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CP3 Medicine > Cardiology p1 > Flashcards

Cardiology p1 Flashcards

1
Q

SOCRATES for MI

A 
S: Central / behind sternum
O: sudden
C: crushing, stabbing
R: neck, shoulder, jaw 
A: sweatiness, SOB, nausea
T: over mins 
E: increases with exercise, decreases with rest 
S: mild-severe
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2
Q

SOCRATES for Aortic dissection

A 
S: central 
O: sudden
C: ripping 
R: back 
A: absent or delayed pulses, unequal upper limb BP, distal ischaemia, shock and neurological signs 
T: seconds
E: 
S: mild-severe
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3
Q

SOCRATES for pleural disease

A 
S: localised to area of chest
O: weeks 
C: sharp
R: ?to shoulder 
A: coughing, pain in shoulder 
T: 
E: worse with breathing and coughing 
S: mild-severe
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4
Q

SOCRATES for oesophageal disease

A 
S: retrosternal 
O: after meals
C: burning 
R: ? 
T: after meals
E: worse lying down / food or bending over 
Better with antacids 
S: mild-severe
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5
Q

SOCRATES for MSK disease

A 
S: Local 
O: following trauma / causative event 
C: sharp / sore
R: ? 
A: ? 
T: ? 
E: with certain movements 
S: mild-severe
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6
Q

What conditions are included in ACS?

A

STEMI
NSTEMI
UA

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7
Q

Describe the pathology of ACS

A
  1. atheromatous plaque formation in coronary arteries
  2. Fissuring/ulceration leads to platelet aggregation
  3. Localised thrombosis, vasoconstriction and distal thromboembolism
  4. Leads to ischaemia of myocardium
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8
Q

What is diagnosis of ACS based on?

A

Cardiac markers - troponin

ECG - ST elevation

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9
Q

Describe the history of a patient presenting with ACS?

A

Central crushing pain, usually >20 mins
not relieved by GTN

Radiates to left arm, neck and jaw

Associated with: SOB, nausea, fatigue, sweaty, palps

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10
Q

What would be the examination findings of a patient presenting with ACS?

A

pulse, BP, O2 sats often normal

pale and clammy
tachycardia

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11
Q

What investigations would you do for a patient with ACS?

what might you find?

A

ECG
Cardiac enzymes: trops (increased in first 4-8 hours, and max at 24 Hours)

FBC, U+E, LFT
glucose (decreases)
lipids (increased)

CXR
Transthoracic echo - helps in ddx of pericarditis, dissection or PE

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12
Q

What is unstable angina?

A

Angina that occurs at rest
increased frequency
increased severity

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13
Q

What is the cause of UA?

A

Fissuring of plaques - total vessel occlusion - progress to AMI

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14
Q

How is MI diagnosed?

A

Increased trops
ECG- ST elevation = STEMI

No ST elevation = NSTEMI

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15
Q

What are the three patterns of MI?

A 
Regional MI (()%)
Regional subendocardial infarction 
Circumferential subendocardial infarction (10%)
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16
Q

What artery causes anterior MI?

A

Left anterior descending

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17
Q

What are the ECG changes on an anterior MI?

A

V1-V4

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18
Q

What artery causes inferior MI?

A

Right coronary

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19
Q

What are the ECG changes on an inferior MI?

A

II, III, aVF

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20
Q

What artery causes lateral changes?

A

left circumflex

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21
Q

What are the ECG changes on lateral MI?

A

lead 1, aVL V5, V6

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22
Q

What are the differences between STEMI and NSTEMI?

A

STEMI = full thickness whereas NSTEMI = partial thickness

no q waves, but can get ST depression and T-wave inversion

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23
Q

What changes occur in 0-12 hours of MI?

A

Infarct not visible

Decreased oxidative enzymes

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24
Q

What changes occur in 12-24 hours of MI?

A

Infarct = pale and blotchy

Intercellular oedema

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25
Q

What changes occur in 24-72 hours of MI?

A

Infarcted area excites acute inflammatory response

dead area soft/yellow with neutrophil infiltration

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26
Q

What changes occur in 3-10 days of MI?

