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Unique
Characteristics of Cardiac Muscle
CV 1. Contrast the duration of the
action potential and the refractory period in a cardiac muscle, a skeletal
muscle, and a nerve. Sketch the temporal relationship between an action
potential in a cardiac muscle cell and the resulting contraction (twitch) of
that cell. On the basis of that graph, explain why cardiac muscle cannot
remain in a state of sustained (tetanic) contraction.
CV 2. State the steps in
excitation‑contraction coupling in cardiac muscle. Outline the sequence of
events that occurs between the initiation of an action potential in a
cardiac muscle cell and the resulting contraction and then relaxation of
that cell. Provide specific details about the special role of Ca2+
in the control of contraction and relaxation of cardiac muscle.
CV 3. Compare cardiac and skeletal muscle with
respect to: cell size, electrical connections between cells, and arrangement
of myofilaments. Based on ion permeability and electrical resistance
describe role of gap junctions in creating a functional syncytium.
CV 4. Identify the role
of extracellular calcium in cardiac muscle contraction. Identify other
sources of calcium that mediate excitation‑contraction coupling, and
describe how intracellular calcium concentration modulates the strength of
cardiac muscle contraction.
CV 5. Describe the role
of Starling’s Law of the Heart in keeping the output of the left and right
ventricles equal.
CV 6. Describe the difference in the way changes in
preload and changes in contractility influence ventricular force
development. Compare the energetic consequences of these two separate
mechanisms of force modulation.
Electrophysiology
of the Heart
CV 7. Sketch a typical action potential in a ventricular muscle and a
pacemaker cell, labeling both the voltage and time axes accurately. Describe
how ionic currents contribute to the four phases of the cardiac action
potential. Use this information to explain differences in shapes of the
action potentials of different cardiac cells.
CV 7A. Describe the ion channels that contribute to each phase of the
cardiac action potential. How do differences in channel population influence
the shape of the action potential in the nodal, atrial muscle, ventricular
muscle, and Purkinje fiber cardiac cells.
CV 8. Explain what accounts for the long duration of the cardiac action
potential and the resultant long refractory period. What is the advantage of
the long plateau of the cardiac action potential and the long refractory
period?
CV 9. Beginning in the SA node, diagram the normal sequence of cardiac
activation (depolarization) and the role played by specialized cells.
Predict the consequence of a failure to conduct the impulse through any of
these areas.
CV 10. Explain why the AV node is the only normal electrical pathway between
the atria and the ventricles, and explain the functional significance of the
slow conduction through the AV node. Describe factors that influence
conduction velocity through the AV node.
CV 11. Explain the ionic mechanism of pacemaker automaticity and rhythmicity,
and identify cardiac cells that have pacemaker potential and their
spontaneous rate. Identify neural and humoral factors that influence their
rate.
CV 12. Discuss the significance of “overdrive suppression” and “ectopic
pacemaker,” including the conditions necessary for each to occur.
CV 13. Contrast the sympathetic and parasympathetic nervous system influence
on heart rate and cardiac excitation in general. Identify which arm of the
autonomic nervous system is dominant at rest and during exercise. Discuss
ionic mechanisms of these effects on both working myocardium and pacemaker
cells.
CV 14. Describe how cell injury, resulting in a less negative resting
potential, alters ionic events in depolarization and repolarization.
CV 15. Define the following terms: decremental conduction, reentry, and
circus movement.
Cardiac
Function
CV 16. Draw and describe the length tension relationship in a single cardiac
cell. Correlate the cellular characteristics of length, tension, and
velocity of shortening with the intact ventricle characteristics of end
diastolic volume, pressure, and dP/dt.
CV17. Define preload and explain why ventricular end-diastolic pressure,
atrial pressure and venous pressure all provide estimates of ventricular
preload. Explain why ventricular end-diastolic pressure provides the most
reliable estimate.
CV18. Define afterload and explain how arterial pressure influences
afterload. Describe a condition when arterial pressure does not provide a
good estimate of afterload.
CV 19. Define contractility and explain why dP/dt is a useful index of
contractility. Explain how the calcium transient differs between cardiac and
skeletal muscle and how this influences contractility.
CV 20. Define the difference between cardiac performance and cardiac
contractility. Describe the impact of changes in preload, afterload, and
contractility in determining cardiac performance.
CV 21. Explain how changes in sympathetic activity alter ventricular work,
cardiac metabolism, oxygen consumption and cardiac output.
