Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Physiology > Cardiac arrythmias epidemiology and Aetiology > Flashcards

Cardiac arrythmias epidemiology and Aetiology Flashcards

1
Q

arrythmia other name

A

dysrhythmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

arrythmia

A

abnormality of electrical rhythm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

types of arrythmia (2)

A

benign and malignant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

arryhmia symptoms

A

palpitations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

palpitation causes (3)

A

critical reduction in cardiac output, altered AP generation or altered AP conduction processes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

ECG

A

electrocardiogram

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

AP

A

action potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

ECG mV

A

1-2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

AP mV

A

100

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

baseline in ECG

A

isoelectric line

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

ECG P

A

atria depolarisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

ECG P to Q

A

AV node delay

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

AV

A

atrioventricular node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

ECG QRS duration

A

ventricle depolarisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what happens just before P in an ECG

A

SA node fires

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

SA

A

sinoatrial node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

ECG T

A

ventricle repolarisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

ECG QT interval

A

ventricular AP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

SA node firing to Q

A

atrial AP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

prevelance of arrythmia

A

high

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what are arrythmias normally

A

asymptomatic without provocation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

arrythmia prevalence in >60 y/o

A

5-9%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

highest mortality of MI caused by

A

arrythmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

getting an arrythmia (2)

A

acquired or genetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

bradyarrythmia

A

too slow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

tachyarrythmia

A

too fast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

fibrillation

A

irregular or unsynchronised electrical activity and

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

arrythmia origin (2)

A

atrial and ventricular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

AF

A

atrial fibrillation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

normal rhythm

A

sinus rhythm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

AF ECG features (3)

A

irregular QRS complexes and no P wave, rough T wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

AF prevalence

A

2-4%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

AF risk factors (2)

A

obesity and age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

AF prevalence att 80 y/o

A

20%, growing health problem

35
Q

VF

A

ventricular fibrillation

36
Q

VF ECG features (2)

A

no QRS complex, squiggly line

37
Q

when is VF most common

A

post MI or stroke

38
Q

MI

A

myocardial infarction or thrombosis

39
Q

does VF need an MI

A

not always

40
Q

Types of AF (3)

A

paroxysmal, persistent, permenant

41
Q

paroxysmal

A

bursts

42
Q

persistent

A

regular

43
Q

permanent

A

constant

44
Q

what makes AF difficult to detect

A

asymptomatic

45
Q

how is AF normally detected

A

investigating other cardiac abnormalities

46
Q

how can AF lead to heart failure

A

tachycardia

47
Q

other causes of VF (3)

A

hypertrophy, hypertension, myocarditis

48
Q

VF results in sudden

A

cardiac and brain death

49
Q

how is automaticiy normally altered (2)

A

unstable rhythm or alternative pacemaker emergence

50
Q

Causes of altered AP generation

A

altered calcium ion homeostasis and unstable RMP

51
Q

types of oscillation in altered AP generation (2)

A

EAD and DAD

52
Q

EAD

A

early afterdepolarisation

53
Q

DAD

A

delayed afterdepolarisation

54
Q

when is AP triggered

A

once threshold is reached -40 mV

55
Q

order of ionic channels in pacemaker cells generating AP

A

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
Q

If

A

net sodium entry

57
Q

Potassium channels role

A

repolarises

58
Q

repolarisation overshoot

A

-60 mV

59
Q

AP depolarisation mV

A

+15 mV

60
Q

what does SA normally do to other pacemakers

A

overdrives

61
Q

sympathetic regulation of pacemakers

A

adrenaline and noradrenaline

62
Q

parasympathetic regulation of pacemakers

A

acetylcholine

63
Q

sympathetic effect on pacemaker

A

increased If and ICa, decreased IK

64
Q

parasympathetic effect on pacemaker

A

decreased If and ICa, increased IK

65
Q

how can abnormality in automaticity occur (3)

A

increased sympathetic effect on latent pacemaker takes over, increased parasympathetic on pacemaker, injured node area

66
Q

what happens if a node area is injured (3)

A

other cells develop pacemaker function, loss of RMP, osciallations

67
Q

what can cause injury to a nodal area

A

Ischaemia

68
Q

normal AP features (3)

A

stable RMP, coverts to pacemaker activity, ventricular longer phase 2 than atrial

69
Q

AP phase 0

A

fast sodium channel opens

70
Q

AP phase 1

A

fast sodium channel closes

71
Q

AP phase 2

A

L type Ca channels open

72
Q

AP phase 3 (2)

A

K channels open, Ca channels close

73
Q

AP phase 4

A

stable RMP

74
Q

triggered impulses

A

EAD and DAD

75
Q

when does EAD occur

A

early in AP repolarisation

76
Q

when is EAD more likely to occur (2)

A

long AP duration or long QT syndromes

77
Q

what causes EAD in long repolarisation

A

voltage gated Ca channels are reactivated

78
Q

EAD can lead to

A

self perpetuating tachyarrythmia

79
Q

sodium channel mutations for EAD

A

SCN5A

80
Q

SCN5A mutation effect (3)

A

channel doens’t stay inactivated, inward current occurs late, extends duration

81
Q

potassium channel mutations for EAD (2)

A

KCNQ1 or HERG

82
Q

KCNQ1 or HERG mutation effects (2)

A

decreased repolarising K efflux and plateau termination delay

83
Q

when does DAD occur

A

after repolarisation

84
Q

what conditions are prone to DAD (2)

A

reliance on Na Ca exchanger for relaxation or RMP depolarised

Physiology (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions