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Phase 3 > Week 5 > Flashcards

Week 5 Flashcards

1
Q

In what situations is ECG first line?

A

for patients with chest pain, palpitations or blackouts

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2
Q

Which are the unipolar ECG leads?

A

Limb leads - aVR, aVL, aVF

chest leads V1-V6

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3
Q

Which are the bipolar leads?

A

Leads I, II and III

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4
Q

What does lead I measure?

A

RA-LA

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5
Q

What does lead II measure?

A

RA-LL

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6
Q

What does lead III measure?

A

LA-LL

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7
Q

Why can atrial depolarisation not be seen in ECG?

A

lost in QRS complex

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8
Q

What is the P wave?

A

atrial depolarisation

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9
Q

What does the QRS complex represent?

A

ventricular depolarisation

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10
Q

What is the ST segment?

A

plateau phase of repolarisation

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11
Q

What is the T wave?

A

Final rapid repolarisation

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12
Q

What is the Q wave?

A

conduction through perkinje fibres

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13
Q

Describe the systemic approach to any ECG

A 
clinical context
date, time, patient details 
assess technical quality 
Identify P /QRS /T
measure heart rate
check ECG intervals
Determine QRS axis
Look at P/QRS /T morphology 
Do not rely on automatic interpretation
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14
Q

How can you quickly determine heart rate from an ECG?

A

300 divided by the number of large squares between each QRS complex
or number of QRS complexes across 10 seconds X 6

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15
Q

What is the normal range for a PR interval?

A

<1 large square

<200ms

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16
Q

What does a prolonged PR interval suggest?

A

heart block

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17
Q

What us the normal range for QRS?

A

<3 small squares

<120ms

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18
Q

What does a prolonged QRS complex mean?

A

bundle branch block

or life threatening hypokalaemia - dehydration, renal impairment

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19
Q

What is the normal QT interval

A

<11 small squares

<440ms

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20
Q

What does a prolonged QT internal suggest?

A

Associated with ventricular tachycardia

can go into VF. young patient with syncope

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21
Q

What is meant by the QRS axis?

A

direction of average depolarisation in the heart - dominated by left ventricular depolarisation

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22
Q

How is the QRS axis determined?

A

from limb leads
relative to lead I
normal is -30 to +90 degress
axis is approximated by dissing the lead with the most +ve QRS

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23
Q

IN a normal axis, where is the QRS positive?

A

I and II

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24
Q

Describe left axis deviation

A

-30 to -90 degrees

positive QRS in I, negative in II and aVF

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25
Q

What does left axis deviation suggest?

A

left ventricular hypertrophy

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26
Q

Describe right axis deviation

A

+90 to +180 degrees

(negative QRS in I, positive in aVF

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27
Q

What does right axis deviation suggest?

A

hypertrophy of the right ventricle - pulmonary hypertension

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28
Q

Describe extreme axis deviation

A

+180 to -90 degrees

(negative QRS in I and II, positive in aVR

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29
Q

What does extreme axis deviation suggest?

A

ventricular tachycardia

paced ryhthm, all impulses could be in ventricle if pace maker is there

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30
Q

Describe normal P/QRS/T morphology

A

P wave is upright in the inferior leads
Normal ST segment is flat
T wave has the same polarity as the QRS

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31
Q

How can P waves be described?

A

positive, negative or biphasic

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32
Q

How are QRS complexes described if the first deflection is negative?

A

Q wave

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33
Q

What is the name for a positive deflection in QRS complex?

A

R wave

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34
Q

Wha t is the name for any negative deflection after R?

A

S wave

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35
Q

How can the ST segment be described?

A

isoelectric, elated or depressed

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36
Q

How can any further positive deflection after R be described in the QRS complex?

A

R’

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37
Q

How can T waves be described?

A

upright, inverted or flat

- also concordant or discordant vs QRS

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38
Q

Describe left bundle branch block

A 
broadening of QRS complex 
characteristic 
negative QRS complex in VI
positive in V6
T waves are discordant
notching of V6
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39
Q

Describe right bundle branch block

A

inverted T waves in VI
V6- no discordant T waves
Left ventricular repolarisation

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40
Q

How do you recognise an arryhtmia?

