AFIATIN
Nephrology and Hypertension Division
Internal Medicine Department
Medical Faculty Padjadjaran University / dr.Hasan
Sadikin Hospital
Bandung
Reference
Lecture Content
Introduction
Epidemiology
Definition
Pathophysiology
Pathogenesis
Pathophysiology of T.O.D
Measurement of blood pressure
History, Physical examination
Treatment
Epidemiology
2 million new cases of hypertension
diagnosed each year in the U.S.
23% of men and 25% of women over the
age of 18 in the U.S. have HTN
The prevalence of HTN among African
Americans is increased 30-50% in each
age group compared to persons of
European descent
Epidemiology cont.
The prevalence of HTN increases steadily with
age; over 70% of women and 50% of men in the
U.S. over the age of 70 have HTN
Linear relationship between the degree of HTN
and the risk for CV and renal disease
Heart disease and stroke are the 1 st and 3rd
leading causes of death in the U.S.
More than $259 billion in direct and indirect
costs
Hypertension
Hypertension is not a disease
It is an arbitrarily defined disorder to which
both environmental and genetic factors
contribute
Major risk factor for:
cerebrovascular disease
myocardial infarction
heart failure
peripheral vascular disease
renal failure
140/90
JNC-VII
140/90
WHO-ISH
Opt <120/<80
140/90
Definition
Based on recommendation JNC VII, The Classification of
BP for adult 18 years :
Normal
diastolic 80 99
Stage-1 : systolic 140 159 or
diastolic 90 99
Stage-2 : systolic equal to or more than 160 or
diastolic equal to or more than 100
Systolic BP
(mm Hg)
Diastolic BP
(mm Hg)
Optimal BP
Normal BP
High-Normal
<120
<130
130-139
<80
<85
85-89
140-159
140-149
160-179
>180
90-99
90-94
100-109
>110
>140
140-149
<90
<90
2. Equipment :
Cuff size : the bladder should encircle and
cover two - thirds of the length of the arm;
if it does not, place the bladder over the
brachial artery. If bladder is too small, high
readings may result.
Manometer : Aneroid gauges should be
calibrated every 6 months against a
mercury manometer.
For infants, use ultrasound equipment (e.g.
the Doppler method)
3. Technique
3.1. Number of readings
On each occasion, take at least two
readings, separated by as much time as is
practical. If readings vary by more than 5
mmHg, take additional readings until two
are close.
For diagnosis, obtain three sets of
readings at least 1 week apart.
Initially, take pressure in both arms; if the
pressures differ, use arm with the higher
pressure.
If the arm pressure is elevated, take
pressure in one leg, particularly in
patients younger than 30.
4. Recordings
Bladder Length
Centre of
bladder must
be over artery
Children > 5
years
12 cm
Usually supplied
Strongly
recommende
d for routine
use
23 cm
35 cm
42 cm
2.
The cuff must be level with
the heart. If Arm
Circumference exceeds 33
cm, a large cuff must be
used. Place stethoscope
diaphragm over brachial
artery
1.
The patient
should be
relaxed and the
arm must be
supported.
Ensure no tight
clothing
constricts the
arm
3.
The column of
mercury must be
vertical. Inflate to
acclude the pulse.
Deflate at 2 to 3
mm/sec. Measure
systolic (first
sound) and
diastolic
(disappearance) to
nearest 2 mmHg.
