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MRCS A > CARDIOLOGY - ACS and Angina > Flashcards

CARDIOLOGY - ACS and Angina Flashcards

1
Q

Broad catergories - chest pain (5)

A

Cardiac
Pulmonary
GORD
MSK
Other

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2
Q

Myocardial ischaemia - SOCRATES

A

S - Retrosternal, central chest pain
O - builds over mins
C - crushing, gripping
R - Neck, shoulder, jaw (C5)
A - paraesthesia arms, sweating, nausea, breathlessness, collapse
T - mins –> hrs
E - Exertion, cold, stress, heavy meal.
S - severe

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3
Q

RF Myocardial ischaemia (10)

A

Hyperlipidaemia
DM
Smoking
FHx
HTN
Obesity
Race
Male
Age
Renal disease

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4
Q

Ix Myocardial ischaemia (5)

A

ECG
Trops
CK
CXR
Ddimers

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5
Q

Type A Aortic Dissection

A

Involves aortic arch and valve proximal to LSCA

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6
Q

Sx from type A Aortic dissection

A

Limb ischaemia
Cerebral ischaemia
Aortic regurg
Cardiac tamponade

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7
Q

Type B Aortic dissection

A

Involves descending thoracic aorta distal to LSCA

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8
Q

Sx from type B Aortic dissection

A

Paraplegia
Ischaemic bowel
Renal aa failure
Lower limb ischaemia

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9
Q

Who gets aortic dissection classically

A

Middle aged HTN males

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10
Q

Other RF Aortic dissection (5)

A

Bicuspid aortic valve disease
Atherosclerosis
Marfan’s
Ehlers Danlos
During pregnancy

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11
Q

Which gene defect is related to aortic dissection?

A

Fibulin-5 –> fibrillin

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12
Q

SOCRATES Aortic dissection

A

S - Central CHx/back/betw shoulder blades
O - V sudden
C - tearing, ripping, searing pain
R - back, shoulders, neck, abdo
A - collapse, sweating, HoTN , ischaemic pain, neuro. Peripheral pulses +/-
T - constant
E - none
S - severe

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13
Q

Ix Aortic dissection

A

CXR/AXR
CT - definitive diagnosis

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14
Q

What is pericarditis

A

Inflammation of the pericardium

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15
Q

Causes pericarditis

A

Idiopathic
Viruses - fl,EBV,mumps, HIV
Bacteria - pneumonia, FR, fever, TB, staph, strep,
Fungi
MI, Dresslers
Dx
RA/SLE, surgery, malig, radioT, sarcoidosis

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16
Q

SOCRATES - Pericarditis

A

S - retrosternal
O - gradual
C - sharp/sore
R - tip L shoulder, back, neck
A - fever, viral Sx, breathless
T - constant + can last days
E/R - worse on insp/lying flat, Relieved by sitting forward + analgesia
S - varies

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17
Q

ECG changes pericarditis

A

Saddle shaped ST elevation

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18
Q

What is pain in shoulder tip suggestive of?

A

Diaphragmatic pleural irritation

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19
Q

SOCRATES PE

A

S - localised to chest wall
O - sudden
C - sharp, pleuritic
R - shoulders/back
A - Dyspnoea, haemoptysis, dizzy, syncope, cough, fever
T - constant
E/R - worse on insp, coughing, moving. R - shallow breaths analgesia
S -varies

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20
Q

GORD and GTN spray

A

Relieves after 20 mins

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21
Q

Definition of ACS

A

Acute central chest pain, lasting > 20 minutes, not relieved by 3x GTN sprays at 5 min intervals

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22
Q

Who gets ACS without chest pain aka silent infarction

A

Elderly
Diabetics

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23
Q

Sympathetic activation Sx ACS

A

Tachycardia
HTN
Pallor
sweatiness

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24
Q

Vagal stimulation Sx ACS

A

Bradycardia
Vomiting

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25
Q

STEMI vs NSTEMI

A

STEMI - ST elevation on ECG + LBBB
= Complete occlusion of coronary aa
+ full thickness MI
NSTEM = elevated troponin but no ST elevation or LBBB
- subtotal occlusion occurs

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26
Q

Def unstable angina

A

Occuring at rest or sudden incr f/severity of existing angina

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27
Q

Blood results UA

A

Plasma Trops and CK = norm

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28
Q

ECG UA

A

Normal
Or ST depression +/- T wave inversion

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29
Q

MI time course - 0-12hrs

A

Infarct not visible
Loss of oxidative enzymes

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30
Q

MI time course - 12-24hrs

A

Infarct pale/blotchy, w/ intracellular oedema

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31
Q

MI time course - 24-72hrs

A

Infarcted area excites acute inflamm response, w/ dead area soft + yellow w/ neutrophilic involvement

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32
Q

MI time course - 3-10days

A

Organisation of infarcted area by vascular granulation tissue

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33
Q

MI time course - 10days to several m

A

Collagen deposition
Infarct replaced by scar

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34
Q

Normal troponin levels

A

<10

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35
Q

How long can troponin stay elevated for?

