Hypertensive crisis: quick reference for acute blood pressure lowering

Key message

The distinction that determines management is: is there acute hypertension-mediated organ damage or not?

A single blood pressure value does not define a hypertensive emergency. Even a blood pressure above 220/120 mmHg can occur without acute organ damage. Conversely, a rapid rise in blood pressure from a previously low level can cause organ damage at lower values, for example in pregnancy, acute glomerular disease or scleroderma renal crisis [1,2].

A hypertensive emergency means a markedly raised blood pressure together with ongoing or new organ damage in which immediate, controlled blood pressure lowering can limit the damage. The choice of drug, the target pressure and the rate of treatment are determined by the affected organ function, not by the blood pressure figure alone [2].

A markedly raised blood pressure without acute organ damage should as a rule not be lowered rapidly with intravenous drugs. Restart or optimise oral treatment and ensure follow-up. Rapid lowering can worsen cerebral, coronary and renal perfusion, particularly in patients with long-standing hypertension and a rightward-shifted autoregulation [1,3].

The term hypertensive urgency is best avoided. It implies that an asymptomatic rise in blood pressure must be treated urgently, which is not supported by evidence. The patient may need active treatment and prompt follow-up, but not necessarily acute normalisation in the emergency department [1,3].

Step 1: confirm the blood pressure and stabilise the patient

Immediate assessment

1. Assess airway, breathing, circulation and level of consciousness.
2. Attach ECG, pulse oximetry and repeated blood pressure measurement when a hypertensive emergency is suspected.
3. Insert a peripheral venous cannula.
4. Measure the blood pressure in both arms at the first assessment, particularly in chest pain, back pain or suspected acute aortic syndrome.
5. Use the correct cuff size. A cuff that is too small overestimates the blood pressure.
6. Repeat the measurement after a few minutes' rest, if the patient's condition allows.
7. With titratable intravenous treatment and an unstable course, an arterial line should be considered.

The blood pressure must not be dismissed as caused merely by pain or anxiety. These factors can affect the pressure, but emergency department studies show that raised values often persist after the visit and predict future hypertension and cardiovascular risk [3].

Questions that rapidly change management

Ask specifically about:

• Neurological symptoms: confusion, visual loss, focal neurological signs, seizures, severe or sudden headache.
• Chest pain, back pain, dyspnoea, orthopnoea and new sweating.
• Oliguria, dark urine or rapidly developing swelling.
• Pregnancy, gestational week and recent delivery. Pre-eclampsia can present postpartum.
• Known hypertension and current antihypertensive treatment.
• Missed doses or abrupt withdrawal of a beta blocker, clonidine or another sympatholytic drug.
• Cocaine, amfetamine, other sympathomimetics, herbal remedies and performance-enhancing preparations.
• Monoamine oxidase inhibitors and recent intake of tyramine-rich food or interacting drugs.
• Corticosteroids, calcineurin inhibitors, erythropoietin, tyrosine kinase inhibitors and drugs directed against vascular endothelial growth factor.
• Episodes of headache, palpitations, sweating and pallor that may suggest phaeochromocytoma.
• Systemic sclerosis, kidney disease, autoimmune disease or previous thrombotic microangiopathy.

Antidepressants can affect the blood pressure in several ways. Monoamine oxidase inhibitors can cause a hypertensive crisis through interactions, while venlafaxine and higher doses of bupropion, among others, can raise the blood pressure. Serotonin syndrome can also cause autonomic instability and hypertension [4].

Step 2: look systematically for acute organ damage

Common hypertensive emergencies are acute pulmonary oedema or heart failure, acute coronary syndrome, ischaemic or haemorrhagic stroke, hypertensive encephalopathy, acute aortic syndrome, acute kidney injury and pregnancy-related severe hypertension [1,5].

Baseline investigations in a suspected hypertensive emergency

A suitable baseline set of investigations is:

• Full blood count and platelet count.
• Sodium, potassium, creatinine and estimated glomerular filtration rate.
• Urine dipstick, and where needed quantification of albumin or protein and urine microscopy.
• ECG.
• Troponin in chest pain, dyspnoea, ECG changes or other suspicion of myocardial injury.
• Liver function tests and LDH in pregnancy, suspected haemolysis or multi-organ involvement.
• Haptoglobin, bilirubin, reticulocytes and a blood film in anaemia or thrombocytopenia.
• A pregnancy test in anyone who may be pregnant when pregnancy cannot be reliably excluded.

