essential hypertension.
The diagnosis of EH
Essential hypertension, also known
as primary hypertension, has no clear cause
and is thought to be linked to genetics, poor
diet, lack of exercise and obesity.
Secondary hypertension can be caused by
conditions that affect your kidneys, arteries,
heart or endocrine system.
ESSENTIAL HYPERTENSION
Approximately 90% of hypertensive patients
have blood pressures that are elevated for no
readily defi nable reason, a condition termed
is one of exclusion; it is the option left to the
clinician after considering the causes of secondary
hypertension described later in this
chapter.
EH is more a description than a diagnosis,
indicating only that a patient manifests
a specifi c physical fi nding (high blood pressure)
for which no cause has been found. In
all likelihood, different underlying defects are
responsible for the elevated pressure in different
subpopulations of patients. Because the
exact nature of these defects is unknown, to
understand EH is to understand the possibilities:
what could go wrong with normal physiology
to produce chronically elevated blood
pressure?
This discussion of EH therefore refl ects
what is currently known about its epidemiology
and genetics, experimental fi ndings, and
natural history. The picture that emerges is
that EH likely results from multiple defects of
blood pressure regulation that interact with
environmental stressors. The regulatory defects
may be acquired or genetically determined
and may be independent of one another. As
a result, EH patients exhibit varied combinations
of abnormalities and, therefore, have
various physiologic bases for their elevated
blood pressures.
Genes regulating the renin–
angiotensin–aldosterone axis have been most
thoroughly studied in hypertensives because of
the central role of this system in determining
intravascular volume and vascular tone. Within
this group, certain polymorphisms in the gene
for angiotensinogen confer an increased risk
of hypertension.
Bruit adalah suara yang terjadi di dalam pembuluh
darah akibat turbulensi, mungkin karena
penumpukan plak atau kerusakan pada pembuluh
darah.
Loud systolic bruits are due to atherosclerotic
plaques within arteries, producing turbulent
flow. These plaques are common in the aorta
and iliac arteries and less common in
the renal arteries. In addition, turbulent flow
within an abdominal aortic aneurysm may
create a bruit.
Aneurisma adalah kelainan pembuluh darah
otak yang muncul akibat penipisan dan
degenerasi dinding pembuluh darah arteri.
Penyebabnya adalah kelainan bawaan,
hipertensi, dan adanya infeksi atau trauma.
Kondisi ini menimbulkan kelemahan pada
dinding pembuluh darah sehingga membentuk
tonjolan seperti balon.
Jugular vein distention is affected by the position of your
body. If the height is greater than 3 to 4 centimeters when
measured while you are in bed with your head elevated 45
degrees, this may signal vascular or heart disease. Smaller
amounts of jugular vein distention can occur in people
without heart or vascular disease.
Increased blood volume, which can occur with heart failure,
or anything that interferes with filling of the right atrium or
movement of the blood into the right ventricle, can increase
the central venous pressure and the amount of jugular vein
distention. For example, jugular vein distention may be
raised by a narrowing or blockage of the superior vena cava,
which can interfere with blood return to the heart. It can also
be caused by constrictive pericarditis (infection of the lining
that surrounds the heart) and cardiac tamponade (filling of
the sac around the heart with blood or other fluid), both of
which restrict the volume of the heart. Right-sided heart
failure is another cause of elevated jugular vein distention.
Common causes of jugular vein distention
Jugular vein distention may be caused by heart conditions
and conditions that affect blood vessels including:
 Congestive heart failure (deterioration of the heart’s
ability to pump blood)
 Constrictive pericarditis (infection or inflammation
of the lining that surrounds the heart that decreases
the lining’s flexibility)
 Hypervolemia (increased blood volume)
 Superior vena cava obstruction (blockage of the
main vein of the upper body that returns blood to
the heart; the jugular veins empty into this vein)
 Tricuspid valve stenosis (narrowing of the valve
between the right atrium and the right ventricle)
Adanya perbedaan tekanan darah antara lengan
kanan dan lengan kiri ini bisa disebabkan oleh
beberapa faktor, diantaranya adalah faktor usia,
adanya oklusi pembuluh darah, penyakit pembuluh
darah perifer, adanya pulsus paradoksus, dan
adanya gangguan pada jantung.
Variasi tekanan darah dapat ditemukan pada arteri
yang berbeda. Variasi normal sering ditemukan
pada kedua lengan, tetapi tidak boleh lebih dari 5 –
10 mmHg. Perbedaan yang lebih dari 10 mmHg
merupakan indikasi terjadinya gangguan vaskuler,
dan bila perbedaan lebih besar dari 20 – 30 mmHg
pada kedua belah lengan menunjukkan suatu
kecurigaan terhadap adanya gangguan organis
aliran darah pada daerah yang tekanan darahnya
rendah
Ada hubungan timbal balik antara kejadian
hipertensi dan penyakit pembuluh darah perifer.
Kerusakan vaskuler akibat hipertensi terlihat jelas
pada seluruh pembuluh perifer. Hipertensi
menyebabkan perubahan struktur dalam arteri-
arteri kecil dan arteriola yang mengakibatkan
terjadinya penyumbatan pembuluh progresif.
Retina
The retina is the only location where systemic
arteries can be directly visualized by physical
examination. High blood pressure induces
abnormalities that are collectively termed
hypertensive retinopathy. Although vision
may be compromised when the damage is extensive,
more commonly the changes serve as
an asymptomatic clinical marker for the severity
of hypertension and its duration.
Severe hypertension that is acute in onset
(e.g., uncontrolled and/or malignant hypertension)
may burst small retinal vessels, causing
hemorrhages, exudation of plasma lipids,
and areas of local infarction. If ischemia of the
optic nerve develops, patients may describe
generalized blurred vision. Retinal ischemia
caused by hemorrhage leads to more patchy
loss of vision. Papilledema, or swelling of the
optic disk with blurring of its margins, may
arise from high intracranial pressure when the
blood pressure reaches malignant levels and
cerebrovascular autoregulation begins to fail.
Chronically elevated blood pressure results
in a different set of retinal fi ndings. Papilledema
is absent, but vasoconstriction results in arterial
narrowing, and medial hypertrophy thickens
the vessel wall, which “nicks” (indents)
crossing veins. With more severe chronic hypertension,
arterial sclerosis is evident as an
increased refl ection of light through the ophthalmoscope
(termed “copper” or “silver”
wiring). Although these changes are not in
themselves of major functional importance,
they indicate that the patient has had longstanding,
poorly controlled hypertension.
The small arrows indicate whether there is a stimulatory () or
inhibitory () effect on the boxed parameters. ADH, antidiuretic
hormone; HR, heart rate; NP, natriuretic peptides; PSNS,
parasympathetic nervous system; SNS, sympathetic nervous
system; SV, stroke volume

Blood pressure (BP) is the product of cardiac

output (CO) and total peripheral resistance
(TPR):

BP = CO x TPR
And CO is the product of cardiac stroke volume
(SV) and heart rate (HR):
CO = SV x HR
As described in Chapter 9, 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).

It follows that at least 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; and
hormones, which modulate the functions of…

• Stroke Volume: It is a volume of blood pumped

out by each ventricle per beat. It is about 70 - 80
ml.

Stroke volume (SV) = EDV – ESV

• End Diastolic Volume: Volume of blood in each

ventricle at the end of diastole. It is about 120 – 130
ml.

• End Systolic Volume: Volume of blood in each

ventricle at the end of Systole. It is about 50 to 60
ml