A

Up to 2 w

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36
Q

What areas of the heart does the R coronary aa supply?

A

RA
RV
Posterior septum
SAN (60%)
AVN (80%)

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37
Q

What type of MI does a RCA give?

A

Post/inferior MI

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38
Q

Which leads does a posterior/inf MI show up in

A

II, III aVF

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39
Q

What 2 aa does the L coronary aa split into?

A

LAD
Circumflex

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40
Q

What areas of the heart does the circumflex artery supply?

A

LA
LV

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41
Q

What type of MI does circumflex aa give?

A

Lateral MI

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42
Q

What ECG leads does a lateral MI show up in

A

I
aVL
V5-6

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43
Q

What areas of the heart dose the LAD aa supply?

A

LV
Anterior septum

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44
Q

What type of MI does LAD aa give?

A

Antero-sepatal MI

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45
Q

What ECG leads does an antero-septal MI show up in?

A

V1-4

46
Q

MI ECG changes at: 5 mins

A

Tall, pointed T-waves

47
Q

MI ECG changes at: 30 mins

A

ST elevation

48
Q

MI ECG changes at: 2+hrs

A

T wave inversion + Q waves develop

49
Q

MI ECG changes at: days after

A

ST segment returns to normal

50
Q

MI ECG changes at: weeks after

A

Q wave remains

51
Q

Which investigation is contraindicated in unstable angina?

A

Stress tests

52
Q

When does troponin levels peak after an MI?

A

24hrs

53
Q

What marker is useful for rapid diagnosis of MI?

A

Myoglobin

54
Q

Why take FBC + U+E for MI Ix

A

Glucose is lowered
Lipids are raised

55
Q

CXR features MI (2)

A

Cardiomegaly
Pulmonary oedema
Widened mediastinum

56
Q

Which test definitively defines presence, extent and severity of CAD?

A

Coronary angiography

57
Q

What is the earliest sign of acute MI on ECG?

A

Hyperacute T waves

58
Q

What leads are hyperacute T waves most evident in?

A

Anterior chest leads

59
Q

What ECG change is often the earliest recognised sign of an acute MI

A

ST elevation

60
Q

What ECG change is DIAGNOSTIC of a STEMI

A

1mm of ST elevation in 2 contingous leads

61
Q

What ECG change is the only firm evidence of myocardial necrosis?

A

Q waves

62
Q

How long may T wave inversion take to resolve?

A

2 weeks

63
Q

Which type of MIs does T wave inversion tend to persist in?

A

Anterior MI

64
Q

Mx STEMI (MOANA)

A

morphine IV 10mg
O2
Antiplaetlets - aspirin (300mg) or clopidogrel (600mg)
Nitrates/GTN
Anti-emetics (10mg metocloperamide)

65
Q

When do you not use GTN spray in STEMI Mx

A

if pt = hypotensive

66
Q

What meds to give post PCI

A

Clopidogrel + abciximab (reduce complication rates)

67
Q

C/I Thrombolysis (6)

A

Haemorrhagic stroke at any time
Ischaemic stroke in last 6 months
CNS damage/neoplasm
Recent trauma (3 weeks)
GI bleed within last month
Bleeding disorder/aortic dissection

68
Q

What is the GRACE score

A

Determines mortality risk in ACS

69
Q

Highest GRACE score risk features in NSTEMI/UA

A

> 6m raised trops
Persistent pain
ST depression
Diabetes

70
Q

Factors taken into account GRACE score

A

Age
HR < BP
class of CHF
Renal fct
ST segment changes
Troponin
Whether there was an arrest at admission

71
Q

Lterm Mx ACS

A

48hr bed rest w/ ECG
U+E’s + cardiac enzymes 3 days
Thromboprophylaxis
Aspirin 75mg OD for life
Clopidogrel 75mg OD 1 yr
Bisoprolol (life)
Start ACEi + statin after 24-48hr
Address RF

72
Q

Immediate complications MI

A

Arrhythmias

73
Q

S term complications MI (6)

A

Pulmonary oedema
Cardiogenic shock
Thromboembolism
Venticulo-septal defect
Ruptured chordae tendinae
Rupture of ventricular wall

74
Q

When does rupture of ventricular wall happen after MI?

A

2-10 days after

75
Q

Why does rupture of ventricular wall post MI happen?

