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Level 2 of 6Must-remember

Hypertensive emergencies

Assess, manage and stay safe — enough on its own

The card — assess, manage, caution

Assessment— look, ask, measure

  • The definition decides the treatment: a hypertensive emergency is severe elevation of blood pressure accompanied by acute, ongoing injury to a target organ — brain, retina, heart, aorta, kidney, microcirculation or placenta; the conventional threshold is a systolic above 180 mmHg or a diastolic above 120 mmHg, but the number is a prompt to look, not the diagnosis itself.
  • Separate the three states: hypertensive emergency (severe hypertension with acute target-organ damage — admission, parenteral therapy, continuous monitoring); hypertensive urgency (usually above 180/120 mmHg with no acute organ damage but a worrying context — oral drugs over 24–48 hours); and severe asymptomatic hypertension (a high reading and nothing else, by a large margin the commonest of the three).
  • Confirm the measurement before you believe it: the cuff bladder must encircle at least 80% of the arm circumference — a cuff that is too small reads falsely high and is the commonest single cause of a spurious crisis; take the reading after at least 5 minutes' rest with the back supported and the arm at heart level, and at least 30 minutes after smoking or coffee.
  • Measure both arms, and the legs if the pulses are weak: the higher reading is the patient's blood pressure and subclavian stenosis should be suspected on the other side, but a difference of more than 20 mmHg with chest or back pain suggests aortic dissection; weak or delayed lower limb pulses mean measuring the leg pressure to exclude coarctation; and the Osler sign — a radial or brachial artery still palpable with the cuff inflated above systolic — warns of pseudohypertension in the elderly.
  • Ask what precipitated it: non-adherence to existing therapy is the commonest precipitant, and abrupt withdrawal of clonidine or a beta-blocker produces a rebound catecholamine surge whose specific treatment is to reinstate the withdrawn drug; then pain, urinary retention, anxiety, hypoxia, hypercapnia, alcohol or opioid withdrawal; then cocaine, amphetamines, decongestants, NSAIDs (which raise pressure by an average of about 5 mmHg), corticosteroids, ciclosporin and tacrolimus, erythropoiesis-stimulating agents, oestrogen-containing contraceptives, atypical antipsychotics, alcohol, and monoamine oxidase inhibitors taken with tyramine-containing food.
  • Neurological — the deficit is global, not focal. Hypertensive encephalopathy evolves insidiously over hours to days with severe headache, nausea and vomiting, visual blurring, restlessness, confusion, drowsiness, seizures and ultimately coma; any focal deficit points instead to stroke or intracerebral haemorrhage, whose management is entirely different.
  • Fundoscopy is the cheapest and most decisive examination available: fresh flame-shaped haemorrhages, cotton-wool spots, hard exudates and papilloedema define the accelerated–malignant phase (Keith–Wagener–Barker grade III and IV) and establish an emergency in sixty seconds, even in a patient who feels well; chronic changes — arteriolar narrowing to less than 50% of venous diameter, copper- and silver-wiring, arteriovenous nipping — indicate long-standing disease but do not themselves establish an emergency.
  • Urine dipstick establishes renal involvement in thirty seconds: blood plus protein indicates glomerular disease or malignant nephrosclerosis, isolated proteinuria in pregnancy supports pre-eclampsia, and a clean stick makes renal involvement unlikely; red-cell casts on microscopy are diagnostic of glomerulonephritis and never normal.
  • Cardiac: breathlessness, orthopnoea, paroxysmal nocturnal dyspnoea, bilateral basal crackles, a third heart sound and hypoxaemia in acute pulmonary oedema; ischaemic chest pain with ECG change; a presystolic (S4) gallop and a left ventricular heave; aortic regurgitation is audible in up to 5% of hypertensive patients.
  • Aortic: sudden, severe, tearing chest or interscapular pain maximal at onset and sometimes migrating, with pulse deficit or inter-arm pressure asymmetry, a new early diastolic murmur, and the paradoxical combination of chest pain with stroke, paraplegia, limb ischaemia or abdominal pain.
  • Renal: oliguria (< 0.5 mL/kg/hour in an adult, < 1 mL/kg/hour in a child), haematuria, frothy urine, peripheral oedema and a creatinine rising hour on hour.
  • Haematological: pallor, jaundice and bruising suggest microangiopathy — look for schistocytes with thrombocytopenia on the blood film.
  • Obstetric — the thresholds in pregnancy are far lower. In pregnancy or up to six weeks postpartum: headache, visual disturbance, epigastric or right upper quadrant pain, brisk reflexes with clonus, oedema, proteinuria and seizure. Any woman of childbearing age with a high blood pressure requires a pregnancy test.
  • One bradycardia inverts everything: bradycardia accompanying the hypertension, with irregular respiration and a falling conscious level, suggests the Cushing response of raised intracranial pressure, in which the hypertension is protective.
  • Age changes the picture: older patients tolerate pressure reduction poorly, have wider autoregulatory shifts, present more often with heart failure than with encephalopathy, and may show only confusion or a fall; younger patients with no previous hypertension have not shifted their autoregulatory curve and develop encephalopathy at lower absolute pressures — 160/100 mmHg may suffice in acute glomerulonephritis or in eclampsia.
  • Children rarely complain, and their definitions are centile-based: hypertension is a pressure at or above the 95th centile for age, sex and height; stage 2 is at or above the 95th centile + 12 mmHg, or ≥ 140/90 mmHg in a child aged 13 years or over, whichever is lower; and a paediatric hypertensive crisis is at or above the 95th centile + 30 mmHg, or any severe elevation with symptoms. Infants present with irritability, poor feeding, failure to thrive, vomiting or seizures; older children with headache, epistaxis, visual symptoms or a facial palsy. Acute post-infectious glomerulonephritis is the classic paediatric hypertensive emergency — a school-age child 1–3 weeks after a sore throat or skin infection with puffy eyes, cola- or tea-coloured urine, reduced urine output, hypertension, and sometimes seizures or pulmonary oedema.