CV 22. Write the formulation of the Law of LaPlace. Describe how it applies
to ventricular function in the normal and volume overloaded (failing)
ventricle.
CV 23. Draw a ventricular pressure volume loop and on it label the phases
and events of the cardiac cycle (ECG, valve movement).
CV 24. Differentiate between stroke volume and stroke work. Identify stroke
volume and stroke work from a pressure-volume loop.
CV 25. Define ejection fraction and be able to calculate it from end
diastolic volume, end systolic volume, and/or stroke volume. Predict the
change in ejection fraction that would result from a change in a) preload,
b) afterload, and c) contractility.
CV 26. Draw the change in pressure volume loops that would result from
changes in a) afterload, b) preload, or c) contractility, for one cycle and
the new steady state that is reached after 20 or more cycles.
Cardiac
Cycle
CV 27. Understand the basic functional anatomy of the atrioventricular and
semilunar valves, and explain how they operate.
CV 28. Draw, in correct temporal relationship, the pressure, volume, heart
sound, and ECG changes in the cardiac cycle. Identify the intervals of
isovolumic contraction, rapid ejection, reduced ejection, isovolumic
relaxation, rapid ventricle filling, reduced ventricular filling and atrial
contraction.
CV 29. Know the various phases of ventricular systole and ventricular
diastole. Contrast the relationship between pressure and flow into and out
of the left and right ventricles during each phase of the cardiac cycle.
CV 30. Understand how and why left sided and right sided events differ in
their timing.
Physiology
of Cardiac Defects (Heart Sounds)
CV 31. Deleted in 2006 revision.
CV32. Know the factors that contribute to the formation of turbulent flow.
CV 33. Describe the timing and causes of the four heart sounds.
CV34. Describe the expected auscultation sounds that define mitral
stenosis, mitral insufficiency, aortic stenosis, and aortic insufficiency.
Explain how these pathologic changes would affect cardiac mechanics and
blood pressure.
The
Normal Electrocardiogram (ECG) and the Electrocardiogram
in Cardiac Arrhythmias and Myopathies
CV 35. Define the term dipole. Describe characteristics that define a
vector. Describe how dipoles generated by the heart produce the waveforms of
the ECG.
CV 36. Describe the electrode conventions used by clinicians to standardize
ECG measurements. Know the electrode placements and polarities for the 12
leads of a 12 lead electrocardiogram and the standard values for pen
amplitude calibration and paper speed.
CV 37. Name the parts of a typical bipolar (Lead II) ECG tracing and explain
the relationship between each of the waves, intervals, and segments in
relation to the electrical state of the heart.
CV 38. Explain why the ECG tracing looks different in each of the 12 leads.
CV 39. Define mean electrical vector (axis) of the heart and give the normal
range. Determine the mean electrical axis from knowledge of the magnitude of
the QRS complex in the standard limb leads.
CV 40. Describe the alteration in conduction responsible for most common
arrhythmias: i.e., tachycardia, bradycardia, A V block,
Wolff-Parkinson-White (WPW) syndrome, bundle branch block, flutter,
fibrillation.
CV 41. Describe electrocardiographic changes associated respectively with
myocardial ischemia, injury, and death. Define injury current and describe
how it is alters the S T segment of the ECG.
Cardiac
Output and Venous Return
CV 42. Understand the principles underlying cardiac output measurements
using the Fick, dye dilution, and thermodilution methods.
CV 43. Know how cardiac function (output) curves are generated and how
factors which cause
hypereffective or hypoeffective changes (contractility) in the heart can
alter the shape of cardiac function curves.
CV 44. Understand the concept of “mean systemic pressure,” its normal value,
and how various factors can alter its value.
CV 45. 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.
CV46. Construct a vascular function curve. Predict how changes in total
peripheral resistance, blood volume, and venous compliance influence this
curve.
CV 46A. Explain why the intersection point of the cardiac function and
vascular function curves represents the steady-state cardiac output and
central venous pressure under the conditions represented in the graph.
CV 47 Use the intersection point of the cardiac function curve and vascular
function curve to predict how interventions such as hemorrhage, heart
failure, autonomic stimulation, and exercise will affect cardiac output and
right atrial pressure. Predict how physiological compensatory changes would
alter acute changes.
Fluid
Dynamics
CV 48. Describe the components of blood (cells, ions, proteins, platelets)
giving their normal values. Relate the three red blood cell concentration
estimates, red blood cell count, hematocrit, and hemoglobin concentration.
