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Lecture 9

EMERGENCY HYPERTENSIONS

Definition
Emergency hypertension is a syndrom characterized by increased systolic blood pressure more
than 230 mmHg and diastolic blood pressure more than 130mmHg, associated with acute significant
target organs damages: brain, heart, kidney, vassels and with immediate threat to life
Mentioned: to the patients without anterior hypertension (ex. children with acute
glomerulonephritis, woman with eclampsia, patients with head trauma) can appear alterated cerebral
status even to values of 150/100 mmHg.

Pathogeny
Usually emergency hypertension appear on most often on a chronic preexistant arterial
hypertension, especially in case of secondary arterial hypertension ( renal diseases, pheocromocitoma),
inssuficient treated or after brutally stopped the medication.
Dangereous tensional values can appear also to the patients without anterior hypertension, like:
- acute glomerulonephritis
- eclampsia
- acute volemic loading
- intra and post surgery
- cerebral trauma

The effects of artertial hypertension on targets organs are:


- increased cerebral flow with acte damage of vascular walls, with increased vascular
permeability and cerebral edema in case of hypertensive encephalopaty,;
- acceleration of atheroclerosis of cerebral vassel, with rupture and intracerebral or
subarahnoidian hemorrhages.
- increased oxigen myocardial needs, left ventricular hypertrophy, with signs of acute
pulmonary edema and acute coronarian ischemia.
- acceleration of aortic atherosclerosis and favorise the intimal rupture.

Classification
Function the emergency , the hypertensions can be classified in:
 emergency (vital)-need to decrease the BP in 1 hour; death can appear in few hours withou
treatment:
- hypertensive encephalopathy
- hemorrhagic stroke
- acute pulmonary edema
- acute dissection of aorta
- eclampsia
- crise of pheocromocitoma
- acute myocardial infarction.
 Urgency (simple, nonvital, comune)- need to decrease the BP in 24 hours
- simple crise of hypertension
- malignant accelerated hypertension
- peri-surgical hypertension
- unstable pectoris angina+ hypertension
- left ventricular failure
- preeclampsia.
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Precipitating factors of the crisis are:
- brutally stopping the antihypertensive treatment
- stopping the administration of betablockers in big doses
- emotional causes- give transitor increased values
- renovascular causes or renoparenchimatous- acute renal failure
- cranial trauma
- drug administration: triciclic antidepresants, sympaticomimetics.

The patients will be hospitalised immediately in cardiology, and the patient evaluation include:
- ECG monitor
- BP monitor
-establish i.v. line
-is necessary : -brief history of hypertension: type of hypertension, evolution, treatment, other previous
diseases;
-clinical examination: exist or not signs of deterioration of brain, heart, kidney,
fundoscopique exam.

Clinical examination:
1. nervous system
- focal neurological signs- exist or not
- consciousness status: alterated or not
- signs of intracranial hypertension-ICHT: headache, vomiting, bradycardia,
ocular disturbances.
- coma- exist or not- usually appears in cerebral tumors, rarely in case of stroke
or ICHT.
- seizures
2. cardiovascular system:
- BP, pulse to both arms, differential pulse femuro-radial
- signs of left ventricular failure (galop, cardiomegaly, dyspneea)
- signs of myocardial infarction, pectoris angina, ECG
- signs of aortic dissection.
- fundoscopique exam
3. renal signs - diuresis- exist or not

Laboratory findings:
- usually exams
- must to be done simultaneously with the emergency treatment
- vanil-mandelic acid, adrenaline , noradrenaline- for pheocromocitoma
- ECG
- serum ureea and creatinine
- urine: small proteinuria, microscopic hematuria.

Clinical forms
I Hypertensive encephalopathy is the biggest hypertensive emergency with risk of death in few
hours. So it needs immediately parenteral antihypertensive treatment. Clinical manifestations appear
due to cerebral edema and difused cerebral ischaemia.
Clinical findings:
- intense headache,
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- vomiting of cental type,
- visual disturbances, paracentral scotom,
- auditive disturbances
- alterated conscious: confusion, obnubilation, rarely profound coma
- seizures.
Abcence of focar neurological signs in presence of this clinical findings, put the diagnosis of
hypertensive encephalopaty. Usually, HTE appears on a chronic old severe hypertension, with big and
persistent values of blood pressure, with IIIrd and IVth degree modifications of fundoscopique exam
like: haemorrhages, exudates and papilledema.

