Cardio · hypertension-aorta-peripheral
Hypertensive emergency and severe hypertension
Fellowship-level guide to hypertensive emergency under the 2024 ESC guideline on elevated blood pressure and hypertension and the 2025 AHA/ACC high blood pressure guideline: definitions and thresholds, acute organ damage, autoregulation, assessment, intensive care, timing of blood pressure (BP) lowering, intravenous drugs by comorbidity, stroke, aortic dissection, phaeochromocytoma and pregnancy, and severe hypertension without acute organ damage.
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Red flags
- Screening office BP of 180/110 mmHg or more: ESC 2024 recommends that hypertensive emergency be excluded (Class I, Level C)
- Nonpregnant, nonstroke adults with a hypertensive emergency (blood pressure [BP] above 180 and/or above 120 mm Hg and evidence of acute target organ damage): AHA/ACC 2025 recommends intensive care unit (ICU) admission for continuous monitoring of BP and target organ damage and for consideration of parenteral administration of appropriate therapy (class of recommendation [COR] 1, level of evidence [LOE] B-NR)
- Nonpregnant, nonstroke adults with a hypertensive emergency but without a compelling condition: AHA/ACC 2025 states that systolic BP (SBP) should be reduced with oral or parenteral therapy by no more than 25% within the first hour; then, if stable, to below 160/100 mm Hg within the next 2 to 6 hours; then cautiously to 130 to 140 mm Hg during the next 24 to 48 hours to limit target organ injury (COR 1, LOE C-LD)
- Nonpregnant, nonstroke adults with a hypertensive emergency related to a compelling condition (e.g. acute aortic syndrome or acute aortic dissection): AHA/ACC 2025 states that SBP should be reduced to below 140 mm Hg for most conditions and to below 120 mm Hg in aortic dissection during the first hour, while monitoring for other target organ dysfunction (COR 1, LOE C-LD)
- Nonpregnant, nonstroke adults hospitalised for noncardiac conditions with severe hypertension (above 180/120 mm Hg) and no evidence of acute target organ damage: AHA/ACC 2025 does not recommend intermittent additional intravenous (IV) or oral antihypertensives to acutely reduce BP (COR 3: Harm, LOE B-NR)
Definitions and classification
Both guidelines build the diagnosis from two parts: a very high BP and acute damage to an organ.[1][2] ESC 2024 sets the BP part at 180/110 mmHg or more, and AHA/ACC 2025 at above 180/120 mm Hg.[1][2] ESC 2024 adds that hypertensive emergencies are potentially life-threatening and require immediate and careful intervention to reduce BP, often with intravenous (i.v.) therapy.[1] AHA/ACC 2025 states that hypertensive emergencies demand immediate reduction of BP to prevent or limit further target organ damage.[2]
ESC 2024
Section 10.1
- Hypertensive emergency: BP of 180/110 mmHg or more associated with acute HMOD, often in the presence of symptoms
- ‘Hypertension urgency’: severe hypertension in patients without clinical evidence of acute organ damage
- Urgency: patients require BP reduction but do not usually require admission to hospital; BP reduction is best achieved with oral medication according to the ESC drug treatment algorithm
AHA/ACC 2025
Section 6.2, What Is New table and Top Take-Home Messages
- Section 6.2: hypertensive emergency is a severe elevation in BP (above 180/120 mm Hg) associated with evidence of acute target organ damage
- Top Take-Home Message 10: severe hypertension in nonpregnant individuals is BP above 180/120 mm Hg without evidence of acute target organ damage
- What Is New table: severe hypertension is the 2025 term; the 2017 guideline used hypertensive urgency
- Top Take-Home Message 10: such patients should be evaluated and treated in the outpatient setting with initiation, reinstitution or intensification of oral antihypertensive medications in a timely manner
- Section 6.2, nonpregnant and nonstroke patients with severe hypertension without evidence of acute target organ damage: reinstitution or intensification of oral antihypertensive medications, preferably in the outpatient setting, is recommended
ESC 2024 defines HMOD, among patients with chronically elevated BP or hypertension, as the presence of specific cardiac, vascular and renal alterations.[1] In a hypertensive emergency, ESC 2024 says the more acute manifestations of organ damage are relevant for management.[1]
For nonpregnant, nonstroke adults, AHA/ACC 2025 sorts emergencies a second way, by whether a compelling condition is present.[2] AHA/ACC 2025 gives acute aortic syndrome or acute aortic dissection as examples of a compelling condition, and in these patients the distinction sets the first-hour target.[2]
[1] [2]Epidemiology and precipitants
A 2020 meta-analysis of eight ED studies included 1970 hypertensive emergencies and 4983 hypertensive urgencies.[6] In that analysis, the prevalence of hypertensive emergencies was 0.3% and of hypertensive urgencies 0.9%.[6] A 2023 meta-analysis that included 15 ED studies reported a prevalence of in-hospital mortality of 9.9% (95% CI 1.4% to 24.6%) among patients with hypertensive emergency.[5]
The two meta-analyses rank the types of acute organ damage differently, so quote each with its source.[6][5]
2020 meta-analysis
ED studies, acute HMOD subtypes
- Pulmonary oedema/heart failure: the most frequent subtype (32%)
- Ischaemic stroke 29%; acute coronary syndrome 18%
- Haemorrhagic stroke 11%
- Acute aortic syndrome 2%; hypertensive encephalopathy 2%
2023 meta-analysis
ED studies, HMOD types
- Ischaemic stroke: the most prevalent (28.1%)
- Pulmonary oedema/acute heart failure 24.1%; haemorrhagic stroke 14.6%
- Acute coronary syndrome 10.8%; renal failure 8.0%
- Subarachnoid haemorrhage 6.9%; encephalopathy 6.1%
- Aortic dissection: the least prevalent (1.8%)
AHA/ACC 2025 states that common forms of acute hypertension-related target organ damage include acute heart failure/pulmonary oedema, neurologic disorders (encephalopathy, intracerebral haemorrhage [ICH], acute ischaemic stroke) and acute kidney injury (AKI).[2] In the same passage, AHA/ACC 2025 names aortic dissection as the least common presentation.[2]
What precipitates it
- Nonadherence: a 2024 review of malignant hypertension names nonadherence to the antihypertensive regimen as the most common cause of malignant hypertension.[9]
- Drugs that trigger emergencies: the same review states that antiangiogenic and immunosuppressant therapy can also trigger hypertensive emergencies.[9]
- Sympathomimetics: ESC 2024 notes that acute and severe increases in BP can sometimes be precipitated by sympathomimetics such as methamphetamine or cocaine, when caution around beta-blocker use is also needed.[1]
- Catecholamine excess: AHA/ACC 2025 Table 26 lists phentolamine for emergencies induced by catecholamine excess: phaeochromocytoma, interactions between monoamine oxidase inhibitors and other drugs or food, cocaine toxicity, amphetamine overdose or clonidine withdrawal.[2]
Pathophysiology
Autoregulation is the ability of an organ or vascular bed to keep its perfusion constant when BP changes.[8] A 1990 paper on cerebral autoregulation states that cerebral blood flow (CBF) autoregulation typically operates between mean pressures of the order of 60 and 150 mm Hg.[8] Chronic hypertension shifts both the lower and the upper limits of CBF autoregulation towards higher pressure.[7][8] A 1995 paper states that CBF in hypertensive and normotensive people without neurological deficit is the same.[7]
