KOMPLIKASI HIPERTENSI

Target
organ
complications
of
hypertension reflect the degree of
chronic blood pressure elevation. Such
organ damage can be attributed to (1)
the increased workload of the heart
and (2) arterial damage resulting from
the combined effects of the elevated
pressure itself (weakened vessel
walls) and accelerated atherosclerosis

 Arteries lined by atherosclerotic plaque

may thrombose or may serve as a source
of cholesterol emboli that occlude distal
vessels, causing organ infarction (such as
cerebrovascular occlusion, resulting in
stroke). In addition atherosclerosis of large
arteries hinders their elasticity, resulting
in systolic pressure spikes that can further
traumatize endothelium or provoke events
such as aneurysm rupture.

 Heart
The major cardiac effects of
hypertension
relate
to
the
increased afterload against which
the heart must contract and
accelerated atherosclerosis within
the coronary arteries.

 Left Ventricular Hypertrophy and Diastolic

Dysfunction The high arterial pressure (heightened
afterload) increases the wall tension of the left ventricle,
which compensates through hypertrophy. Concentric
hypertrophy (without dilatation) is the normal pattern of
compensation, although conditions that elevate blood
pressure by virtue of increased circulating volume (e.g.,
primary aldosteronism) may instead cause eccentric
hypertrophy with chamber dilatation . Left ventricular
hypertrophy (LVH) results in increased stiffness of the
left ventricle with diastolic dysfunction, manifested by
elevation of LV fi lling pressures that can result in
pulmonary congestion.

Systolic Dysfunction
Although LVH initially serves a compensatory role,
later in the course of systemic hypertension, the
increased LV mass may be insufficient to balance
the high wall tension caused by the elevated
pressure. As LV contractile capacity deteriorates,
findings of systolic dysfunction become evident
(i.e., reduced CO and pulmonary congestion).
Systolic dysfunction is also provoked by the
accelerated development of coronary artery
disease with resultant periods of myocardial
ischemia.

Coronary Artery Disease

Chronic hypertension is a major contributor to the
development of myocardial ischemia and infarction.
These complications reflect the combination of
accelerated
coronary
atherosclerosis
(decreased
myocardial oxygen supply) and the high systolic
workload (increased oxygen demand). In addition,
hypertensives
have
a
higher
incidence
of
postmyocardial infarction complications such as rupture
of the ventricular wall, LV aneurysm formation, and
congestive heart failure. In fact, 60% of patients who
die of transmural myocardial infarctions have a history
of hypertension.

Cerebrovascular System
Hypertension-induced strokes can be hemorrhagic or,
more commonly, atherothrombotic.
Hemorrhagic
CVAs
result
from
rupture
of
microaneurysms induced in cerebral parenchymal
vessels
by
long-standing
hypertension.
Atherothrombotic (also called thromboembolic) CVAs
arise when portions of atherosclerotic plaque within the
carotids or major cerebral arteries, or thrombi that form
on those plaques, break off, and embolize to smaller
distal vessels. Additionally, intracerebral vessels may
be directly occluded by local atherosclerotic plaque
rupture and thrombosis.
Occlusion of small penetrating brain arteries can result
in multiple tiny infarcts. As these lesions soften and are
absorbed by phagocytic cells, small (3 mm diameter)
cavities form, termed lacunae. These lacunar
infarctions are seen almost exclusively in patients with

Aorta and Peripheral Vasculature

The accelerated atherosclerosis associated with
hypertension may result in plaque formation and
narrowing throughout the arterial vasculature. In
addition to the coronary arteries, lesions most
commonly appear within the aorta and the major
arteries to the lower extremities, neck, and brain.
Chronic hypertension may lead to the development of
aneurysms, particularly of the abdominal aorta. An
abdominal aortic aneurysm (AAA) represents
prominent dilatation of the vessel, usually located
below the level of the renal arteries, contributed to by
the mechanical stress of the high pressure on an
arterial wall already weakened by medial Damage
and atherosclerosis. Aneurysms greater than 6 cm in
diameter have a very high likelihood of rupture within
2 years if not surgically corrected.

Another
life-threatening
vascular
consequence of high blood pressure is
aortic
dissection.
Elevated
blood
pressure, especially in the highest ranges,
accelerates degenerative changes in the
media of the aorta. When the weakened
wall is further exposed to high pressure,
the intima may tear, allowing blood to
dissect into the aortic media and
propagate in either direction within the
vessel wall, clipping off and obstructing
major branch vessels along the way
(including coronary or carotid arteries).
The mortality rate of aortic dissection is

Kidney
Hypertension-induced
kidney
disease
(nephrosclerosis)
is a leading cause of renal failure that results from
damage to the organs vasculature. Histologically,
the vessel walls become thickened with a hyaline
infi ltrate, known as hyaline arteriolosclerosis .
Greater levels of hypertension can induce smooth
muscle hypertrophy and even necrosis of
capillary walls, termed fi brinoid necrosis. These
changes result in reduced vascular supply and
subsequent ischemic atrophy of tubules and, to a
lesser extent, glomeruli. Because intact nephrons
can usually compensate for those damaged by
patchy ischemia, mild hypertension rarely leads
to renal insuffi ciency in the absence of other

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

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) acrossing 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.

REFERENCE
Lilly, Leonard S. Patofisiologi of heart
disease fifth edition. 2011. Lippincott
Williams & Wilkins, a Wolters Kluwer
business. US.