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CVS > CVS 9 Chest Pain + Acute Coronary Syndromes > Flashcards

CVS 9 Chest Pain + Acute Coronary Syndromes Flashcards

1
Q

Areas which can cause chest pain

A

Cardiac- cardiac muscle + pericardial sac
Respiratory - lungs + pleura
Gastro-intestinal - Oesophagus + Peptic ulcer disease
Vascular - Aortic dissection
MSK - muscle, bone, costochondritis, cartilage
Skin

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2
Q

What could a patient with a respiratory condition present with that a patient with acute contrary syndrome wouldn’t?

A

Coughing
Fever

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3
Q

Difference in location of chest pain caused by cardiac vs respiratory issues?

A

Cardiac - central
Respiratory - antero-lateral

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4
Q

Features of pleuritic chest pain

A
  • Sharp, well localised
  • Antero-lateral
  • Worsening with breathing in or coughing
  • Indicates involvement of structures with somatic innervation e.g. lung pleura, MSK structures, pericardial sac
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5
Q

What nerves innervate cardiac chest pain?

A

Visceral nerves

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6
Q

What nerves innervate pleuritic chest pain?

A

Somatic nerves

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7
Q

Features of cardiac chest pain

A

Dull/heaving
Poorly localised
Central
Can radiate to jaw, neck, shoulder + arm
Worsens with exercise
Indicates involvement of heart muscle (visceral nerves)

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8
Q

Why is cardiac chest pain felt centrally (+ radiation to arm)?

A
  • Cardiac ischaemia stimulates visceral nerve endings
  • signals sent to spinal cord segments T1-T4/5
  • sensory afferent from T1-T4/5 Dermatomes of skin
  • brain interprets pain as arising from skin
  • pain perceived as arising from chest (+ limbs innervated by T1-T4/5)
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9
Q

What Dermatomes are involved in cardiac chest pain?

A

T1-T4/5

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10
Q

Cardiac causes of chest pain

A

Pericardium - pericarditis
Cardiac muscle - stable angina
- acute coronary syndromes

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11
Q

Typical history of pericarditis

A

Male > female
Often virally caused
Previous viral infection
Eased with sitting forwards
Worsened when lying supine/flat

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12
Q

What worsens the pain of pericarditis?

A

Lying supine/flat

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13
Q

What eases the pain of pericarditis?

A

Sitting forwaeds

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14
Q

Further investigations of pericarditis

A

ECG
Blood tests

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15
Q

ECG of pericarditis

A

Saddle shape ST elevation
PR depression
Widespread - across all leads

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16
Q

What causes ischaemic heart disease?

A

Insufficient blood supply to heart muscles due to atherosclerotic disease of coronary arteries

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17
Q

Risk factors of acute coronary syndrome

A

Age
Gender
Smoking
Hypertension
Diabetes mellitus
Alcohol
Infection
Obesity
Lack of exercise
Hyperlipidaemia

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18
Q

Describe the plaque in stable angina

A

Plaque is fixed - stable occlusion

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19
Q

What happens if an atherosclerotic plaque ruptures in a stable occlusion in stable angina?

A

Thrombus formation
Sudden increased occlusion
Acute coronary syndrome occurs

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20
Q

Describe a thrombus in a STEMI

A

Complete conclusion of vessel

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21
Q

What eases stable angina pain?

A

Relieved by rest

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22
Q

Key differential between stable angina and acute coronary syndrome

A

Stable angina - pain relieved by rest
ACS - pain at rest

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23
Q

Are there any associated autonomic features with stable angina?

A

No

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24
Q

What feature causes increased troponin in blood?

A

Muscle death

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25
Q

Similarities between pains of acute myocardial infarction + pericarditis

A

Felt centrally

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26
Q

Differences between pains of acute myocardial infarction + pericarditis

A

MI - pain radiates to left arm + jaw
Pericarditis - worsens on lying down
- eases when leaning forward

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27
Q

Differences between ECGs of STEMI + pericarditis

A

STEMI - ST elevation
Pericarditis - widespread saddle shaped ST elevation

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28
Q

What autonomic features can occur with STEMI/NSTEMI?

