FRCA Notes

Hypertensive Emergencies

This topic is probably outwith the requirements of the FRCA, although could fall under the old ICM-in-anaesthetic-training curriculum item "recognises and manages circulatory failure".

Resources

  • Hypertensive emergencies are common and carry a high mortality if untreated (80% at 12 months)
  • They are defined by the presence of acute hypertension-mediated organ damage (HMOD), rather than by an absolute blood pressure value
  • Management balances blood pressure reduction against the risk of organ hypoperfusion from overtreatment
  • For chronic essential hypertension, its end-organ effects and perioperative management, see hypertension


Term Definition
Severe hypertension Systolic BP ≥180mmHg and/or diastolic BP ≥110mmHg
Hypertensive crisis Severe, abrupt rise in BP with impending or progressive HMOD
Encompasses emergencies and urgencies
Hypertensive urgency Severe hypertension without HMOD
The term is falling out of favour
Hypertensive emergency Severe hypertension with acute HMOD of the heart, brain, retina, kidneys or large arteries
Malignant hypertension Hypertension (not necessarily severe) complicated by hypertensive microangiopathy
e.g. grade III/IV retinopathy or thrombotic microangiopathy

  • HMOD can occur without severe BP elevation as it is the rate of rise which matters more than any specific threshold
  • Hypertensive urgency does not require immediate BP reduction or hospital admission as outcomes do not differ from uncontrolled hypertension managed in primary care

Chronic hypertension

  • Essential hypertension may progress to crisis through missed diagnosis, undertreatment or non-adherence
  • Up to 40% of hypertensive emergencies have a secondary cause, which should be screened for e.g.

Drugs

  • Intoxication with sympathomimetics:
    • Therapeutic e.g. noradrenaline, adrenaline
    • Recreational e.g. cocaine, methamphetamine
    • MAOIs in combination with a tyramine-rich diet
  • Withdrawal of antihypertensives (e.g. β-blockers) or sedatives (e.g. clonidine, dexmedetomidine, benzodiazepines); rebound hypertension may exceed pre-treatment levels

Other acute causes


Respiratory

  • Pulmonary oedema
  • Respiratory compromise secondary to reduced conscious level

Cardiovascular

  • Raised LV afterload increases myocardial oxygen demand and reduces myocardial perfusion, causing ischaemia and LV dysfunction
  • Shear stress on vessel walls (often at junctions) causes new or worsening tears, e.g. aortic dissection

Neurological

  • Hypertensive encephalopathy:
    • Severe hypertension with seizures, lethargy, cortical blindness or coma, without alternative explanation
    • Occurs when high BP overwhelms cerebral autoregulation
    • Present in 15% of cases of malignant hypertension
  • PRES is a clinico-radiological diagnosis with focal vasogenic oedema on imaging although may also occur in normotensive patients
  • Ischaemic or haemorrhagic stroke
  • Retinopathy: exudates, haemorrhages, papilloedema

Renal

  • AKI, proteinuria, haematuria
  • Pressure natriuresis commonly leads to intravascular volume depletion

Gastrointestinal

  • Gastrointestinal upset

Haematological

  • Thrombotic microangiopathy, a feature of malignant hypertension:
    • High pressure forces blood into the subendothelial space, activating coagulation and platelets
    • Diagnosed by severe hypertension, haemolysis with a negative DAT, and thrombocytopenia, which improve with antihypertensive therapy
    • Exclude TTP early (ADAMTS13 assay)

  • Aim to establish the extent of HMOD and the underlying cause
  • BP stabilisation may need to take priority over extensive work-up

Target Investigations
Heart and great vessels ECG, troponin, BNP, echocardiography, CXR, CT aortogram
Brain and retina Neurological examination, fundoscopy, CT/MRI brain
Kidneys U&E, urine dipstick and microscopy, urine albumin:creatinine ratio
Microangiopathy FBC, coagulation screen, blood film, LDH, bilirubin, haptoglobin, DAT
Pregnancy Pregnancy test ± CTG

