Transcript Cardiovascular System

Left- Versus Right-Side
Heart Failure
 Right-sided disease –
tends to result in a buildup of blood flowing into
the right side of the heart.
This build-up results in
edema of the ankles,
distention of the neck
veins, and enlargement of
the spleen because of
congestion in the veins
that cannot empty
properly into the heart.
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 Left-sided failure – leads
to a build-up of fluid in the
lungs or pulmonary
edema, which causes
shortness of breath.
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Figure 7-13: (a) Left-sided congestive heart failure. (b)
Right-sided congestive heart failure.
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Normal ventricular wall
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Hypertrophied ventricular wall.
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Congenital Heart Disease
 Most congenital abnormalities are in the
septum that separates the right and left
side of the heart.
 An opening in this septum allows a mixing
of deoxygenated and oxygenated blood,
which causes the heart to overwork in an
attempt to compensate for lower oxygen
levels.
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of congenital heart disease.
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Septal Defects
 Failure of the Foramen Ovale to Close
– Least serious, but most common defect
 Atrial Septal Defect
 Ventral Septal Defect
– May lead to left ventricular failure
– Cyanosis may develop if deoxygenated blood
from the right side of the heart enters the
general circulation
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Figure 7-14: Effect of septal defects (a) Normal shunt - no cyanosis. (b)
Increased pressure in right ventricle. ( c ) shunt reversal - cyanosis
develops.
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Tetralogy of Fallot
 Pulmonary stenosis
– “Blue baby” cyanosis, because of poorly oxygenated
blood.
– The union of oxygen with hemoglobin gives normal
arterial blood its bright, scarlet red color.
 Large ventricular septal defect
 Ventricular hypertrophy
 Misplaced aorta
– Secondary polycythemia, dyspnea after any exertion
– Clubbed fingers
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Figure 7-15: Tetralogy of Fallot (top) compared to normal
anatomy (bottom).
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Treatment – Tetralogy of Fallot
 Surgical repair of the problem consists of
patching the ventricular septal defect
 Opening the narrowed passageway from
the right ventricle and the narrowed
pulmonary valve
 Closing any abnormal connection made
between the aorta and the pulmonary
artery
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Patent Ductus Arteriosus (PDA)
 The ductus arteriosus is a fetal blood vessel that
connects the pulmonary artery and the aorta, shunting
blood from the nonfunctional fetal lungs.
 Soon after birth, it normally closes, but if it remains open
or patent, blood intended for the body flows from the
aorta to the lungs overloading the pulmonary artery.
 This blood is oxygenated so there is no cyanosis. There
is long-term danger of heart failure and infection at the
site of the lesion.
 The ductus may be closed surgically by dividing the
connection between the pulmonary artery and the aorta.
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Figure 7-16: Patent ductus arteriosis.
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Coarctation of the Aorta
 A narrowing, or stricture, of the artery that provides blood
to the entire body.
 The stricture, possibly near the ductus arteriosus, occurs
beyond the branching of blood vessels to the head and
arms, so the blood supply to the upper part of the body is
adequate.
 Less blood, however, flows through the constricted area
to the abdomen and legs.
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Coarctation of the Aorta
(continued)
 Blood pressure is significantly reduced in the
legs, but is high in the arms.
 Many collateral blood vessels develop to
compensate for this poor blood supply.
 The coarctation can be corrected surgically by
cutting out (excising) the narrow segment and
resectioning the aorta together.
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Heart Valve Disorders
 Stenosis: opening too small for sufficient
blood flow
 Insufficiency: opening too large
 Heart murmur: characteristic sounds that
indicate the nature of the defect
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Figure 7-17: Effect of mitral valve stenosis on the heart.
