C h a p t e r 1 8
Disorders of Blood Flow and Blood Pressure
429
trials, antihypertensive therapy has been associated with
reductions in stroke incidence averaging 30% to 40%;
myocardial infarction, 20% to 25%; and heart failure,
more than 50%.
29
Hypertension increases the workload of the left ven-
tricle by increasing the pressure against which the heart
must pump as it ejects blood into the systemic circula-
tion.
30
As the workload of the heart increases, the left
ventricular wall hypertrophies to compensate for the
increased pressure work. Despite its adaptive advan-
tage, left ventricular hypertrophy is a major risk factor
for coronary heart disease, cardiac arrhythmias, sud-
den death, and congestive heart failure. Hypertensive
left ventricular hypertrophy regresses with therapy.
Regression is most closely related to systolic pressure
reduction and does not appear to reflect the particular
type of medication used.
Chronic hypertension can lead to nephrosclerosis, a
common cause of chronic kidney disease (see Chapter
25). Hypertensive kidney disease is more common in
blacks than whites. Hypertension also plays an impor-
tant role in accelerating the course of other types of kid-
ney disease, particularly diabetic nephropathy. Because
of the risk for diabetic nephropathy, the American
Diabetes Association recommends that persons with
diabetes maintain their blood pressure at levels less than
130/80 mm Hg
31
(see Chapter 33).
Dementia and cognitive impairment occur more com-
monly in persons with hypertension.
29
Hypertension,
particularly systolic hypertension, is a major risk factor
for ischemic stroke and intracerebral hemorrhage
30
(see
Chapter 37). Narrowing and sclerosis of small penetrat-
ing arteries in the subcortical regions of the brain are
common findings on autopsy in persons with chronic
hypertension.
29
These changes are thought to contribute
to hypoperfusion, loss of autoregulation of blood flow,
and impairment of the blood–brain barrier, ultimately
leading to subcortical white matter demyelination.
Magnetic resonance imaging studies have revealed
more extensive white matter lesions and brain atrophy
in hypertensive versus normotensive persons. Effective
antihypertensive therapy strongly reduces the risk of
development of significant white matter changes; how-
ever, existing white matter changes, once established, do
not appear to be reversible.
29
Diagnosis andTreatment
Unlike disorders of other body systems that are diag-
nosed by methods such as radiography and tissue
examination, hypertension and other blood pressure
disorders are determined by repeated blood pressure
measurements. Laboratory tests, x-ray films, and other
diagnostic tests usually are done to exclude secondary
hypertension and determine the presence or extent of
target-organ damage.
The increased availability of hypertensive screening
clinics provides one of the best means for early detec-
tion. Because blood pressure in many individuals is
highly variable, unless the pressure is extremely elevated
or associated with symptoms it should be measured
on different occasions over a period of several months
before a diagnosis of hypertension is made.
Ambulatory and self/home measurement of blood
pressure may provide valuable information outside the
clinician’s office regarding a person’s blood pressure and
response to treatment. Self/home measurement can help
detect “white coat hypertension,” a condition in which
the blood pressure is consistently elevated in the health
care provider’s office but normal at other times; it can
also be used to assess the response to treatment measure,
motivate adherence to treatment regimes, and eventu-
ally reduce health care costs.
29,30
The main objective for treatment of hypertension is
to achieve and maintain arterial blood pressure below
140/90 mm Hg, with the goal of preventing morbidity
and mortality. In persons with hypertension and diabe-
tes or renal disease, the goal is blood pressure below
130/80 mm Hg. Treatment methods include lifestyle
modification and, when necessary, pharmacologic
agents to achieve and maintain blood pressure within
an optimal range.
29
Lifestyle Modification.
Lifestyle modification has been
shown to reduce blood pressure, enhance the effects of
antihypertensive drug therapy, and prevent cardiovas-
cular risk. Major lifestyle modifications shown to lower
blood pressure include weight reduction in persons who
are overweight or obese, regular physical activity, reduc-
tion of dietary sodium intake, and limitation of alcohol
intake to no more than two drinks per day for most
men and one drink for women and persons of lighter
weight.
48
Pharmacologic Treatment.
The decision to initiate
pharmacologic treatment is based on the severity of the
hypertension, the presence of target-organ disease, and
the existence of other conditions and risk factors.
29,48
Drug selection is based on the stage of hypertension.
Among the drugs used in the treatment of hyperten-
sion are diuretics,
β
-adrenergic receptor inhibitors, ACE
inhibitors or angiotensin II receptor blockers, calcium
channel blockers, central
α
2
-adrenergic agonists,
α
1
-
adrenergic receptor blockers, and vasodilators.
The physiologic mechanisms whereby the different
antihypertension drugs produce a reduction in blood
pressure differ among agents.
Diuretics
lower blood
pressure initially by decreasing vascular volume (by sup-
pressing renal reabsorption of sodium and increasing
sodium and water excretion) and cardiac output. With
continued therapy, a reduction in peripheral resistance
becomes a major mechanism of blood pressure reduc-
tion. The
β
-adrenergic receptor inhibitors
are effective in
treating hypertension because they decrease heart rate,
cardiac output, and renin release by the kidney. The
ACE
inhibitors
act by inhibiting the conversion of angiotensin
I to angiotensin II, thus decreasing angiotensin II levels
and reducing its effect on vasoconstriction, aldosterone
levels, intrarenal blood flow, and glomerular filtration
rate. The
calcium channel blockers
decrease periph-
eral vascular resistance by inhibiting the movement of
calcium into arterial smooth muscle cells. The centrally
