Hypertension in the ED

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

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

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

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

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

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

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

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

Precipitants

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

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

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

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

• 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

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

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

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

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

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

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

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

Treatment targets

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

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)

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

Vasodilators

• Hydralazine
  • Predictable BP lowering
  • Direct arteriolar vasodilation
  • Reduces diastolic > systolic
  • Risk of reflex tachycardia
  • 5mg increments IV

Phentolamine

• Useful in sympathetic crises
• Bolus 1-5mg IV then 0.2-0.5mg/min

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

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

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

Last Updated on October 28, 2020 by Andrew Crofton