HYPERTENSION

dr. I Kadek Susila Surya Darma, SpJP

FIHA

Bagian / SMF Kardiologi dan Kedokteran Vaskular

FK Udayana RSUP Sanglah Denpasar
 Approximately 60 million Americans, and 1 billion people
throughout the world, have hypertension

Framingham Heart Study indicate that 90% of people over age

55 will develop hypertension during their lifetimes

More than two thirds of hypertensive persons are either unaware

of their elevated blood pressure or are not treated adequately to
minimize the cardiovascular risk.
PREVALENSI HT AGE 20 YEAR OLD
NHANES (NATIONAL HEALTH & NUTRITION EXAMINATION SURVEY )
2007 - 2010
 90% of affected patients cause of the blood pressure
elevation is unknown, a condition termed primary or essential
hypertension (EH).

High blood pressure attributed to a definable cause is termed

secondary hypertension.
 WHAT IS HYPERTENSION?

Hypertension a diastolic pressure 90 mm Hg

Or
a systolic pressure 140 mm Hg
CLASSIFICATION OF BLOOD PRESSURE
(JNC VII)
DEFINITIONS AND CLASSIFICATION OF BLOOD
PRESSURE LEVELS (ESC 2013)
STRATIFICATION OF TOTAL CV RISK
 FACTORS OTHER THAN BP INFLUENCING
PROGNOSIS; USED FOR STRATIFICATION OF TOTAL CV RISK
 FACTORS OTHER THAN BP INFLUENCING
PROGNOSIS; USED FOR STRATIFICATION OF TOTAL CVRISK
 HOW IS BLOOD PRESSURE REGULATED?

BP = CO x TPR
CO = SV x HR
SV is determined by
(1) cardiac contractility
(2) the venous return to the heart (the preload)
(3) the resistance the left ventricle must overcome to eject blood
into the aorta (the afterload)
REGULATION OF SYSTEMIC BLOOD PRESSURE
 Four systems are directly responsible for blood pressure regulation:
the heart, which supplies the pumping pressure
the blood vessel tone, which largely determines systemic resistance
the kidney, which regulates intravascular volume
hormones
The cardiovascular system is endowed with feedback mechanisms
that continuously monitor arterial pressure baroreceptor reflex
 ESSENTIAL HYPERTENSION

EH is more a description than a diagnosis, indicating

only that a patient manifests a specific physical finding
(high blood pressure) for which no cause has been
found.
 EPIDEMIOLOGY AND GENETICS

Heredity appears to play an important role in EH, but definite

genetic markers have not been consistently identified

Furthermore, an uneven distribution of EH exists among

different racial groups

Blacks are significantly more likely to be hypertensive than

persons of other races.
 SYSTEMIC ABNORMALITIES

The heart can contribute to a high CO based hypertension owing to

sympathetic overactivity.

The blood vessels may contribute to peripheral vascular resistance based

hypertension by constricting in response to:
increased sympathetic activity
abnormal regulation of vascular tone by local factors
ion channel defects in contractile vascular smooth muscle.
The kidney can induce volume-based hypertension by retaining
excessive sodium and water as a result of:
failure to regulate renal blood flow appropriately
ion channel defects (e.g., reduced basolateral NaK-ATPase),
which directly cause sodium retention
inappropriate hormonal regulation.
 INSULIN RESISTANCE, OBESITY,
AND THE METABOLIC SYNDROME
Elevated insulin levels may contribute to hypertension via
increased sympathetic activation or by stimulation of vascular
smooth muscle cell hypertrophy, which increases vascular
resistance.
Obesity is associated with hypertension, by:
(1) the release of angiotensinogen from adipocytes as substrate for
the reninangiotensin system
(2) augmented blood volume related to increased body mass
(3) increased blood viscosity caused by adipocyte release of profi -
brinogen and plasminogen activator inhibitor 1.
POTENTIAL PRIMARY ABNORMALITIES IN
ESSENTIAL HYPERTENSION
 NATURAL HISTORY

EH characteristically arises after young adulthood.

Its prevalence increases with age and more than 60% of
Americans older than 60 years are hypertensive.
Accordingly, diastolic hypertension is more common in young
people, while a substantial number of hypertensive patients
over age 50 have isolated systolic hypertension with normal
diastolic values
Categories of blood pressure elevation in untreated hypertensive
patients(NHANES III). Hypertension. 2001;37:869874.)
HEMODYNAMIC PROGRESSION OF
ESSENTIAL HYPERTENSION
 SECONDARY HYPERTENSION

The usual clinical evaluation of a patient with recently

diagnosed hypertension begins with a careful history and
physical examination, including a search for clues to the
secondary forms.
repeated urinary tract infections
Excessive weight loss
excessive alcohol
Obstructive
sleep apnea
CAUSES OF HYPERTENSION
PATIENT EVALUATION
PERSONAL AND FAMILY MEDICAL HISTORY
PERSONAL AND FAMILY MEDICAL HISTORY
 PHYSICAL EXAMINATION FOR SECONDARY
HYPERTENSION, ORGAN DAMAGE AND OBESITY
 PHYSICAL EXAMINATION FOR SECONDARY
HYPERTENSION, ORGAN DAMAGE AND OBESITY
LABORATORY INVESTIGATIONS
LABORATORY INVESTIGATIONS
 EXOGENOUS CAUSES

