HYPERTENSIVE

EMERGENCIES

Diagnosis and treatment

 Defining the hypertensive emergency

1. Hypertensive urgencies
Persistent BP increase (dBP > 120 mmHg and/or sBP
> 220 mmHg)
2. Hypertensive emergencies
Persistent BP increase + acute or severe target organ
damage

SEVERITY is influenced by:

Speed and persistence of systolic and diastolic BP rise

BP level
Degree and extension of vascular lesions, especially
fibrinoid necrosis
 Important messages

The emergency is not determined by the

level of BP but rather by the clinical status
of the patient!

The degree of target organ damage

determines the speed of BP lowering!
 Hypertensive emergencies

Hypertensive encephalopathy
HTN with left ventricular failure
HTN with acute myocardial infarction
HTN with unstable angina
HTN with aortic dissection
Severe HTN with subarachnoid hemorrhage or stroke
Hypertensive crisis associated with
Pheochromocytoma
HTN associated with surgery
HTN in preeclampsia eclampsia
Drug related HTN (amphetamines, LSD)
 Incidence of hypertensive
emergencies
5-10% of general hypertensive population
depends on:
HTN etiology higher frequency in:
Severe HTN (dBP >130 mmHg)
Renal HTN
Reno-vascular HTN
Pheochromocytoma
Antihypertensive treatment
Association of HTN with other cardiovascular risk
factors
 Pathophysiological factors

Are the ones that determine acute BP

increases (dBP = 105-114 mmHg)
Neurogenic factors:
Central nervous system
Sympathetic nervous system

Vasoactive hormones (vasopressin, opioid

peptides)
Renin-angiotensin-aldosterone system
Vascular hyperreactivity
Pathogenic factors:
Salt excess or sudden interruption of low salt
diet
Sodium retention

Hypercatecholamine state in
pheochromocytoma or prolonged stress
Sudden interruption of antihypertensive
therapy
Increase in renin secretion
 Physiopathological profiles
1. Hypervolemia associated with sodium
retention:
GNDA
Heart failure
Primary hyperaldosteronism
Interruption of diuretic treatment
2. Significant arteriolar vasoconstriction:
Renovascular HTN
Accelerated HTN
Pheochromocytoma
 Severe hypertension
BP > 180/110 mm Hg

Target organ damage?

Yes No
Hypertensive 1st episode Frequent episodes
Emergency HTN Urgency Uncontrolled HTN

I.v. treatment p.o treatment p.o. treatment

ICU admission Reevaluation in 24h Reevaluation in 24h
 Patient evaluation

History
Etiology of HTN, duration, current treatment
Sympatomimetic drug treatment
Symptoms consistent with cerebral, cardiac or eye
damage
Clinical
Cardio-pulmonary status
Neurological exam
Evaluating edema/pleural effusion/pericardial effusion
Fundoscopic examination
 Clinical characteristics of hypertensive
emergencies

BP usually > 220/140 mmHg

Fundoscopic examination hemorrhages,
exudates, papillary edema
Neurologic exam headache, confusion,
eyesight impairment, convulsions, coma
Cardiac heart failure
Renal retention of waste products,
proteinuria, oliguria
Gastrointestinal - nausea, vomiting
Fundoscopic examination

Retinopathy K-W grade 4 papillary edema

Fundoscopic examination - soft
exudates
Fundoscopic examination
hemorrhages
Fundoscopic examination
papillary edema
 Patient evaluation

Paraclinic
HLG
Urea , creatinine, glucose, serum electrolytes
Urine exam (including urinary metanefrines)
ECG
Chest X-ray
 Treatment objectives

Obtaining a progressive reduction and control of

BP values
NOT NORMALIZATION OF BP
purpose minimization of cerebral, coronary and
renovascular hypoperfusion risk

Risks of rapid decrease of BP:

Acute renal failure
Cardiac ischemic events
Cerebral ischemic events
Retinal artery occlusion (blindness)
 Acute left ventricular failure
(Hypertensive pulmonary edema)

Occurs in the setting of hypertensive cardiopathy

and diastolic dysfunction systolic dysfunction

The main role is played by the myocardial factor,

rather than the pressure factor, but decrease of
BP is a major objective

LVH More frequent pulmonary edema because

of low compliance
Hypertensive acute pulmonary edema
Etiopathogenic particularities

BP values must be very high

PTDVS and pulmonary wedge pressure
HTN associates other factors with negative effect on
the myocardial function:
Coronary ischemia
Supraventricular and ventricular rhythm disorders
valvulopathies
Toxic, degenerative myocardial damages

