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Human Physiology Study Guide 3 (Guyton 11th Ed.)
Cardiac Muscle- specialized and contractile cells of the heart.
1. Describe the electrical and mechanical features of myocardial (contractile) cells.
2. What is the structure and role of intercalated disks? How do these disks account for the term “functional
syncytium?”
3. Review the structure and function of the heart (fibrous skeleton, chambers, valves, septa, papillary muscle,
chordae tendinae, coronary circulation, etc.) You should know the path of blood flow in adult and fetus, and
anatomy of the conductive system. Ref. any good anatomy text.
4. Understand the principles behind the terms autorhythmicity / intrinsic rhythm. What is the ionic explanation
for this phenomenon? Do specialized cells have a resting membrane potential? Why or why not? How would
heart function be different if these fibers were absent in a heart?
5. Compare the AP profiles of skeletal muscle fibers and cardiac contractile and specialized fibers, and note their
similarities and differences.
6. Note the phases of each AP (specialized and contractile) and give the ionic basis for the voltage changes.
7. What is the "pacemaker potential" or prepotential? List ways in which the rhythmicity of the nodal fibers can
be affected (drugs and autonomic nervous system effects)
8. What is the normal intrinsic rhythm of each region of the conductive system?
9. Indicate the specific connections of the ANS on the heart, the types of receptors for each NTS, and the effects
of each system on chronotropy and inotropy. (for chronotropic effects: how exactly does each system affect
the nodal prepotential?)
10. Which of the specialized cells acts as the pacemaker? Why?
11. Do contractile cells have a resting membrane potential? Why or why not?
12. Where is there a delay in the transmission of the depolarization event? List the two big reasons why.
13. Review autonomic tone: understand that we can speed up or slow down the heart in a variety of ways (i.e.,
increase sympathetic input or, conversely inhibit parasympathetic input, etc.).
14. What differences are there in cardiac muscle (exchangers, location of calcium, etc.) compared to skeletal
muscle (see chapter 5).
The Cardiac Cycle
1. Be able to walk yourself through one complete cardiac cycle. Know the timing of pressure, volume changes,
isovolumic contraction and relaxation, timing of valve openings/closings while understanding the pressure
differences that create those openings/closings, overlap of A and V diastole, heart sounds and EKG events. Be
able to recreate the cardiac cycle graph demonstrated in class from your knowledge of each event.
2. Discuss the Frank-Starling Law of the heart and relate it to what you know about the skeletal muscle lengthtension relationship. What is the relationship between SV and EDV? Can the ANS affect this relationship?
What contributes to EDV?
3. Discuss the advantages to having a strong heart during exercise. Make reference to Starling’s Law of the heart
and importance of long diastolic time.
4. What is the basis for the heart sounds? Do any of the valves actively close? Do they passively close?
5. What is cardiac output? What is EDV? What is ESV? What is ejection fraction?
6. What happens to the heart cycle when heart rate increases? Which part of the cycle is compromised the most?
Why can tachycardia ultimately lead to a reduced cardiac output?
7. How does digitalis cause a (-,+) effect on the heart? What effects do atropine, pilocarpine, and propranolol
have on the heart?
The EKG and mean electrical axis.
1. Give a clear and detailed description of the path of current through the heart. Draw a vector diagram of these
events (that is, draw the 5 vectors of the heart presented in class).
2. What is a lead?
3. Name the three different sets of leads that can be applied in an EKG (i.e., bipolar, augmented, Precordial).
4. List the types of information that can be gathered about the heart by reading an EKG. Should a diagnosis be
based on a single EKG?
5. An EKG reading is an extracellular recording of charge differences. Explain this statement.
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Strictly speaking, does an EKG provide direct information about mechanical (contractile) events in the
heart?
Be able to draw your hexaxial diagram (that is, be able to draw the bipolar and augmented leads in a circle
with proper orientation of their arrow heads and proper orientation of their “degrees” in a protractor.
Draw the normal EKG profile and define each wave, interval and segment of the profile. Then describe the
events which occur in each of these periods, and give the normal time frames for as many as possible.
Which bipolar lead should give the largest QRS wave in a normal EKG? Why?
Which of the 6 leads (bipolar and augmented) should give an inverted QRS wave in a normal EKG? Why?
What about the Precordial leads?
What is meant by “mean electric axis” of the heart?
What conditions might result in a shift in mean electric axis?
Define the terms bradycardia and tachycardia, and give values for each. Can bradycardia be normal for some
people?
Define first, second and third degree AV nodal block. How might they appear on an EKG?
If I give you a reading lead and the 5 cardiac vectors of the heart, can you tell me if your pen would deflect
upward or downward?
Review questions for Cardiac problems and fetal blood flow
1. Review your normal heart sounds and be able to properly fill them in on a graph showing the cardiac
cycle (figure 9-5 from Guyton and Hall).
2. What is a prolapsed valve? What is regurgitation? What is a stenotic valve?
3. Understand how the streptococcal organism can lead to an immune response against the mitral and
aortic valves. (What “fever” causes this? Yes, it is in the book!)
4. Be able to address the following for ALL FOUR valves:
 If a valve is stenotic, where is pressure building up? Where would pressure be low? What
would CO be like? Where could edema develop? When would you hear the abnormal heart
sound—ventricular diastole or systole?
 If a valve is prolapsed, where is pressure building up? Where would pressure be low? What
would CO be like? Where could edema develop? When would you hear the abnormal heart
sound—ventricular diastole or systole?
5. Review normal fetal circulation. What structures are in place to bypass the liver and the lungs? At
birth, be able to describe the changes that SHOULD occur to convert from fetal circulation to adult
circulation.
