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IPE revision CARDIOLOGY > acute coronary syndromes and angina > Flashcards

acute coronary syndromes and angina Flashcards

1
Q

describe the pathogenesis behind acute coronary syndromes

A

Atherosclerosis:

  1. damage to endothelium
  2. lipids infiltrate
  3. macrophages engulf oxidised lipids and become foam cells
  4. macrophages release cytokines and inflam process
  5. smooth muscle cells respond and migrate from media to intima
  6. Fibrosis occurs around lipids leading to fibrotic cap surrounding lipid core - plaque

Plaque ruptures, platelets aggregate and thrombus forms –> ischaemia

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2
Q

compare STEMI, NSTEMI and angina in terms of pathogenesis, markers and ECG changes

A

Angina = partial occlusion, no infarction, no troponin
ECG changes = none/ ST depression when symptomatic

NSTEMI = occlusion with only part of myocardial wall infacted, troponin increase
ECG changes = ST depression

STEMI = ischaemia across the full width of the myocardial wall, troponin greatly increased
ECG changes = ST elevation in corresponding leads

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3
Q

what are the signs and symptoms of MI

A
  • Central crushing chest pain which can radiate up neck to jaw and down left arm for >20min, progressively getting worse and not relieved by GTN
  • palpitations
  • feeling of impending doom / anxiety
  • sympathetic drive - sweat, cold/clammy, tachypnoea, tachycardia, pallor, N+V

signs of heart failure

  • Breathlessness
  • Raised JVP
  • crackles
  • signs of shock - syncope, hypotension

old people and diabetics can present with back pain or no pain at all

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4
Q

list the non modifiable risk factors in developing MI

A
  1. genetic predisposition - familial hyperlipidaemia
  2. male
  3. old
  4. ethnicity
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5
Q

list the modifiable risk factors for developing MI

A
  1. Smoking
  2. T2DM
  3. hyperlipidaemia
  4. Hypertension
    extra:
    obesity, alcohol, stress, lack of exercise
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6
Q

which coronary artery is affected and what section of heart if ST changes are seen in..

a) V1, V2, V3, V4
b) V1, V2
c) I, aVL, V5, V6
d) II, III, aVF
e) aVR and V1

A

a) anterior (LAD)
b) septal (LAD)
c) left lateral (left circumflex)
d) inferior (RCA)
e) right atrium (RCA)

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7
Q

explain the coronary artery vasculature and describe which regions each vessel supplies

A 
LAD = septum, LV + RV
left circumflex = left atria, LV
left marginal = LV
RCA = RA, RV, SAN/AVN
Right marginal = RV
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8
Q

describe in detail ECG changes that can be associated with STEMI

A

Initially:
tall T wave
ST elevation

Days later:
Inverted T
flattened R
Pathological Q
reversal of ST elevation to normal
can also get reciprocal changes (ST depression) in other leads dependant on anastomoses 
associated features:
New LBBB
bradycardia
heart block
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9
Q

Describe ECG changes seen in NSTEMI

A

ST Depression

T wave inversion

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10
Q

what defines a pathological Q wave

A

> 25% of QRS and >1 small square

or >2 small squares

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11
Q

describe the difference between transmural and sub-endocardial myocardial injury

A

Transmural - full thickness ischaemia and necrosis as seen in STEMI - get ST elevation

Sub-endocardial = partial thickness ischaemia and necrosis - get ST depression

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12
Q

what investigations would you order in someone with suspect ACS?

A

Bloods - FBC (anaemia), U&E (HyperK+), LFT (baseline for drugs)
Cardiac Troponin levels, CK levels, AST levels, lactate dehydrogenase
ECG - monitor changes in what leads
CXR - complications e.g. pul oedema
Glucose and lipids for risk factors
ECHO - for complications

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13
Q

explain the reason for the following investigations in ACS..

  • FBC
  • LFT
  • Urea and electrolytes
  • glucose and lipids
A

FBC = anaemia
LFT = baseline for drugs (statin), Ticagrelor (antiplatelet) is contraindicated in hepatic impairment
U+E = HyperK+ and other disturbances
glucose and lipids to monitor risk factor levels

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14
Q

what are the markers of myocardial infarction? state when then peak and fall?

A

Troponin I + T
Rises in the first 3 hours, peaks at 24hours before gradually falling

other markers inc: CK, AST, lactate dehydrogenase

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15
Q

how can troponin distinguish between MI, angina and myocarditis ?

A 
Angina = no troponin
MI = lots of troponin rising and falling again quickly
myocarditis = low level troponin over long period
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16
Q

what CXR changes may you see with MI?

