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 = I x R
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 = Cardiac output x Peripheral resistance
Hypertension = Increased CO and/or Increased PR
Preload
Fluid volume
Renal sodium
retention
Excess
sodium
intake
Genetic
factors
Contractility
Heart rate
Vasoconstriction
Sympathetic
nervous
system
Renin-
angiotensin-
aldosterone
system
Kaplan (1994)
Hypertension
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
Cardiac
Output
Systemic Vascular
Resistance
Hypertension Guidelines
BP Classification WHO-ISH 2003 ESH-ESC 2003 BP-J NC 7
Optimal

<120 / <80 <120/<80 Normal

Normal <130 / <85 120-129 /80-84
Prehypertension
High normal 130-139 / 85-89 130-139 / 85-89
Grade 1 Hypertension
(mild)
140-159 / 90-99
(140-149 / 90-94)
140-159 / 90-99 Stage 1 Hypertension
Grade 2 Hypertension
(moderate)
160-179 /100-109 160-179/100-109 Stage 2 Hypertension
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
Optimal BP: <120/80 mmHg; normal BP: 120-129/80-84
mmHg; high-normal BP: 130-139/85-89 mmHg
Cumulative
incidence of
CV events
(%)
16
12
10
8
6
4
2
0
14
Optimal BP
Normal BP
12
10
8
6
4
2
0
0 2 4 6 8 10 12
Years
Optimal BP
Normal BP
High-normal BP
Women
Men
Cumulative
incidence of
CV events
(%)
High-normal 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
Ca
2+
Channel blockers
Dilate resistance vessels
Ca
2+
Channel blockers
Renin-angiotensin system blockers

1
adrenoceptor blockers
Nitrates
Reduce vascular volume
Diuretics
Direct vasodilators

Anti-Hypertensive Drugs: Sites of Action
BLOCKERS
Calsium Antagonist
+
BLOCKERS
HYDRALAZINE
Symphatetic
Activity
Cardiac
Output
Renin
PERIPHERAL
VASCULAR
RESISTENCE
Thiazids
ACE-i
ARBs
Renin inhibitors
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/
ARB/- blockers

BPH - blockers

-blockers/ ACE-i/ ARB/
Diuretics/ CCBs
Initial Drug Choices
Drug(s) for the
compelling indications
Other antihypertensive
drugs (diuretics, ACEI,
ARB, BB, CCB) as
needed
With Compelling Indications
Stage 2 Hypertension
(SBP >160 or DBP >100
mmHg)
2-drug combination for
most (usually thiazide-
type diuretic and ACEI
or ARB or BB or CCB)
Stage 1 Hypertension
(SBP 140159 or DBP
9099 mmHg)
Thiazide-type diuretics
for most. May consider
ACEI, ARB, BB, CCB,
or combination
Without Compelling Indications
Not at Goal BP
Optimize dosages or add additional drugs
until goal BP is achieved.
Consider consultation with hypertension
specialist.
JNC 7 Medication Algorithm
Antihypertensive: Side-effects and Contraindications
Class of
drugs
Main side-effects Contraindications/
Special Precautions
Diuretics
(e.g. HCT)
Electrolyte
imbalance,
level of total and
C-LDL,, glucose
levels, UC, C-
HDL
Hypersensitivity, Anuria
-blockers
(e.g. atenolol)
Impotence,
Bradycardia,
fatique
Hypersensitivity, Bradycardia,
Conduction disturbances,
Diabetes, Asthma, Severe
cardiac failure
Class of drugs Main side-effects Contraindications/
Special Precautions
CCB (e.g.
Amlodipine,
Diltiazem)
Pedal edema,
Headache
Non-DHP CCBs (e.g diltiazem)
Hypersensitivity, Bradycardia,
Conduction disturbances, CHF, LV
dysfunction.
DHP CCBsHypersensitivity
-blockers (e.g.
Doxazosin)
Postural hypotension Hypersensitivity
ACE-inhibitors
(e.g. Lisinopril)
Cough, Hypertension,
Angioneurotic edema
Hypersensitivity, Pregnancy,
Bilateral renal artery stenosis
A-II RB Headache, Dizziness

Hypersensitivity, Pregnancy,
Bilateral renal artery stenosis
Antihypertensive: Side-effects and Contraindications
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 emergency : severe HTN +
TOD
Pathogenesis
Untreated essential hypertension
Sudden 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