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Physiology > Electricity and the heart > Flashcards

Electricity and the heart Flashcards

1
Q

what are the types of muscle?

A

cardiac
skeletal
smooth

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2
Q

what are the important features of cardiac muscle?

A

timing
togetherness
achieved by sophisticated electrical mechanisms

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3
Q

what are the specific needs of the heart?

A

simultaneous, intermittent contraction of all fibres
prevention of sustained (tetanic) contraction
ability to change rate according to circumstances

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4
Q

ion distribution in cardiac myocyte

A

Na+/K+ ATPase- powered pump maintains the high sodium ion conc outside the cell and high potassium ion conc inside the cell
to sustain the calcium gradient an antiport system exchanges calcium ions for sodium ions

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5
Q

Action potential of a cardiac myocyte

A 
depolarisation - fast inflow of sodium
calcium inflow - T type
potassium outflow 
calcium inflow - L-type, continues to create action potential so causes plateau
repolarisation
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6
Q

what is the role of calcium in the cardiac myocyte action potential

A

extended duration of AP

esnures total ventricular depolarisation

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7
Q

Refractory period of AP in cardiac myocyte

A

prolonged refractory period
ion channel inactivation
prevents tetany

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8
Q

pacemaker

A 
specialised cells in atria, especially SAN and AVN 
automatic firing, without stimulus
results from continuous slow ionic leak
natural rate is highest in SAN 
other areas become active if SAN fails
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9
Q

pacemaker cell action potential

A

no resting phase

calcium not sodium inflow responsible for main depolarisation

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10
Q

heart rate

A 
pacemaker cycle length determines HR
varies under influence of autonomic NS
natural rate - 100-110 bpm 
parasympathetic normally dominant 
very sensitive to change - even respiration alters HR - sinus arrhythmia
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11
Q

sympathetic influence on heart

A

slow sodium ion channel permeability increases
slope of phase 4 becomes steeper
threshold reached sooner, increasing HR

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12
Q

where is phase 4 on a cardiac AP?

A

the first ascending part

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13
Q

parasympathetic influence on heart

A

increases resting potassium ion channel permeability
trough potential is lowered and slope of phase 4 becomes flatter
threshold reached later and so decreases HR

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14
Q

intra-cardiac conduction

A

non-specific conduction in atria
AVN acts as a gate in the firewall between atria and ventricles
Bundle of His-Purkinje system supplies the ventricles

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15
Q

what direction does depolarisation happen?

A

from in to out

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16
Q

what direction does perfusion happen

A

from out to in

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17
Q

what does the AVN do?

A

slows conduction
allows time for atrial emptying
protects ventricles from atrial tachyarrhythmias
also affected by autonomic NS

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18
Q

conduction from the AVN

A

Left bundle branch has 2 fascicles for conduction
there is 1 right bundle branch
the branching nature of cardiac muscle enables the depolarisation to spread and so the ventricles contract simultaneously

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19
Q

electrocardiogram

A

surface recording of electrical activity
series of electrodes allows multiple views
magnitude = 1-2mV

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20
Q

polarity of impulses on ECG

A

positive if the impulse moves towards the recording electrode
negative if the impulse moves away from the recording electrode

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21
Q

what colour are the limb leads?

A

yellow and green for left

red and black for right

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22
Q

which lead goes on the left wrist?

A

yellow

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23
Q

which lead goes on the right wrist?

A

red

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24
Q

how many ECG leads are there?

A

10
4 limb
6 chest

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25
Q

what are the planes in which an ECG shows the heart?

A

vertical and horizontal

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26
Q

which electrode provides the best recording?

A

2

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27
Q

what happens at the 3rd electrode of an ECG?

A

main electrical flow is at 90 degress to the lead so the signal is minor, no QRS complex and minimal T wave

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28
Q

which leads give a lateral view of the heart?

A

I,aVL,V5,V6

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29
Q

which leads give a reciprocal view of the heart?

A

aVR

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30
Q

which leads give an inferior view of the heart?

A

II,III,aVF

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31
Q

which leads give an antero-septal view of the heart?

A

V1,V2

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32
Q

which leads given an anterior view of the heart?

A

V4,V3

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33
Q

what needs to analysed from an ECG?

A

rate
rhythm
axis
morphology

34
Q

how to calculate rate from an ECG?

A

count number of large squares between QRS complexes
divide this number into 300
if using small squares divide into 1500

35
Q

what should the PR interval be?

A

<200ms

36
Q

How long should the QRS complex be?