Chest radiography, natriuretic peptides, echocardiography, CT and MRI are directed by the symptoms and findings. Routine broad testing in entirely asymptomatic patients without suspicion of organ damage has not been shown to improve outcome. The history, repeated correct blood pressure measurements and a targeted examination are central [3].

Fundoscopy still matters

Bilateral retinal haemorrhages or exudates, with or without papilloedema, in the presence of severe hypertension indicate advanced hypertension-mediated vascular damage. Historically this has been called malignant or accelerated hypertension. The retinopathy can resolve relatively quickly after treatment, which makes early examination valuable [6].

A finding of papilloedema or marked retinopathy should lead to active investigation of concomitant cerebral, renal and haematological organ damage. The absence of papilloedema does not, however, exclude a hypertensive emergency.

Step 3: choose the target according to the condition

Overview

The general rule outside the specific exceptions

In hypertensive encephalopathy and several other hypertensive emergencies, a reasonable general rule is:

1. Lower the mean arterial pressure by no more than about 20 to 25 per cent during the first hour.
2. Thereafter lower it gradually towards about 160/100 to 110 mmHg over the following 2 to 6 hours.
3. Once the patient is stable, the pressure can approach the usual treatment target over 24 to 48 hours.

The rule does not apply unchanged in acute aortic syndrome, ischaemic stroke, intracerebral haemorrhage, pregnancy-related severe hypertension or scleroderma renal crisis. These conditions have targets of their own [2,3,7].

Chronic hypertension shifts autoregulation so that the brain and the kidneys can become dependent on a higher perfusion pressure. This is the explanation for why a forceful normalisation within minutes can precipitate cerebral ischaemia, myocardial ischaemia or acute kidney injury [3].

Condition-specific management

Hypertensive encephalopathy and PRES

Hypertensive encephalopathy causes acute or subacute headache, confusion, impaired consciousness, visual disturbance and seizures. Focal neurological deficits can occur, but they require stroke and other structural pathology to be excluded.

PRES, posterior reversible encephalopathy syndrome, is a clinical and radiological syndrome with vasogenic oedema, often parieto-occipital. It occurs in, among other settings, severe hypertension, renal failure, pre-eclampsia, eclampsia, sepsis, autoimmune disease and treatment with immunosuppressive or cytotoxic drugs [8,9].

CT of the brain is performed urgently to exclude haemorrhage and other gross pathology. MRI is more sensitive for PRES and often shows symmetrical changes consistent with vasogenic oedema. A normal CT does not exclude PRES.

Treat with a titratable intravenous drug and lower the mean arterial pressure by about 20 to 25 per cent in the first hour. Avoid large swings in blood pressure. Treat seizures and correct precipitating factors, for example renal failure, eclampsia or drug toxicity. Most patients improve, but intracerebral haemorrhage, cerebral ischaemia, status epilepticus and persistent epilepsy can occur [8,9].

Acute aortic syndrome

Suspect acute aortic syndrome in sudden severe chest, back or abdominal pain, particularly together with syncope, a pulse difference, neurological deficits, aortic regurgitation, limb ischaemia or a blood pressure difference between the arms.

CT angiography of the thorax and usually also the abdomen is the standard investigation in a haemodynamically stable patient. Acute aortic syndrome comprises aortic dissection, intramural haematoma and penetrating aortic ulcer. These conditions have a high mortality and non-specific symptoms, which makes diagnostic delay dangerous [10].

Management must reduce both the blood pressure and the force of left ventricular ejection:

1. Give effective analgesia.
2. Give intravenous beta blockade, usually esmolol or labetalol according to the local protocol.
3. Once rate control has been achieved, a titratable vasodilator can be added if the blood pressure is still too high.
4. Aim for a systolic pressure of 100 to 120 mmHg and a heart rate of around 60/min, provided organ perfusion is preserved [10].
5. Contact a cardiothoracic surgeon immediately in type A. Complicated type B requires urgent vascular surgical or endovascular assessment.