A

vascular granulation tissue in infarcted area

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27
Q

What changes occur in 10+ days of MI?

A

Collagen deposits become scar tissue

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28
Q

What is the management of ACS?

A

A-E + ECG and trops

MOANA: 
M - morphine (5mg titrated up) 
O - oxygen If sats <94%
A: anti-emetic - 10mg metoclopramide 
N: nitrates - GTN spray or IV nitrates 
A: Aspirin 300mg chewable
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29
Q

What is the management of STEMI?

A

CHECK local guidelines

PCI: gold standard treatment if available in timely fashion - i.e. under 2 hours -
praugrel + aspirin if not taking oral anticoagulant
Clopidogrel + aspirin if they are taking an oral anticoagulant

If you can’t get PCI in 2 hours, THROMBOLYSIS:
ticagrelor. If ECG after 90 minutes shows this hasn’t worked –> PCI

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30
Q

What is the management of NSTEMI?

A 
BROMANCE: 
Beta blocker
Reassurance
O2
Morphine 5mg
Aspirin 300mg
Nitrates
Clopidogrel 300mg
Enoxaparin - NOTE NOW FONDAPARINOUX

Assess using grace score.

Only give oxygen if sats below 95%

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31
Q

What is the GRACE score?

A

This scoring system gives a 6-month risk of death or repeat MI after having an NSTEMI:

<5% Low Risk
5-10% Medium Risk
>10% High Risk
If they are medium or high risk they are considered for early PCI (within 4 days of admission) to treat underlying coronary artery disease.

> 3% = PCI within 72 hours
<3%: Ticagrelor

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32
Q

What is the management if the grace score indicates high risk?

A

(>5-10% in 6 months, increased troponin or ST depression, diabetes)

Semi-elective PCI as inpatient

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33
Q

What is the management if the grace score = low risk?

A

Discharge with long term meds

Outpatient stress test/angiography or elective PCI

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34
Q

What is the long term management of ACS?

A 
48 hours bed rest 
daily U+Es and cardiac enzymes
thromboprophylaxis (fondaparinoux) 
Aspirin 75mg for life 
Clopidogrel 75mg for 1 year 
Bisoprolol 
statin + ACEi

Oral nitrates
D/c on COBRAA

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35
Q

COBRAA?

A 
5-7 days post discharge: 
Clopidogrel (75mg) - N.B. now ticagrelor 
Omega 3
Bisoprolol 
Ramipril (2.5mg) 
Atorvastatin (80mg) 
Aspirin 75mg
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36
Q

What lifestyle advice immediately after MI?

A

Smoking cessation
No sex for 1 month
No air travel for 2 months
diet + exercise

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37
Q

What are the immediate complications of Acute MI?

A

Cardiac arrest - VF (most common cause of death)
VF
Bradyarrhythmia

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38
Q

What are the short term complications of MI?

A

Pulmonary oedema
Cardiogenic shock
Thromboembolism
VSD –> pan systolic murmur
Ruptured chordae tendinea –> Mitral regurg
Ruptured ventricle wall –> cardiac tamponade

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39
Q

How does pulmonary oedema occur following MI?

A

LH fails to pump

Dilation of LV causes back pressure on pulmonary veins causing Extravasation of low protein fluid into the alveoli

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40
Q

How does cardiogenic shock occur following MI?

A

Decreased BP and decreased coronary flow = pump failure

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41
Q

What are the long term complications of MI?

A

Heart failure
Dressler’s syndrome (immune mediated pericarditis)
Pericarditis
Ventricular aneurysm - Thrombus may form within the aneurysm increasing the risk of stroke

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42
Q

What is Dressler’s syndrome?

A

Immune-mediated pericarditis

Sharp chest pian, increased lying down

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43
Q

What is the management of Dressler’s?

A

high dose aspirin and NSAIDs - n.b. now aspirin and colchicine

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44
Q

What is angina caused by?

A

Narrowing of the coronary arteries reduces blood flow to the myocardium. During times of exercise, there is inefficient blood to meet the demands causing pain.