A 
What is the QRS rate
are the QRS complexes regular?
is the QRS board or narrow?
Are there P waves
What is the P:QRS relation?
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41
Q

What types of bradyarrythmias are there?

A

sinus bradycardia
junctional bradicardia
atrioventricular block - first degree, second degree, Mobitz I/II, third degree

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42
Q

Describe sinus bradycardia

A

rate <60bpm
regular, narrow QRS
P waves present
P:QRS is 1:1

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43
Q

Describe junctional bradycardia

A

rate <60bpm
regular, narrow QRS
No P waves present

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44
Q

Describe second degree AV block - mobitz type 1

A

slowest rate <60bpm
irregular narrow QRS
P:QRS not 1:1
regularly irregular

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45
Q

Describe second degree AV block - mobitz type II

A

slowest rate <60bpm
irregular narrow QRS
P:QRS not !:!
often indication for pace maker

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46
Q

Describe complete AV block

A

rate <60bpm
regular broad QRS
no relation between P and QRS

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47
Q

What drug may be used to treat bradyrhythmias?

A

atropine

anticholinergic - decreases vagal tone

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48
Q

What appearance does a pacemaker have on ECG?

A

looks like left bundle branch block

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49
Q

Give examples of regular narrow complex tachycardias

A

sinus/junctional

SVT

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50
Q

Give examples of irregular narrow tachycardias

A

AF

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51
Q

Give examples of broad complex regular tachycardias

A

monomorphic VT

SVT with BBB

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52
Q

Give examples of broad complex irregular tachycardias

A

polymorphic VT
AF with BBB
pre-excited AF

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53
Q

Describe sinus tachycarida

A

rate >100 bpm
regular, narrow QRS
P waves present
P:QRS is I:I

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54
Q

Describe atrial fibrillation

A

rate variable - fast
irregular, narrow QRS
no P waves

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55
Q

Describe atrial flutter

A

macro-reentrant atrial tachycardia
regular narrow QRS
sawtooth atrial activity - about 300bpm
may get variable AV block

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56
Q

Describe supraventricular tachycardia

A 
rate - more than 150bpm
regular, narrow QRS
P waves present
P:QRS is 1:1
AVRT, AVNRT or atrial tachycardia
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57
Q

Describe broad complex tachycardia

A 
regular borad QRS
P waves may still be seen
ventricular tachycardia
SVT with BBB
SVT over an accessory pathway
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58
Q

How can VT and SVT be differentiated?

A

fusion beats, capture beats, AV dissociation, extreme rightward or NW axis, or QRS concordance more likely to be VT
if in doubt always treat as VT

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59
Q

What does ST elevation in the anterior leads suggest?

A

MI in left anterior descending artery

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60
Q

What does ST elevation in lateral leads suggest?

A

MI is distal, left anterior descending artery or circumflex artery

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61
Q

What does ST elevation in the inferior leads suggest?

A

MI in right coronary artery or circumflex

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62
Q

What is heart failure?

A

failure of the heart to pump blood at a rate sufficient to meet the metabolic requirements of the tissues - caused by an abnormality of any aspect of cardiac function and with adequate cardiac filling pressure

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63
Q

How is heart failure characterised?

A

by typical haemodynamic changes (systemic vasoconstriction) and neurohumoral activation

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64
Q

What does heart failure cause clinically?

A

breathlessness, effort tolerance, fluid retention, and is associated with frequent hospital admission and poor survival

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65
Q

What are common causes of heart failure in the UK?

A 
coronary artery disease 
hypertension
idiopathic
toxins 
genetic
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66
Q

What are the less common causes of heart failure in the UK?

A 
valve disease
infections
congenital heart disease
metabolic 
pericardial disease (e.g. TB)
endocardial disease
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67
Q

Describe HF-REF

A

systolic HF
younger
more often male
coronary aetiology

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68
Q

Describe HF-PEF

A

diastolic HF
older
more often female
hypertensive aetiology

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69
Q

Describe chronic (congestive) heart failure

A

present for a period of time

may have been acute or become acute

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70
Q

Describe acute (decompensated) heart failure

A

usually admitted to hospital
worsening of chronic
new onset

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71
Q

Describe the pathophysiology of heart failure

A

myocardial injury
left ventricular systolic dysfucntion
perceived reduction in circulating volume and pressure
neurohumoral activation
systemic vasoconstriction renal sodium and water retention
which leads to further left ventricular systolic dysfuction

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72
Q

What hormones are related in response to heart failure?

