Krisis Hypertensi

Sigit Widyatmoko
Fakultas Kedokteran
Universitas Muhammadiyah Surakarta

Pendahuluan

Definisi: peningkatan hebat tekanan

darah, biasanya diambil patokan
tekanan diastolik > 120 mmHg.
Gejala dan kerusakan organ target
yang disebabkan TD tidak selalu
berhubungan dengan tingginya TD
Penderita hipertensi kronik TD sistolik
dapat mencapai 120 140 mmHg tanpa
adanya gejala

Oscillometric Devices

Measure mean arterial pressure (MAP) and

calculates SBP and DBP

The algorithms used are proprietary and NOT

standardized
Results can vary widely and they do not always
closely match BP values obtained by auscultation
These machines must be calibrated regularly

MAP = CO x SVR DP + 1/3 (SP-DP)

MAP= mean arterial pressure
CO= cardiac output
SVR= systemic vascular resistance
DP= diastolic pressure
SP= sistolic pressure

Manual vs. Automatic

Manual is the gold standard

Oscillometric measurements preferred in
infants and ICU settings ONLY
All high readings should be confirmed
with a manual

Confirming High BPs

Repeat BP in both arms and one leg

(both not usually necessary)
Repeat 3 times to assure accurate
Dx of HTN requires elevated BPs on 3
separate occasions

Epidemiology

Why should we care about hypertension?

30% of the population is unaware they have

hypertension
Control rates for known cases is about 50%
(we dont do a great job at controlling BP)

Risk Factors

If >50, systolic BP > 140 is a more concerning

risk factor for cardiovascular disease than
diastolic BP.
The risk of cardiovascular disease doubles for
every increase in BP of 20/10 over 115/75.

Definitions

Hypertension (according to JNC VII)

Normal BP
Prehypertension
Stage I HTN
Stage II HTN
(Severe HTN

<120/<80
121-139/80-89
140-159/90-99
>160/>100
>180/>110)

Severe HTN is not a JNC VII defined

entity

Definitions

Hypertensive Emergency

Acute, rapidly evolving end-organ damage

associated with HTN (usu. DBP > 120)
BP should be controlled within hours and
requires admission to a critical care setting

Hypertensive Urgency

DBP > 120 that requires control in BP over

24 to 48 hours
No end organ damage

Other Terminology

Severely elevated BP (JNC VII)

accelerated HPT

Defined as BP > 180/120

term used to describe individuals with

chronic hypertension with associated group 3
Keith-Wagener-Baker retinopathy

malignant HPT

describe those individuals with group 4 KWB

retinopathy changes + papilledema no
longer used

Etiology
1.

2.

3.

Non-compliance with medications in a

chronic hypertensive patient
Those with secondary hypertension (e.g.
pheochromocytoma, reno-vascular
hypertension, Cushings)
Hypertension during pregnancy is a
major risk factor for women

Other causes

Renal parenchymal disease (80% of

sec.causes)
Systemic disorders with renal involvement
(SLE)
Renovascular disease
(Atheroscleroses/fibromuscular dysplasia)
Endocrine ( phaeochromocytoma/cushing
syndrome)
Drugs (cocaine/amphetam/clonidine
withdrawal/diet pills)
CNS (trauma or spinal cord disorders GuillainBarre
Preeclampsia/Eclampsia
Postop. HPT

Pathophysiology

Not well understood

Failure of normal autoregulation + abrupt rise in SVR
Increase in SVR due to release of humoral vasoconstrictors
from the stressed vessel wall.
Endothelium plays a central role in BP homeostasis via
substances as Nitric oxide and prostacyclin
Increased pressure starts a cycle of
- endothelial damage
- local activation of clotting cascade
- fibrinoid necrosis of small vessels
- release of more vasoconstrictors
Process leads to progressive increase in resistance and
further endothelial dysfunction

End Organ Damage

Cerebral infarction 24%

Hypertensive encephalopathy16%
Intracranial hemorrhage4.5%
Acute aortic dissection2%
Acute coronary syndrome/myocardial infarction12%
Pulmonary edema with respiratory failure22%
Severe eclampsia/HELLP syndrome2%
Acute congestive heart failure14%
Acute renal failure9%

