Hypertension (HTN) in the ward setting generally refers to severe blood pressure (BP) elevations (SBP >180mmHg and/or DBP >110mmHg) that cause or increase the risk of end-organ damage.
Initial evaluation aims to differentiate patients into the three categories defined below. These categories guide both the choice and the urgency of treatment. True hypertensive emergencies are uncommon and overzealous reduction of an elevated blood pressure may cause more harm than good. (1)
Hypertensive Emergency – BP > 180/110 with new or worsening end-organ damage. (1,4)
Hypertensive Urgency – BP > 180/110 without acute end-organ damage seen in hypertensive emergencies but with significant risk factors (see Box. 1) OR symptoms of hypertension (i.e headache, dizziness) (1,4)
Severe Asymptomatic Hypertension – BP > 180/110 with no symptoms of hypertension and no evidence of acute end-organ damage. (1,4)
|Symptoms||Acute End-organ dysfunction [NB1]||Management|
|Severe Asymptomatic Hypertension||Not present||Not present||If persistent, aim to reduce BP to safe level (usually < 160 systolic) over 1-2 days with oral agent. F/u with primary care within 1 week.|
|Hypertensive Urgency||✓||Mild/mod non-acute organ dysfunction may be present [NB2]||Reduce BP to safe level over several hours using oral/topical agent.|
|Hypertensive Emergency||✓||✓||IMMEDIATE LIFE THREATEscalate to senior staff.BP must be lowered over minutes to hours with parenteral medications in an intensive care setting. Avoid lowering BP by more than 25% in the first 2 hours.|
|[NB1] Acute end-organ damage or dysfunction may include acute pulmonary oedema, acute aortic dissection, hypertensive encephalopathy, papilledema or cerebrovascular haemorrhage.|
[NB2] e.g. chronic heart failure, ischaemic heart disease, chronic kidney disease, previous stroke/TIA. (Presence confers increased risk of acute end-organ dysfunction)
Table 1. Based on Table 3.6 from eTG complete (1)
- There is little evidence to guide the management of HTN in hospitalised patients. The benefit of aggressive BP reduction in patients without acute end-organ dysfunction is uncertain. (2)
- Conversely, rapid BP lowering may precipitate renal, cerebral or coronary ischaemia as well as increase risk of falls – especially in elderly patients. (3,4)
- Check that elevated BP is real by measuring in both arms using an appropriately sized manual BP cuff.
- Consider common causes of elevated BP in hospitalised patients (e.g pain, missed regular antihypertensive dose) before instituting antihypertensive pharmacotherapy.
- The presence of acute end-organ dysfunction in a patient with severe hypertension is a medical emergency requiring immediate escalation.
- Involve senior clinicians in special populations including pregnant women, spinal cord injuries, post stroke. Do not use this guideline in these patient groups.
- Consider risk factors and clues for secondary hypertension and investigate appropriately (clinical indicators of secondary hypertension)
It is vitally important to organise adequate follow-up with primary care to review chronic HTN management. HTN is a significant and modifiable risk factor for many chronic diseases.
- Hypertension > 180/110 will generally require a rapid review (attend within 15 minutes).
- A phone call/message to clarify pertinent features (i.e is the patient symptomatic?) may be sufficient to further stratify urgency of physical review and management.
Box.1 Consider more prompt review if factors present that increase the risk of acute end-organ dysfunction (1,4)
Extreme blood pressure elevation (> 220/140 mmHg)Patient requiring tight blood pressure control (recent vascular procedure, known aneurysm, aortic dissection)Patient with abnormal coagulation (Recent or imminent fibrinolysis, anticoagulant or antiplatelet therapy, coagulopathy)Presence of mild/mod non-acute organ dysfunction (Heart failure, ischaemic heart disease, chronic kidney disease, history of stroke/TIA )
Life-threatening conditions associated with marked increase in BP (5)
- Aortic Dissection
- Myocardial infarction
- Acute Pulmonary Oedema
- Subarachnoid Haemorrhage
- Ischaemic stroke
- Raised ICP (Cushing’s reflex of hypertension and bradycardia)
- Malignant Hypertension/Hypertensive Encephalopathy*
- Acute kidney injury
- Catecholamine crisis (Pheochromocytoma/sympathomimetic overdose)
*Hypertensive Encephalopathy – severe hypertension with headache, vomiting, visual disturbance, mental status changes, seizure, and papilloedema. (Most often due to secondary hypertension)
Causes of hypertension (5,6)
- Essential Hypertension
- Undiagnosed chronic hypertension
- Inadequate or poor adherence with treatment
- Incorrectly charted medications
- Secondary Hypertension
- Renal artery stenosis / thrombosis
- Coarctation of the aorta
- Mineralocorticoid excess
- Cushing’s syndrome
- Renal parenchymal disease
- Obstructive sleep apnoea
- Other transient precipitants
- Anxiety and pain
- Bladder distension
- White coat hypertension
- Neurological disorders (increased ICP, quadriplegia, dysautonomia)
- Medications (NSAIDs, corticosteroids, oestrogens)
- Drug overdose (cocaine, amphetamine, ecstasy)
- Medication withdrawal (ETOH, beta-blocker, clonidine or ACE-inhibitor)
- Drug interactions (MAOI antidepressant)
Clinical features (5) #
Box.2 Red Flags (4)
Acute head injury/trauma Generalised neurological symptoms (agitation/delirium/seizures) Focal neurological symptoms consistent with stroke Acute dyspnoea Nausea/vomiting Chest pain Acute severe back pain Recent drug withdrawalDecreased urine outputPregnancy (this guideline should NOT be used for this population)Spinal cord injury (autonomic dysreflexia)
- Determine if symptoms are present (i.e headache, dizziness)
- Confirm absence of red flags (Box 2)
- Review current antihypertensive management
- Check medication adherence / correctly charted regular antihypertensives
- Check previous blood pressure trends during admission. Previously high blood pressure without concern is unlikely to require urgent investigation and management.
