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Cardiology > Acute Coronary Syndromes > Flashcards

Acute Coronary Syndromes Flashcards

1
Q

What are the acute coronary syndromes?

A
  • Unstable angina
  • NSTEMI
  • STEMI
  • Sudden cardiac death
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2
Q

What is the unstable angina?

A

Defined by the absence of biochemical evidence of myocardial damage. It is characterised by specific clinical findings of:

  • Prolonged (>20 minutes) angina at rest
  • New onset of severe angina
  • Angina that is increasing in frequency, longer in duration, or lower in threshold
  • Angina that occurs after a recent episode of MI.
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3
Q

What is an NSTEMI?

A

Non-ST elevated myocardial infarction

MI, but without ST-segment elevation. May have other ECG changes, such as ST-segment depression or T-wave inversion. Will have elevated cardiac biomarkers.

This pathologyically results in a subendocardial infarct - partial thickness infarct

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4
Q

What is a STEMI?

A

ST elevation myocardial infarction

MI as defined as in acute myocardial infarction, with ST-segment elevation more than 0.1 mV in two or more contiguous leads, and elevated cardiac biomarkers.

Pathologically this is classed by a transmural infarct

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5
Q

What happens phsyiologically within a few minutes of infarction?

A

All these effects are reversible

Within seconds - Cell switches to anaerobic metabolism -> ATP depletion

<2 minutes - Myocardial contractility decreases -> Heart failure

Within 5 minutes - Myofibrillar relaxation, glycogen depletion, cell and mitochondrial swelling

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6
Q

What happens pathologically after about 20-40 minutes of infarction?

A

Effects of this stage are irreversible

Myocardial necrosis - Sarcolemmal integrity disrupted, leading to leakage of intacellular macromolecules

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7
Q

What happens phsyiologically 24-48 hours after an infarct has happened?

A

Macroscopically pale infarct appears

Acute inflammatory reaction begins at the edge of the infarct

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8
Q

After the first 20-40 minutes of infarction, what happens in the follwoing 24 hours from a pathological point of view?

A
  • Early coagulation necrosis
  • Oedema and haemorrhage
  • Early neutrophil infiltration
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9
Q

What happens pathologically 3-7 days after an infarct?

A
  • Disintegration of dead myofibres
  • Dying neutrophils
  • Early phagocytosis by infiltrating macrophages
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10
Q

What occurs pathologically after 7-10 days of infarction?

A

Granulation tissue begins to form at the margins of the infarct

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11
Q

What pathologically occurs 2-8 weeks after infarction?

A

Increased collagen deposition and decreased cellularity

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12
Q

What happens pathologically after 2 months post infarct?

A

Dense collagenous scar formation

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13
Q

What is coagulative necrosis?

A

Characterised by the formation of gelatinous substance in dead tissue in which the architecture of the tissue is still maintained. Coagulation occurs as a result of protein denaturation, causing albumin in proteins to form a firm and opaque state. .

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14
Q

How does infarction occur?

A

Coronary artery obstruction or rupture

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15
Q

What is the difference between an NSTEMI and Unstable angina?

A

NSTEMI there are biochemical signs of infarction (troponin rise), whereas in unstable angina there are not

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16
Q

What are modifiable risk factors for ACS?

A
  • Smoking
  • Alcohol intake
  • Calorie intake
  • Sedentary lifestyle
  • Diabetes
  • Obesity
  • Hyperlipidaemia/Dyslipidaemia
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17
Q

What are non-modifiable risk factors for ACS?

A
  • Increasing age
  • Sex - male
  • FH
  • Ethnicity
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18
Q

What are symptoms of an acute coronary syndrome?

A
  • Chest pain - crushing, radiates to jaw, neck and arm, not relieved by rest or GTN
  • Dyspnoea
  • Diaphoresis
  • Nausea
  • Palpitations
  • Syncope
  • Sense of impending doom
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19
Q

What signs may be seen in someone with an acute coronary syndrome?

A
  • Brady/tachycardia
  • Signs of HF - Increased JVP, basal creps, 3rd heart sound etc
  • Pallor, sweatiness
  • 4th heart sound
  • Pansystolic murmur
  • Late signs - Pericardial rub, Peripheral oedema
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20
Q

What causes a 3rd heart sound?

A

A dull, low-frequency extra heart sound heard in the rapid filling phase of early diastole. The cadence of the heart sounds in a patient with an S3 is said to be similar to the word ‘Ken-tuck-y’.