Do not give a pure vasodilator before rate control. Reflex tachycardia and increased contractility can increase the shear stress on the aortic wall.

Acute hypertensive pulmonary oedema

Acute hypertensive pulmonary oedema can develop within minutes through a markedly increased afterload and a redistribution of fluid into the pulmonary circulation. The patient therefore need not be generally fluid overloaded. Only about half of the patients with this phenotype have a clear volume excess [11].

Treatment comprises:

• Sitting the patient up.
• Oxygen in hypoxaemia.
• Early continuous positive airway pressure or another form of non-invasive ventilation in marked respiratory failure.
• Intravenous nitroglycerin with rapid titration according to the local protocol, if there are no contraindications.
• A loop diuretic where there are clinical signs of fluid overload or known fluid retention.
• Simultaneous treatment of the precipitating cause, for example ischaemia, arrhythmia, infection, renal failure or interrupted medication.

Nitroglycerin reduces preload and, at higher infusion rates, also afterload. Intravenous administration gives a rapid and titratable effect. The evidence for very high doses or repeated boluses consists largely of small studies and observational data, so the regional emergency protocol must be followed [12,13].

Furosemide must not be used as a general acute antihypertensive. Its effect on the blood pressure is slower and less predictable. In a euvolaemic or hypovolaemic patient, unnecessary diuresis can worsen renal function and perfusion [3,11].

Nitroglycerin is contraindicated after recent intake of a phosphodiesterase-5 inhibitor and must be used with great caution in right ventricular infarction, severe aortic stenosis, hypertrophic obstructive cardiomyopathy and hypotension [12].

Acute coronary syndrome

In acute coronary syndrome the aim is to reduce myocardial oxygen demand and relieve ongoing ischaemia without lowering the diastolic perfusion pressure too far.

Manage according to the standard acute coronary syndrome protocol. Where there is concomitant hypertension with persistent ischaemia or heart failure, sublingual or intravenous nitroglycerin can be used if there are no contraindications. Intravenous treatment is easier to titrate than repeated oral doses [12].

A beta blocker may be appropriate in tachycardia with a preserved circulation, but must be avoided or given with great caution in acute pulmonary oedema, bradycardia, conduction disturbance, bronchospasm or signs of cardiogenic shock. Do not normalise the blood pressure abruptly. Treatment must be guided by the ischaemia, the heart rate, the chest findings and the perfusion.

Ischaemic stroke without reperfusion treatment

Acute ischaemic stroke is an important exception to the general rule of rapid blood pressure lowering. The ischaemic penumbra may lack functioning autoregulation and be directly dependent on the systemic pressure.

In patients who are not to undergo thrombolysis or thrombectomy, no acute lowering is generally recommended during the first 24 hours if the blood pressure is no more than about 220/120 mmHg and there is no other concurrent indication, for example aortic dissection, acute coronary syndrome, pulmonary oedema or eclampsia. At higher values a cautious reduction, of around 15 per cent during the first 24 hours, may be considered [14].

Randomised trials have not shown an improved functional outcome from routine early blood pressure lowering in ischaemic stroke without reperfusion treatment. Large or rapid falls in blood pressure can be harmful [14].

Ischaemic stroke before thrombolysis or thrombectomy

Before intravenous thrombolysis the blood pressure must be below 185/110 mmHg. After thrombolysis it must be kept below 180/105 mmHg according to the stroke protocol. Intensive lowering well below these limits has reduced the frequency of certain intracerebral haemorrhages in trials but has not improved the overall functional outcome [14].

In thrombectomy, hypotension must be avoided before reperfusion, since collateral flow may be pressure-dependent. After successful reperfusion a lower systolic target may be reasonable, but the optimal target has not been reliably established and must be individualised by the stroke team [15].

Follow the local stroke pathway and the current regional reperfusion protocol. Swedish national thresholds may be updated more quickly than international reviews.

