15
Structural Cardiac
Disorders
Textbook Readings for Lesson 15:
Structural Cardiac Disorders
Topics Textbook Pages
Review 598–604
Pericarditis 667–669
Cardiomyopathies 669–670
Valvular Dysfunction 670–674
Rheumatic Fever/Rheumatic Heart Disease 674–677
Endocarditis 677–679
Congenital Heart Defects 710–720
Key Terms
Vascular Resistance
Pressure against which a cardiac chamber must eject blood
Resistance varies with the size of the vessel and changes in the opening and closing
of channels
High resistance impedes blood flow, low encourages blood flow
Narrow tube means greater resistance
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Oxygen Saturation (SaO2)
Percent of available hemoglobin that is bound to oxygen
Oxygen Content
Normally higher in the left side of the heart-blood is returning from the lungs (about
95%)
Normally lower in the right side–venous blood is returning from the body (about
72–80%)
Chamber Pressure
atria—thin-walled chambers, low pressure,
ventricles—thicker walled with high pressure
left ventricle has the greatest pressure because it must
pump blood into the high-pressure systemic circulation
Cardiac Shunt
Left to right-oxygenated blood from left side of heart goes into right side of heart
Right to left—less oxygenated blood goes from the right side of the heart into the
left side or systemic circulation
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Cyanosis
Bluish discoloration of the skin due to decreased oxygen levels in the arterial blood
Murmur
A blowing or swishing sound that occurs with turbulent blood flow in the heart or
great vessels
Fetal Circulation
Structures Important for Normal Fetal Circulation
Ductus Venosus
connects umbilical vein to inferior vena cava. Takes oxygenated blood from the
placenta to fetus, closes at birth.
Foramen Ovale
opening between right & left atria, blood goes through and bypasses fetus lungs
closes 15-18 hours after birth.
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Ductus Arteriosus
joins pulmonary artery to distal aortic arch
bypasses fetus lungs; circulates oxygenated blood to body, closes 10-21 days after
birth.
Congenital Heart Disease
Etiology: Multifactorial—drugs, diseases, heredity, environment
Acyanotic Heart Disease
The 3 "Acyanotic" defects are Atrial Septal Defect, Ventricular Septa Defect, and
Coarctation of the aorta. Note that all 3 defects have left-to-right shunts. Blood in
the left side of the heart has just been through the lungs where it got oxygenated.
So, left-to-right shunts (where oxygenated blood abnormally moves to the right
side), do NOT cause low O2 (cyanotic) problems. You should see more problems
related to pressure changes.
Atrial Septal Defect
Left to Right Shunt. An abnormal opening between atria leads to increased pressure and
oxygenation in right side of heart. Females 3:1.
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Ventricular Septal Defect
Left to Right Shunt. An abnormal opening between the ventricles leads to increased
pressure and oxygenation in the right side of the heart. Frequently associated with other
defects. Most close spontaneously.
Left to Right Shunt
The failure of the fetal structure to close after birth. Blood shunted from high-pressure
aorta to lower pressure pulmonary artery.
In premature babies, it may stay open due to low oxygen saturation. Indomethacin
given to close PDA.
Surgery rarely needed.
Females 3:1.
Survival Rate: 99–100% on all three types
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Coarctation of Aorta
Acyanotic heart disease. A localized narrowing of the aorta.
2 types
Preductal: between the ductus arteriosus and the subclavian artery
Postductal: distal to the ductus arteriosus
Increased pressure proximal to the defect causing high blood pressure and bounding
pulses in upper extremities and head with dizziness, headaches, fainting and
epistaxis
Decreased blood supply distal to the defect causing decreased or absent femoral
pulses, muscle cramps and coolness in lower extremities.
Males 4:1
Survival 99% in older child
83% in infants
Diagnosis/Management of Coarctation of Aorta
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Echocardiogram and/or cardiac catheterization
Surgical correction if needed.
Cyanotic Heart Disease (low O2)
Two "cyanotic" defects are Tetralogy of Fallot and Transposition of Great Vessels. Note
that both of these have right-to-left shunts.
Right to Left Shunt: Desaturated venous blood flows into the left side
of the heart, bypassing the lungs, because the pressure on the right side is
greater than the left, or the vessels are misplaced.
