Cardiovascular Part 2 Lecture - Physio

Front 1

SAN is located at the

Back 1

junction of the right atrium & vena cava

Front 2

SAN node is what kind of cardiac AP?

Back 2

pacemaker= sponteous APs occur here

Front 3

Impulses from the SAN spread to the right atria via

Back 3

radial spread

Front 4

To get the left atrium to depolarize, impulses are brought from the SAN node via

Back 4

Bochmann's bundle.

Front 5

Once Bochmann's bundle brings impulses to the left atrium, then what will take over?

Back 5

radial spread -

Front 6

What is the AVN?

Back 6

gateway of electrical depolarization to the ventricles

Front 7

How many internodal pathways go from the SAN to AVN

Back 7

3

Front 8

Is there radial spread in the internodal pathways?

Back 8

not clear

Front 9

What is the purpose of the internodal tracts?

Back 9

to bring impulses to AVN

Front 10

Fibers of the AVN are

Back 10

long and thin

Front 11

What has the longest conduction time of any cardiac tissue?

Back 11

AVN

Front 12

How do you ensure that the atria depolarize and contract before ventricular depolarization?

Back 12

by impulses being brought to the AVN and by having a slow conduction time via AVN and the rest of the pathway.

Front 13

Special properties of AVN that cause slowing of conduction time:

Back 13

long fibers w/ smaller diameters

Front 14

Longer fibers of the AVN node cause impulses to take

Back 14

Longer

Front 15

Beginning to end of AVN introduces a

Back 15

100 ms delay.

Front 16

Delay of AVN allow

Back 16

atria to contract prior to ventriculatr contraction.

Front 17

After the AVN, impulses go down the

Back 17

Bundle of His

Front 18

After the Bundle of His, the impulse go

Back 18

down right & left bundle branches, purkinje fibers, then ventricular muscles.

Front 19

Diameter of Purkinje fibers

Back 19

large: quickly bring impulses from bundle branches to ventricular muscle - so that you have a quick depolarization.

Front 20

Function of Purkinje Fibers

Back 20

quick depolarization of massive ventricles

Front 21

Left ventricular muscle mass is greater than the right b/c the left has to generate

Back 21

higher pressure

Front 22

Right bundle branch of common branch/Bundle of His looks like a

Back 22

twig.

Front 23

Entire conduction pathway

Back 23

SAN - LA via Bocchman's bundle -depolarize atrial muscle
SAN via radial spread depolarizes atrial muscle
Impulses go to the ventricle via internodal pathways - depolarizes AVN
AVN node/100 ms delay:go to bundle of His, divide into left/right bundle branches
Purkinje fibers then ventricular muscle

Front 24

Because of the electrical conduction pathway, muscles of the heart

Back 24

depolarize

Front 25

Depolarizations of cardiac muscle is what is seen on an

Back 25

EKG - not conduction pathway.

Front 26

EKG monitors

Back 26

electrical events of the heart - only looking at depolarizations of the muscle.

Front 27

From depolarization of muscle, you can

Back 27

infer what is happening in the conduction system.

Front 28

in order to understand EKG, you need to understand the

Back 28

vectors that are set up.

Front 29

Atrial vector goes from

Back 29

SAN across inter-atrial septum towards the left ventricle
=atrial depolarization.

Front 30

atrial vector is a ______ vector and gives rise to the _____ wave

Back 30

slow
P

Front 31

Atrial vector is the origin of the

Back 31

P wave - one vector - gradual depolarization going.

Front 32

first region of the heart to depolarize is

Back 32

across the ventricular septum going from left to right side of th heart = septal depolarization.

Front 33

septal vector is

Back 33

a small vector - quickly over

Front 34

What happens after septal depolarization?

Back 34

apical depolarization

Front 35

What is the major event of ventricular depolarization?

Back 35

apical depolarization.

