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Accelerated Hypertension

Key facts:

Authors: John Soong and Lavanya Pelluri
Top Tip: The initial aim is NOT to achieve normal BP, but to ensure a controlled lowering of BP to a safe level

Key Differential Diagnoses

  • Severe chronic hypertension ('Hypertensive Urgency')
  • White-coat hypertension
  • Intracerebral disease (eg CVA/haemorrhage, mass, post-ictal, raised ICP)
  • Other (see Investigations)

Key Investigations

  • FBC, U+E, LFT, Bone, Glucose
  • CXR
  • ECG
  • Urinalysis

Key Treatment

Hypertensive Urgency

  • PO anti-hypertensives, eg PO NIFEDIPINE 10-20mg bd, RAMIPRIL 5mg od, BISOPROLOL 5 mg od

Hypertensive Emergency

  • In general, use oral therapy. If IV drugs are required:
  • IV SODIUM NITROPRUSSIDE 0.5-8.0mcg/kg/min, titrate at 0.5mcg/kg/min every 5 min
  • IV LABETOLOL 20–40mg boluses every 10 min, or 2mg/min infusion
  • IV GTN 10-200mcg/min
    Note: if IV drugs are used, consultant involvement is required, with the patient on ITU, HDU or CCU

Key Management Decisions

  • PO or IV anti-hypertensives
  • ITU/HDU/CCU or not


If the patient is drowsy, do a CT head and exclude hypoglycaemia


  • Accelerated hypertension (also called 'hypertensive emergency') is a condition in which elevated blood pressure results in end-organ damage. In 'hypertensive urgency' there is no evidence of end-organ damage
  • Headache, epistaxis, psychomotor agitation and arrythmia make end-organ damage more likely
  • Fundoscopy is important in the differentiation of hypertensive emergency from urgency
  • The systems primarily involved include CNS, CVS and renal. CVA, CCF and hypertensive encephalopathy are the commonest examples of end-organ damage
  • <1% of patients with essential hypertension develop accelerated hypertension, but the reason some patients develop it whereas others do not is unknown
  • The characteristic vascular lesion is fibrinoid necrosis of arterioles and small arteries, which causes the clinical manifestations of end-organ damage
  • Red blood cells are damaged as they flow through vessels obstructed by fibrin deposition, resulting in microangiopathic haemolytic anaemia (MAHA)
  • Another pathological process is the dilatation of cerebral arteries following a breakthrough of normal autoregulation of cerebral blood flow
  • Causes of accelerated hypertension are listed below. Any cause of secondary hypertension can cause it but rarely do so
  • Hypertensive emergencies require rapid therapy to decrease blood pressure within minutes to hours
  • But, in general, use oral therapy first; in both hypertensive emergency and urgency
  • Rapidly reducing blood pressure in patients with hypertensive urgency (definition, see below) may harm the patient, resulting in cardiac, renal, or cerebral hypoperfusion

Distinction between Hypertensive 'Emergency' and 'Urgency'

  • This is not as clearcut as the terms would suggest. There are patients 'on their way' from 'Urgency' to 'Emergency'
  • It is also not true that, in terms of treatment, 'Emergency' requires IV drugs and 'Urgency' requires oral ones
  • Often oral therapy if the first line treatment for 'Hypertensive Emergency', and IV drugs only used, if these do not work


Accelerated Hypertension (or 'Hypertensive Emergency')
Is a severe elevation in blood pressure, normally in excess of 220/140 mmHg, associated with impending progressive end organ damage. It can cause a range of hypertensive emergencies, including:
1. Hypertensive encephalopathy
2. Hypertensive retinopathy (papilloedema, and retinal haemorrhages)
3. Intracerebral haemorrhage/infarction
4. Acute myocardial infarction
5. Acute LVF/pulmonary oedema ('hypertensive acute heart failure)
6. Dissecting thoracic aneurysm
7. Pre-eclampsia of pregnancy
8. AKI ('malignant nephrosclerosis'). This may be the presentation of another disease, either primary (eg IgA Nephropathy or secondary, eg Systemic Sclerosis) 
9. Adrenergic crisis