The shift matters when BP is lowered.[7][2] Acute BP reduction lowers CBF only if pressure is taken below the lower limit of autoregulation, and in chronic hypertension that limit sits higher.[7] AHA/ACC 2025 warns that rapid correction of BP to the normal range in patients with longstanding hypertension may result in vital organ hypoperfusion due to loss of autoregulation.[2] With chronic antihypertensive treatment, CBF autoregulation may re-adapt towards normal.[7]
At the other end of the curve, the 1990 paper states that acute hypertensive encephalopathy is thought to be due to autoregulatory failure at very high pressure.[8] In malignant hypertension, ESC 2024 describes acute microvascular damage with small-artery fibrinoid necrosis in the kidneys, retina and brain.[1] A 2024 review adds that malignant hypertension is characterised by acute microvascular damage and autoregulation failure affecting the retina, brain, heart, kidney and vascular tree.[9] The same review states that both absolute BP levels and the pace of BP rise determine the risk of target-organ damage.[9]
Acute ischaemic stroke needs a different approach.[8][1] The 1990 paper states that autoregulation is lost in acute ischaemic stroke, leaving surviving brain tissue unprotected against the potentially harmful effect of BP changes.[8] ESC 2024 bases its more conservative approach to acute BP management in acute ischaemic stroke without i.v. thrombolysis or mechanical thrombectomy on cerebral autoregulation that may be impaired in acute stroke, with cerebral perfusion relying on systemic BP.[1] AHA/ACC 2025 describes autoregulation in the ischaemic penumbra as grossly abnormal, and says rapid reduction of BP, even to levels within the hypertensive range, can be detrimental.[2]
[8] [7] [2]Clinical presentation
ESC 2024 states that the symptoms depend on the organs affected.[1] ESC 2024 lists headache, visual disturbances, chest pain, shortness of breath, dizziness and other neurological deficits as symptoms that may occur.[1]
In hypertensive encephalopathy, ESC 2024 lists somnolence, lethargy, tonic–clonic seizures and cortical blindness as features that may precede a loss of consciousness.[1] Focal neurological lesions are rare in encephalopathy, and ESC 2024 says they should raise the suspicion of stroke.[1]
ESC 2024 states that the acute microangiopathy of malignant hypertension is typically characterised clinically by retinopathy: flame haemorrhages, cotton wool spots and/or papilloedema.[1] ESC 2024 states that other manifestations of the microangiopathy include disseminated intravascular coagulation, encephalopathy (in about 15% of cases), acute heart failure and acute deterioration in renal function.[1]
Posterior reversible encephalopathy syndrome (PRES) is a neurological disorder of (sub)acute onset with varied symptoms.[10] A 2017 paper on PRES lists headache, impaired visual acuity or visual field deficits, disorders of consciousness, confusion, seizures and focal neurological deficits among them.[10] The same paper states that in a majority of patients the presentation includes elevated BP up to hypertensive emergencies.[10]
In the 2020 ED meta-analysis, patients with hypertensive urgency were younger than those with hypertensive emergency by 5.4 years.[6] In the same analysis, patients with hypertensive urgency more often complained of nonspecific symptoms and/or headache, whereas specific symptoms were more frequent in hypertensive emergency.[6]
[1]Differential diagnosis: is this really an emergency?
Both guidelines separate very high BP with acute organ damage from very high BP without it, and other situations also need separating.[1][2]
Situations to separate before labelling a hypertensive emergency
| Situation | What distinguishes it | Source |
|---|---|---|
| Hypertensive emergency | BP of 180/110 mmHg or more (ESC 2024) or above 180/120 mm Hg (AHA/ACC 2025) with acute organ damage | ESC 2024; AHA/ACC 2025 |
| Severe hypertension without acute organ damage (ESC: ‘hypertension urgency’) | Severe hypertension without clinical evidence of acute organ damage; oral treatment (ESC 2024: usually without admission; AHA/ACC 2025, nonpregnant, nonstroke adults: preferably in the outpatient setting) | ESC 2024; AHA/ACC 2025 |
| Acute pain or distress in the ED | Many such patients may have acutely elevated BP that will normalise when the pain and distress are relieved, rather than requiring any specific intervention to lower BP | ESC 2024 |
| Asymptomatic severe hypertension in an inpatient | Spontaneous falls in BP without any antihypertensive agents occur commonly, at a rate of 40% to 50% | AHA/ACC 2025 |
| Stroke versus hypertensive encephalopathy | Focal neurological lesions are rare in encephalopathy and should raise the suspicion of stroke (ESC 2024); ICH and acute ischaemic stroke are themselves among the common forms of acute target organ damage (AHA/ACC 2025) | ESC 2024; AHA/ACC 2025 |
| Catecholamine excess (a cause of emergencies, not a look-alike) | AHA/ACC 2025 Table 26 lists phentolamine for hypertensive emergencies induced by catecholamine excess (phaeochromocytoma, monoamine oxidase inhibitor interactions with other drugs or food, cocaine toxicity, amphetamine overdose or clonidine withdrawal) | AHA/ACC 2025 Table 26 |
The reading itself does not settle the question.[6] In the 2020 ED meta-analysis, no clinically meaningful difference was found for BP levels at presentation.[6] The 2020 meta-analysis concluded that BP levels alone do not reliably predict acute HMOD, which should be suspected according to the presenting signs and symptoms.[6]
Clinical and bedside assessment
ESC 2024 rows on a very high screening reading and on fundoscopy (Recommendation Tables 6 and 10)
| ESC 2024 recommendation | Class, level |
|---|---|
| Where screening office BP is 160/100 mmHg or more: BP 160–179/100–109 mmHg should be confirmed as soon as possible (e.g. within 1 month), preferably by home or ambulatory BP measurements; when BP is 180/110 mmHg or more, hypertensive emergency should be excluded (both bullets are one row) | I, C |
| Fundoscopy if BP is above 180/110 mmHg in the work-up of hypertensive emergency and malignant hypertension, as well as in hypertensive patients with diabetes | I, C |
ESC 2024 text adds that, for BP of 180/110 mmHg or more, assessment for hypertensive emergency is recommended.[1] In a hypertensive emergency, ESC 2024 recommends immediately starting BP-lowering treatment.[1] For individuals with BP above 180/110 mmHg at screening but without a hypertensive emergency, prompt confirmation (preferably within a week) can be considered before starting treatment.[1]
ESC 2024 links fundoscopy directly to this diagnosis.[1] ESC 2024 Table 9 lists optional tests that may be used as clinically indicated in the initial work-up of a patient with elevated BP or hypertension to assess HMOD or established cardiovascular disease.[1] Table 9 lists fundoscopy for assessing HMOD (hypertensive retinopathy) and for diagnosing hypertensive emergency/malignant hypertension (haemorrhages and exudates, papilloedema).[1] A diagnostic work-up is necessary for patients with a suspected hypertensive emergency, and ESC 2024 sets it out in supplementary Table S12.[1]
Investigations
