This document discusses hypertensive emergencies and urgencies. It defines severe hypertension and distinguishes between emergencies and urgencies. Hypertensive emergencies involve acute severe hypertension with signs of damage to target organs, while urgencies involve acute severe hypertension without organ damage. The document provides epidemiological data and discusses the etiology, pathophysiology, evaluation, and management of hypertensive crises. Management depends on the clinical presentation and involves rapidly reducing blood pressure in emergencies but more slowly in urgencies.

1. Hypertensive emergency

2. DEFINITION HYPERTENSION

3. SEVERE HYPERTENSION
• Severe hypertension is defined as persistent
elevated SBP >180 mmHg and/or DBP >110
mmHg.
Hypertensive urgency Hypertensive emergency
Acute severe hypertension without
any signs of damage to target
organs
Acute severe hypertension with
signs of progressive damage to
target organs

5. EPIDEMIOLOGY
• In a recent large series, only a minority of
patients admitted (5.1%) had hypertensive
crises. Of those more than three quarters
(76.6%) constitute hypertensive emergencies.

6. ETIOLOGY
• Essential hypertension : non-compliance with
antihypertensive medication and inadequate
blood pressure control
• Secondary hypertension

8. Pathophysiology

9. EVALUATION
• A complete history should include:
• • duration and level of elevated BP if known
• • symptoms of secondary causes of hypertension
• • symptoms of target organ complications (i.e. renal failure and heart
failure)
• • symptoms of cardiovascular disease (e.g. CHD and cerebrovascular
disease)
• • symptoms of concomitant disease that will affect prognosis or treatment
e.g.
• diabetes mellitus, heart failure, renal disease and gout
• The evaluation of these patients should include a thorough history and
• physical examination, particularly looking for signs of acute target organ
damage /
• complication and causes of secondary hypertension.

10. • • family history of hypertension, CHD, stroke, diabetes, renal
disease or dyslipidaemia
• • dietary history including salt caffeine, liquorice and alcohol intake
• • drug history of either prescribed or over-the-counter medication
(NSAIDs, nasal
• decongestants) and traditional or complementary medicine
treatment
• • lifestyle and environmental factors that will affect treatment and
outcome (e.g.
• smoking, physical activity, work stress and excessive weight gain
since childhood)
• • presence of snoring and or day time somnolence which may
indicate sleep
• apnoea

12. MANAGEMENT
• Management of these patients depends on
the clinical presentation and laboratory
• investigations.

13. HYPERTENSIVE URGENCY
• Initial treatment should aim for about 25%
reduction in BP over 24
• hours but not lower than 160/90 mmHg

15. HYPERTENSIVE EMERGENCY
• The BP needs to be reduced rapidly. It is
• suggested that the BP be reduced by 25%
depending on clinical scenario over 3 to 12
• hours but not lower than 160/90 mmHg

17. • Rapid reduction of BP (within minutes to hours) in
asymptomatic severe hypertension or
• hypertensive urgencies is best avoided as it may precipitate
ischaemic events.102
• Oral or sublingual drugs with rapid onset of action can
result in an uncontrolled BP
• reduction. Several serious side effects have been reported
with the administration of
• sublingual fast-acting nifedipine and therefore this is no
longer recommended.103 (Level III)
• However oral nifedipine retard can be used and has been
recommended as first line
• therapy for hypertensive urgencies.

18. HYPERTENSIVE CRISIS
• Hypertensive emergency :. These include
patients with complications of severe
hypertension such as acute heart
• failure, dissecting aneurysm, acute coronary
syndromes, hypertensive encephalopathy,
subarachnoid haemorrhage and acute renal
failure.

19. Hypertensive emergency
• Target organ damage:
• Brain:
• Hypertensive encephalopathy is characterized by
lethargy, dullness, headache, seizures and visual
disturbances including blindness. • Cerebral
infarction, hemorrhage and facial nerve palsy
may occur.
• Neuroimaging shows features of white matter
degeneration in the parieto-occipital area
(posterior leukoencephalopathy), which are
reversible with treatment.

21. • Retina

22. Grade 1 Generalised arteriolar constriction - seen as `silver wiring` and Vascular
tortuosities. Grade 2 + irregularly located, tight constrictions - `AV nicking` or `AV
Nipping` Grade 3 + with cotton wool spots and flame-haemorrhages Grade 4 + with
swelling of the optic disk (papillodema) only 8.6% had evidence of retinopathy
diagnosed with an ophthalmoscope