Severe Chronic Hypertension (or 'Hypertensive Urgency')
This is characterised by a severe elevation of blood pressure, often over 180/120 mmHg, which can be symptomatic or asymptomatic, with or without evidence of non-progressive end organ damage. Symptoms may include:
1. Headache
2. Shortness of breath
3. Pedal oedema
Note: or there may be no symptoms, and no signs (other than the hypertension)

Malignant Hypertension
Some use this term used to encompass severe elevations of blood pressure associated with retinal haemorrhages, exudates and papilloedema, thought to be a sign of impending hypertensive encephalopathy (Ahmed, 1986). It may be the same thing as the more modern term, accelerated hypertension (or hypertension emergency)

Note 1: It should be noted there is no definition based on absolute blood pressure measurements alone, and the diagnosis relies on the clinical presentation, symptoms and evidence of end organ damage

Note 2: A continuum exists between the clinical syndromes of hypertensive 'urgency' and 'emergency' (accelerated hypertension); hence, the distinction between the 2 syndromes may not always be clear and precise in practice


  • 1% hypertensive adults
  • 25% patients referred to Emergency Department with hypertension (Zampaglione, 1996)

Risk Factors


  • Low birth weight


  • Uncontrolled Stage I and II hypertension
  • Sedentary lifestyle
  • Stress (Kyrou, 2006)
  • Obesity (85% of BMI>25 have hypertension)
  • Metabolic syndrome
  • Underlying renovascular disease
  • Hypokalaemia
  • High alcohol intake (Djoussé, 2009)
  • Vitamin D Deficiency (Lee, 2008)


  • The commoner causes are essential hypertension on non-compliance (70%), renovascular (10%), Neurogenic (7%), Phaeochromocytoma (3%), Conn's Syndorme (0.6%) (Chobanian, 2003)
  • Adrenergic crisis may be caused by recreational drug use (cocaine, ecstasy, metamphetamines), non-compliance to dietary/drug restrictions of monoamine oxidase inhibitors and phaeochromocytoma
    Note: ask about recreational drug use
  • Other secondary causes of hypertension rarely present as a hypertensive emergencies. They include: 


  • Cushing’s Syndrome/Hyperaldosteronism
  • Apparent mineralocorticoid excess syndromes
  • Phaeochromocytoma
    Note: the triad of headaches, palpitations and sweating makes this (very rare) diagnosis more likely


  • Polycystic Kidney Disease
  • Glomerulonephritis
  • Renovascular disease
  • Hyper-reninaemic syndromes
  • Any cause of CRF


  • Co-arctation of the aorta


  • Steroids
  • Sudden withdrawal of antihypertensives (eg beta-blockers) or other drugs (alpha-stimulants, alcohol); ie rebound hypertension
  • Oral contraceptive



  • Obtructive Sleep Apnoea/Obesity-hypoventilation syndrome
  • Arsenic exposure


  • Characteristic vascular lesion is fibrinoid necrosis of arterioles and small arteries
  • Red blood cells are damaged as they flow through vessels obstructed by fibrin deposition, resulting in microangiopathic haemolytic anaemia (MAHA)


Clinical presentation of accelerated hypertension has been reviewed by Elliott (2006)


  • Visual loss
  • Headache
  • Drowsy


  • Chest pain
  • SOB
  • Leg oedema


  • Poor urine output


  • Nausea and vomiting


  • Collapse
  • Nose-bleeds

Key Questions

  • "Have you been diagnosed with hypertension (high blood pressure)?"
  • "If so, have you been prescribed tablets for it? If so, have you been taking them regularly?”


Blood Pressure

  • Usually in excess of 220/140


  • Grade I = Minimal changes. Tortuous arteries, silver wiring. No exudates
  • Grade II = Arteriolar sclerosis ± haemorrhages (flame shaped). AV nipping. No exudates 
  • Grade III = Exudates (cotton) ± haemorrhages
  • Grade IV = Papilloedema


  • Confusion
  • Drowsiness, coma
  • Seizures
  • Focal deficits


  • Prominent apical pulsation, displaced apical impulse
  • LVF/pulmonary oedema
  • Unequal/absent peripheral pulses (aortic dissection)