Pathophysiology
BP=TPR X CO (blood pressure is
the product of total peripheral
resistance and cardiac output)
Autoregulation
BLOOD PRESSURE = CARDIAC OUTPUT X PERIPHERAL RESISTANCE
Hypertension
Preload
Fluid
Volume
Contractility
Increased PR
Functional
Constriction
Structural
Hypertrophy
Volume
Redistribution
Renal
Sodium
retention
Excess
sodium
intake
= Increased CO and/or
Descreased
filtration
surface
Genetic
alteration
Sympathetic
nervous
overactivity
Stress
Reninangiotensin
excess
Cell
membrane
alteration
Hyperinsuli
nemia
Genetic
alteration
Obesity
Endothelium
derived
factors
Causes of Sympathetic
Nervous System (SNS)
Activation Genetic
Diet
Factors
SNS
Activation
Acute
Physical
Stressors
Psychosocial
Stress
Catecholamine levels
Heart
rate
Cardiac
output
Blood
pressure
Platelet
aggregation
ANGIOTENSINOGEN
Renin
ANGIOTENSIN I
Converting
enzyme
ANGIOTENSIN II
ANGIOTENSIN III
ANGIOTENSINASE A
Adrenal
cortex
Kidney
Intestine
CNS
Vascular
smooth
muscle
Peripheral nervous
system
Heart
Adrenergic
facilitation
Contractility
Aldosterone
Sympathetic
discharge
Distal
nephron
reabsorption
Maintain or increase
ECFV
Thirst salt
appetite
Vasopressin
release
Vasoconstriction
Total peripheral
resistance
Cardiac
output
Angiotensinogen
Renin
Angiotensin I
ACE
vasoconstriction
Angiotensin II
aldosterone (inc. reabsorp of Na)
Inc. PVR
Pre
hypertension
Established hypertension
30-50 years
10-30 years
CO
Complicated hypertension
40-60 years
(T. O. D)
HEREDITY - ENVIRONMENT
Age
PRE - HYPERTENSION
0 - 30
30 - 50
COMPLICATED
Accelerate CARDIAC
LARGE CEREBRAL
dHypertroph
VESSEL
Ischemia
malignant
y Failure
Aneurysm Thrombosis
course
Infarction Dissection Hemorrhag
e
RENAL
Nephrosclerosi
s Failure
Causes of Hypertension
Essential or Primary
Underlying pathophysiologic alteration
of unknown cause;
95% of cases of HTN
Secondary-Resulting from a specific cause
such as renal or endocrine disorders;
5% of cases
Primary Hypertension
Is usually of gradual onset
Usually develops between the ages of 30 and 50
Tends to remain asymptomatic for 10 to 20
years
Triggers include obesity, psychological stress,
high-sodium intake, and alcohol intake over 1
ounce per day
Aetiology of essential
hypertension
The aetiology of hypertension is
polyfactorial
polygenic
Likely causes:
Increased reactivity of resistance vessels and
resultant increase in peripheral resistance
as a result of an hereditary defect of the smooth
Other factors
Age : BP tends to rise with age, possibly as a
result of decreased arterial compliance and
should be treated agressively as in the young
Environment
Mental and physical stress both increase
blood pressure
However removing stress does nor
Sodium Intake
The SALT study and more recently the DASH
study have confirmed a strong relationship
between hypertension, stroke and salt intake
Reducing salt intake in hypertensive
individuals does lower blood pressure
However reducing salt intake in normotensives
appears to have no effect
Reducing salt intake to 60-80mmol/day does
lower BP
However there are real difficulties in achieving
this level of salt restriction (fast food)
Alcohol
The most common cause of hypertension in
the young Scot
Affects 1% of the population
Small amounts of alcohol tend to decrease
BP
Large amounts of alcohol tend to increase BP
If alcohol consumption is reduced BP will fall
over several days to weeks.
Average fall is small 5/3 mmHg
Weight
Obese patients have a higher BP
Up to 30% of hypertension is
attributable in part or wholly to obesity
If a patient loses weight BP will fall
In untreated patients a weight loss of
9Kg has been reported to produce a fall
in BP of 19/18 mmHg
Weight reduction is the most important
non-pharmacological measure available
Race
Caucasians have a lower BP than black
populations living in the same environment
Black populations living in rural Africa have a
lower BP than those living in towns
Reasons are not clear
Possibly black populations are more susceptible
to stress when living in towns
Respond in different ways to changes in diet
Black populations are genetically selected to be
salt retainers and so are more sensitive to an
increase in dietary salt intake
Secondary
Hypertension
5-10% of all hypertension has an identifiable
cause
Removal of the cause does not guarantee that
the hypertension or risk will return to normal
Sustained hypertension produces end-organ
damage to blood vessels, heart and kidney
This type of damage tends to increase BP
further and so a vicious self-propagating cycle
is established
Renal disease
Drug Induced
NSAIDs
Oral contraceptive
Corticosteroids
Pregnancy
pre-eclampsia
Endocrine
Conns Syndrome
Cushings disease
Phaeochromocytoma
Hypo and hyperthyroidism
Acromegaly
Vascular
Coarctation of the aorta
Sleep Apnea
Hypertension Syndrome
Its More Than Just Blood Pressure
Obesity
Decreased
Arterial
Compliance
Endothelial
Dysfunction
Abnormal
Lipid
Metabolism
Accelerated
Atherogenesi
s
Abnormal
Glucose
Metabolism
HYPERTENSION
LV Hypertrophy
and Dysfunction
Abnormal
Insulin
Metabolism
BloodClotting
Mechanism
Changes
Neurohormo
nal
Dysfunction
RenalFunction
Changes
Kannel WB. JAMA. 1996;275:1571-1576. Weber MA et al. J Hum Hypertens. 1991;5:417423. Dzau VJ et al. J Cardiovasc Pharmacol. 1993;21(suppl 1):S1-S5.