CV 49. Identify the source, stimulus for formation, and function of the
hormone erythropoietin. Relate the rate of red blood cell synthesis to the
normal red blood cell life span and the percentage of immature reticulocytes
in the blood.
CV 50. Describe the functional consequence of the lack of a nucleus,
ribosomes, and mitochondria for a) protein synthesis and b) energy
production within the red blood cell.
CV 51. Discuss the normal balance of red blood cell synthesis and
destruction, including how imbalances in each lead to anemia or polycythemia.
CV 52. Explain how red blood cell surface antigens account for typing of
blood by the A B O system and rhesus factor. Based on these antigens,
identify blood type of a “universal donor” and a “universal recipient.”
CV53 Know the factors that determine the total energy of the flowing blood
and the relationship among these factors. Describe the usual reference point
for physiological pressure.
CV 54. Be able to differentiate between flow and velocity in terms of units
and concept.
CV 55. Understand the relationship between pressure, flow, and resistance in
the vasculature and be able to calculate for one variable if the other two
are known. Apply this relationship to the arteries, arterioles, capillaries,
venules, and veins. Explain how blood flow to any organ is altered by
changes in resistance to that organ.
CV 56. Explain how Poiseuille’s Law influences resistance to flow. Use it to
calculate changes in resistance in a rigid tube (blood vessel). Explain the
deviations from Poiseuille's law predictions that occur in distensible blood
vessels.
CV 57. Understand the relationship between flow, velocity, and
cross-sectional area and the influence vascular compliance has on these
variables. Explain how hemodynamics in blood vessels, especially
microcirculation, deviate from theory due to anomalous viscosity,
distensibility, and the glycocalyx.
CV 58. Define resistance and conductance. Understand the effects of adding
resistance in series vs. in parallel on total resistance and flow. Apply
this information to solving problems characterized by a) resistances in
series and b) resistances in parallel. Apply this concept to the
redistribution of flow from the aorta to the tissues during exercise.
CV 59. List the factors that shift laminar flow to turbulent flow. Describe
the relationship between velocity, viscosity, and audible events, such as
murmurs and bruits.
CV 60. Understand the principles of flow through collapsible tubes, the
Starling resistor, and what pressure gradient determines flow for different
relative values of inflow, surrounding, and outflow pressures.
CV 61. Explain how hemodynamics in blood vessels, especially
microcirculation, deviates from theory due to anomalous viscosity,
distensibility, axial streaming, and critical closing behavior.
Arterial
Pressure and the Circulation
CV 62. Describe the organization of the circulatory system and explain how
the systemic and pulmonary circulations are linked physically and
physiologically.
CV 63. Deleted in 2006 revision.
CV 64. Describe blood pressure measurement with a catheter and transducer
and explain the components of blood pressure waveform. Contrast that with
the indirect estimation of blood pressure with a sphygmomanometer. Explain
how each approach provides estimates of systolic and diastolic pressures.
Given systolic and diastolic blood pressures, calculate the pulse pressure
and the mean arterial pressure.
CV 65. Describe how arterial systolic, diastolic, mean, and pulse pressure
are affected by changes in a) stroke volume, b) heart rate, c) arterial
compliance, and d) total peripheral resistance.
CV 66. Contrast pressures and oxygen saturations in the 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.
CV 67. Identify the cell membrane receptors and second messenger systems
mediating the contraction of vascular smooth muscle by norepinephrine,
angiotensin II, and vasopressin.
CV 68. Identify the cell membrane receptors and second messenger systems
mediating the relaxation of vascular smooth muscle by nitric oxide,
bradykinin, prostaglandins, and histamine.
The
Microcirculation and Lymphatics
CV 69. 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. Define and give examples of diffusion-limited and flow-limited
exchange.
CV 70. Describe how changes in capillary surface area affect the capacity
for fluid exchange.
CV 71. Define the Starling equation and discuss how each component
influences fluid movement across the capillary wall.
CV 72. Describe the pathway for leukocyte migration across the
microcirculation, including leukocyte expression of cellular adhesion
molecules, and recognition sites in the vascular endothelial cells.
CV 73. Starting at the post capillary venule, describe the process of
angiogenesis, including the stimulus that initiates new vessel growth.
CV 74. Describe the Donnan effect and its importance in capillary dynamics.
CV 74A. Describe how smooth muscle contractile mechanisms differ from the
contractile mechanisms of skeletal and cardiac muscle.
CV 74B. Describe the involvement of G protein-coupled receptors and signal
transduction pathways in the regulation of smooth muscle contraction.
