathophysiological changes that occur in relation to any brain injury. Cerebral autoregulation is disrupted and adequate perfusion of the injured area relies heavily on mean arterial pressure; therefore, even in the absence of precipitating hypertension, a hypertensive response occurs in the majority of patients.
This presents a challenge in the management of hypertensive crises, where on one hand blood pressure reduction is necessary, but excessive lowering will exacerbate ischemia and secondary brain injury.
Acute coronary syndromes (ACS) constitute unstable angina, non-ST-elevation myocardial infarction (NSTEMI) and ST-elevation MI (STEMI). MIs may be asymptomatic, particularly in susceptible groups such as the elderly or diabetics, or may present with chest pain and/or dyspnea, particularly in the context of low-cardiac-output states, pulmonary edema or congestive cardiac failure.
Back pain with or without chest pain should alert the physician to the possibility of aortic dissection. Other symptoms and signs related to acute aortic dissection will depend upon the location and extent of tearing and can result in ischemia of any organ or limb.
A syndrome of excessive catecholamine release, myocardial stunning and heart failure is a recognized complication of SAH. This completely reversible neurogenic myocardial stunning is associated with a wide spectrum of left ventricular wall motion abnormalities.
It also includes a subset of patients who exhibit classical tako-tsubo cardiomyopathy (a complex of apical ballooning and akinesia with basal sparing and hyperkinesis), which typically affects postmenopausal women in response to stress.
After diabetes mellitus, hypertension is the second most common cause of chronic renal impairment. The earliest signs of renovascular disease will be reductions in glomerular filtration rate (GFR) and microproteinuria.
Severe renal failure may present with a range of clinical symptoms, including general malaise, uremic delirium and fluid overload. Patients are often oligurio-anuric; laboratory tests will show elevations in urea and creatinine, and electrolyte abnormalities frequently include hyperkalemia. In scleroderma renal crisis urine output may be normal.
Key management points
Therapeutic priority is to reduce blood pressure to a pre-determined safe range promptly. The desired speed and degree of reduction will depend on the presence and type of end-organ damage.
In essential hypertension, blood pressure control can be achieved over a period of weeks to months with the aim of minimizing the long-term complications of chronic hypertension. In hypertensive urgencies it is adequate to reach target parameters over a period of hours to days. Oral medication is used, the choice of which will depend on patient demographics and underlying comorbidities.
Conversely, in hypertensive emergencies blood pressure reduction is required within minutes or hours at the most. The patient should be managed in a level 2 or 3 environment, invasive blood pressure monitoring is paramount, and short-acting intravenous drugs that can easily be titrated should be used.
In the absence of RCT evidence, a generally recommended goal is to reduce mean arterial pressure by 20-25% or diastolic pressure to 100-110mmHg. Excessive lowering of BP may lead to organ ischemia and infarction.
2. Emergency management
The patient should be stabilized according to the established principles of airway and breathing, and then attention can be focused on the circulation.
The history, examination and investigations obtained (as detailed below under ‘diagnosis’) will guide clinicians as to the precise nature of the problem and help establish specific therapeutic targets.
Hypertensive encephalopathy: is entirely reversible and symptoms should begin to resolve within 6-12 hours of blood pressure control. MAP should be reduced by 25% over a few hours but no more than 20% in the first hour.
Acute ischemic strokes: treatment is not indicated unless the SBP is greater than 220 mmHg or DBP is greater than 120 mmHg. If a patient fulfills the criteria for thrombolysis, then BP should be reduced to SBP less than 185 mmHg and DBP less than 110 mmHg before fibrinolytics are administered and then maintained at SBP less than 180 mmHg and DBP less than 105 mmHg for the next 24 hours.
Intracerebral hemorrhage: new evidence using target SBP of 140 mmHg suggests that early BP control is well tolerated and can limit hematoma size. Current guidelines, however, recommend maintaining MAP less than 110 mmHg or SBP less than 160 mmHg except where radiological evidence of raised intracranial pressure exists, where targets will be higher: MAP less than 130 mmHg or SBP less than 180 mmHg.