Tetralogy of Fallot
One of the most common cyanotic heart diseases. Increased pressure in the right
ventricle results in hypertrophy, deoxygenated blood is shunted into the overriding aorta
and left ventricle because of septal defect and pulmonary stenosis.
4 defects present
Ventricular septal defect
Pulmonary stenosis
Overriding aorta
Right ventricular hypertrophy
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Manifestation/Management
Polycythemia
Anoxic spells
Decreased physical growth
Murmur
Treatment
Palliative surgery
to increase pulmonary blood flow
Corrective surgery
to correct all of the defects
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Survival Rate
95% or better after Neonatal Period
Transposition of Great Vessels
2 separate circulations. The pulmonary artery leaves the left ventricle and the aorta
leaves the right ventricle.
Must have a defect present to allow communication between the 2 circulations in
order to have extrauterine life.
Associated defects may be an atrial septal defect, ventricular septal defect or patent
ductus arteriosus
Predominately in males
Significant number have history of familial diabetes
Congestive heart failure
Tachycardia
Tachypnea
Hepatomegaly
Cardiomegaly
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Surgery
Palliative—to increase pulmonary blood flow
Corrective—new procedure switches vessels
Survival rates vary with procedure and age—85-90%
Manifestations/Management
Depends on size and type of associated defects
Infections/Inflammation of the Heart
Infective Endocarditis
Inflammation of the endocardium (inner lining of the heart), especially involves the valve
tissues.
Etiology
Causal agents: Microorganisms. Most commonly streptococcus or
staphylococcus, but can be any virus, bacteria, fungus, etc.
Pathophysiology
The key to understanding the patho of endocarditis is that there needs to be TWO
things: Endothelial damage and bugs ( microorganisms). So the main part of the
patho is understanding HOW this endothelial damage can occur. After the damage
occurs, THEN bugs (microorganisms) have to come along before infective
endocarditis develops.
Risk Factors— (for endothelial damage of myocardial tissue)
1. Turbulent blood flow
—valve disease, prosthetic heart valves
2. Infection risk factors
—long term indwelling lines, dental work, GU procedure
3. Autoimmune Diseases
—deposition of immune complexes in the tissues
4. HIV—associated cardiac involvement
Non-bacterial thrombotic activity—This is an inflammation reaction in response
to the endothelial damage. The endothelial damage (remember the examples above
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for how this can occur) exposes the basement membrane of the endothelium
(which contains a type of collagen that actually attracts platelets).
Pathology steps
1. Endocardium must be "prepared" for colonization. The endothelial damage
does this—see risk factors above. Remember that you have to have BOTH
damage AND bugs....
2. Colonization. Microorganisms (bugs) circulating in the bloodstream must
adhere to the damaged endothelial surface. This is GREATLY facilitated by
the non-bacterial thrombotic process described above.
3. Infective vegetation forms (usually on and around the valves). This occurs
by:
(a.) bacteria stimulating the clotting cascade. This leads to increased fibrin
formation around the colonies.
(b.) then the bacterial colonies are embedded in these protective fibrin clots.
This makes them less accessible to host defenses. Another way to say this is
that these bacterial colonies are underneath the clots, which protects them
from the person's immune cells.
4. Valve dysfunction occurs due to the infective vegetation. Take a look at
some of the website pictures at the end of the lesson. Compare a nice
normal valve to one that is all full of vegetation. No wonder the valves don't
work well!
Vegetation may break off and become embolus- causing other symptoms. 2 types:
Subacute Bacterial Endocarditis (SBE)—develops gradually
(weeks/months)
Acute Bacterial Endocarditis (ABE)
More severe develops in days to months
Other Risk Factors
Heart disease (CAD, rheumatic fever, degenerative, valvular)
Cardiac surgery
Chronic debilitating diseases
Intravenous drug abuse
Immunosuppression
Manifestations
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Splinter hemorrhages (micro-emboli that look like splinters in the nail beds)
Osler's Nodes (painful due to inflammation around small infected emboli)
Janaway Lesions (flat, small non-tender red spots)
Possible Emboli Manifestations in main organs or systems
(CNS, Splenic, Renal, Pulmonary, Cardiac)
Diagnosis/Management of Endocarditis:
Echocardiogram
Antibiotics
Antimicrobial agents for 4-6 wks
Valve replacement
Prophylaxis with antibiotics for invasive procedures
Use the Web Resources links found at the unit level of your online
course for more information on the topics covered in this section.
