Hypertension

and
Hypertensive Crisis

Hypertension

Blood pressure

Pressure is generated when the heart contracts against the

resistance of the blood vessels.

Ohm's Law can be applied as follows:

V=IxR
MAP = CO x SVR
MAP = Estimated by DBP + (SBP - DBP)/3
CO = cardiac output
SVR = systemic vascular resistance

Cardiac output can be broken down as:

CO = SV x HR
SV = Dependent on pre-load, contractility, after-load

Control of blood pressure

Blood pressure
Hypertension

=
=

Cardiac output x Peripheral resistance

Increased CO and/or Increased PR
Vasoconstriction

Preload

Contractility
Heart rate

Fluid volume
Sympathetic
nervous
system

Renal sodium
retention
Excess
sodium
intake

Reninangiotensinaldosterone
system

Genetic
factors
Kaplan (1994)

Hypertension
Systemic Vascular
Resistance

Cardiac
Output

Hypervolemia
- Renal artery stenosis
- Renal disease
- Hyperaldosteronism
- Aortic coarctation
Stress
- Sympathetic activation
Pheochromocytoma
- Increased
cathecholamines

Stress
- Sympathetic activation
Atherosclerosis
Renal artery disease
- Increased Ang II
Pheochromocytoma
- Increased cathecholamine
Thyroid dysfunction
Diabetes
Cerebral ischemia

Hypertension Guidelines
BP Classification

WHO-ISH 2003

ESH-ESC 2003

BP-JNC 7

Optimal

<120 / <80

<120/<80

Normal

Normal

<130 / <85

120-129 /80-84

Prehypertension

130-139 / 85-89

130-139 / 85-89

140-159 / 90-99
(140-149 / 90-94)

140-159 / 90-99

Stage 1 Hypertension

160-179/100-109

Stage 2 Hypertension

High normal
Grade 1 Hypertension
(mild)
Grade 2 Hypertension
(moderate)

160-179 /100-109

Grade 3 Hypertension
(severe)

> 180 / >110

> 180 / >110

Isolated Systolic
Hypertension

> 140 / < 90

>140 / < 90

Isolated Systolic
Hypertension

Essential (Primary)
Hypertension

Primary or Essential Hypertension

1. Etiology - unknown
2. Accounts for approximately 90% of hypertension
3. Onset typically in the fifth or sixth decade of life
4. Strong family history - 70-80% positive family history
BP

correlations are stronger among parent and child than

between spouses, suggesting that environmental factors
are less important than genetic ones

Certain

races (e.g. African Americans) are at much

higher risk of HT

Risk factors

Race (More common and more severe in blacks)

Age > 60 years
Sex (men and postmenopausal women)
Family history of CVD
Smoking
High cholesterol diet
Co-existing disorders such as diabetes, obesity
and hyperlipidemia
Sodium intake
High intake of alcohol
Sedentary life style

Secondary Hypertension

Secondary Hypertension
1. Identifiable underlying cause:
kidney disease
renal artery stenosis
hyperaldosteronism
pheochromocytoma
2. Represents approximately 10% of all hypertension
3. Has specific therapy, and is potentially curable
4. Often distinguishable from essential hypertension on
clinical grounds

Endocrine hypertension
Secondary hypertension
6-8%
Renal
4-5%
Miscellaneous
~2%
Endocrine
1-2%
Primary hyperaldosteronism 0.3%
Cushings syndrome
<0.1%
Pheochromocytoma
<0.1%

COMPLICATIONS

The risks of hypertension

The

risks of hypertension are well recognised

Cerebrovascular

disease: Thromboembolic,

Intra cranial bleed, TIA

Cardiovascular disease: MI, HF, CAD
LVH

-- enhanced incidence of HF, ventricular

arrhythmias, death following MI, and sudden
cardiac death.
Peripheral vascular disease
Renal failure

Impact of high-normal BP on CV risk

16
14
Cumulative 12
10
incidence of 8
CV events
6
(%)
4
2
0
12
Cumulative 10
incidence of 8
CV events 6
4
(%)
2
0

High-normal BP

Men

Normal BP
Optimal BP

Women

High-normal BP
Normal BP

6
Years

Optimal BP: <120/80 mmHg; normal BP: 120-129/80-84

mmHg; high-normal BP: 130-139/85-89 mmHg

10

12

Optimal BP

Vasan RS, et al. N Engl J Med 2001;345:1291-1297

DIAGNOSIS

Diagnosis
Based

upon the average of > 2 properly

measured readings at each of > 2 visits (at least
3 to 6 visits, spaced over a period of weeks to
months)
Apply to adults on no antihypertensive
medications and who are not acutely ill.
If there is a disparity in category between the
systolic and diastolic pressures, the higher value
determines the severity of the hypertension.