  • Oliguria
  • Abdominal bruits - make renovascular disease more likely 


  • Nausea, vomiting 


If hypokalaemia is not present, Cushing's and Conn's Syndromes are unlikely 


  • FBC - anaemia (haemolytic, of MAHA), low platelets (MAHA)
  • U+E - end organ damage, ie AKI or AKI on CKD
    Note: hypokalaemia may indicate diuretics, Conn's syndrome, Cushing's syndrome or renovascular disease
  • Magnesium – hypomagnesaemia-induced dysrhythmias
  • LFTs (HELLP syndrome?), Bone, Glucose
  • Fasting lipids, 10am cortisol, TFTs 


  • Urinalysis – significant proteinuria and haematuria
    Note: absence of blood and protein in the urine makes glomerular disease unlikely
  • Urine microscopy - red blood cells, cellular casts (renal parenchymal disease)
  • CXR - cardiac sihouette shape/size (left ventricular hypertrophy), rib notching and 'figure 3 sign' (coarctation of aorta; see below), mediastinal size (aortic dissection)
  • ECG - left ventricular hypertrophy, myocardial infarction
    Note: LVH on CXR or ECG favours essential hypertension; and may be a 'bad thing' implying lack of treatment and chronicity

Coarctation of the Aorta (rib notching)

Coarctation of Aorta (aortic knuckle has a 3-shaped left sided contour = 'figure 3 sign')

Key Investigations

  • The basics:
  • FBC, U+E, LFTs, urinalysis, ECG and CXR 

Specialist Investigations

Investigations for secondary causes of hypertension do not have to be done immediately. It may more appropriate that they are done later (primarily as outpatient), if there is clinical suspicion:

  • Endocrine: plasma and 24 hour urine metanephrines plasma, and urine catecholamines(phaeochromocytoma); 24 hour urine free cortisol (Cushings); plasma renin and aldosterone levels, and 24 hour urine aldosterone (Conn's); 123-I-MIBG scan (phaeochromocytoma)
  • Renal: renal ultrasound (PCKD), MRA/CTA ± renal angiogram (renovascular disease), plasma urate
  • Cardiac - ECHO, cardiac catheter (coarctation)

Differential Diagnoses

  • Severe chronic hypertension ('Hypertensive Urgency')
  • White-coat hypertension
  • Intracerebral disease (eg CVA/haemorrhage, mass, head injury, post-ictal, raised ICP)
  • Other
     - Connective-tissue disease (especially lupus with cerebral vasculitis)
     - Drug overdose or withdrawal
     - Cocaine or amphetamine ingestion
     - Acute anxiety
     - Thrombotic thrombocytopenic purpura



If the patient is fluid overloaded, also give IV FUROSEMIDE 40-80mg

Treatment Principles - Hypertensive Emergency

  • Target: the initial aim in a hypertensive emergency is NOT to achieve a NORMAL blood pressure but to ensure a controlled progressive lowering of blood pressure to a safe level (Vaughan, 2000)
  • So, in general, use oral therapy (as for hypertensive urgency, see below)
  • Under normal circumstances, autoregulatory processes ensure that blood flow to the vital organs (cerebral, renal and coronary circulation) remain constant, despite fluctuations in blood pressure. In severe hypertension, these autoregulatory processes are set to a much higher blood pressure than normally tolerated
  • Sudden drops in blood pressure may then compromise vital organ perfusion. Studies suggest that the lower limit of autoregulation of cerebral blood flow is set at approximately 25% below the mean arterial pressure of normotensives or patients with uncomplicated blood pressure (Strandgaard, 1992)
  • Most centres, therefore, suggest that initial lowering of blood pressure should NOT exceed 25% of the pre-treatment blood pressure, with initial reduction targets of 20 - 25% of pre-treatment blood pressure, or a diastolic blood pressure of 100–110 mmHg, as being safer in minimising the risk of vital organ hypoperfusion. Blood pressure can then be normalised slowly
  • In some patients, IV therapy (and more rapid control of BP) is required. The choice of drug and how rapidly the initial blood pressure lowering should be, depends on the specific hypertensive emergency (see below). Broadly speaking, the initial lowering of blood pressure to the above targets should take place over 1–2 hours, with further reduction in blood pressure done over the following 24 hours, depending on the patients clinical state and the adequacy of end organ perfusion with close clinical monitorin
  • Angelats EG (2010) has reviewed the treatment of accelerated hypertension in the Emergency Department