  • Fundoscopy is underused, being performed in only 10% of cases

A hypertensive emergency is a medical emergency and I would seek senior support as well as making a rapid but thorough assessment of the patient

  • Management has two linked aims:
    • Control BP to limit HMOD
    • Treat the underlying cause e.g. analgesia, anxiolysis, treating intoxication

Timeframe for BP reduction

  • Some conditions require BP control within 1hr:
    • Acute aortic syndromes
    • Acute coronary syndromes
    • Acute cardiogenic pulmonary oedema
    • Severe pre-eclampsia
    • Phaeochromocytoma crisis
    • Malignant hypertension with encephalopathy

  • In other hypertensive emergencies, reduce BP more gradually:
    • ≤25% reduction in the first hour
    • Then to 160/100mmHg over the next 2-6hrs if stable
    • Normalise over 24hrs

Practical points

  • IV agents are preferred for their rapid onset and titratability, and a continuous infusion is preferable to bolus dosing (avoids over-correction of BP)
  • Treat hypovolaemia before or alongside antihypertensives
  • Where the premorbid BP is unknown, aim for the upper end of the target range
  • Hypertensive emergencies are generally treated to a systolic target but organ perfusion is generally protected using a MAP target
  • Most antihypertensives are arteriolar vasodilators that reduce SVR although the exceptions are β-blockers and non-dihydropyridine calcium channel blockers (e.g. diltiazem)

Complications of treatment

  • Overtreatment (an inappropriately low target) or overshoot (an unintended precipitous fall) causes organ hypoperfusion:
    • Watershed cerebral infarction
    • Myocardial infarction
    • AKI
    • Mesenteric ischaemia
  • Those with chronic hypertension and cerebrovascular disease are particularly vulnerable, as their autoregulatory curves are right-shifted
  • Hydralazine and sodium nitroprusside are more prone to overshoot than labetalol or clevidipine
  • Sublingual nifedipine should be avoided due to serious adverse effects and increased mortality


Drug (onset) Advantages Disadvantages
Esmolol
(1-2 min)		 Avoids vasodilation
Ideal for acute aortic syndromes		 Bradycardia (inc. fetal)
Bronchospasm
Negative inotropy
Labetalol
(5-10 min)		 Preserves cerebral autoregulation
Negligible placental transfer		 Fetal bradycardia if overshoot
Reduced limb blood flow
Clevidipine/nicardipine
(2-15 min)		 Nicardipine: coronary and cerebral selectivity
Clevidipine: useful in heart failure and cardiac surgery		 Reflex tachycardia
Headache, increased CBF
Limited availability
Magnesium sulphate
(<1 min)		 Anti-epileptic
Bronchodilation
Anti-arrhythmic		 Weakness
Conduction disorders
Neonatal hypotonia
Sodium nitroprusside
(<1 min)		 Immediate preload and afterload reduction Cyanide toxicity
Coronary steal
Overshoot
GTN
(1-5 min)		 Reduces preload and myocardial oxygen demand Tachyphylaxis
Raised ICP, headache
Reflex tachycardia
High doses needed for afterload effect
Phentolamine
(1-2 min)		 Ideal for catecholamine-induced emergencies Tachycardia
Angina
Urapidil
(3-5 min)		 α1-blockade without reflex tachycardia Limited availability

  • Agents with slow onset, long duration or unpredictable response are less suitable for infusion e.g. metoprolol, enalaprilat
  • Centrally acting α2-agonists (clonidine, dexmedetomidine) can be useful adjuncts


Condition Target in first hour (mmHg) First-line infusion Avoid
Acute aortic syndrome SBP <120 and HR 60-80 Esmolol, labetalol
ACS SBP <140 GTN, labetalol SNP
Acute cardiogenic pulmonary oedema SBP <140 GTN, SNP
Pre-eclampsia <160/105 Labetalol, nicardipine SNP
Phaeochromocytoma crisis SBP <140 Phentolamine, then β-blocker β-blockade alone
Malignant hypertension with encephalopathy MAP reduction 20-25% Labetalol, nicardipine
Sympathomimetic intoxication Benzodiazepine, then phentolamine