A

SNS
RAAS
ET, AVP etc
natriuretic peptides

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73
Q

What are the symptoms of heart failure?

A

dyspnoea and cough
ankle swelling
fatigue/ tiredness

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74
Q

What are the signs of heart failure?

A 
peripheral oedema
elevated JVP
third heart sound
displaced apex beat
pulmonary oedema
pleural effusion
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75
Q

Describe NYHA class I

A

no symptoms and no limitation in ordinary physical activty

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76
Q

Describe NYHA class II

A

mild symptoms (shortness of breath or angina) and slight limitation during normal activity

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77
Q

Describe NYHA class III?

A

marked limitation in activity due to symptoms, even less than ordinary activity - walking short distances
only comfortable at rest

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78
Q

Describe class IV NYHA

A

severe limitations

experience symptoms even while at rest. mostly bedbound

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79
Q

What investigations will all patients receive for heart failure?

A 
ECG
CXR
echocardiogram
blood chemistry
haematology
natriuertic peptides
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80
Q

What investigations will selected patients get for heart failure?

A 
coronary angiography
exercise test
adulatory ECG monitoring
myocardial biopsy
genetic testing
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81
Q

Describe the treatment of heart failure

A 
Beta blocker and ACE inhibitor (or ARB)
MRA
sacubitril/valsartan 
ICD or CRTP/CRTD, ivabradine
digoxin
consider transplant
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82
Q

What affect does angiotensin II have on the blood vessels?

A 
vasoconstriction
SMC hypertrophy 
superoxide generation
enodthelin secretion
monocyte activation
inflammatory cytokines 
reduced fibrinolysis
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83
Q

What affect does angiotensin II have on the kidneys?

A

sodium and water retention
efferent arterial vasoconstriction
globular and interstitial fibrosis

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84
Q

What affect does angiotensin II have on the heart?

A 
cellular hypertrophy
myocyte apoptosis
myocardial fibrosis
inflammatory cytokines 
coronary vasoconstriction 
positive isotropy
proarrythmia
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85
Q

What affect does angiotensin II have on the adrenal gland?

A

aldosterone secretion

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86
Q

What affect does angiotensin II have on the brain?

A

vasopressin secretion

sympathetic activation

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87
Q

What do natriuretic peptides do?

A

vasodilation
natriuresis
diuresis
inhibition of pathologic growth/fibrosis

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88
Q

What does neprilysin do?

A

breaks down natriuretic peptides

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89
Q

What can be seen in chest X-ray in stage I heart failure?

A

redistribution pulmonary vessels

cardiomegaly

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90
Q

What can be seen on chest X-ray in stage 2 heart failure?

A

kerely lines
peribronchial cuffing
hazy contours of vessels
thickened interlobar fissures

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91
Q

What can be seen on chest x-ray in stage 3 heart failure?

A

consolidation
air bronchogram
cottonwool appearance
pleural effusions

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92
Q

Describe redistribution of pulmonary vessles

A

in the normal chest x-ray vessels in lower zones are larger than equivalent vessels in upper zones
if vessels in upper zones are enlarged them elevated pulmonary venous pressure should be considered

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93
Q

What are kerley B lines?

A

spatial lines - fid leakage into interlobular septa
seen at bases perpendicular to the pleural surface
if transient or rapidly developing virtually diagnostic of pulmonary oedema

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94
Q

What are kerly A lines?

A

caused by distension of the anastomotic channels between the peripheral and central sympathetic
oblique

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95
Q

What are kerly c lines?

A

reticular opacities at the lung bases

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96
Q

What are the signs of interstitial oedema?