Therefore, exertional chest pain

45
Q

What causes decreased perfusion in angina?

A 
Atheroma
Embolus 
Thrombosis 
Inflammation of coronary arteries
Decreased BP
46
Q

How does tissue demand increase in Angina?

A

Cardiac hypertrophy

Increased CO

47
Q

What is the cause of stable angina?

A

Decreased flow in atherosclerotic coronary arteries

48
Q

Describe the Pathology of stable angina?

A

Arteriosclerosis: thickening and hardening of walls, decreased contractility and elasticity and decreased blood flow

Atheroma: thickening and hardening of walls so decreased tissue perfusion

49
Q

How does atheroma formation occur?

A

Damage to endothelium
Entry of LDLs in the intima, macrophages form a fatty streak

Cytokines stimulated by macrophages: collagen deposition –> plaque

50
Q

What are the risk factors for stable angina?

A 
Increasing age
Males
FH
Smoking
Diet high in fat / low in fruit 
obesity
increased BP
lipidaema 
DM
51
Q

How is diagnosis of angina done?

A

Clinical: mild ache - severe pain
Sweating/fear
increased with exercise, meals, cold, emotion
fades after rest

CT Coronary Angiography - Gold Standard diagnostic investigation. This involves injecting contrast and taking CT images timed with the heart beat to give a detailed view of the coronary arteries, highlighting any narrowing

52
Q

What ix would you do for ?angina?

A 
Physical Examination (heart sounds, signs of heart failure, BMI)
ECG
FBC (check for anaemia)
U&Es (prior to ACEi and other meds)
LFTs (prior to statins)
Lipid profile
Thyroid function tests (check for hypo / hyper thyroid)
HbA1C and fasting glucose (for diabetes)
53
Q

What is the NICE tool for CAD?

A 
clinical assessment of CAD:
>90% - stable angina treatment
61-70%: coronary angiography indicated
31-60: SPECT myocardial scan, exercise echo, stress MRI
10-30: CT calcium scoring 
<10: investigate other cause
54
Q

What are the indications for Stress ECG?

A

If resting ECG normal
ST depression >1mm shows ischaemia
+ve within 6 mins - angiography indicated

55
Q

What is the first management of Angina?

A

Immediate: GTN N.B. nitrates are contraindicated in aortic stenosis

Long term: Beta-blocker / Calcium channel blocker (verapamil or diltiazem if mono therapy)
If disease not treated with one, add the other

(refractory disease - nicorandil)

Secondary prevention: Aspirin (75mg), atorvastatin, ACEi and they are already on beta blocker

56
Q

What is given for secondary prevention of Angina?

A

Statin
Low dose aspirin
ACEi

57
Q

How should the patient be counselled when starting a nitrate

A

sublingual GTN
Advise to sit down after spray
wait 5 mins and spray again
999 if still in pain after 10 mins - may be having an MI

Can use prophylactically

Nitrate free period if standard release isosorbide mononitrate

58
Q

How do nitrates act?

A 
Cause venorelaxation (decrease pre-load)
beware of venous pooling therefore dizziness on standing

Decreased aortic pressure
overall decreased O2 requirement of myocardium
coronary vasodilation - increased O2 delivery

59
Q

How do b-blockers work?

A

work on b1 receptors to decrease HR and SV

60
Q

What are the S/E of b-blockers

A

bronchoconstriction - don’t use in asthma, COPD
cardiac depression / bradycardia
hypoglycaemia
fatigue

61
Q

Give some examples of CCB

A

dihydropyridines: amlodipine or nifedipine

rate limiting agents: verapamil/diltiazem

62
Q

How do CCB work?

A

prevent SM contractions: decreased after load and CA vasodilation

Acton AVN to decrease HR

63
Q

What are the S/E of CCB?

A

flushing
headache
ankle swelling

64
Q

What are the procedural / surgical treatments for angina?

A

Percutaneous Coronary Intervention (PCI) with coronary angioplasty (dilating the blood vessel with a balloon and/or inserting a stent: catheter into brachial or femoral artery, feeding that up to the coronary arteries under xray guidance + contrast This can then be treated with balloon dilatation followed by insertion of a stent

PCTA

Co-prescribe aspirin and clopidogrel

CABG

65
Q

What are the risks of angioplasty?