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Mitral Stenosis
 Cusps that form the valve become rigid
and fuse together
 A deep funnel shaped valve is formed
 Increased resistance of blood flow from
the left atrium to the left ventricle
 Often follows rheumatic fever
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Complications of Valvular Stenosis
 Tendency for thrombus to form
 Clotting elements form over the
malfunctioning valve
 Distention of veins delivering blood
through the heart
 Edema, poor circulation, cyanosis, heart
failure
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Mitral Insufficiency
 Blood leaks back through the mitral valve each
time the ventricle contracts
 As the left ventricle pumps blood out of the heart
and into the aorta, some blood leaks back into
the atrium, increasing the pressure and volume
there
 This backflow, in turn, increases blood pressure
in the vessels leading from the lungs to the
heart, resulting in lung congestion. This
occurrence is exacerbated if the cusps become
hardened, sclerotic, and retract.
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Mitral Insufficiency (continued)
 Another cause for leakage is the failure of specialized
muscles in the ventricle, called papillary muscles, to
contract. These muscles are attached to the underside of
the cusps by means of small cords (chorda tendinae)
that normally prevent the cusps from flipping up into the
atria when the ventricles contract. If the papillary
muscles fail to contract, the cusps open upward toward
the atria under the force of expelled ventricular blood.
This failure is commonly referred to as mitral valve
prolapse (MVP).
 Most individuals with MVP are asymptomatic and lead
fairly normal lives. Those who have moderate or more
severe cases of MVP take antibiotics like amoxicillin as a
prophylaxis measure. If the case worsens, then a valve
reconstruction or replacement may be in order.
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Aortic Stenosis
 Narrowing of the valve leading into the aorta,
occurs more often in men than in women and
most frequently in men over 50 years old.
 It may result from rheumatic fever but not as
frequently as does mitral stenosis.
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Aortic Stenosis (continued)
 Sometimes it is a congenital defect or it may occur with
hardening of the arteries; the cusps become rigid and
adhere together. Masses of hard, calcified material are
deposited, giving a warty appearance to the valve.
Because the left ventricle of the heart must pump
through this valve into the aorta, this chamber
hypertrophies greatly through overwork. An inadequate
amount of blood may be pumped into the aorta to meet
the requirements of the body.
 An insufficient blood supply to the brain can cause
syncope (fainting). This valve defect, like others, can be
corrected surgically.
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Aortic Insufficiency
 The valve does not close properly. Each
time the left ventricle relaxes, blood flows
back in from the aorta. This condition can
result from inflammation within the heart,
endocarditis, or a dilated aorta, in which
the ring around the valve is too large.
Backflow of blood causes the ventricle to
dilate, become exhausted, and eventually
fail.
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Rheumatic Heart Disease
 Rheumatic fever is an autoimmune
disease.
– Results from a reaction between
streptococcal antigens and the patient’s
own antibodies against them
– There seems to be an attraction of the
antigen-antibody complex for the mitral
valve. The aortic semilunar valve is also
affected at times
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Rheumatic Heart Disease
 The valves become inflamed as a result of the infection,
and clotting elements are deposited by blood flowing
over the valves. Small nodular structures called
vegetations form along the edge of the cusps. The
normally delicate cusps thicken and adhere to each
other. Later, fibrous tissue develops, which has a
tendency to contract.
 If the adhesions of the cusps seriously narrow the valve
opening, the mitral valve becomes stenotic. An
inadequate amount of blood flows from the left atrium to
the left ventricle. Stasis, or slowed blood flow, frequently
causes thrombus formation.
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Rheumatic Heart Disease
(continued)
 It is possible for the cusps to retract to the extent
that they fail to meet, and the valve cannot
close. The mitral valve is then insufficient, or
incompetent. There is a backflow of blood,
regurgitation, from the left ventricle into the left
atrium, when the ventricle contracts. Fortunately,
rheumatic fever is not as common today as it
once was. This is because of the widespread
use of antibiotics in treating streptococcal
infections (e.g., penicillin).
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Infectious Endocarditis
 Inflammation of the endocardium caused by a
strain of Streptococcus
 Organisms enter the blood stream from various
routes
 Friable nodules form on the endocardium
– Risk for emboli to vital organs
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Figure 7-18: Infections resulting in bacterial endocaritis.
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Figure 7-19: Bacterial endocarditis.