Hypertensive encephalopathy

Clinical manifestation of cerebral edema

and microhemorrhages seen with
dysfunction of cerebral autoregulation

Defined as an acute organic brain

syndrome or delirium in the setting of
severe hypertension

HPT Encephalopathy

Not adequately treated cerebral

heamorrhage, coma and death.
BUT with proper treatment
completely reversible
Clinical diagnoses (exclusion)

HPT Retinopathy - Fundoscopy

Keith-Wagener classification

Stage I arteriolar sclerosis with thickening,

irregularity and tortuosity
Stage II AV dipping or compression
Stage III Flame shaped haemorrhages and
cotton wool spots
Stage IV Papilledema

presence of stage III and IV lesions

implies failure of the CNS vascular
autoregulation and makes the Dx of
Malignant HPT definitive

HPT Retinopathy

Cotton wool spot (soft exudates)

Cotton wool spots

Hard exudates

Retinal Hemorrhage

HPT retinopathy

Pathophysiology

A loss of cerebral autoregulation.

Autoregulation is best studied in the
brain but present in heart and kidneys
as well
Represents the bodys attempt to
maintain constant FLOW of blood to
perfuse the cells

Autoregulation

In the uninjured, normotensive brain,

autoregulation is effective over MAP
ranging from about 50 150
In the chronic hypertensive, this range
is increased (e.g. 80 180)

Autoregulasi serebral

Merupakan suatu mekanisme dimana aliran

darah serebral (CBF/cerebral blood flow)
tetap konstan pada tekanan perfusi
serebral (CPF/cerebral perfusion
pressure/CPP) yang disebabkan oleh refleks
vasokontriksi atau vasodilatasi arterole
serebral sebagai repon terhadap perubahan
tekanan perfusi
CPP = MAP ICP
ICP = intracranial pressure

Autoregulation

Pada hipertensi kronis, kurva bergerak ke

kanan, sehingga autoregulasi mulai
terganggu pada CPP (cerebral perfussion
pressure) yang lebih tinggi.

Aliran darah serebral normal 50

ml/100g/menit.
TD MAP dan CPP kontriksi arteriole
untuk CVR (cerebrovascular resistance)
TD dilatasi arteriole
MAP di bawah 50-60 mmHg vasodilatasi max
CBF iskemia
MAP > 140-160 kelelahan vasokontriksi
arteriole tekanan hidrostatik edema
serebral dan kerusakan blood brain barrier

Pathophysiology

Loss of autoregulation leads to:

Cerebral hyper-perfusion
Vascular permeability
Cerebral edema
Vasospasm
Ischemia
Punctuate hemorrhages

Cerebrovascular Hypertensive
Emergencies

Cerebral
Infarct

Intracerebral
Hemorrhage
Hypertensive
Encephalopathy

Cerebral Edema

Ischemic CVA

Tx controversial

Risk increasing ischemic penumbra

Cardiovascular Hypertensive
Emergencies

Aortic
Dissection

Congestive
Heart Failure

Acute MI

Congestive Heart Failure

Elevated BP
often present
w/ CHF

Vol. Overload
renal failure
Flash Pulm.
Edema

Acute Coronary Syndrome

Reduce
myocardial work
dec. infarct size

Aortic Dissection

Intimal tear w/
extension of
dissection
Mortality 1 2%/hr.

Diagnosis and Recognition

Presentation

Always present with a new onset

symptom

Take a good history

History of HTN and previous control

Medications with dosage and compliance
Illicit drug use, OTC drugs

Diagnosis and Recognition for

Hypertension Crisis

Physical

Confirm BP in more than one extremity

Ensure appropriate cuff size
Pulses in all extremities
Lung examlook for pulmonary edema
Cardiacmurmurs or gallops, angina, EKG
Renalrenal artery bruit, hematuria
Neurologicfocal deficits, HA, altered MS
Fundoscopic examretinopathy, hemorrhage

Diagnosis and Recognition

Laboratory/Radiologic evaluations

Basic Metabolic Panel (BUN, Cr)

CBC with smear (hemolytic anemia)
Urinalysis (proteinuria, hematuria)
EKG to look for ischemia
CXR to look for pulmonary edema if dyspnea
Head CT for hemorrhage if HA or altered MS
MRI chest if unequal pulses and wide
mediastinum to look for aortic dissection

General Management Goals

Reduce BP so autoregulation can be reestablished

Typically, this is a ~25% reduction in
MAP
Or, reduce MAP to 110-115
Avoid

Lowering the BP too much or too fast.

