Electricity and the heart Flashcards

(81 cards)

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
what are the planes in which an ECG shows the heart?
vertical and horizontal
26
which electrode provides the best recording?
2
27
what happens at the 3rd electrode of an ECG?
main electrical flow is at 90 degress to the lead so the signal is minor, no QRS complex and minimal T wave
28
which leads give a lateral view of the heart?
I,aVL,V5,V6
29
which leads give a reciprocal view of the heart?
aVR
30
which leads give an inferior view of the heart?
II,III,aVF
31
which leads give an antero-septal view of the heart?
V1,V2
32
which leads given an anterior view of the heart?
V4,V3
33
what needs to analysed from an ECG?
rate rhythm axis morphology
34
how to calculate rate from an ECG?
count number of large squares between QRS complexes divide this number into 300 if using small squares divide into 1500
35
what should the PR interval be?
<200ms
36
How long should the QRS complex be?
<120ms
37
Timing
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
what can cause abnormalities in the morphology of an ECG?
ischaemia/ infarction hypertrophy electrolyte disturbance metabolic disturbance
39
ischaemia/ infarction on ECG
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
acute coronary syndrome
can be reversible
41
full thickness damage
ST elevation
42
subendocardial damage
ST depression
43
coronary artery for inferior heart
right coronary
44
coronary artery for antero-septal heart
left anterior descending
45
coronary artery for antero-apical
left anterior descending
46
coronary artery for antero-lateral
circumflex
47
coronary artery for posterior
right coronary
48
why are there abnormal Q waves in infarcts?
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
what are other causes of ST changes?
trauma pericarditis hyperkalaemia digoxin
50
what happens to ECG trace during hyperkalaemia?
high peaked T waves and QRS widening
51
hypertrophy on ECG
negative deflection in V1 and positive deflection in V5 | large amplitude QRS complexes
52
fibrillation
rapid uncoordinated contraction | atrial or ventricular
53
atrial fibrillation
AV node prevents ventricular fibrillation cardiac output decreased thrombo-embolism risk
54
ventricular fibrillation
no cardiac output | rapidly fatal if not treated
55
AF on ECG
No P waves QRS normal irregularly irregular
56
how is AF managed?
anti-thrombotic - warfarin or aspirin cardioversion - synchronised shock to prevent VF rate control - beta blocker, calcium antagonist amiodarone digoxin deal with underlying cause
57
What does digoxin do?
slows conduction through AVN | reduces ventricular rete in AF
58
how does digoxin work?
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
VF on ECG
``` continuous bizarre irregular trace no baseline no P ot T waves can cause sudden death if not treated ```
60
how to manage VF?
defibrillation - unsychronised, 150-200J
61
AED
external and internal
62
External AED
used by paramedics and in public
63
internal AID
implanted for high risk patients more long-term
64
where do conduction defects occur?
SAN AVN Intra-ventricular
65
SAN conduction defects
pacemaker failure | lower site normally takes over
66
AVN conduction defects
heart block
67
Intra-ventricular conduction defects
bundle branch block
68
what is heart block?
problem with conduction through AVN | 3 degrees
69
1st degree heart block
delayed transmission but it is all transmitted.
70
1st degree heart block ECG
long P-R interval | Normal QRS complexes
71
2nd degree heart block
partial AVN transmission
72
2nd degree heart block ECG
some P waves without associated QRS complex Some P waves not conducted regular or variable
73
3rd degree heart block
no AVN transmission
74
3rd degree heart block ECG
no link between P waves and QRS complexes | Wide QRS complexes
75
What is bundle branch block?
a problem with conduction through the R or L bundle branch | This means 1 ventricle depolarises slightly after the other
76
How does bundle branch block appear on an ECG?
Wide QRS complex after normal P wave
77
Right bundle branch block
M pattern in V1 and W pattern in V6
78
Left bundle branch block
M pattern in V6
79
How does asystole appear on an ECG?
no waves
80
How does ventricular ectopic appear on an ECG?
No P wave | Wide, bizarre QRS complex
81
Pacing impulse - artefact on ECG
very brief impulse, external impulse stimulates ventricle and sometimes atrium cause abnormal, wide QRS complexes