Treatment - Hypertensive Emergency - IV Drugs

  • IV SODIUM NITROPRUSSIDE (0.5-8.0 mcg/kg/min, titrate at 0.5mcg/kg/min every 5 min) is a commonly used medication. Vasodilator. It is a short-acting agent, and the BP response can be titrated from minute to minute. However, patients must have constant monitoring in an intensive care unit. The potential exists for thiocyanate and cyanide toxicity with prolonged use or if the patient has renal or hepatic failure. Problems: thiocyanide toxicity, B12 deficiency, avoidance of sudden withdrawal, special giving equipment, methaemo-globinaemia
  • IV LABETOLOL (20 – 40mg boluses every 10 min, or 2mg/min infusion) is particularly preferred in patients with acute dissection. Adrenergic inhibitor by alpha- and beta-blockade. Once an adequate BP level is obtained, oral hypertensive therapy should be initiated, and patients are gradually weaned from parenteral agents. Problems: bronchoconstriction, brady-arrhythmias, severe hepatocellular damage
  • IV GTN 10-200mcg/min. Vasodilator. Problems: prolonged use may cause methaemo-globinaemia, acute angle closure glaucoma (rare), tachyphylaxis
  • IV PHENTOLAMINE 2–5mg, repeat as necessary. Adrenergic inhibitor via alpha-blockade. Avoid beta-blockers before administering phentolamine. Usually given with LABETOLOL. Problems: quick onset (1-2 min) and offset (10-30 min), sulphites in ampoules may trigger hypersensitivity (esp in asthmatics). Very irritant to tissues, avoid in porphyria, contact sensitisation
  • IV DIAZOXIDE may also be used in hypertensive crisis. Small boluses of 100 mg are administered every 5 minutes, as indicated. Diazoxide is not preferred with concomitant congestive heart failure or low cardiac output

Neurologic Emergencies

  • Rapid BP reduction may be indicated in neurologic emergencies, such as hypertensive encephalopathy, acute ischaemic stroke, acute intracerebral hemorrhage, and subarachnoid hemorrhage
  • In hypertensive encephalopathy, the treatment guidelines are to reduce the MAP 25% over 8 hours. Labetalol and nicardipine are the preferred medications; nitroprusside and hydralazine should be avoided
  • For most cases of acute ischaemic stroke, no anti-hypertensive treatment is recommended. But if there is evidence of accelerated hypertension, the preferred medications are labetalol and nicardipine
  • For acute intracerebral haemorrhage, again, anti-hypertensive agents are usually avoided. If necessary, the preferred medications are labetalol and nicardipine; nitroprusside and hydralazine should be avoided
  • In subarachnoid haemorrhage, nicardipine and labetalol, are also the preferred agents; again, nitroprusside and hydralazine should be avoided. Maintain the SBP < 160 mm Hg until the aneurysm is treated or cerebral vasospasm occurs. Although oral nimodipine is used to prevent delayed ischemic neurologic deficits, it is NOT indicated for treating acute hypertension

Cardiovascular Emergencies

  • Rapid BP reduction may be indicated in cardiovascular emergencies, such as aortic dissection, acute coronary syndrome, and acute heart failure
  • In aortic dissection, the preferred medications are labetalol, nicardipine, nitroprusside (with beta-blocker) and morphine sulphate. However, avoid beta-blockers if there is aortic regurgitation or suspected cardiac tamponade. Maintain the SBP at < 110 mm Hg, unless signs of end-organ hypoperfusion are present
  • For acute coronary syndrome, beta blockers and SL or IV GTN are the preferred drugs
  • In acute heart failure, SL or IV sublingual GTN are the preferred drugs

Adrenergic Crisis (eg, Phaeochromocytoma, Cocaine toxicity)

  • Diazepam, phentolamine, and GTN/nitroprusside are the preferred drugs. Avoid beta-adrenergic antagonists before administering phentolamine
  • Hypertension and tachycardia from cocaine toxicity rarely require specific treatment. Alpha-adrenergic antagonists (phentolamine) are the preferred agents for cocaine-associated acute coronary syndromes
  • Phaeochromocytoma treatment guidelines are similar to that of cocaine toxicity. Only after alpha blockade can beta blockers be added for BP control