Intracerebral haemorrhage

In spontaneous intracerebral haemorrhage, early, smooth blood pressure lowering can reduce haematoma expansion. For patients with a systolic blood pressure of around 150 to 220 mmHg and without contraindications, a target of around 140 mmHg is often used according to the stroke protocol. Avoid excessive lowering, hypotension and large variations.

A meta-analysis using individual patient data from randomised trials showed that active or intensive blood pressure lowering reduced the risk of both absolute and relative haematoma growth. No definite improvement in functional outcome or mortality was seen in the pooled analysis [16].

The choice of target is influenced by the size of the haemorrhage, the intracranial pressure, the level of consciousness, anticoagulant treatment, renal function and any neurosurgical intervention. Contact the neurologist, the on-call stroke physician or the neurosurgeon according to local procedures.

Subarachnoid haemorrhage

In suspected subarachnoid haemorrhage, urgent neurosurgical or neurological contact is required. Before an aneurysm has been secured, the risk of rebleeding must be weighed against the risk of cerebral hypoperfusion. There is no single well-founded blood pressure target that suits every patient.

Avoid both marked hypertension and hypotension. Give analgesia and antiemetics, treat agitation, and use a short-acting titratable drug if blood pressure lowering is needed. The target is decided together with the responsible neurovascular centre.

Pre-eclampsia and eclampsia

Severe hypertension in pregnancy is usually defined as a blood pressure of at least 160 mmHg systolic or 110 mmHg diastolic, confirmed within about 15 minutes. In pre-eclampsia or after gestational week 20, such a blood pressure must be treated within 30 to 60 minutes to reduce the risk of maternal stroke, heart failure and renal injury [17].

Acute treatment is usually with intravenous labetalol, intravenous hydralazine or oral immediate-release nifedipine according to the obstetric protocol. An initial target of approximately 130 to 150 mmHg systolic and 80 to 100 mmHg diastolic is used in several international guidelines. Too rapid a reduction can impair uteroplacental blood flow [17,18].

Magnesium sulfate is not primarily an antihypertensive drug. It is used to prevent and treat eclamptic seizures and has better documented efficacy than phenytoin or diazepam in eclampsia [17].

Pre-eclampsia does not require proteinuria if other typical organ damage is present. Consider:

• Headache and visual phenomena.
• Epigastric pain or pain below the right costal margin.
• Thrombocytopenia or haemolysis.
• Raised liver function tests.
• Renal failure.
• Pulmonary oedema.
• Neurological symptoms or seizures.

The condition can present after delivery. Recently delivered patients with headache, visual disturbance, dyspnoea or a high blood pressure must therefore be assessed with the same vigilance as pregnant women [17,19].

Phaeochromocytoma and other catecholamine crises

Phaeochromocytoma and paraganglioma are uncommon but can cause a life-threatening catecholamine crisis with a markedly labile blood pressure, tachycardia, sweating, pallor, headache, cardiomyopathy and multi-organ failure.

In a suspected crisis, alpha blockade or titratable vasodilator treatment is used in consultation with intensive care and endocrinology. Beta blockade may be added only after adequate alpha blockade if the tachycardia persists. Pure beta blockade first can leave the alpha stimulation unopposed and cause a further rise in blood pressure [20].

Labetalol has both alpha- and beta-blocking properties but proportionally stronger beta blockade. It must therefore not be used uncritically as the sole first-line agent in a suspected phaeochromocytoma crisis [20].

Cocaine, amfetamine and other sympathomimetics

In sympathomimetic toxicity, agitation, hyperthermia, seizures and ischaemia must be treated in parallel. Benzodiazepines are often the first-line treatment, since they reduce central sympathetic activation, but they do not always normalise the hypertension, the tachycardia or the vasospasm [21].

Where severe hypertension or coronary vasospasm persists, nitroglycerin, a calcium channel blocker or alpha-blocking treatment may be indicated depending on the clinical picture and local toxicological advice. The systematic literature on cocaine toxicity shows limited but overall supportive evidence for benzodiazepines, nitrates and certain calcium channel blockers. Combined alpha and beta blockade has not shown the same clear risk as pure beta blockade, but treatment should be discussed with your national or regional poison control centre in serious toxicity [21].

