Answers
Session 2 /
Heart Physiology I
M.A.S.T.E.R. Learning Program, UC Davis School of MedicineDate Revised: 1/11/02
Revised by: Andrew Dao and Reza Danesh1. 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
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.
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?
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 200300ms, 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 heart failure, for example) is more likely to suffer myocardial ischemia than a person with a nondilated heart?
The Law of Laplace: T=Tension, P = Pressure, r = radius, h = wall thickness
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 / MUSCLE CONTRACTIONLENGTH OF TIME / short / long
REFRACTORY PERIOD / yes / no
ALL OR NONE? / yes / no
DEPOLARIZATION BEFORE REACTIVATION OF FAST Na+ CHANNELS. / nothing / tetany/summation
8. Fill in the chart below concerning types of muscle fibers:
TYPE I / TYPE Ila / TYPE IIBRate of Contraction / slow / fast / fast
ATP production / ox. Phos. / Ox. Phos. / glycolysis
# of mitochondria / many / many / few
Rate of fatigue / slow / intermediate / fast
Fiber Size / small / intermediate / large
Function: / long duration, posture / rapid cont. sustained over time / 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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