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Cardiovascular Learning Objectives
Updated 1/24/2008
1. Apply hemodynamic laws to pressure, flow, and resistance in the peripheral circulation.
Understand the relationship between flow, velocity, and cross sectional area and the
influence vascular compliance has on these variables. Apply this relationship to the various
segments of the circulation, arteries, capillaries and veins. Explain how Poiseuille’s Law
represents resistance to flow. Understand the effects of adding resistances in series or in
parallel on total peripheral resistance and flow.
2. List the factors that shift laminar flow to turbulent flow. Describe the relationship between
velocity, viscosity, and audible elements, such as murmurs and bruits.
3. Describe the organization of the circulatory system and explain how the systemic and
pulmonary circulations are linked physically and physiologically.
4. Describe how arterial systolic, diastolic, mean, and pulse pressures are affected by changes in
a) stroke volume, b) heart rate, c) arterial compliance, and d) total peripheral resistance.
5. Contrast pressures and oxygen saturations in the arteries, arteries, arterioles, capillaries,
venules and veins of both the systemic and pulmonary circulations. Repeat that process for
velocity of blood flow and cross sectional area, and volume.
7. Identify the cell membrane receptors and G-protein second messenger systems mediating the
contraction of vascular smooth muscle by norepinephrine, angiotensin II, and vasopressin.
8. Identify the cell membrane receptors and second messenger systems mediating the relaxation
of vascular smooth muscle by nitric oxide, bradykinin, prostaglandins and histamine.
9. Describe the involvement of endothelial cells in the regulation of vascular diameter and
inflammatory responses.
10. Learn how the anatomical- physiological characteristics of arteries and veins contribute to
their distribution of blood flow.
11. Explain how water and solutes traverse the capillary wall. Use Fick’s Equation for diffusion
to identify the factors that will affect the diffusion-mediated delivery of nutrients from the
capillaries to the tissues.
12. Define the Starling Law for Transcapillary Exchange, and discuss how each component
influences fluid movement across the capillary wall.
13. Explain how edema develops in response to: a) venous obstruction, b) lymphatic obstruction,
c) increased capillary permeability, d) heart failure, e) tissue injury or allergic reaction, and f)
14. Describe the pathway for leukocyte migration across the microcirculation, including
leukocyte expression of cellular adhesion molecules, and recognition sites in the vascular
endothelial cells.
15. Describe the direct consequences of the loss of circulating blood volume on cardiac output,
central venous pressure, and arterial pressure. Describe the compensatory mechanisms
activated by these changes.
16. Starting at the post-capillary venule, describe the process of angiogenesis, including the
stimulus that initiates new blood vessel growth.
17. Define venous return. Understand the concept of “resistance to venous return” and know
what factors determine its value theoretically, what factors are most important in practice and
how various interventions would change the resistance to venous return.
18. Remember the (open loop) vascular function curve is a predictive tool that, when combined
with the (open loop) cardiac function curve, this combination represents the (closed loop)
intact cardiovascular system. Together they can help to understand physiological interactions
between the peripheral circulation and the heart.
19. Construct a vascular function curve, and predict how changes in vascular resistance, blood
volume and vascular compliance influence this curve.
20. Using the combined cardiac function and vascular function curves, use the intersection point
to predict how interventions to the cardiovascular system such as hemorrhage, heart failure,
autonomic stimulation or exercise will affect cardiac output and right atrial pressure. Predict
how physiological compensatory changes would alter acute changes.
21. Predict how, in an intact cardiovascular system, blood pressure homeostasis is affected by
changes in the:
Radii of resistance vessels
Capacitance of veins or resistance of arteries
Sympathetic-parasympathetic nervous system synergy
Adrenal (medullary) gland function
Kidney regulation of blood volume
Nitric oxide modulation of vsm tone
22. List the anatomical components of the arterial and cardiopulmonary baroreceptor reflexes
23. Explain the sequence of events in the baroreceptor reflex that occur after an increase or
decrease in arterial blood pressure. Include receptor response, afferent nerve activity, CNS
integration, efferent nerve activity to the SA node, ventricles, arterioles and hypothalamus.
24. Explain the sequence of events mediated by cardiopulmonary (atrial “volume”) receptors that
occur after an acute increase or decrease in arterial pressure. Include receptor response,
afferent nerve activity, CNS integration, efferent nerve activity to the heart, kidney,
hypothalamus, and vasculature.
25. Contrast the sympathetic and parasympathic divisions of the ANS in control of heart rate,
contractility, total peripheral resistance, and venous capacitance. Predict the cardiovascular
consequence of altering sympathetic nerve activity and parasympathetic nerve activity.
26. Contrast the relative contribution of short and long term mechanisms in blood pressure
regulation and blood volume regulation.
27. Outline the cardiovascular reflexes initiated by decreases in blood O2 and increases in blood
28. Describe the release, the cardiovascular target organs, and mechanisms of the cardiovascular
effects for angiotensin, atrial naturetic factor, bradykinin and nitric oxide (EDRF or
endothelial-derived relaxing factor).
29. Define “autoregulation” of blood flow. Compare and contrast the myogenic and metabolic
theories of autoregulation. Identify which mechanism would predominate at high and low
mean arterial pressures.
30. Describe how the theory of metabolic regulation of blood flow accounts for active and
reactive hyperemia. Identify the role of PO2, PCO2, pH, adenosine and K+ in the metabolic
control of blood flow to specific tissues.
