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CDHB

Hypertension

Classification

• Primary: Idiopathic, 'essential'.
• Secondary: Renal, endocrine or neurological disease, diabetes mellitus, coarctation of the aorta, drug induced.
• Malignant: Severe hypertension with rapidly progressive end organ damage e.g., acute left ventricular dysfunction, encephalopathy, retinopathy (haemorrhages, exudates and papilloedema) and renal failure.

Aetiology of secondary hypertension

• Renal: Acute or chronic disease, renovascular disease and volume overload (especially dialysis patients).
• Endocrine: Cushing's syndrome, phaeochromocytoma, hyperaldosteronism, hyperthyroidism, acromegaly.
• Neurological: Raised intracranial pressure.
• Diabetes Mellitus: Both Type I and II patients are commonly hypertensive.
• Coarctation of the Aorta.
• Respiratory: Obstructive sleep apnoea.
• Drugs: NSAIDs, steroids, sympathomimetics including non-prescription drugs, alcohol, liquorice, cocaine, erythropoietin, cyclosporin. Clonidine withdrawal.
• Obesity.

Investigations

• Blood pressure measurement: Systolic BP is more accurately measured than diastolic and correlates more reliably with end-organ damage. Measure lying and standing BP. Blood pressure is variable and so several measurements should be made over a period of days or weeks before deciding on long term treatment. Elderly patients with postural hypotension should not be treated. Consider not only the magnitude of systolic BP but also end-organ damage, cardiovascular risk, and side-effects of treatment. Whitecoat hypertension in hospital patients is very common and if there is uncertainty consider a 24 hour ambulatory BP.
• CBC and blood film for microangiopathic changes.
• ECG and CXR.
• Urinalysis (diptest for proteinuria/haematuria, microscopy for cells and casts).
• Na, K, Cl, creatinine, glucose, TFTs.
• Other tests for secondary causes (e.g., if patient <40 years, has resistant hypertension, or has clinical features that suggest a secondary cause):
  • Phaeochromocytoma: obtain a 24 hour urine for catecholamines and metanephrines (into an acid bottle) or blood for plasma metanephrines (4 mL blood into green lithium heparin tube).
  • Hyperaldosteronism: aldosterone-renin ratio. ACE-inhibitors, AT2 blockers and thiazide diuretics can falsely lower the aldosterone-renin ratio.
  • Cushing's syndrome: 24 hour urine cortisol or low dose overnight dexamethasone suppression test.
  • Renal disease: renal ultrasound for renal size and calcification.
  • Renal artery stenosis: renal MRA or CT angiogram. Vascular intervention is generally only appropriate in younger patients with fibromuscular dysplasia.

Management of Acute Hypertensive Crisis

Monitor blood pressure frequently:

• The excessive use of powerful IV antihypertensive agents may lead to severe cerebral and myocardial insufficiency. Gentle reduction over hours and days enables compensatory vasodilatation and cardiovascular changes to develop and decreases possibility of end organ damage.
• Hypertensive encephalopathy in adults is usually associated with systolic BP >200 mm Hg and diastolic >130 mm Hg but can occur at lower levels if there has been a rapid rise in pressure. Aim to reduce diastolic to around 100 mm Hg only. Oral therapy is generally best but patients with evidence of hypertensive encephalopathy (confusion, restlessness, convulsions, hypoventilation, papilloedema) require IV treatment. Consider admission to ICU or CCU.
• Oral therapy - a calcium antagonist (e.g., felodipine 2.5 mg) or an alpha-antagonist (e.g., doxazosin 1 mg) can be used. Alternatively captopril 6.25 mg PO may be used but should be avoided in the presence of hyponatraemia. Labetalol gives combined alpha- and beta-blockade and may be used if no contraindications to beta-blockade (200 mg PO stat then repeat as required up to 1200 mg daily). Avoid a beta-blocker alone if phaeochromocytoma is a possibility. In this situation, labetalol is generally a good choice.
• IV therapy - for true acute hypertensive encephalopathy, i.e., sudden severe rise in diastolic blood pressure, give a labetalol infusion. Add 500 mg (100 mL) of labetalol to 400 mL sodium chloride 0.9% giving a concentration of 1 mg/mL. Start infusion at 2 mg/min (120 mg/hour). The usual dose needed to control BP is from 50 to 200 mg/hour. An alternative is nitroprusside 100 mg in 500 mL 5% glucose, starting at 0.5 microgram/kg/min and titrating against BP. Only given in the CCU or ICU.

Note:

• Do not treat acute cerebrovascular accidents with IV therapy - oral therapy is best as this will result in a slower reduction in blood pressure and preserve cerebral autoregulation. Refer to Acute Management of Ischaemic Stroke.
• If hypertension is associated with acute LVF or volume overload IV frusemide should be used along with an ACE inhibitor or an angiotensin II receptor antagonist (e.g., losartan).
• Phaeochromocytoma, if suspected, requires alpha-blockade (phenoxybenzamine) or the combination of alpha- plus beta-blockade (e.g., labetalol). Avoid beta-blocker monotherapy as it may cause paradoxical hypertensive crisis via unopposed alpha adrenergic activity.
• Plasma sodium gives some index of volume depletion and activity of the Renin-Angiotensin-Aldosterone system (RAAS) in hypertension. A low sodium usually indicates low circulating volume and high RAAS activity. The use of ACE inhibitors may produce profound hypotension in this situation.
• If hypertension is associated with withdrawal of clonidine or other centrally acting drugs used in hypertensive treatment, avoid giving a beta-blocker alone. Stopping clonidine may induce a phaeo-like state which is exacerbated by giving a beta-blocker. Labetalol is recommended as it provides alpha- and beta-blockade.

Topic Code: 1338