  • Normal blood pressure in a pregnant woman is <120/70
  • >140/90 is a medical sub-emergency
  • The preferred medications are methyldopa, hydralazine, labetalol, and nifedipine. Avoid nitroprusside and angiotensin-converting enzyme inhibitors
  • Seizures should be treated with IV MAGNESIUM SULPHATE, 4g bolus, followed by 1g/hour
  • In women with eclampsia or pre-eclampsia, the SBP should be < 160 mm Hg and the DBP should be < 110 mm Hg in the antepartum and intrapartum periods

Perioperative hypertension

  • Nitroprusside and IV GTN are preferred. Target the perioperative BP to within 20% of the patient's baseline pressure, except if there is the potential for life-threatening arterial bleeding
  • Perioperative beta blockers are the first choice in patients undergoing vascular procedures or in patients with an intermediate or high risk of cardiac complications

Treatment - Hypertensive Emergency - Procedures

  • Consider arterial and CVP lines, and urinary catheter, if patient needs ITU/HDU/CCU
  • ECG monitor

Treatment - Hypertensive Urgency



Mechanism of action

Special considerations

Nifedipine SR or MR

10-20 mg od

Dihydropyridine calcium channel antagonist

Oedema; rarely gynaecomastia, rash


1.25-10 mg od

Angiotensin converting enzyme inhibitor

Hyperkalaemia,   angioedema, rash, cautioned in renovascular disease, poor response on   Afro-carribeans, >55 years and primary hyperaldosteronism


2.5-10 mg od

Cardioselective beta blocker

With thiazides may cause deterioration in glucose tolerance, cautioned in   peripheral vascular disease, bronchospasm


25-100 mg od

Angiotensin II receptor blocker (ARB)

See Ramipril


50-100 mcg tds to a max of 1.2 mg daily

Centrally acting antihypertensive

Drowsiness, confusion, abrupt withdrawal may precipitate hypertensive crisis


1-16 mg od


Fatigue, asthenia, paraesthesia, urinary tract infections


200-300 mcg bd

Centrally acting antihypertensive

Indicated if failure to control blood pressure with above drug classes, abrupt   withdrawal may trigger hypertensive crisis, severe bradyrhythmias (not to be   used with beta blocker), contraindicated in epilepsy, Parkinsons’ disease,   depression and pregnancy

Prescribing Issues



  • Centrally acting antihypertensives and beta blockers tend to trigger rebound hypertension and possibly a hypertensive crisis if withdrawn abruptly. If alteraltions in medication are needed, they should be weaned off, then replaced

Key Management Decisions

  • PO or IV anti-hypertensives
  • ITU/HDU/CCU or not


  • Hypertensive urgency: usually
     - The management of severe hypertension depends on the availability of early review. Larger centres with available rapid review would be able to discharge patients after commencing oral antihypertensive medication, with monitoring of response in the department for 3–12 hours (depending on symptoms and presence of non-progressive end organ damage), and rapid follow up within 3–7 days
      - Centres with no facility for acute follow up may have to admit the patient overnight for review of response to oral treatment, in keeping with good risk management practice
  • Hypertensive emergency: always

Bed Plan

  • AMU (then ?cardiac, endocrine, renal or obstetric wards, depending on cause)



  • Cardiac, endocrine, renal or obstetric


The Rest

A blood pressure of > 140/90 in pregnancy is a medical sub-emergency and requires rapid action


  • "If BP control is good, hypertensive emergency is unlikely"


Severe hypertension may progress to a hypertensive emergency if untreated. The following are clinical sequalae of severe hypertension:


  • Left ventricular hypertrophy
  • Diastolic dysfunction
  • Congestive cardiac failure
  • Coronary artery disease
  • Arrhythmias

Peripheral vascular disease


  • Cerebrovascular disease (TIA/CVA)
  • Intracerebral haemorrhage
  • Hypertensive encephalopathy
  • Impaired cognition


  • Fibrinoid necrosis of afferent arterioles (malignant hypertension)
  • Glomerulosclerosis


  • Papilloedema
  • Micro and macro aneurysms
  • Ischaemia
  • Haemorrhages
  • Exudates
  • Central or branch vein occlusions


  • GP ±
  • Cardiology, endocrine, renal, obstetrics (as appropriate)

Risk Stratification

  • If there is no evidence of end-organ damage, a slower approach is appropriate. This may involve largely outpatient management