An abrupt limitation of left ventricular inflow during early diastole causes vibration of the entire heart and its blood contents, resulting in the S3. In heart failure with systolic dysfunction there is elevated atrial pressure. When the mitral valve opens there is rapid filling down the pressure gradient into the stiffened dysfunctional ventricle.

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21
Q

What causes a 4th heart sound?

A

An S4 is typically found in conditions that cause a decrease in compliance of the left ventricle or diastolic dysfunction. Any condition causing stiffening of the left ventricle may cause an S4.

Forceful contraction of the atrium pushes blood into a non-compliant left ventricle. The sudden deceleration of blood against the stiff ventricular wall produces a low-frequency vibration, recognised as the fourth heart sound.

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22
Q

Why might you get a pansystolic murmur in an MI?

A

Papillary muscle rupture or a VSD

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23
Q

What patient groups may present without chest pain but have a MI?

A

Reduced sensation in mediastinal area

  • Elderly
  • Diabetics
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24
Q

How might an elderly or diabetic patient present with an MI?

A
  • Syncope
  • Pulmonary oedema
  • Epigastric pain and vomiting
  • Acute confusional state
  • Stroke
  • Diabetic hyperglycaemia
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25
Q

If you suspected an ACS, what investigations would you do?

A
  • 12 lead ECG, then continuous cardiac monitoring
  • Bloods - FBC, U+E’s, LFTs, CRP, Glucose, Troponin, magnesium, phosphate, lipid profile, CK-MB, myoglobin
  • CXR
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26
Q

What are the features of NSTEMI on an ECG?

A

Horizontal/downsloping ST depression >0.5 mm in > 2 leads

  • ST depression ≥ 1 mm is more specific and conveys a worse prognosis.
  • ST depression ≥ 2 mm in ≥ 3 leads associated with a high prob. of NSTEMI

T wave inversion/flattening at least 1mm deep in > 2 leads with dominant R-waves

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27
Q

What are the features of a STEMI on ECG?

A
  1. ST elevation in >/=2 adjacent chest leads of >/=0.2mV in leads V1, 2 or 3
  2. ST elevation in >/= 2 adjacent limb leads of >/=0.1 mV in other leads
  3. Pathological Q waves
  4. T-wave inversion
  5. New LBBB/RBBB
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28
Q

What would indicate a septal infarct?

A

Maximal ST elevation in V1-2

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29
Q

What would indicate an anterior infract on ECG?

A

Maximal ST elevation ST elevation in V2-V5

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30
Q

What would indicate an anterioseptal infarct on ECG?

A

Maximal ST elevation in leads V1-4

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31
Q

What would indicate an anterolateral infarct on ECG?

A

Maximal ST elevation in V3-6, 1 and aVL

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32
Q

Why when lookign at cardiac enzymes would you take an immediate level then take a level 12 hours later?

A

It can take 10–12 hours after a heart attack for troponin levels to rise, so 2 troponin tests are carried out (10–12 hours apart) to see if there is a change in troponin level

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33
Q

What would indicate purely lateral infarct on ECG?

A

Maximal ST elevation in I and aVL

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34
Q

What would indicate an inferior infract on ECG?

A

Maximal ST elevation on II, III and aVF

35
Q

What changes would you see in an ECG minutes after an infarction begins?

A

T waves become tall, pointed and upright and there is ST segment elevation

36
Q

What changes would you see in an ECG after a few hours following an infarction?

A

T waves invert, the R wave voltage is decreased and Q waves develop.

37
Q

What changes would you see in an ECG a few days following an infarct?

A

After a few days the ST segment returns to normal, but T waves may still be inverted and pathological Q-waves may be present

38
Q

What changes in an ECG might you see in someone weeks after having a STEMI?

A

T wave may return to upright but the Q wave remains.

39
Q

How would you initially manage someone with an Acute coronary syndrome?

A

ABCDE

Gain IV access

Give MONACT

  • DiaMorphine - 2.5 - 10mg in 10 ml slowly IV + 10 mg Metoclopramide IV
  • Oxygen - 94-98%
  • Nitrates - Sublingual GTN spray x2 if not hypotensive
  • Aspirin - 300mg loading dose, then 75 mg OD
  • Clopidogrel - 300-600 mg loading dose, then 75 mg OD, or Ticagrelor - 180 mg loading dose, then 90 mg OD
40
Q

In the initial management of an ACS, what dose of morphine would you give?

A

http://oscestop.com/ACS.pdf

2.5 - 10 mg in 10 ml - titrate to the pain

41
Q

What oxygen saturations would you aim for in someone with ACS?