Do not routinely give a pure beta blocker as the sole initial treatment during marked ongoing sympathomimetic effect.

Acute kidney injury and thrombotic microangiopathy

Severe hypertension can cause endothelial injury, glomerular ischaemia, haemolysis and thrombocytopenia. At the same time, a primary thrombotic microangiopathy can cause both renal failure and severe hypertension. The causal relationship can therefore run in either direction.

Suspect thrombotic microangiopathy in the presence of:

• Microangiopathic haemolytic anaemia.
• Schistocytes on the blood film.
• Thrombocytopenia.
• A raised LDH and bilirubin.
• A low haptoglobin.
• Acute kidney injury.
• Neurological or other ischaemic organ damage.

Start blood pressure control immediately, but investigate in parallel for TTP, complement-mediated thrombotic microangiopathy, pregnancy-related disease, drug-induced disease and other secondary causes. A normal platelet count or the absence of clear haemolysis does not exclude kidney-limited thrombotic microangiopathy [22].

If the platelet count and renal function do not improve despite adequate blood pressure control over the following days, complement-mediated disease must be considered early together with nephrology and haematology. In such cases severe hypertension may be a symptom of the underlying disease [22].

Scleroderma renal crisis

In a patient with systemic sclerosis, particularly early diffuse disease, new-onset hypertension and a rising creatinine must be regarded as possible scleroderma renal crisis. Microangiopathic haemolysis and thrombocytopenia are often present but are not obligatory. About 10 per cent of cases may be normotensive in absolute terms, but the blood pressure has then often risen clearly from the patient's usual low level [23].

Start an ACE inhibitor immediately and titrate according to the specialist protocol. The creatinine may continue to rise despite an improved blood pressure, which is not in itself a reason to stop treatment. The ACE inhibitor should usually be continued even if dialysis becomes necessary, since renal function can recover late [23,24].

Beta blockers should be avoided in scleroderma renal crisis, since a reduced cardiac output and increased peripheral resistance can worsen renal perfusion. Contact nephrology and rheumatology early. The condition still carries a high mortality despite modern treatment [23].

Drugs

Intravenous drugs must be given where continuous monitoring and rapid dose adjustment are possible. The evidence is not sufficient to identify a single agent as best in all hypertensive emergencies. The choice must be made on the basis of the organ damage, the heart rate, cardiac function, renal function, pregnancy and contraindications [3,7].

Nicardipine, clevidipine, labetalol and esmolol are common titratable options internationally. Availability varies between Swedish regions. Nitroprusside is now used more rarely because of its toxicity and the need for intensive monitoring [3,7].

Doses

Doses are not given here. Intravenous antihypertensives are titrated to a condition-specific target, and the availability of agents differs between regions. Follow the local emergency protocol, the Swedish medicines compendium (FASS) and the responsible specialist service.

When there is no acute organ damage

Do not normalise the blood pressure acutely

In a stable patient without acute organ damage, rapid blood pressure lowering in the emergency department has not been shown to improve clinical outcome. It can, however, worsen organ perfusion. Avoid intravenous drugs and rapid-acting oral preparations given merely to obtain a lower figure before discharge [1,3].

A blood pressure of, for example, 220/120 mmHg without acute organ damage is therefore not automatically a hypertensive emergency. It is at the same time a serious finding that requires verification, assessment of adherence, an oral treatment plan and secure follow-up.

Practical management

1. Repeat the blood pressure with the correct cuff and correct positioning.
2. Assess whether symptoms or findings after all suggest organ damage.
3. Treat pain, hypoxia, withdrawal, urinary retention and other concurrent problems.
4. Check the medication list and adherence.
5. Restart missed regular treatment if this is medically appropriate.
6. Consider starting or adjusting long-acting oral treatment, particularly if the patient has no reliable access to primary care.
7. Arrange blood pressure monitoring and medication follow-up, usually within a few days to at most one or two weeks depending on the values, comorbidity and treatment.
8. Check the creatinine and electrolytes after starting or increasing the dose of a drug that affects the renin–angiotensin system or the electrolyte balance.
9. Give clear advice on when the patient should seek emergency care.