LVF may appear on:

Normal sized LV, but with concentric LVH and stiffness
syndrome
Dilated LV
 HTN with Left Ventricular Failure
- Clinic

Specific:
Persistency of high BP values, even with the reduction of
LVF signs
Other clinical signs associated with target organ damage

!!! Other types of acute pulmonary edema can be

accompanied by temporary significant BP increase in the
course of the sympathetic reflex, but BP tends to rapidly go
back to normal, together with the remission of the
pulmonary edema, even without specific BP-lowering drugs
Acute LVF (Hypertensive Acute
Pulmonary Edema)
Classic treatment
Oxygen
Mialgin
Inotropes + diuretic
bleeding
Specfic treatment
Nitroglycerin
Diuretic
Other antihypertensives: nicardipine,
clonidine, labetalol
Bleeding
! To be avoided: Dihydralazine
 Acute coronary
syndromes (ACS)

No ST elevation ST elevation
NSTEMI

Unstable angina Myocardial infarction

AMI AMI-
non-Q Q
 Hypertension with acute
coronary syndrome (unstable
angina, myocardial infarction)
 Mechanism

1. Coronary atherosclerosis (mandatory for MI) -

hypertension risk factor for IC
2. Small coronary occlusive disease due to the specific
structural lesions of hypertensive vascular disease
(predominantly muscular hypertrophy)
3. Inadequate development of microcirculation
4. Increased coronary resistance, especially extravascular
5. Reduction of coronary reserve
6. Spasm in the microcirculation
7. Increased oxygen demand due to LVH

Subendocardium = vulnerable area

Accentuated increase of the BP leads to increased
demand over supply, with severe ischemia and even
necrosis, to non-Q MI (more often) or transmural AMI

Severe complications of MI
Rupture
LVF
Sudden death due to arrhythmias

Acute coronary syndrome hypertensive

crisis due to hypercatecholamine state and
increased sympathetic tonus
 HTN with ACS
Treatment
reducing the BP with caution to avoid compromising the
coronary perfusion
the importance of maintaining BP within normal limits - useful
for reperfusion therapy; thrombolysis - not recommended if
BP> 200/120 mmHg
agents that reduce afterload and improve coronary flow
nitroglycerin i.v. of choice
dilatation of intercoronary collaterals more than the small resistance
vessels;
also decreases the preload
nitroprusside
predominant effect on resistance vessels, can cause coronary theft
phenomenon
only to cases refractory to treatment with nitrates
 HTN with ACS
Treatment
beta-blockers
might not efficiently control the BP
reduce myocardial oxygen consumption and heart rate
using the beta-blocker early post-infarction reduces infarct size and mortality

!!! Afterload reduction carefully; myocardial perfusion - dependent on

the coronary perfusion pressure

hBP episodes may worsen myocardial ischemia and infarct

expansion

Vasodilators - diazoxide, hydralazine, short-acting dihydropyridines -

contraindicated
determines reflex sympathetic activation
Increases myocardial oxygen demand
 HTN in stroke

Types of stroke:
Intracerebral
hemorrhage
Subarachnoid hemorrhage
Atherothrombotic cerebral infarction
 HTN and Central Nervous
System
Chronical Sympathetic
RAAS
HTN NS
ASC endothelial dysfunction vascular remodeling media hypertrophy

large brain small brain a. Cerebral VR

a.

DSC (chronic)
stenosis
ulcerated
haemorrhage
ulcerated plaque Leucoaraiosis
plaques
thrombus

Cognitive and motor disorders

lacunar
Embolism
infarction vascular dementia
or
thrombosis
What are the target levels of BP
in hypertensive crisis with
stroke?
170-160mmHg
 Current recommendations
Hemorrhage

Increased blood pressure may increase bleeding:

reducing BP = benefits:
recurrent bleeding
further vascular damage

BUT: BP may lead to ischemia by inadequate perfusion

and concurrent cerebral vasospasm

cerebral perfusion pressure (CPP) = medium BP - intracranial pressure

maintenance of high medium BP may be the only way to keep CPP> 60
mmHg
It is not clear which is the optimal therapeutic attitude !
 Current recommendations
Ischemic stroke

NO antihypertensives at least 10 days after stroke!