SAH: management presents a particular challenge as blood pressure needs to be reduced to prevent re-bleeding but maintained high enough to minimize vasospasm. This problem is abolished following successful protection of the lesion, such as clipping or coiling of an aneurysm, when BP priorities will shift to vasospasm prevention. Nimodipine is used to help prevent vasospasm and will cause hypotension, especially if given intravenously; however, it is not indicated for the treatment of hypertension with SAH per se.
ACS: Treatment is indicated if SBP is greater than 160 mmHg or DBP is greater than 100 mmHg. Myocardial work reduction can be achieved by reducing heart rate and blood pressure, and in combination will limit infarct size.
While vasodilation is desirable, diastolic pressure should be adequate to support coronary perfusion and drugs that cause coronary artery dilatation are preferred. Thrombolysis is contraindicated if SBP is greater than 180 mmHg or DBP is greater than 100 mmHg.
Use: GTN + beta blocker +/- analgesia.
Acute left ventricular failure: hypertension increases myocardial work and exacerbates diastolic dysfunction; thus, vasodilation is the treatment of choice. It is a great misconception that immediate diuresis is necessary, as these patients are often intravascularly depleted from renin-induced natriuresis as well as catecholamine and angiotensin II-mediated vasoconstriction.
A rapid relief of symptoms may be observed with furosemide, but this is largely due to its pulmonary and systemic vasodilatory properties. Cardiac output monitoring should be employed to make accurate assessment of volemic status to determine whether the patient will benefit from fluid challenging or diuresis.
Use: Vasodilator +/- diuretic +/- ACE inhibitor.
Aortic dissection: vasodilators that cause a reflex tachycardia will increase the rate of pressure change (dP/dt) and risk tear extension. The aim is for SBP less than 110 mmHg.
Use: Analgesia + beta-blocker with vasodilator. Avoid beta-blocker with aortic regurgitation or cardiac tamponade. Calcium channel blockers can be used to control heart rate when beta-blockade is undesirable.
Evaluation to establish the cause/effect relationship is crucial. Blood pressure should be lowered using vasodilators but in specific situations alternative drugs may be indicated. In scleroderma renal emergencies ACE inhibitors are effective in 90% of cases and can promote renal recovery.
Usually ACE inhibitor use in the acute setting is contraindicated as renal dysfunction is exacerbated, particularly in patients with hyperkalemia and uremia. Post renal transplantation, calcium channel blockers, which may reverse cyclosporine-associated renal vasoconstriction, are preferred.
Management points not to be missed
Some neurological emergencies may be masked by cardiovascular complications – for example, a patient with severe acute heart failure and left bundle branch block (LBBB) who was thought to have an acute MI may have been thrombolysed as her drowsiness was thought to be due to a low-cardiac-output state. Further history determined that the patient was well until sudden onset of severe headache and vomiting, after which she became short of breath. A CT brain scan revealed a subarachnoid hemorrhage.
Drugs and dosages
Contraindications: Neurological emergencies: cerebral vasodilation and worsen edema.
Name: Nitroglycerin/glyceryl trinitrate
Action: Venodilator at low dose. At higher doses: dilator of both veins and arteries, including coronary arteries.
Indication: ACS, aortic dissection, heart failure.
IV Dose: Initial: 0.25-0.5 mcg/kg/min, Max: 8-10 mcg/kg/min.
Action: Arteriolar and venous vasodilator
Indication: Most hypertensive emergencies
Contraindication: Pregnancy. Caution in ACS.
IV Dose : 0.25-10 mcg/kg/min
Other: Risk of cyanide toxicity with doses greater than 2 mcg/kg/min, prolonged infusions lasting more than 24-28 hours and in renal impairment.
Action: Arteriolar dilator.
Indication: Pre-eclampsia. Pregnancy.
Contraindication: Neurological emergencies.
IV Dose: 0-10 mg every 20-30 min. Max: 20 mg.
Action: Alpha and beta adrenoceptor blockade.
Indication: Most hypertensive emergencies.
Contraindication: Acute heart failure, asthma.
IV Dose: Infusion: 0.5-2 mg/min; Bolus: 5-80 mg every 10 min.
Action: Short-acting selective beta-1 blockade (t1/2 is 8 minutes).