CV 74C. Describe the involvement of endothelial cells in the regulation of
vascular diameter and inflammatory responses.
CV 75. Predict how altering pressure or resistance in pre- and
post-capillary regions alters capillary pressure and the consequence of this
change on transmural fluid movement.
CV 76. Using the components of the Starling equation, explain why fluid does
not usually accumulate in the interstitium of the lungs.
CV 77. Describe how histamine alters the permeability of the post capillary
venules, and how the loss of albumin into the interstitial space promotes
localized edema.
CV 78. Describe the lymphatics, and explain how the structural
characteristics of terminal lymphatics allow the reabsorption of large
compounds, such as proteins.
CV 79. Contrast the structure of lymphatic capillaries and systemic
capillaries, including the significance of the smooth muscle in the walls of
the lymphatic vessels.
CV 80. Identify critical functions of the lymphatic system in fat
absorption, interstitial fluid reabsorption, and clearing large proteins
from the interstitial spaces.
CV 81. Diagram the relationship between interstitial pressure and lymph
flow. Explain why edema does not normally develop as interstitial pressure
increases.
CV 82. 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) malnutrition.
Regulation
of Arterial Pressure
CV 83. List the anatomical components of the baroreceptor reflex.
CV 84. Explain the sequence of events in the baroreflex that occur after an
acute increase or decrease in arterial blood pressure. Include receptor
response, afferent nerve activity, CNS integration, efferent nerve activity
to the SA node, ventricles, arterioles, venules, and hypothalamus.
CV 85. Explain the sequence of events mediated by cardiopulmonary (volume)
receptors that occur after an acute increase or decrease in arterial blood
pressure. Include receptor response, afferent nerve activity, CNS
integration, efferent nerve activity to the heart, kidney, hypothalamus, and
vasculature.
CV 85A. Explain the sequence of events mediated by cardiopulmonary (volume)
receptors that occur after an acute increase or decrease in central venous
pressure. Include receptor response, afferent nerve activity, CNS
integration, efferent nerve activity to the heart, kidney, hypothalamus, and
vasculature.
CV 86. Contrast the sympathetic and parasympathetic nervous system control
of heart rate, contractility, total peripheral resistance, and venous
capacitance. Predict the cardiovascular consequence of altering sympathetic
nerve activity and parasympathetic nerve activity.
CV 87. Contrast the relative contribution of short- and long-term mechanisms
in blood pressure and blood volume regulation.
CV 88. Outline the cardiovascular reflexes initiated by decreases in blood
O2 and increases in blood CO2.
CV 89. Describe the release, cardiovascular target organs, and mechanisms of
cardiovascular effects for angiotensin, atrial natriuretic factor,
bradykinin, and nitric oxide.
Local
Control of Blood Flow
CV90 Define autoregulation of blood flow to the brain. Distinguish between
short-term and long-term autoregulatory responses and the mechanisms
responsible for each.
CV 91. Describe how the theory of metabolic regulation of blood flow
accounts for active hyperemia and reactive hyperemia.
CV 92. Identify the role of PO2 , PCO2 , pH, adenosine, and K+ in the
metabolic control of blood flow to specific tissues.
CV 93. Diagram the synthetic pathway for nitric oxide (EDRF, endothelial
derived relaxing factor), including substrate and the interplay between
endothelium and vascular smooth muscle.
CV 94. Discuss the circumstances and the mechanisms whereby humoral
substances contribute to regulation of the microcirculation.
CV95 Discuss the interaction of a) intrinsic (local), b) neural, and c)
humoral control mechanisms and contrast their relative dominance in the CNS,
coronary, splanchnic, renal, cutaneous, and skeletal muscle vascular beds.
CV 96. Describe the role of angiogenesis in providing a long term match of
tissue blood flow and metabolic need.
Fetal
and Neonatal Circulation
CV 97. Describe the progressive changes in maternal blood volume, cardiac
output, and peripheral resistance during pregnancy and at delivery.
CV 98. Contrast the blood flow pattern in the fetus with that of a normal
neonate, including the source of oxygenated blood.
CV 99. Describe the function in utero of the fetal ductus venosus, foramen
ovale, and ductus arteriosus. Explain the mechanisms causing closure of
these structures at birth.
CV 100. Discuss the relative differences in oxygen saturation and pressure
for blood in the major blood vessels and cardiac chambers of the fetus.
Explain how these values change at birth.
CV 101. Explain the unfavorable consequences to the neonate if either the
ductus arteriosis or the foramen ovale fails to close.