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Figure 7-20:Thrombus formation in an atherosclerotic
vessel. Depicted are the initial clot formation (a) and the
varying degrees of occlusion (b).
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Thrombosis
 Formation of clots in areas of turbulence
and slow blood flow (diseased valve)
 Thrombus breaks free and forms an
embolus
– Emboli may be septic or contain pyogenic
bacteria.
– Emboli may be fatal.
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Aneurysm
 A weakening in the wall of a blood vessel can cause
localized dilation
 Most commonly occur in the abdominal aorta or brain
and result primarily from arteriosclerosis
 Aneurysms can also develop in arteries other than the
aorta.
 The danger of an aneurysm is its tendency to increase in
size and rupture, resulting in hemorrhage, possibly in a
vital organ such as the heart, brain, or abdomen.
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Aneurysm (continued)
 Aneurysms usually produce no symptoms and are
detected by an x-ray or routine physical exam.
Ultrasound techniques can diagnose and measure
aneurysms. A computed tomography or CT scan is
accurate in determining the shape and size of an
aneurysm. Early detection prevents rupture.
 Surgical procedures have been very successful in
repairing blood vessels affected by aneurysm formation.
The diseased area of the vessel is removed and
replaced with an artificial graft or segment of another
blood vessel. This procedure reduces the risk of
hemorrhage and thrombus formation.
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Raynaud’s Disease
 A condition in which small arteries or arterioles
in the fingers and toes constrict.
 Symptoms are spasms including numbness,
discoloration of the local skin of the fingers and
toes, and pain.
 Spasms come and go and are most commonly
triggered by cold. As vessels constrict, blood
flow temporarily decreases causing the fingers
and toes to turn white. As the episode resolves,
the affected areas may turn pink or bluish in
color.
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Raynaud’s Disease (continued)
 Raynaud’s disease can usually be controlled by
protection from cold. Smoking should be
avoided as it constricts blood vessels regardless
of environmental conditions. Relaxation
techniques can help reduce stress, which may
bring about an attack. Cigarette smoking must
stop to ensure best results.
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Figure 7-21: Raynaud’s disease.
(Courtesy of Jason L. Smith, M.D.)
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Phlebitis
 An inflammation of a vein, usually in the leg
 Veins are both superficial and deep. It is only
when the deep veins are affected that the
condition is considered potentially serious.
Several factors may cause phlebitis: injury,
general infection, poor circulation, and obesity,
to name a few.
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Phlebitis (continued)
 The greatest danger in the deep veins is
thrombus formation, and the condition is then
called thrombophlebitis.
– Edema develops once a vein becomes occluded as
fluid tends to leak out of the vessel.
– The blood cannot return properly to the heart, the
veins become congested with blood, and fluid seeps
out into the tissues.
– It is important that the clot does not become
dislodged and travel as an embolism. Anticoagulants,
e.g. aspirin, may be administered to prevent further
clot formation, and antibiotics are administered to
prevent infection. Surgery is sometimes required to
remove the thrombus.
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Varicose Veins
 Develop in the superficial veins of the leg
 Veins become swollen, painful, and appear
knotty under the skin. The condition is caused by
stagnation of blood in the veins that can result
from several factors
– Incompetent valves (pooling of blood)
– Pregnancy, tumor
 Treatment: elastic hose, ligation, compression
sclerotherapy
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Figure 7-22: Thrombophlebitis
(Courtesy of Jason L. Smith, M.D.)
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Figure 7-23: Development of varicose veins
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Figure 7-24: Spider veins
(Courtesy of Jason L. Smith, M.D.)
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Hemorrhoids
 Varicose veins of the rectum
 Cause pain, itching, and bleeding
 Can develop from pressure on the veins
– Straining due to constipation, pressure on the
veins from a pregnant uterus, or a tumor may
promote their development
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Esophageal Varices
 Varicose veins of the esophagus frequently accompany
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cirrhosis of the liver.
They result from pressure that develops within the veins
as they try to empty.