Indication: ACS. Unknown beta-blocker tolerance.
Contraindication: Severe heart failure.
IV Dose: 25-50 mcg/kg/min. Loading dose 250-500 mcg/kg over 3 minutes.
Other classes of drugs
Action: Calcium channel blocker.
Indication: Most hypertensive emergencies.
Contraindication: Acute heart failure. Caution in ACS..
IV Dose: 5-15 mg/hr.
Action: Peripheral dopamine-1 antagonist.
Indication: Most hypertensive emergencies.
Contraindication: Caution in glaucoma.
IV Dose: 0.1 mcg/kg/min.
Action: Alpha-adrenergic blocker.
Indication: Catecholamine excess: pheochromocytoma, cocaine.
IV Dose: 5-10 mg every 5-15 minutes.
Action: Short-acting ACE inhibitor.
Indication: Acute LV failure, scleroderma crisis.
Contraindication: Non-scleroderma renal failure. Caution in ACS.
Oral Dose: 1.25-5 mg every 6 hours.
Action: Calcium channel blocker, reduces A-V nodal conduction, causes coronary artery dilatation.
Indication: Aortic dissection.
Contraindication: Acute heart failure, ACS.
Oral Dose: 30-120 mg q6-8h. Modified-release preparation not indicated in the acute setting.
A detailed history and examination are the first steps in establishing a diagnosis. Thereafter a list of differentials will guide the choice of investigations. All patients presenting acutely will have ‘routine’ observations and investigations performed.
Hypertension history should include previous diagnosis and duration of hypertension; medication and compliance with medication; use of over-the-counter drugs that are sympathomimetic or illicit drugs, particularly cocaine; enquire about herbal remedies. Establish the presence of chronic end-organ damage, previous hospitalization or emergency treatment.
Routine observations: GCS, BM for glucose, respiratory rate, oxygen saturations, heart rate, BP.
Routine investigations: Electrolytes, urea and creatinine, full blood count. ECG and CXR
Establishing a specific diagnosis
Blood pressure parameters should be confirmed by at least two separate readings and should be measured in both arms. A difference of more than 20 mmHg would raise the suspicion of aortic dissection. If the patient is well enough the supine and standing or supine and sitting BP measurements may help determine if the patient is intravascularly fluid depleted.
If there is doubt about the accuracy of the recordings, as with cuff/patient size incompatibility or severe arrhythmias, intra-arterial blood pressure measurement should be considered.
Salient points in the history and examination not to be missed are described below, but the points listed are by no means exhaustive.
Diagnostic approach to a patient with this problem
History: Time of onset may be crucial (e.g. for ischemic stroke thrombolysis). Speed of onset and evolution of symptoms. Presence of visual disturbance, meningismus or seizure activity.
Examination: Establish pupillary size and reflexes; ocular palsies; presence of focal deficits. Fundoscopy for papilloedema or retinal changes may help distinguish a hypertensive emergency from an urgency.
CT brain scan: is the initial investigation of choice in most countries and will usually demonstrate the presence of any blood. Ischemic lesions often do not show up on early imaging, and thus CT may need to be repeated at a later date. CT signs of generalized cerebral edema include loss of gray/white matter differentiation, effacement of sulci and compression of ventricles.
Localized edema is represented by the above as well as areas of low attenuation. Unilateral lesions associated with significant mass effect may cause midline shift. CT imaging cannot exclude the presence of raised intracranial pressure, but the absence of radiological signs makes it less likely. A finding of posterior leukoencephalopathy (edema of the subcortical white matter in the parieto-occipital region) is characteristic of hypertensive encephalopathy.
Other imaging: Rarely necessary in the immediate setting but may help establish definitive diagnosis.
MRI will delineate cortical lesions more accurately than CT. Diffusion-weighted imaging (DWI) can show ischemic abnormalities very early and is the gold standard in some centers. CT angiography is required to look for cerebral aneurysms or arteriovenous malformations. Future stroke protocols will incorporate CT perfusion and angiography when a patient suspected of having a stroke has a normal plain CT.
History: Onset and nature of chest pain. Presence or absence of back pain is essential as many aortic dissections may mimic ACS. Anticoagulation in aortic dissection can have catastrophic consequences.