Remodelling
Ventricular dilation/
cognitive dysfunction
Myocardial
infarction &
stroke
Atherosclerosis and
left ventricular
hypertrophy
Endothelial
dysfunction
Risk factors*:
hypertension, diabetes,
obesity, smoking, age
Macroproteinuria
Nephrotic
proteinuria
End-stage
renal
disease
End-stage
heart disease,
brain damage
and dementia
Cardio/
cerebrovascular
death
Dzau VJ, et al. Circulation 2006;114:28502870; Figure adapted from Dzau V, Braunwald E.
Am Heart J 1991;121:12441263; Yusuf S, et al. Lancet 2004;364:937952
Management
The most essential element in reducing
the morbidity and mortality associated
with hypertension is long term
compliance/adherence
achieved through life style modification
alone or in combination with
pharmacologic therapy (stepped care)
Lifestyle modification
weight reduction
sodium restriction
dietary fat modification
exercise
alcohol restriction
caffeine restriction
relaxation techniques
potassium supplementation
Hypertension With
Compelling Indications
Hypertension Without
Compelling Indications
Stage 1 Hypertension
(systolic BP 140-159 mm Hg
Or Diastolic BP 90-99 mm Hg)
Thiazide type diuretics for most
may consider ACE inhibitor, ARB,
-blocker, CCB, or Combination
Stage 2 Hypertension
(systolic BP 160 mm Hg
Or Diastolic BP 100 mm Hg)
2-Drug
2-Drug combination for most
(usually thiazide - type diuretic
and ACE inhibitor or ARB or
-blocker, CCB)
Not at Goal BP
Optimize Dosages or Add Additional Drugs Until Goal BP is Achieved
Consider Consultation With HypertensionSpecialist
BP > 180/110 mm Hg
Pospone Op
AHA/JNC 7
Elective Op
Evaluation :
therapy
BP measurement confirmation
Target organ damage ?
Yes
Pospone op
BP
Optimalizing
No
Performe op
Emergency Op
Performe op
BP Monitoring
ECG monitoring
Admit to ICU pre and post op
Give antiischemia (beta blocker)
Consider spinal/epidural
anesthesia
Avoid increase or decrease of BP
> 20 % baseline
EKG post op dan periksa
troponin
AFIATIN
Bagian/UPF Ilmu Penyakit Dalam
FK. UNPAD / RSUP dr.Hasan Sadikin
Bandung
FENOMENA
GUNUNG
ES
PGK tahap 5
PGK Tahap 4
PGK Tahap 3
PGK Tahap 2
PGK Tahap 1
ANATOMI GINJAL
2 buah
retroperitoneal
FUNGSI GINJAL
EKSKRESI
MENGATUR KESEIMBANGAN
CAIRAN DAN ELEKTROLIT
MENGATUR TEKANAN DARAH
ENDOKRIN :
menghasilkan hormon-hormon :
aldosteron, renin, eritropoetin
Gout
Lupus
LFG
(ml/menit/1.73 m2
90
60 80
30 59
15 29
< 15
PGK Tahap 1
R Konservatif
PGK Tahap 5
Cuci Darah
Hemodialisis
CAPD
Gagal
Cangkok
Ginjal
Berhasil
Evaluasi
4. Program Penyuluhan
4.1 Tujuan :
a. Mengenal penyebab PGK :
* Dapat diobati dengan obat/tindakan bedah
* Menghambat perjalanan penyakit sehingga
terhindar dari tahapan 5 PGK
b. Mengenal beberapa prinsip terapi konservatif
(tabel)