A

Nausea + sweating

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29
Q

ECG in unstable angina

A

ST depression
T wave inversion

30
Q

ECG in NSTEMI

A

ST depression
T wave inversion

31
Q

What distinguishes between unstable angina and NSTEMI

A

Both have ST depression + T wave inversion

Unstable angina - normal troponin
- no autonomic feature
NSTEMI - raised troponin
- associated autonomic features

32
Q

Autonomic features in acute coronary syndromes

A

Pallor
Sweating
Nausea

33
Q

What are critical test if acute coronary syndrome is suspected?

A

ECG
Troponin

34
Q

What is stable angina characterised by?

A

Cardiac sounding pain only on exertion
Relieved by rest
Pain settles <15 minutes

35
Q

What are acute coronary syndromes characterised by?

A

Cardiac sounding chest pain at rest
Pain >15 mins
Possible associated autonomic features

36
Q

Pathology of an acute coronary syndrome

A

Atheromatous plaque rupture
Thrombus formation
Partial or full occlusion

37
Q

What causes a type 1 myocardial infarction?

A

Atherosclerotic plaque rupture, ulceration, erosion or dissection > thrombus in coronary arteries > decrease in blood flow / distal embolisation > myocardial necrosis > myocardial infarction

38
Q

What is type 2 myocardial infarction?

A

A condition other than coronary plaque instability contributes to decreased myocardial O2 supply
e.g.
Coronary artery spasm
Coronary endothelial dysfunction
Tachyarrthymias, bradyarrthymias
Anaemia
Respiratory failure

39
Q

Describe the assessment needed for acute coronary syndromes

A

Cardiac sounding?
Radiation?
What eases pain?
What worsens the pain?
How long does it last?
Relieved with GTN?
Pleuritic? (Pain when breathing)
Any other symptoms

40
Q

What is GTN?

A

Glyceryl trinitrate
Vasodilator

41
Q

What is used to treat angina?

A

GTN

42
Q

What does a ST elevation imply?

A

Sudden occlusion

43
Q

What does a T wave inversion imply?

A

Under supply of blood to myocardium
Not sudden occlusion

44
Q

What does a ST depression imply?

A

Under supply of blood to myocardium
Not sudden coronary occlusion

45
Q

Blood test for NSTEMI

A

Troponin - raised
Cholesterol
Renal function
HbA1C (blood glucose)
Haemoglobin (anaemic?)

46
Q

How is troponin measured?

A

Immunoassay

47
Q

When is troponin raised after cardiac muscle death?

A

3 hours

48
Q

How long does troponin remain elevated for after cardiac muscle death?

A

2+ weeks

49
Q

Management of STEMI

A
  • transfer to catheter lab
  • IV morphine with metoclopramide
  • Chewable aspirin 300mg > 75mg od for life
  • 60mg prasugrel/600mg clopidogrel/180mg ticagrelor
  • PCI
  • full biochemical screen on admission (lipidprofile, glucose, HbA1c + FBC)
  • B blocker, ACEi, ARB
  • statin if needed
  • smoking cessation
50
Q

Management of NSTEMI/unstable angina

A
  • pain relief morphine
  • aspirin 300mg loading dose > 75mg od
  • LMWH
  • repeat ECG
  • risk assessment if elevated has-TnIgraace score
  • ticagrelor if risk is >3% 180mg loading
  • anti-anginals: nitrates (GTN), CCBs
51
Q

When is urgent PCI needed in NSTEMIs?