Examination: Feel peripheries to assess perfusion, look for signs of RV and LV failure. Palpate bilaterally upper limb and lower limb pulses.
Investigations: ECG should be compared with any previous records in the patient’s notes. Serial ECGs may be required to distinguish old from evolving ischemic changes. Arrhythmias and LVH may be apparent. A chest radiograph may show an enlarged cardiac profile, pulmonary edema or widened mediastinum.
Echocardiography will provide information about regional wall motion abnormalities, structural abnormalities and cardiac function. CT angiography is the gold standard for diagnosing aortic dissection, although a dissection flap may be visualized with TTE but more so with TOE.
Often diagnosed after laboratory investigation results have been obtained. Other investigations include: Urinalysis (UA) to detect hematuria or proteinuria. Urine microscopy to detect small quantities of RBC not detected on UA or RBC casts. A 24-hour urine collection is required to quantify micro-albuminuria. A renal USS may be required to exclude urinary tract obstruction.
Urinary toxicology screen.
Urinary beta-HCG for pregnancy.
Urinary catecholamines for suspected pheochromocytoma.
CTA or Doppler USS of renal arteries or renal biopsy for suspected primary renal disease.
Endocrine tests may be indicated to establish etiology of hypertension.
Following stabilization of the patient, the etiology of the hypertensive crisis needs to be established to guide further management.
Table III. Causes of hypertensive emergencies
Elevations in systemic vascular resistance are responsible for arterial hypertension, but the precise pathophysiological mechanisms are incompletely understood. Three processes account for the raised systemic vascular resistance:
Increased concentrations of circulating catecholamines.
Increased activity of the sympathetic nervous system.
Activation of the renin-angiotensin system.
Hypertension can also occur as a result of augmented left ventricular contractility or substantial intravascular volume expansion. Blood pressure is related to cardiac output by the following equation:
Mean Arterial Pressure = Cardiac Output x Systemic Vascular Resistance
Failure of the delicate homeostatic mechanisms that control these systems precipitates the hypertensive crisis. As SVR rises, the stressed vessel wall releases humoral vasoconstrictors, initiating a perpetual cycle of endothelial damage with subsequent activation of intravascular clotting cascades, the development of obliterative vascular lesions, proliferative arteritis and ultimately fibrinoid necrosis with further release of vasoactive mediators.
If this cycle is not interrupted, the vascular injury and autoregulatory dysfunction lead to a state of relative organ ischemia.
The latest data show that the majority of patients (83%) presenting with an hypertensive emergency will exhibit single-organ dysfunction, 14% will have two-organ involvement, while multiorgan manifestations are uncommon. Cerebrovascular manifestations predominate, followed closely by cardiovascular disorders.
Table IV. Manifestations of hypertensive emergencies in order of frequency
Central nervous system (CNS)
Cerebral blood flow is normally maintained at constant levels through a wide range of perfusion pressures, approximately between MAP 50-150 mmHg. This autoregulation is maintained by myogenic, metabolic and humoral mechanisms.
Myogenic: wall stress is preserved in accordance with LaPlace’s law, which describes the relationship between the transmural pressure difference, the vessel radius, the wall thickness and wall tension, and is summed up by the following equation: Tension= (Pressure difference x Radius) ÷ Thickness.
Metabolic: At areas of low flow, substances such as nitric oxide, hydrogen ions, carbon dioxide and adenosine will accumulate, resulting in vasodilation with subsequent washout.
In addition to this metabolic build-up, during inflammation kinins are produced that also act to relax smooth muscle. Cerebral autoregulation is disrupted by brain injury; therefore, cerebral blood flow relies more heavily on perfusion pressure.
Cerebral Blood flow = Mean Arterial Pressure – Intracranial Pressure.
Patients with longstanding hypertension have the higher cerebrovascular resistance resulting in a right shift of the flow-pressure curve in the central nervous system. They can tolerate higher MAPs before there is disruption of their autoregulatory systems, but are more prone to ischemia at lower pressures.