Management— do this, in order

  • Decide first whether this is an emergency at all. With no acute organ damage the correct management is rest, re-measurement, treatment of pain, anxiety or retention, reinstatement or adjustment of oral therapy, and follow-up within a few days — there is no evidence that acute parenteral reduction improves outcome in hypertensive urgency or severe asymptomatic hypertension, and considerable evidence that it causes harm.
  • Set a ceiling on the rate of reduction before giving any drug: for all emergencies except the named exceptions, reduce the mean arterial pressure by no more than 20–25% in the first hour, or to a diastolic of about 100–110 mmHg, whichever represents the *smaller* fall. Never take the diastolic below 100 mmHg in the first hour.
  • Calculate the MAP explicitly: MAP = diastolic + (systolic − diastolic) ÷ 3. At 240/140 mmHg the MAP is 173 mmHg; a 25% fall is 43 mmHg, giving a one-hour target MAP of about 130 mmHg, roughly 170/110 mmHg.
  • Then go slowly: over the following 2–6 hours aim for approximately 160/100–110 mmHg if this is tolerated, and normalise cautiously with oral agents over 24–48 hours.
  • Use a titratable intravenous agent with a short half-life and continuous monitoring — the virtue of intravenous therapy is not speed but reversibility; where continuous titration is not feasible, intermittent boluses whose effect can be observed are safer than an unmonitored infusion.Doctor / NurseNot available at your setup — Infusion pump. Where continuous titration is not feasible, intermittent boluses whose effect can be observed are safer than an unmonitored infusion.
  • Labetalol is the workhorse: 20 mg IV over 2 minutes, then 20–80 mg every 10 minutes to a maximum cumulative 300 mg, or an infusion of 0.5–2 mg/min; onset 5–10 minutes, duration 3–6 hours. Avoid in asthma, COPD with wheeze, acute decompensated heart failure, second- or third-degree block and bradycardia below 50/min.Doctor / Nurse
  • Alternatives by availability: nicardipine 5 mg/hour IV increasing by 2.5 mg/hour every 5–15 minutes to a maximum of 15 mg/hour; esmolol 500 microgram/kg IV over 1 minute then 50–200 microgram/kg/min; glyceryl trinitrate 5 microgram/min increasing by 5–10 microgram/min every 5 minutes to a usual maximum of 200 microgram/min; hydralazine 5–10 mg IV over 5–10 minutes repeated every 20–30 minutes to a total of 20 mg, then an infusion of 200–300 microgram/min titrated down to 50–150 microgram/min; clevidipine 1–2 mg/hour IV doubling every 90 seconds to a usual maximum of 16–32 mg/hour.Doctor / NurseNot available at your setup — Infusion pump.
  • Encephalopathy and malignant hypertension with retinopathy: labetalol or nicardipine with the standard 20–25% ceiling; improvement in conscious level within hours supports the diagnosis, and failure to improve or deterioration should prompt reconsideration and imaging.Doctor / Nurse
  • Aortic dissection — the exception to every rule about gentleness: reduce the systolic to 100–120 mmHg with a heart rate below 60/min within about 20 minutes, give adequate opioid analgesia because pain drives the pressure, and give the beta-blocker first (labetalol, or esmolol 500 microgram/kg over 1 minute then 50–200 microgram/kg/min), adding a vasodilator only once the rate is controlled.Doctor / Nurse
  • Acute ischaemic stroke: the hypertension largely protects the ischaemic penumbra — do not lower the pressure unless it exceeds 220/120 mmHg, and then by no more than 15% in the first 24 hours; if thrombolysis is to be given the threshold falls to 185/110 mmHg before treatment and below 180/105 mmHg for the following 24 hours. Labetalol and nicardipine are preferred.Doctor / Nurse