31. Discuss the interactions of a) intrinsic (local), b) neural and, c) humoral, cardiovascular
control mechanisms and contrast their relative dominance in the CNS, coronary, splanchnic,
renal, cutaneous and skeletal muscle circulations.
32. Describe how the muscle “pump” and local metabolic vasodilation improve venous return to
the heart.
33. List the components of the cardiac conduction system. Describe the functions of the
intercalated disks and gap junctions in cardiac muscle cells.
34. Describe the sequence of activation of the heart beginning at the sino-atrial (SA) node.
35. Draw a typical cardiac ventricular action potential, properly labeling the horizontal and
vertical axes. Identify the resting membrane potential and label the phases.
36. Describe the sequence of events that generates a typical cardiac action potential including the
changes that take place in the membrane conductances for Na+, K+, and Ca++. Draw a typical
pacemaker potential, properly labeling the horizontal and vertical axes. Show the location of
the threshold potential. Describe the sequence of events that generates a typical pacemaker
potential including the changes that take place in the membrane conductances for Na+, K+,
and Ca++. Describe how increasing or decreasing sympathetic and parasympathetic input
alters the heart rate.
37. Describe the sequence of events that results in the contraction and relaxation of cardiac
muscle. Define the refractory period of the heart.
38. Describe the blood pressure changes that occur in the left atrium, left ventricle, and central
aorta during the cardiac cycle. Identify the periods of time when the various cardiac valves
are either open or closed and when the heart sounds associated with the cardiac cycle occur.
39. Define the terms end diastolic volume, end systolic volume, stroke volume, and ejection
40. Describe a typical cardiac pressure-volume loop and explain the underlying events
represented by the loop.
41. Identify the differences between the pressure changes that take place on the right side of the
heart compared to those changes on the left side of the heart during the cardiac cycle.
42. Define the term “cardiac output” and describe how it can be calculated.
43. Draw a ventricular function curve and describe the Frank-Starling mechanism for increasing
stroke volume. On that same diagram, show the effect of increasing the activity of cardiac
sympathetic nerves.
44. Define and use in the proper context
pressure overload
Aschoff body
Prinzmetal angina
central venous pressure
spiral septum
contraction band necrosis
stable angina pectoris
cor pulmonale
Swan-Ganz catheter
Eisenmenger syndrome
ejection fraction
torsade de pointes
endocardial cushion
unstable angina pectoris
Libman-Sacks endocarditis
variant angina pectoris
ostium secundum
ostium primum
volume overload
45. Discuss the genetic factors, environmental factors, and common extracardiac defects that
may be involved in congenital heart disease.
46. Describe the differences and clinical significance between the fetal blood circulation and the
adult blood circulation
47. Describe the normal embryologic development of the heart and great vessels
48. Discuss the embryologic derivation and the clinical features, significance, and complications
of atrial septal defect, atrioventricular septal defect, coarctation of the aorta, patent ductus
arteriosus, persistent truncus arteriosus, tetralogy of Fallot, transposition of the great vessels,
and ventricular septal defect.
49. Compare and contrast left-to-right intracardiac shunts and right-to-left intracardiac shunts
50. List the major predisposing factors to atherosclerosis and discuss their role in the
development of atherosclerotic plaques
51. Discuss the normal mechanisms of lipid transport and clearance in humans
52. Discuss the pathogenesis of atherosclerotic lesions and their potential complications.
Recognize the morphologic (gross and microscopic) changes of the arterial walls produced
by atherosclerosis.
53. Describe the role of the clinical laboratory in the diagnosis of cardiovascular disease and
discuss the significance of elevated concentrations of HDL, LDL, VLDL, homocysteine, Creactive protein
54. Discuss the physiologic compensatory mechanisms of the heart in response to myocardial
55. Compare and contrast myocardial ischemia and myocardial infarction in terms of
predisposing factors, morphologic (gross and microscopic) changes to the tissue, clinical
features, ECG findings, and laboratory findings.
56. List the major causative factors and describe the clinical and morphologic features associated
with valvular diseases.
57. Discuss the reasons for and clinical significance of abnormal heart sounds
58. Compare and contrast acute rheumatic fever and rheumatic heart disease in terms of etiology,
pathogenesis, morphologic features, laboratory findings, clinical features, and potential
59. Compare and contrast forms of endocarditis in terms of predisposing factors, etiology,
organisms, and clinical outcomes.
60. Discuss the similarities and differences between the different cardiomyopathies.
62. Describe the morphologic changes that occur in the heart and vasculature in patients with
systemic hypertension.
63. List the major primary neoplasms that arise in the heart and vasculature, and discuss their
clinical significance.
64. Compare and contrast “acute” pericarditis and “chronic”pericarditis in terms of predisposing
factors, causative agents, morphologic (gross and microscopic) features, clinical
manifestation, and clinical outcome.
65. List the major types of vascular aneurysms and discuss their similarities and differences in
terms of etiology, pathogenesis, distribution, gross and microscopic appearance, and clinical
66. Discuss aortic dissection in terms of pathogenesis, morphologic appearance, clinical features
and potential outcomes.
67. Describe the morphologic and clinical features of peripheral vascular disease
68. Describe the underlying mechanisms responsible for the common forms of cardiac
69. Discuss the factors that may lead to heart failure in terms of etiology, compensatory
mechanisms, clinical features, and potential outcome.
70. List the etiologic factors that can produce shock. Discuss the chain of events that occur in
patients in shock and discuss the body’s physiologic compensatory responses to those events.
71. Discuss the pharmacological management of cardiovascular diseases.