A

peribronchial cuffing

hazy contour of vessles

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97
Q

Describe peribronchial cuffing

A

normally walls of bronchi are invisible

when fluid collects in peribronchial interstitial space the bronchial walls become visible

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98
Q

Describe hazy contour of vessels

A

not only enlarged but lose their defined margin due to surrounding oedema
requires previous examinations

99
Q

Describe subpleural pulmonary oedema

A

fluid can accumulate in the loose connective tissue beneath the visceral pleura
seen as a sharply defined band on increased density

100
Q

Describe alveolar oedema

A

represents spill of fluid from interstitial into alveolar spaces resulting in airspace opacity
bilateral usually
butterfly distribution
rapid change - infection slower than HF

101
Q

Describe pleural effusions

A

fluid within potential space between parietal and visceral layers
divided into transudates and exudates

102
Q

When are transudates found in pleural effusions?

A

LVF, cirrhosis, nephrotic syndrom

myxoedema, PE, sarcoidois

103
Q

When are exudates found in pleural effusions?

A

PE, bacterial infection, bronchial ca

fungal/viral infection. lymphoma

104
Q

What is the appearance of pleural effusions on chest X-ray?

A

homogenous lower zone opacity with a curvilinear upper border
large effusions obscure heart border and displace mediastinum, airways and diaphragm

105
Q

Describe subpolmonic effusion

A

fluid can accumulate in a subpulmonic location
can be difficult to detect as upper edge of fluid mimics contour of diaphragm
principle sign is apparent elevation of hemidiaphragm

106
Q

What is a valve?

A

a device for controlling the passage of fluid thorough a pipe or duct, especially an automatic device allowing movement in one direction only

107
Q

What can go wrong with valve leaflets?

A 
calcification
thickening
degeneration
infection
prolapse
108
Q

What can go wrong with the valve apparatus or annulus?

A

annular dilitation
annular calcification
apparatus tethering/thickeing/ rupture
regional wall motion abnormality

109
Q

What does stenosis cause?

A

pressure overload
increased pressure in LV
hypertrophy

110
Q

What does regurgitation cause?

A

volume overload

ventricles start to dilate due to increased volume

111
Q

Describe rheumatic valve disease

A

acute rheumatic fever
mainly strep pyrogens throat infections
antibody cross reactivity affecting connective tissue
cardiac injury generated by recurrent inflammation and fibrinous repair and scarring
less prevalent in antibiotic age

112
Q

Describe the aortic valve

A

lies between LV and aorta
3 cusps
right, less, non coronary

113
Q

What can cause aortic stenosis?

A

thickening
calcification
rheumatic valve disease
congenital

114
Q

What are the symptoms of aortic stenosis?

A

shortness of breath
pre syncope
chest pain
reduced exercise capacity

115
Q

What can cause aortic regurgitation?

A 
degeneration
rheumatic valvular disease
aortic root dilatation
systemic disease
endocarditis
116
Q

Which systemic diseases can cause aortic regurgitation?

A

marfan’s syndrome
ehlers danlos syndrome
ankylosing spondyltis
SLE

117
Q

What are the symptoms of aortic regurgitation?

A

shortness of breath

reduced exercise capacity

118
Q

Describe bicuspid aortic valves

A

prone to premture dysfunction
associated with aortic abnormalities
genetic component

119
Q

Describe the mitral valve

A

lies between LA and LV
2 leaflets
anterior and posterior

120
Q

Describe mitral stenosis

A 
rheumatic valve disease
pressure overload
dilated LA
atrial fibrilation
pulomary hypertension
secondary right heart dilatation
121
Q

What are the symptoms of mitral stenosis?

A 
shortness of breath
palpitation
chest pain
haemoptysis
right heart failure symptoms
122
Q

Describe mitral regurgitation?

A 
volume overload - LA/LV
LV and LA dilatation
pulomary hypertension
secondary right heart dilatation
atrial fibrillation
123
Q

What are the symptoms of mitral valve regurgitation?

A

shortness of breath
palpitation
right heart failure symptoms

124
Q

Describe the pulmonic valve

A

3 leaflets

lies between RV and pulmonary artery

125
Q

Describe the tricuspid valve

A

3 leaflets

lies between RA and RV

126
Q

How are valve defects assessed?

A 
history 
examination
blood pressure
ECG
echo
CT
MRI
exercise tolerance tesr
CPET
stress echo
catheterisation
127
Q

What is infective endocarditis?