  • Intracerebral haemorrhage: presenting within 6 hours with a systolic of 150–220 mmHg, a target systolic of 140 mmHg achieved smoothly over the first hour is reasonable, avoiding a fall below 130 mmHg; smoothness matters more than the number.Doctor / Nurse
  • Acute pulmonary oedema: glyceryl trinitrate infusion is first-line, reducing preload and afterload; add furosemide 40–80 mg IV over 1–2 minutes only where there is genuine congestion; nitroprusside or clevidipine are alternatives.Doctor / NurseNot available at your setup — Infusion pump.
  • Pre-eclampsia and eclampsia: treat any pressure ≥ 160/110 mmHg, aiming for 140–150/90–100 mmHg, and do not allow the diastolic to fall below 80 mmHg because placental perfusion depends on maternal pressure. First line is labetalol 20 mg IV, then 40 mg, then 80 mg at 10-minute intervals to a maximum of 300 mg (or 200 mg orally), hydralazine 5 mg IV every 20 minutes to a maximum of 20 mg, or nifedipine 10 mg orally, swallowed.Doctor / Nurse
  • Eclamptic seizures — magnesium sulphate is the anticonvulsant of choice, superior to both diazepam and phenytoin in randomised trials: 4 g IV over 5–15 minutes, then 1 g/hour for 24 hours, with 2 g IV over 5 minutes for a recurrent seizure. Definitive treatment of eclampsia is delivery.Doctor / Nurse
  • Catecholamine excess: in stimulant toxicity a benzodiazepine first (for example diazepam 5–10 mg IV, repeated) often controls both agitation and pressure; phentolamine 2–5 mg IV every 5–10 minutes is the specific alpha-blocker, with nitrates, nicardipine or nitroprusside as alternatives; in clonidine or beta-blocker withdrawal, reinstate the withdrawn drug.Doctor / Nurse
  • Scleroderma renal crisis is the one place an ACE inhibitor is the specific treatment: give captopril 6.25–12.5 mg orally, up-titrated every 4–8 hours as pressure allows — a rising creatinine is expected and is not a reason to stop. Patients present with accelerated hypertension, generally > 150/90 mmHg, and progressive oliguric renal insufficiency.Doctor / Nurse
  • Children — reduce more cautiously than adults: no more than 25% of the total planned reduction in the first 8 hours, and the remainder over the following 24–48 hours. Confirm the weight before drawing up any drug. Labetalol 0.2–1 mg/kg per dose IV over 2 minutes (maximum 20–40 mg per dose) every 10 minutes, or infusion 0.25–3 mg/kg/hour; nicardipine infusion 0.5–1 microgram/kg/min titrated to 4–5 microgram/kg/min; hydralazine 0.1–0.2 mg/kg per dose IV (maximum 20 mg) every 4–6 hours; esmolol 100–500 microgram/kg/min; furosemide 1 mg/kg IV (maximum 2 mg/kg per dose) for the fluid-overloaded child; seizures — lorazepam 0.1 mg/kg IV (maximum 4 mg) or diazepam 0.25–0.5 mg/kg rectally, unless the patient is a pregnant or recently delivered adolescent, in which case eclampsia is the diagnosis and magnesium sulphate is the drug.Doctor / Nurse
  • If the pressure will not fall: confirm the measurement with a correctly sized cuff or an arterial line; look for an untreated driver (pain, retention, hypoxia, hypercapnia, agitation, withdrawal); reconsider the diagnosis (phaeochromocytoma, cocaine, autonomic dysreflexia, raised intracranial pressure); reconsider volume status; then add a second agent from a different class rather than escalating the first indefinitely. Sodium nitroprusside 0.25–0.5 microgram/kg/min, titrated to a usual maximum of 8–10 microgram/kg/min (paediatric 0.3–0.5 microgram/kg/min to a maximum of 8 microgram/kg/min) is the most reliable rescue agent but demands invasive arterial monitoring.Doctor / NurseNot available at your setup — Infusion pump.