Patients who are discharged must understand that the absence of acute organ damage does not mean that the blood pressure is harmless in the longer term. Repeated high values in the emergency department often predict persistent hypertension [3].

Monitoring during acute treatment

A hypertensive emergency usually requires a monitored bed, high-dependency care or intensive care, depending on the organ damage and the drug used.

Monitor:

• Blood pressure frequently during titration.
• Level of consciousness and neurological status.
• Heart rate and ECG.
• Work of breathing and oxygenation.
• Urine output and renal function.
• Chest pain and signs of myocardial ischaemia.
• Signs of cerebral, coronary or peripheral hypoperfusion.
• Electrolytes and acid–base status in a serious course.
• Fetal monitoring according to obstetric procedures in pregnancy.

A rapidly falling blood pressure together with new confusion, focal neurological signs, chest pain, oliguria, a cold periphery or a rising lactate must raise the suspicion of overshoot. Pause or reduce the infusion and reconsider the target pressure.

After initial stabilisation, intravenous treatment must be replaced with long-acting oral treatment. The transition must be planned so that the blood pressure does not rise again when the infusion is stopped.

Red flags and pitfalls

• Treating the figure instead of the patient. A very high blood pressure without acute organ damage is not in itself an indication for intravenous treatment.
• Missing organ damage at lower pressures. Pregnancy, acute kidney disease and scleroderma renal crisis can cause serious organ damage at lower absolute values.
• Lowering too rapidly. Chronic hypertension shifts autoregulation. Abrupt normalisation can cause cerebral, coronary or renal ischaemia.
• Dismissing the blood pressure as pain or anxiety. Treat the precipitating factors, but repeated high values require continued assessment and follow-up [3].
• Aortic dissection. Give analgesia and beta blockade before a vasodilator, otherwise reflex tachycardia and contractility can increase the load on the aortic wall.
• Phaeochromocytoma. Do not give pure beta blockade before adequate alpha blockade.
• Ischaemic stroke. Do not routinely lower the blood pressure to normal values. The penumbra may be pressure-dependent.
• Pulmonary oedema. Not every patient is fluid overloaded. Vasodilatation and respiratory support may be more important than large doses of diuretic.
• Intracerebral haemorrhage. Aim for smooth, controlled lowering. Large variations and hypotension must be avoided.
• Pregnancy and the postpartum period. Always ask about pregnancy and recent delivery. Pre-eclampsia can present after delivery.
• Thrombocytopenia and haemolysis. Investigate for thrombotic microangiopathy. Do not automatically assume that all the findings are caused by the hypertension.
• Systemic sclerosis. New-onset hypertension and renal failure are scleroderma renal crisis until proven otherwise. Start an ACE inhibitor early.
• Sublingual short-acting nifedipine. This must not be used in a hypertensive emergency because of the risk of an uncontrolled fall [20].
• Nitroglycerin after a phosphodiesterase-5 inhibitor. This can cause marked hypotension.
• The wrong cuff size. A cuff that is too small can give falsely high values.
• Missing a withdrawal reaction. Abrupt withdrawal of clonidine or a beta blocker can cause marked sympathetic activation.
• Forgetting the long-term plan. The acute episode is often an expression of inadequate chronic treatment, poor adherence, secondary hypertension or a lack of continuity of care.

A short management algorithm

1. Confirm the blood pressure, measure in both arms and use the correct cuff.
2. Assess ABC and identify immediately life-threatening conditions, particularly aortic syndrome, pulmonary oedema, acute coronary syndrome, stroke and eclampsia.
3. Look for acute organ damage with a targeted history, examination, fundoscopy, ECG, laboratory tests and imaging.
4. If there is organ damage, choose a titratable intravenous drug and a condition-specific target. Place the patient at an appropriate level of monitoring.
5. If there is no organ damage, avoid rapid lowering. Restart or optimise long-acting oral treatment.
6. Arrange secure follow-up, including monitoring of blood pressure, renal function and electrolytes.
7. Investigate the precipitating cause, for example an interruption of treatment, kidney disease, pregnancy, drugs, a drug interaction, endocrine disease or thrombotic microangiopathy.

References

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