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 BP’s

 Repeat BP in both arms and one leg

(both not usually necessary)
 Repeat 3 times to assure accurate
 Dx of HTN requires elevated BP’s 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 don’t 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 <120/<80
 Prehypertension 121-139/80-89
 Stage I HTN 140-159/90-99
 Stage II HTN >160/>100
 (Severe HTN >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)

 Defined as BP > 180/120
 “accelerated HPT”
 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. Non-compliance with medications in a

chronic hypertensive patient
2. Those with secondary hypertension (e.g.
pheochromocytoma, reno-vascular
hypertension, Cushing’s)
3. 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 – Guillain-
Barre
- 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 encephalopathy……………………16%
 Intracranial hemorrhage……………………………4.5%
 Acute aortic dissection………………………………2%
 Acute coronary syndrome/myocardial infarction…12%
 Pulmonary edema with respiratory failure…………22%
 Severe eclampsia/HELLP syndrome………………2%
 Acute congestive heart failure……………………14%
 Acute renal failure……………………………………9%
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 body’s 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 Intracerebral Cerebral Edema

Infarct Hemorrhage

Hypertensive
Encephalopathy
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 exam—look for pulmonary edema
 Cardiac—murmurs or gallops, angina, EKG
 Renal—renal artery bruit, hematuria
 Neurologic—focal deficits, HA, altered MS
 Fundoscopic exam—retinopathy, 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 re-

established
 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
 Obat yang ada di Indonesia:
nikardipin, diltiazem, nitrogliserin,
clonidin
 Vaidya & Quelette (2008):
 Turunkan MAP 10% pada jam 1 diikuti
15% pada 2-3 jam berikutnya
 Penurunan tidak boleh drastis agar
tidak terjadi komplikasi hipoperfusi
 Pemantauan ketat dilakukan tiap 15
menit.
 Bila target TD tercapai tetesan secara
bertahap diturunkan
 Target TD tidak boleh lebih dari 25%
dalam 2 jam
 TD 160/100 diharapkan tercapai
dalam 2-6 jam
 Pemberian diuretik bermanfaat 
mengurangi cairan dan retensi Na
Treatment

 Medication options

1. Oral antihypertensives
• Chronic hypertensive
• Hypertensive urgency

2. IV antihypertensives
• Hypertensive emergency
 Medications
 IV, short acting, titratable.
 Arterial Vasodilators
 Hydralazine, fenoldepam, nicardipine, enalapril
 Venous Vasodilators
 Nitroglycerine
 Mixed Arterial and Venous Vasodilators
 Sodium nitroprusside
 Negative Inotrope/Chronotrope
 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 MI—Labetolol or Esmolol
 Hypertensive Encephalopathy—Labetolol
 Acute Aortic Dissection—Labetolol
 Eclampsia—Labetolol or Nicardipine
 Acute Renal Failure—Fenoldopam
 Sympathetic Crisis/Cocaine—Verapamil 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 10-20 mg up to 80 mg 3-5 min 3-6 h
every 10 minutes
i.v. infusion 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 1 mg/kg for 1 min 1-2 min 20-30 min
i.v. infusion 150-300 mcg/kg/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-to-

titrate 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 β-blocker with associated α-

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 β-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 mild-
moderate 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 4-
15mg/hr
Acute Left Ventricle Failure
Signs and Symptoms

 Abrupt and severe dyspnea,

tachypnea, and diaphoresis
 Rales, wheezes, distant breath
sounds, frothy sputum, and gallop
rhythm
Therapy

 Nitroglycerin
 Arterial (especially coronaries) and veno-
dilator, reducing preload and afterload
 Lasix
 Initially a vasodilator, then diuretic
 Morphine
 Vasodilator and sympatholytic
 ACE inhibitor
 Interrupts the renin-angiotensin-aldosterone
axis
Acute Coronary Syndrome

 Elevated BP significantly increases

LV wall tension
 Wall tension is one of main
determinants of myocardial oxygen
demand.
ACS therapy goals

 Goal is to decrease wall tension by

decreasing preload and afterload.
 Typical agents do this well:
Nitroglycerin, beta-blockers,
morphine
 Avoid hydralazine and minoxidil, as
they increase myocardial oxygen
demand.
Aortic Dissection
Diagnostics

 CXR
 may be normal in up to 12% !!
 Wide mediastinum
 Deviation of trachea or NG tube
Diagnostics - CXR
Therapy

 Goal is to reduce both the BP and

the slope of the pulse wave!
 If patient presents with normal BP,
still need to decrease the shear
forces!!
Therapy
 BP goal is SBP of 100-120
 Beta-blocker (e.g. esmolol)
 Nitroprusside for BP reduction
(started after or with the beta-
blocker to avoid reflex tachycardia)
 Labetalol as monotherapy
Pregnancy and Hypertension

 Complicates 5% of pregnancies
 Risk factors:
 Nulliparity
 Age >40
 African American
 Chronic renal failure
 Diabetes mellitus
 Multiple gestations
Pregnancy and Hypertension

 Accounts for 18% of maternal

deaths
 Most common risk factor for
placental abruption
 Defined as:
 Greater than 140/90
 SBP increased >20 from baseline
 DBP increased >10 from baseline
 Pregnancy and Hypertension

 Pre-eclampsia  Eclampsia
 Hypertension  Pre-eclampsia +
 Proteinuria >300mg seizures – This is an
per 24 hr. emergency !!!!
 Peripheral edema or  HELLP syndrome
weight gain >5 lbs in  Variant of pre-
1 week eclampsia
 Presents >20 weeks  Blood pressure lower
except in gestational
 Predilection for
trophoblastic disease
multigravid
Prinsip Terapi

 Persalinan merupakan terapi yang

tepat untuk ibu, tetapi belum tentu
cocok untuk bayi
 Perfusi buruk merupakan penyebab
mortalitas dan morbiditas
 Dapat dilakukan terapi paliasi
terhadap ibu yang memnungkinkan
pematangan janin dan penipisan
servik
Terapi dengan Obat
 Indikasi: TD diastolik menetap ≥ 105-110
mmHg
 Target: TD diastolik 95 – 105 mmHg
 ACE inh, ARB, diuretik: jangan diberikan
 Jika persalinan > 48 jam: metil dopa,
labetalol, nifedipin
 Persalinan < 48 jam: parenteral
 Magnesium sulfat: mencegah PE menjadi
Eklampsia
Pheochromocytoma

 Is a tumor of adrenergic cells

 Most common site is adrenal
medulla
 Increased risk in patients with von
Recklinhausen’s disease
(neurofibromatosis)
 Treatment of Hypertensive
Urgencies

 Goal: Gradual reduction of blood

pressure over 24 hours target TD
160/100
 Treatment:
 Restart prescribed anti-hypertensive
medications for the non-compliant patient
 Clonidine
 Captopril
 Losartan
 Follow up within 24 hours
alhamdulillah