ESC 2024 lists the diagnostic work-up for a suspected hypertensive emergency in supplementary Table S12; the tests and findings below are those named in the main texts and reviews.[1]
- Fundoscopy: ESC 2024 recommends it if BP is above 180/110 mmHg in the work-up of hypertensive emergency and malignant hypertension, as well as in hypertensive patients with diabetes (Class I, Level C). ESC 2024 Table 9 lists it among optional tests that may be used as clinically indicated in the initial work-up of a patient with elevated BP or hypertension to assess HMOD or established cardiovascular disease. Table 9 lists fundoscopy for assessing HMOD (hypertensive retinopathy) and for diagnosing hypertensive emergency/malignant hypertension (haemorrhages and exudates, papilloedema).[1]
- Evidence of acute kidney injury: AKI is one of the common forms of acute hypertension-related target organ damage in AHA/ACC 2025, and ESC 2024 lists acute deterioration in renal function among the manifestations of the microangiopathy of malignant hypertension.[2][1]
- Disseminated intravascular coagulation: ESC 2024 lists it among the manifestations of the microangiopathy of malignant hypertension.[1]
- Brain imaging: in PRES, neuroimaging, in particular magnetic resonance imaging, frequently shows a distinctive parieto-occipital pattern with a symmetric distribution of changes reflecting vasogenic oedema (2017 paper).[10]
- In pregnancy: ESC 2024 defines pre-eclampsia as gestational hypertension accompanied by any of the following of new onset: proteinuria (above 0.3 g/day or 30 mg/mmol albumin:creatinine ratio [ACR] or more), other maternal organ dysfunction, or uteroplacental dysfunction.[1]
Management: the first hours
ESC 2024 frames treatment around three key considerations.[1]
- Establishing the affected target organ(s) and whether they require any specific interventions other than BP lowering.[1]
- Determining whether there is a precipitating cause for the acute rise in BP and/or another concomitant health condition that might affect the treatment plan (e.g. pregnancy).[1]
- The recommended timing and magnitude of BP lowering required for safe BP reduction.[1]
ESC 2024 states that these considerations inform the type of BP-lowering treatment required.[1] ESC 2024 adds that i.v. treatment with a short half-life drug is typically ideal, to allow careful titration of the BP response.[1] ESC 2024 states that this requires a higher dependency clinical area with facilities for continuous or near-continuous haemodynamic monitoring.[1]
AHA/ACC 2025 states its approach in formal recommendation rows.[2] AHA/ACC 2025 gives the therapeutic goal as minimising target organ damage safely by rapid recognition of the problem and early start of appropriate antihypertensive treatment.[2] To achieve rapid BP control and avoid large swings in BP, AHA/ACC 2025 says continuous infusion of short-acting titratable antihypertensive agents is often preferable in the intensive care setting.[2]
AHA/ACC 2025: hypertensive emergencies and severe hypertension in nonpregnant and nonstroke patients (all four rows)
| AHA/ACC 2025 Section 6.2 recommendation | COR, LOE |
|---|---|
| In adults with a hypertensive emergency (BP above 180 and/or above 120 mm Hg and evidence of acute target organ damage), admission to an ICU is recommended for continuous monitoring of BP and target organ damage and for consideration of parenteral administration of appropriate therapy (Tables 26 and 27) | 1, B-NR |
| For adults with a hypertensive emergency related to a compelling condition (e.g. acute aortic syndrome or acute aortic dissection), SBP should be reduced to below 140 mm Hg for most conditions and to below 120 mm Hg in aortic dissection during the first hour, while monitoring for other target organ dysfunction | 1, C-LD |
| For adults with a hypertensive emergency but without a compelling condition, SBP should be reduced with oral or parenteral therapy by no more than 25% within the first hour; then, if stable, to below 160/100 mm Hg within the next 2 to 6 hours; and then cautiously to 130 to 140 mm Hg during the next 24 to 48 hours, to limit target organ injury | 1, C-LD |
| For adults with severe hypertension (above 180/120 mm Hg) who are hospitalised for noncardiac conditions without evidence of acute target organ damage, intermittent use of additional intravenous (IV) or oral antihypertensive medications is not recommended to acutely reduce BP | 3: Harm, B-NR |
AHA/ACC 2025 handles hypertensive emergencies in acute ICH and acute ischaemic stroke in its cerebrovascular section, and in pregnant adults in its pregnancy section.[2] This topic covers those settings under Specific scenarios and Special populations below.
AHA/ACC 2025 timing in nonpregnant, nonstroke adults with a hypertensive emergency but without a compelling condition (Section 6.2 row 3; COR 1, LOE C-LD), to limit target organ injury
- 1
First hour
Reduce SBP by no more than 25%, with oral or parenteral therapy
- 2
Next 2 to 6 hours
Then, if stable, to below 160/100 mm Hg
- 3
Next 24 to 48 hours
Then cautiously to 130 to 140 mm Hg
Why not lower faster without a compelling condition?[2] AHA/ACC 2025 notes there is no randomised controlled trial (RCT) evidence for treating other forms of hypertensive emergency without a compelling indication.[2] ESC 2024 text likewise does not recommend rapid and uncontrolled or excessive BP lowering, because this can lead to further complications.[1]
[2] [1]Drug choice
AHA/ACC 2025 says drug selection should rest on the drug’s pharmacology and the underlying mechanisms of hypertension.[2] AHA/ACC 2025 adds the degree of progression of target organ damage, the desirable rate of BP decline and the presence of comorbidities.[2] AHA/ACC 2025 states that clinical trials suggested IV nicardipine is more effective than labetalol in reaching a short-term BP target, and that clevidipine induced faster BP reduction than nicardipine.[2]
ESC 2024 puts its recommended drug treatments for specific hypertensive emergencies in supplementary Table S13.[1] In its main text, ESC 2024 states that i.v. drug administration is recommended for most hypertensive emergencies.[1] ESC 2024 adds that oral angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs) or beta-blockers (shorter-acting formulations like captopril or metoprolol) can also be effective.[1] ESC 2024 advises low initial doses, because these patients can be very sensitive to these agents, and treatment in hospital.[1]
AHA/ACC 2025 Table 26: intravenous drugs for hypertensive emergencies
| Class and drug | Usual dose range (AHA/ACC 2025) | Comments (AHA/ACC 2025) |
|---|---|---|
| Dihydropyridine calcium channel blocker (CCB): nicardipine | Initial 5 mg/h, increasing every 5 min by 2.5 mg/h to maximum 15 mg/h | Contraindicated in advanced aortic stenosis; no dose adjustment needed for persons aged 65 years or more. No negative inotropic or chronotropic effects. |
| Dihydropyridine CCB: clevidipine | Initial 1–2 mg/h, doubling every 90 s until BP approaches target, then increasing by less than double every 5–10 min; maximum dose 21 mg/h; maximum duration 72 h | Contraindicated in soybean, soy product, egg and egg product allergy and in defective lipid metabolism (e.g. pathological hyperlipidaemia, lipoid nephrosis [minimal change disease] or acute pancreatitis). No negative inotropic or chronotropic effects. Decreased risk of reflex tachycardia. |
