Cardiac arrythmias epidemiology and Aetiology Flashcards
1
Q
arrythmia other name
A
dysrhythmia
2
Q
arrythmia
A
abnormality of electrical rhythm
3
Q
types of arrythmia (2)
A
benign and malignant
4
Q
arryhmia symptoms
A
palpitations
5
Q
palpitation causes (3)
A
critical reduction in cardiac output, altered AP generation or altered AP conduction processes
6
Q
ECG
A
electrocardiogram
7
Q
AP
A
action potential
8
Q
ECG mV
A
1-2
9
Q
AP mV
A
100
10
Q
baseline in ECG
A
isoelectric line
11
Q
ECG P
A
atria depolarisation
12
Q
ECG P to Q
A
AV node delay
13
Q
AV
A
atrioventricular node
14
Q
ECG QRS duration
A
ventricle depolarisation
15
Q
what happens just before P in an ECG
A
SA node fires
16
Q
SA
A
sinoatrial node
17
Q
ECG T
A
ventricle repolarisation
18
Q
ECG QT interval
A
ventricular AP
19
Q
SA node firing to Q
A
atrial AP
20
Q
prevelance of arrythmia
A
high
21
Q
what are arrythmias normally
A
asymptomatic without provocation
22
Q
arrythmia prevalence in >60 y/o
A
5-9%
23
Q
highest mortality of MI caused by
A
arrythmia
24
Q
getting an arrythmia (2)
A
acquired or genetic
25
bradyarrythmia
too slow
26
tachyarrythmia
too fast
27
fibrillation
irregular or unsynchronised electrical activity and
28
arrythmia origin (2)
atrial and ventricular
29
AF
atrial fibrillation
30
normal rhythm
sinus rhythm
31
AF ECG features (3)
irregular QRS complexes and no P wave, rough T wave
32
AF prevalence
2-4%
33
AF risk factors (2)
obesity and age
34
AF prevalence att 80 y/o
20%, growing health problem
35
VF
ventricular fibrillation
36
VF ECG features (2)
no QRS complex, squiggly line
37
when is VF most common
post MI or stroke
38
MI
myocardial infarction or thrombosis
39
does VF need an MI
not always
40
Types of AF (3)
paroxysmal, persistent, permenant
41
paroxysmal
bursts
42
persistent
regular
43
permanent
constant
44
what makes AF difficult to detect
asymptomatic
45
how is AF normally detected
investigating other cardiac abnormalities
46
how can AF lead to heart failure
tachycardia
47
other causes of VF (3)
hypertrophy, hypertension, myocarditis
48
VF results in sudden
cardiac and brain death
49
how is automaticiy normally altered (2)
unstable rhythm or alternative pacemaker emergence
50
Causes of altered AP generation
altered calcium ion homeostasis and unstable RMP
51
types of oscillation in altered AP generation (2)
EAD and DAD
52
EAD
early afterdepolarisation
53
DAD
delayed afterdepolarisation
54
when is AP triggered
once threshold is reached -40 mV
55
order of ionic channels in pacemaker cells generating AP
T type Ca open and If opens, some Ca open If closes, lots of L type Ca open, Ca open and K open, K closes and If opens
56
If
net sodium entry
57
Potassium channels role
repolarises
58
repolarisation overshoot
-60 mV
59
AP depolarisation mV
+15 mV
60
what does SA normally do to other pacemakers
overdrives
61
sympathetic regulation of pacemakers
adrenaline and noradrenaline
62
parasympathetic regulation of pacemakers
acetylcholine
63
sympathetic effect on pacemaker
increased If and ICa, decreased IK
64
parasympathetic effect on pacemaker
decreased If and ICa, increased IK
65
how can abnormality in automaticity occur (3)
increased sympathetic effect on latent pacemaker takes over, increased parasympathetic on pacemaker, injured node area
66
what happens if a node area is injured (3)
other cells develop pacemaker function, loss of RMP, osciallations
67
what can cause injury to a nodal area
Ischaemia
68
normal AP features (3)
stable RMP, coverts to pacemaker activity, ventricular longer phase 2 than atrial
69
AP phase 0
fast sodium channel opens
70
AP phase 1
fast sodium channel closes
71
AP phase 2
L type Ca channels open
72
AP phase 3 (2)
K channels open, Ca channels close
73
AP phase 4
stable RMP
74
triggered impulses
EAD and DAD
75
when does EAD occur
early in AP repolarisation
76
when is EAD more likely to occur (2)
long AP duration or long QT syndromes
77
what causes EAD in long repolarisation
voltage gated Ca channels are reactivated
78
EAD can lead to
self perpetuating tachyarrythmia
79
sodium channel mutations for EAD
SCN5A
80
SCN5A mutation effect (3)
channel doens't stay inactivated, inward current occurs late, extends duration
81
potassium channel mutations for EAD (2)
KCNQ1 or HERG
82
KCNQ1 or HERG mutation effects (2)
decreased repolarising K efflux and plateau termination delay
83
when does DAD occur
after repolarisation
84
what conditions are prone to DAD (2)
reliance on Na Ca exchanger for relaxation or RMP depolarised
