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Guided Lecture Notes, Chapter 24, Disorders of Cardiac Function
Learning Objective 1. Characterize the function of the pericardium.
 Describe to the students the general anatomy of the pericardial sac and list its functions.
Use “fist in a water balloon” as an example of the positioning of the pericardium. (Refer
to PowerPoint slide 2.)
Learning Objective 2. Compare the clinical manifestations of acute pericarditis and chronic
pericarditis.
 Describe the manifestations of acute versus chronic disease process. Emphasize the
immediacy of the acute onset versus the silence of the chronic presentation. (Refer to
PowerPoint slides 3 to 5.)
Learning Objective 3. Describe the physiologic impact of pleural effusion on cardiac function
and relate it to the life-threatening nature of cardiac tamponade.
 Explain how the effusion puts pressure on the heart and restricts the contractile ability,
but does not affect the electrical activity. It results in pulse electrical activity. (Refer to
PowerPoint slides 5 and 6.)
Learning Objective 4. Describe blood flow in the coronary circulation and relate it to the
determinants of myocardial oxygen supply and demand.
 Describe the anatomy of coronary vessel arrangement, emphasizing the points on the
heart where each artery feeds the muscle. Relate this to the site of blockage as the
determinate of tissue damage. (Refer to PowerPoint slides 7 to 10.)
Learning Objective 5. Define the term acute coronary syndrome and distinguish among chronic
stable angina, unstable angina, non–ST-segment elevation myocardial infarction, and STsegment elevation myocardial infarction in terms of pathology, symptomatology, ECG changes,
and serum cardiac markers.
 Briefly review the normal physiology of ECG. Base the lecture discussion on what the
ECG shows the clinician and then what abnormalities can demonstrate. Then, correlate
these changes to the developing pathologies that can be described using these methods.
(Refer to PowerPoint slides 11 to 20.)
Learning Objective 6. Define the treatment goal for acute coronary syndrome.
 For ACS, the disease has progressed to a more serious condition and needs prevention at
the cellular level via pharmacological interventions. (Refer to PowerPoint slides 22 to
27.)
Learning Objective 7. Define the term cardiomyopathy as it relates to both the mechanical and
electrical function of the myocardium.
 Describe cardiomyopathy in terms of inappropriate ventricular hypertrophy and dilation.
(Refer to PowerPoint slides 28 and 29.)
Learning Objective 8. Differentiate among the pathophysiologic changes that occur with
hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, dilated
cardiomyopathies, and myocarditis.
 Explain how the different cardiomyopathies develop from specific mechanisms. For
example, the arrhythmogenic RVC arises from abnormal conduction versus myocarditis
from inflammatory destruction. The result is the same, but how the disease progresses is
specific. (Refer to PowerPoint slides 31.)
Learning Objective 9. Describe the treatment strategies of both primary and secondary
cardiomyopathy.
 Explain that despite the large variety of causes, the result of each is very similar;
therefore, the treatment is very similar. Treatment is aimed at adding compensation
and/or alleviating symptoms. (Refer to PowerPoint slides 31 to 34.)
Learning Objective 10. Distinguish between the roles of infectious organisms in infective
endocarditis and rheumatic fever.
 Describe to the students that the organism is the stimulating agent, but the damage is
derived from immune-mediated reactions. (Refer to PowerPoint slide 36.)
Learning Objective 11. Describe the relation between the infective vegetations associated with
infective endocarditis and the extracardiac manifestations of the disease.
 Describe to the students that the manifestations systemically arise due to the exposure of
the blood stream to the infective organism and the immune activity in the heart. (Refer
to PowerPoint slide 36.)
Learning Objective 12. Describe the long-term effects of rheumatic fever and primary and
secondary prevention strategies for rheumatic fever and rheumatic heart disease.
 Describe the primary effects are damage to the valvular structure. This can lead to many
different conditions such as MI, cardiomyopathy, and CHF. Describe how the pathology
arises from the breakdown of heart tissue. (Refer to PowerPoint slide 37.)
Learning Objective 13. State the function of the heart valves and relate alterations in
hemodynamic function of the heart that occur with valvular disease.
 Describe the structure of the valves. Explain that they are pressure-sealed valves and
prevent retrograde blood flow. When the valves leak, the resulting pathologies directly
arise from the heart having to compensate for retrograde blood flow. (Refer to
PowerPoint slide 38.)
Learning Objective 14. Compare the effects of stenotic and regurgitant mitral and aortic
valvular heart disease on cardiovascular function.
 Describe the concepts of stenosis and regurgitant mechanisms. Explain how the
pathologies arise from the increase workload that is placed on the heart. In stenosis, the
heart has to work harder to move blood out of the ventricle. In regurgitation, the blood
must be pumped twice. (Refer to PowerPoint slides 38 and 39.)
Learning Objective 15. Describe the flow of blood in the fetal circulation, state the function of
the foramen ovale and ductus arteriosus, and describe the changes in circulatory function that
occur at birth.
 Describe the fetal circulation differences that are present due to differences in
oxygenation via placenta versus pulmonary. Explain that the foramen ovale and ductus
arteriosus are adaptations to the parallel blood flow. (Refer to PowerPoint slide 44.)
Learning Objective 16. Describe the anatomic defects and altered patterns of blood flow in
children with atrial septal defects, ventricular septal defects, endocardial cushion defects,
pulmonary stenosis, tetralogy of Fallot, patent ductus arteriosus, transposition of the great
vessels, coarctation of the aorta, and single-ventricle anatomy.
 Have the students work through these many conditions. Break them into small groups and
have them discuss the diseases. (Refer to PowerPoint slide 46.)
Learning Objective 17. Describe the manifestations related to the acute, subacute, and
convalescent phases of Kawasaki disease.
 Explain how the inflammatory changes will have systemic manifestations. The most
significant is the progressive vasculitis and the effects that will be seen. Use this as an
opportunity to review vasculitis. (Refer to PowerPoint slide 47.)