Pericarditis
Inflammation of the sac around the heart
Acute or chronic (healed form of acute that results in a chronic
pericardial dysfunction)
Etiology
Infections, myocardial injury, hypersensitivity reactions, metabolic disorders,
neoplasms
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Classifications according to exudate
Serous
Fibrinous
Purulent
Hemorrhagic
Pathophysiology-Inflammatory process:
WBC collect where tissue injury occurred and produces an exudate in the sac
around the heart.
The accumulating exudate may limit the heart function and thus decrease cardiac
output.
Manifestations
Severe chest pain radiating to the back, presence of a friction rub (pericardial layers
rub together during movement)
Sysphagia
Weakness
Malaise
Restlessness
Weight loss
Fever
Sinus tachycardia
Management
Treat underlying cause
Symptomatic treatment (ASA, NSAIDs, analgesics)
If this is chronic, may have to remove the pericardium
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Cardiomyopathies
Definition
Disease of the myocardium itself—affects the pumping ability of the heart—fibers
cannot contract well.
Etiology
Most are idiopathic! May be secondary to toxins, infections, immunological
disorders, nutritional disorders (alcoholism), and genetics.
Classes
Dilated (congestive)—enlarged heart due to degeneration to the heart fibers. Both
RV and LV balloon out. Immense cardiomegaly. You see manifestations of both LV
Failure and RV Failure.
Hypertrophic—Ventricular SEPTUM and LV hypertrophy leads to altered shape of
chambers and poorly coordinated contractions. You see manifestations of LV
Failure.
Restrictive—This is the clinical picture of constrictive pericaditis. The myocardial
muscle becomes INFILTRATED with abnormal substances, causing dysfunction of
the ventricles. You see manifestations of both LV Failure and RV Failure.
Manifestations
LV Failure:
Dyspnea on exertion
Fatigue
Orthopnea
Fluid in lungs, crackles
RV Failure:
Edema
Jugular vein distention
Liver congestion
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Management
Treat CHF symptomatically for each type using various drugs
Diuretics
Beta blockers (decrease hypercontractibility)
Calcium channel blockers (to enhance diastolic relaxation)
Heart transplant
Valvular Disorders
Valvular disorders are usually caused by inflammation or infections (remember infective
endocarditis and rheumatic fever?), trauma, degeneration and age, or connective tissue
disorders. Look at a picture of the valve leaflets or cusps. In order to understand the
valve problems, you have absolutely GOT to remember the normal flow of blood
through the heart, where the valves are, when they are open, and when they are closed.
An absolute MUST to remember this.
Stenosis
Valve opening (orifice) is narrowed and/or constricted. Therefore the blood flow through
the valve is impeded. When the valve should be wide open, it cannot be wide open. This
can lead to increased pressure and workload of the chamber that is trying to eject blood
through the stenotic valve.
Regurgitation or Insufficiency
Another word is Incompetence. A regurgitant or insufficient or incompetent valve is one
whose leaflets do not close as tightly as they should. During systole blood can leak back
through the valves that are supposed to be closed (back into the atria). In essence, this
means that the chambers behind and in front of the valve are pumping some of the blood
again! So, there is increased volume to pump, and increased workload of both the atria
and ventricle.
Aortic Valve Stenosis
Increased LV pressure and LV hypertrophy and LV workload
Narrowed pulse pressure
Systolic murmur
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Mitral Valve Stenosis
Increased LA pressure
Pulmonary hypertension, edema, RV Failure
Diastolic murmur
Aortic Regurgitation
Increased LV volume and overload, LV hypertrophy, and LV workload
Diastolic murmur
Mitral Regurgitation
LA and LV hypertrophy to increase cardiac output
LV Failure
Systolic murmur
Management
Valve repair or replacement for severe cases. Prophylactic antibiotics before surgery
and dental work.