A

shadowing over lung if pulmonary oedema present
widened mediastitum
cardiomegaly

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17
Q

describe the emergency treatment for STEMI

A

ABCDE approach - call help, establish peripheral access
12-lead ECG and take bloods on admission

ROMANCE mnemonic
R = reassure
O = O2 (only give if hypoxic as vasoconstricts if hyperoxic)
M = morphine IV and cyclizine (antiemetic)
A = Aspirin 300mg
N = nitrates (GTN) 2puffs or sublingual tab
C = Clopidogrel
E = enoxaparine (LMWH)

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18
Q

state two options for definitive treatment after STEMI

A

PCI or thrombolysis

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19
Q

what is PCI?

A

Access through femoral artery back via aorta to coronary artery
dye injected to see where thrombus is
balloon inflated at area and stent placed in coronary artery to allow the blood flow to pass

Anticoagulants needed for prophylaxis:

  • Bivalirudin
  • Ticagrelor
  • Clopidogrel
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20
Q

what are the complications of PCI?

A

can detached thrombus leading to emboli
reperfusion arrhythmia (reactive hyperaemia)
bleeding

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21
Q

what is Thrombolysis?

A

administering drugs which mimic the work of tPa to break down clots
- Alteplase/Reteplase
Converts plasminogen to plasmin
Plasmin can then break down fibrin

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22
Q

what are the indications for thrombolysis

A

if can be given within 12 hours of the first onset of chest pain + any of:

  • > 1mm in 2 consecutive limb leads
  • > 2mm in 2 consecutive chest leads
  • new LBBB
  • posterior infarct
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23
Q

what are the absolute contraindications of thrombolysis

A
  1. recent haemorrhage in last 6 months
  2. GI bleed in the last month
  3. intracranial malignancy
  4. aortic dissection
  5. recent trauma/surgery
  6. Bleeding disorder
24
Q

what are the relative contraindications of thrombolysis

A
  1. warfarin
  2. pregnancy
  3. infective endocarditis
  4. advanced liver disease
25
Q

what are the complications of thrombolysis?

A 
Bleeding (esp subarachnoid)
hypotension
allergic reaction (streptokinase esp)
embolization of thrombi
reperfusion arrhythmia
26
Q

describe the long term management of an STEMI

A 
5 key meds:
B blockers
Aspirin indefinetely
Statin (80mg simvastatin)
Clopidogrel (30days - 12months)
ACEi (prevents remodelling to stop HF - give within 24hrs)

assess risk factors
no work or sex for 1 month
no driving for 1 month and must inform DVLA

27
Q

when should STEMI patients be followed up?

A

at 5 weeks if any signs of angina, breathlessness or palpitations (complications post-MI)
At 3 months to test LFTs because of statin use and re-check lipid levels

28
Q

describe management of a NSTEMI

A

analgesia - morphine and cyclizine

anti-ischaemic:
B blockers
Nitrates
consider ACEi
Statin

antiplatelet:
Aspirin and Clopidogrel

Antithrombotic
Fondaparinux (used instead of LMWH - heparin like drug)

29
Q

how do we decide if a NSTEMI is high or low risk?

+ how do we manage each risk?

A

GRACE score
low risk = discharge if troponin I negative
high risk = clopidogrel and aspirin, GPIIb or IIIa antagonist, consider PCI

30
Q

when is PCI considered for NSTEMIs

A 
Previous PCI or CABG
ECG changes or recurrent angina despite treatment
Troponin I raised
Features of HF
Haemodynamically unstable
31
Q

State the complications of an MI

A 
Mnemonic SPREAD
S = Sudden cardiac death 
P = pericarditis or pump failure
R = rupture septum, papillary muscles
E = Emboli - DVT/P.E
A = Aneurysms, Arrhythmias
D = Dressler's syndrome
32
Q

what is dresslers syndrome and how is it treated?

A

Dressler’s = 5 days - 10week presentation of chronic pericarditis due to autoimmune response to inflammation
Raised ESR, fever and anaemia
Treated with NSAIDs, steroids and colchine

33
Q

explain the different arrhythmias that can result from an MI

A

sinus tachy - due to stress

VT - damaged myocytes with ectopics

VF - early (reperfusion >48hours) or chronic (no coordination of myocytes due to damage)

Brady - SAN damage (RCA inferior MI)

Heart block - AVN damage (RCA inferior MI)

new LBBB

34
Q

what type of MI is rupture of papillary muscles most common in?

A

Inferior/posterior MI

35
Q

how would rupture of papillary muscles post MI present?

A

Mitral regurgitation - patient with 3rd heart sound
pulmonary oedema
signs of HF

36
Q

how would ventricular septal rupture post MI present?

A

Pansystolic murmur

acute HF

37
Q

how can left ventricular rupture post MI present?