A

infection of the endocardium and/or intra-cardiac devices

can lead to formation of vegetation and destruction of cardiac tissue

128
Q

What are the cardiac risk factors for infective endocarditis?

A 
existing valvular heart disease
congenital heart disease
prosthetic heart valves
indwelling cardiac devices
`past history of IE
129
Q

What are the non-cardiac risk factors for infective endocarditis?

A 
immunodeficiency
diabetes
alchohol dependency
indwelling IV lines
IV drug use (mostly right sides IE)
130
Q

How do people get IE?

A 
dental manipulation 
dental disease
extra-cardiac infection
invasive procedure
cardiac surgery
IV drug use
no clear cause
131
Q

Describe staphylococci in endocarditis

A

aureas - 26.6% - IVDU

coagulase negative staph - epidermis, device/line related or early PVE

132
Q

Describe streptococci and enterococci in IE

A

oral stereo - 18.7%
non-oral - associated with colorectal cancer
enterococci - 10.5%

133
Q

What does HACEK stand or?

A

haemophilus, aggregatibacter, cardiobacterium, eikenella corrodens, kingella

134
Q

how does IE develop?

A

endothelial injury caused by valve sclerosis, rheumatic valvulitis or direct bacterial activty
development of non-infected platelet thrombus
bacterial adherence to thrombus and colonisation
further cycles of endothelial injury and thumbs deposition leads to formation of bacterial vegetation

135
Q

Describe acute IE

A

acute and aggressive onset of symptoms
often due to staph areas
progressive valve destruction and metastatic infection

136
Q

Describe subacute IE

A

insidious, non specific presentation
strep viridian’s most commonly
metastatic infection uncommon

137
Q

What are the symptoms of IE?

A 
fever
fatigue
anorexia
weight loss
night sweats
dyspnoea
138
Q

What are the symptoms of embolic phenomena in IE?

A

stroke, meningitis,
lung assess, emboli
abdominal pain
back pain - osteomyelitis

139
Q

When should IE be considered?

A

fever in presence of risk factors
sepsis of unknown origin
evidence of embolic phenomena
history,

140
Q

What are the vascular phenomena in IE?

A 
septic embolism - stroke, digital gangrene
spilnter haemorrhages
laneway lesions 
conjunctival haemorrhages 
pulmonary , renal or splenic infarcts 
petechial rash
141
Q

What are the immunological phenomena in IE?

A

glomerulonephritis
oslers nodes
roth spots

142
Q

What are some other sign’s of IE?

A

murmur
splenomegaly
neurological signs
nail clubbing

143
Q

What are osier’s nodes?

A

painful, eryhtmetous nodular lesions, necrotising vasculitis

144
Q

What are janeway lesions?

A

non painful, erythematous, blanching macule , embolic microabscesses

145
Q

What are splinter haemorrhages?

A

non-blanching, linear, reddish-brown lesions - not full length of nail

146
Q

Describe roth spots

A

retinal haemorrhages with pale centres

147
Q

What can cause nail clubbing?

A

atrial myxoma, cyanotic congenital heart disease, bronchietactis, interstitial lung disease and lung cancer

148
Q

What are the major clinical criteria in modified duke diagnosis of IE?

A

blood cultures positive for infective endocarditis

evidence of endocardial involvement - echo / valvular regurgitation

149
Q

what are the minor clinical criteria in the diagnosis of IE?

A 
predisposition
fever
vascular phenomena
immunological phenomena
microbiological eveidence
150
Q

When is IE diagnosis definite ?

A

two major criteria
one major and three minor criteria
5 minor criteria

151
Q

What antibiotics are used fro NVE?

A

amoxicillin / flucloxacilin/ gent

152
Q

What antibiotics are used for PVE?

A

vancomycin/gentamycin/rifampicin

153
Q

What are the indications for cardiac surgery in IE?

A

valve dysfunction leading to heart failure
uncontrolled infection
prevention of embolism

154
Q

What are the symptoms of MI?

A 
chest pain
back pain
jaw pain
indigestion
sweetness/claminess
shortness of breath
none (diabetes / dementia)
death
155
Q

What are the signs of MI?