Acute elevations in blood pressure disrupt the balance between myocardial oxygen supply and demand. Supply depends upon coronary blood flow, oxygen content of arterial blood and the position of the oxy-hemoglobin dissociation curve. Demand is determined by afterload (systolic arterial pressure), preload (left ventricular end-diastolic pressure), myocardial contractility and heart rate.
Acute hypertension can cause acute myocardial dysfunction. In chronic hypertension, left ventricular wall hypertrophy occurs, necessitating higher filling pressures resulting in relative diastolic dysfunction. LaPlace’s law can also be applied to explain left ventricular dysfunction in dilated cardiomyopathy; the increased radius requires the ventricle to generate greater tension in order to produce the same pressure.
Both these scenarios increase myocardial work and predispose to ischemia and ventricular failure. In primary myocardial dysfunction, hypertension occurs as a result of the sympathoadrenal response to pain, anxiety, hypoxemia and increased work of breathing.
Acute aortic dissection initiates with vessel wall tearing, which results in blood flow between the inner smooth intimal layer and the tunica media. Extension of the tear depends on the rate of change of aortic pressure (dP/dt) influenced by blood pressure, myocardial stroke volume and heart rate.
Blood pressure parameters will vary depending on the extent and location of the tear, and while hypertension may be present, a significant proportion of cases may present with severe hypotension, especially in the context of aortic rupture.
Renal blood flow is also autoregulated in a manner similar to CBF. Alterations in renal blood flow affect the renin-angiotensin system, which regulates the release of potent vasoconstrictors.
Renovascular disorders can occur secondary to systemic hypertension; as a result of renal artery stenosis; and due to intrinsic renal disease such as glomerulonephritis, particularly in younger patients or less frequently in association with specific disease processes such as scleroderma.
Hypertension is common following renal transplantation; however, in the early post-transplant period it may be a manifestation of graft ischemia, rejection or immunosuppressant toxicity.
Pre-eclampsia is a severe form of pregnancy-induced hypertension (i.e. that occurring after 20 weeks’ gestation) associated with multiple organ dysfunction. It is a common complication, occurring in 7% of pregnancies, and is the second most common cause of maternal mortality after thromboembolic disease.
Diagnostic features are high blood pressure (SBP > 160 and DBP > 110) and proteinuria greater than 5 g in 24 hours. Severe peripheral edema occurs but as edema is very common in pregnancy it is no longer used as a disease hallmark.
Oliguria fewer than 500 mls in 24 hours and thrombocytopenia (platelets < 100,000) are common. Other features are headaches, visual disturbances, hyper-reflexia, clonus, and seizures (eclampsia); pulmonary edema; epigastric or hypochondrial pain and HELLP (hemolysis, elevated liver enzymes and low platelets) may occur.
Pre-eclampsia is an ischemic condition that can affect any organ; however, the precise etiology remains unclear. Pathophysiological changes include:
Uteroplacental inadequacy: the normal vasodilatation of the placental vessels after the third trimester does not occur. Instead, vasoconstrictors are released to ensure placental perfusion; these vasoactive drugs have been identified in the placental and amniotic fluid as well as the blood. The vessels may become atherosclerotic.
Primary endothelial damage: results in increased production of thromboxane A2 and decreased prostacyclin, leading to further vasoconstriction.
Ischemic damage: increased platelet turnover and deposition of microvascular thrombin can lead to disseminated intravascular coagulation. Fibrinoid ischemic necrosis occurs in the placenta, cerebral, hepatic and renal vascular beds, causing multiple organ failure.
Immune complexes: occur due to inadequate maternal antibody response to the antigenic fetus.
Treatment: Magnesium sulfate infusion is the initial treatment of choice and is continued for 72 hours. Magnesium levels may be monitored in the laboratory, with the targets being 2-4 mmol/l; nevertheless, clinical monitoring of power and reflexes for signs of toxicity is essential.
Labetalol and hydralazine are second-line agents. Delivery of the fetus is the only cure and will be undertaken in severe life-threatening cases regardless of gestation.
Pheochromocytomas are benign neuroendocrine tumors that arise from chromaffin cells, 90% of which occur within the adrenal glands. Excess catecholamine release causes high blood pressure with periodic attacks of severe hypertension, tachycardia and diaphoresis that can last minutes or days.