A

If patient has ongoing CP with dynamic ECG changes
If patient develops arrythmias with compromise

52
Q

Management of acute coronary syndromes

A

Lifestyle changes - low fat + salt diet, regular exercise
Dual anti platelets for 12 months
Aspirin for life
Statins to lower cholesterol
Bisoprolol
ACE inhibitors

53
Q

Why does chest pain in a patient with stable angina come on with exercise?

A

Blood flow through the left coronary artery is compromised due to shorter diastole + O2 demand has increased

54
Q

What is the primary mechanism by which GTN spray alleviates myocardial ischaemia in a patient with stable angina?

A

Dilation of systemic veins

55
Q

Why is cardiac chest pain poorly localised whereas pleuritic chest pain is well localised?

A
  • Cardiac chest pain is innervated by visceral nerves which arises from splanchnic part of lateral plate mesoderm
  • whereas pleuritic chest pain is somatic nerves
56
Q

What order of ADP receptor antagonist should be given in management of STEMIs?
What loading dose for each?

A

Prasugrel 60mg
Clopidogrel 600mg
Ticagrelor 180mg

57
Q

Why are ACEi given in STEMI management?

A

To prevent muscle over damage

58
Q

Causes of non-cardiac chest pain

A
  • costrochondritis
  • GORD
  • PE
  • pneumonia
  • pneumothorax
  • shingles
59
Q

Investigations of angina

A
  • physical exam
  • ECG
  • FBC + U&Es
  • LFTs + lipid profile
  • thyroid function test
  • HbA1C + fasting glucose
60
Q

Management of stable angina

A

RAMPS
- Refer to cardiology
- Advise about diagnosis + managment
- Medical treatment
- Procedural or surgical interventions: PCI or CABG
- Secondary prevention

61
Q

Medical management of stable angina

A
  • sublingual glycerol trinitrate
  • beta blocker +/- CCB e.g. Diltiazem or verapamil (both avoided in HFrEF
62
Q

Surgical interventions of stable angina

A
  • percutaneous coronary intervention (balloon + stent)
  • coronary artery bypass graft
63
Q

What are the 3 main options for graft vessels in a coronary artery bypass graft?

A

Saphenous vein
Internal thoracic artery
Radial artery

64
Q

What is involved in a coronary artery bypass graft?

A
  • midline sternotomy incision to open chest along sternum
  • graft vessel is attached to affected coronary artery > bypasses stenotic area
  • options for graft vessels: saphenous vein, internal thoracic artery or radial rtery
65
Q

Compare PCI vs CABG scars

A
  • PCI: brachial or femoral artery access
  • CABG: midline sternotomy, scar on inner leg (saphenous vein harvesting)
66
Q

Causes of raised troponin

A
  • NSTEMI/STEMI
  • chronic kidney disease
  • myocarditis
  • sepsis
  • aortic dissection
  • PE
67
Q

Investigations of ACS

A
  • FBCs
  • U&Es
  • LFTs
  • lipids
  • glucose
  • CXR
  • echocardiogram
68
Q

Complications of myocardial infarction

A
  • death
  • rupture of heart septum or papillary muscles
  • heart failure
  • arrhythmias + aneurysm
  • Dressler’s syndrome
69
Q

What is Dressler’s sydrome?

A
  • ‘post myocardial infarction syndrome’
  • occurs 2-3 weeks after acute MI
  • caused by localised immune response > pericarditis
70
Q

Presentation of Dressler’s syndrome

A
  • pleuritic chest pain
  • low grade fever
  • pericardial rub
71
Q

Managment of Dressler’s syndrome

A
  • NSAIDs
  • steroids if more severe
  • pericardiocentesis if pericardial effusion occurs
72
Q

Types of myocardial infarction

A
  • type 1: traditional MI - sudden occulsion of vessel
  • type 2: ischamia secondary to increased demand or reduced supply of O2
  • type 3: sudden cardiac death or caridac arrest suggestive off ischaemic event
  • type 4: MI assocaited with procedures such as PCI, CABG… (iatrogenic)

CVS (22 decks)

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