• Note that it is not the absolute BP level that dictates the need for intervention, but rather the threat to organ dysfunction

Non-life threatening asymptomatic hypertension management overview

  1. Recheck manual BP/different arm
  2. Check for end-organ damage
  3. PRN anti-hypertensives if any or once off dose of existing anti-hypertensives if applicable
  4. Amlodipine/GTN patch

Phone Call/Presentation Questions

  • How high is the BP and what has it been previously?
  • What was the reason for admission?
  • Is the patient pregnant? ⇒ pre-eclampsia
  • Does the patient have symptoms suggestive of a hypertensive emergency?
    • Sudden onset chest or back pain ⇒ aortic dissection
    • Chest pain, arrhythmia or dyspnoea ⇒ Acute Coronary Syndromes and or Acute Pulmonary Oedema
    • Sudden headache, vomiting, confusion, seizure ⇒ SAH or hypertensive encephalopathy
  • What antihypertensive medication has the patient been taking?
  • Is the patient taking a MAOI antidepressant

Instructions Over the Phone

  • If features of hypertensive emergency or pregnant:
    • Ask the nurse to stay by the patient’s bedside and get help from additional nursing staff
    • Administer oxygen to maintain saturation >94%
    • Attach ECG and pulse oximetry monitoring to the patient
    • Request an IV trolley at the patient’s bedside with a selection of cannulae ready for insertion if not already in place
    • If asymptomatic and no abnormal clinical signs, ask the nurse to check the BP again in 10 minutes and call you back with the result
    • Ensure that the patient’s regular antihypertensive medication has not been missed recently
  • Hypertension associated with acute end-organ damage needs to be seen immediately (hypertensive emergency)
  • Hypertension in an asymptomatic patient does not need to be assessed immediately irrespective of how high the BP is; the BP can be safely brought under control over the following hours or days1

Common Causes (Corridor Thoughts)

  • Essential Hypertension
    • Especially outpatient anti-hypertensives being withheld
  • Secondary hypertension
    • Obstructive uropathy, renal artery stenosis, chronic pyelonephritis
    • Glomerulonephritis, diabetic renal disease, polycystic kidney disease
    • Endocrine disease such as Cushing’s syndrome, Conn’s syndrome, acromegaly, thyrotoxicosis, myxoedema
    • Autoimmune disease such as SLE or scleroderma
  • Medications
    • Corticosteroids, oral contraceptive pill, NSAIDs
    • Serotonin syndrome
    • Neuroleptic malignant syndrome
  • Catecholamine related
    • Phaeochromacytoma
    • Drug overdose (especially cocaine, amphetamines, ecstasy)
  • Medication withdrawal
    • Abrupt withdrawal from a beta-blocker, clonidine or ACE inhibitor resulting in a rebound hypertensive crisis
  • Drug interaction
    • MAOI antidepressant in combination with a sympathomimetic or other psychoatcive drug or a food containing tyramine (e.g. cheese or wine)
  • Neurogenic
    • Anxiety (e.g. white coat hypertension, unexpected/distressing hospital admission)
    • Raised intracranial pressure (e.g. Cushing’s reflex of hypertension and bradycardia)
    • Cerebral ischaemia (e.g Stroke)
    • Autonomic dysreflexia (e.g. following high spinal cord injury)
  • Other
    • Preeclampsia
    • Coarctation of the aorta
    • Polycytheaemia
    • Hypercalcaemia
    • Hyperparathyroidism
    • Sleep apnoea
    • Hyperactive delirium
  • Other miscellaneous that cause transient ↑ BP: pain, bladder distension, alcohol or nicotine withdrawal, agitation and anxiety

Assessment

NOTE

It is important to distinguish hypertension as the complication of a suspected disease from the aetiologies of hypertension and importantly not mutually exclusive

End of Bed

  • The initial appearance often undermines the situation; even a patient with hypertensive encephalopathy may look deceptively well

A → E Assessment

  • Blood pressure?
    • Retake the blood pressure in both arms (lower pressure in one arm can indicate aortic coarctation)
  • Heart rate?
    • Bradycardia and hypertension in a patient not on beta-blockers ⇒ ? ↑ICP
    • Tachycardia and hypertension ⇒ catecholamine related cause
  • Respiratory rate?
    • Dyspnoea may indicate pulmonary oedema with acute LVF → listen at lung bases for confirmatory basal crackles

