What is a hypertensive crisis/emergency vs hypertensive urgency?
A hypertensive emergency is defined by severe elevations in blood pressure (>180/120mmHg) with evidence of impending, or progressive target organ dysfunction
Target organ dysfunction includes:
Neurological:
Hypertensive encephalopathy
Intracerebral haemorrhage
Papilloedema, retinal haemorrhages
Cardiac:
Acute MI/Unstable angina pectoris
Tachy/bradyarrhythmia
Left ventricular failure
Dissecting aortic aneurysm
Eclampsia
Respiratory:
Acute pulmonary oedema
Renal failure
A hypertensive urgency is when there is severe BP elevation without target organ dysfunction
Headache, SOB, epistaxis, chest pain, severe anxiety may occur
Examining the patient
So you've been called to see Mrs J whose blood pressure is now 220/116mmHg and the nurse sounds understandably worried over the phone. What do you do?
Firstly, to establish whether this is a hypertensive emergency or urgency, you need to quickly assess the patient for end organ damage:
Symptoms and signs of heart failure (oxygen saturations, breathlessness, rales, basal crepitations, elevated jugular venous pressure, pedal oedema)
Assess their GCS and perform a basic neurological exam (to rule out a haemorrhagic stroke/encephalopathy)
Check for differential pulses/BP on bilateral limbs to rule out aortic dissection
Fundoscopy to look for papilloedema, flame haemorrhages
Urine microscopy/dipstick - proteinuria/haematuria
Blood investigations to consider: Full blood count, Urea and electrolytes, Troponin
Consider a chest radiograph - look for evidence of acute pulmonary oedema or a widened mediastinum
Immediate Management
Patient should be resting supine
If there is evidence of major end organ dysfunction - an ICU/HD setting should be considered
Initial goal of therapy is to reduce mean arterial BP (MAP) by not more than 25% within 1 hour (aim 10-20% in the first 1-2 hours)
One year mortality after an episode of hypertensive urgency is about 9%. (Guiga et al. 2017)
In hospital mortality in HTN emergency is 13%, one year mortality is 39%
Note that MAP = ((2xDBP) + SBP) / 3
Subsequently if the patient is stable, reduce the BP to 160/100-110mmHg within the next 2-6 hours
Blood pressure should not be reduced too drastically as this could precipitate renal, cerebral or coronary ischaemia
If the patient continues to remain stable, then BP can be further reduced to the normal range in the next 24-48 hours
Exceptions to the above:
Ischaemic stroke: allow permissive hypertension unless the patient has just had thrombolysis in which strict BP targets should be ensured SBP<160mmHg
Aortic dissection: reduce SBP to < 100mmHg if tolerated
In phaeochromocytoma crisis reduce SBP to 140mmHg within the first hour
In pre-eclampsia and eclampsia, reduce SBP to 140mmHg within the first hour
Medications to use:
Alpha blockers (particularly if a pheochromocytoma is suspected):
Phentolamine
0.5mg IV test dose, followed by a 0.5mg/hr infusion titrating up as required to 40mg/hr
1-5mg IV bolus followed by 1mg/hour continuous infusion up to 40mg/hour
Phenoxybenzamine (oral)
10mg BD up to 40mg TDS
Vasodilators:
Nitrates:
Glyceryl trinitrate: IV infusion of 5-100mcg/min or topical patch
Sodium nitroprusside: IV infusion 0.3-10mcg/kg/min increasing every 5min until the target BP is reached
Hydralazine: IV bolus 10-50mg Q4-6H
Calcium channel blockers:
Amlodipine up to 10mg/day, nifedipine LA up to 60mg BD
Beta blockers:
IV labetalol (should not be used if there is no initial alpha blockade if there are concerns for a phaeochromocytoma)
10-20mg over 2minutes followed by 0.5-2.0mg/minute
IV esmolol (can reduce HR and shear stresses in aortic dissection)
250-500mcg/kg over one min loading dose then 25-50mcg/kg/min cont, titrate every 5 minutes as required.
Adjuncts:
Magnesium sulphate: IV 4g bolus over 10min followed by 1-4g/hr
Special scenarios:
For phaeochromocytomas, always consider fluid resuscitation as patients are very volume constricted, consider central venous pressure monitoring for accurate volume status assessment. Fluid resuscitation should be done BEFORE initiating alpha blockade as otherwise the patient's BP may crash
Not all hypertension is essential hypertension
As endocrinologists, we are always vigilant for other secondary causes of hypertension. In particular, when there are severe elevations in blood pressure, causes other than essential hypertension should be considered and investigated. These include:
Endocrinological causes:
Phaeochromocytomas
Hyperthyroidism
Cushing's syndrome
Primary hyperaldosteronism
Non classical congenital adrenal hyperplasia (NCCAH) - particularly 17a OH and 11b OH deficiency (which present with hypertension and hypokalaemia)
Acromegaly
Hypercalcaemia (due to Increased vascular smooth muscle contraction, increased renin production and decreased nitric oxide production)
Non-endocrinological causes
Obstructive Sleep Apnoea (OSA)
Aortic coarctation
Renal parenchymal disease
Renal artery stenosis (e.g. in NF-1 look out for café au lait spots/neurofibromas)
Illicit drug use: cocaine/amphetamines
Pregnancy (pre-eclampsia/eclampsia)
It is essential to find the underlying cause so that it can be adequately treated and the blood pressure sufficiently controlled to avoid end organ damage.
Possible exam questions:
In the special case of a phaeochromocytoma crisis, what other features might you expect to see?
Fever > 40c due to IL-6 secretion by the tumour
Labile BP with fluctuation between hyper and hypotension
Multi-organ failure due to severe vasoconstriction
Renal failure with anuria
Gut: pseudoobstruction, megacolon, ischaemic bowel, perforation
Hepatic: Ischaemic/congestive liver injury
Vascular/Musculoskeletal: Peripheral gangrene, rhabdomyolysis
Lactic acidosis due to Type A hypoperfusion
Hyperglycaemia leading to DKA/HHS
References:
Guiga et al. Hospital and out-of-hospital mortality in 670 hypertensive emergencies and urgencies. J Clin Hypertens (Greenwich). 2017;19(11):1137-1142.
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