A

local dissection or CA or CA occlusion
1% mortality, 2% AMI

increased symptoms but no prognostic benefit

66
Q

What are the indications for CABG?

A

Severe stenosis: symptom control for patients unsuitable for PCI

improved survival after MI

67
Q

What are the employment and driving limitations following ACS?

A

2 months return to work
(not pilots/drivers, and heavy labour should seek lighter work)

Travel - avoid air travel for 2 months
sex - 1 month off

Driving: PCI - 1 week, and if not, 4 weeks

Angina - stop

68
Q

What are the driving limitations for AAA?

A

notify DVLA if >6cm

Disqualified if >6.5cm

69
Q

What does the left circumflex artery supple?

A

Left atrium and left ventricle

70
Q

What does the right coronary artery supply?

A

Right atrium and right ventricle

71
Q

What does the left anterior descending artery supply?

A

left ventricle and inter ventricular septum

72
Q

what does the left marginal artery supply?

A

left ventricle

73
Q

What does the tricuspid valve separate

A

RA and RV

74
Q

What does the mitral valve separate?

A

LA and LV

75
Q

What does the left heart go to?

A

AORTA - BODY

76
Q

What does the right heart go to?

A

pulmonary artery - lungs

77
Q

What are the major branches of the aortic arch?

A

BCC: right CC and subclavian
Left common carotid
left subclavian

78
Q

What is the management of blunt cardiac trauma?

A

CXR in resus
CT often needed
ECG
conservative

79
Q

What is the management of Penetrating cardiac trauma?

A

complex ix and management
surgery
CXR

80
Q

What is the presentation of cardiac tamponade?

A

Becks triad: hypotension
JVP increased
muffled heart sounds

CXR- rounded heart border
ECG: alternans QRS
Confirm with USS
Mx - pericardiocentesis and sternotomy and repair

81
Q

What is myxoma? what are the signs?

A 
Cardiac tumour
Signs - similar to infective endocarditis
MS
confirm on echo 
mx = excision
82
Q

What are the causes of constrictive pericarditis?

What are the signs?

Tx?

A

TB, RA, trauma

dyspnoea
right heart failure: elevated JVP, ascites, oedema, hepatomegaly
JVP shows prominent x and y descent
pericardial knock - loud S3
Kussmaul's sign is positive

Excision of pericardium

83
Q

What are the differences between cardiac tamponade and constrictive pericarditis?

A

JVP: Absent Y descent. X and Y present in constrictive pericarditis

pulsus paradox - present in cardiac tamponade, absent in constrictive pericarditis

Kussmaul sign: rare in cardiac tamponade but present in constrictive pericarditis

84
Q

What is the pathophysiology of pulmonary oedema?

A

Increase in fluid in the alveolar wall
most common = LVF
increased pressure in alveolar capillaries and leakage of fluid

85
Q

What is the presentation of pulmonary oedema?

A

dyspnoea
paroxysmal nocturnal SOB
orthopnoea
cough - frothy, blood stained sputum

ACUTE PRES: SOB, cough, anxiety, cheyne stokes breathing

86
Q

What are the examination features of pulmonary oedema?

A 
increased RR
increased HR and gallop rhythm
increased venous pressure 
peripheral shut down
widespread crackles / wheeze
87
Q

What investigations would you do for pulmonary oedema? What might you find?

A

ABG: T1RF or T2 due to impaired gas exchange

Bloods - FBC, U+E. glucose, D-dimer and CRP to rule out.
BNP

CXR: diffuse haziness/batwing oedema / Kerley B lines

ECG: tachycardia, arrhythmias
Echo

88
Q

What are the causes of pulmonary oedema?

A
  1. Increased capillary pressure: LVF, valve disease, arrhythmia, VSD, pulmonary venous obstruction, MI
    fluid overload
  2. Increased capillary permeability: ARDS, infection, DIC, toxins
  3. Decreased plasma oncotic pressure: Renal/liver failure - hypoalbuminaemia
  4. Lymph obstruction - tumour
  5. Other: neuro/head injury / raised ICP
    PE, altitude
89
Q

What is the management of pulmonary oedema?