Immediate Management

  • If acutely symptomatic or suggestive of a serious cause:
    • Call for senior help
    • Oxygen to maintain the saturation >94%
    • Attach cardiac monitoring and pulse oximeter to the patient
    • Establish IV access
    • Acute lowering of the BP may be required but only when critical hypertensive emergency is diagnosed
      • The choice of antihypertensive agent otherwise depends on cause of the hypertension, age and medical history

Selective History and Chart Review

  • Signs of end-organ damage indicating a hypertensive emergency?
    • Sudden onset tearing chest or back pain ⇒ Aortic Dissection
    • Focal weakness or sensory symptoms ⇒ Aortic Dissection
    • Shortness of breath, orthopnoea ⇒ Acute Pulmonary Oedema
    • Chest pain ⇒ myocardial ischaemia
    • Sudden headache, confusion ⇒ Subarachnoid haemorrhage
    • Headache, nausea and vomiting, confusion, blurred vision ⇒ Hypertensive encephalopathy
  • Does the patient have a history of hypertension or any risk factors for hypertension?
    • Ask specifically about previously diagnosed renal, autoimmune or endocrine disease, amphetamine or cocaine use, steroid therapy or progressive uraemia (renal hypertension)
  • Was the patient taking antihypertensive medications prior to coming to hospital?
    • Prescribed antihypertensive agents
      • Also consider over-the-counter remedies containing ephedrine, liquorice, St John’s wort
    • Check medication chart to ensure the patient’s normal antihypertensive medications have been charted
    • Discontinuation of an antihypertensive medication often happens at admission → look back in the chart or for a GP’s letter
  • Charts
    • Observation chart
      • Check previous BP measurements and confirm that is abnormally high for the patient (check modifications)
      • Decide whether there has been a sudden or slow change
      • Check the HR (is the hypertension associated with tachycardia or bradycardia)
    • Medication chart
      • Check for prescribed agents that cause hypertension:
        • Corticosteroid
        • Amphetamine derivative (usually prescribed for appetite suppression or narcolepsy)
        • NSAIDs
        • Nasal decongestants (e.g. pseudoephidrine within 14 days of a MAOI)
        • Oral contraceptive pill
        • MAOI

Examinations

ExaminationNotes
VitalsRepeat now and check BP in both arms
MentalAgitation, confusion ⇒ ↑ ICP, SAH, hypertensive encephalopathy
FundoscopyAssess fundi for hypertensive changes (arteriolar narrowing, flame shaped haemorrhages near the disc, exudates and ischaemic changes ‘cotton wool spots’)
Papilloedema is a bad sign as it indicates hypertensive encephalopathy with cerebral oedema
Severe hypertension may not show marked encephalopathy or papilloedema but will usually show retinal haemorrhages or exudates
RespTachypnoea, crackles, pleural effusion ⇒ APO
CardiovascularS3 gallop, elevated JVP ⇒ LVF and biventricular Heart Failure
Absent pulse, new murmur ⇒ Aortic Dissection
NeuroHyperreflexia, clonus, headache and visual disturbances ⇒ pre-eclampsia, hypertensive encephalopathy
Focal neurological defecits ⇒ Aortic Dissection, late sign of hypertensive encephalopathy

Investigations

  • Bedside
    • ECG
    • Urinalysis - Urinary beta-hCG in women of childbearing age (pre-eclampsia) - Proteinuria (pre-eclampsia, nephrotic syndrome, glomerulonephritis) - Haematuria (renal hypertension, glomerulonephritis, nephritic syndrome)
  • Bloods
    • FBC (polycythaemia, anaemia with chronic renal disease)
    • U&E to determine renal function (cause or effect of hypertension)
    • LFTs including urate (pre-eclampsia)
  • Imaging
    • CXR may show
      • Cardiomegaly
      • Evidence of heart failure
      • Widened mediastinum