A

B/C reorganisation + softening of wall
–> haemopericardium, cardiac tamponade + rapid death

76
Q

L term complications MI (3)

A

Heart failure
Dressler’s syndrome
Ventricular aneurysm formation

77
Q

What is Dressler’s syndrome

A

Immune mediated pericarditis post MI

78
Q

Sx Dressler’s syndrome

A

Sharp chest pain
Exaccerbated by movement + lying down
Relieved by sitting forward

79
Q

Tx Dresslers’ syndome

A

High dose aspirin / NSAIDs

80
Q

Define angina

A

Chest pain precipitated by exercise and relieved by rest.
Usually fades within mins
Caused by heart not getting enough O2

81
Q

Causes angina (11)

A

Coronary aa disease
Aortic stenosis
LVH
Anaemia/carboxyhaemoglobinaemia
Atheroma
Embolus
Thrombosis
Spasm
Inflammation coronary aa
Generalised HoTN
Tachyarrhythmia
Hyperthyroidism

82
Q

What is atherosclerosis

A

Non-specific thickening of walls of aa –> loss of contractility + elasticity decreased blood flow

83
Q

What is an atheroma

A

Specific degenerative disease affecting large/med size aa

84
Q

Pathology of Angina

A

LDLs into intima
LDLs taken up by macrophages –> fatty streak
Macrophages stimulate cytokines –> collagen deposition –> plaque becomes fibrotic
–> pressure atrophy
Endothelium is fragile, ulcerates

85
Q

RF Angina (9)

A

Age
Male
FH
Smoking
Diet
Obesity
HTN
Hyperlipidaemia
DM

86
Q

What is decubitus angina

A

Angina precipitated by lying down as there is increased venous return to heart

87
Q

Prinzmetal’s angina

A

Occurs without provocation at rest as result of coronary aa spasm

88
Q

Ix that show Prinzmetal’s angina

A

ST elevation
But no trops rise

89
Q

PS Angina (socrates)

A

S- retrosternal
O - builds over mins
C- dull ache constriction, heavy
R - l arm, shoulders, neck, jaw
A - usually none
T - mins
E - exertion, stress, cold, food
(R - rest, nitrates)
S - mild

90
Q

Ix Angina

A

Clinical assessment
FBC,gluc, lipids, TFTs
Resting 12 lead ECG lead
Stress-12 lead ECG (if resting is normal)
Nuclear medical testing
CT angiography
Coronary angiography
scintigraphy
Stress echo
Stress perfusion MRI
FFR
FFI

91
Q

NICE tool - likelihoodness of CAD

A

 >90%: treat as stable angina
 61-90%: coronary angiography = indicated
 31-60%: functional imaging = indicated – SPECT myocardial perfusion scan, exercise echo, stress MRI
 10-30%: CT Ca scoring = used
 <10%: investigate for another cause

92
Q

FFR value that is significant in Angina

A

<0.75

93
Q

FFI value that is significant in Angina

A

<0.89

94
Q

Mx angina

A

Mx risk factors
1st line = GTN + B blocker or CCB

95
Q

Mx - angina (refractory disease)

A

Combination therapy
Or
Nicorandil

96
Q

2’ prevention angina

A

Statin
Low dose aspirin

97
Q

SE aspirin

A

GI ulcer
Bleeding

98
Q

effect nitrates

A

Decrease pre-load and afterload - decr O2 req of myocardium
–> VD
–> Incr O2 delivery

99
Q

SE nitrates (2)

A

Headache
HoTN

100
Q

effect B blockers

A

Negative inotroic and chronotropic effects
Slow HR
Reduces contractility
Reduce aa pressure

101
Q

SE b blockers (5)

A

GI problems
Fatigue
Poor perfusion
Bronchoconstriction
Hypoglycaemia

102
Q

Effect CCB

A

Inhibit excitability of cardiac mm
Prevents SM contraction, reduce afterload and –> coronary VD

103
Q

What do rate limiting blockers (CCBs) do

A

Inhibit conduction through AVN and cause bradycardia

104
Q

What does dihydropyrmidine blockers do

A

Reduce contractility but may –> reflex tachy C

105
Q

Which Dx is 1st line in prinzmetal angina

A

CCB

106
Q

SE CCB

A

Dizziness
Flushing
Headache
Peripheral oedema

107
Q

effect nicorandil

A

Combined NO donor + activator ATP sensitive K channels on vascular SM –> hypoerpolarisation + marked VD

108
Q

What is PCTA

A

Dilate coronary atheromatous obstructions
Inflate catheter-mounted balloon w/ obstruction using fluoroscopy

109
Q

Risks PCTA (2)

A

Local dissection
Acute coronary occlusion

110
Q

When is CABG indicated

A

For sx control in patients unsuitable for PCI

111
Q

How long after ACS should you avoid air travel

A

2 months

112
Q

How long after ACS should you avoid intercourse

A

1 month

MRCS A (36 decks)

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