This document discusses systemic hypertension, including: - Definitions of different classifications of hypertension according to WHO and AHA guidelines. - Differences between hypertensive emergencies and urgencies. - Common causes and clinical presentations of secondary hypertension. - Recommended treatment approaches for various hypertensive crises and emergencies, including targets for blood pressure reduction. - Drugs commonly used to lower blood pressure such as labetalol, nicardipine, nitroglycerin, and sodium nitroprusside.

1. Systemic hypertension
Dr Andrew Crofton
ED Registrar
Disclaimer: https://criticalcarecollaborative.com/disclaimer/

2. Introduction
 30% of population
 Elderly females most resistant to pharmacological control
 Systolic rises with age and diastolic stable or falls
 CVD risk most closely aligned with systolic BP >50yo and diastolic BP if <50yo
 1-6% of ED presentations will have severe HTN
 1/3 to ½ of these will have end-organ damage

3. Introduction
 WHO Classification of chronic hypertension
 Prehypertension – 120/139 or 80-89
 Mild Stage 1 – 140-159 or 90-99
 Moderate Stage 2 -160 – 179 100-109
 Severe >180/110
 AHA 2017 classification
 Normal <120/80
 Elevated 120-130/<80
 Stage 1 - 130-140/80-90
 Stage 2 - >140/>90

4. Introduction
 Hypertensive emergency
 Acute elevation of BP (>180/120) associated with end-organ damage (brain, heart, aorta,
kidneys or eyes
 Hypertensive urgency
 BP >180/120 without evidence of end-organ damage
 No evidence that rapid pharmacological reduction in BP results in any meaningful
outcomes
 Prompt therapy with oral agents to reduce BP over days to weeks is preferred

5. HTN
 Primary most common (essential)
 Secondary
 Chronic renal disease, renal artery stenosis, phaeochromocytoma, Cushing’s, thyrotoxicosis,
sleep apnoea, coarctation of aorta, stimulant use, NSAID’s, hypercalcaemia
 Investigation for secondary causes indicated if:
 Drug-resistant HTN
 Abrupt onset HTN
 Onset <30yo
 Exacerbation of previously controlled HTN
 Onset of diastolic HTN in adults >=65yo
 Unprovoked or excessive hypokalaemia

6. Chronic HTN management
 Non-pharmacological
 1kg weight loss reduces systolic BP by 1mmHg
 30 min daily aerobic exercise reduces SBP by 5mmHg
 Salt restriction
 <100mmol/day reduces SBP by 5mmHg
 <50mmol/day eliminates primary HTN
 High potassium diet
 Each increase of 100mmol/day reduces SBP by 10mmHg
 Alcohol restriction
 <=2 standard drinks per day for adult males and <=1 for females reduced SBP by 2mmHg

7. Chronic HTN management
 Pharmacological control
 Alpha blockers should not be first-line as increase mortality
 Good BP control more important than choice of agent
 Thiazide/CCB/ACEi/ARB first-line
 Thiazide/CCB if dark skin (ACEi less effective)
 Chronic renal disease – ACEi/ARB

8. Hypertensive crises
 Acute aortic dissection
 Acute pulmonary oedema
 Acute MI
 Acute renal failure – check for renal bruits, proteinuria, creatinine
 Severe pre-eclampsia/HELLP/eclampsia – proteinuria, haemolysis, LFT, plt’s
 Hypertensive retinopathy – Retinal haemorrhages, cotton-wool spots, hard exudates
 Hypertensive encephalopathy
 Epistaxis
 Subarachnoid haemorrhage
 ICH
 Acute ischaemic stroke
 Acute perioperative hypertension – failure to control bleeding with direct pressure
 Sympathetic crisis – Drugs or phaeochromocytoma

9. Pathophysiology
 Mechanical wall stress and endothelial injury leads to increased vascular
permeability, excessive perfusion of organ beds, activation of coagulation cascade
and inflammatory pathways
 Manifested as haematuria or arterial haemorrhages on fundoscopy
 RAS activation due to reduced organ perfusion (due to above damage) results in
further vasoconstriction
 Pressure natriuresis occurs with volume depletion and further vasoconstrictor
release
 Results in hypoperfusion, ischaemia, dysfunction and endothelial dysfunction that
can last for years after acute episode

10. Precipitants
 Usually idiopathic acute on chronic HTN
 Sudden withdrawal of antihypertensives
 Worsening renal function
 Vasculitis and connective tissue disorders
 Sympathomimetics
 Phaeochromocytoma

11. Clinical features
 BP in both arms
 >10-20mmHg difference is significant and for every 10mmHg, risk of death is increased
 Treat higher blood pressure and measure on the higher arm each time
 DDx – Aortic dissection, coarctation, peripheral vascular disease, age, normal
 Proportion of patients presenting with elevated BP with specific diagnoses
 Subarachnoid haemorrhage – 100% >140mmHg
 Ischaemic stroke – 77-82% >140mmHg
 Intracerebral haemorrhage – 75% >140mmHg
 Type B aortic dissection – 67-77% >140/>90
 Type A aortic dissection – 36-74% >150
 Acute heart failure – 54% >140
 NSTEMI – 60% >140