Specific Management

NOTE

  • Overly aggressive treatment may cause syncope, cortical blindness with occipital stroke, myocardial ischaemia. Do not treat the BP reading, only treat the complication(s) associated with it
    • Typically reduce by 10-20% within first hour and another 5-15% within the next day
  • Severe hypertension (SBP>180 mmHg) is common in hospitalised patients and usually has no features of a hypertensive emergency and a high reading alone does not require urgent treatment
  • Isolated hypertension
    • Exclude end-organ dysfunction: history, examination, urinalysis, ECG, renal function
    • Identify precipitating cause:
      • Non-compliance, incorrect dose, drug interaction
      • Secondary cause (as outlined earlier)
    • Gain control gradually over 48 hours or more using oral antihypertensive medications:
      • Review the patient’s current antihypertensive treatment and consider in dose or one-off dose making a clear note in the patient’s chart
      • A decision to use a new agent can usually await the patient’s regular medical care team (i.e. don’t change much on an overnight/on call shift) but can consider among: beta-blockers, diuretics, ACE inhibitors, ARBs, and CCBs
        • Amlodipine 5mg or GTN patch 5mcg or 10mcg instructing nursing staff to check BP every 30 minutes and remove patch when SBP <100
        • Can also consider Hydralazine 12.5mg PRN for hypertension if already on amlodipine
  • Aortic Dissection Management

Hypertensive Encephalopathy

  • Arrange an urgent CT brain scan to exclude alternative causes of confusion (e.g. SAH, space-occupying lesion, intracranial infection or stroke) and consider postictal state or non-convulsive status epilepticus
  • Look for evidence of renal disease
    • Check for proteinuria on urinalysis and send a sample for microscopy
  • Look for retinal haemorrhages, exudates or papilloedema on fundoscopy
    • If present, the BP should be carefully lowered over the next 2-4 hours; call for senior help
  • Aim to initally reduce the MAP by 25% or for a DBP of 100-110 mmHg within the first 24 hours
    • Start oral therapy:
      • Atenolol 50mg, labetalol 100mg, amlodipine 5-10mg or felodipine sustained-release 5-10mg
    • If unsuccessful, give hydralazine 5-10mg slow IV boluses every 15-30 minutes
    • If still unsuccessful, arrange for admission to the ICU
      • In ICU start sodium nitroprusside 0.25-10 mcg/kg/min IV with intra-arterial BP monitoring
  • Once controlled, the usual medical team can continue oral therapy to maintain satisfactory BP control

Catecholamine Crisis

  • Consider other presentations with sudden hypertension, headache, diaphoresis, anxiety, palpitations, nausea or abdominal pain which are more likely than phaeochromocytoma:
    • Cocaine, ecstasy and amphetamine misuse
      • In cocaine-induced hypertension, use high-dose titrated benzodiazepines such as diazepam 0.1-0.2mg/kg or midazolam 0.1mg/kg IV
        • Check ECG and measure troponin to exclude myocardial damage
    • Abrupt antihypertensive medication withdrawal (clonidine)
    • Interaction between MAOI and tyramine-containing foods (e.g. cheese or wine) and/or sympthaomimetic or other psychoactive drugs
      • Call senior and transfer to ICU/CCU
      • Phentolamine or nitroprusside may be used by beta-blockers should be avoided because of the risk of unopposed alpha stimulation causing increased BP
  • If phaeochromocytoma suspected, call your senior and transfer the patient to the ICU/CCU for ECG and intra-arterial BP monitoring followed by alpha-adrenergic blockade

Pre-eclampsia and Eclampsia

  • The treatment of choice near term is immediate delivery of the baby and magnesium sulfate IV. Call for senior help including the obstetric team, and commence magnesium for any complications:
  • Give magnesium sulfate 4 g IV over 10–15 minutes, followed by maintenance infusion 1 g/hour continued for at least 24 hours after delivery.
  • Magnesium sulfate does not significantly lower the BP. Therefore, other drugs such as hydralazine or labetalol are given according to local practice.
  • Diuretics are avoided as the patient is already volume-depleted from an activated renin–angiotensin system, despite being hypertensive.

Sources

  1. FRCEM AFTBAFFF, FFSEM MCMMbcF, FACEM ACMMc. Marshall & Ruedy’s On Call: Principles & Protocols. 3rd edition. Elsevier; 2016. Chapter 19 Hypertension
  2. Acute Hypertension - Strong Medicine | Youtube

Footnotes

Footnotes

  1. According to On Call