II. Cerebrovascular accidents - stroke


Hypertension can determine:
- cerebral infarction,
- intracerebral or subarahnoidian haemorrhage,
- transitory ischaemic stroke.
All these are directly corelated with systolic blood pressure value.
a. subarahnoidian haemorrhage: intense headache, photophobia, signs of meningeal irritation,
haemorrhagic cerebral fluid, loose of consciousnes untill coma.
b. intracerebral haemorrhage: focar motor deficites, eventually signs of meningeal irritation, alterated
consciousness status (usually more precocious and more severe in intracerebral haemorrhages)
c. cerebral infarction is an hypertensive emergency only if exist excesive raised BP which aggravates
neurological status (by aggravating the edema from infarction zone, or by haemorrhagic transformation
of the lesion).
Cerebral fluid is clear in cerebral infarction and cerebral haemorrhage without ventricular flood and the
differention between these two forms is made on CT or magnetic resonance exam.

III. Hypertensive pulmonary edema


Onset of typical syptomatology is preceded hours or days by appearance or aggravation of
effort or nocturnal dyspneea, palpitations, precordial pain.
The oset is relatively brutally with intense dyspneea, ortopneea, tachypneea. Cough is initial
nonproductive, then become productive with pinky frothy sputum. The patient is anxious, pale, cold
sweating, cyanosis of the extremities.
The physical findings reveals pulmonary subcrepitant rales in both pulmonary basis, which tend
to raise to the apex. Often the rales can be heard without stetoscope, next to the mouth of patient.
Sometimes can be associated sibilants , Wheezing.

IV. Acute coronarian accidents with hypertension: unstable angina, myocardial infarction
See lecture nr. 3

V. Hypertensive crisis of pheocromocitoma


Is characterised by: headache, sweating, palpitations, anxiety, palor, piloerection; and is
favorised by: stress, palpation of lombar region, anestezia, aortography.

VI. Acute dissection of aorta


In acute dissection of aorta, hypertension interfere in 2 ways:
- directly, because brutally and severe increased hydrostatic pressure can
produce rupture of intima
- indirectly, hypertension is the major factor of atherosclerosis.
Symptomatology can variate function the localisation and extension of dissection – see lecture nr. 3.
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VII.Eclampsia and preeclampsia
These represents big emergencies for pregnant woman, due to risk sometimes vital, for both
mother and foetus.
Preeclampsia represents raised BP>= 140/90 mmHg, appeared after 20 weeks of pregnancy, associated
with proteinuria and edema.
Eclampsia is characterized by appearance of seizures to a preeclamptic woman. Frequently appear
oliguria, acute pulmonary edema, disseminated intravascular coagulation.
Alarm symptoms to a pregnant woman with preeclampsia are:
- diastolic BP>=110mmHg
- recent important proteinuria >2g/24h
- elevated value of serum creatinine level >2mg%
- thrombocitopenia<100.000/mm3 or signs of angiopatic hemolitic anemia
- pain in superior abdomen
- headache, visual disturbances, signs of central nervous system affectation
- cardiac failure
- haemorrhages, exudates or papiledema
- delay of fetal growth.

VIII. Malignant/ accelerated HTA is defined on next criterias:


- diastolic BP >=130mmHg
- sistolic BP permanently increased
- fundoscopic exam: III-IV degree modifications
- resistant to the treatement
- proggresive affectation of target organs:
- renal nephroangiosclerosis, oliguria, azotemic retention, proggresiv renal
failure
- cerebral edema, neurologic manifestations: headache, confusion, severe
encephalopathy
- left ventricular failure, acute pulmonary edema
- gastrointestinal reactions: nausea, vomiting
- angiopatic hemolitic anemia.