White coat hypertension

"white-coat"

or isolated office HT
Approximately 20 to 25 % of pts
persistent office HT but repeatedly normal
when measured at home, at work, or by
ABPM
more common in the elderly, but is infrequent
(< 5%) in pts with office DP 105 mmHg.
Taken by a nurse or technician, rather than
the physician

Masked hypertension
Elevated

out-of-office readings despite

normal office readings
Cardiovascular risk: similar as patients
with sustained HT
This is consistent with the risk of
hypertensive cardiovascular complications

Indications for ABPM

Suspected

white coat HT
Suspected episodic HT (eg, pheochromocytoma)
HT resistant to increasing medication
Hypotensive symptoms while taking
antihypertensive medications
Autonomic dysfunction

EVALUATION

Aim
To determine

the extent of target organ

damage.
To assess the patient's overall
cardiovascular risk status.
To rule out identifiable and often curable
causes of hypertension

If HT diagnosed
Evaluate

for Cardiovascular Risk Factors

Age,Fm Hx, Lipids, Obesity, microalbuminuria,
Inactivity, Smoking

Evaluate

for Target Organ Damage (TOD)

LVH or reduced EF, Angina, stroke, Kidney disease,
PAD, retinopathy

Think

about Secondary Hypertension with any new

onset Hypertension or uncontrolled hypertension

Physical examination
Goal

is to assess for target organ damage

(such as retinopathy) and clues to secondary
causes
BP, P, R
Vascular (including check all pulses)
Thyroid
Heart and Lungs
Abdomen
Neurologic

Testing
Hematocrit,

urinalysis, and routine blood

chemistries (glucose, creatinine, electrolytes)
Fasting lipid profile (total and HDL-C, TG)
Electrocardiogram
Testing for microalbuminuria
Echocardiography - detect left ventricular
hypertrophy.

Testing for renovascular hypertension

Severe or refractory HT
An acute rise in BP over a previously stable baseline
Proven age of onset before puberty or above age 50.
An acute Cr that is either unexplained or occurs after the
institution of therapy with an ACE-i or AIIRB
Moderate to severe HT in a patient with diffuse atherosclerosis
or an incidentally discovered asymmetry in renal disease.
A systolic-diastolic abdominal bruit that lateralizes to one side.
Negative family history for HT.
Moderate to severe HT in patients with recurrent episodes of
acute pulmonary edema or otherwise unexplained CHF.

Testing for other causes of identifiable

hypertension

Elevated creatinine, a calculated GFR < 60 mL/min per 1.73

m2, or proteinuria.
Pheochromocytoma: paroxysmal elevations in BP - triad of
headache, palpitations, and sweating.
Low-renin forms of hypertension (primary
hyperaldosteronism): unexplained hypokalemia
Measurement of plasma renin activity (PRA) and
aldosterone concentration.
Cushing's syndrome: cushingoid facies, central obesity,
ecchymoses, and muscle weakness.
Coarctation of the aorta: decreased peripheral pulses and a
vascular bruit over the back.

TREATMENT

JNC VI and WHOISH

blood pressure targets

JNC VII targets

<140/90 mmHg in uncomplicated hypertension
<130/85 mmHg in patients with diabetes or renal
disease
<125/75 mmHg in patients with renal insufficiency
and proteinuria >1 g/24 hours

WHOISH targets
<130/85 mmHg in young, middle-aged and diabetic
patients
<140/90 mmHg in elderly patients
JAMA. 2003; 289:2560-2572
J Hypertens 1999;17:151183

Lifestyle Modification
Modification

Approximate SBP reduction

(range)

Weight reduction

520 mmHg/10 kg weight loss

Adopt DASH eating

plan

814 mmHg

Dietary sodium
reduction

28 mmHg

Physical activity

49 mmHg

Moderation of
alcohol consumption

24 mmHg

Drug treatment

Factors affecting choice of

antihypertensive drug
The

cardiovascular risk profile of the

patient
Coexisting disorders
Target organ damage
Interactions with other drugs used for
concomitant conditions
Tolerability of the drug
Cost of the drug

