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Flashcards in Hypertensive emergencies Deck (12):

Causes of

essential and

secondary hypertension

Essential hypertension

(primary, cause unknown). ~95% of cases.

Secondary hypertension

~5% of cases. Causes include:

    • Renal disease: The most common secondary cause. 75% are from intrinsic renal disease: glomerulonephritis, polyarteritis nodosa (pan), systemic sclerosis, chronic pyelonephritis, or polycystic kidneys. 25% are due to renovascular disease, most frequently atheromatous (elderly ♂ cigarette smokers, eg with peripheral vascular disease) or rarely fibromuscular dysplasia (young ♀).

    • Endocrine disease: Cushing’s ([link]) and Conn’s syndromes ([link]), phaeochromocytoma ([link]), acromegaly, hyperparathyroidism.

    • Others: Coarctation, pregnancy (ohcs p48), steroids, maoi, ‘the Pill’.


Target blood pressures

Target pressure is <140/90mmHg,

but in diabetes mellitus, aim for <130/80mmHg,

and <125/75 if proteinuria.


lifestyle changes

↓Concomitant risk factors: stop smoking; low-fat diet. Reduce alcohol and salt intake; increase exercise; reduce weight if obese.



If ≥55yrs, and in Black patients of any age, 1st choice is a Ca2+ channel blocker or thiazide.


If <55, 1st choice is ACEI (or ARB if ace–i intolerant, eg cough).

β-blockers are not 1st-line for hypertension, but consider in younger people, particularly: if intolerance or contraindication to ace-i/arb (angiotensin receptor blockers) exists,

or she is a women of child-bearing potential, or there is ↑sympathetic drive.


Combination therapy

ACEI + a Ca2+-channel blocker or diuretic is logical, and has been commonly done in trials.

There is little evidence on using 3 drugs so the recommendation is based on the most straightforward option: try ACEI, Ca2+-channel blocker and thiazide.

If bp still uncontrolled on adequate doses of 3 drugs, add a 4th (consider: higher-dose thiazide, or another diuretic, eg spironolactone (monitor u&e), or β-blockers, or selective α-blockers) and get help.

If only on a β-blocker and a 2nd drug is needed, add a Ca2+ blocker, not a thiazide to ↓ risk of developing diabetes.


Thiazides SE

 SEs: K+↓, Na+↓, postural hypotension, impotence. ci: gout.


Ca2+ blockers SE

se: flushes, fatigue, gum hyperplasia, ankle oedema; avoid short acting form.



when 1st choice?



 ace-i may be 1st choice if co-existing lvf, or in diabetics (esp. if microalbuminuria,)or proteinuria.

SE: cough, K+↑, renal failure, angio-oedema.

CI bilateral renal artery or aortic valve stenosis


Beta blockers




bisoprolol 2.5–5mg/24h po.

SE: bronchospasm, heart failure, cold peripheries, lethargy, impotence.

CI: asthma; caution in heart failure.



MALIGNANT hypertension

In general, use oral therapy, unless there is encephalopathy or ccf. The aim is for a controlled reduction in blood pressure over days, not hours. Avoid sudden drops in bp as cerebral autoregulation is poor (so stroke risk↑).

  • Bed rest;
  • there is no ideal hypotensive, but atenolol or long-acting Ca2+ blockers PO.


Encephalopathy (headache, focal cns signs, seizures, coma):

  • aim to reduce bp to ~110mmHg diastolic over 4h.
  • Admit to monitored area.
  • Insert intra-arterial line for pressure monitoring.
  • Furosemide 40–80mg iv; then either iv labetalol (eg 50mg iv over 1min, repeated every 5min, max 200mg) or sodium nitroprusside infusion (0.5μg/kg/min ivi titrated up to 8μg/kg/min, eg 50mg in 1L dextrose 5%; expect to give 100–200mL/h for a few hours only, to avoid cyanide risk).

Never use sublingual nifedipine to reduce bp (∵ big drop in bp and stroke risk)


hypertensive crisis

Hypertensive crisis is defined as a severe elevation in BP (SBP >200mmHg, DBP >120mmHg). Rate of change in BP is important. A rapid rise is poorly tolerated and leads to end-organ damage, whereas a gradual rise in a patient with existent poor BP control is tolerated better.


hypertensive crisis classification

    • Hypertensive emergency, where a high BP is complicated by acute target-organ dysfunction and includes:

        • Hypertensive emergency with retinopathy, where there is marked elevation in BP (classically DBP >140mmHg) with retinal haemorrhages and exudates (previously called accelerated hypertension) and

        • Hypertensive emergency with papilloedema, with a similarly high BP and papilloedema (previously called malignant hypertension).

    • Hypertensive urgency, where there is a similar rise in BP, but without target organ damage.