| Nitric-oxide-dependent vasodilator: sodium nitroprusside | Initial 0.3–0.5 mcg/kg/min; increase in increments of 0.5 mcg/kg/min every 5 min to achieve BP target; maximum dose 10 mcg/kg/min; duration of treatment as short as possible | Intra-arterial BP monitoring recommended, because of potency, to prevent overshoot. Lower dose required for older adults. Tachyphylaxis common with extended use. Avoid in acute cerebrovascular disease (increased mortality risk) unless other agents are not available. Use cautiously in pregnancy or older adults. Cyanide and thiocyanate toxicity: see Complications. |
| Nitric-oxide-dependent vasodilator: nitroglycerin | Initial 5 mcg/min; increase in increments of 5 mcg/min every 3–5 min to a maximum rate of 200 mcg/min | Use only in patients with acute coronary syndrome and/or acute pulmonary oedema. Do not use in volume-depleted patients. Tachyphylaxis common with extended use. |
| Direct vasodilator: hydralazine | Initial 10 mg via slow IV infusion (maximum initial dose 20 mg); repeat every 4–6 h as needed; total cumulative dose up to 200 mg/24 h | BP begins to decrease within 10–30 min, and the fall lasts 2–4 h. An undesirable first-line agent for acute treatment in most patients, because of unpredictable response and prolonged duration of action. |
| Beta-1 selective blocker: esmolol | Loading dose 500–1,000 mcg/kg/min over 1 min, then 50 mcg/kg/min infusion; for additional dosing, repeat the bolus and increase the infusion in 50 mcg/kg/min increments as needed to a maximum of 300 mcg/kg/min | Contraindicated with concurrent beta-blocker therapy, bradycardia or decompensated heart failure. Monitor for bradycardia. Higher doses may block beta-2 receptors and impact lung function in reactive airway and obstructive pulmonary disease. |
| Combined alpha-1 and nonselective beta blocker: labetalol | Initial 0.3 to 1.0 mg/kg dose (maximum 20 mg) slow IV injection at 10-min intervals, or 0.4–1.0 mg/kg/h IV infusion up to 3 mg/kg/h; total cumulative dose up to 300 mg/24 h | Contraindicated in reactive airway or obstructive pulmonary disease. Especially useful in hyperadrenergic syndromes. May worsen heart failure; should not be given with second- or third-degree heart block or bradycardia. |
| Nonselective alpha blocker: phentolamine | IV bolus 5 mg; additional bolus doses every 10 min as needed to lower BP to target; total cumulative dose up to 50 mg/24 h | Used in hypertensive emergencies induced by catecholamine excess (phaeochromocytoma, monoamine oxidase inhibitor interactions with other drugs or food, cocaine toxicity, amphetamine overdose, or clonidine withdrawal). |
| Dopamine-1 selective agonist: fenoldopam | Initial 0.1–0.3 mcg/kg/min; may be increased in increments of 0.05–0.1 mcg/kg/min every 15 min until target BP is reached; maximum infusion rate 1.6 mcg/kg/min | Contraindicated in patients at risk of increased intraocular pressure (glaucoma) or intracranial pressure, and in sulfite allergy. |
| ACE inhibitor: enalaprilat | Initial 1.25 mg over 5 min; doses can be increased up to 5 mg every 6 h as needed to achieve BP target; total cumulative dose up to 50 mg/24 h | Contraindicated in pregnancy; should not be used in acute myocardial infarction (MI) or bilateral renal artery stenosis. Mainly useful in emergencies with high plasma renin activity. Poorly defined dose adjustments for kidney failure; may worsen kidney injury in chronic kidney disease (CKD). Relatively slow onset (15 min) and unpredictable BP response. |
*AHA/ACC 2025 Table 27: IV drugs for hypertensive emergencies in patients with selected comorbidities (listed in alphabetical order, not in order of preference; † agent of choice for acute coronary syndromes)
| Comorbidity | Preferred drug(s)* | Comments |
|---|---|---|
| Acute aortic dissection | Esmolol, labetalol | Requires rapid lowering of SBP to 120 mm Hg or less. Beta blockade should precede vasodilator (e.g. nicardipine or nitroprusside) administration, if needed for BP control or to prevent reflex tachycardia or inotropic effect; SBP of 120 mm Hg or less should be achieved within 20 min. |
| Acute pulmonary oedema | Clevidipine, nitroglycerin, nitroprusside | Beta blockers contraindicated. |
| Acute coronary syndromes | Esmolol†, labetalol, nicardipine, nitroglycerin† | Nitrates given with phosphodiesterase type-5 (PDE-5) inhibitors may induce profound hypotension. Contraindications to beta blockers include moderate-to-severe left ventricular (LV) failure with pulmonary oedema, bradycardia (below 60 beats/min), hypotension (SBP below 100 mm Hg), poor peripheral perfusion, second- or third-degree heart block and reactive airways disease. |
| Acute kidney injury | Clevidipine, fenoldopam, nicardipine | None given |
| Eclampsia or preeclampsia | Hydralazine, labetalol, nicardipine, nifedipine | Requires rapid BP lowering. ACE inhibitors, ARBs, renin inhibitors and nitroprusside contraindicated. |
| Perioperative hypertension (BP of 160/90 mm Hg or more, or SBP elevation of 20% or more of the preoperative value, persisting for more than 15 min) | Clevidipine, esmolol, nicardipine, nitroglycerin | Intraoperative hypertension is most frequently seen during anaesthesia induction and airway manipulation. |
| Acute sympathetic discharge or catecholamine excess states (e.g. phaeochromocytoma, post-carotid endarterectomy status) | Clevidipine, nicardipine, phentolamine | Requires rapid lowering of BP. |
| Acute ICH | Clevidipine, nicardipine, esmolol, labetalol, hydralazine | AHA/ACC Section 5.3.9.1 |
| Acute ischaemic stroke | Clevidipine, nicardipine, esmolol, labetalol, hydralazine | AHA/ACC Section 5.3.9.2 |
Severe hypertension without acute organ damage
In the 2020 ED meta-analysis, hypertensive urgencies were more common than emergencies (0.9% versus 0.3%).[6] ESC 2024 says these patients require BP reduction but do not usually require admission to hospital.[1] ESC 2024 states that BP reduction in these patients is best achieved with oral medication according to its drug treatment algorithm, and that they may need more urgent outpatient review to ensure their BP is controlled.[1]
For nonpregnant, nonstroke adults with severe hypertension without evidence of acute target organ damage (previously called hypertensive urgency), AHA/ACC 2025 states that these patients should not have aggressive BP lowering in the short-term or be given parenteral antihypertensive drug therapy.[2] AHA/ACC 2025 recommends reinstitution or intensification of oral antihypertensive medications for these nonpregnant, nonstroke adults, preferably in the outpatient setting.[2]
Inpatients are a special case.[2] In nonpregnant, nonstroke adults hospitalised for noncardiac conditions with severe hypertension (above 180/120 mm Hg) and no evidence of acute target organ damage, AHA/ACC 2025 does not recommend intermittent additional IV or oral antihypertensive medications to acutely reduce BP (COR 3: Harm, LOE B-NR).[2] AHA/ACC 2025 cites observational studies linking such use to increased in-hospital mortality, AKI and prolonged hospital stay.[2] AHA/ACC 2025 says asymptomatic patients with severe hypertension can be treated with careful and frequent monitoring, using standing medications and avoiding as-needed medications.[2]
Specific scenarios
Acute aortic dissection