12. Clinical features
 Chest pain
 Most commonly ACS with hypertension vs. aortic dissection
 Aortic dissection
 Typical tearing sudden onset pain radiating to interscapular region
 <25% have neurological deficit or pulse deficit >20mmHg
 1/3 have diastolic murmur
 CXR abnormal in most but usually non-specific
 25% have widened mediastinum
 ECG changes are non-specific but <10% demonstrate findings consistent with MI

13. Clinical features
 Acute neurological symptoms
 Focal neuro deficits strongly suggest ischaemic or haemorrhagic stroke
 Hypertensive encephalopathy is a clinical diagnosis of exclusion after
haemorrhage/infarct ruled out. Characterised by ALOC, headache, vomiting, seizures or
visual disturbances
 Most patients will have papilloedema
 If MRI shows reversible ischaemia primarily focused posteriorly = PRES (posterior reversible
encephalopathy syndrome)
 Takes hours/days to resolve after BP control
 Acute renal failure and peripheral oedema
 May be asymptomatic or show oedema, ALOC, oliguria, anorexia, nausea or vomiting
Clinical features
´ Ac ute neurological symptoms
´ Focal neuro defic its strongly suggest ischaemic or haemorrhagic stroke
´ Hypertensive encephalopathy is a c linical diagnosis of exc lusion after
haemorrhage/ infarct ruled out. Charac terised by ALOC, headache, vomiting,
seizures or visual disturbances
´ Most patients will have papilloedema
´ If MRI shows reversible ischaemia primarily focused posteriorly = PRES(posterior reversible
encephalopathy syndrome)
´ Takes hours/ days to resolve after BP control
´ Ac ute renal failure and peripheral oedema
´ May be asymptomatic or show oedema, ALOC, oliguria, anorexia, nausea or
vomiting

14. Clinical features
 Sympathetic crisis
 Abrupt discontinuation of clonidine (potentiated by beta-blocker use due to unopposed
alpha agonism)
 Phaeochromocytoma
 5-20% of tumours are malignant
 Headache, alternating periods of normal and elevated BP, tachycardia, flushing and
asymptomatic periods
 Sympathomimetics
 Cocaine, amphetamine, PCP, LSD
 MAOi-associated tyramine reaction
 Autonomic dysfunction due to spinal cord or severe head injury or chronic spinal
disorders

15. Asymptomatic patients
 There are no formal recommendations currently for the asymptomatic hypertensive
patient
 Clinically meaningful results obtained in only 6% of patients
 ED evaluation should be based on patient complaint, history and review of systems
with selected testing for end-organ damage

16. Treatment
 Goal is to minimise end-organ damage while avoiding hypoperfusion of cerebral,
coronary and renovascular beds
 Acute aortic dissection is the exception as risk of morbidity and mortality
associated with uncontrolled hypertension/tachycardia is far greater than risks of
hypoperfusion syndromes
 Aortic dissection
 Target HR <60 and SBP 100-140
 Fentanyl 50mcg IV q10min targeting comfort
 Metoprolol 5mg q5min until HR <60
 Hydralazine 10mg IV q10min until SBP <120

17. Treatment
 Acute hypertensive pulmonary oedema
 GTN 400mcg 5 sprays S/L stat
 CPAP 5cmH20 rapidly titrated up to 15cmH20 on FiO2 1,0 as tolerated
 GTN infusion 40mcg/min titrated up to 200mcg/min as required to achieve target SBP
<150
 UpToDate states 15-30% drop is usually sufficient. Tintinalli states target <150/100
 Remember, aim is reduction of afterload vs. in hypertensive encephalopathy need to
avoid sudden drop for cerebral perfusion to be maintained
 Acute MI
 Nitrates first-line
 IV beta-blockade only if severe hypertension

18. Treatment
 Sympathetic crisis
 IV benzodiazepines if cocaine/amphetamine-related
 Nitroglycerin or phentolamine second-line
 CCB third-line
 Beta-blockers can result in unopposed alpha agonism (labetalol is preferred in this case)
 Phaeo
 Phentolamine first-line
 MAO toxicity
 IV benzodiazepine
 Phentolamine, nitroglycerine and nitroprusside next line

19. Treatment
 Acute renal failure
 Fenoldopam ideal (improves natriuresis and CrCl) but may not be available
 Nicardipine reduces systemic vascular resistance with preservation of renal blood flow
 Nitroprusside is an alternative
 Eclampsia/pre-eclampsia
 Magnesium infusion + see guideline

20. Treatment
 Hypertensive encephalopathy
 IV nicardipine, labetalol
 Do not use nitroglycerin as dilates cerebral arteries, alters global and regional flow and may
worsen autoregulatory failure
 Target DBP <110mmHg
 Subarachnoid haemorrhage
 IV nicardipine/labetalol
 Oral nimodipine for modest BP reduction and prevention of vasospasm to improve
neurological outcomes
 Intracerebral haemorrhage
 Labetalol, nicardipine, esmolol
 Lowering from >180 to 120-160mmHg may improve clinical outcomes

