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
because of the stable resting membrane potential of the ventricular AP
unless it receives external stimulus, it will not contract therefore relies on pacemaker cells
26
ventricular AP: phase 0
electrical activity passes to ventricular myocyte through gap junction, rapid depolarisation goes to 20/30mV
27
ventricular AP: phase 1
early repolarisation slight repolarisation before plateau reached
28
ventricular AP: phase 2
plateau phase longer 200/300millisendocnds allows for duration of mechanical event: contraction of myocytes
29
ventricular AP: phase 3
repolarsation back to-90mV
30
ventricular AP (permeability changes): phase 0
controlled by increase in Na+ permeability
31
ventricular AP (permeability changes): phase 1
sudden decrease in Na+ permeability increase in K+ permeability + ions leave cell cell MP becomes more -
32
ventricular AP (permeability changes): phase 2
increase in Ca2+ permeability, Ca2+ entering cell decrease in K+ permeability, K+ leaving cell
33
ventricular AP (permeability changes): phase 3
increase in K+ permeability, decrease Ca2+ permeability more + ions leaving, less entering allows us to reach resting mp
34
ventricular AP (permeability changes): phase 4
increase permeability of K+ lots of + ions leaving cell helps to keep - MP
35
Ventricular AP refractory period
must reach back to resting membrane potential before AP can be reactivated length in which it takes cell to mechanically contract
36
firing of electrical activity leads to
mechanical event: contraction
37
how does electrical activity turn into mechanical action
excitation contraction-coupling
38
AP opens
opens calcium channels within T Tubules calcium enters diads
39
calcium entering diads causes
further calcium release from viandadeen receptors more calcium being released from internal stores within cell elevates intercellular calcium level
40
once intercellular calcium level in high,
binds to troponin C on thick and thin myosin filaments cross-bridged can occur allow for contraction to occur
41
why and how must calcium levels drop again
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
spread of excitation through myocardium creates...
small currents that can be detected on the body's surface
43
Einthoven's triangle
created through electrodes created on left arm right arm and left leg creates triangle around heart
44
Einthoven's triangle lead 1
right arm to left arm
45
Einthoven's triangle: lead 2
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
Einthoven's triangle: lead 3
left arm to left leg
47
ECG: upward deflection on ECG
positive signal moving towards left leg OR negative signal moving towards negative electrode
48
ECG: negative deflection on ECG
positive signal moving away from + electrode
49
ECG: P wave
atrial excitation small + wave
50
ECG: short flat area between P wave and QRS complex
delay at the AV node occurs
51
ECG: QRS complex
ventricular excitation ventricular depolarsation large + defelction at end of S, all ventricles fully depolarised
52
ECG: T wave
ventricular repolarisation small + deflection larger than P wave
53
ECG: flat area after T wave
heart at rest waiting until next beat
54
ECG: P-Q interval
measures delay between atrial and ventricular depolarisation includes AV nodal delay
55
ECG: Q-T interval
measure of the duration of ventricular systole how long they are in mechanical contraction phase
56
ECG: T-Q interval
measure of the duration of ventricular diastole relaxation phase
57
ECG: R-R interval
measure of heart rate
58
caridac cyle
alternates periods of systole(contraction and ejection) and diastole (relaxation and filling)
59
two heart sounds
heart sound 1: lup heart sound 2: dup
60
heart sound 1: lup associated with
closure of AV valves at the start of ventricular systole
61
heart sound 2: dup associated with
closure of the semi-lunar valves at the start of the ventricular diastole
62
other heart sounds
associated with rapid ventricular filling or atrial contraction only heard during pathological conditions or particular circumstances
63