Within AHA/ACC 2025 Section 6.2 recommendation 2, aortic dissection has the lowest first-hour target.[2] AHA/ACC 2025 Section 6.2 recommendation 2 covers nonpregnant, nonstroke adults with a hypertensive emergency related to a compelling condition (e.g. acute aortic syndrome or acute aortic dissection).[2] For these nonpregnant, nonstroke adults, AHA/ACC 2025 states that SBP should be reduced to below 140 mm Hg for most conditions and below 120 mm Hg in aortic dissection during the first hour, while monitoring for other target organ dysfunction (COR 1, LOE C-LD).[2] AHA/ACC 2025 Table 27 lists esmolol and labetalol as the preferred drugs in acute aortic dissection, with beta blockade before any vasodilator if one is needed, and SBP of 120 mm Hg or less achieved within 20 min.[2]
AHA/ACC 2025 notes that, other than for stroke/ICH, there is no RCT evidence comparing different strategies to reduce BP acutely; for the aortic dissection target it cites observational studies.[2] AHA/ACC 2025 cites observational studies showing an exponential dose-response relationship between SBP and the risk of aortic dissection and death, with a hazard ratio of more than 2-fold for SBP above 120 mm Hg.[2] AHA/ACC 2025 notes that BP in those studies was not measured during hospitalisation or IV drug treatment.[2]
Acute pulmonary oedema and acute coronary syndromes
AHA/ACC 2025 Table 27 lists clevidipine, nitroglycerin and nitroprusside for acute pulmonary oedema, and states that beta blockers are contraindicated.[2] AHA/ACC 2025 cites small clinical trials in acute heart failure with severe hypertension that showed less dyspnoea when SBP fell by 15% (20 to 40 mm Hg) within 30 minutes, without increased adverse events.[2]
For acute coronary syndromes, AHA/ACC 2025 Table 27 lists esmolol, labetalol, nicardipine and nitroglycerin, with esmolol and nitroglycerin marked as agents of choice.[2] The same row warns that nitrates given with PDE-5 inhibitors may induce profound hypotension.[2]
Acute intracerebral haemorrhage
ESC 2024 states that, in acute ICH, an increased BP is common and is associated with a greater risk of haematoma expansion and death and a worse prognosis for neurological recovery.[1] In trials testing immediate BP lowering (within 6 h) to a systolic target below 140 mmHg, ESC 2024 reports that achieved systolic BP in the intervention group was typically 140–160 mmHg and was reported to reduce the risk of haematoma expansion.[1]
Acute ICH: the ICH rows of ESC 2024 Recommendation Table 32 and all three AHA/ACC 2025 Section 5.3.9.1 rows
| Recommendation | Class or COR, level |
|---|---|
| ESC 2024: in patients with ICH, immediate BP lowering (within 6 h of symptom onset) should be considered to a systolic target of 140–160 mmHg, to prevent haematoma expansion and improve functional outcome | IIa, A |
| ESC 2024: in patients with ICH presenting with systolic BP of 220 mmHg or more, acute reduction in systolic BP of more than 70 mmHg from initial levels within 1 h of starting treatment is not recommended | III, B |
| AHA/ACC 2025: for adults with acute spontaneous ICH presenting with SBP between 150 and 220 mm Hg, it can be beneficial to immediately lower SBP to 130 to below 140 mm Hg for at least 7 days after ICH, to improve functional outcomes, but stop antihypertensive medications if SBP is below 130 mm Hg | 2a, A |
| AHA/ACC 2025: in adults with acute spontaneous ICH requiring acute BP lowering, careful titration to ensure smooth, nonlabile and sustained BP control, avoiding peaks and large variability in SBP, can be beneficial for improving functional outcomes | 2a, B-NR |
| AHA/ACC 2025: for adults with acute spontaneous ICH presenting with SBP above 220 mm Hg, SBP should not be lowered below 130 mm Hg, to reduce adverse events | 3: Harm, B-NR |
The two guidelines set different systolic targets for ICH, so name the body: compare the ESC 2024 and AHA/ACC 2025 ICH rows in the table above, each with its own conditions.[1][2]
- INTERACT2: 2839 patients with spontaneous ICH within the previous 6 hours and elevated SBP were randomised to intensive treatment (target SBP below 140 mm Hg within 1 hour) or guideline-recommended treatment (target SBP below 180 mm Hg), with agents of the physician’s choosing.[3]
- INTERACT2 primary outcome (death or major disability, modified Rankin score 3 to 6 at 90 days), among 2794 participants with the outcome determined: 52.0% with intensive and 55.6% with guideline-recommended treatment (odds ratio 0.87; 95% confidence interval [CI] 0.75 to 1.01; P=0.06), not a significant reduction.[3]
- INTERACT2 prespecified ordinal analysis: significantly lower modified Rankin scores with intensive treatment (odds ratio for greater disability 0.87; 95% CI 0.77 to 1.00; P=0.04). INTERACT2 mortality was 11.9% with intensive and 12.0% with guideline-recommended treatment.[3]
- ATACH-2: 1000 eligible participants with ICH (volume below 60 cm³, Glasgow Coma Scale 5 or more; mean baseline SBP 200.6 mm Hg) were randomised to an SBP target of 110 to 139 mm Hg (intensive) or 140 to 179 mm Hg (standard), with IV nicardipine given within 4.5 hours after symptom onset.[4]
- ATACH-2 primary outcome (death or disability, modified Rankin score 4 to 6 at 3 months): 38.7% (186 of 481) intensive versus 37.7% (181 of 480) standard (relative risk 1.04, adjusted for age, initial Glasgow Coma Scale score and intraventricular haemorrhage; 95% CI 0.85 to 1.27). Enrolment stopped for futility after a prespecified interim analysis.[4]
- ATACH-2, post hoc analysis of grouped adverse events: renal adverse events within 7 days 9.0% with intensive versus 4.0% with standard treatment (P=0.002).[4]
AHA/ACC 2025 adds that a meta-analysis of INTERACT-2 and ATACH-2 showed improved 90-day global disability with incrementally lower achieved SBP up to 130 mm Hg.[2] AHA/ACC 2025 states that any antihypertensive drug with rapid onset and short duration of action, allowing easy titration and sustained BP control with minimal SBP variability, seems appropriate, although venous vasodilators may be harmful.[2]
Acute ischaemic stroke
ESC 2024 states that the benefit of BP reduction in acute ischaemic stroke remains unclear.[1] ESC 2024 states that patients treated with i.v. thrombolysis or mechanical thrombectomy (or both) should have more proactive management of severe hypertension, because of their increased risk of reperfusion injury and intracranial haemorrhage.[1]
Acute ischaemic stroke: the acute ischaemic stroke rows of ESC 2024 Recommendation Table 32 and all six AHA/ACC 2025 Section 5.3.9.2 rows
| Recommendation | Class or COR, level |
|---|---|
| ESC 2024: in acute ischaemic stroke, early BP lowering should be considered in the first 24 h in patients eligible for reperfusion therapy with intravenous thrombolysis or mechanical thrombectomy, with BP carefully lowered and maintained at below 180/105 mmHg for at least the first 24 h after treatment | IIa, B |
| ESC 2024: in acute ischaemic stroke, early BP lowering should be considered in the first 24 h in patients not receiving reperfusion treatment with BP of 220/110 mmHg or more, with BP carefully lowered by approximately 15% during the first 24 h after stroke onset | IIa, C |
| ESC 2024: for patients with ischaemic stroke or transient ischaemic attack (TIA) and an indication for BP lowering, BP-lowering therapy should be started before hospital discharge | I, B |
| AHA/ACC 2025: in acute ischaemic stroke, hypotension and hypovolaemia should be corrected to maintain systemic perfusion levels necessary to support organ function | 1, C-LD |
| AHA/ACC 2025: patients with elevated BP otherwise eligible for IV thrombolytics should have BP lowered to SBP below 185 mm Hg and diastolic BP (DBP) below 110 mm Hg before thrombolysis, and maintained below 180/105 mm Hg for at least the first 24 hours after starting it, to avoid complications | 1, B-NR |
| AHA/ACC 2025: in patients who undergo endovascular treatment, it is reasonable to maintain BP at 180/105 mm Hg or less during and for 24 hours after the procedure, to improve long-term functional outcomes and prevent death | 2a, B-NR |
| AHA/ACC 2025: with BP of 220/120 mm Hg or more, no IV thrombolytic or endovascular treatment and no comorbid condition requiring acute antihypertensive treatment, it might be reasonable to lower BP by 15% during the first 24 hours after onset, to improve outcomes | 2b, C-LD |
| AHA/ACC 2025: with BP below 220/120 mm Hg, no IV thrombolysis or endovascular treatment and no comorbid condition requiring urgent antihypertensive treatment, starting or restarting treatment of hypertension within the first 48 to 72 hours is not effective to prevent death or disability | 3: No Benefit, A |
| AHA/ACC 2025: after successful brain reperfusion with endovascular treatment for a large vessel occlusion, lowering SBP below 140 mm Hg within the first 24 to 72 hours after reperfusion can worsen long-term functional outcome | 3: Harm, A |
AHA/ACC 2025 notes that early treatment of hypertension is indicated when required by comorbid conditions.[2] AHA/ACC 2025 gives as examples a concomitant acute coronary event, acute heart failure, aortic dissection, post-fibrinolysis symptomatic ICH or pre-eclampsia/eclampsia.[2] AHA/ACC 2025 notes that patients with severe hypertension (most commonly SBP/DBP above 220/120 mm Hg) were excluded from trials of BP lowering after acute ischaemic stroke.[2] For these patients, AHA/ACC 2025 says management should be individualised, with an initial BP reduction of 15% a reasonable goal.[2] AHA/ACC 2025 warns that an excessive drop in BP could result in complications such as stroke progression, by compromising penumbral perfusion, and AKI from renal hypoperfusion.[2]
Phaeochromocytoma and other catecholamine excess
ESC 2024 states that adrenergic crises cause hypertensive emergencies and should be treated with an i.v. alpha-1-blocker, such as phentolamine, doxazosin or terazosin, or labetalol.[1] AHA/ACC 2025 considers phaeochromocytoma hypertensive crisis a medical emergency that requires prompt lowering of BP.[2] AHA/ACC 2025 adds that the relationship between BP and mortality risk during adrenergic crisis has not been characterised.[2]
AHA/ACC 2025 states that phaeochromocytoma should not be considered a compelling indication to reduce SBP immediately to below 120 or 140 mm Hg in the first hour.[2] AHA/ACC 2025 states this despite potential cardiovascular complications such as a takotsubo-like cardiomyopathy.[2] With sympathomimetics such as methamphetamine or cocaine, ESC 2024 advises caution around beta-blocker use.[1]
Malignant hypertension
A 2024 review calls malignant hypertension a hypertensive emergency with excessive BP elevation and accelerated disease progression.[9] The review states that BP must be lowered within hours to mitigate risk, and that parenteral or oral therapy can be used to start, depending on the clinical presentation.[9] The review also notes that evidence-based outcome data are spotty or lacking.[9]
PRES
The 2017 paper states that PRES frequently develops with cytotoxic medication, (pre)eclampsia, sepsis, renal disease or autoimmune disorders.[10] According to that paper, treatment is symptomatic and determined by the underlying condition.[10] The 2017 paper describes the overall prognosis as favourable, with symptoms and imaging lesions reversible in most patients, although neurological sequelae including long-term epilepsy may persist in individual cases.[10]
Complications and pitfalls
- Lowering too fast: ESC 2024 does not recommend rapid and uncontrolled or excessive BP lowering; AHA/ACC 2025 warns that rapid correction to the normal range in longstanding hypertension may cause vital organ hypoperfusion due to loss of autoregulation.[1][2]
- Kidney injury from intensive lowering: in its supporting text for the compelling-condition row, AHA/ACC 2025 states that clinical trials in patients without aortic dissection or phaeochromocytoma showed increased risk of adverse kidney events with early intensive SBP lowering to 110 to 139 mm Hg, particularly with initial SBP above 220 mm Hg. The two studies it cites for this are in intracerebral haemorrhage, one a post hoc analysis of a randomised clinical trial.[2]
- ICH: ESC 2024 says excessive acute systolic drops (above 70 mmHg) may be associated with acute renal injury and early neurological deterioration and should be avoided.[1]
- Nitroprusside toxicity: cyanide toxicity (increased risk in liver dysfunction and CKD) and thiocyanate toxicity (increased risk in kidney dysfunction, sCr above 3) may occur at infusion rates of 3 mcg/kg/min or more and/or durations of 3 days or more (AHA/ACC 2025 Table 26).[2]
- Both toxicities may present with metabolic acidosis, altered mental status and cardiac arrhythmia; AHA/ACC 2025 says to stop nitroprusside and give sodium thiosulfate or cyanocobalamin.[2]
- Wrong drug for the organ: in a hypertensive emergency with acute pulmonary oedema, beta blockers are contraindicated (AHA/ACC 2025 Table 27, IV drugs for hypertensive emergencies in patients with selected comorbidities), and, due to increased mortality risk, nitroprusside should be avoided in acute cerebrovascular disease unless other agents are not available (Table 26).[2]
- Hydralazine as first line: AHA/ACC 2025 calls it an undesirable first-line agent for acute treatment in most patients, because of unpredictable response and prolonged duration of action.[2]
- Treating the number in an inpatient without acute organ damage: for nonpregnant, nonstroke adults with severe hypertension (above 180/120 mm Hg) hospitalised for noncardiac conditions without evidence of acute target organ damage, AHA/ACC 2025 does not recommend intermittent additional IV or oral antihypertensives to acutely reduce BP (COR 3: Harm, LOE B-NR).[2]
- Missing the pain: ESC 2024 notes that BP raised by acute pain or distress in the ED may normalise when these are relieved.[1]
Prognosis and follow-up
AHA/ACC 2025 reports an in-hospital mortality rate of 10% in hypertensive emergencies, with a 1-year cardiovascular morbidity and mortality rate of 20% to 30%.[2] ESC 2024 states that survival after hypertensive emergencies has improved over the past few decades.[1] ESC 2024 adds that these patients remain at high risk and should be screened for secondary hypertension.[1]
For malignant hypertension, a 2024 review states that prognosis has improved with effective treatment, but patients remain at high risk of adverse cardiovascular and kidney outcomes.[9] ESC 2024 says patients with severe hypertension but no acute organ damage do not usually require admission; for nonpregnant, nonstroke adults, AHA/ACC 2025 recommends reinstitution or intensification of oral antihypertensive medications, preferably in the outpatient setting.[1][2] ESC 2024 adds that these patients may need more urgent outpatient review to ensure their BP is controlled.[1] ESC 2024 also reports a high prevalence of hyperaldosteronism (up to 12%) in patients with BP above 180/110 mmHg, when describing primary aldosteronism as a common cause of secondary hypertension.[1]