Examination (Focus on excluding end-organ dysfunction)
- Signs of myocardial ischemia/infarction
- Signs of aortic dissection (pulse/BP differential, new aortic regurgitation)
- Signs of decompensated cardiac failure
- Mental status change, decreased GCS, seizures
- Focal neurological deficits
- Papilloedema, retinal haemorrhages and/or exudates
Initial investigations (4, 5)
|ECG||Exclude left ventricular hypertrophy or ischaemic changes|
|UEC||Renal impairment may be a cause or a consequence of hypertension|
|Urinalysis||Proteinuria, microscopic haematuria, red blood cells, and hyaline casts in urine suggests a renal cause. (7)|
Further investigations (4, 5)
|Troponin||If chest pain and cardiovascular risk factors|
|Chest X-ray||Useful to screen for pulmonary oedema, left ventricular hypertrophy, and aortic dissection. (7)|
|Non-contrast CT-brain||If history/exam suspicious for intracranial pathology|
|Thoracic CT or TOE||If history/exam suspicious for aortic dissection|
|B-HCG||In woman of child-bearing age to rule out pregnancy|
|Secondary hypertension screen||If there are clinical indicators of secondary hypertension, consider additional investigations (see link).|
Management – acute end-organ dysfunction #
Hypertensive Emergency (1, 4)
- STEP 1: Initiate MET call (if in ward setting)
- STEP 2: Immediately escalate to senior registrar/consultant and inform ICU/HDU
- STEP 3^: Commence frequent NIBP monitoring at least every 5 minutes
- STEP 4^: Commence neurological observations
- STEP 5: Gain IV access
- STEP 6*: Commence IV antihypertensive as per senior registrar/consultant instructions.
|These medications should only be given in the presence of a senior/ICU colleague|
*Hydralazine 1 mg IV bolus, repeated every minute as required up to a maximum total dose of 5 mg OR*Metoprolol Tartrate 1 mg IV bolus, repeated every minute as required up to a maximum total dose of 5 mg
- STEP 7: Ensure transfer of care to appropriate setting for invasive BP monitoring and antihypertensive infusion (ED/ICU/CCU).
Management – NO acute end-organ dysfunction #
Hypertensive Urgency (1,4)
- STEP 1: Document absence of acute end-organ dysfunction
- STEP 2: Document blood pressure target and rate of blood pressure reduction. Aim for reduction in BP to 160/110mmHg over several hours. (no more than 25 to 30 percent lower than the baseline blood pressure) (2)
- STEP 3^: Commence 2 hourly BP monitoring
- STEP 4: Correct any readily reversible underlying causes. (e.g. pain, anxiety, missed anti-hypertensives, drug withdrawal, fluid overload, recent institution of medication associated with hypertension).
- STEP 5: Administer STAT antihypertensive. In patients already on antihypertensive therapy, earlier dosing of regular medications is a suitable alternative. STAT dose can be repeated or an alternative agent added if required. This should be done with consideration of the onset and duration of action of each drug.
|Amlodipine 5mg PO|
Onset: > 2 hours, Peak: 6-12 hours, Duration: 24 hours (8)ORPrazosin 1-2mg POOnset: 2 hours, Peak: 2-4 hours, Duration: 10-24 hours (9)ORGlyceryl Trinitrate Patch 5-15mg/24 hours TOP. Patch can be removed if there is an undesirable drop in BP.Onset: Upto 30 minutes, Peak: 2 hours (10)
Note: Some antihypertensives may interfere with the interpretation of the aldosterone-renin ratio. If secondary hypertension is suspected, discuss with a renal physician before instituting treatment.
- STEP 6a: If BP unchanged or increasing, reassess patient, discuss with registrar
- STEP 6b: If BP decreasing, recommence regular BP monitoring interval. Ensure adequate follow-up with primary care within a week for review of chronic hypertension management.