21. Treatment
 Ischaemic stroke
 Moderate elevations may be beneficial and will spontaneously decrease within 90 minutes of
acute stroke onset
 Labetalol and nicardipine are recommended
 Fibrinolytic therapy is contraindicated if BP >185/110 after antihypertensive therapy
 If tPA candidate
 Treat if BP >185/110 and aim 141-150mmHg
 If not a tPA candidate
 Treat if >220/120 on 3 measurements
 Do not lower >10-15% in first 24 hours
 Goal should be <180/105 if patient has received fibrinolysis
 Measure q15min for 2 hours then q30min for 6 hours, then hourly for 16 hours

22. Treatment targets
Disorder Target
Aortic dissection HR <60, SBP <120
Acute hypertensive APO Reduce SBP 30%
SBP <150/100 often mentioned
Acute MI MAP reduction by 30%
Acute renal failure Reduce SBP by 20% maximum
Hypertensive encephalopathy 20-25% MAP reduction in first hour
SAH SBP <160 to prevent rebleeding
Once secured, depends on vasospasm
ICH Treat if SBP>200 or MAP >150
Early aggressive BP control to SBP 120-
160 may have morbidity/mortality benefit
Acute ischaemic stroke If fibrinolysis planned - <185/110
Otherwise only if >220/>120

23. Beta-blockers
 Labetalol
 Modest selective alpha-1 blocker (1:7 alpha:beta)
 Recommended for all hypertensive emergencies except for cocaine intoxication or systolic dysfunction in decompensated HF
 10-20mg IV bolus over 2 minutes, then 40-80mg at 10 minute intervals up to 300mg total dose
 Continuous infusion 2mg/min titrated up to 300mg total dose if required
 Oral metoprolol recommended for ACS and can consider IV formulation if BP control is required
 Esmolol has a very short half-life and is rapidly titratable and may be of benefit in those with severe asthma or
COAD
 Difficult to set up infusions in ED
 Beta-1 selective
 250-500mcg/kg over 1-3min IV
 Infusion 50mcg/kg/min IV over 4 minutes
 If adequate effect not observed, repeat loading dose and increase infusion rate in increments of 50mcg/kg/min repeated up to 4
times and infusion rate up to 300mcg/kg/min

24. Calcium channel blockers
 Nicardipine
 Onset of action 5-15min, titrated at 15 minute intervals
 Safe and effective in neurological hypertensive emergencies
 5mg/hr infusion increased by 2.5mg/hr every 15 minutes up to 15mg/hr
 Nifedipine use is discouraged in hypertensive emergencies except peripartum
 Nimodipine for SAH to prevent vasospasm and reduce BP (modest)

25. Vasodilators
 Nitroglycerin
 Arterial dilator at very high doses
 Venous > arteriolar dilatation
 Also dilates bronchial and GIT smooth muscle
 First-line only in acute heart failure or ACS
 Primary benefit seen in reduced venous return to heart
 Start at 5-20mcg/min and can titrate up to 200mcg/min
 Sodium nitroprusside
 Good as second-line agent. Venous > arteriolar vasodilation
 Cyanide toxicity concern heightened in renal/liver failure patients
 Combination therapy is most common i.e. with esmolol for aortic dissection
 0.5mcg/kg/min IV increased by 0.5mcg/kg/min
 Risk of cyanide toxicity at >2mcg/kgmin and thiosulfate infusion should be initiated if infusion 4-10mcg/kg/min

26. Vasodilators
 Hydralazine
 Predictable BP lowering
 Direct arteriolar vasodilation
 Reduces diastolic > systolic
 Risk of reflex tachycardia
 5mg increments IV

27. Phentolamine
 Useful in sympathetic crises
 Bolus 1-5mg IV then 0.2-0.5mg/min

28. Treatment of asymptomatic severe
hypertension
 Acute treatment does not prevent or reduce short-term morbidity or mortality
 If 120-160/80-100: Advise follow-up within 2 months
 >160/>100 – Advise follow-up within 1 month
 >180 or >110: Consider initiation of therapy and follow-up within 1 week
 >200 or >120: Initiate therapy and follow-up within 1 week
 Can initiate outpatient regimes in ED based on study showing increased risk of
cardiovascular events within 4 years of ED presentation in hypertensive urgency
patients compared to control patients
 Once daily, inexpensive and checking of renal function/pregnancy
status/ECG/electrolytes/asthma/COAD are crucial

29. Treatment options
 Non-black individuals
 Thiazide e.g. hydrochlorothiazide 25mg daily or
 ACEi e.g. lisinopril 10mg daily or
 CCB
 Black individuals
 Thiazide diuretic or
 CCB
 Or Both

30. Treatment options
 Chronic kidney disease with or without diabetes
 ACEi or ARB
 Heart failure
 Diuretic + ACEi
 Post-MI
 Beta-blocker or ACEi
 High coronary artery disease risk
 Beta-blocker
 Educate re: common adverse effects