Mitral Valve Prolapse
Most common valvular disorder in the U.S.
Up to 30% of young women have this disorder.
Usually asymptomatic and it is suggested that this may be a normal variant.
Usually diagnosed incidentally on physical exam.
May be associated with connective tissue diseases such as Marfan's Syndrome or
scoliosis.
May show some symptoms of mitral regurgitation if prolapse is sufficient enough.
No treatment is usually necessary.
May use prophylactic antibiotics.
Acute Rheumatic Fever
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Etiology
Group A Beta hemolytic streptococcus (after a pharyngeal infection).
Risk groups
Individuals with either untreated strept throat or those who do not complete the
prescribed medications; others living in crowded sub-standard conditions.
Pathophysiology
Diffuse inflammatory disease involving the heart, joints, subcutaneous tissue, CNS
and skin. Usually seen in ages 3-15 yr.
Manifestations
RF is diagnosed if strept throat and 2 major or 1 major and 2 minor manifestations are
present.
Major manifestations
Carditis or Rheumatic Heart Disease—In app. 10% of cases strept has
affinity to endocardium. Bacterial vegetation forms on the valve leaflets—
causing swelling—and on the myocardium, causing it to become fibrotic and
necrotic (called Aschoff Bodies). Tachycardia is in proportion to the fever.
Migratory polyarthritis—Large joints are painful with no permanent
disability.
Syndenham's Chorea—Largely females, self-limiting, purposeless
movements, no permanent disability.
Subcutaneous nodules—Small painless nodules on the extensor tendons on
knees, knuckles, and elbows.
Erythema marginatum—Nonpruretic, transient rash on trunk and proximal
extremities
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Minor manifestations
Fever
Documented history of strept throat through screening such as C-reactive
protein, ASO titer
Arthralgia
Increased Sedimentation Rate
Management
Antibiotics for strept infection ASA or anti-inflammatory agent
Bed rest in cardiac involvement Long-term SBE prophylaxis
Use the Web Resources links found at the unit level of your online
course for more information on the topics covered in this section.
When you have completed your assigned textbook readings and the course discussion
for this lesson, be sure to complete the Self-Check Test before you begin the next
lesson.
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NURS325B04, Lesson 15 Self-Check
Questions in the online course are randomized to provide a more comprehensive learning
experience. The questions listed below are the same ones that you will use in the Lesson
15 Self-Check test of the online course, though the order of the questions and/or answers
may be different.
Question 1
Which of the following would cause the LEAST amount of hypoxemia?
a ductus arteriosus that remains patent months after birth
atrial septal defect
Tetralogy of Fallot
transposition of the great vessels
Question 2
The oxygen content of the blood on the LEFT side of the heart is
about 75%.
decreased due to the high pressure.
about 95%.
heading to the lungs to become oxygenated.
Question 3
Which of the following is considered a cyanotic congenital heart defect?
atrial septal
ventricular septal
patent ductus arteriosus
Tetralogy of Fallot
Question 4
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Ventricular Septal Defect, an abnormal opening between the ventricles,
demonstrates which of the following?
cyanotic disorder
a localized narrowing of the aorta
two separate circulations
left to right shunt
Question 5
What abnormal heart sound would you auscultate with pericarditis?
murmur
pericardial friction rub
S3
S4
Question 6
Inflammation of the inner lining of the heart is called what?
cardiomyopathy
endocarditis
mitral stenosis
pericarditis
Question 7
The class of cardiomyopathy that is due to a thickened ventral septum is
dilated.
congestive.
hypertrophic.
restrictive.
Question 8
Which of the following would confirm the diagnosis of Rheumatic fever?
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strept throat, migratory polyarthritis, subcutaneous nodules
strept throat, tachycardia, fever
Carditis, fever, arthralgia
carditis, migratory polyarthritis, increased sedimentation rate
Question 9
Which of the following manifestations is most likely for pericarditis?
accumulation of fluid in the pericardial sac
Osler's nodes
emboli formation in the major organ systems
vegetation formation on the cardiac valves
Question 10
Which of the following would cause the MOST amount of hypoxemia?
right to left cardiac shunt
mitral valve stenosis
a foramen ovale that closes off after birth
left to right cardiac shunt
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