Hypertensive emergencies are those situations where very high blood pressure (BP) values are associated with acute organ damage, and therefore, require immediate, but careful BP reduction.ESC Council on hypertension has released its latest position document on the management of hypertensive emergencies or high blood pressure related emergencies that has appeared in European Heart Journal Cardiovascular Pharmacotherapy.
- Patients with a hypertensive emergency or High Blood Pressure related emergencies should be admitted for close monitoring and, in most cases, treated with intravenous blood pressure (BP)-lowering agents to reach the recommended BP target in the designated time-frame.
- The type of acute organ damage is the principal determinant of (i) the drug of choice, (ii) the target BP, and (iii) the timeframe in which BP should be lowered. Key target organs are the heart, retina, brain, kidneys, and large arteries.
- Patients that lack acute hypertension-mediated end-organ damage to the heart, retina, brain, kidneys, or large arteries do not have a hypertensive emergency and can be treated with oral BP-lowering agents and usually discharged after a brief period of observation.
- Hypertensive emergencies are situations where very high Blood Pressure values are associated with acute hypertension-mediated organ damage, and therefore, require immediate BP reduction to limit extension or promote regression of target organ damage.
- Key target organs of acute High Blood Pressure mediated damage are the heart, retina, brain, kidneys, and large arteries.
- Malignant hypertension is a hypertensive emergency characterized by the presence of a severe BP elevation (usually >200/120 mmHg) and advanced retinopathy, defined as the bilateral presence of flame-shaped haemorrhages, cotton wool spots, or papilloedema. Sodium nitroprusside, labetalol, nicardipine, and urapidil all appear to be safe and effective for the treatment of malignant hypertension.
- Hypertensive encephalopathy is a hypertensive emergency characterized by severe hypertension and (one or more of the following): seizures, lethargy, cortical blindness and coma, and in the absence of an alternative explanation.
- Thrombotic microangiopathy: any situation where severe BP elevation coincides with a Coombs-negative haemolysis (elevated lactic dehydrogenase levels, unmeasurable haptoglobin, or schistocytes) and thrombocytopenia in the absence of another plausible cause and with improvement during BP-lowering therapy.
- Acute management of hypertensive emergencies-There is general agreement that patients without acute hypertension-mediated organ damage usually can be treated with oral BP-lowering medication or adaptation of their current BP-lowering medication. Rapid BP lowering is not recommended, as this can lead to cardiovascular complications. Among the different oral BP lowering drugs captopril, labetalol, and nifedipine retard have been proposed.
- For acute ischaemic stroke and an indication for thrombolytic therapy, lowering BP to <185 mmHg systolic and 110 mmHg diastolic is recommended before thrombolysis is given.
- In case severe hypertension is associated with the acute coronary syndrome, both nitroglycerine and labetalol have been used to lower BP in patients with an acute coronary event.
- Haemoglobin, platelet count
- Creatinine, sodium, potassium, lactic dehydrogenase (LDH), haptoglobin
- Quantitative urinalysis for protein, urine sediment for erythrocytes, leucocytes, cylinders and casts
- ECG (ischaemia, arrhythmias, left ventricular hypertrophy)
- Troponin-T, CK, CK-MB
- Peripheral blood smear (for assessment of schistocytes)
- Chest X-ray (fluid overload)
- Transthoracic echocardiography (cardiac structure and function) or point of care cardiac and lung ultrasound (cardiac pulmonary oedema)
- CT (or MRI)-brain (intracranial haemorrhage)
- CT-angiography of thorax and abdomen (acute aortic disease)
- Renal ultrasound (postrenal obstruction, kidney size, left to right difference)
|Clinical presentation||Time line and target BP||1st line treatment||Alternative|
|Malignant hypertension with or without TMA or acute renal failure||Several hours, MAP −20% to −25%||Labetalol||Nitroprusside|
|Hypertensive encephalopathy||Immediate, MAP −20% to −25%||Labetalol||Nitroprusside|
|Acute ischaemic stroke and BP >220 mmHg systolic or >120 mmHg diastolic||1 h, MAP −15%||Labetalol||Nitroprusside|
|Acute ischaemic stroke with indication for thrombolytic therapy and BP >185 mmHg systolic or >110 mmHg diastolic||1 h, MAP −15%||Labetalol|
|Acute haemorrhagic stroke and systolic BP >180 mmHg||Immediate, systolic 130<BP <180 mmHg||Labetalol||Urapidil|
|Acute coronary event||Immediate, systolic BP <140 mmHg||Nitroglycerine||Urapidil|
|Acute cardiogenic pulmonary oedema||Immediate, systolic BP <140 mmHg||Nitroprusside or Nitroglycerine (with loop diuretic)||Urapidil (with loop diuretic)|
|Acute aortic disease||Immediate, systolic BP <120 mmHg and heart rate <60 b.p.m.||Esmolol and Nitroprusside or Nitroglycerine or Nicardipine||Labetalol or Metoprolol|
|Eclampsia and severe pre-eclampsia/HELLP||Immediate, systolic BP < 160 mmHg and diastolic BP <105 mmHg||Labetalol or Nicardipine and Magnesium sulphate|
BP, blood pressure; HELLP, haemolysis, elevated liver enzymes and low platelets; TMA, thrombotic microangiopathy.
