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  • pg 1
            Structural Cardiac
       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
   Normally lower in the right side–venous blood is returning from the body (about

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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   Bluish discoloration of the skin due to decreased oxygen levels in the arterial blood

   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

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
   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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    Anoxic spells
    Decreased physical growth

    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

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      Palliative—to increase pulmonary blood flow
      Corrective—new procedure switches vessels
      Survival rates vary with procedure and age—85-90%

      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

     Causal agents: Microorganisms. Most commonly streptococcus or
     staphylococcus, but can be any virus, bacteria, fungus, etc.

     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

NURS325B04                                 10                                   Lesson 15
     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
           (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
           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


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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:
  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.

Inflammation of the sac around the heart
      Acute or chronic (healed form of acute that results in a chronic
                      pericardial dysfunction)

     Infections, myocardial injury, hypersensitivity reactions, metabolic disorders,

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Classifications according to exudate

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

  Severe chest pain radiating to the back, presence of a friction rub (pericardial layers
rub together during movement)
  Weight loss
  Sinus tachycardia

     Treat underlying cause
     Symptomatic treatment (ASA, NSAIDs, analgesics)
     If this is chronic, may have to remove the pericardium

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    Disease of the myocardium itself—affects the pumping ability of the heart—fibers
    cannot contract well.
    Most are idiopathic! May be secondary to toxins, infections, immunological
    disorders, nutritional disorders (alcoholism), and genetics.

    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
    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.

    LV Failure:

             Dyspnea on exertion
             Fatigue
             Orthopnea
             Fluid in lungs, crackles

    RV Failure:

             Edema
             Jugular vein distention
             Liver congestion

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     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.

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

   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
   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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    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.

   Diffuse inflammatory disease involving the heart, joints, subcutaneous tissue, CNS
   and skin. Usually seen in ages 3-15 yr.

RF is diagnosed if strept throat and 2 major or 1 major and 2 minor manifestations are
   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
          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

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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

      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

NURS325B04                                18                                 Lesson 15
      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

NURS325B04                                  19                                 Lesson 15
   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?
              pericardial friction rub

 Question 6
   Inflammation of the inner lining of the heart is called what?
              mitral stenosis

 Question 7
   The class of cardiomyopathy that is due to a thickened ventral septum is
 Question 8
   Which of the following would confirm the diagnosis of Rheumatic fever?

NURS325B04                                20                                  Lesson 15
               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

NURS325B04                                   21                                  Lesson 15

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