Hypertensive Emergency

Last Updated on by frcemuser

Hypertensive emergency is defined as severely elevated blood pressure (BP) associated with new or progressive target organ dysfunction (e.g. signs of papilloedema or retinal haemorrhage, or the presence of clinical conditions such as acute coronary syndromes, acute aortic dissection, acute pulmonary oedema, hypertensive encephalopathy, acute cerebral infarction, intracerebral or subarachnoid haemorrhage, eclampsia, or rapidly progressing renal failure). Although the absolute value of the BP is not as important as the presence of end-organ damage, the systolic BP is usually >180 mmHg and/or the diastolic BP is >120 mmHg. Hypertensive urgency is defined as a BP above 180/120 mmHg but the patient is stable and there is no organ dysfunction.

Causes

Essential hypertension that is either undiagnosed or inadequately treated is a common cause of hypertensive emergency. Another common cause is secondary and resistant hypertension.

Systemic disorders that can lead to a presentation of hypertensive emergency include:

  • Renal disease (underlying chronic disease, renal artery stenosis, acute glomerulonephritis, collagen-vascular diseases, kidney transplantation)
  • Neurological (head trauma, spinal cord injury, autonomic dysfunction)
  • Respiratory (obstructive sleep apnoea)
  • Immunological (scleroderma, vasculitis)
  • Endocrine (primary hyperaldosteronism, phaeochromocytoma, thyrotoxicosis, Cushing’s syndrome, acromegaly, hyperparathyroidism, carcinoid tumour, congenital adrenal hyperplasia, or renin-secreting tumour)
  • Coarctation of the aorta
  • Pregnancy-related pre-eclampsia, HELLP syndrome, and eclampsia

Diagnosis

The key to diagnosis of hypertensive emergency is a rapid but thorough evaluation. The main areas of focus should be the neurological, cardiovascular, and renal systems.

Clinical features that may identify specific organ compromise include:

  • Neurological compromise; for example, blurry vision, dizziness, headache, seizures, change in mental status from baseline, dysphagia, loss of sensation, paraesthesia, or loss of movement
  • Cardiac compromise; for example, chest pain, shortness of breath, diaphoresis, orthopnoea, paroxysmal nocturnal dyspnoea, palpitations, or oedema
  • Renal compromise; for example, decrease in urine output

Physical examination:

  • BP readings should be taken from both arms and readings repeated after 5 minutes to confirm. If there is a more than 20 mmHg pressure difference between arms, aortic dissection should be considered.
  • A fundoscopic examination should be performed, looking for the presence of arteriolar spasm, retinal oedema, retinal haemorrhages, retinal exudates, papilloedema, or engorged retinal veins.
  • A rapid bedside neurological examination is also required, including testing cognition, cranial nerve function, dysarthria, motor strength, gross sensory function, upper extremity pronator drift, and gait.
  • Cardiopulmonary status should be assessed, examining in particular for the presence of new murmurs, friction rubs, additional heart sounds, lateral displacement of the apex beat, jugular venous distension, carotid or renal artery bruits, rales, and lower extremity oedema.

Investigations

  • Baseline blood and urine samples must be collected prior to administration of treatment, including:
    • Blood chemistry panel, including creatinine and electrolytes
    • Full blood count, including peripheral blood smear
    • Urinalysis with microscopy.
  • In some circumstances, the following may also be indicated:
    • Cardiac enzymes and/or brain natriuretic peptide, if acute coronary syndrome or acute heart failure is suspected
    • A urine drug screen, if illicit drug use is suspected
    • Plasma renin activity and aldosterone levels, if primary aldosteronism is suspected (e.g. in patients with diastolic hypertension with persistent hypokalaemia and metabolic alkalosis)
    • Plasma renin activity before and 1 hour after 25-mg captopril is administered, if renovascular hypertension is suspected (e.g. in patients with severe hypertension who have abdominal bruits and/or unexplained renal deterioration with angiotensin-converting enzyme (ACE) inhibitor treatment)
    • Spot urine or plasma-free metanephrine levels, if phaeochromocytoma is suspected (e.g. in patients with hypertension and palpitations, headaches and/or diaphoresis)
  • Further investigation:
    • Electrocardiogram (ECG) and chest x-ray should be strongly considered. If aortic dissection is considered possible, an urgent thoracic CT scan with contrast or a transoesophageal echocardiogram should also be obtained.
    • Renal angiography is the gold standard for diagnosing renal artery stenosis but is invasive and may not be readily available. Renal ultrasound and Doppler provides a non-invasive functional assessment of the renal arteries when evaluating for renovascular hypertension.
    • If ischaemic stroke or intracranial haemorrhage is suspected (e.g. in patients with decreased consciousness or those with focal neurological deficits), an urgent non-contrast CT scan of the head and/or an MRI should be requested, depending on local availability.

Management

If hypertensive emergency is suspected, treatment should not be delayed while conducting a full diagnostic evaluation.

