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CVS physiology > Origin and conduction of cardiac impulse (CVS2&3) > Flashcards

Origin and conduction of cardiac impulse (CVS2&3) Flashcards

1
Q

autorythmicity

A
  • the heart is an electrically controlled muscular pump
  • the electrical signals which control the heart are generated within the heart itself
  • the heart is capable of beating rhythmically in the absence of external stimuli, this is called autorythmicity
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2
Q

how is an ECG (electrocardiogram) obtained

A

it is possible to record the spread of electrical activity through the heart from the skin surface to obtain an ECG

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3
Q

normal origin of excitation within the heart

A

in the pacemaker cells in the sinoatrial node/SA node

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4
Q

how is heart beat initiated

A

by the cluster of specialized pacemaker cells in the sinoatrial node

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5
Q

location of sinoatrial node

A

in the upper right atrium close to where the superior vena cava enters the right atrium

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6
Q

tricuspid valve

A

between right atrium and right ventrical

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7
Q

mitral valve

A

between left atrium and left ventricle

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8
Q

what drives/sets the pace for the entire heart

A

sinoatrial node

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9
Q

what does it mean if a heart is said to be in sinus rhythm

A

it is controlled by the sinoatrial node

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10
Q

properties of cells in the sinoatrial node

A
  • they do not have a stable resting membrane potential

- they exhibit spontaneous pacemaker potential

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11
Q

function of spontaneous pacemaker potential exhibited by cells within sinoatrial node

A

takes the membrane potential to a threshold to generate an action potential in the SA nodal cells

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12
Q

pacemaker potential

A
  • slow depolarization of membrane potential to a threshold, due to a decrease in K+ efflux superimposed on a slow Na+ influx (funny current)
  • the permeability to K+ within the pacemaker cells does not remain constant between action potentials
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13
Q

efflux

A

inside to outside

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14
Q

influx

A

outside to inside

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15
Q

what causes the rising phase of the action potential/depolarization in pacemaker cells

A

activation of voltage gated calcium ion channels, resulting in calcium(Ca++) influx

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16
Q

depolarization

A

rising phase of action potential

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17
Q

what causes the falling phase of the action potential/repolarization in pacemaker cells

A

activation of K+ channels, resulting in K+ efflux

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18
Q

intracellular recording from SA node cell/graph of action potential

A
  • pacemaker potential causes slow depolarization of membrane potential to a threshold (from -60 to -40)due to a decrease in K+ efflux superimposed on a slow Na+ influx
  • once the threshold is reached, activation of voltage gated calcium ion channels, resulting in calcium(Ca++) influx causes the rising phase of the action potential/depolarization (from-40 to 0)
  • the activation of K+ channels, resulting in K+ efflux which is responsible for the falling phase of the action potential/repolarization (from 0 to -60)
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19
Q

how does cardiac excitation normally spread across the heart

A
  • from SA node to AV node via cell-cell conduction (from one myocardial cell to another myocardial cell and so on and so on)
  • through SA node through both atria via gap junctions
  • and within ventricles via gap junctions
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20
Q

atrioventricular node

A
  • small bundle of specialized cardiac cells (AV node cells are small in diameter and have slow conduction velocity which allows for delay of action potentials, allowing heart to conduct in contracted manner- atria first then ventricles)
  • ONLY point of electrical contact between atria and ventricles
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21
Q

pathway through heart that the spread of excitation follows

A

-originate in sinoatrial node, travel to atrioventricular node via cell-cell conduction, then to the bundle of His conductive pathways and down their divided left and right branches, before reaching purkinje fibres and spreading through out ventricle

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22
Q

gap junctions

A
  • part of intercalated discs (a specialized intercellular attachment of cardiac muscle cells comprising gap junctions, fascia adherens, and occasionally desmosomes)
  • cell-cell current flow
  • allow action potentials to spread from cell-cell
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23
Q

how do action potentials spread from cell-cell

A

cell-cell conduction via action potentials

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24
Q

location of AV node

A

base of right atrium, just above the junction of atria and ventricles

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25
Q

systole

A

contraction

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26
Q

dyastole

A

relaxation

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27
Q

spread of excitation across atria

A

mainly cell-cell conduction via gap junctions

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28
Q

spread of excitation from SA node to AV node

A

mainly cell-cell conduction via gap junctions but there is also some internodal pathways

