Cardiovascular Physiology
419
maximum heart rate (and thus cardiac output) achievable. This
results in particular from increased stiffness of the heart, and
thus a decrease in the ability to rapidly fi ll during diastole.
Hypertension
Hypertension
is defi ned as a chronically increased systemic
arterial pressure. Although the clinical defi nition of hyperten-
sion is a blood pressure above 140/90 mmHg, new guidelines
suggest that interventions to lower blood pressure should be
instituted at systolic pressures of 130 to 139 mmHg, and
diastolic pressures of 85 to 89 mmHg.
Theoretically, hypertension could result from an increase
in cardiac output or in total peripheral resistance, or both. In
reality, however, the major abnormality in most cases of well-
established hypertension is increased total peripheral resistance
caused by abnormally reduced arteriolar radius.
What causes the arteriolar constriction? In only a small
fraction of cases is the cause known. For example, diseases that
damage a kidney or decrease its blood supply are often associ-
ated with
renal hypertension
.
The cause of the hypertension
is increased release of renin from the kidneys, with subsequent
increased generation of the potent vasoconstrictor angioten-
sin II. However, for more than 95 percent of the individuals
with hypertension, the cause of the arteriolar constriction is
unknown. Hypertension of unknown cause is called
primary
hypertension
(formerly “essential hypertension”).
Many hypotheses have been proposed to explain the
increased arteriolar constriction of primary hypertension.
At present, much evidence suggests that excessive sodium
retention is a contributing factor in genetically predisposed
(“salt-sensitive”) persons. Many people with hypertension show
a drop in blood pressure after being on low-sodium diets or
receiving drugs, called
diuretics,
that cause increased sodium
and water loss in the urine. Low dietary intake of calcium
has also been implicated as a possible contributor to primary
hypertension. Obesity and a sedentary lifestyle are defi nite risk
factors, and weight reduction and exercise are frequently effec-
tive in causing some reduction of blood pressure in people with
hypertension. Cigarette smoking, too, is a defi nite risk factor.
Hypertension causes a variety of problems. One of the
organs most affected is the heart. Because the left ventricle
in a hypertensive person must chronically pump against an
increased arterial pressure (afterload), it develops an adap-
tive increase in muscle mass called
left ventricular hypertro-
phy
.
In the early phases of the disease, this hypertrophy helps
maintain the heart’s function as a pump. With time, however,
changes in the organization and properties of myocardial cells
occur, and these result in diminished contractile function and
heart failure. The presence of hypertension also enhances the
possible development of atherosclerosis and heart attacks, kid-
ney damage, and
stroke
—the rupture of a cerebral blood ves-
sel, causing localized brain damage. Long-term data on the
link between blood pressure and health show that for every
20 mmHg increase in systolic pressure and every 10 mmHg
increase in diastolic pressure, the risk of heart disease and
stroke doubles.
The major categories of drugs used to treat hypertension
are summarized in
Table 12–8
. These drugs all act in ways
that reduce cardiac output and/or total peripheral resistance.
You will note in subsequent sections of this chapter that these
same drugs are also used to treat heart failure and in both
the prevention and treatment of heart attacks. One reason
for this overlap is that these three diseases are causally inter-
related. For example, as noted in this section, hypertension is
a major risk factor for the development of heart failure and
heart attacks. But the drugs often have multiple cardiovascu-
lar effects, which may play different roles in the treatment of
the different diseases.
Heart Failure
Heart failure
(also called
congestive heart failure
) is a collec-
tion of signs and symptoms that occur when the heart fails to
pump an adequate cardiac output. This may happen for many
reasons; two examples are pumping against a chronically elevated
arterial pressure in hypertension, and undergoing structural
damage due to decreased coronary blood fl ow. It has become
125
70
70
200
5
20
25
Work rate
Trained
Untrained
Trained
Untrained
Work rate
Untrained
Trained
O
2
consumption
Stroke volume (ml)
Heart rate (beats/min)
Cardiac output (L/min)
Figure 12–64
Changes in cardiac output, heart rate, and stroke volume with
increasing workload in untrained and trained individuals.
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