  • Depends on the degree of end organ damage
  • Mortality is high
  • Without treatment, the 6-month mortality rate for Hypertensive Emergencies is 50%, and the 1-year mortality rate approaches 90%
  • Risk increases with age, essential hypertension, raised urea or creatinine, increasing duration fd known hypertension and Grade II-IV hypertensive retinopathy

2° Prevention + Health promotion

  • Most who present with hypertensive emergency and severe hypertension will need multiple classes of antihypertensive medication to control their blood pressure (unless a reversible secondary cause can be found)
  • However, non-pharmacological measures should not be forgotten:

Patient Information

  • The British Hypertension Society suggests the following non-pharmacological strategies be explored for all patients with hypertension:
    - Weight Reduction
    - Regular aerobic (low intensity) exercise
    - Reduction in dietary sugar and salt intake
    - DASH (Dietary Approaches to Stop Hypertension) diet (rich in fruit and vegetables, low in fat)
    - Cessation of cigarette smoking and alcohol consumption
    - Stress reduction techniques

Don't Forget

  • The initial aim in a hypertensive emergency is NOT to achieve a normal blood pressure, but to ensure a controlled progressive lowering of blood pressure to a safe level
  • In most patients, use oral drugs first
  • A blood pressure of > 140/90 in pregnancy is a medical sub-emergency and requires rapid action
  • In pregnancy, the preferred medications are methyldopa, hydralazine, labetalol, and nifedipine. Avoid nitroprusside and angiotensin-converting enzyme inhibitors
  • Ask about recreational drug use (eg cocaine, ecstasy)

Red Flags

  • AKI
  • Chest pain (?dissection ?MI)
  • SOB (CCF? AKI?)
  • Drowsiness/seizures (hypertensive encephalopathy)
  • Anaemia/low platelets (MAHA)


international guidelines US/NHLBI. Chobanian AV, Bakris GL, Black HR et al. Seventh report of the joint National Committee on Prevention, Detection, and Treatment of High Blood Pressure. Hypertension; 42(6): 1206-52, 2003

national guidelines UK/BHS. Williams B et al. Guidelines for management of hypertension. Report of the fourth working party of the British Hypertension Society, BHS 2004 - IV

UK/NICE. CG127. Hypertension: clinical management of primary hypertension in adults, August 2011

UK/MIMS. Clinical Management of Primary Hypertension in Adults. Good summary of UK/NICE CG127, August 2011

reviews James PR, Nelson-Piercy C. Management of hypertension before, during, and after pregnancy. Heart; 90(12): 14991504, 2004

Vaughan CJ, Delanty N. Hypertensive emergencies. Lancet; 356: 411, 2000

Angelats EG, Baur EB. Hypertension, hypertensive crisis, and hypertensive emergency: approaches to emergency department care. Emergencias; 22: 209-219, 2010

articles Ahmed ME, Walker JM, Beevers DG, Beevers M. Lack of difference between malignant and accelerated hypertension. Br Med J; 292: 235, 1986

Zampaglione B et al. Hypertensive urgencies and emergencies: Prevalence and clinical presentation. Hypertension; 27: 144-147, 1996

Davis BA, Crook JE, Vestal RE, Oakes JA. Prevalence of renovascular hypertension in patients with grade III or IV retinopathy. N Engl J Med; 301: 1273, 1979

Kyrou I, Chrousos GP, Tsigos C. Annals of the New York Academy of Sciences; 1083: 77-110, 2006

Strandgaard S, Paulson OB. Regulation of cerebral blood flow in health and disease. J Cardiovasc Pharmacol; 9: S89-S93, 1992

Elliott WJ. Clinical features in the management of selected hypertensive emergencies. Prog Cardiovasc Dis; 48: 316-325, 2006

Young DB. Potassium Depletion and Diastolic Dysfunction. Hypertension; 48: 201, 2006

Djouss L, Mukamal KJ. Alcohol Consumption and Risk of Hypertension: Does the Type of Beverage or Drinking Pattern Matter? Rev Esp Cardiol; 62 (6): 603605, 2009

Lee JH, O'Keefe JH, Bell D, Hensrud DD, Holick MF. Vitamin D deficiency an important, common, and easily treatable cardiovascular risk factor? J. Am. Coll. Cardiol; 52 (24): 194956, 2008