topic.9. powerpoint 9.2

Question 1

What is the main difference between neurogenic and myogenic hearts?

Answer 1

Neurogenic hearts are controlled by the nervous system, while myogenic hearts have contractions initiated within the heart.

Question 2

Gap junctions are found where?

Answer 2

gap junctions are located in the intercalated discs of cardiac muscle cells.

Question 3

What is the function of intercalated discs in cardiac muscle cells?

Answer 3

Intercalated discs allow action potentials to spread between cardiac cells[due to ion movement], due to ga junctions that produce uniform depolarization of the heart muscle.

Question 4

Intercalated disc are found where?

Answer 4

cardiac muscle cells, more specifically the Z line of sarcomere

Question 5

Draw the parts of a sarcomere

Answer 5

z-disk, actin filament, I band, A Band, H zone, M line

Question 6

Auto-rhythmicity

Answer 6

The ability of the heart to stimulate itself to contract at regular intervals.

Question 7

How is the heart able to stimulate itself to contract at regular intervals[auto-rhythmicity]?

Answer 7

uses pacemaker cells aka excitable cells in the sinoatrial (SA) node of the heart to spontaneously generate action potentials to regulate the heartbeat. Action potentials occur pacemaker specialized cell membrane that allow Na+, K+, Ca++ to cross

Question 8

T/F only parasymapehtic nerve fibers influence SA nerve?

Answer 8

false, both can.
-Sympathetic input increases, and norepinephrine binds to receptors on the SA node, leading to an increase in the permeability of sodium (Na+) and calcium (Ca++) channels in pacemaker cells. Depolarization

-parasympathetic input increases, acetylcholine (ACh)binds to receptors on the SA node cells. This binding leads to a decrease in the permeability of sodium (Na+) and calcium (Ca++) ions, as well as an increase in the permeability of potassium (K+) ions. Hyperolarization

Question 9

Sino Atrial Node found in what part of the heart?

Answer 9

right atrium

Question 10

WHat is another name for heart muscle cells?

Answer 10

cardiomyocytes

Question 11

How do cardiomyocytes move ions across cell membranes in order to generate AP?

Answer 11

depolarization and repolarization of cell membranes

Question 12

Summarize heart electrical acitivty in SA node

Answer 12

Pacemaker cells in SA spontaneously generate AP, spread slowly through atria to AV then rapid spread of AP to large connecting fibers[Bundle of His] then to L and R bundle branches to the Purkinje fibers that goes to ventricular wall to causing rapid ventricular contraction

Question 13

T/F There is electrical connection between the muscle cells of
the atria and the muscle cells of the ventricles.

Answer 13

false; There is no electrical connection between the muscle cells of
the atria and the muscle cells of the ventricles. There is (just
connective tissue between them)

Question 14

How can AP rapidly spread down connective tissue if there is is no electrical connection between the muscle cells of the atria and the muscle cells of the ventricles?

Answer 14

The rapid spread of action potentials down connective tissue in the heart is facilitated by specialized conducting fibers. These conducting fibers have small diameters, allowing for the rapid transmission of electrical signals between the atria and the ventricles.

Question 15

What effect will the small diameter have on the conduction
velocity of the action potential?

Answer 15

increases the velocity of the action potential

Question 16

Why would you want the action potential to go though
the atria to the ventricles slowly? in SA node

Answer 16

When discussing heart electrical activity, pacemaker cells in SA spontaneously generate AP and spread slowly through atria to AV. There is a delay between the contraction between the atria
and the ventricle because you don’t want the atria and ventricles to
pump at the same time

Question 17

Explain AP in SA node

Answer 17

1.permeability to K+[flows out], gradual rise in MP
2.Na+ travel through funny channels which are open at low MP and close as MP rises
3.Funny channels close and Ca++ enters
4. Threshold reached due to Ca++ influx
5. Repolarization K+ out

Question 18

Explain how AP in SA Node spread slowly through atria to AV then rapid spread of AP to large connecting fibers[Bundle of His] then to L and R bundle branches to the Purkinje fibers that goes to ventricular wall to causing rapid ventricular contraction

Answer 18

2 voltage-dependent calcium channels impact cardiac muscle
-L-type, respond to higher MP, open slowly and remain open longer than the T-type
-L-type sustains AP which t-type initiate AP

Question 19

What are funny channels?