Because of blocked blood vessels within the damaged
liver, there is a backup of blood and general congestion.
A fatal hemorrhage from these varices can occur.
Treatment: endoscopic sclerotherapy
– In this procedure, a retractable needle is guided into the
esophagus by means of a fiberoptic endoscope. The
gastroenterologist punctures the varicosities and injects a
caustic sclerosis (hardening) solution to occlude the swollen
veins. This prevents engorgement, rupture, and hemorrhage, or
stops a hemorrhage that has already begun.
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Hypertension or
“High Blood Pressure”
 A condition of abnormally high blood pressure in
the arteries
 Primary – unknown causes
– Aggravated by obesity, lack of exercise, and
excessive alcohol and salt intake
 Secondary – due to brain tumors, kidney
disease, endocrine disorder
 Hypertension may have a gradual onset and
continue for a long time, or it may be malignant,
with sudden onset and rapid progression
resulting in death if not treated immediately.
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Table 7-4: Risk of Stroke and Heart Disease Increase
with Increasing Blood Pressure
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Control Mechanisms
– Blood Pressure
 Adjustments of blood pressure are
governed by changes in kidney function
and nervous system.
– Sympathetic nervous system
– Kidneys
– Parasympathetic nervous system
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Control Mechanism
 Sympathetic Nervous System – Constricts
Arteries
–
Greater force through less space or constricted
arteries
– Fluid is added to the system, the blood pressure
increases until arteries dilate or expand, and the
kidneys are able to excrete the excess fluid.
– During the “fight or flight” response, the
sympathetic nervous system temporarily
increases blood pressure.
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Control Mechanisms –
Kidney
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Decrease in blood volume by secreting a substance
called renin
Renin activates angiotensin, arteries constrict, and
increase blood pressure.
Angiotensin also triggers the release of
aldosterone, which causes the kidneys to retain salt
(sodium) and water, thus expanding blood volume
and further increasing blood pressure.
Vasoconstriction of blood vessels due to high blood
pressure causes increased renin, angiotensin, and
aldosterone secretion.
If this cycle is not broken, blood pressure continues
to increase.
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Control Mechanisms –
Parasympathetic Nervous System

Works antagonistically to the sympathetic nervous
system and decreases blood pressure
 Reduces blood pressure by reducing blood volume
via a capillary shift mechanism
 Blood volume is high, the pressure in the arteries is
higher than that of the tissue outside
 The high blood pressure forces the fluid through the
walls of the capillaries into the tissue spaces, thus
reducing blood volume and pressure.
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Hypertensive Heart Disease
 This condition is caused by long-standing high
blood pressure or hypertension.
 The heart naturally pumps against resistance of
the narrowing blood vessels farther from the
heart.
– In the hypertensive heart, it struggles to enlarge as it
tries to meet the demands of the body by pumping
harder to force the blood through abnormally
narrowed blood vessels.
– The left ventricle that does most of the work finally
enlarges or dilates, becomes exhausted, and
eventually fails to pump blood adequately.
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Hypertension and Kidney Disease
 Hypertension can contribute to kidney disease,
and kidney disease can contribute to
hypertension.
 Decreased function of the kidneys leads to water
and salt retention, causing increased blood
volume and elevated blood pressure levels.
 Long-standing hypertension causes
arteriosclerosis of the renal artery, which
reduces blood flow to the kidneys and damages
them.
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High Blood Pressure and Morbidity
 Increases the risk of heart disease, kidney disease, and
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stroke. Increased blood pressure damages all arteries of
the body, including the coronary arteries.
Damaged arteries become sclerotic (hardened) and
weak.
Thrombi form in weakened vessels leading to ischemia
and necrosis with loss of function in vital organs.
Left ventricular hypertrophy
Angina pectoris
Stroke and damage to vital organs
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signs.
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signs.
Mulvihill, Zelman, Holdaway, Tompary, and Raymond
Human Diseases: A Systemic Approach, 6e
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Insert T 07-03 Table of blood pressure
ranges
Table 7-3: Blood Pressure Guidelines.
