Definitions
- A fair bit of crossover!
- Hypertensive emergency
-
- BP > 180/120 with new or worsening target organ damage
- 40% previous HTN diagnosis, 60% de novo
- 30% have secondary cause
-
- Hypertensive urgency / uncontrolled HTN
-
- BP > 180/120 without target organ damage
-
- Malignant / accelerated HTN
-
- Severe HTN (>180/120) + grade 3 or 4 hypertensive retinopathy
- May progress to hypertensive emergency
- Rare
- 80% mortality at 2 years without treatment. Survival 90% at 5 years with treatment
- If not an emergency – give oral agents and don’t lower BP too quickly
-
Assessment
- Use large cuff for large patient, check both arms and check for postural drop (especially in the elderly)
- Ask about vision, headaches, chest/back pain, vomiting
- Examine CV, respiratory system, neurological system (document GCS) and fundi
- Look for secondary causes and signs of end organ damage
-
- Urine – dip for blood/protein (send urine PCR if present), pregnancy test
- ECG
- CxR
- Eyes – changes can be absent in presence of organ damage elsewhere. Can be unilateral.
- Bloods – U&Es (creat, K+), BNP, trop, TSH, clotting, blood film if haemolysis
- Consider
-
- CT head / CTA (for CVA, bleeds, PRES). Always if depressed GCS.
- Full renal screen
- Echo
- Metanephrines, autoantibodies
-
-
- Consider secondary causes (more here)
-
- Drugs (recreational, withdrawal, OCP, steroids, psychiatric, immunosuppressants, anti-cancer drugs)
- CNS (head injury, CVA, raised ICP)
- Renal (primary, renovascular)
- Endocrine (hyperaldosteronism, phaeo, cushings, thyroid)
- Other (coarctation, eclampsia)
-
- Consider urgent management in the absence of end organ damage, emergency management if present
- However… Isolated hypertensive retinopathy, renal dysfunction, LVH on ECG, proteinuria or cerebral microbleeds does not constitute an emergency
Complications (defines hypertensive emergency)
- CV
-
- Aortic dissection
- ACS
- Acute LV failure / pulmonary oedema
-
- Neuro
-
- Hypertensive encephalopathy
- Intracranial haemorrhage
- Acute ischaemic CVA
-
- Other
-
- AKI
- Pre-eclampsia
- Thrombotic microangiopathy (low platelets, fragments on film)
-
- Notes on hypertensive encephalopathy
-
- Headache, vomiting, confusion, seizures, visual disturbance
- Insidious onset
- Can be evidence of PRES on imaging (often on CT, though MRI is better)
- Causes vasogenic oedema secondary to failure of cerebral autoregulation
- More common in lupus, cryoglobulinaemia, haemolytic uraemic syndrome, cyclosporine, cisplatin and tacrolimus tx, CKD
- Aim to reduce BP by 20% during first hour, and to 160/100 by 4 hours
-
Lowering the Blood Pressure in A Hypertensive Emergency
- Usual strategy
-
- Lowering BP too fast can be life-threatening
- In first hour aim to reduce MAP by 15% or 20% (or to maybe 160-180 systolic – then keep it there)
- Over next 23 hours, aim to gradually reduce MAP by 10%
- Can give IV treatment initially, then oral at 6 hours and then wean IV (but must give an oral agent at some point or you won’t be able to wean the IV)
- Should be on HDU with arterial line ideally
-
- Exceptions
-
- Acute ischaemic stroke – only lower acutely if BP > 220 systolic (or > 180 if candidate for thrombolysis) to prevent watershed infarction. Aim 15% reduction in MAP
- Aortic dissection – you should rapidly lower BP, aim systolic of 120 within 20 minutes and HR < 60. Use betablocker first, then a vasodilator.
- Acute intracerebral haemorrhage – decrease BP to 150 systolic within an hour and < 140 in 6 hours. Maybe don’t drop BP by > 60 (risk of AKI). If large haematoma and signs of raised ICP, can reduce BP more slowly
- ACS or heart failure – some guidelines suggest decrease systolic BP to 140 within an hour
-
- Labetalol infusion
-
- Usually first line
- Infusion 200mg in 200ml. 0.5-2mg/min, or 30-300mg/hr. Start at 120mg/hour and double rate every 15 mins to 480mg/hr max.
- Don’t give more than 200mg
- Can give 20mg IV bolus first if need to bring BP down faster in first hour
- Can be used in aortic dissection, CVA and encephalopathy especially
- Increase by 15-30mg/hr every 15-30 minutes
- Can cause bradycardia and bronchoconstriction
- Lasts 3-6 hours
- Not recommended in
-
- Uncontrolled heart failure
- 2nd or 3rd degree HB, bradycardia, sick sinus syndrome
- Asthma
- Severe peripheral artery disease
- Untreated pheochromocytoma
- Metabolic acidosis
- Be cautious if already on betablocker, digoxin or CCB
-
-
- IV GTN
-
- An alternative (but could also be used with labetalol)
- Best in aortic dissection and ACS
- 50ml GTN in 50ml normal saline. Rate is 2mg/min, titrating to max 10mg/min. Increase rate every 15 mins
- Lasts minutes so easier to titrate
- Then once controlled, wean rate and add in oral antihypertensives.
- Side effects – headache, reflex tachycardia
- Becomes less effective over time
- Not recommended in
-
- PRES (can increase oedema)
- RV infarct
- Severe aortic stenosis
- Mitral stenosis
- Tamponade / constrictive pericarditis
- HOCM
- Marked anaemia or severe volume depletion
- Cerebral haemorrhage
- Use of sildenafil
- Raised ICP
-
-
- Other IV options
-
- Nitroprusside – option in heart failure, avoid in liver and renal dysfunction or acute MI
- Nicardipine – useful in encephalopathy
- Esmolol – useful for aortic dissection. Very short acting
- Phentolamine – alpha blocker, useful for phaeo, cocaine, clonidine withdrawal. Can cause reflex tachycardia
-
- If using oral agents as well, choose long-acting ones Amlodipine, bisoprolol, bendroflurazide, ramipril
- For cocaine toxicity – diazepam. Avoid betablockers.
- For pre-eclampsia – magnesium and labetolol. See PET
Lowering BP in hypertensive urgency (or ‘uncontrolled HTN’)
- No acute end organ damage with BP > 180 systolic (Ensure normal ECG, urine dip, fundi, no symptoms)
- Can often be managed as outpatient but seen in ambulatory care within 48 hours of starting therapy
- Consider referral to complex HTN clinic – esp if young, or already on 3 agents
- Aim to reduce MAP by no more than 20% in first 48 hours (or to 160/100). Aiming to control BP in days to weeks.
- Check postural BP
- Drug treatment
-
- Consider
-
- Diltiazem (Tildium LA) 200-300mg OD
- Doxazocin 8mg BD
- Nifedipine MR 10mg BD (not s/l prep which can be dangerous and drops BP too fast). Can increase to 20mg BD
-
- Then
-
- Metoprolol 12.5mg initially, then up titrate to 25mg BD
-
- Then
-
- Add in ACE-I or alpha blocker or diuretic
-
- Amlodipine – takes 8 hours to reach peak concentration, and about 1 week to reach steady-state effect. Therefore not recommended in this scenario (although often given)
- Might avoid diuretics – can exacerbate volume depletion and hypokalaemia
- Can use ACE-I and betablockers but be careful, patients can be very sensitive, start at a low dose
- Avoid betablocker if suspected pheochromocytoma
- Avoid ACE-i if suspected bilateral RAS
- Consider
-