Treating non-emergent hypertension

Treatment

Medication options

1.

Oral antihypertensives

Chronic hypertensive
Hypertensive urgency

IV antihypertensives

2.

Hypertensive emergency

Medications

IV, short acting, titratable.

Arterial Vasodilators

Venous Vasodilators

Sodium nitroprusside

Negative Inotrope/Chronotrope

Nitroglycerine

Mixed Arterial and Venous Vasodilators

Hydralazine, fenoldepam, nicardipine, enalapril

Labetolol (also vasodilates), Esmolol

Alpha blockers (inc. sympathetic activity)

Phentolamine

Medications

Preferred agents by usage

Labetolol>Esmolol>Nicardipine>Fenoldopam (esp in
pheochromocytoma)

Preferred agents by end organ damage

Pulmonary Edema (systolic)Nicardipine

Pulmonary Edema (diastolic)Esmolol
Acute MILabetolol or Esmolol
Hypertensive EncephalopathyLabetolol
Acute Aortic DissectionLabetolol
EclampsiaLabetolol or Nicardipine
Acute Renal FailureFenoldopam
Sympathetic Crisis/CocaineVerapamil or Diltiazem

Pharmacodynamic characteristics of
antihypertensive drugs
Drug

Route

Dosage

Onset

Duration

Nitroprusside

i.v. infusion

0.25-10 mcg/kg/min

Immediate 1-2 min

Labetalol

i.v. bolus

3-5 min

3-6 h

i.v. infusion

10-20 mg up to 80 mg
every 10 minutes
0.5-2 mg/min

Nitroglycerin

i.v. infusion

5-300 mcg/min

1-2 min

1-3 min

Nicardipine

i.v. infusion

5-15 mg/h

5-10 min

15-40 min

Fenoldapam

i.v. infusion

0.1-1.6 mcg/kg/min

15 min

30-60 min

Esmolol

i.v. loading
i.v. infusion

1 mg/kg for 1 min

150-300 mcg/kg/min

1-2 min

20-30 min

Phentolamine

i.v. bolus

5-10 mg every 10 min

1-2 min

10-30 min

Enalaprilat

i.v. bolus

0.625-1.25 every 6h

10-15 min

6-8 h

Hydralazine

i.v. bolus

5-20 mg

10-30 min

3-6 h

Nitroprusside

The prototype of a short-acting easy-totitrate arteriolar and venous

vasodilator.
Most common adverse effect is
hypotension which can be treated by
reducing dosage and administering
fluids if needed (lasts 1-2 min)
Other adverse effects include reflex
tachycardia and
cyanide/thiocyanate toxicity

Nitroprusside

Nitroprusside is metabolized non-enzymatically

through combination with hemoglobin to
produce cyanomethemoglobin.
A mitochondrial enzyme in the liver
(rhodanase), catalyzes the reaction of cyanide
with thiosulphate to produce thiocyanate
Thyocyanate is then excreted in the urine
So hepatic insufficiency leads to cyanide
accumulation whereas renal insufficiency leads
to thiocyanate accumulation

Labetalol

A non-selective -blocker with associated blocking activity, in a 7 to 1 ratio in i.v.

formulation.

Reduces peripheral vascular resitance with mild

reduction in heart rate while maintaining cardiac
output.

Contraindicated in reactive airway disease or

second to third degree heart block.

Should be used with caution in patients with

second to thir degree heart block.

Nitroglycerin

A venous and coronary artery dilator.

Can dilate systemic arteries at higher doses.

Indicated in patients with acute coronary

syndromes; has also been used in perioperative
hypertension.
Side effects include headache, nausea,
bradycardia, hypotension, and
methemoglobinemia.
Prlonged use may cause tachyphylaxis.

Esmolol

Short-acting cardioselective -blocker

that can be used in perioperative
hypertension and tachycardia.
If no other agents are used , a
prolonged esmolol infusion is a
relatively expensive means of blood
pressure control

Enalaprilat

The IV formulation and active

metabolite of enalapril.
Its long duration of action and variable
response, do not make it an ideal
candidate for hypertensive
emergencies.
Contraindicated during preganancy,
and in renal failure, esp. in renal
artery stenosis.

