Chapter 18
The Cardiovascular System: The Heart
If the right side of the heart fails,
peripheral congestion
curs. Blood stagnates in body organs, and pooled fluids in the
tissue spaces impair the ability of body cells to obtain adequate
nutrients and oxygen and rid themselves of wastes. Te result-
ing edema is most noticeable in the extremities (feet, ankles,
and fingers).
Failure of one side of the heart puts a greater strain on the
other side, and ultimately the whole heart fails. A seriously
weakened, or
, heart is irreparable. ±reatment is
directed primarily toward (1) removing the excess leaked fluid
(drugs that increase the kidneys’ excretion of Na
and water), (2) reducing a²erload with drugs that drive down
blood pressure, and (3) increasing contractility with digitalis
derivatives. Heart transplants and other surgical or mechanical
remedies to replace damaged heart muscle provide additional
hope for some cardiac patients.
Check Your Understanding
After running to catch a bus, Josh noticed that his heart was
beating faster than normally and was pounding forcefully in
his chest. How did his increased HR and SV come about?
What problem of cardiac output might ensue if the heart
beats far too rapidly for an extended period, that is, if
tachycardia occurs? Why?
For answers, see Appendix H.
Developmental Aspects
of the Heart
Describe the development of the heart, and indicate how
the fetal heart differs from the adult heart.
Provide examples of age-related changes in heart function.
Te human heart, derived from mesoderm and guided by
powerful signaling molecules, begins as two simple endothe-
lial tubes. Tey quickly fuse to form a single chamber or heart
tube that is busily pumping blood by the 22nd day of gestation
(Figure 18.24)
Before Birth
Te tube develops four slightly bulged areas that represent the
earliest heart chambers. From tail to head, following the direc-
tion of blood flow, the four primitive chambers are the following
(Figure 18.24b):
Sinus venosus
sus). Tis chamber initially re-
ceives all the venous blood of the embryo. It will become
the smooth-walled part of the right atrium and the coro-
nary sinus. It also gives rise to the sinoatrial node, which
“takes the baton” and sets heart rate early in embryonic
Tis embryonic chamber eventually becomes the
pectinate muscle–ridged parts of the atria.
It is a known, and desirable, consequence of endurance train-
ing. With physical and cardiovascular conditioning, the heart
hypertrophies and SV increases, allowing a lower resting heart
rate while still providing the same cardiac output. However, in
poorly conditioned people persistent bradycardia may result in
grossly inadequate blood circulation to body tissues, and brady-
cardia is o²en a warning of brain edema a²er head trauma.
Homeostatic Imbalance of Cardiac Output
Te heart’s pumping action ordinarily maintains a balance be-
tween cardiac output and venous return. Were this not so, a
dangerous damming up of blood (blood congestion) would oc-
cur in the veins returning blood to the heart.
congestive heart failure (CHF)
, the heart is such an inef-
ficient pump that blood circulation is inadequate to meet tissue
needs. Tis progressively worsening disorder reflects weakening
of the myocardium by various conditions that damage it in dif-
ferent ways. Let’s take a look.
Coronary atherosclerosis.
Coronary atherosclerosis, essen-
tially fatty buildup that clogs the coronary arteries, impairs
blood and oxygen delivery to cardiac cells. Te heart becomes
increasingly hypoxic and begins to contract ineffectively.
Persistent high blood pressure.
Normally, pressure in the
aorta during diastole is 80 mm Hg, and the le² ventricle ex-
erts only slightly over that amount of force to eject blood
from its chamber. When aortic diastolic blood pressure rises
to 90 mm Hg or more, the myocardium must exert more
force to open the aortic valve and pump out the same amount
of blood. If a²erload is chronically elevated, ESV rises and
the myocardium hypertrophies. Eventually, the stress takes
its toll and the myocardium becomes progressively weaker.
Multiple myocardial infarctions.
A succession of MIs (heart
attacks) depresses pumping efficiency because noncontrac-
tile fibrous (scar) tissue replaces the dead heart cells.
Dilated cardiomyopathy (DCM)
Te cause of this condition, in which the ventricles stretch
(dilate) and become flabby and the myocardium deteriorates,
is o²en unknown. Drug toxicity (alcohol, cocaine, excess cat-
echolamines, chemotherapeutic agents) and inflammation of
the heart following an infection are implicated in some cases.
Te heart’s attempts to work harder result in increasing
levels of Ca
in cardiac cells. Te Ca
activates calcineurin,
a calcium-sensitive enzyme that initiates a cascade which
switches on genes that enlarge the heart. CO is poor because
ventricular contractility is impaired, and the cardiomyopathy
progressively worsens.
Because the heart is a double pump, each side can initially
fail independently of the other. If the le² side fails,
occurs. Te right side continues to propel blood
to the lungs, but the le² side does not adequately eject the re-
turning blood into the systemic circulation. Blood vessels in
the lungs become engorged with blood, the pressure in them
increases, and fluid leaks from the circulation into the lung tis-
sue, causing pulmonary edema. If the congestion is untreated,
the person suffocates.
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