Hypertensive

Emergencies
Prof. EL-Metwally EL-Shahawy
Head of Internal Medicine &
Nephrology Departments
Benha Faculty of Medicine
Definition
Hypertensive Emergency
• Diastolic BP >130 mm Hg
• Clinical symptomatology is evident
• Often acute end-organ damage
• Requires immediate BP reduction
 Definitions

Hypertensive Urgencies
• Diastolic BP > 110 mm Hg, Systolic BP >180
• Mild or no acute end- organ damage
• No clinical symptoms
• BP should be lowered within a few hours
Definitions
Accelerated Hypertension
• Svevere elevation of BP, Diastolic >140
• Vascular damage manifested by retinal
hemorrhages and exudates
Malignant Hypertension
• Accelerated Hypertension
• Papilledema
Prevelance
Percentage of all medical emergencies:
• Hypertensive crisis 28%
• Hypertensive urgency: 21%
• Hypertensive emergency 7%
Causes of Hypertensive
Emergencies
Essential hypertension
Renal parenchymal disease:
Acute glomerulonephritis,
Vasculitis,Haemolytic uraemic syndrome,
TTP
Renovascular disease:
Renal-artery stenosis
 Causes of Hypertensive
Emergencies Cont
Pregnancy:
Eclampsia
Endocrine:
Phaeochromocytoma
Cushing's syndrome,
Renin-secreting tumours
Mineralocorticoid hypertension
 Causes of Hypertensive
Emergencies Cont
Drugs :
Cocaine, sympathomimetics, erythropoietin,
cyclosporin, antihypertensive withdrawal
Interactions with monoamine-oxidase inhibitors
(tyramine),amphetamines,
lead intoxication
Autonomic hyper-reactivity:
Guillain-Barré syndrome, acute intermittent
porphyria
Central-nervous-system disorders:
Head injury, cerebral infarction/ haemorrhage
 Pathophysiology
• Abrupt rise in vascular resistance
• Mechanical stretching
• Proinflammatory response,secretion of cytokines
(IL-6)
• Increased endothelial cell cytosolic Ca
• Increased vascular resistance by:
1- Increased production of ATII,
norepinephrine, endothelin, ADH, thromboxane
and aldosterone
2- Low production of VD: NO and PGI2
Pathophysiology Cont

• Acute or severe elevation of BP >

expression of CAMs
• Endothelial dysfunction, increase in its
permeability, fibrinoid necrosis
• Loss of endothelial fibrinolytic activity
coupled with activation of coagulation and
platelets promotes DIC
Vascular Pathophysiology of
Hypertensive Emergencies
Hyprertensive Emergencies
• Hypertensive Encephalopathy 16.3%
• Cerebral infarction 24.5%
• Intracerebral or subarachnoid haemorrhage
4.5%
• Renal insufficiency
• Acute pulmonary edema 22.5%
• Myocardial ischemia or infarction 12%, HF
14.3%
• Dissecting aortic aneurysm 2%
• Eclampsia 4.5%
 Hypertensive Encephalopathy

• Definition:
1- Reversible alteration in neurologic function
due to abrupt BP elevation.
2- Acute organic brain syndrome ( acute
encephalopathy or delirium) occurring as a
result of failure of the upper limit of cerebral
vascular autoregulation (autoregulation
breakthrough)
Autoregulation of cerebral blood
flow:
Pathogenesis of Hypertensive
Encephalopathy
• Autoregulation failure
• Cerebral hyperperfusion
• Increased permeability
• Cerebral oedema
• Microhaemorrhage
Pathogenesis of Hypertensive Encephalopathy cont
Posterior leukoencephalopathy
• MRI shows bilateral
Leukoencephalopathy:
• Affects the white matter of the parieto-
occipital region , and other posterior
structures: cerebellum and brain stem
• The cortex of temporal and frontal regions
are involved in occasional cases
Pathogenesis of Hypertensive Encephalopathy cont
Posterior leukoencephalopathy

hypertensive reversible posterior

leukoencephalopathy syndrome {PLS})
• Non-hypertensive causes of PLS:
Cyclosporin, tacrolimus,
cisplatin,interferon-alfa, AIDS, TTP and
blood transfusion
Clinical manifestations of Hypertensive
Encephalopathy

• Acute or subacute onset of lethargy, confusion,

headache, visual disturbances and seizures
• If not treated can progress to cerebral
haemorrhage , coma and death
• It is associated with untreated or undertreated
hypertension
• It is associated with known causes of severe
hypertension :Renal disease,
immunosuppressive
therapy ,erythropoietin,TTP,pre-eclampsia and
eclampsia
 Approach to the Patients with
Hypertensive Emergencies
Distinguish between hypertensive emergency and
hypertensive urgency
History: • Hypertension • Renal diseases
• Cardiac or CNS symptoms
• Medications
Examination: BP Supine and upright, left & right
• Funduscopic examination
• Cardiovascular examination
• Neurological examination
Approach to the Patients with
Hypertensive Emergencies
• Laboratory tests
Urine: proteinuria & RBCs
Serum: Electrolytes, BUN ,Creatinine
CBC: RBCs, Leucocytes, Platelets
• ECG: LVH, strain, Ischemia or

infarction
• Chest X-ray Cardiomegaly and or
pulmonary edema
Treatment for Hypertensive
Urgencies
• Oral medications preferred
• Usually, short- acting meds given in
repeated doses: ACEI, CCBs, β-blockers,
alpha-blockers or a combination
• Close monitoring for overshoot
hypotension
• Quick (next day) follow-up
Treatment of Hypertensive
Emergency
Management Principles:

• The patient should be admitted to ICU

• Establish IV access
• Insert an arterial line to monitor BP
• IV administration of antihypertensive drugs
Management Principles
• The goal of therapy is to reduce mean BP by no
more 25% ( within minutes to 2 hours), then
toward 160/100 mmHg within 2 to 6hours
• Avoid excessive fall in BP that may precipitate
renal, cerebral, or coronary ischemia.
• Age: Caution when lowering BP in elderly
patients. They autoregulate poorly and may >
cerebrovascular events
Management Principles
• For most patients, the greatest risk in
treating hypertensive emergency is the
risk accompanying HYPOTENSION ( not
hypertension
• Parenteral medications, short acting,
easily titrated
• Use of nifedipine capsule is discouraged
(denied in 1985 by FDA)
Commonly used parenteral
antihypertensive drugs
Adverse
Duration Onset Dose Drug
effects
Hypotension, 0·25­10 µg kg-1
1­2 min Immediate Sodium
nausea, min-1
vomiting, cyanate nitroprusside
toxicity
Nausea, vomiting, 2­6 h 5­10 min 20­80 mg bolus Labetalol
heart block, (every 10 min)or
2 mg/min
bronchospasm
infusion
Reflex tachycardia 2­6 h 10 min 10­20 mg bolus Hydralazine
0·1­0·6 µg kg-1
Hypotension, 10­15 min 5­10 min Fenoldopam
min-1
headache
 5­15 min
Headache, vomiting 1­3 min 5­100 µg/min Glyceryl

trinitrate
15 min
Hypotension, renal 4­6 h 1·25­5·00 mg bolus Enalaprilat

failure
5­10 min
Reflex tachycardia, 2­4 h 2­10 mg/h Nicardipine

flushing
1­2 min
Reflex tachycardia 3­5 min 5­10 mg/min Phentolamin

Drug Dose Onset Duration Adverse effects

Management:
Special settings
 Treatment of Hypertensive
Encephalopathy
• Early recognition
• Withdrawal of exacerbating factors
• Parenteral anticonvulsant treatment
• Suitable antihypertensive drugs: Sodium
nitroprusside, labetolol, enalapril and
hydralazine
• Clonidine should be avoided
Treatment:
Acute stroke
• Antihypertensive therapy is not routinely
recommended for patients with stroke and
hypertension
• Failure of cerebral autoregulation after a
stroke, within the infarct area and in the
surrounding ischaemic penumbra, so this
area more prone to hypoperfusion during
BP reduction
Treatment: Acute stroke
• Optimum management of BP in acute
stroke in:
• Intracerebral or subarachnoid
haemorrhage
• Diastolic BP 130 mm Hg
Treatment: Pre-eclampsia
• Parental Mg to prevent the evolution of
pre-eclampsia to eclampsia
• The parenteral antihypertensive drugs
most commonly used during pregnancy
are hydralazine and labetalol
• ACEI & ARBS are contraindicated
Treatment:Myocardial ischaemia
• IV nitrate: Improve coronary perfusion,
decrease LV preload and have a moderate
hypotensive action
• IV B-blockers leads to reduction in both
HR and BP
• Vasodilators should be avoided
• LV failure: IV glyceryltrinitrate or sodium
nitroprusside + loop diuretics
Treatment: Aortic dissection
SBP should be decreased as rapidly as
possible to 100-110 mm Hg with a
combination of β-blockers or labetalol
and sodium nitroprusside
 Treatment: Renal Insufficiency
• Renal insufficiency can be a cause or a
consequence of hypertensive emergency
• Hypertensive emergencies are common
in patients with:
Haemodialysis and particularly those
receiving erythropoietin
Renal transplantation especially those
receiving cyclosporin and corticosteroid
Treatment: Renal Insufficiency
• Antihypertensive drugs that preserve renal blood
flow: Ca antagonists and alpha-adrenergic
blocking agents
• Sodium nitroprusside, fenoldopam, or
hydralazine can be used if hypertension remains
severe or refractory
• Diuretic use may be beneficial or deleterious
depending on patient’s volume status
 Summary

End-organ complications and

therapeutic considerations of
Hypertensive Emergencies
 End
Therapeutic considerations Complications
organ

β-blockade, labetalol , sodium Aortic dissection Aorta

nitroprusside with ß-blockade, avoid

isolated use of pure vasodilators

Avoid centrally acting

Hypertensive
antihypertensive drugs, such as
encephalopathy Brain
clonidine

Cerebral
Avoid centrally acting agents; avoid infarction
rapid decreases in BP or haemorrhage
 Myocardial
ischaemia,
Intravenous glyceryl trinitrate, ß- Myocardial
Heart
blockade infarction

Diuretics and ACE inhibitors , ß-

blockers with caution Heart failure

Diuretics with caution, calcium

Renal
antagonists Kidney
insufficiency

Hydralazine, labetalol, calcium

antagonists.
Eclampsia Placenta
Avoid sodium nitroprusside
and ACE inhibitors