Hydralazine

An arteriolar vasodilator.

Difficult to use due to its variable magnitude and

rate of response.

Improves placental blood flow so good for

preeclampsia/eclampsia

Side effects include tachycardia, and increased

CO/myocarial oxygen consumption.

Should therefore not be used in aortic dissection or

myocardial ischemia.

Manifestasi Lain
Krisis Hipertensi

Stroke Syndromes

Terdapat 2 tipe jejas pada neuron:

Pertama, nekrosis seluler dan menetap pada

bagian pusat atau inti dari jaringan saraf yang
mengalami jejas
Kedua, penumbra, yaitu daerah iskemik di
sekeliling inti dan merupakan fokus penanganan
strok iskemik akut

Daerah penumbra bisa kembali berfungsi

normal bila terjadi perbaikan aliran darah,
sehingga penurunan TD dapat
memperburuk hipoperfusi dan
menyebabkan infark

Peningkatan tekanan darah pada stroke

iskemik akut menunjukkan kompensasi
tubuh untuk mempertahankan CPP
Tetapi TD menimbulkan risiko edema
serebral dan transformasi hemoragik pada
daerah yang mengalami infark
Pada beberapa kasus TD dalam beberapa
jam/hari menunggu merupakan pilihan
terbaik

Thrombo-Embolic CVA

Represent 85% of all strokes

BP elevations are generally mildmoderate and represent a
physiologic response to maintain
cerebral perfusion pressure to the
penumbra, which has lost its ability
to autoregulate

Embolic CVA - Dilemma

Inappropriate lowering of the BP

may convert the potentially
salvageable ischemic penumbra to
true infarction.
However, persistent BP >185/110 is
a contraindication to thrombolytic
therapy (it significantly increases
risk of intra-cranial bleeding)

Embolic CVA When to Rx HTN

For thrombolytic candidates, 1-2

doses of labetalol (5mg) or
nitroglycerin paste may be used in
attempt to get BP <185/110
If thrombolytics are given, then the
BP MUST be aggressively kept
below 185/110!

Embolic CVA When to Rx HTN

According to National Institutes of

Neurologic Disorders and Stroke:

SBP <220, no treatment

DBP <120, no treatment
End Organ Damage (+) LVH, aorta
dissection, lung edema, acute renal
failure treatment

Others use MAP <130

Embolic CVA When to RX

If complicated by:

Aortic dissection
Hypertensive encephalopathy
AMI
Renal failure

Embolic CVA How to Rx HTN

Goal: reduce MAP 10-20% or BP

15% in first 24 hours in:

uncomplicated embolic CVA with

markedly elevated pressures
End Organ Damage (+)

Hemorrhagic CVA

Unlike embolic CVA, BP elevations

in hemorrhagic CVA are profound
However, this again represents a
physiologic response to increased
intracranial pressure (and free
blood irritating the autonomic
nervous system)
Typically is transient

Hemorrhagic CVA When to Rx

However, modest reductions of

~20% MAP have not been show to
adversely affect outcome
More aggressive than CVA emboli
no penumbra:
SBP > 200 mmHg or MAP > 150

Hemorrhagic CVA - Rx

Labetalol is agent of choice

ACE inhibitor can be used but not as
well studied.
Vasodilators such as nitroprusside
and nitroglycerin are
contraindicated because they may
raise the ICP

Subarachnoid Hemorrhage

A special subset of hemorrhagic CVA.

Evidence suggests that there may be
less vasospasm and less re-bleeding
if SBP <160 or MAP <110
Target: SBP 120-150 mmHg
Agents:

Oral nimodipine 60mg q 4hr x 21 days

IV nicardipine 2mg bolus, then 415mg/hr

Treatment of Hypertensive
Urgencies

Goal: Gradual reduction of blood

pressure over 24 hours
Treatment:

Restart prescribed anti-hypertensive

medications for the non-compliant patient
Clonidine
Sublingual nitroglycerine
Captopril
Nifedipine (dont use)
Losartan

Follow up within 24 hours

alhamdulillah