|Drug||Onset of action||Duration of action||Dose||Contraindications||Adverse effects|
|Esmolol||1–2 min||10–30 min||0.5–1 mg/kg as bolus; 50–300 mg/kg/min as continuous infusion||History of 2nd or 3rd degree AV block (and in the absence of rhythm support), systolic heart failure, asthma, and bradycardia||Bradycardia|
|Metoprolol||1–2 min||5–8 h||15 mg intravenous (iv), usually given as 5 mg iv, and repeated at 5 min intervals as needed||History of 2nd or 3rd degree AV block, systolic heart failure, asthma, and bradycardia||Bradycardia|
|Labetalol||5–10 min||3–6 h||0.25–0.5 mg/kg; 2–4 mg/min until goal BP is reached, thereafter 5–20 mg/h||History of 2nd or 3rd degree AV block, systolic heart failure, asthma, and bradycardia||Bronchoconstriction and foetal bradycardia|
|Fenoldopam||5–15 min||30–60 min||0.1 µg/kg/min, increase every 15 min until goal BP is reached|
|Clevidipine||2–3 min||5–15 min||2 mg/h, increase every 2 min with 2 mg/h until goal BP||Headache and reflex-tachycardia|
|Nicardipine||5–15 min||30–40 min||5–15 mg/h as continuous infusion, starting dose 5 mg/h, increase every 15–30 min with 2.5 mg until goal BP, thereafter decrease to 3 mg/h||Liver failure||Headache and reflex-tachycardia|
|Nitroglycerine||1–5 min||3–5 min||5–200 mg/min, 5 mg/min increase every 5 min||Headache and reflex tachycardia|
|Nitroprusside||Immediate||1–2 min||0.3–10 mg/kg/min, increase by 0.5 mg/kg/min every 5 min until goal BP||Liver/kidney failure (relative)||Cyanide intoxication|
|Enalaprilat||5–15 min||4–6 h||0.62–1.25 mg iv||History of angioedema|
|Urapidil||3–5 min||4–6 h||12.5–25 mg as bolus injection, 5–40 mg/h as continuous infusion|
|Clonidine||30 min||4–6 h||150–300 µg iv in 5–10 min||Sedation and rebound hypertension|
|Phentolamine||1–2 min||10–30 min||0.5–1 mg/kg bolus injections OR 50–300 µg/kg/min as continuous infusion||Tachyarrhythmias and chest pain|
Types of Hypertensive Emergencies encountered across all specialities are-
The retinal abnormalities associated with malignant hypertension consist of flame-shaped hemorrhages, cotton wool spots (Grade III) with or without the presence of papilloedema (Grade IV).
Both high BP and angiotensin II have been associated with activation of pro-inflammatory and pro-coagulant pathways.25,26 Endothelial detachment is one of the pathological hallmarks of hypertensive microangiopathy and is thought to result from high-shear forces.
When BP is markedly elevated and cerebral autoregulation cannot prevent a rise in intracranial pressure cerebral edema may develop, especially in the posterior areas of the brain where sympathetic innervation is less pronounced leading to less effective damping of BP oscillations. pressure, cerebral edema may develop, especially in the posterior areas of the brain where sympathetic innervation is less pronounced leading to less effective damping of BP oscillations.
4.Acute cardiogenic pulmonary edema
In patients with acute pulmonary edema caused by hypertensive heart failure, both nitroglycerine and sodium nitroprusside can be used as they will optimize preload and decrease afterload. Nitroprusside is the drug of choice as it will acutely lower ventricular pre- and afterload. In patients with autonomic hyper-reactivity because of suspected (meth)amphetamine or cocaine intoxication, treatment with benzodiazepines should be initiated first. In case additional BP-lowering treatment is needed phentolamine, a competitive alpha-blocking agent for intravenous use, nicardipine or nitroprusside can be considered. Alternatively, clonidine can be used, which apart from its sympathicolytic action also has sedative effects.
5.Acute aortic disease
In patients with acute aortic disease (dissection or rupture) systolic BP and heart rate need to be immediately reduced to 120 mmHg or lower and 60 b.p.m. or less to reduce aortic wall stress and disease progression. Beta-blockers are therefore considered first-line treatment. Esmolol can be used together with ultra-short acting vasodilating agents such as nitroprusside or clevidipine.
6.Eclampsia and severe pre-eclampsia
In patients with eclampsia or severe pre-eclampsia (with or without hemolysis, elevated liver enzymes, and low platelets syndrome), BP-lowering therapy is given next to intravenous magnesium Sulfate and delivery needs to be considered after the maternal condition has stabilized.
The management of hypertensive emergencies is mainly based on consensus from clinical experience, observations, and comparisons on intermediate outcomes. Acute hypertension-mediated organ damage includes stroke (ischemic or hemorrhagic), acute hypertensive microangiopathy and encephalopathy, cardiogenic pulmonary oedema, coronary ischemia, and acute aortic disease. The treatment goal is to prevent or limit the further hypertensive damage by a controlled BP reduction.
For reference log on to https://doi.org/10.1093/ehjcvp/pvy032