Hypertension is treated only if it is a vital emergency:
severe heart failure
aortic dissection

acute cardiogenic pulmonary edema

OR
BP > 220/120 mmHg
In case of administering thrombolytic therapy: the
antihypertensive therapy is instituted 24 hours after
thrombolysis if BP> 180/110mmHg
Hypertensive encephalopathy

Clinical syndrome resulted by acute organic

brain damage due to the disturbance
of cerebral flow autoregulation phenomenon
hyperperfusion and cerebral edema
 Hypertensive encephalopathy
clinical syndrome: headache, nausea, vomiting,
confusion, drowsiness, agitation, visual disturbances,
seizures coma

NB!: there are no persistent focal neurological symptoms

in the context of severe hypertension
Fundoscopic examination: retinal angiopathy HTN
stage III-IV
physiopathological substrate: cerebral edema
overcoming of cerebral circulation self-regulation mechanism
injury of the capillary endothelium with an increased permeability
 Autoregulation of cerebral flow in chronic hypertension

Cerebral
blood flow 100
(mL/min/100 g)

normotensive
50
hypertension

0 100 200

TA medie (mm Hg)

 Messages
Encephalopathy dg.- a diagnosis of exclusion
Dif. dg. with other CNS injuries: ischemic stroke,
subarachnoid hemorrhage, encephalitis, vasculitis,
tumors, seizure diseases.
Major hypertensive emergency; requires parenteral
treatment!!! Avoid very fast BP decreases,
especially in the elderly.
medium BP - decreased by 25% in the first 1-2
hours or DBP decreased at approximately 100
mmHg
Reduction of medium BP with > 40% in the early
hours - associated with neurological complications.
Hypertensive encephalopathy Medication
of choice

Recommended:
nicardipine
sodium nitroprusside

labetalol
fenoldopamul

Avoid:
central adrenergic inhibitors sedative effect
(clonidine, methyl-dopa, reserpine, beta-blockers)
direct vasodilators (diazoxide, hydralazine) may
increase cerebral vasodilation.
 10 days hypertension is not
Thromboembolic
treated
stroke
Labetalol
Nitroprusside

Intracerebral Nitroprusside, Nicardipine,

hemorrhage Labetalol

Hypertensive Subarachnoid Labetalol, Nimodipine

crisis hemorrhage NOT Nitroprusside,
NTG

Hypertensive Labetalol, Nicardipine, Nitroprusside,

encephalopathy NTG
AORTIC DISSECTION
 Signs and symptoms
Acute Aortic PE Pneumoth Pneumonia/ Radiculop Acute
coronary dissection orax pleuresy athy pericarditis
syndromes

Character of +++ +++ + +++ + ++ ++

the pain continuous
Vegetative ++ +++ ++ + + + +
symptoms

Dyspnea +++ +++ _

(Pulmonary
edema)
Hemoptysis ++ _ _ _ _
(Pulmonary
edema)
Cyanosis _ ++ _ _ _
(Pulmonary
edema)
 Clinical examination
ACS Aortic PE Pn.thora Pneumonia/ Radiculitis Acute
dissection x pleuresy pericarditis

BP () N

Pulse N

Left ventricular
dysfunction EPA _ _ _ _
unilat
Right _
ventricular ++ _ _
dysfunction
Condensation
syndrome _ _ _ +++ _ _

Hyperresonanc _ _ _ ++ _ _
e
 Classification of aortic dissection

type I: double lumen

separation intima-media (false
one often thrombosed)

type II: intramural hematoma

type III: limited intimal lesion

(without hematoma)

type IV: atherosclerotic

plaque with
subadventiceal penetrating
ulceration and intramural
hematoma

type V: post-traumatic or
iatrogenic dissection (eg
coronary catheterization)
Aortography :
Acute aortic dissection
Acute aortic dissection
Acute aortic dissection
 Pre-eclampsia and eclampsia

Clinical syndrome characterized by::

HBP moderately severe
Proteinuria NS

Edematous syndrome

Papilloedema

Tonic-clonic seizures confusion

High frequency in primiparous after the

20th week of pregnancy
Pre-eclampsia and eclampsia

HTN background:
HTN preexisting pregnancy
eHTN
Secondary HTN
Renoparenchymal
Renovascular
Pheochromocytoma

Pregnancy toxemia
Pathogenesis of hypertension in eclampsia
(Sperloff)
Utero-placental ischemia

RAAS activation Reduced placental PG

synthesis

+ TxA2
PVR

HBP
 Pre-eclampsia and eclampsia
Treatment

MgSO4 seizure control

Labetalol bolus
Nifedipine po
Nicardipine preferable
Hydralazine - not recommended
-unpredictable response
Angiotensin converting enzyme inhibitors
fetal abnormalities

