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physiology and anatomy > week 5: cardiac physiology: structure of the lungs and heart and activity of the heart > Flashcards

week 5: cardiac physiology: structure of the lungs and heart and activity of the heart Flashcards

1
Q

the heart is myogenic meaning

A

contacts by itself

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2
Q

why is the heart myogenic

A

pacemaker cells within the heart

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3
Q

SAN cells

A

0.1 mm in length
spontaneously beat

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4
Q

cardiac AP originates

A

SA node
not dependent on neuronal stimulation
myogenic
generated own firing rate

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5
Q

myogenic tissue within heart

A

SA node
AV node
bundle of his

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6
Q

dominant pacemaker

A

SA node as it’s at the highest frequency firing rate

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7
Q

delay from propagation of electrical signal

A

100 millisecond

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8
Q

how is heart muscle connected

A

electrically
electrical connection between cardiomyocytes
gap junctions

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9
Q

electrical connection between cardiomyocytes allows AP generated in pace maker cells to

A

spread through to adjacent cells
electrical current passes through gap junctions in intercalated discs

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10
Q

gap junctions in intercalated discs forms a

A

low resistance pathway

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11
Q

frequency in which AP fires controls

A

heart rate

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12
Q

pacemaker potential is controlled by

A

different levels of permeability to different ions

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13
Q

maximum diastolic potential

A

phase 4
lowest part of AP
can move which changes frequenxy heart rate
ussually sits around -70mV

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14
Q

why does membrane potential begin to rise in stage 4

A

due to declining permeability to K+ and increasing permeability to Na+ and Ca2+
more + ions moving into cell faster than Na+ moving out

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15
Q

-40mV reached

A

threshold reached
rapid increase in Ca2+ permeability through altide calcium channles
generate upstroke in AP

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16
Q

peak of AP

A

associated in decrease in Ca2+ permeability, channels shut
increased permeability to K+, K+ channels open
K+ leaves faster than Ca2+ enter,
causes membrane to become more negative
decrease in membrane potential

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17
Q

membrane potential reaches -55/60mV

A

permeability to K+ starts to decrease
re-entry of Na+ and Ca2+
restarting pacemaker potential

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18
Q

AP spreads…..

A

spreads through atrial tissue to AV node via internodial tracts
propagates to all of atiral but specifically goes down internodial tracts to stimulate AV node

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19
Q

cells in atrioventricular node AP

A

slower
cause delay of impulse transmitting down further- 100 milliseconds

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20
Q

after impulse reaches AV node,

A

passed to bundle of His from AV node
only electrical connection between atrial tissue and ventricular tissue

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21
Q

after bundle of His,

A

electrical tissue splits into two branches:
right and left bundle branch

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22
Q

where does electrical activity run down to from left and right bundle branches

A

apex of heart

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23
Q

electrical activity after apex of heart,

A

spread throughout ventricular tissue through Purkinje fibers

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24
Q

ventricular action potential has a stable:

A

resting membrane potential
-90mV

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25
Q

because of the stable resting membrane potential of the ventricular AP

A

unless it receives external stimulus, it will not contract therefore relies on pacemaker cells

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26
Q

ventricular AP: phase 0

A

electrical activity passes to ventricular myocyte through gap junction,
rapid depolarisation
goes to 20/30mV

27
Q

ventricular AP: phase 1

A

early repolarisation
slight repolarisation before plateau reached

28
Q

ventricular AP: phase 2

A

plateau phase
longer
200/300millisendocnds
allows for duration of mechanical event: contraction of myocytes

29
Q

ventricular AP: phase 3

A

repolarsation
back to-90mV

30
Q

ventricular AP (permeability changes): phase 0

A

controlled by increase in Na+ permeability

31
Q

ventricular AP (permeability changes): phase 1

A

sudden decrease in Na+ permeability
increase in K+ permeability
+ ions leave cell
cell MP becomes more -

32
Q

ventricular AP (permeability changes): phase 2

A

increase in Ca2+ permeability,
Ca2+ entering cell
decrease in K+ permeability, K+ leaving cell

33
Q

ventricular AP (permeability changes): phase 3

A

increase in K+ permeability,
decrease Ca2+ permeability
more + ions leaving, less entering
allows us to reach resting mp

34
Q

ventricular AP (permeability changes): phase 4

A

increase permeability of K+
lots of + ions leaving cell
helps to keep - MP

35
Q

Ventricular AP refractory period

A

must reach back to resting membrane potential before AP can be reactivated
length in which it takes cell to mechanically contract

36
Q

firing of electrical activity leads to

A

mechanical event: contraction

37
Q

how does electrical activity turn into mechanical action

A

excitation contraction-coupling

38
Q

AP opens

A

opens calcium channels within T Tubules
calcium enters diads

39
Q

calcium entering diads causes

A

further calcium release from viandadeen receptors
more calcium being released from internal stores within cell
elevates intercellular calcium level

40
Q

once intercellular calcium level in high,

A

binds to troponin C on thick and thin myosin filaments
cross-bridged can occur
allow for contraction to occur

41
Q

why and how must calcium levels drop again

A

allow for cell to relax
Ca2+ extruded back out through na/ ca channels into extracellular are
or pumped back into intercellular stores within sarcoplasmic reticulum

42
Q

spread of excitation through myocardium creates…

A

small currents that can be detected on the body’s surface

43
Q

Einthoven’s triangle

A

created through electrodes created on left arm right arm and left leg
creates triangle around heart

44
Q

Einthoven’s triangle lead 1

A

right arm to left arm

45
Q

Einthoven’s triangle: lead 2

A

right arm to left leg
used to represent net amplitude and direction of electrical activity of heart
runs in line in same direction in whihc heart is directed, base to apex

46
Q

Einthoven’s triangle: lead 3

A

left arm to left leg

47
Q

ECG: upward deflection on ECG

A

positive signal moving towards left leg
OR
negative signal moving towards negative electrode

48
Q

ECG: negative deflection on ECG

A

positive signal moving away from + electrode

49
Q

ECG: P wave

A

atrial excitation
small + wave

50
Q

ECG: short flat area between P wave and QRS complex

A

delay at the AV node occurs

51
Q

ECG: QRS complex

A

ventricular excitation
ventricular depolarsation
large + defelction
at end of S, all ventricles fully depolarised

52
Q

ECG: T wave

A

ventricular repolarisation
small + deflection
larger than P wave

53
Q

ECG: flat area after T wave

A

heart at rest
waiting until next beat

54
Q

ECG: P-Q interval

A

measures delay between atrial and ventricular depolarisation
includes AV nodal delay

55
Q

ECG: Q-T interval

A

measure of the duration of ventricular systole
how long they are in mechanical contraction phase

56
Q

ECG: T-Q interval

A

measure of the duration of ventricular diastole
relaxation phase

57
Q

ECG: R-R interval

A

measure of heart rate

58
Q

caridac cyle

A

alternates periods of systole(contraction and ejection) and diastole (relaxation and filling)

59
Q

two heart sounds

A

heart sound 1: lup
heart sound 2: dup

60
Q

heart sound 1: lup associated with

A

closure of AV valves at the start of ventricular systole

61
Q

heart sound 2: dup associated with

A

closure of the semi-lunar valves at the start of the ventricular diastole

62
Q

other heart sounds

A

associated with rapid ventricular filling or atrial contraction
only heard during pathological conditions or particular circumstances

63
Q
A

physiology and anatomy (31 decks)

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