Special populations
Pregnancy
Pregnancy has its own thresholds and drugs, and both guidelines treat it separately.[1][2] ESC 2024 defines severe hypertension in pregnancy, in general, as systolic BP above 160 mmHg and diastolic BP above 110 mmHg.[1] ESC 2024 links it with adverse maternal and perinatal outcomes, independent of pre-eclampsia and potentially as large as with eclampsia itself.[1] ESC 2024 considers acute onset of severe hypertension persisting for more than 15 min a hypertensive emergency in pregnancy.[1]
AHA/ACC 2025 defines severe hypertension in pregnancy as SBP of 160 mm Hg or more or DBP of 110 mm Hg or more.[2] AHA/ACC 2025 states that, when left untreated, it can result in maternal stroke, renal insufficiency or kidney failure, myocardial infarction, heart failure, placental abruption, preterm birth and fetal growth restriction.[2] The same passage adds maternal death from intracerebral haemorrhage and/or stillbirth or perinatal death.[2]
Selected pregnancy rows: ESC 2024 Recommendation Tables 22 and 33 and AHA/ACC 2025 Section 5.5
| Recommendation | Class or COR, level |
|---|---|
| ESC 2024: systolic BP of 160 mmHg or more or diastolic BP of 110 mmHg or more in pregnancy can indicate an emergency, and immediate hospitalisation should be considered | IIa, C |
| ESC 2024: in pre-eclampsia or eclampsia with hypertensive crisis, drug treatment with i.v. labetalol or nicardipine and magnesium is recommended | I, C |
| ESC 2024: in pre-eclampsia or eclampsia associated with pulmonary oedema, nitroglycerin given as an i.v. infusion is recommended | I, C |
| ESC 2024: in severe hypertension in pregnancy, drug treatment with i.v. labetalol, oral methyldopa or oral nifedipine is recommended; i.v. hydralazine is a second-line option | I, C |
| AHA/ACC 2025: pregnant individuals with SBP of 160 mm Hg or more or DBP of 110 mm Hg or more confirmed on repeat measurement within 15 minutes should receive antihypertensive medication (Table 23) to lower BP to below 160/110 mm Hg within 30 to 60 minutes, to prevent adverse events | 1, B-R |
| AHA/ACC 2025: individuals with hypertension who are planning a pregnancy or who become pregnant should not be treated with atenolol, ACE inhibitors, ARBs, direct renin inhibitors, nitroprusside or mineralocorticoid receptor antagonists (MRAs), to avoid fetal harm | 3: Harm, C-LD |
ESC 2024 lists this pregnancy row in its Table 4 of revised recommendations.[1] ESC 2024 Table 4 shows that the 2018 version called systolic BP of 170 mmHg or more or diastolic BP of 110 mmHg or more in a pregnant woman an emergency, with admission recommended (Class I, Level C).[1] The 2024 version is the Class IIa, Level C row above.[1]
In pre-eclampsia, ESC 2024 states that the condition is cured by delivery and that most international societies, including the ESC, recommend an intensive approach to BP lowering.[1] ESC 2024 notes that the 2018 ESC/ESH and 2022 ESC pregnancy guidelines recommended immediately reducing systolic BP below 160 mmHg and diastolic BP below 105 mmHg with i.v. labetalol or nicardipine in pre-eclampsia with severe hypertension.[1] ESC 2024 adds that those earlier recommendations included magnesium sulfate if appropriate and consideration of delivery if appropriate.[1] For women with pre-eclampsia and severe hypertension, ESC 2024 text sets the objective of lowering BP within 150–180 min.[1]
- Magnesium sulfate (ESC 2024 text): 4 g i.v. over 5 min, then 1 g/h i.v.; or 5 g intramuscularly (i.m.) into each buttock, then 5 g i.m. every 4 h. ESC 2024 recommends magnesium sulfate for eclampsia treatment and also for women with pre-eclampsia who have severe hypertension and proteinuria or hypertension and neurological symptoms or signs.[1]
- ESC 2024 warns of a risk of hypotension when magnesium is given concomitantly with nifedipine.[1]
- In pre-eclampsia, if BP control is not achieved by 360 min despite two medications, ESC 2024 recommends consulting critical care for ICU admission, stabilisation and delivery (if appropriate).[1]
- Because plasma volume is reduced in pre-eclampsia, ESC 2024 says diuretic therapy should be avoided.[1]
- In severe hypertension in pregnancy, ESC 2024 notes differences in the rate of BP control between i.v. labetalol and i.v. hydralazine, that hydralazine may be associated with more perinatal adverse events than other drugs (evidence is conflicting), and that nifedipine seems to give lower BP with fewer neonatal complications than labetalol.[1]
AHA/ACC 2025 Table 23: agents for urgent BP control in pregnancy
| Drug | Dose | Comments | Onset of action |
|---|---|---|---|
| Labetalol | 10–20 mg IV, then 20–80 mg every 10–30 min to a maximum cumulative dosage of 300 mg; or constant infusion 1–3 mg/min IV | Tachycardia is less common, with fewer adverse effects. Avoid in women with asthma, pre-existing myocardial disease, decompensated cardiac function, heart block and bradycardia. | 1–2 min |
| Hydralazine | 5 mg IV or intramuscular (IM), then 5–10 mg IV every 20–40 min to a maximum cumulative dosage of 20 mg; or constant infusion of 0.5–10 mg/h | Higher or frequent dosage associated with maternal hypotension, headaches and abnormal fetal heart rate tracings; may be more common than with other agents. | 10–20 min |
| Nifedipine (immediate release) | 10–20 mg orally, repeat in 20 min if needed; then 10–20 mg every 2–6 h; maximum daily dose 180 mg | May observe reflex tachycardia and headaches. | 5–10 min |
AHA/ACC 2025 notes that immediate-release oral nifedipine was associated in a meta-analysis with faster time to target BP specifically in pregnancy, although it is not generally recommended for the acute treatment of other types of hypertension.[2] ESC 2024 defines pre-eclampsia as gestational hypertension accompanied by any of the following of new onset: proteinuria (above 0.3 g/day or 30 mg/mmol ACR or more), other maternal organ dysfunction, or uteroplacental dysfunction.[1]
Older adults and organ dysfunction
- Nitroprusside: AHA/ACC 2025 Table 26 says a lower dose is required for older adults and that it should be used cautiously in pregnancy or older adults; AHA/ACC 2025 Table 27 lists nitroprusside as contraindicated in eclampsia or preeclampsia.[2]
- Nicardipine: no dose adjustment is needed for persons aged 65 years or more (AHA/ACC 2025 Table 26).[2]
- Enalaprilat: dose adjustments for kidney failure are poorly defined, and it may worsen kidney injury in CKD (AHA/ACC 2025 Table 26).[2]
- Nitroprusside: cyanide toxicity (increased risk in liver dysfunction and CKD) and thiocyanate toxicity (increased risk in kidney dysfunction, sCr above 3) may occur at infusion rates of 3 mcg/kg/min or more and/or durations of 3 days or more (AHA/ACC 2025 Table 26).[2]
Evidence, guidelines and regional differences