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29
Q

why is the conduction delayed in the AV node

A

allows atrial systole (contraction) to precede ventricular systole (spreads in contracted manner)

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30
Q

role of bundle of His and its branches (right and left) and the network of purkinje fibres

A

allow rapid spread of action potential to the ventricles

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31
Q

spread of excitation through ventricular muscle

A

via cell-cell conduction

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32
Q

ventricular muscle action potential

A
  • action potential in contractile cardiac muscle cells differs considerably from the action potential in the pacemaker cells
  • resting membrane potential remains at -90 (instead of -60 in pacemaker cells) until the cell is excited
  • no pacemaker potential present
  • switches on systole(contraction- explained more in next lecture)
33
Q

what causes the rising phase of the action potential/depolarization in ventricular muscle (contractile muscle) cells

A
  • fast Na+ influx (rapidly reverses the membrane potential from -90 to 30)
  • known as phase 0 of action potential in contractile cardiac muscle cells
34
Q

phases of ventricular muscle action potential

A
  • PHASE 0= fast Na+ influx (rapidly reverses the membrane potential from -90 to 30mV)
  • PHASE 1= closure of Na+channels and transient K+efflux (membrane potential decreases slightly)
  • PHASE 2=plateau phase, mainly due to Ca++ influx, very characteristic of cardiac muscle action potential(membrane potential decreases to around 0mV)
  • PHASE 3= due to closure of Ca++ channels and K+ efflux (membrane potential decrease from around 0 to -90mV)
  • PHASE 4= resting membrane potential (-90mV)
35
Q

phase 0 of ventricular muscle action potential

A

fast Na+ influx (rapidly reverses the membrane potential from -90 to 30mV)

36
Q

phase 1 of ventricular muscle action potential

A

closure of Na+channels and transient K+efflux (membrane potential decreases slightly)

37
Q

phase 2 of ventricular muscle action potential

A

plateau phase, mainly due to Ca++ influx, very characteristic of cardiac muscle action potential(membrane potential decreases to around 0mV)

38
Q

phase 3 of ventricular muscle action potential

A

due to closure of Ca++ channels and K+ efflux (membrane potential decrease from around 0 to -90mV)

39
Q

phase 4 of ventricular muscle action potential

A

resting membrane potential (-90mV)

40
Q

time between phase 0 and phase 4 of ventricular muscle action potential

A

250msec’s

41
Q

units of membrane potential

42
Q

plateau phase of action potential (in ventricular muscle)

A
  • where the membrane potential is maintained near the peak of action potential for a few hundred milliseconds
  • unique characteristic of contractile cardiac muscle cells
  • mainly due to influx of Ca++ through voltage gated Ca++ channels (also decrease in NA+ influx)
43
Q

what causes the falling phase of the action potential/repolarization in ventricular muscle (contractile muscle) cells

A

-inactivation of Ca++ channels and activation of K+ channels, resulting in K+ efflux

44
Q

what is heart rate mainly influenced by

A

autonomic nervous system

45
Q

how does sympathetic stimulation affect heart rate

A

increases heart rate (also caused by a decrease in parasympathetic stimulation)

46
Q

how does parasympathetic stimulation affect heart rate

A

decreases heart rate (also caused by a decrease in sympathetic stimulation)

47
Q

parasympathetic supply to the heart

A
  • vagus nerve (CNX)
  • exerts a continuous influence on the SA node under resting conditions, if you remove the influence of CNX and parasympathetics, the heart will spead up
48
Q

influence of autonomic nervous system on the normal resting heart rate

A
  • vagus nerve exerts a continuous influence on the SA node under resting conditions (vagal tone dominates under normal resting conditions- vagal tone is more dominant in athletes)
  • vagal tone slows intrinsic heart rate from ~100bpm to produce a normal resting heart rate of ~70bpm
49
Q

effect of vagal tone on intrinsic heart rate

A

slows intrinsic heart rate from ~100bpm to produce a normal resting heart rate of ~70bpm

50
Q

normal resting heart rate

A
  • ~70bpm

- (considered to be normal if it is between 60-100bpm)

