Hypertension · 12
Chapter 12: Hypertensive urgencies and emergencies
Hypertensive emergencies are among the most challenging situations in acute care. The clinician must distinguish a severe blood pressure reading accompanied by immediate cardiovascular or renal risk from a severe reading without evidence of acute harm. A hypertensive emergency is generally a grade 3 elevation with acute hypertension-mediated organ damage (HMOD). It is life-threatening and usually requires prompt, carefully monitored treatment, most often with an intravenous drug. The speed of the rise may be as important as the absolute value.
Typical presentations include acute stroke or intracranial haemorrhage, acute aortic syndrome or dissection, acute heart failure and pulmonary oedema, acute coronary syndrome, acute kidney injury, catecholamine excess from cocaine, amphetamines or pheochromocytoma, and severe hypertensive disorders of pregnancy, including pre-eclampsia, eclampsia and HELLP syndrome. Malignant hypertension may occur with or without thrombotic microangiopathy and acute kidney injury; it can be associated with fibrinoid arteriolar necrosis, severe retinal changes, disseminated intravascular coagulation, encephalopathy or acute heart failure.
Symptoms may include headache, visual disturbance, dizziness, focal neurological symptoms, chest pain and shortness of breath. Hypertensive encephalopathy may cause drowsiness, confusion, generalised tonic-clonic seizures or cortical blindness. Focal deficits should raise concern for stroke. Suspected acute stroke should be managed in a specialised stroke unit, using the blood pressure strategy appropriate to the type of stroke and any reperfusion treatment.
The term hypertensive urgency is used for severe blood pressure elevation without acute HMOD, but its definition is inconsistent and its clinical value is limited. Most such patients do not require hospital admission solely because of the number. After repeated accurate measurements and clinical assessment, treatment is usually adjusted with oral medication and a gradual reduction over 24–48 hours. Sublingual or immediate-release nifedipine should be avoided because an uncontrolled fall can cause cerebral, coronary or renal hypoperfusion.
Diagnostic assessment
The initial assessment should identify both the affected organ and a possible precipitating cause. Common investigations include:
- fundoscopy for haemorrhages, exudates, papilloedema and other severe hypertensive retinal changes;
- an ECG, full blood count with platelets, fibrinogen and peripheral blood smear;
- serum creatinine, estimated GFR, electrolytes, LDH and haptoglobin;
- urine albumin-to-creatinine ratio and urine microscopy; and
- a pregnancy test when relevant.
Additional tests should be guided by the presentation. Troponin and NT-proBNP are useful when acute coronary syndrome or heart failure is suspected; chest radiography or lung ultrasound can assess pulmonary oedema; echocardiography can evaluate ventricular function, ischaemia and aortic pathology; CT angiography of the chest and abdomen is used when acute aortic disease is suspected; CT or MRI of the brain is indicated for neurological involvement; renal ultrasound can help evaluate acute kidney injury or renal artery disease; and toxicology testing may be appropriate when cocaine or methamphetamine exposure is possible.
Hospital treatment and rate of reduction
Patients with a hypertensive emergency should be admitted to a setting that permits continuous or very frequent monitoring. In pregnancy, a persistent pressure around 170/110 mmHg or higher requires urgent assessment. Treatment should begin only after identifying the likely organ injury and reversible causes. Intravenous agents with a short half-life are useful because they can be titrated and stopped quickly. The first dose should be conservative, and rapid, uncontrolled normalisation should be avoided.
| Clinical situation | Usual first options | Initial objective |
|---|---|---|
| Malignant hypertension, with or without acute kidney injury | Labetalol or nicardipine; nitroprusside or urapidil may be alternatives | Reduce mean arterial pressure by about 20–25% over several hours |
| Hypertensive encephalopathy | Labetalol or nicardipine; nitroprusside may be an alternative | Reduce mean arterial pressure by about 20–25% promptly but in a controlled manner |
| Acute coronary syndrome | Labetalol or nitroglycerin; urapidil may be an alternative | Usually aim for systolic pressure below 140 mmHg, guided by ischaemia and perfusion |
| Acute cardiogenic pulmonary oedema | Nitroglycerin or labetalol with a loop diuretic; urapidil with a loop diuretic may be an alternative | Usually aim for systolic pressure below 140 mmHg while treating congestion |
| Acute aortic dissection | Esmolol followed by nitroprusside, nitroglycerin or nicardipine; labetalol, urapidil or metoprolol may be alternatives | Urgently target systolic pressure below 120 mmHg and heart rate below 60/min, if tolerated |
| Eclampsia, severe pre-eclampsia or HELLP syndrome | Labetalol or nicardipine plus magnesium sulfate; delivery should be considered with the obstetric team | Reduce blood pressure promptly, commonly below 160/105 mmHg, while protecting the mother and fetus |
These are clinical frameworks, not substitutes for local emergency protocols or specialist assessment. The safe target depends on the organ involved, the duration of hypertension, cerebral and coronary perfusion, and whether aortic disease or pregnancy is present. After stabilisation, patients need early post-discharge review and, in many cases, at least monthly follow-up with a hypertension specialist or dedicated centre until control and the cause are clear.
Severe readings in the emergency department
Emergency-department blood pressure measurements are often affected by pain, anxiety, recent exertion, incorrect cuff size or an unsuitable measurement technique. In one year-long review, 48% of emergency-department patients had an elevated reading. The value often falls after pain and anxiety resolve, but this cannot be assumed. Medication review should include NSAIDs, decongestants, stimulants and recreational drugs. If there is no evidence of emergency, repeat unattended measurements in a quiet room and reassess at intervals; the source describes an approximate 30% fall toward grade 2 or lower within 30 minutes as a possible reassuring trend, not a universal treatment target.
Perioperative hypertension
Hypertension is common before surgery, and severe uncontrolled hypertension may increase bleeding and cardiovascular risk. Before an operation, confirm the pressure with accurate technique and classify the severity. Elective surgery generally need not be delayed solely for untreated grade 1 hypertension or for near-controlled hypertension. Untreated grade 2 or grade 3 hypertension, particularly systolic pressure above 180 or diastolic pressure above 110 mmHg, should prompt discussion about postponing elective surgery while considering white-coat hypertension and home or ambulatory measurements.
Antihypertensive therapy is usually continued, especially beta-blockers; abrupt withdrawal should be avoided. Anaesthetic induction, intubation, vasoconstrictors and pain can produce sharp rises, whereas anaesthesia, blood loss and volume depletion can cause hypotension. There is no single perioperative target for every patient. The practical objective is a stable, safe range with avoidance of large fluctuations. Beta-blockers should be restarted promptly after surgery, while diuretics and renin–angiotensin-system blockers are commonly restarted within 48 hours after reassessing volume status, renal function and blood pressure.
Evidence context
Randomised evidence is limited for many emergency presentations, and targets are not interchangeable across organ syndromes. Management therefore combines the affected organ, pharmacology, specialist consensus and close monitoring. The numerical objectives above should be interpreted as syndrome-specific starting points rather than universal rules.