Answer 19

allow the passage of both sodium (Na+) and potassium (K+) ions
-activated by voltage and cAMP

Question 20

What if the permeability to Na+ and Ca2+ was increased?

Answer 20

Sympathetic effect
-slow rise to depolarization become quicker due to increase in channels openings Na+ and Ca2+
**norepinephrine is responsible

Question 21

What can we expect in term of the permeability of Na+ and Ca2+ is we think about the parasympathetic effect?

Answer 21

Decrease permeability o Na+ and Ca2=, aka channels close and a slower rate of depolarization

Question 22

How does AP in skeletal muscle differ from cardiac muscle?

Answer 22

AP in cardiac muscle longer than because it has a longer refractory period, meaning it can’t generate another AP until the muscle is finished contracting.

Question 23

What would we expect if cardiac muscle AP has a shorter refractory period?

Answer 23

Another AP generated before muscle finished contracting, meaning ventricles won’t fill up completely with blood from atrium

Question 24

What is the difference between cardiac muscle AP and SA node AP?

Answer 24

cardiac muscle AP are driven by the
output from the SA node
1. K+ flows out in Ap in SA node but in cardiac muscle AP some K+ channels actually close, increase in permeability to k+ is delayed
2.When Na+ travel through funny channels in SA node AP, the AP in ventricular muscle peaks.
3.plateaus after peak in cardiac muscle AP is explained by Ca+ channels opening for long time
4. Permeability to K+ is delayed, causing repolarization to take long time

Question 25

How does SA node relate to long refractory period in cardiac muscle AP?

Answer 25

-Tetanus not possible: Heart contracts long
enough to pump blood, then relaxes to fill
- Normally, no self-re-excitation, rate set by
pacemaker

Question 26

Explain difference of Excitation-contraction coupling in cardiac muscle vs skeletal muscle

Answer 26

In general AP spread from PM to interior of cells via t-tubules

Skeletal muscle: AP in t-tubules open Ca++ in sarcoplasmic reticulum, Ca+ bind to troponin, initiate muscle contraction

Cardiac muscle: AP can travel through t-tubules, primarily relies on AP opening voltage-gated channels in t-tubule membrane allowing influx of extracellular Ca+. These calcium ions then bind to calcium receptors on the sarcoplasmic reticulum, causing the release of stored calcium ions into the cytosol

Question 27

ECG/EkG

Answer 27

Electrocardiogram is a measure of electrical activity that can be
measured at the surface of your body

Question 28

How do you measure ekg?

Answer 28

Electrodes: conductive pads in contact with the body that
makes an electrical circuit with the electrocardiograph
Lead: provide a comparison between electrodes by recording the electrical activity of the heart from a different angle

Question 29

In an EKg, label 1-4 and P/Q/R/S/T/P

Answer 29

P wave is step 1 and 2
Pacemakers in SA node generate a wave of signals to contract. Straight+curved rise
Signals are delayed between A and V, completed curved
QRS is step 3 depolarization of ventricles
AV node cells are stimulated to produce signal, travel along Purkinje to bottom of heart, sharp upside down V[QRS]]
T and P are in step 4
Signals spread from the bottom of heart upward, causing ventricles to contract. Straight +completely curve straight

Question 30

In ekg, explain all the intervals?

Answer 30

p-QRS is time impulse travels within AV node
P-R interval, 0.12 to 0.2 represents time between onset of atrial depolarization and onset of ventricular depolarization
S-T: ventricles are completely depolarized
T: ventricles repolarize
Q-T: time for ventricular depolarization and repolarization aka avg ventricular AP

Question 31

What would happen to the
EKG if the spread of the AP
though the Av node were
slowed down more than
normally?
What part of the EKG
would get longer?

Answer 31

The space between the p
wave and the qrs would
get longer because it
would take longer for the
excitation potential to get
to the ventricle.

Question 32

What if the ventricular action potential had a shorter
duration?
The flat line between the qrs and the T wave (ST
segment) would be shorter because repolarization
happens sooner.

Answer 32

The flat line between the qrs and the T wave (ST
segment) would be shorter because repolarization
happens sooner.