6. What is a patent ductus arteriosus and what problems would you expect the child to present with?
What can be done about this problem? Does surgery always need to be done?
7. What is Tetralogy of Fallot? Why is it called “blue baby syndrome?” What classic four abnormal
heart features are associated with this syndrome? Will a baby necessarily present with all four?
8. Review the types of shock discussed in class.
9. What is hypertension vs. hypotension?
Vessels and Flow dynamics:
1. Be able to describe the vessels blood travels through starting with the aorta and finishing with the
inferior/superior vena cava.
2. What purpose do these vessels serve?
3. Why are arterioles called resistance vessels? Why are veins called capacitance vessels? Why are capillaries
called exchange vessels?
4. What types of capillaries are there? Which one is most abundant? Where would you find fenestrated or
sinusoidal capillary beds?
5. What tunics are in each of the vessel types? What other structure do veins have that work in a similar way to
the semilunar valves of the heart?
6. What is central venous pressure (CVP?) What factors can change CVP? What symptoms would a patient
present with if they had elevated CVP?
7. What is the Ohm’s law for describing flow in the cardiovascular system?
8. Understand the equations CO = HR X SV, and BP = CO X TPR. Know how to use them. Ex: for any given
CO, what will happen to BP if TPR increases by 20 %? (On slide 13 and 14 of your vessels and flow
dynamics lecture, I gave you examples of changes to flow if resistance or pressure changed….now I’m simply
asking you to describe what would happen to BP if resistance changed).
9. What is laminar vs. turbulent flow of blood? Why can turbulent blood be harmful to blood vessels? What can
cause blood flow to be turbulent?
10. What is blood pressure? How do you calculate MAP?
11. What is pulse pressure? How do you calculate it? What factors influence pulse pressure?
12. What is pulse pressure velocity? Does blood flow in the vessel flow with the same rate?
13. Why is it important to have the pulse pressure fluctuation dampened by the time the blood arrives at the
capillary bed? Which vessels takes most of the “hit” off of the pulse pressure?
14. Why does the right side of the heart generate less pressure than the left and yet the same amount of blood gets
ejected from both sides of the heart?
15. What is Poiseuille's Law? From this law, what is the most significant way to change blood pressure and flow?
16. Define resistance. Which vessels are mostly responsible for producing changes in TPR?
17. What other factors will contribute to resistance? How does the length of a vessel contribute? Hematocrit?
Control of blood flow and pressure (short term effects: local (intrinsic) and extrinsic mechanisms).
1. Why is controlling blood flow and pressure important? Hint: Perfusion vs. ischemia vs. hypoxia vs. anoxia
vs. infarction.
Review the following:
Tissue Perfusion Dependent on:
 Cardiac output
 Peripheral resistance
 Blood pressure
Regulation of perfusion dependent on:
 Autoregulation (Acute, local)—what factors help with autoregulation? (i.e., what factors cause local
vasoconstriction or vasodilation). Review oxygen lack vs. vasodilator theory.
 Neural mechanisms (acute)
 Endocrine mechanisms (long-term)
Understand, that for this unit, you have only been taught the local and extrinsic (acute, short term) mechanisms.
Long term maintenance of blood pressure will be covered in the renal physiology section).
2. What is the effect of the SNS (sympathetics) on BP? How does the SNS acts on the heart and blood vessels.
How does this affect HR, SV, TPR?
3. Review the mechanism by which the nervous system regulates acute changes in blood pressure. Detail the path
of the baroreceptor reflex for maintenance of BP. Review the nerves that are involved.
4. How does the baroreceptor reflex respond to sudden changes in BP (how does it “compensate” or correct), for
example, upon standing after lying down? What is “orthostatic hypotension?” Why is this reflex NOT useful
in long-term control of blood pressure? Where is the CMV control center of the brain?
5. What is the role of the kidney, adrenal cortex and hypophysis as well as the lung in the long term maintenance
of blood pressure? (review the hormones I briefly introduced in class).
6. What other types of receptors are found in the aortic bodies and carotid sinuses besides baroreceptors? What
do these receptors respond to and how would the heart rate/contractility change?
7. what receptors do the right atria and pulmonary artery have? What is the Bain-bridge effect? How does it
work in concert with the Frank-Starling mechanism? What hormone does the right atrium release? What
other hormones would this hormone be antagonistic toward?
Capillary Hemodynamics
1. Describe the structure of a capillary wall. Describe the routes by which fluid and solutes can make their way
across this wall
2. How do capillaries vary in different organs (which are most/least permeable?) Why do they differ in different
organs?
3. What is colloid osmotic pressure? What is hydrostatic pressure?
4. What are the Starling Forces that determine fluid movement across capillaries?
5. What is protein concentration in plasma and in interstitial fluid? What is the principal protein in plasma? Where
is it made? It accounts for what percentage of total protein in plasma?
6. Identify each of the forces across a capillary wall. Determine in which direction each force directs fluid flow.
7. What are the net forces at the arteriolar and venous ends of the capillary?
8. What is the effect of each of the following situations on capillary forces: liver damage, protein depletion,
elevated blood pressure, lymphatic blockage, increased permeability of capillary walls due to burns or due to
histamine release in allergic reactions?
9. How are lymphatic capillaries designed to collect leaked proteins and fluid from interstitial fluid?
10. Describe the structure of lymphatic capillaries. Review the anatomy of the lymphatic system: vessels, ducts,
valves, etc. Where do they join the cardiovascular system.
11. How does the lymphatic system pump material against gravity (where’s the pump?)
12. What is edema? Which compartments lose fluid and which gain fluid and protein in edema?
13. What is the difference between systemic edema? pulmonary edema? How is each produced? What is
elephantiasis? How does this result in edema?