For nonpregnant, nonstroke patients, AHA/ACC 2025 says directly that high-quality RCT evidence in hypertensive emergency is lacking.[2] In that section, AHA/ACC 2025 states there is no RCT evidence that antihypertensive drugs reduce morbidity or mortality in patients with hypertensive emergencies.[2] AHA/ACC 2025 adds that there is no high-quality RCT evidence on which first-line drug class provides more benefit than harm, a gap it relates to small trials, lack of double-blinding, lack of long-term follow-up and failure to report outcomes.[2] Other than for stroke and ICH, AHA/ACC 2025 states there is no RCT evidence comparing strategies to reduce BP acutely.[2]
ESC 2024 updates the 2018 ESC/ESH hypertension guideline, and the 2025 AHA/ACC guideline retires and replaces the 2017 ACC/AHA guideline.[1][2]
ESC 2024 and AHA/ACC 2025 side by side (each cell from that body’s own text)
| Question | ESC 2024 | AHA/ACC 2025 |
|---|---|---|
| BP threshold for an emergency | 180/110 mmHg or more with acute HMOD | Above 180/120 mm Hg with evidence of acute target organ damage |
| Name for very high BP without acute organ damage | ‘Hypertension urgency’ | Severe hypertension (replaces hypertensive urgency) |
| Where to manage an emergency | i.v. treatment with a short half-life drug is typically ideal for careful titration; this requires a higher dependency area with continuous or near-continuous haemodynamic monitoring (text); with oral therapy, treatment should take place in hospital (text) | Nonpregnant, nonstroke adults with a hypertensive emergency (BP above 180 and/or above 120 mm Hg and evidence of acute target organ damage): ICU admission for continuous monitoring of BP and target organ damage and for consideration of parenteral administration of appropriate therapy (COR 1, LOE B-NR) |
| Speed of lowering | Rapid and uncontrolled or excessive lowering not recommended (text); recommended drug treatments for specific emergencies in supplementary Table S13 | Nonpregnant, nonstroke adults. With a compelling condition: SBP below 140 mm Hg for most conditions and below 120 mm Hg in aortic dissection during the first hour, while monitoring for other target organ dysfunction; without a compelling condition: with oral or parenteral therapy, no more than 25% within the first hour, then, if stable, below 160/100 mm Hg within the next 2 to 6 hours, then cautiously 130 to 140 mm Hg during the next 24 to 48 hours to limit target organ injury (each COR 1, LOE C-LD) |
| Acute ICH systolic target | In ICH, immediate lowering (within 6 h of symptom onset) to 140–160 mmHg should be considered, to prevent haematoma expansion and improve functional outcome (IIa, A) | In acute spontaneous ICH presenting with SBP between 150 and 220 mm Hg, immediately lowering SBP to 130 to below 140 mm Hg for at least 7 days can be beneficial, to improve functional outcomes, stopping antihypertensives if SBP falls below 130 mm Hg (2a, A) |
| Pregnancy: SBP 160 or more or DBP 110 or more | Systolic 160 mmHg or more or diastolic 110 mmHg or more in pregnancy can indicate an emergency, and immediate hospitalisation should be considered (IIa, C) | SBP 160 mm Hg or more or DBP 110 mm Hg or more confirmed on repeat measurement within 15 minutes: antihypertensive medication to lower BP to below 160/110 mm Hg within 30 to 60 minutes, to prevent adverse events (1, B-R) |
In Australia and New Zealand
No Australian or New Zealand guideline specific to hypertensive emergency was found in a PubMed search on 6 October 2026. The PubMed search found one Australian and New Zealand guideline covering part of this topic: the 2023 Society of Obstetric Medicine of Australia and New Zealand (SOMANZ) hypertension in pregnancy guideline.[11] The SOMANZ summary states that the guideline updates the 2014 SOMANZ guidelines and has been approved by the National Health and Medical Research Council.[11] The SOMANZ summary reports 39 recommendations on screening, preventing, diagnosing and managing hypertensive disorders of pregnancy, especially pre-eclampsia.[11] The summary abstract does not give the acute treatment recommendations, so this topic teaches acute pregnancy management from ESC 2024 and AHA/ACC 2025.[11]
Exam pearls
- Thresholds: ESC 2024 180/110 mmHg or more; AHA/ACC 2025 above 180/120 mm Hg. Both need acute organ damage.[1][2]
- AHA/ACC 2025, nonpregnant, nonstroke adults without a compelling condition: SBP should be reduced with oral or parenteral therapy by no more than 25% within the first hour; then, if stable, to below 160/100 mm Hg within the next 2 to 6 hours; then cautiously to 130 to 140 mm Hg during the next 24 to 48 hours to limit target organ injury (COR 1, LOE C-LD).[2]
- AHA/ACC 2025, nonpregnant, nonstroke adults with a compelling condition: SBP should be reduced to below 140 mm Hg for most conditions and to below 120 mm Hg in aortic dissection during the first hour, while monitoring for other target organ dysfunction (COR 1, LOE C-LD).[2]
- ICH systolic targets differ. ESC 2024: in ICH, immediate lowering (within 6 h of symptom onset) to 140–160 mmHg should be considered, to prevent haematoma expansion and improve functional outcome (IIa, A). AHA/ACC 2025: in acute spontaneous ICH presenting with SBP between 150 and 220 mm Hg, immediately lowering SBP to 130 to below 140 mm Hg for at least 7 days can be beneficial, to improve functional outcomes, stopping antihypertensives if SBP falls below 130 mm Hg (2a, A).[1][2]
- ESC 2024 Class III, Level B: in ICH presenting with systolic BP of 220 mmHg or more, acute reduction in systolic BP of more than 70 mmHg from initial levels within 1 h of starting treatment is not recommended.[1]
- AHA/ACC 2025 Table 27 (IV drugs for hypertensive emergencies in patients with selected comorbidities): with acute pulmonary oedema, beta blockers are contraindicated; in acute aortic dissection, beta blockade should precede vasodilator administration, if needed for BP control or to prevent reflex tachycardia or inotropic effect.[2]
- AHA/ACC 2025: phaeochromocytoma should not be considered a compelling indication to reduce SBP immediately to below 120 or 140 mm Hg in the first hour.[2]
References11ShowHide
- [1]McEvoy JW, et al. 2024 ESC Guidelines for the management of elevated blood pressure and hypertension. Eur Heart J, 2024.PMID 39210715
- [2]Jones DW, et al. 2025 AHA/ACC/AANP/AAPA/ABC/ACCP/ACPM/AGS/AMA/ASPC/NMA/PCNA/SGIM Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol, 2025.PMID 40815242
- [3]Anderson CS, et al. Rapid blood-pressure lowering in patients with acute intracerebral hemorrhage. N Engl J Med, 2013.PMID 23713578
- [4]Qureshi AI, et al. Intensive Blood-Pressure Lowering in Patients with Acute Cerebral Hemorrhage. N Engl J Med, 2016.PMID 27276234
- [5]Siddiqi TJ, et al. Clinical Outcomes in Hypertensive Emergency: A Systematic Review and Meta-Analysis. J Am Heart Assoc, 2023.PMID 37421281
- [6]Astarita A, et al. Hypertensive emergencies and urgencies in emergency departments: a systematic review and meta-analysis. J Hypertens, 2020.PMID 32510905
- [7]Strandgaard S, et al. Cerebral blood flow in untreated and treated hypertension. Neth J Med, 1995.PMID 8538822
- [8]Paulson OB, et al. Cerebral autoregulation. Cerebrovasc Brain Metab Rev, 1990.PMID 2201348
- [9]Boulestreau R, et al. Malignant Hypertension:A Systemic Cardiovascular Disease: JACC Review Topic of the Week. J Am Coll Cardiol, 2024.PMID 38658108
- [10]Fischer M, et al. Posterior reversible encephalopathy syndrome. J Neurol, 2017.PMID 28054130
- [11]Shanmugalingam R, et al. A summary of the 2023 Society of Obstetric Medicine of Australia and New Zealand (SOMANZ) hypertension in pregnancy guideline. Med J Aust, 2024.PMID 38763516