A 
tachycardia
distressed patient
heart failure(crackles, raised  JVP)
shock 
arrhythmia 
none
156
Q

What is troponin?

A

part of cardiac myocyte

release in blood stream is a marker of cardiac necrosis

157
Q

What is the universal definition of MI?

A

any elevation in troponin in clinical setting consistent with MI

158
Q

What is type 1 MI?

A

spontaneous MI due to primary coronary event

159
Q

What is type 2 MI?

A

increased oxygen demand /decreased supply - heart failure, sepsis, anaemia, arryhtmias, hypertension or hypotension

160
Q

What is type 3 MI?

A

sudden cardiac death

161
Q

What is type 4a MI?

A

MI associated with PCI

162
Q

What is type 4b MI?

A

Stent thrombosis documented by angiography or PM

163
Q

What is type 5 MI?

A

MI associated with CABG

164
Q

What are cases of type 2 MIs?

A 
congestive heart failure
tachyarrythmias
PE
sepsis
apical ballooning syndrome
anything that stresses the heart
165
Q

What can cause chronic troponin elevation (not MI)

A

renal failure
chronic heart failure
infiltrative cardiomyopathies

166
Q

What is unstable angina?

A

an acute coronary event without rise in tropnin

167
Q

how can a stem in posterior wall be detected in ECG?

A

anterior ST depression

168
Q

what is the immediate management of a STEMI?

A 
ABCD
ambulance, defib
aspirin 300mg PO
UF heparin 
morphine 
anti-emetics
clopidogrel
ticagrelor (in hospital) 
activate PPCI team
169
Q

How does primary PCI compare to thrombolysis?

A 
improves survival
reduced strokes
reduces repeated MI
reduces further angina
speeds up reconvery
shortens time in hospital
170
Q

What is the subsequent management of a STEMI?

A

coronary care unit
drugs for secondary prevention
echo for LV function and cardiac structure
cardiac rehab

171
Q

What drugs are used for secondary prevention of MI?

A

ACE inhibitors
BB
statins
eplerenone (diabetes / clinical heart failure)

172
Q

When would an ICD be considered following an MI?

A

if LVSD > 9 months

173
Q

What are the complications of an MI?

A 
arrthymias
heart failure
cariogenic shock 
myocardial rupture
psychological
174
Q

What is the definition of hypertension?

A

persistant elevevation in retrial blood pressure >140/90
a BP level that increases the vascular risk in patients sufficient to require intervention
the threshold at which benefits of action exceed those of inaction

175
Q

What is optimal BP?

A

<120/ <80

176
Q

What is normal BP?

A

120-129

80-84

177
Q

What is high normal BP?

A

130-139

85-89

178
Q

What is grade 1 hypertension?

A

140-159

90-99

179
Q

What is grade 2 hypertension?

A

160-179

100-109

180
Q

What is grade 3 hypertension?

A

> 180

>110

181
Q

What is isolated systolic hypertension?

A

> 140

<90

182
Q

What are the non-modifiable risk factors for primary hypertension?

A

age
gender
ethnicity
genetic factors

183
Q

What are the modifiable risk factors for primary hypertension?

A 
diet
physical activity
obesity 
alcohol excess
stress
184
Q

What are the causes of secondary hypertension?

A 
hyperaldosteronism
thyroid disorders
phaeochromocytoma
renal artery stenosis
exogenous steroid use
NSAIDs
herbal remedies 
cocaine
185
Q

What are the two out of office BP measurement techniques?

A

24 hour ambulatory blood pressure monitoring

home blood pressure monitoring

186
Q

What initial investigations can be carried out in a patient with hypertension?

A 
U&amp;Es
electrolytes
glucose
lipid profile
TFTs
LFTs
urine dipstick 
12 lead ECG
187
Q

What additional tests can be used in the elevation of hypertension?

A 
renin and aldosterone
25 hour urine catecholamines
echo
renal ultrasound
MRA renal
188
Q

How is the cardiovascular risk assessed in hypertension?

A 
BP category
presece of end organ damage
presence of diabetes 
CV
renal disease
189
Q

How can hypertension be managed?

A

lifestyle measures
pharmacological management
renal denervation

190
Q

What medications can be used to treat hypertension?