A

Acute cardiac tamponade - sudden death

38
Q

when do aneurysms post MI present?

A

4-6 weeks

39
Q

how are the following MI complications managed:

a) pulmonary oedema
b) LVF
c) cardiogenic shock

A

Pulmonary Oedema:
- resuscitation (o2 and sit up), opiates (calm), GTN spray, furosemide, CPAP if required

LVF:
- diuretics and ACEi

Cardiogenic shock:
- iontropes and intra-aortic balloon pump

40
Q

describe the pathogenesis behind angina

A

Atherosclerosis:

  1. damage to endothelium
  2. lipids infiltrate
  3. macrophages engulf oxidised lipids and become foam cells
  4. macrophages release cytokines and inflam process
  5. smooth muscle cells respond and migrate from media to intima
  6. Fibrosis occurs around lipids leading to fibrotic cap surrounding lipid core - plaque (AS, anaemia, arteritis , tachyarrhythmias)

blocks part of vessel

other causes: Aortic Stenosis, anaemia, arteritis, tachyarrhythmias

41
Q

what are the symptoms of angina

A

Central chest pain on exertion relieved by GTN spray/rest
(can be worse after a meal, cold, emotion)

dyspnoea, sweating, nausea

42
Q

what is the difference between a stable and unstable plaque?

A

stable = thick fibrous cap unlikely to rupture

unstable = thin fibrous plaque as inflammatory process has not occurred properly so more likely to ulcerate and thrombose

43
Q

what investigations would you do in someone presenting with angina?

A

Bloods:
FBC (anaemia), U&E (hyperK+), LFT (baseline).
Troponin I test to look for ischaemic damage
(Can also look at AST, lactate dehydrogenase for damage)
TFT - thyrotoxicosis
Lipids and glucose - risk factors
ECG - look at changes associated
Exercise stress test (not recommended by NICE)
Coronary angiography

44
Q

what would the ECG show in someone with angina

A

Normal

or ST depression, T wave flattening/inversion in symptomatic at the time

45
Q

why may an ECHO be indicated in someone presenting with angina like symptoms?

A
  • Aortic stenosis gives very similar symptoms to angina

- HOCM - hypertrophic obstructive cardiomyopathy (presents with angina like symptoms)

46
Q

how is angina managed?

A

modifiable risk factors - smoking, diabetes, weight loss, statins (high lipids), BP, exercise

Pharma:
- Aspirin 75-150mg daily
- B Blockers (Ca blockers if B blockers contraindicated)
- Nitrates:
GTN spray or sublingual tablets (up to every 1/2 hour)or prophylaxis with oral nitrate (isosorbide mononitrate)
- Omega 3
- ACEi if angina and diabetes

Emergency setting:
- Give ACEi and Clopidogrel for unstable angina

Definitive treatments:

  • PTCA
  • CABG
47
Q

what is PTCA?

A

Balloon dilation of stenotic vessels + stenting

indicated if poor medical response and not suitable for CABG

48
Q

what are the complications of PTCA and how are these minimised?

A

Re-stenosis
- Emergency CABG required or will result in death

Minimalised by placing patients on duel antiplatelet therapy to prevent thrombosis:
- Clopidogrel and Aspirin

49
Q

what is CABG?

A

Harvested vein (mainly) or artery is used as a graft to divert blood around the blockage in a coronary artery (bypass)

Usually used are reversed great saphenous vein of the leg or internal mammary artery

50
Q

when is CABG indicated?

A
  1. left main stem disease
  2. severe stenosis
  3. triple vessel disease
  4. unsuitable or failed angioplasty
  5. Abnormal LV function
51
Q

what after care is required after CABG?

A

No driving for 1 month, no work for 3 months

no smoking or exercise

Aspirin (clopidogrel if aspirin CI)

52
Q

what is crescendo and decubitus angina?

A

Crescendo = gradually gets worse each time patient exercises and they can do less each time until pain symptom onset

Decubitus = angina symptoms on lying down

53
Q

what is prinzmental angina?

A

usually in young females in the morning.

Angina symptoms with no associated risk factors of atherosclerosis present.
Caused by coronary spasms.
ST elevation which resolves when pain subsides

54
Q

how is prinzmental angina treated? what should be avoided?

A

Treated with Calcium channel blockers and long acting nitrates

BB and aspirin must be avoided in these patients as they aggravate the coronary spasms

55
Q

what is syndrome X?

A

angina pain and ST elevation on exercise but no evidence of coronary atherosclerosis – probably represents small vessel disease

56
Q

what are the complications of CABG?

A 
MI
stroke
pericardial tamponade
post perfusion syndrome
post op AF
graft stenosis

IPE revision CARDIOLOGY (9 decks)

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