Any type of sustained nontreated hypertension can develop malignant hypertension.


The characteristic morphopathologic lesion is fibrinoid necrosis of small arteries and arterioles.
Without treatment the death appears in 6-12 months by renal failure, cardiac failure or stroke.
With sustained treatment (included hemodialisis) we can control the values of BP; can transform in
benign form of hypertension and the lesions can regress.

ANTIHYPERTENSIVE DRUGS
The majority of hypertensive emergencies is treated , at least in first few hours, parenterally, with:

1. Sodium nitroprusiate- Niprid, Niprus- 1 f=50 mg


Action: direct venodilation (lower preload, do not influence inotropism) and direct arteriolodilation
(reflex tachycardia, decrease BP and cardiac output).
Administration: - perfusion i.v. under control BP from 5 to 5 min.
- dose 0,5-10microg/kg/min

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- advantages: imediately effect 1-2-3 min., don’t produce sedation and
tachyphylaxy.
Side effects: hypotension, nausea, vomiting, parestesis, psyhic disturbances, tiociant intoxication
(antidote= sodium tiosulphate).
Contraindications: renal failure, imposibility of monitoring BP, stroke
Specific indications: acute pulmonary edema, aortic dissection, hipertensive encephalopaty.

2. Diazoxide - 1 f= 300 mg
Act: direct arteriolodilation (reflex tachycardia, increase inotropism, lower peripheral resistance,
increase cardiac output)
Adm.: - 50-100mg bolus i.v. rapidly, repeated after 10 min., max 300 mg
- then perfusion 10-30 mg/min.
SE : brutally hypotension, tachycardia, nausea, hyperglicemia, stop the uterine work.
CI: diabetics, myocardial infarction, aortic aneurysm, myocardial ischemia.
Specific indications: hypertensive encephalopaty.

3. Labetolol
Act: alpha and beta blocker
Adm: - 20 mg bolus i.v.; can repeat after 10 min. Max. 100mg
- then perfusion 1-2 mg/min
- lower BP in 5-10 min.
- alpha effect >beta effect, you can give in left ventricular failure
- advantages: don’t give tachycardia.
SE: rebound in case of pheocromocitoma, vomiting, bradycardia, ortostatic hypotension.
CI: asthma, AV block, sinusal bradiarrythmias, congestive heart failure.
Specific indications: dissection aneurysm, stroke, eclampsia, myocardial infarction.

4. Nytroglicerine
Act: in big doses- venodilation (decrease preload, don’t influence inotropism) and arteriolodilation
(increase cardiac frequence and cardiac output).
Adm: perfusion i.v.10-100 microg/min. BP decrease in 2-5 min.
SE: headache, hypotension, tachycardia.
CI: intracranian hypertension.
Specific indications: acute pulmonary edema, perisurgery hypertension.

5. Hydralasine, Hypopresol, Alazine


Act: direct arteriolar dilator
Adm: - 5-10-20 mg.i.v. bolus, repeated in 20-30 min. Max. 40 mg.
- effect appear in 10-30 min.
SE: reflex tachycardia, headache, hypotension, facial eritema, increase oxygene needs of myocardium.
CI: aortic aneurysm, intracranial hypertension.
Specific indications: eclampsia.

6. Nicardipine
Act: calcium blocker
Adm: - 1mg/min.over 10 min. , then 5-10 mh/h.
- effect appear in 5-10 min.
SE: tachycardia, headache, local flebitis.
Indications: all hypertensive emergencies.
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7. Phentolamine, Regitine
Act: nonselective alpha blocker , arteriolar dilatation (reflex tachycardia, increase cardiac output, don’t
influence inotropism)
Adm: - 5-10 mg. bolus i.v. repeated to 5-10 min. until BP decrease.
- effect appear in 1-3 min.
SE: tachycardia, facial eritema
Specific indications: pheocromocitoma, rebound to clonidine, adrenergic crisis.