A

A-E

POUR SOD: Pour away fluids PLUS:
Sit upright
Oxygen
Diuretics - IV furosemide

If severe 
IV diamorphine 
IV furosemide
GTN spray 2 puffs 
NIV

SBP >100: IV infusion of nitrate and CPAP if no improvement

DBP <100: treat as cardiogenic shock
alert ICU

90
Q

What are the complications of ARDS?

A

Prolonged oedema –> pulmonary HTN which leads to irreversible structural changes to pulmonary arteries

Increased pressure to RV leads to RV hypertrophy leading to RHF and Cor Pulmonale

91
Q

What is ARDS caused by?

A

Lungs responding to direct inhalation or blood-bourne insults.

Direct:
aspiration of gastric contents, smoke/toxins
pneumonia
near drowning

Indirect: 
sepsis
trauma
pancreatitis
transfusion reaction
anaphylaxis
92
Q

What is the pathophysiology of ARDS?

A

damage to type 2 pneumocystis - surfactant depletion and alveolar collapse

non-cardiogenic pulmonary oedema

93
Q

What are the features of ARDS?

A

Decreased O2
absence of increased arterial pressure
CXR: bilateral ground glass appearace
decreased lung compliance

94
Q

What is the management of ARDS?

A 
Admit to ICU
100% O2
CPAP
IV nitrates
IV furosemide
Morphine and metoclopramide
Aminophylline if bronchospasm
95
Q

What is open heart surgery?

How is this different from closed heart surgery?

A

Any surgery requiring cardio-pulmonary bypass, whereas closed heart surgery does not require a bypass

96
Q

What is the function of a cardiopulmonary bypass?

A

Takes over the function of the heart and lungs, allowing a motionless blood-free field for operation

97
Q

What happens during a cardiopulmonary bypass?

A

Ascending aorta is clamped and cannulated and a venous Line inserted into the right atrium to drain venous blood

System involves a heat exchanger to regulate temperature, an oxygenator, an arterial pump and a filter

98
Q

How is potential for ischaemic damage minimised in cardiopulmonary bypass?

A

(no coronary blood supply)

potential for ischaemic damage is minimised by arresting the heart in a high potassium solution and also cooling the myocardium to between 4 and 12 degrees

99
Q

What are the main complications of a cardiopulmonary bypass?

A

Due to activation of the clotting cascade, within the bypass machine, with consumes clotting factors and platelets

This is prevented with high dose systemic heparin biro cannulation, reversed after this operation with protamine sulphate

Blood products may also be needed to reverse this

100
Q

What is a median sternotomy?

A

Most common approach for operations on The heart and aortic arch - with any chamber or surface of the heart operable

101
Q

When might an anterolateral thoracotomy be used?

A

Access to the right side of the heart

102
Q

When might a Posterolateral thoracotomy be used?

A

Access to the distal aortic arch and descending thoracic aorta

103
Q

When might a bilateral transverse thoracotomy be used?

A

Double lung transplants or heart-lung transplants

104
Q

Which is better - CABG or PCI?

A

CABG provides better symptomatic relief and requires fewer late re-interventions than PCI

105
Q

How is CABG performed?

A

Median sternotomy incision with CPB
Left internal mammary artery os the most common artery used as a conduit - harvested from the chest wall

Enlarges in response to demand, resistant to atheroma formation

106
Q

Which vein was previously used for CABG?

A

Saphenous vein harvest - good secondary targets, however results are less good than IMA

107
Q

What are the complications of CABG?

A 
MI
bleeding
stroke
arrhythmias
tamponade
aortic dissection 
respiratory / systemic complications
108
Q

What are the two different types of valves?

A

Man made: ball in cage / bileaflet
durable BUT thrombogenic and require anti-coagulation with warfarin

Tissue valves: homographs / xenographs
Anticoagulation not required BUT more prone to degenerative failure

CP3 Medicine (19 decks)

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