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Midterm

BPK 306 Study Guide - Midterm Guide: Cardiac Muscle Cell, Ryanodine Receptor 2, Resting Potential


Department
Biomedical Physio & Kines
Course Code
BPK 306
Professor
Mike Walsh
Study Guide
Midterm

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KIN 305 Mdtm 1 Study Questions
1. Explain the ionic basis of the resting membrane potential of a cardiac myocyte.
gK>>gNa>gCa at rest in a semipermeable cell membrane
K concentration is very high intracellular, Na concentration very high extracellular
Ek = -95 according to Nernst equation (if only K+ was present and pK = 1, fully permeable
membrane) K+ will exit cell, and make it more negative inside
Ena = +70 (if only Na+ was present and pK = 1, fully permeable membrane) Na+ will enter cell
and make it more positive inside
Chord conductance equation: shows that the resting membrane potential will be dominated by
the greatest conductance (gK) at rest.
Hence, in a cardiac myocyte, the resting Vm is -90, closest to gK because K+ will exit the cell
most and make it very negative
Other ions affect the resting Vm, such as Cl-, and Ca++.
Na/K pump also maintains the electrochemical gradient by taking out 3 Na+ for 2K+ (makes
inside cell more negative due to the trade off)
2. Differentiate between the absolute and relative refractory period of a cardiac ventricular
myocyte AP.
Absolute/Effective Refractory period:
oH-gate channels are closed
oThere cannot be any new AP when H-gates are closed b/c it is impossible for Na+
influx through the fast voltage gated Na+ channels
Relative Refractory period:
oH-gates and M-gates have begun to reset (M-gates closed, H-gates open)
oA stronger stimulation would be needed for a new AP
oThe AP will be weaker
oThe longer you wait through phase 3, the stronger the new AP will be
oOnce phase 4 is reached, you can achieve a full new AP
3. Why does the speed of the AP conduction differ between the AV node and purkinje cells?
Why is this physiologically significant?
Teliological: Heart needs time for atrial systole to complete contraction before ventricles can
begin contraction otherwise we will have heart arrhythmia
Physiological reason:
oLesser diameter in AV node = greater resistance = lesser field effect = slower
conduction
oLack of fast Na channels in AV node, only slower Funny current channels
oLess negative resting Vm produces a weaker AP that has lesser field effect and slower
conduction
oLower density of gap junctions which aid in conduction of APs, so slower conduction
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4. Describe the ionic events that occur during Phase 2 of the cardiac ventricular myocyte AP.
Explain their physiological significance.
Physiological significance: Ca++ needs to be brought into the cell to activate CICR from SR
that will increase [Ca++]i and activate muscle contraction mechanism
Vm remains fairly constant
Ik1 is not very significant because of inward rectifying. Its role is reduced at 0mV and more
positive Vm.
Ito, and Ik are actively causing K+ efflux down conc’n gradient and electrical gradient
Ca++ influx through L-type channel occurring to offset the K+ channels. Ca++ flowing down
conc’n gradient, but against electrical gradient
5. How do pacemaker cells (such as those of the SA node) trigger their own depolarization?
During phase 4, Funny Current channels activate at <-50mV, and T type Ca++ channels
activate at >-55mV
This is self activating from its own K+ outward repolarizing currents during phase 4
1. Draw and label a “normal” (Lead II) ECG tracing. Explain why the QRS complex and the T-
wave both produce positive deflections in the ECG.
2. Describe what the electrical vector of Einthoven’s Triangle represents. Describe two situations
that cause this vector to shift.
Electrical vector is downwards and to the left of the heart. This is the direction the
depolarization is traveling
Ventricle Hypertrophy and Systemic hypertension causes left axis shift
Heart may be displaced
3. In the absence of extracellular calcium, explain what happens to cardiac contraction. How (and
why) does this effect differ from skeletal muscle contraction?
Luminar Ca++ can bind to L-site of a RYR2 channel causing release of Ca++ into cell. Now
that Ca++ can bind to A-sites of RYR2 channels causing further Ca++ release into the cell for
muscle contraction
Skeletal muscle cannot be used in absence of extracellular Ca++ b/c it has no RYR2 channels
4. Draw a “normal” volume-pressure diagram for the left ventrical. Label all values and axes.
Indicate where the following are located or occur:
a. Opening and closing of the AV valve
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