A

<120ms

37
Q

Timing

A

mechanical contraction lags behind depolarisation
QRS complex starts with Phase 0 of ventricular action potential
T wave ends with phase 3 of ventricular AP

38
Q

what can cause abnormalities in the morphology of an ECG?

A

ischaemia/ infarction
hypertrophy
electrolyte disturbance
metabolic disturbance

39
Q

ischaemia/ infarction on ECG

A

typically produce ST segment changes acutely
damaged cells repolarise early so ST segment is out of step with normal areas
division between ischaemia and infarction is now less clear

40
Q

acute coronary syndrome

A

can be reversible

41
Q

full thickness damage

A

ST elevation

42
Q

subendocardial damage

A

ST depression

43
Q

coronary artery for inferior heart

A

right coronary

44
Q

coronary artery for antero-septal heart

A

left anterior descending

45
Q

coronary artery for antero-apical

A

left anterior descending

46
Q

coronary artery for antero-lateral

A

circumflex

47
Q

coronary artery for posterior

A

right coronary

48
Q

why are there abnormal Q waves in infarcts?

A

act as an electrical window, where there is no electrical activity
electrode records depolarisation of opposite wall, which goes from inside to out and causes a negative deflection - Q wave

49
Q

what are other causes of ST changes?

A

trauma
pericarditis
hyperkalaemia
digoxin

50
Q

what happens to ECG trace during hyperkalaemia?

A

high peaked T waves and QRS widening

51
Q

hypertrophy on ECG

A

negative deflection in V1 and positive deflection in V5

large amplitude QRS complexes

52
Q

fibrillation

A

rapid uncoordinated contraction

atrial or ventricular

53
Q

atrial fibrillation

A

AV node prevents ventricular fibrillation
cardiac output decreased
thrombo-embolism risk

54
Q

ventricular fibrillation

A

no cardiac output

rapidly fatal if not treated

55
Q

AF on ECG

A

No P waves
QRS normal
irregularly irregular

56
Q

how is AF managed?

A

anti-thrombotic - warfarin or aspirin
cardioversion - synchronised shock to prevent VF
rate control - beta blocker, calcium antagonist
amiodarone
digoxin
deal with underlying cause

57
Q

What does digoxin do?

A

slows conduction through AVN

reduces ventricular rete in AF

58
Q

how does digoxin work?

A

increases myocardial contractility
sodium/ potassium pump is inhibited, increasing conc of Na+ inside cell
the sodium/ calcium pump becomes less efficient so intracellular calcium increases and is stored in sarcoplasmic reticulum
force of subsequent contractions are enhanced

59
Q

VF on ECG

A 
continuous
bizarre
irregular trace 
no baseline
no P ot T waves
can cause sudden death if not treated
60
Q

how to manage VF?

A

defibrillation - unsychronised, 150-200J

61
Q

AED

A

external and internal

62
Q

External AED

A

used by paramedics and in public

63
Q

internal AID

A

implanted
for high risk patients
more long-term

64
Q

where do conduction defects occur?

A

SAN
AVN
Intra-ventricular

65
Q

SAN conduction defects

A

pacemaker failure

lower site normally takes over

66
Q

AVN conduction defects

A

heart block

67
Q

Intra-ventricular conduction defects

A

bundle branch block

68
Q

what is heart block?

A

problem with conduction through AVN

3 degrees

69
Q

1st degree heart block

A

delayed transmission but it is all transmitted.

70
Q

1st degree heart block ECG

A

long P-R interval

Normal QRS complexes

71
Q

2nd degree heart block

A

partial AVN transmission

72
Q

2nd degree heart block ECG

A

some P waves without associated QRS complex
Some P waves not conducted
regular or variable

73
Q

3rd degree heart block

A

no AVN transmission

74
Q

3rd degree heart block ECG

A

no link between P waves and QRS complexes

Wide QRS complexes

75
Q

What is bundle branch block?

A

a problem with conduction through the R or L bundle branch

This means 1 ventricle depolarises slightly after the other

76
Q

How does bundle branch block appear on an ECG?

A

Wide QRS complex after normal P wave

77
Q

Right bundle branch block

A

M pattern in V1 and W pattern in V6

78
Q

Left bundle branch block

A

M pattern in V6

79
Q

How does asystole appear on an ECG?

A

no waves

80
Q

How does ventricular ectopic appear on an ECG?

A

No P wave

Wide, bizarre QRS complex

81
Q

Pacing impulse - artefact on ECG

A

very brief impulse, external impulse stimulates ventricle and sometimes atrium
cause abnormal, wide QRS complexes

Physiology (46 decks)

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