Hemostasis
and Injury, Hemorrhage, Shock
CV 102. Diagram the enzymes and substrates involved in the formation of
fibrin polymers, beginning at prothrombin. Contrast the initiation of
thrombin formation by intrinsic and extrinsic pathways.
CV 103. Contrast the mechanisms of anticoagulation of a) heparin, b) EGTA,
and c) coumadin. Identify clinical uses for each agent.
CV 104. Describe the mechanisms of fibrinolysis by TPA, tissue plasminogen
activator and urokinase.
CV 105. Explain the role of the platelet release reaction on clot formation.
Distinguish between a thrombus and an embolus.
CV 106. Explain why the activation of the clotting cascade does not
coagulate all of the blood in the body.
CV 107. Describe the direct cardiovascular consequences of the loss of 30%
of the circulating blood volume on cardiac output, central venous pressure,
and arterial pressure. Describe the compensatory mechanisms activated by
these changes.
CV 108. Explain three positive feedback mechanisms activated during severe
hemorrhage that may lead to circulatory collapse and death.
CV 109. Contrast the change in plasma electrolytes, hematocrit, proteins,
and colloid osmotic pressure following resuscitation from hemorrhage using
a) water, b) 0.9% NaCl, c) plasma, and d) whole blood.
Coronary
and Skeletal Muscle Circulations
CV 110. Describe the phasic flow of blood to the ventricular myocardium
through an entire cardiac cycle. Contrast this cyclic variation in
myocardial flow a) in the walls of the right and left ventricles and b) in
the subendocardium and subepicardium of the left ventricle. Identify the
area of the ventricle most susceptible to ischemic damage and why the risk
is increased at high heart rates.
CV 111. Explain how arterio venous O2 difference and oxygen extraction in
the heart is unique when compared with other body organs.
CV 112. Explain the mechanism whereby coronary blood flow is coupled to
myocardial workload, and identify stimuli that cause increases in coronary
blood flow to occur.
CV 113. Explain how sympathetic stimulation alters heart rate,
contractility, and coronary vascular resistance, as well as both directly
and indirectly to change coronary blood flow. Identify the relative
importance of the direct and indirect SNS effects in determining coronary
blood flow during exercise.
CV 114. Describe what is meant by coronary vascular reserve and the role of
collateral blood vessels. Discuss physiological and pathological events that
decrease coronary vascular reserve.
CV 115. Contrast the neural and local control of skeletal muscle blood flow
at rest and during exercise.
CV 116 Contrast the effect of phasic and sustained skeletal muscle
contraction on extravascular compression of blood vessels and on central
venous pressure.
Cerebral,
Splanchnic and Cutaneous Circulation
CV 117. Contrast the local and neural control of cerebral blood flow.
Discuss the relative important of O2, CO2, and pH in regulating cerebral
blood flow.
CV 118. Describe the structural components of the blood brain barrier and
how this barrier impedes the movement of gases, proteins, and lipids from
the blood to neurons. Identify the differences in cerebrospinal fluid and
plasma relative to protein concentration, and describe the function of
cerebrospinal fluid.
CV 119. Contrast the mechanisms of the two major types of stroke,
hemorrhagic and occlusive stroke.
CV 120. Contrast the local and neural control of the splanchnic circulation.
Describe the role of the hepatic portal system and the hepatic artery in
providing flow and oxygen to the liver.
CV 121: Describe the blood pressure in the hepatic portal vein, hepatic
sinusoids, and the vena cava. Given an increase in central venous pressure,
predict how hepatic microcirculatory fluid exchange will be altered,
including the development of ascites.
CV 122. Describe how the GI circulation is adapted for secretion and
absorption. Explain the enterohepatic circulation.
CV 123. Contrast local and neural control of cutaneous blood flow.
CV 124. Discuss the unique characteristics of skin blood flow that are
adaptive for body temperature regulation.
Exercise
(also see Integration)
CV 125. Describe the cardiovascular consequences of exercise on peripheral
resistance, cardiac output, A V oxygen difference, and arterial pressure.
CV 126. Describe the redistribution of cardiac output during exercise to the
CNS, coronary, splanchnic, cutaneous, and skeletal muscle vascular beds
during sustained exercise (distance running). Explain the relative
importance of neural and local control in each vascular bed.
CV 127. Discuss four adaptations to physical training on the cardiovascular
system. Explain the mechanisms underlying each.
CV 128. Contrast the effects of static vs. dynamic exercise on blood
pressure.
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Unique
Characteristics