A

diuretics
ACE inhibitor /ARBs
vasodilators- calcium channel blockers, beta blockers, alpha blockers

191
Q

IN a patient under the age of 55, what are the steps in the pharmacological management of hypertension?

A

ACE inhibits or ARB
then add calcium channel blocker
then add thiazide diuretic
consider alpha or beta blocker

192
Q

What are the stages in the pharmacological management of patients over 55 or black patients with hypertension?

A

calcium channel blocker
then add ACEI
then add thiazide diuretic
then consider beta/alpha blocker s

193
Q

How is AF diagnosed?

A

irregularly irregular rhythm
no discernible P waves
>30 seconds

194
Q

What are the other key ECG changes in AF?

A

absence of isoelectric baseline

fibrillary waves may be present

195
Q

What is atrial flutter?

A

caused by re-entry circuit within RA
length of re-entry circuit corresponds to size of RA
predictable atrial rate about 300bpm
ventricular rate determined by AV conduction ratio
i.e. if 2:1 then ventricular rate will be about 150bpm

196
Q

What is meant by a type 1 flutter?

A

typical
IVC and tricuspid isthmus in circuit
anti-clockwise or clockwise

197
Q

What is a type 2 flutter?

A

atypical
does not fit typical criteria
less amenable to ablation

198
Q

How is AF classified?

A

paroxysmal (<48 hours)
persistent (>7 days or requires CV)
long standing (>1 year)
permanent (accepted)

199
Q

Describe the pathophysiology of AF

A

progressie remodelling of atrial structure and ion channel function
provoked by numerous stressors
structural remodelling usually develops before the onset of AF

200
Q

What are the hallmarks of AF pathophysiology

A

activation of fibroblasts, enhanced connective tissue deposition, and fibrosis

201
Q

What is theory A in the electrophysiological mechanism of AF?

A

a focal source in pulmonary veins can trigger AF
heirarchic organisation of AF with rapidly activated areas driving the arrhythmia documented in paroxysmal AF, but less obvious in persistent

202
Q

What is theory B in the electrophysiological mechanism of AF

A

perpetuated by continuous conduction of several independent wavelets propagating through atrial musculature in seemingly chaotic manner

203
Q

What are the cardiac causes of AF?

A 
coronary artery disease
conduction disease
structural heart disease
cardiomyopathy
heart failure
valvular disease
hypertension
204
Q

What are the endogenous causes of AF?

A 
thyroid dysfunction
COPD
PE
sleep apnoea 
diabetes
CKD
electrolyte disturbances 
obesity 
acid base disturbances
205
Q

What are the exogenous causes of AF?

A

infection
alcohol - chronic excess/binges
smoking
caffeine

206
Q

What investigations are needed in AF?

A 
ECG
TFTs
echo
LFTs
electrolytes
CRP/blood cultures
207
Q

What are the symptoms of AF?

A

palpitations
dyspnoea
chest tightness
pre-syncope

208
Q

What are the major complications of AF?

A

thromboembolism

heart failure

209
Q

What is used to assess whether AF patients need stroke prevention?

A

ChA2DS2VASc risk scores

210
Q

What can be used as stroke prevention in AF?

A 
vitamin K antagonists
DOACs
antiplatelet agents 
transcatheter therapy 
surgical therapy
211
Q

Which treatment strategy should be used in which AF patients?

A

offer rate control as 1st line strategy, except -
new onset
secondary reversible cause
HF thought primarily due by AF

212
Q

Give an example of a class 1 antiarrythmic drug

A

flecainide

sodium channel blocker

213
Q

Give examples of class II anti arrhythmic drugs

A

beta blockers
bisprolol
carvedilol

214
Q

Give examples of class III anti arrhythmic drugs

A

k+ channel blockers

amioderone

215
Q

Give examples of class IV anti arrhythmic drugs

A

Ca2+ Channel blockers
diltiazem
verapamil

216
Q

Give examples of class V anti arrhythmic drugs

A

amiodarone

217
Q

What are the main rhythm control drugs?

A

flecainide

amioderone

218
Q

What are the main rate control drugs?

A

beta blockers
digoxin
calcium channel blockers

219
Q

What are the risks associated with flecainide?