8. Enalapril
Act: converting enzyme inhibitor
Adm: - 1,25-5 mg. i.v.every 6 hours
- effect appear in 15 min.
SE: hypotension in case of hypertension with hyperreninemia.
Indications: acute pulmonary edema, myocardial infarction.

9. Trimetaphan
Act: ganglioplegia
Adm: 0,5-1 mg/min.perfusion i.v.
SE: intestinal and urinary bladder paresis
CI: eclampsia, perisurgery hypertension.
Indications: dissection of aorta, cerebrovascular emergencies.

10. Propranolol
Act: beta blocker
Adm: - 1-5 mg i.v., then 3mg/h.
- effect appear in 1-2 min.
SE: those of betablockers.
CI: those of betablockers, cerebrovascular events.

11. Urapidil
Act: alfablocker
Adm: - 25mg. bolus i.v., repeated after 10 min., then 2 mg/min.
- effect appear in 10-20 min.
Indications: acute pulmonary edema, perisurgery hypertension.

The next drugs have slower action of decreasing BP:

1. diuretics: Furosemide
- don’t have immediate effect (20 min)
- don’t give like unic treatment
- effect: diuretic and venodilator
- CI: malignant hypertension, pregnancy, renal failure with hypertension.
2. Clonidine
- alpha adrenergic stimulant, predominant on central nervous system
- effect appear in 15-30 min.
- 0,15-0,3 mg in 5 min. i.v., i.m.
- SE: hypotension, sedation can mask encephalopaty.
- CI: hypertensive encephalopaty, cerebrovascular emergencies.
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3. Rezerpine, Raunervil, Hiposerpil
- 2,5-5mg.i.m.
- decrease slowly BP, can mask encephalopaty.

Therapeutical particularities function clinical form

Type of HT emergency Preferated drug Avoided drug


HT encephalopaty Sodium nitroprusiate Rezerpine- sedation
Trimethaphan Clonidine- sedation
Diazoxide Metildopa- sedation
Nicardipine Hydralazine- increase cerebral
vasodilation

Malignant HT Labetolol
Nicardipine
Stroke Trimethaphan Metildopa
Nicardipine Rezerpine
Labetolol Clonidine
Hydralazine- increase ICHT
Diazoxide
Left ventricular failure- acute Sodium nitroprusiate Propranolol
pulmonary edema Nytroglicerine Esmolol
Urapidil Labetolol
Trimetaphan
Acute myocardial infarction Nitroprusiate Hydralazine
Nitroglicerine Diazoxide
Labetolol
Urapidil
Aortic dissection Nitroprusiate +betablocker Hydralazine
Trimetaphan Diazoxide - increase cardiac
Nicardipine output
Excess of cathecolamines Phentolamine All the others have small
Labetolol specificity
Postsurgery HT Nitroprusiate Trimethaphan- intestinal and
Nytroglicerine urinary bladder atonia
Diazoxide
Esmolol
Labetolol
Urapidil
Eclampsia Hydralazine
Labetolol
Magnesium sulphate

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Diseases which contraindicates some antihypertensive drugs in emergency

Asthma beta blockers


Ortostatic hypotension guanetidine, prazosin. Caution with captopril,
enalapril.
Stroke hydralazine, diazoxide, guanetidine
Colagenosis hydralazine
Congestive cardiac failure beta blockers
Unstable angina, guanetidine, hydralazine, diazoxide
myocardial infarction
Diabetes propanolol, beta blockers, tiazidic diuretics,
diazoxide
Gout tiazidic diuretics, diazoxide
Hyperpotasemia spironolactona, triamteren
Hypopotasemia other diuretics
Chronic hepatitis alpha metil dopa

Particular treatment function clinical form

I. Hypertensive encephalopaty
- Sodium nitroprusiate- ideal drug
- Diuretics- Furosemide 40-60 mgi.v.- 120mg.
Etacrinic acid 50-200mg
- Alternatives: - Diazoxide 100mg.i.v.
- Nifedipine 10-20mg. sublingual
- Labetolol, Urapidil
- Treat ICHT - Hiperventilation
- Manitol 20% 100-150 ml perfusion i.v.
- Glucose 33% 100ml i.v.
- Magnesium sulphate 10ml=1f=2 g perfusion i.v.
- Corticoids
- Adjuvants drugs: Diazepam 10mg. i.v.

