Study Guides (238,105)
Canada (114,924)
BPK 306 (9)

Midterm Study Questions

5 Pages
Unlock Document

Simon Fraser University
Biomedical Physio & Kines
BPK 306
Mike Walsh

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: o H-gate channels are closed o There 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: o H-gates and M-gates have begun to reset (M-gates closed, H-gates open) o A stronger stimulation would be needed for a new AP o The AP will be weaker o The longer you wait through phase 3, the stronger the new AP will be o Once 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: o Lesser diameter in AV node = greater resistance = lesser field effect = slower conduction o Lack of fast Na channels in AV node, only slower Funny current channels o Less negative resting Vm produces a weaker AP that has lesser field effect and slower conduction o Lower density of gap junctions which aid in conduction of APs, so slower conduction 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 -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 b.
More Less

Related notes for BPK 306

Log In


Don't have an account?

Join OneClass

Access over 10 million pages of study
documents for 1.3 million courses.

Sign up

Join to view


By registering, I agree to the Terms and Privacy Policies
Already have an account?
Just a few more details

So we can recommend you notes for your school.

Reset Password

Please enter below the email address you registered with and we will send you a link to reset your password.

Add your courses

Get notes from the top students in your class.