A

hypotension
atrial flutter
QT prolongation
avoid in patents with IHD or significant structural heart disease

220
Q

What are the risks associates with amiodarone?

A 
phlebitis
hypotension
bradycardia/AV block
will slow ventricular rate
delated conversion to sinus rhythm
221
Q

For which patients in catheter ablation used in AF?

A

with paroxysmal or persistent AF who fail AAD

222
Q

What are the surgical options in AF treatment?

A

maze procedure

223
Q

Describe ablation of AV node

A

ablation results in iatrogenic 3rd degree heart block
controls ventricular rate in AF when medications fail to do so
patients pacemaker dependent for life

224
Q

Describe the RA

A

sinoatrial node

broad appendage

225
Q

Describe the LA

A

narrow, long appendage

pulmonary venous confluence

226
Q

Describe the RV

A

trabeculated endocardium

insertion of chord to IVS, moderator band

227
Q

Describe the LV

A

smooth endocardium, ellipsoid cavity

228
Q

What are the categories of cyanotic CHD?

A

no shunt and shunt

229
Q

Give examples of no shunt CHDs

A 
correction of aorta
abstain's anomaly
pulmonary stenosis
bicuspid aortic valve
subaortic membrane
ccTGA
230
Q

Give example of shunt CHDs

A 
atrial septal defect
ventricular septal defect
AVSD
patent ductus arterioles
aortopulmonary window 
partial anomalous pulmonary venous drainage
231
Q

Give examples of cyanotic CHDs

A 
Eisenmenger syndtome
tetralogy of fallot
transposition of the great arteries
tricuspid atresia
pulomary atresia
combined lesions - ASD with severe pulmonary stenosis
232
Q

What is ccTGA?

A

congenitally correction transposition of the great arteries

usually not in isolation

233
Q

What are the special considerations in arrhythmia in CHD?

A 
common
scar related
haemodynamic 
lesion related
emergency if fontan
234
Q

What are the special considerations in pregnancy in CHD?

A 
higer risk
volume shift 
arrhythmia
dissection risk
outflow obstruction - CO can't be increased
235
Q

Describe secundum ASD

A

shunts left to right in isolation
right heart volume loading
pulmonary flow murmur
fixed, split second heart sound

236
Q

What can secundum ASD lead to?

A 
RV failure
tricuspid regurgitation
atrial arrhythmias
pulmonary hypetension
Eisenmenger syndrome
237
Q

Describe transposition of the great arteries

A

oxygenated blood from pulmonary veins is re-ciculated to lungs
deoxygenated blood from the body is recirculated to the body
duct dependent circulation

238
Q

Describe foetal circulation

A

in-utero oxygenation is by the maternal placenta
pulmonary circulation is minimal and at high resistaance
oxygenated blood returns to RA bia IVS
it bypasses the RV/PA bia the foramen ovale
of the blood that is pumped to the PA, most passes to the aorta via the ductus arteriosus

239
Q

What are the consequences on surgery to treat transposition of the great arteries?

A

atrial switch

systemic RV- dilatation, tricuspid regurgitation, heart failure, atrial arrhythmias

240
Q

Describe tetralogy of fallot

A

ventricular septeal defect
overriding arota
RVOT obstruction
right ventricular hypertrophy

241
Q

How is tetralogy of ballot repaired?

A

pulmonary artery and right ventricle enlarged using a patch
muscular obstruction removed
VSD closed with patch

242
Q

What is the repaired history of tetralogy of fallot?

A

significant pulmonary regurgitation
intrinsic iatrogenic arryhmia risk
residual VSD
pulmonary arterial/branch PA stenoses

243
Q

Describe fontal/TCPC

A

single ventricle supports systemic circulation
systemic venous return is directed to pulmonary arteries, bypassing the ventricular mass
pulmonary circulation relies on maintained systemic venous pressure and low pulmonary vascular resistance
dehydration, arrhythmia, bleeding and pulmonary embolus all potentially catastrophic

244
Q

Describe coarction of the aorta

A

age at presentation depends on position and severity
pre-ductal may cause lower limb cyanosis
upper body hypertension, berry aneurisms, claudication and renal insufficiency may ensure

Phase 3 (15 decks)

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