II. Hemorrhagic stroke


BP must to be reduced with prudence, under continous control of neurological status.
Do not lower BP less than 170/100mmHg. – exception – sure diagnosis of intracerebral hematoma.
Give:
- Sodium nitroprusiate
- Trimethaphan
- Labetolol
Avoid: direct vasodilator drug- accentuate cerebral edema
betablockers- produce spasm on cerebral arteries
central adrenergic inhibitors- give sedation.

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III. Hypertensive pulmonary edema
- sitting position
- oxygen
- flebotomy
- Nitroprusiate
- Diazoxide
- Diuretics- Furosemide
- Opioids
- Aminophiline
- Cardiotonic

IV. Acute myocardial infarction


To the patients with unstable angina or development of myocardial infarction, hypertension can
be:
- primary factor
- reflex factor- reactional hypertension due to sympatetic stimulation, due to
pain and excess of cathecolamines.
To the hypertensive patients, the rhythm of atherogenesis is increased and also exist concentric
ventricular hypertrophy with big risk of non Q myocardial ischemia.
Reduce BP with prudence, not to decrease coronarian perfusion and to maintain the diuresis.
Give: - Nitroglicerine perfusion i.v.
- Diuretic
- Betablockers
- Sodium Nitroprusiate
- Treat myocardial infarction
- Alternative: Nifedipine 60-80 mg sublingual

V. Aortic dissection
Must to decrease BP immediately and brutally, untill small levels (sBP=100mmHg), to lower the
posibility of extending the dissection, but with maintenance of diuresis.
Give Nitroprusiate + Propranolol.
Contraindications: vasodilators which produce reflex tachycardia: Diazoxide, calcium blocker,
Hydralazine.

VI. Eclampsia
a. Preeclampsia without alarm signs:
- weekly measure BP, weight, proteinuria
- normal diet
- If dBP >=100 mmHg give medical treatment: Metiladopa, Labetolol,
calcium blockers.
Avoid: Nitroprusiate- toxic for foetus
Selective betablocker- fetal mental retardation
Diuretics- placentary hypoperfusion
Converting enzyme inhibitors- hypotension and renal failure to the new birth.
b. Preeclampsia with signs of alarm:
- hospitalization
- maintain BP 90-100 mmHg
- Hydralazine 5-10 mg repeated after 20-30 min.
- Diazoxide or labetolol if no efficiency appear
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- Nicardipine
- Prevent convulsions with magnesium sulphate i.v. or perfusion
c. Eclampsia
In this case you must to reduce BP very fast to avoid hypertensive encephalopaty and renal damages.
- maintain opened airways
- oxygen
- i.v. line- magnesium sulphate 1g i.v., then perfusion max. 6-8 g/day.
- Hydralazine 10-20 mg i.v repeated if dBP>=110mmHg.
- Alternative: Labetolol
- In case of convulsions- Diazepam 10mg i.v. repeated
- The solution is evacuation of uterus: caesarian section if foetus is alive;
abortion if foetus is dead.

VII. Pheocromocitoma
- phentolamine 5-10 mg. i.v., repeated after 30 min., then perfusion, with
labetolol.

VIII. Malignant hypertension


-Nitroprusiate
-Labetolol 20mg. i.v.bolus repeated after 10 min.
-Diazoxide 50-100 mg i.v. bolus repeated after 10 min.
-Hydralazine 5-10 mg. repeated after 20-30 min.
-If exist signs of cerebral edema, give furosemide in small doses.
After 12-24 hours you can give orally treatment:
a. - diuretic 20mg/day
- peripheral dilators: Hydralazine 75-100mg or Prazosine
-cental sympatetic inhibitor- Clonodine.
b. -diuretic20 mg/day
- converting enzymes inhibitors: Captopril 25mg.x3times/day or Enalapril 10-40 mg/day.
- selective betabloker: Metoprolol 100-200 mg

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