Physiology 8-9

Front 1

a. Once an action potential is generated in one cardiac myocytes, how does it travel so quickly through other cardiac myocytes?

Back 1

Intercalated disks w/ gap junctions

Front 2

b. How is the action potential in the cardiac myocytes different from skeletal muscle and conduction system?

Back 2

1. gap junctions 2. one myocyte depolarizes soon they all depolarize 3. non-synaptic 4. non-spontaneous 5. stable RMP at -90mv

Front 3

c. What is the resting membrane potential in cardiac myocytes?

Back 3

-90 mv

Front 4

d. For each phase, what current, due to what ion, moving in what direction, through what channel causes the change from resting membrane potential?

Back 4

0- Na+ ion channel, inward flow/current, ECF to ICF. 1- K+ ion channel, outward current, ICF to ECF, repolarization 2. Ca+2 L-type or slow channels, ECF to ICF, inward current, activates cytosol SR fast Ca+ channels, plateau effect. 3- further increase open probability of K+ channels same as 1. 4- RMP reached as decrease Na+, Ca+ is stored, and decrease in ICF to ECF flow of K+ prevents hyperpolarization.

Front 5

e. For each phase what is the permeability of the membrane to Na+, K+, Ca+2? and open probability (high/low) of each channel in each phase?

Back 5

0- high perm/open probability for Na+, low perm/open for K+. 1- high perm/open for K+. 2- high perm/open for Ca+2, high perm for Na+. 3- high perm/open for K+. 4- low perm/open for K+

Front 6

f. Where does the calcium released by the calcium-induced calcium-release mechanism come from?

Back 6

Sarcoplasmic reticulum in the cytosol

Front 7

g. What is the significance of the plateau for myocytes contraction? How long does it last?

Back 7

Sustained contraction allows all the blood to be pumped out, lasts 200-250msec

Front 8

h. What is meant by ‘cardiac muscle has a more sustained contraction than skeletal muscle?

Back 8

Does not repolarize as fast, keeps a depolarized state longer due to Ca+ L-type and fast channels

Front 9

i. How would altering cytoplasmic [Ca+2] during the plateau (either high or low) affect myocyte contraction?

Back 9

Decrease ICF Ca+ contraction time shortens, increase it contraction time increases

Front 10

a. Once intracellular calcium is high, it binds what protein to start contraction?

Back 10

troponin

Front 11

b. Decreased intracellular calcium concentration as compared to normal results in what effect on myocyte contraction?

Back 11

Decreases strength and time of contraction

Front 12

c. Where does intracellular calcium go during repolarization?

Back 12

Pumped back into SR

Front 13

d. What is the overall effect of ‘Caliuim-pumps’ on the plasma membrane and on the sarcoplasmic reticulum?

Back 13

To increase ICF Ca+ concentration and thus depolarize the cell slightly (plateau)

Front 14

a. What is positive chronotropic effect and what effects/factors can causes it? Give an example.

Back 14

Increased SA node rhythm (time), sympathetic stimulation such as by Epinephrine

Front 15

b. What is negative chronotropic effect and what effects/factors can cause it? Give an example.

Back 15

Decrease in heart rate (time) by parasympathetic action through acteylcholine

Front 16

c. What is positive inotropic effect and what effects/factors can causes it? Give an example.

Back 16

Increase contraction by ionic effect, cardiac glycosides

Front 17

d. What is negative inotropic effect and what effects/factors can cause it? Give an example.

Back 17

Decrease contraction by blocking ion channels, Calcium-channel blockers

Front 18

a. What are nifedipine, diltiazem, and verapamil prescribed for?

Back 18

Decrease strength and contraction time

Front 19

b. What channels do they block?

Back 19

calcium

Front 20

c. What is the effect of these blockers on intracellular calcium and myocytes contraction?

Back 20

Slow Ca+ are blocked less ICF Ca+ and less activation of fast channels(SR), myocytes contract less.

Front 21

d. What are cardiac glycosides prescribed for?