BP goals:
<160/110 mm Hg
<150/100 mm Hg if platelets < 100000/mm
 Hypertension associated with
Cocaine / Amphetamines

Benzodiazepines
sometimes can end the crisis
Nitroglycerin
Phentolamine
NO -blockers like labetalol
-adrenergic effects
vasoconstriction
paradoxical increase of BP
 Symptomatic HTN crisis

dBP 120 mmHg and / or sBP 220 mmHg

Variable clinical signs:
headache
epistaxis
palpitations
anxiety
chest pain
bleeding on recent vascular suture line
 Symptomatic HTN crisis
Clinical circumstances of occurrence:
1. Postoperative hypertension (especially
cardiovascular interventions)
2. Cerebral injury (due to IC HT and stimulation
of vegetative superior nervous centers)
3. Acute hypervolaemia in ADGN or iatrogenic
4. Rebound after abrupt discontinuation of
antihypertensive treatment with certain drugs:
clonidine, methyldopa, guanfacine, guanabenz
5. BP leap when installing AMI
6. The use of monoamine oxidase inhibitors
(MAOIs)
7. Pheochromocytoma, etc..
 Postoperative BP leap
Induced by:
Physical or mental stress
Hypoxia

Hypercapnia
fluid overload
Hypersympathetic plasmacatecholamine,
especially after aorto-coronary bypass on
the left coronary artery at patients who
were treated with beta-blockers
Increased activity of plasma reninemia
Adrenergic hyperreactivity
 Rebound to clonidine
Mechanism: sympathetic sudden interruption
with the increase of central sympathetic flow
often associated with the interruption of
clonidine and propranolol
mecanism: sympathetic interruption + sudden
unblock of peripheral beta-adrenergic receptors
that become hyperreactive
Treatment:
Clonidine
Propranolol 1-4 mg i.v.
Labetalol
 Symptomatic HTN crisis
No signs or symptoms of acute target organ
damage
Gradual decrease of BP within 24-48 h
Usually - oral medication:
Captopril oral or sublingual
Furosemide i.v.
Amlodipine

BP may decrease spontaneously by resting in a

quiet room!
NO sublingual Nifedipine!
 Accelerated and malign
hypertension

Diagnostic criteria(OMS)
A. Accelerated hypertension:
dBP 130 mmHg
Fundoscopic examination IIIrd degree
relative resistance to treatment
rapid development of histological lesions in target organs
heart or renal failure
B. Malign hypertension :
above criteria
in addition: papillary edema and fibrinoid necrosis lesions
in the retinal microcirculation
! there is a tendency to equate the two
pathological conditions
 Accelerated and malign
hypertension
Physiopathological particularities of malign
hypertension :
negative sodium balance
hypovolemia
hiperreninemia
increased plasma levels of vasoactive factors
increased PVR
normal or low CD
histological lesions of fibrinoid necrosis and
miointimal proliferation
DIC
microangiopathic hemolytic anemia
 Accelerated and malign
hypertension

Etiologic
conditions of developing
malign hypertension
CGN
scleroatrophic CPN

polyarteritis nodosa

scleroderma

renovascular hypertension

Severe primary hypertension etc.

 Accelerated and malign
hypertension

Aggravation of ischemia
renin hypersecretion RAAS

Treatment
Vasodilator + beta-blocker + diuretic
 Principles of treatment

BP reduction is done progressively to values of DBP = 100-110

mmHg (risk of tissue ischemia at sudden drop of BP)

In patients with severe tension leap, but without neurological or

cardiac manifestations, initially are used oral antihypertensive

Avoid parenteral vasodilators association with beta-blockers or

other drugs that prevent reflex sympathetic stimulation
(reduces CD and hypotension occurs; beta-blocker iv leads to
cerebral vasoconstriction). Exception: aortic dissection

In case of diffuse cerebral edema - direct vasodilators are

contraindicated

Special attention to those with previous cardiovascular disease

(cerebral infarction or TIA) - vulnerable to sudden reduction of
BP
Antihypertensive treatment according to the type of
hypertensive emergencies
Antihypertensive treatment according to the type of
hypertensive emergencies(continued)
 Conclusions
Hypertensive emergencies treatment

Treatment goal
Prevent target organ damage
NOT immediate normalization of the BP (except
dissection of the aorta)

Requires lowering BP, but not brutal, within 24-48h, usually

with parenteral administered therapy in monitoring conditions.

Aggressive reduction of BP may contribute to further damage

of target organs by losing the autoregulation phenomenon!!!
THANK YOU FOR YOUR
ATTENTION!