Severe Asymptomatic Hypertension (1,4)
- STEP 1: Document absence of acute end-organ dysfunction and symptoms
- STEP 2: Allow a period of observation with repeated measurement to see if BP settles without intervention.
- STEP 3: Correct any readily reversible underlying causes (e.g. pain, anxiety, missed anti-hypertensives, drug withdrawal, fluid overload, recent institution of medication associated with hypertension).
- STEP 4: Consider the need to start or add new therapy with standard BP-lowering drugs. This does not need to occur urgently and JMOs should consult with staff who are more experienced or familiar with the patient before prescribing a new drug. (1)
- STEP 5: Reassure patient and nursing staff that isolated hypertension without end-organ dysfunction does not require immediate resolution and gradual reduction is safest.
- STEP 6: Ensure adequate follow-up with primary care within a week to review chronic hypertension management. This is the most important management step for asymptomatic hypertension.
Additional Notes: Management of HTN associated with specific clinical conditions #
Acute Pulmonary Oedema
- Glyceryl trinitrate (GTN) is the preferred agent to reduce HTN associated with acute pulmonary oedema (1, 5) (see guideline on Acute Pulmonary Oedema)
- Avoid aggressive BP management in acute phase of stroke as it may reduce cerebral perfusion and worsen ischaemia. (1) (see guideline on Stroke)
- In a patient with aortic dissection it is important to give a beta blocker before giving a vasodilator to reduce BP (1). (see guideline on Aortic Dissection) Reflex tachycardia in response to vasodilation has the potential to increase shear stress on the aorta.
- Adrenergic crisis is most commonly precipitated by stimulant overdose (e.g cocaine, amphetamine) or pheochromocytoma. (1)
- A direct alpha blocker such as phentolamine is the preferred agent to lower BP in an adrenergic crisis. (1)
- Beta blockers must not be used alone. Unopposed alpha stimulation may paradoxically increase BP. (1)
- Benzodiazepines can be a useful adjunct to BP-lowering therapy as they can reduce catecholamine-induced tachycardia and hypertension. (1)
- eTG complete [Internet]. Melbourne (Vic): Therapeutic Guidelines Ltd; 2021. Urgent control of elevated blood pressure [cited 2021 Aug 31]. Available from: https://tgldcdp-tg-org-au.ezproxy-f.deakin.edu.au/viewTopic?topicfile=urgent-control-severe-bp-elevation&guidelineName=Cardiovascular
- Varon J, Elliott WJ. Uptodate [Internet]. 2021. Management of severe asymptomatic hypertension (hypertensive urgencies) in adults; [cited 2021 Aug 31]. Available from: https://www.uptodate.com/contents/management-of-severe-asymptomatic-hypertension-hypertensive-urgencies-in-adults
- Rastogi R, Sheehan MM, Hu B, Shaker V, Kojima L, Rothberg MB. Treatment and Outcomes of Inpatient Hypertension Among Adults With Noncardiac Admissions. JAMA internal medicine. 2021 Mar 1;181(3):345-52.
- South Eastern Sydney Local Health District. Management of Hypertension in the SESLHD Ward Settings. New South Wales, Australia. NSW Government; 2018 Sep [cited 2021 Aug 31]. Available from: https://www.seslhd.health.nsw.gov.au/sites/default/files/documents/SESLHDGL068.pdf
- Marshall S, Ruedy J. On Call: Principles and Protocols (3rd Edition). In: Brown AF, Cadogan M, Celenza A, editors. On Call: Principles and Protocols. Pennsylvania W.B. Saunders & Company
- Mansoor A . Frameworks for internal medicine . Philadelphia, PA: Wolters Kluwer, 2019.
- Nadar S, Lip GYH. Assessment of hypertension. In BMJ Best Practice [Internet]. London: BMJ Publishing Group; c2021. [updated 2021 July; cited 2021 Aug 31]. Available from: BMJ Best Practice.
- MIMS Online [Internet]. Sydney: MIMS Australia; c2010. MIMS Full Prescribing Information ‘Amlodipine APOTEX’ [cited 2021 Sep 21]. Available from: https://www.mimsonline.com.au
- Minipress, Prazin (prazosin) dosing, indications, interactions, adverse effects, and more [Internet]. Reference.medscape.com. 2021 [cited 21 September 2021]. Available from: https://reference.medscape.com/drug/minipress-prazin-prazosin-342352#10
- Ambulance Victoria (AU). Clinical practice guidelines ambulance and MICA paramedics. Medications: Glyceryl Trinitrate [Internet]. Version 5.0.1 Doncaster (AU): Ambulance Victoria; 2021 [cited 2021 Nov 30]. 433 p. Available from: https://www.ambulance.vic.gov.au/paramedics/clinical-practice-guidelines/.
Reviewing Consultant/Senior Registrar
Dr William Semple
Dr Adam Steinberg