Caution— what harms

  • Sublingual or bite-and-swallow nifedipine capsules must never be used — the fall is precipitous, uncontrollable and unpredictable, and has caused stroke, myocardial infarction and death; if an oral calcium channel blocker is appropriate, use a swallowed preparation (amlodipine 5–10 mg once daily, or nifedipine 10 mg orally) and wait for it to work.
  • Do not lower the pressure in the Cushing response — hypertension with bradycardia and irregular respiration is compensating for raised intracranial pressure and is protective; lowering it removes cerebral perfusion pressure and infarcts the brain.
  • Never give unopposed beta-blockade in catecholamine excess — including labetalol as a single agent — in phaeochromocytoma, cocaine or amphetamine toxicity, or MAOI crisis: blocking beta-2-mediated vasodilation leaves alpha-mediated vasoconstriction unopposed and the pressure rises further.
  • Beta-blockers, including labetalol, are contraindicated in acute decompensated left ventricular failure.
  • Nitrates are absolutely contraindicated within 24–48 hours of a phosphodiesterase-5 inhibitor, and glyceryl trinitrate causes headache, tachyphylaxis within 24 hours and a rise in intracranial pressure.
  • Never give a vasodilator before beta-blockade in suspected dissection — it causes reflex tachycardia, increases dP/dt and extends the tear.
  • Diurese only the genuinely congested. Patients with malignant hypertension are frequently volume-depleted from pressure natriuresis, so furosemide given to a patient who is not congested activates the renin–angiotensin system and drives the pressure *up* while the kidney fails. Do not give a fluid bolus to a hypertensive, oedematous, oliguric child unless volume depletion is certain; in acute glomerulonephritis restrict fluid and salt.
  • ACE inhibitors and angiotensin receptor blockers are contraindicated in pregnancy, and enalaprilat (1.25 mg IV over 5 minutes, repeated every 6 hours) is absolutely contraindicated in pregnancy, risky in bilateral renal artery stenosis and unpredictable in high-renin states.
  • Never stack hydralazine doses at short intervals — its effect is unpredictable and long-lasting, with reflex tachycardia, headache and fluid retention.
  • Sodium nitroprusside: requires invasive arterial monitoring, must be protected from light, and causes cyanide and thiocyanate toxicity above 2 microgram/kg/min or beyond 24–48 hours, especially in renal impairment; it also raises intracranial pressure and causes coronary steal.Not available at your setup — Infusion pump.
  • Magnesium must be monitored: patellar reflexes (lost first), respiratory rate (> 12/min) and urine output (> 30 mL/hour); the antidote is calcium gluconate 1 g (10 mL of 10%) IV over 10 minutes.
  • Deterioration during treatment means you have lowered the pressure too far or too fast — new confusion, a new focal deficit, chest pain or falling urine output. Stop the infusion and give a cautious fluid challenge, for example 250 mL of 0.9% sodium chloride — do not give a vasopressor. Watershed cerebral infarction and cortical blindness are the classic iatrogenic complications.
  • Check the glucose before blaming the blood pressure for any confused, drowsy or fitting patient, and do a pregnancy test in every woman of childbearing age whatever the menstrual history.
  • Do not measure catecholamines or aldosterone during a crisis or while the patient is receiving vasoactive drugs — the results are uninterpretable and must be deferred until the patient is stable.

Refer / escalate

Admit and escalate any patient with demonstrable acute target-organ damage — reduced or falling conscious level, seizure or focal deficit; new retinal haemorrhages, cotton-wool spots, hard exudates or papilloedema; acute pulmonary oedema or ischaemic chest pain with ECG change; tearing chest or interscapular pain with an inter-arm difference > 20 mmHg, pulse deficit or a new aortic regurgitant murmur; oliguria or a creatinine rising hour on hour; schistocytes with thrombocytopenia; or pregnancy or recent delivery with headache, visual disturbance, epigastric pain or clonus — and transfer urgently for CT, CT aortography, surgery, dialysis or delivery where these cannot be provided locally.

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