Several medications can elevate blood pressure

oral contraceptives
glucocorticoids, cyclosporine, erythropoietin
sympathomimetic drugs
Nonsteroidal anti-infl ammatory drugs

Two other substances that may contribute to hypertension are

ethanol (i.e., chronic excessiveconsumption) and cocaine.
 RENAL CAUSES

renal disease contributes to two important endogenous causes of secondary

hypertension: renal parenchymal disease, accounting for 2% to 4% of
hypertensive patients, and renal arterial stenosis, which accounts for
approximately 1%.
Damaged nephrons are unable to excrete normal amounts of sodium and
water, leading to a rise in intravascular volume, elevated CO, and hence
increased blood pressure.
The elevated blood pressure in RH arises from reduced renal blood flow to
the affected kidney, which responds to the lower perfusion pressure by
secreting renin. The latter raises the blood pressure through the subsequent
actions of angiotensin II (vasoconstriction) and aldosterone (sodium retention
THE RENINANGIOTENSINALDOSTERONE SYSTEM
 COARCTATION OF THE AORTA

COA relative obstruction to flow, the blood pressure in the aortic arch,
head, and arms is higher than that in the descending aorta and its branches
and in the lower extremities.
If coarctation involves the origin of the left subclavian artery causing
lower pressure in the left arm compared with the right arm.
Hypertension in this condition arises by two mechanisms:
reduced blood fl ow to the kidneys stimulates the renin angiotensin system
Second, high pressures proximal to the coarctation stiffen the aortic arch through
medial hyperplasia and accelerated atherosclerosis
 ENDOCRINE CAUSES

conditions is evaluated in four ways:

1. History of characteristic signs and symptoms
2. Measurement of hormone levels
3. Assessment of hormone secretion in response to
stimulation or inhibition
4. Imaging studies to identify tumors secreting the
excessive hormone
 PHEOCHROMOCYTOMA

Pheochromocytomas are catecholaminesecreting tumors of

neuroendocrine cells (usually in the adrenal medulla) that cause
approximately 0.2% of cases of hypertension.
The release of epinephrine and norepinephrine by the tumor
results in intermittent or chronic vasoconstriction, tachycardia,
and other sympathetic mediated effects
 ADRENOCORTICAL HORMONE EXCESS

Mineralocorticoids, primarily aldosterone, increase blood

volume by stimulating reabsorption of sodium into the circulation
by the distal portions of the nephron.

Glucocorticoids, such as cortisol, elevate blood pressure

when present in excess amounts, likely via blood volume
expansion and stimulated synthesis of components of the renin
angiotensin system
 THYROID HORMONE ABNORMALITIES

Approximately one third of hyperthyroid and one fourth of hypothyroid

patients have significant hypertension.
Thyroid hormones exert their cardiovascular effects by:
(1) inducing sodiumpotassium ATPases in the heart and vessels
2) increasing blood volume
(3) stimulating tissue metabolism and oxygen demand, with secondary
accumulation of metabolites that modulate local vascular tone.

Hyperthyroid patients develop hypertension through cardiac hyperactivity

with an increase in blood volume.
Hypothyroid patients demonstrate predominantly diastolic hypertension and
an increase in peripheral vascular resistance.
CLINICAL INDICATIONS AND DIAGNOSTICS OF SECONDARY
HYPERTENSION
CONSEQUENCES OF
HYPERTENSION
 CLINICAL SIGNS AND SYMPTOMS

In the past, classic symptoms of hypertension were considered

to include headache, epistaxis (nose bleeds), and dizziness. The
usefulness of these symptoms has been called into question

In general, however, most hypertensive patients are

asymptomatic and are diagnosed simply by blood pressure
measurement during routine physical examinations.
 PATHOGENESIS OF THE MAJOR
CONSEQUENCES OF ARTERIAL HYPERTENSION
TARGET ORGAN DAMAGE IN HYPERTENSION
INITIATION OF ANTIHYPERTENSIVE DRUG
TREATMENT
INITIATION OF LIFESTYLE CHANGES AND
ANTIHYPERTENSIVE DRUG TREATMENT
BLOOD PRESSURE GOALS IN HYPERTENSIVE
PATIENTS
CLASSES OF ANTIHYPERTENSIVE MEDICATIONS
PHYSIOLOGIC EFFECTS OF ANTIHYPERTENSIVE
MEDICATIONS
ADOPTION OF LIFESTYLE CHANGES
COMPELLING AND POSSIBLE CONTRA-INDICATIONS TO THE
USE OF ANTIHYPERTENSIVE DRUGS
DRUGS TO BE PREFERRED IN SPECIFIC CONDITIONS
POSSIBLE COMBINATIONS OF CLASSES OF
ANTIHYPERTENSIVE DRUGS.
EVIDENCE-BASED DOSING FOR ANTIHYPERTENSIVE DRUGS
(JNC VIII)
2014 HYPERTENSION GUIDELINE MANAGEMENT ALGORITHM
(JNC VIII)
2014 HYPERTENSION GUIDELINE MANAGEMENT ALGORITHM
STRATEGIES TO DOSE ANTIHYPERTENSIVE DRUGS
TERIMA KASIH