Management of high blood pressure emergencies -ESC Council guidelines

Published On 2018-09-03 13:33 GMT | Update On 2018-09-03 13:33 GMT

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.

Key messages

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.

Proposed diagnostic studies in patients with suspected hypertensive emergency

Laboratory analysis

Haemoglobin, platelet count

Creatinine, sodium, potassium, lactic dehydrogenase (LDH), haptoglobin

Quantitative urinalysis for protein, urine sediment for erythrocytes, leucocytes, cylinders and casts

Diagnostic examination

ECG (ischaemia, arrhythmias, left ventricular hypertrophy)

Fundoscopy

On indication

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)

Hypertensive emergencies requiring immediate BP lowering

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
	Several hours, MAP −20% to −25%	Nicardipine	Urapidil
Hypertensive encephalopathy	Immediate, MAP −20% to −25%	Labetalol	Nitroprusside
Hypertensive encephalopathy	Immediate, MAP −20% to −25%	Nicardipine	Nitroprusside
Acute ischaemic stroke and BP >220 mmHg systolic or >120 mmHg diastolic	1 h, MAP −15%	Labetalol	Nitroprusside
	1 h, MAP −15%	Nicardipine	Nitroprusside
Acute ischaemic stroke with indication for thrombolytic therapy and BP >185 mmHg systolic or >110 mmHg diastolic	1 h, MAP −15%	Labetalol
	1 h, MAP −15%	Nicardipine	Nitroprusside
Acute haemorrhagic stroke and systolic BP >180 mmHg	Immediate, systolic 130<BP <180 mmHg	Labetalol	Urapidil
Acute haemorrhagic stroke and systolic BP >180 mmHg	Immediate, systolic 130<BP <180 mmHg	Nicardipine	Urapidil
Acute coronary event	Immediate, systolic BP <140 mmHg	Nitroglycerine	Urapidil
Acute coronary event	Immediate, systolic BP <140 mmHg	Labetalol	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.

Intravenous drugs for the treatment of hypertensive emergencies

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-

1.Hypertensive retinopathy

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).

2.Thrombotic microangiopathy

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.

3.Hypertensive encephalopathy

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

Article Source : With inputs from European Heart Journal Cardiovascular Pharmacotherapy

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