Hypertensive emergency — viva

Stem

Practice viva. You are the cardiology registrar called to the emergency department about a patient with BP 226/132 mm Hg. The examiner works through definitions, acute organ damage, autoregulation, the timing of BP lowering, drug choice, aortic dissection, intracerebral haemorrhage and the asymptomatic inpatient. Answer for a non-pregnant adult unless stated.

Branch A — Is this an emergency?

Examiner: What makes very high BP a hypertensive emergency?

Strong answer:

• ESC 2024 defines hypertensive emergency as BP of 180/110 mmHg or more associated with acute hypertension-mediated organ damage, often in the presence of symptoms.^[1]
• AHA/ACC 2025 defines hypertensive emergencies as severe elevations in BP (above 180/120 mm Hg) associated with evidence of acute target organ damage.^[2]
• For severe hypertension without clinical evidence of acute organ damage, ESC 2024 uses the term ‘hypertension urgency’; AHA/ACC 2025 uses severe hypertension, its replacement for the 2017 term hypertensive urgency.^[1][2]
• BP levels alone do not reliably predict acute HMOD; the 2020 ED meta-analysis advises suspecting it according to the presenting signs and symptoms.^[6]

Follow-up: Which acute manifestations of organ damage does ESC 2024 list?^[1]

• ESC 2024 says they include severe acute hypertension with other clinical conditions likely to require urgent reduction in BP, e.g. acute onset of aortic dissection, myocardial ischaemia, eclampsia or heart failure.^[1]
• ESC 2024 also lists malignant hypertension, defined as extreme BP elevations and acute microvascular damage (microangiopathy) affecting various organs, with small-artery fibrinoid necrosis in the kidneys, retina and brain as its hallmark.^[1]
• ESC 2024 lists sudden severe hypertension due to phaeochromocytoma, which can result in severe acute organ damage.^[1]

Branch B — Why not normalise BP quickly?

Examiner: Why do we not bring the BP straight down to normal?^[2][1]

Strong answer:

• Cerebral blood flow autoregulation typically operates between mean pressures of the order of 60 and 150 mm Hg, and chronic hypertension shifts the lower and upper limits towards higher pressure.^[8][7]
• Acute BP reduction lowers cerebral blood flow only if pressure is taken below the lower limit of autoregulation.^[7][8]
• AHA/ACC 2025 states 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]
• ESC 2024 text states that rapid and uncontrolled or excessive BP lowering is not recommended in hypertensive emergency, as this can lead to further complications.^[1]

Branch C — How fast?

Examiner: He has encephalopathy but no aortic dissection, and the team judges that no compelling condition is present. Where is he managed, and how fast do you lower his BP?^[2]

Strong answer:

• In nonpregnant, nonstroke adults with a hypertensive emergency (BP above 180 and/or above 120 mm Hg and evidence of acute target organ damage), AHA/ACC 2025 recommends 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).^[2]
• For nonpregnant, nonstroke adults with a hypertensive emergency but without a compelling condition, AHA/ACC 2025 states that 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 (COR 1, LOE C-LD). For an SBP of 226 mm Hg, 25% is 56.5 mm Hg, so the first-hour SBP should not fall below 169.5 mm Hg.^[2]
• ESC 2024 says i.v. treatment with a short half-life drug is typically ideal to allow careful titration, and that this requires a higher dependency clinical area with facilities for continuous or near-continuous haemodynamic monitoring.^[1]

Follow-up: What changes if he has an acute aortic dissection?^[2]

• For nonpregnant, nonstroke adults with a hypertensive emergency related to a compelling condition, 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).^[2]
• AHA/ACC 2025 Table 27 lists esmolol and labetalol as the preferred IV drugs in acute aortic dissection; beta blockade should precede vasodilator (e.g. nicardipine or nitroprusside) administration, if needed for BP control or to prevent reflex tachycardia or inotropic effect, and SBP of 120 mm Hg or less should be achieved within 20 min.^[2]

Branch D — Nitroprusside

Examiner: What are the hazards of sodium nitroprusside?

Strong answer:

• AHA/ACC 2025 Table 26 recommends intra-arterial BP monitoring because of its potency, to prevent overshoot, and notes that a lower dose is required for older adults.^[2]
• 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.^[2]
• Both may present with metabolic acidosis, altered mental status and cardiac arrhythmia; nitroprusside should be discontinued and sodium thiosulfate or cyanocobalamin given.^[2]
• Nitroprusside should be avoided in acute cerebrovascular disease (increased mortality risk) unless other agents are not available, and used cautiously in pregnancy or older adults.^[2]

Branch E — Intracerebral haemorrhage

Examiner: The CT instead shows a spontaneous intracerebral haemorrhage, 2 hours after onset, with SBP 196 mm Hg. What do the guidelines say?

Strong answer:

• 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 (Class IIa, Level A).^[1]
• AHA/ACC 2025: in 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, to improve functional outcomes, but to stop antihypertensive medications if SBP falls below 130 mm Hg (COR 2a, LOE A).^[2]
• INTERACT2 (systolic target below 140 mm Hg within 1 hour versus below 180 mm Hg) did not significantly reduce death or major disability at 90 days (52.0% versus 55.6%; P=0.06), although a prespecified ordinal analysis showed significantly lower modified Rankin scores (P=0.04).^[3]
• ATACH-2 (SBP target 110 to 139 versus 140 to 179 mm Hg) did not lower death or disability at 3 months (38.7% versus 37.7%; adjusted relative risk 1.04, 95% CI 0.85 to 1.27), and enrolment was stopped for futility. In a post hoc analysis of grouped adverse events, renal adverse events within 7 days were more frequent with intensive treatment (9.0% versus 4.0%; P=0.002).^[4]

Follow-up: And if the SBP had been 230 mm Hg?^[1][2]

• ESC 2024: 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 (Class III, Level B).^[1]
• AHA/ACC 2025: for acute spontaneous ICH presenting with SBP above 220 mm Hg, SBP should not be lowered below 130 mm Hg, to reduce adverse events (COR 3: Harm, LOE B-NR).^[2]

Branch F — The ward call

Examiner: A patient admitted for pneumonia has BP 188/122 mm Hg, no symptoms and no evidence of acute target organ damage. The nurse asks for an IV bolus. What do you say?

Strong answer:

• 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 antihypertensive medications to acutely reduce BP (COR 3: Harm, LOE B-NR).^[2]
• AHA/ACC 2025 notes that spontaneous falls in BP without any antihypertensive agents occur commonly in hospitalised patients with asymptomatic severe hypertension, at a rate of 40% to 50%.^[2]
• AHA/ACC 2025 cites observational studies linking such use to increased in-hospital mortality, AKI and prolonged hospital stay, and says asymptomatic patients with severe hypertension can be treated with careful and frequent monitoring using standing medications and avoiding as-needed medications.^[2]