Back 21

(in general) increase heart contraction strength and time

Front 22

e. What molecule is affected and how by cardiac glycosides?

Back 22

Na/K atpase channel is shutdown

Front 23

f. What is the effect of cardiac glycosides on cytoplasmic concentration of Na+, K+, Ca+2 (higher/lower)?

Back 23

Na is higher, K is lower, Ca is higher

Front 24

g. What is the effect of cardiac glycosides on myocyte contraction? How does this affect the amount of blood that leaves the ventricles (more/less)?

Back 24

The plateau and strength of contraction will increase, giving the ventricles greater ability to pump more blood out.

Front 25

a. What is the difference between a wave and an isoelectric line?

Back 25

Wave is recording of electrical activity, isoelectric line no electrical activity can be recorded

Front 26

b. What cardiac electrical events does the p-wave, QRS-complex and T-wave represent?

Back 26

p-wave=atria depolarize, QRS=ventricles depolarize, T=ventricles repolarize

Front 27

c. During what segment do the atria undergo systole?

Back 27

Isoelectric line seen after P wave and before Q

Front 28

d. During what segment do the ventricles undergo systole?

Back 28

Isoelectric line seen after S and before T wave

Front 29

e. Can the strength of systole and diastole be measured with an EKG?

Back 29

The notes seem to indicate NO

Front 30

a. What are the two types of cardiac regulation?

Back 30

Intrinsic and extrinsic

Front 31

b. Define stroke volume, heart rate and cardiac output?

Back 31

amount of blood pumped by ventricles per beat (ml/beat), amount of beats per minute, amount of blood pumped by heart per minute (ml/min

Front 32

c. What portions of the ANS affect heart rate and stroke volume?

Back 32

Sympathetic and Parasympathetic

Front 33

d. How does end diastolic volume affect cardiac output?

Back 33

Directly related, as EDV increases so does CO and vice versa

Front 34

e. How does an increase or decrease in cardiac rate, stroke volume, sympathetic or parasympathetic activity, or stretch of ventricular myocytes affect cardiac output?

Back 34

An increase in all except psym will increase CO, an increase in psym will decrease CO, and vice-versa

Front 35

f. Memorize formula and units for cardiac output and be able to calculate cardiac output given heart rate and stroke volume.

Back 35

ml/min, beats/min, ml/beat respectively

Front 36

d. During what segment do the ventricles undergo systole?

Back 36

Isoelectric line seen after S and before T wave

Front 37

e. Can the strength of systole and diastole be measured with an EKG?

Back 37

The notes seem to indicate NO

Front 38

g. What is the normal cardiac output for an average, well-hydrated individual at rest?

Back 38

5-5.5 L/min

Front 39

h. How does exercise affect stroke volume, heart rate and cardiac output? Increase/decrease.

Back 39

Increases all

Front 40

i. Name the 2 phases included in the ventricular systole portion of the cardiac cycle.

Back 40

E1=isovolumetric ventricular contraction, E2=blood ejection

Front 41

j. Name the 3 phases included in the ventricular diastole portion of the cardiac cycle.

Back 41

E3=isovolumetric ventricular relaxation, E4=Passive filling, E5=active ventricular fillng/atrial systole

Front 42

k. For each of the 5vphases named above, describe the whether AV and SL valves are opened or closed, the changes (increase, decrease, same) seen for intraventricular pressure, ventricular blood volume and presence of heart sounds (systolic and diastolic).

Back 42

E1=both closed, InterVentricular pressure increases, blood volume stays the same, S1 heard. E2=AV closed SL open, pressure max and drop, volume decrease. E3=both closed, pressure decreases, volume stays the same, S2 heard. E4= AV open SL closed, pressure same, volume increases.

Front 43

l. In which of the 5 phases above, do you see an increase, a decrease in intraventricular pressure? During which phase does intraventricular pressure reach the highest level?

Back 43

IV pressure reaches max at E2. Increase at E1, decrease at E3