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SECTION VI
Cardiovascular Physiology
ATRIAL SYSTOLE
Contraction of the atria propels some additional blood into
the ventricles. Contraction of the atrial muscle narrows the or-
ifices of the superior and inferior vena cava and pulmonary
veins, and the inertia of the blood moving toward the heart
tends to keep blood in it. However, despite these inhibitory in-
fluences, there is some regurgitation of blood into the veins.
VENTRICULAR SYSTOLE
At the start of ventricular systole, the AV valves close. Ventric-
ular muscle initially shortens relatively little, but intraventric-
ular pressure rises sharply as the myocardium presses on the
blood in the ventricle (Figure 31–2). This period of
isovolu-
metric (isovolumic, isometric) ventricular contraction
lasts
about 0.05 s, until the pressures in the left and right ventricles
exceed the pressures in the aorta (80 mm Hg; 10.6 kPa) and
pulmonary artery (10 mm Hg) and the aortic and pulmonary
valves open. During isovolumetric contraction, the AV valves
bulge into the atria, causing a small but sharp rise in atrial
pressure (Figure 31–3).
When the aortic and pulmonary valves open, the phase of
ventricular ejection
begins. Ejection is rapid at first, slowing
down as systole progresses. The intraventricular pressure rises
to a maximum and then declines somewhat before ventricular
systole ends. Peak pressures in the left and right ventricles are
about 120 and 25 mm Hg, respectively. Late in systole, pres-
sure in the aorta actually exceeds that in the left ventricle, but
for a short period momentum keeps the blood moving for-
ward. The AV valves are pulled down by the contractions of
the ventricular muscle, and atrial pressure drops. The amount
of blood ejected by each ventricle per stroke at rest is 70 to 90
mL. The
end-diastolic ventricular volume
is about 130 mL.
Thus, about 50 mL of blood remains in each ventricle at the
end of systole
(end-systolic ventricular volume),
and the
ejection fraction,
the percent of the end-diastolic ventricular
volume that is ejected with each stroke, is about 65%. The
ejection fraction is a valuable index of ventricular function. It
can be measured by injecting radionuclide-labeled red blood
cells and imaging the cardiac blood pool at the end of diastole
and the end of systole (equilibrium radionuclide angiocardio-
graphy), or by computed tomography.CLINICAL BOX 31–1
Heart Failure
Heart failure occurs when the heart is unable to put out an
amount of blood that is adequate for the needs of the tissues. It
can be acute and associated with sudden death, or chronic. The
failure may involve primarily the right ventricle (cor pulmo-
nale), but much more commonly it involves the larger, thicker
left ventricle or both ventricles. Heart failure may also be sys-
tolic or diastolic. In
systolic failure,
stroke volume is reduced
because ventricular contraction is weak. This causes an increase
in the end-systolic ventricular volume, so that the
ejection
fraction
falls from 65% to as low as 20%. The initial response to
failure is activation of the genes that cause cardiac myocytes to
hypertrophy, and thickening of the ventricular wall
(cardiac re-
modeling).
The incomplete filling of the arterial system leads
to increased discharge of the sympathetic nervous system and
increased secretion of renin and aldosterone, so Na
+
and water
are retained. These responses are initially compensatory, but
eventually the failure worsens and the ventricles dilate.output may be elevated in absolute terms but still be inade-
quate to meet the needs of the tissues
(high-output failure).
Treatment of congestive heart failure is aimed at improving
cardiac contractility, treating the symptoms, and decreasing
the load on the heart. Currently, the most effective treatment
in general use is inhibition of the production of angiotensin II
with angiotensin-converting enzyme (ACE) inhibitors. Block-
ade of the effects of angiotensin II on AT
1
receptors with non-
peptide antagonists is also of value. Blocking the production
of angiotensin II or its effects also reduces the circulating al-
dosterone level and decreases blood pressure, reducing the
afterload against which the heart pumps. The effects of aldos-
terone can be further reduced by administering aldosterone
receptor blockers. Reducing venous tone with nitrates or hy-
dralazine increases venous capacity so that the amount of
blood returned to the heart is reduced, lowering the preload.
Diuretics reduce the fluid overload. Drugs that block
β
-adre-
nergic receptors have been shown to decrease mortality and
morbidity. Digitalis derivatives such as digoxin have classi-
cally been used to treat congestive heart failure because of
their ability to increase intracellular Ca
2+
and hence exert a
positive inotropic effect, but they are now used in a secon-
dary role to treat systolic dysfunction and slow the ventricular
rate in patients with atrial fibrillation.In
diastolic failure,
the ejection fraction is initially main-
tained, but the elasticity of the myocardium is reduced so fill-
ing during diastole is reduced. This leads to inadequate stroke
volume and the same cardiac remodeling and Na
+
and water
retention that occur in systolic failure. It should be noted that
the inadequate cardiac output in failure may be relative
rather than absolute. When a large arterior venous fistula is
present, in thyrotoxicosis and in thiamine deficiency, cardiac