Antihypertensive drug strategies

Reduce

cardiac output

-adrenergic

blockers
Ca2+ Channel blockers
Dilate

resistance vessels

Ca2+

Channel blockers
Renin-angiotensin system blockers
1 adrenoceptor blockers
Nitrates
Reduce

vascular volume

Diuretics
Direct

vasodilators

Anti-Hypertensive Drugs: Sites of Action

Symphatetic
Activity

Renin inhibitors

Renin

BLOCKERS
Cardiac
Output

Thiazids

ACE-i
ARBs

Calsium Antagonist+

BLOCKERS
HYDRALAZINE

PERIPHERAL
VASCULAR
RESISTENCE

Choosing the right antihypertensive

Condition

Preferred drugs

Other drugs that can

be used

Drugs to be
avoided

Asthma

CCBs

-blockers/ARB/Diuretics/
ACE-i

-blockers

Diabetes
mellitus

-blockers/ACE-i/
ARB

CCBs

Diuretics/
-blockers

High
cholesterol
levels

-blockers

ACE-i/ARB/ CCB

-blockers/
Diuretics

Elderly
patients

CCBs

-blockers/ACE-i/

BPH

- blockers

ARB/- blockers
-blockers/ ACE-i/ ARB/
Diuretics/ CCBs

JNC 7 Medication Algorithm

Initial Drug Choices

Without Compelling Indications

Stage 1 Hypertension
(SBP 140159 or DBP
9099 mmHg)
Thiazide-type diuretics
for most. May consider
ACEI, ARB, BB, CCB,
or combination

With Compelling Indications

Stage 2 Hypertension
(SBP >160 or DBP >100
mmHg)
2-drug combination for
most (usually thiazidetype diuretic and ACEI
or ARB or BB or CCB)

Drug(s) for the

compelling indications
Other antihypertensive
drugs (diuretics, ACEI,
ARB, BB, CCB) as
needed

Not at Goal BP
Optimize dosages or add additional drugs
until goal BP is achieved.
Consider consultation with hypertension
specialist.

Antihypertensive: Side-effects and Contraindications

Class of
drugs
Diuretics
(e.g. HCT)

Main side-effects

Contraindications/
Special Precautions

Electrolyte
Hypersensitivity, Anuria
imbalance,
level of total and
C-LDL,, glucose
levels, UC, CHDL

Impotence,
-blockers
(e.g. atenolol) Bradycardia,
fatique

Hypersensitivity, Bradycardia,
Conduction disturbances,
Diabetes, Asthma, Severe
cardiac failure

Antihypertensive: Side-effects and Contraindications

Class of drugs
CCB (e.g.
Amlodipine,
Diltiazem)

Main side-effects
Pedal edema,
Headache

Contraindications/
Special Precautions
Non-DHP CCBs (e.g diltiazem)
Hypersensitivity, Bradycardia,
Conduction disturbances, CHF, LV
dysfunction.
DHP CCBsHypersensitivity

-blockers (e.g. Postural hypotension Hypersensitivity

Doxazosin)
ACE-inhibitors Cough, Hypertension, Hypersensitivity, Pregnancy,
(e.g. Lisinopril)
Angioneurotic edema Bilateral renal artery stenosis
A-II RB

Headache, Dizziness

Hypersensitivity, Pregnancy,
Bilateral renal artery stenosis

Hypertensive Crises

Definitions:
Acute

life-threatening increase in BP

Hypertensive

urgency: severe
hypertension (usually SBP > 180 and DBP
> 120 mmHg) without acute target organ
damage (TOD)

Hypertensive

TOD

emergency : severe HTN +

Pathogenesis
Untreated

Sudden

essential hypertension

withdrawal / non-adherence to

antihypertensive drug therapy

Increase

in sympathetic tone (stress, drugs)

Renovascular

hypertension, renal parenchymal

diseases, pheochromocytoma, or primary
hyperaldosteronism.
Pressure damages vascular endothelium
Platelets and fibrin activate

Clinical Manifestations
Encephalopathy
AMI/USA
Nephropathy
Aortic

dissection
LV failure/cardiac decompensation
Eclampsia

Patient evaluation
Medical

history
Physical examination
Laboratory evaluation
serum
urine
Medication profile
Drug use
Fundoscopy
EKG, CXR, head CT, echo

Laboratory evaluation
Urinalysis:

protein, RBC, casts

Cardiac enzymes- CKMB, troponins
Electrolytes, BUN, creatinine
Toxicology screen
EKG, echo, angiography, X-ray
Thyroid, cortisol, BG
LFTs