Front 36

Apical depolarization is when

Back 36

majority of ventricle tissue depolarizes. Apical b/c ventricles depolarize simulateneously from base of ventricle to apex of ventricles

Front 37

Due to ______, you can bring impusles to all regions of the heart

Back 37

Purkinje fibers

Front 38

left ventricular mass takes longer to depolarize on a cell by cell basis b/c

Back 38

the left ventricular muscle mass is much greater

Front 39

What is left late depolarization?

Back 39

region of the left ventricular wall near its base - is last to depolarize.

Front 40

4 vectors in ventricular muscle:

Back 40

septal
apical
left ventricular
late left ventricular

Front 41

normal heart rate is

Back 41

60-100 bpm

Front 42

How to control Heart rate:

Back 42

control rate of diastolic depolarization /slope
changing threshold potential
nt alteration.
hyperpolarizing
starting at a more depolarized state.

Front 43

Controlling the rate of diastolic depolarization or the slope:
by increasing the rate/steepness of diastolic depolarization you would

Back 43

increase the rate of spontaneous APs b/c threshold potentials would be more easily/quickly achieved.

Front 44

Raising the threshold potential would:

Back 44

slow the rate:slow the rate of APs by raising the threshold.

Front 45

Decreasing the threshold potential would:

Back 45

increase rate of AP production

Front 46

Hyperpolarization will ______ the heart

Back 46

slow: takes longer time to reach threshold potential

Front 47

Depolarization will ______ the heart

Back 47

increase:

Front 48

how do you affect depolarization of the heart?

Back 48

by changing K concentrations in the blood stream.

Front 49

Increasing K concentration in the bloodstream causes:

Back 49

the cells to increase K inside the cell thereby decreasing RMP, bringing it closer to threshold.

Front 50

If you raise the RMP above the threshold potential, you may

Back 50

may not get APs at all - so be careful about potassium

Front 51

epinepherine does what to heart rate?

Back 51

increases

Front 52

ACh does what to heart rate?

Back 52

decreases

Front 53

vagal stimulation is the ____

Back 53

brake

Front 54

Heart is innervated by the

Back 54

vagus nerve

Front 55

vagus nerve produces

Back 55

ACh.

Front 56

converting a perkinje fiber non pacemaker cell into a pacemaker AP via

Back 56

epinepherine

Front 57

a sponteneous depolarization will give rise to AP, no linger would need

Back 57

electrical depolarizations to stimulate AP.

Front 58

membrane potenial of a pacemaker AP is

Back 58

-60/-50mV rather than -90 mV

Front 59

do non pacemaker cells actually have the ability to become pacemaker cells?

Back 59

unknown.

Front 60

SAN is the normal pacemaker & AVN is it's slave b/c of

Back 60

overdrive suppression.

Front 61

inherent drive of AVN will be lower b/c it is driven by

Back 61

the higher rate of SAN.

Front 62

If AVN is stopped from being driven by the higher rate it will

Back 62

eventually recover
long time for first spontaneous AP to come out - initially, then time interval will shorten until inherent rate of 50 bpm will be reached.

Front 63

increasing rate of driven activity - the amount of time needed for recovery for the first spontaneous AVN pacemaker cell will be

Back 63

increased.

Front 64

The higher the frequency of overdrive suppression, the ________ to obtain the first spontaneous cell

Back 64

longer the delay/latency

Front 65

how can you increase latency of the AVN pacemaker cell?

Back 65

by increasing the number of depolarizations that occur prior to spontaneous AP.

Front 66

series of APs termed:

Back 66

trains.

Front 67

series of APs termed:

Back 67

trains.

Front 68

A long train of impulses causes overdrive: the longer the train - the longer the

Back 68

latency until you get the first spontaneous impulse.

Front 69

What prevents AVN from acting as the pacemaker of the heart?

Back 69

overdrive suppression

Front 70

SAN has a higher

Back 70

higher rate of firing overdrive: suppresses the AVN

Front 71

If you lose impulses from the SAN, what will take over?

Back 71

AVN