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Human Diseases: A Systemic Approach, 6e
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Treatment of Hypertension
 A combination of medication, diet changes, and exercise is the ideal
method for controlling high blood pressure. Because there are
usually no symptoms of high blood pressure, treatments that make
people feel bad or interfere with lifestyle are avoided.
 Overweight individuals are advised to reduce their weight. Changes
in diet for those who have diabetes and high cholesterol levels are
important for overall cardiovascular health. Cutting down on salt and
alcohol intake may make drug therapy for high blood pressure
unnecessary. Moderate exercise can help control weight and
improve circulation.
 Treatment of secondary hypertension depends on the underlying
cause. For example, treatment of kidney disease, when recognized,
can help normalize and lower blood pressure. If the blood vessels
are examined and found to be partially occluded using angiography
(dye flow), then angioplasty is called upon subsequently.
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Abnormalities in Heart
Conduction
 Heart block
 Atrial fibrillation and atrial flutter
 Ventricular fibrillation
 Cardiac arrhythmia or dysrhythmia
 Beats may be skipped or come
prematurely; these beats are called
premature ventricular contractions (PVCs).
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Heart Block
 Heart block can result from scar tissue
interfering with the conduction bundle
 May be necessary to implant an electric
pacemaker if the block is complete
 Graded
– First degree
– Second degree
– Third degree
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Atrial Fibrillation and Atrial Flutter
 The impulse for contraction spreads over
the atria and the ventricle in an
uncoordinated fashion.
 Atrial fibrillation and atrial flutter are very
fast impulses.
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Ventricular Fibrillation
 Potentially fatal
 A series of uncoordinated impulses spreads over the
ventricles, causing them to twitch or quiver rather
than contract. The ventricle does not carry out
effective coordinated contractions. Because no blood
is pumped from the heart, ventricular fibrillation is a
form of cardiac arrest. Immediate attempts at
resuscitation must be made or death will result.
Permanent damage to other organs, particularly the
brain, results when blood supply to them is
compromised.
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Human Diseases: A Systemic Approach, 6e
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Dysrhythmia
 Heart beat rhythm may become irregular and is
known as cardiac arrhythmia or dysrhythmia.
– Beats may be skipped
– Or come prematurely – premature ventricular
contractions (PVCs).
– Additional irregularities include significant increases in
heart rate, called tachycardia, or abnormally slow
rate, called bradycardia
– Medications typically control the irregularities.
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Human Diseases: A Systemic Approach, 6e
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Shock
 A life-threatening condition in which blood
pressure is too low to sustain life
 Hypovolemic (hemorrhagic) shock results from
fluid volume loss after severe hemorrhage or
loss of plasma in burn patients. Treatment
includes administration of plasma or whole
blood.
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Human Diseases: A Systemic Approach, 6e
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Shock (continued)
 Neurogenic shock is due to generalized vasodilation,
resulting from decreased vasomotor tone. The reduced
blood pressure causes poor venous return to the heart
and, hence, poor cardiac output. The decreased
vasomotor tone may be due to spinal anesthesia, spinal
cord injury, or certain drugs.
 Anaphylactic shock accompanies a severe antigenantibody reaction, such as occurs in an incompatible
blood transfusion.
 Cardiogenic shock is the result of extensive myocardial
infarction. It is often fatal, but there are drugs to combat
it.
Mulvihill, Zelman, Holdaway, Tompary, and Raymond
Human Diseases: A Systemic Approach, 6e
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Click on the screenshot to view an animation showing
hypovolemic shock.
Mulvihill, Zelman, Holdaway, Tompary, and Raymond
Human Diseases: A Systemic Approach, 6e
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Figure 7-25: Various types of shock
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Diagnostic Procedures
 Auscultation
 ECG electrical recording
 Echocardiography
 Color Doppler echocardiography
 Exercise tolerance test
 Cardiac catheterization
 X-rays of the heart and great vessels, coronary
arteriography
Mulvihill, Zelman, Holdaway, Tompary, and Raymond
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