Therapeutic approach
Time

frame - consider risk level

BP goal
Urgency:

gradual; DBP to 110 in 24-48 hours

Emergency: MAP < 20 to 25% in 1 to 2 hours
Drug

selection
Route

Complications of rapid BP reduction in

severe hypertension
Widening

neurologic deficits
Retinal ischemia: blindness
Acute myocardial infarction
Deteriorating renal function

Drug treatment of
hypertensive emergencies

Nitroprusside
Potent

arterial and venous dilator

Onset seconds, duration 1-2 minutes
Immediate rebound
ADR:
coronary

steal
cyanide toxicity
Hepatic

conversion to thiocyanate
Less toxic
Cleared renally
Na thiosulfate antidote
ototoxicity,

encephalopathy, seizures
Increase mortality post MI

 May

drop cerebral blood flow

May increase intracranial pressure
Recommended vs. toxic dose!
Approved dose max 10mcg/kg/min
Toxic at 4mcg/kg/min for 2-3 hrs
Protect from light

Nicardipine
Water

soluble DHP CCB

IV infusion, titratable effects
As effective as nitroprusside
Onset 5-15min, dur 4-6h
Dose independent of pt wt (5-15mg/h)

Parenteral drugs for treatment of hypertensive emergencies

Parenteral drugs for treatment of hypertensive emergencies

Nifedipine
Given

SL, absorbed PO
onset 5min, peak 30-60, duration 6h
direct arterial dilation, decrease PVR
unpredictable BP lowering
cerebral, renal, cardiac ischemia- fatal!
Elderly most prone to ADR
Do not use!

Oral agents

Limitation: slower onset of action and an inability to control

the degree of BP reduction.
May be useful when there is no rapid access to the
parenteral medications.
Nifedipine SL (10 mg) and captopril SL (25 mg) lower the
BP within 10 to 30 minutes in many patients.
Major risk with these drugs is ischemic symptoms (eg, AP,
MI, or stroke) due to an excessive and uncontrolled
hypotensive response.
Should be avoided if more controllable drugs are available.

Treatment of specific
hypertensive emergencies

Ischemic stroke or subarachnoid or

intracerebral hemorrhage
The

benefit of reducing the BP in these

disorders must be weighed against possible
worsening of cerebral ischemia induced by
the thrombotic lesion or by cerebral
vasospasm.
These cerebrovascular events are
characterized by the abrupt onset of usually
focal neurologic findings.

Acute pulmonary edema

Hypertension

in patients with acute LF failure due

to systolic dysfunction should be principally treated
with vasodilators.
Nitroprusside or nitroglycerin with a loop diuretic is
the regimen of choice for this problem.
Drugs that increase cardiac work (hydralazine) or
decrease cardiac contractility ( labetalol or other
beta blocker) should be avoided.

Angina pectoris or AMI

Acute

coronary insufficiency frequently increases

the systemic BP.
Intravenous parenteral vasodilators, principally
nitroprusside and nitroglycerin, are effective and
reduce mortality in patients with AMI, with or
without hypertension.
Labetalol is also effective in this setting.
Drugs that increase cardiac work (hydralazine) are
contraindicated

Withdrawal of antihypertensive therapy

Abrupt discontinuation of a short-acting
sympathetic blocker (such as clonidine or
propranolol) can lead to severe hypertension and
coronary ischemia due to upregulation of
sympathetic receptors.
Control of the BP can be achieved in this setting by
readministration of the discontinued drug and, if
necessary nitroprusside, or labetalol

Pregnancy
Usually

due to preeclampsia or preexistent

hypertension
Hydralazine is the treatment of choice
Nicardipine or labetalol are alternatives in patients
who do not achieve adequate BP control with
hydralazine.
Nitroprusside, ACE inhibitors, and A II RB are
contraindicated
ACE inhibitors and AII RB can impair renal function
in the fetus

Nah gambar di atas ada dua,Tata Surya dan Pulau Jawa. Takaran Alam ini
kira2 kalau dihitung pakai matematika hasilnya:
Tata Surya dibanding Galaksi Bima Sakti = 1 cm dibanding 1000 km
Jadi = sebuah neker dibanding sebuah pulau Jawa sebagai radiusnya.
Kalau Tatasurya sebesar kelereng, maka Galaksi Bima Sakti adalah sebesar
Bola dengan Radius sepanjang pulau Jawa pokoknya bayangin sendiri
ajakarena saat itu kita ndak jelas seberapa ukuran kita..???
Padahal Galaksi tidak sekedar satu namun Milyaran