51
Q

bradycardia/bradycardic patient

A

-slow resting heart rate, less than 60bpm

52
Q

tachycardia/tachycardic patient

A

-fast resting heart rate, more than 100bpm

53
Q

effect of vagal stimulation on heart

A
  • vagus nerve supplies SA node and AV node

- slows heart rate(by slowing rate SA node fires action potentials) and increases AV nodal delay

54
Q

2 ways heart rate is slowed

A
  • slowing the rate SA node fires action potentials

- increasing delay of impulse in AV node

55
Q

parasympathetic neurotransmitter

A

acetylcholine (acting through M2/muscarinic receptors)

56
Q

atropine

A
  • competitive inhibitor of acetylcholine
  • blocks effect of acetylcholine to speed up heart rate
  • used in extreme bradycardia (slow HR)
57
Q

effect of vagal stimulation on pacemaker potentials

A
  • causes cell hyperpolarization (An increase in polarization of membranes of nerves or muscle cells; the reverse change from that associated with excitatory action) therefore takes longer to reach threshold
  • slope of pacemaker potential decreases
  • frequency of action potential (AP) decreases
  • negative chronotropic effect (slows down HR)
58
Q

chronotropic effect (positive and negative)

A

relates to heart rate (positive speeds up HR, negative slows down HR)

59
Q

positive chronotropic effect

A

speeds up HR

60
Q

negative chronotropic effect

A

slows down HR

61
Q

sympathetic supply to heart

A

-cardiac sympathetic nerves supply SA node, AV node and myocardium (ventricular muscle itself)

62
Q

effect of myocardium (ventricular muscle) on HR

A

-can influence heart rate itself and degree of contraction

63
Q

effect of sympathetic stimulation on the heart rate

A
  • increases heart rate and decreases AV nodal delay, therefore spread of action potentials is faster
  • also increases force of contraction (more in next lecture)
64
Q

sympathetic neurotransmitter

A

noradrenaline (acting through beta adrenoreceptors)

65
Q

effect of noradrenaline on pacemaker cells (and pacemaker potentials)

A
  • slope of pacemaker potential increases
  • pacemaker potential reaches threshold quicker
  • frequency of action potentials increases - positive chronotropic effect (speeds up HR)
66
Q

effect of sympathetic stimulation/noradrenaline on slope of pacemaker potential

67
Q

effect of parasympathetic (vagal) stimulation/acetylcholine on slope of pacemaker potential

68
Q

effect of sympathetic stimulation/noradrenaline on heart rate

69
Q

effect of parasympathetic (vagal) stimulation/acetylcholine on heart rate

70
Q

effect of parasympathetic (vagal) stimulation/acetylcholine on Pk+ of pacemaker cells (efflux)

71
Q

effect of parasympathetic (vagal) stimulation/acetylcholine on PNa+ and PCa++ of pacemaker cells (influx)

72
Q

effect of parasympathetic (vagal) stimulation/acetylcholine on AV nodal delay

73
Q

effect of sympathetic stimulation/noradrenaline on Pk+ of pacemaker cells (efflux)

74
Q

effect of sympathetic stimulation/noradrenaline on PNa+ and PCa++ of pacemaker cells (influx)

75
Q

effect of sympathetic stimulation/noradrenaline on AV nodal delay

76
Q

electrocardiogram (ECG)

A
  • ECG is a record of depolarization and repolarization cycle of cardiac muscle obtained from skin surface
  • the wave of depolarization and repolarization moves across the heart and sets up electrical currents which can be detected by surface electrodes
77
Q

how do we record ECG (standard limb leads)

A
  • measure potential difference between two electrodes
  • limb lead= imaginary line between 2 electrodes
  • lead I: RA (right arm) - LA (left arm)
  • lead II: RA (right arm) - LL (left leg)
  • lead III: LA (left arm) - LL (left leg)
78
Q

different points/ intervals on ECG graph recorded from skin surface

A

-P: atrial depolarization
-QRS complex: ventricular depolarization
-T:ventricular repolarization
-PR interval: largely AV node delay
-ST segment: ventricular systole/contraction
-TP interval: diastole/ relaxation
(P->Pr->QRS->ST->T->TP->P…)
REFER TO GRAPH IN LECTURE

CVS physiology (11 decks)

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