  • Appropriate facilities
    • Patients with hypertensive emergencies should be admitted to an intensive care unit for continuous monitoring of blood pressure (BP) and target organ damage and for parenteral administration of appropriate therapeutic agent(s).
  • Choice of agents
    • The specific parenteral agents used for treating a hypertensive emergency should be dictated by the end-organ systems that have been damaged, patient comorbidities, and overall clinical condition. Oral therapies are generally discouraged as first-line treatment options.
  • Rate of BP reduction
    • Excessive falls in pressure may precipitate renal, cerebral, or coronary ischaemia and so should be avoided. The general rules are:
      • The initial goal of therapy is to reduce mean arterial BP by no more than 25% (within minutes to 1 hour).
      • If the patient remains stable, further reduce the BP to 160 mmHg systolic and 100-110 mmHg diastolic within the next 2 to 6 hours.
      • If the initial level of reduced BP is well tolerated and the patient is clinically stable, further gradual reductions towards a normal BP can be implemented over the next 24-48 hours.
  • Specific conditions
    • Accelerated (malignant) hypertension, hypertensive encephalopathy or intracranial haemorrhage
      • The term ‘accelerated hypertension’ (also known as malignant hypertension) is a subcategory of hypertensive emergency where severe hypertension occurs with retinopathy of grade III (flame haemorrhages, dot and blot haemorrhages, hard and soft exudates) or grade IV (papilloedema).
      • Hypertensive encephalopathy encompasses the transient neurological symptoms that occur with malignant hypertension, which are usually reversed by prompt treatment and lowering of BP.
      • Labetalol is the first-line treatment for accelerated (malignant) hypertension, hypertensive encephalopathy, or intracranial haemorrhage.
    • Acute ischaemic stroke
      • Treating a hypertensive emergency with an associated acute ischaemic stroke warrants greater caution in reducing BP than in other types of hypertensive emergency. Overly rapid or large reductions of mean arterial pressure (MAP) may decrease cerebral perfusion pressure (CPP) to a level that could theoretically worsen brain injury.
    • Myocardial ischaemia/infarction
      • First-line treatment of hypertensive emergency complicated by myocardial ischaemia or infarction is the combination of esmolol (a selective beta-blocker) plus glyceryl trinitrate (a peripheral vasodilator, which affects venous vessels more than arterial). Esmolol acts to reduce the heart rate and glyceryl trinitrate acts to decrease preload and cardiac output, and increases coronary blood flow.
    • Left ventricular failure and/or pulmonary oedema
      • First-line treatment of hypertensive emergency with left ventricular failure and/or pulmonary oedema is glyceryl trinitrate or clevidipine.
    • Suspected aortic dissection
      • If aortic dissection is suspected in a hypertensive emergency, the BP should be lowered quite aggressively, typically with a target of reducing the systolic BP to <120 mmHg within 20 minutes. Medical therapy aims to both lower the BP and decrease the velocity of left ventricular contraction, so decreasing aortic shear stress and minimising the tendency for propagation of the dissection. First-line treatment choice is beta-blockers, either labetalol or esmolol, administered intravenously. If there is no significant improvement, nitroprusside or nicardipine can be added to the beta-blocker. The beta-blockade should precede vasodilator (nicardipine or nitroprusside) administration to prevent reflex tachycardia and worsen shear stress on the intimal flap.
    • Acute kidney injury
      • Fenoldopam is the first-line treatment choice of hypertensive emergency complicated by acute kidney injury. This drug (a selective peripheral dopamine-1-receptor agonist with arterial vasodilator effects) is particularly useful in renal insufficiency because it acts to both decrease afterload and increase renal perfusion.
    • Hyperadrenergic states
      • If the hyperadrenergic state is due to sympathomimetic drug use, the first-line agents are benzodiazepines, and antihypertensive medications are given only if the BP response is inadequate. In all other clinical situations (e.g. phaeochromocytoma), the first-line treatment choice is phentolamine (which acts by blocking alpha-adrenoceptors) or calcium-channel blockers (clevidipine and nicardipine). A beta-blocker (such as labetalol) can be added after sufficient alpha-adrenoceptor blockade. The administration of a beta-blocker alone is contraindicated, since inhibition of beta-adrenoceptor-induced vasodilation results in unopposed alpha-adrenergic vasoconstriction and a further rise in BP.
    • Severe hypertension in pregnancy (pre-eclampsia and eclampsia)
      • The first-line treatment choices in this situation are intravenous hydralazine or labetalol. Immediate-release oral nifedipine may also be considered first-line therapy, particularly when intravenous access is not available. A guide target in these patients is to maintain a systolic BP of 140-150 mmHg and a diastolic BP of 90-100 mmHg. Magnesium sulfate is not recommended as an antihypertensive agent, but remains the drug of choice for treatment of eclampsia and/or seizure prophylaxis for women with acute-onset severe hypertension during pregnancy and the postnatal period.

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