Download 4. In-Class Worksheet Answers - CIM

IN-CLASS
Answers
Session 2
HEART PHYSIOLOGY I
M.A.S.T.E.R. Learning Program, UC Davis School of Medicine
Date Revised: 1/11/02
Revised by: Andrew Dao and Reza Danesh
1. Draw the length tension curves for total, passive, and active force generated by isometric contraction. What
determines maximum tension and why?
During an isometric contraction, the tension produced
is proportional to the number of crossbridges
produced between actin and myosin. Max tension is
determined by the muscle's resting length in the body.
It has been found experimentally that it is at this value
that the most actin myosin interaction is possible; that
is, the greatest number of crossbridges can be formed.
When a muscle is stretched beyond its resting length,
the overlap between actin and myosin is reduced and
the number of crossbridges is reduced. Hence, less
tension can be produced. Similarly, if the length is
decreased to smaller than Lo(Lo = Optimum length),
tension declines because the overlapping of the two
sets of thin filaments interfere with crossbridge
formation on these two areas.
ELECTROPHYSIOLOGY OF THE HEART
2. Pacemaker Action Potential
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The resting potential of pacemaker cells is less negative than ventricular cells due to increased Na+
conductance at rest.
Phase 4: These cells undergo a spontaneous, gradual depolarization due to progressive decline in K+
conductance and a small increase in Ca++ conductance (and also a slow Na+ influx called the “funny” Na
current)..
Phase 0: once the AP threshold is reached at –50m there is Ca++ influx. Because the threshold potential is
less negative in the pacemaker cells, the fast Na+ channels are inactive. The major contributing current is a
slow inward Ca++ current (rather than the fast Na current),
Phase 3: is characterized by increased K+ efflux from the cell.
0
Membrane
Potential
(mV)
-50
-70
0
The rate at which the conductance of K+ decreases is reduced by parasympathetic stimulation
Parasympathetic
-50
-70
0
Conductance to Ca++ is increased by sympathetic stimulation
Sympathetic
-50
-70
3. A) Draw the ventricular and atrial action potentials. B) Describe each phase in terms of ion conductance. C)
How do the two differ from each other and from an AP of skeletal muscle?
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A) Drawn above
B) Phase 4- Resting membrane potential; -90mV, membrane most permeable to K+
Phase 0- voltage dependent activation of fast Na+ channels, Na+ enters cell depolarization to +20mV.
Phase 1 - Rapid decrease in Na+ conductance, brief outward K+ current causes decline in potential.
Phase 2- Voltage dependent activation of slow inward Ca++ current, slow inward Na+ current, and
slow outward K+ current. These flows of charges balance each other for approximately 200-300ms,
which causes prolongation of the depolarization.
Phase 3- Slow Na+ and Ca++ channels are inactivated, and there is an increase in outward K+ current,
membrane moves toward K+ equilibrium potential.
C) The ventricular action potential is much longer in duration thant the AP of skeletal muscle and even
atrial AP. The significance of this is that there is a more prolonged refractory period in which the
ventricular muscle cannot be restimulated. This allows the ventricles to empty and refill before the next
ventricular contraction.
CARDIAC CYCLE & CARDIAC OUTPUT
4. Cardiac Cycle
5. Using the theory behind the law of Laplace, explain why a person with a dilated heart (due to congestive
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heart failure, for example) is more likely to suffer myocardial ischemia than a person with a non-dilated
heart?
The Law of Laplace: T 
Pr
T=Tension, P = Pressure, r = radius, h = wall thickness
2h
The reason that this law is so important when dealing with the heart is because the amount of tension that
the heart must produce is one of the main determinants of how much oxygen it requires. The more tension
produced by the myocardium, the greater the oxygen requirement; and in a person with, say,
atherosclerosis, blood flow and oxygen delivery to the heart might be limited. The law of Laplace puts into
numbers the fact that the larger the heart, the more tension it must produce in order to overcome a given
aortic pressure (for a given P. if you increase r and/or decrease h, then T increases. ) It is important to note
that this refers to the entire ventricle being stretched (increased radius & decreased wall thickness – both
factors inversely related and very important in determining Tension), and is separate from the length
tension relationship in individual myocytes described earlier.
6. In a normal heart, what type of contraction is occurring in the left ventricular muscle before the aortic valve
opens?
Before the aortic valve opens, there is an increase in pressure but no change in volume. This is isovolumic
contraction, and is caused by the interaction of actin/myosin without sliding of the myofilaments. Sound
familiar?
What type of contraction are we looking at after the aortic valve opens? (That is, in the left ventricle.)
When the isovolumic contraction of the L. ventricle results in a tension that exceeds the aortic pressure, the
aortic valve opens. At this point, the muscle fibers begin to shorten, which decreases the volume of the
ventricle, and results in the ejection of blood. Initially, this is an isotonic contraction, because the ventricle
must work against a given afterload albeit not a constant one as the aortic pressure is changing
continuously during eject.
What determines how much the ventricular muscle fibers will shorten?
Afterload: As in skeletal muscle, the fibers will shorten until they reach the length according to the length
tension relationship at which the peak tension is equal to afterload.
Contractility: Any increase in myocardial contractility (positive inotropic effect) is usually defined as any
intervention that increases peak isometric tension development in cardiac muscle at a fixed length. For
example, Norepinephrine is the most important regulator of myocardial contractility. At any given resting
muscle length or volume, the ventricle will generate greater ventricular tension and pressure in the
presence of NE than it will when it is not present. Similarly, the muscle will be able to shorten to a greater
extent against the same afterload in the presence of NE.
Please note the below information was NOT covered in your syllabus this year. Skeletal muscle and reflexes will be
covered in the Spring Quarter. However, it would be advisable for you to obtain an understanding of this material
which is briefly presented below. An understanding of muscle contraction will help you better understand the
cardiophysiology. Dr. Carlsen advises you to read the recommended textbook on the subject matter.
SKELETAL MUSCLE
7. Compare and contrast depolarization in a muscle fiber action potential versus muscle fiber shortening upon
contraction in terms of the following:
AP
LENGTH OF TIME
REFRACTORY PERIOD
ALL OR NONE?
DEPOLARIZATION BEFORE
REACTIVATION OF FAST Na+
short
yes
yes
nothing
MUSCLE CONTRACTION
long
no
no
tetany/summation
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CHANNELS.
8. Fill in the chart below concerning types of muscle fibers:
Rate of Contraction
ATP production
# of mitochondria
Rate of fatigue
Fiber Size
Function:
TYPE I
slow
ox. Phos.
many
slow
small
long duration,
posture
TYPE Ila
fast
Ox. Phos.
many
intermediate
intermediate
rapid cont.
sustained over
time
TYPE IIB
fast
glycolysis
few
fast
large
short duration,
high resistance
9. What are three ways to increase the force of a muscle contraction?
a. Increase the frequency of activation of the motor unit (tetany!)
b. Increase the # of motor units recruited.
c.
Stretch the muscle to Lo “Optimum length” (but not beyond it!)
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