Treatment is surgical excision; however, perioperative control of blood pressure is crucial, as both the surgical incision and handling of the tumor can result in a hypertensive crisis. The preferred agent is phentolamine, a potent alpha-adrenergic antagonist, with or without beta-adrenergic blockade. Labetalol is safe; however, beta-blockade without alpha-blockade is absolutely contraindicated.
Preoperative hypertension is often due to anxiety, and it is important to allow the patient some time to relax before a second measurement is obtained. Such acute elevations can be successfully treated with anxiolytic medication such as temazepam.
Preoperative hypertension is associated with significant cardiovascular morbidity; therefore, in patients with persistently elevated blood pressure, current recommendations are to postpone elective surgery if SBP is greater than 180 or DBP is greater than 110 mmHg and refer the patient for blood pressure management.
Postoperative hypertension may be due to pain, nausea, anxiety, hypoxemia, hypercarbia or hypervolemia. These reversible causes should be considered and treated before pharmacological agents are used.
The World Health Organisation (WHO) has listed high blood pressure as the first cause of death worldwide.
The incidence of chronic hypertension among adults in the developed world is approximately 30% and has been increasing over the past three decades in North America, probably because of the strong association with obesity, whereas it has remained stable in England since 2003.
In all other aspects, statistics from both the USA and the UK largely concur, but the precise figures depend on the definition of hypertension, the values of which are lower in the USA. The prevalence of hypertension is up to 4% higher in men than in women, particularly in the younger and middle-aged groups. Westerners of African or Caribbean descent have 1.5-2.0 times greater risk of developing hypertension than Caucasians.
Universally blood pressure increases with age; it is more pronounced in females and it rises most rapidly over the age of 60. Systolic hypertension is more prevalent in the elderly and has a greater association with cardiovascular disease than diastolic hypertension.
It is well recognized that the monitored treatment of hypertension reduces the risk of subsequent complications. In people over 60, treatment reduced the risk of myocardial infarction, stroke and all-cause mortality if only the systolic value or both systolic and diastolic values were targeted. In those over 80, treatment did not reduce the risk of death but reduced stroke.
Estimates suggest that between 1% and 5% of hypertensive people will develop a hypertensive crisis. There are no data to prove that treating chronic hypertension prevents hypertensive crises, but this would be a reasonable extrapolation since over 90% of patients presenting with a hypertensive emergency have had a previous diagnosis of hypertension.
The prevalence of hypertensive emergencies is reflected by the prevalence of chronic hypertension in the community; therefore, hypertensive emergencies are more common in the elderly, in males and in those of Afro-Caribbean origin.
What's the evidence?
“The task force for the Management ofArterial Hypertension of the European Society of Hypertension (ESH) andof the European Society of Hypertension. 2007 Guidelines for the Management of Arterial Hypertension”. European Heart Journal. vol. 28. 2007. pp. 1462-536.
Aram, V. Chobanian, George, L. Bakris, Henry, R. Black. “The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure: The JNC7 Report”. JAMA. vol. 289. 2003. pp. 2560-72.
Fink, MP, Abraham, E, Vincent, JL, Kochanek, PM. Textbook of Critical Care. 2005. pp. 21-26.
Vaughan, CJ, Delanty, N. “Hypertensive Emergencies”. Lancet.. vol. 256. 2000. pp. 411-7.
Flanigan, JS, Vitburg, D. “Hypertensive Emergencies and Severe Hypertension: What to Treat, Who to Treat and How to Treat”. Med Clin North Am.. vol. 90. 2006. pp. 439-51.
Panioli, AM. “Hypertension Management in Neurological Emergencies”. Ann Emerg Med. vol. 51. March 2008. pp. S24-7.
Anderson, CS, Huang, Y, Wang, JG. “Intensive blood pressure reduction in acute cerebral haemorrhage trial (INTERACT): a randomised pilot trial”. Lancet Neurol. vol. 7. May 2008. pp. 391-9.
Marik, PE, Varon, J. “Hypertensive crises: challenges and management”. Chest. vol. 131. 2007. pp. 1949-62.
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- 1. Description of the problem
- 3. Diagnosis
- What's the evidence?