A

94-98% unless COPD (aim 88-92% using 24-28% through venturi mask)

42
Q

What dose of GTN would you give someone initially with ACS?

A

2 puffs (unless hypotensive), then PRN

43
Q

When would you not give nitrates as part of the initial management of an ACS?

A

If they are hypotensive

44
Q

What dose of aspirin would you give someone in the initial management of ACS?

A

300 mg loading dose, then 75 mg OD

45
Q

What dose of clopidogrel would you give someone in the initial management of ACS?

A

300-600 mg loading dose, then 75 mg OD

46
Q

After initial management, how would you manage someone with a STEMI?

A
  • Admit to CCU
  • Reperfusion ASAP - PCI (gold standard) or Thrombolysis
  • Medications - add B-blockers and ACEi
47
Q

When performing a rapid examination in someone with ACs, what specific things are you looking for?

A
  • Hypotension
  • Murmurs
  • Acute pulmonary oedema
  • Signs of dissection - AR + unequal BP in both arms
48
Q

Following administering MONACT as part of your initial management of ACS, what should you start someone on asap if they were having a STEMI?

A

B-blockers - reduce cardiac workload

49
Q

What reperfusion options are there in ACS?

A
  • PCI
  • Thrombolysis
50
Q

When would you consider giving thrombolysis in someone with a STEMI?

A

No PCI available, plus STEMI with:

  • STE in two adjacent ECG leads
    • > 1mm in limb leads
    • >2 mm in chest leads
  • Or, new LBBB
51
Q

What are contraindications for thrombolysis?

A

AGAINST

  • Aortic dissection
  • GI bleed
  • Allergic Reaction
  • Iatrogenic: recent surgery
  • Neuro: cerebral neoplasm/CVA
  • Severe hypertension
  • Trauma
52
Q

What mnemonic can you use for remembering the absolute contraindications of thrombolysis?

A

AGAINST

53
Q

What are examples of different thrombolytic agents?

A
  • Alteplase
  • Streptokinase
  • Reteplase
  • Tenectaplase
54
Q

If thrombolysing someone, what would you start them on post thrombolysis?

A

LMWH - except with SK use

55
Q

What are the complications of thrombolysis?

A
  • Bleeding
  • Hypotension - SK
  • Allergic reactions - SK
  • Systemic embolisaton
  • Intracranial haemorrhage
  • Reperfusion arrhythmia
56
Q

What are the indications for primary PCI?

A
  • Chest pain + STT or new LBBB
  • Contraindications to thrombolysis
57
Q

In someone with STEMI who has already had B-Blockers, antiplatelet therapy and reperfusion therapy, what long term management would you continue them on?

A
  • Continue B-blockers - 12 months
  • Continue ACEi
  • GTN spray PRN
  • CVS risk reduction regime
    • Dual antiplatelet - aspirin + clopidogrel
    • Statin
    • BP control
    • Lifestyle modification
    • Cardiac rehab
58
Q

What are the components of CVS risk reduction therapy?

A
  1. Dual antiplatelet
  2. Statins
  3. Lifestyle modification
  4. Cardiac rehabilitation
  5. BP control
59
Q

When should someone with a STEMi be started on B-blockers?

A

As soon as possible

60
Q

When would you start someone on ACEi if they had a STEMI?

A

Within 24 hours MI - After starting aspirin, B-blockers and reperfusion

61
Q

After initially managing someone (using MONACT) with an NSTEMI/UA, how would you manage them?

A

GIVE MEDICATIONS

  • Continue aspirin, clopidogrel and Nitrates
  • B-blockers
  • High dose Statins - reduce mortality and recurrent MI
  • Fondaparinaux/LMWH - if no PCI/CABG in next 24 hrs

THEN PERFORM EARLY RISK STRATIFICATION - GRACE Score - divide into high and low risk

62
Q

After risk stratifying using the GRACE scoring system, if someone with an NSTEMI/UA was found to be high risk, how would you manage them?

A

Move to CCU

Medications

  • Continue Dual antiplatelet, LMWH and anti-ischaemic meds - b-blocker and GTN
  • Add Glycoprotein IIb/IIIa inhibitor

Aim for PCI/angiogrpahy

63
Q

If someone with NSTEMI/UA was deemed to be low/intermediate risk, how would you manage them?

A

Admit for monitoring in step down ward. If still symptomatic, treat as high-risk; if not, continue on:

  • Dual antiplatelet
  • LMWH
  • Anti-ischaemic hterapy - B-blockers, GTN

Then perform 2nd risk assessment - If high risk go for in-patient angiography; if low risk for outpatient angiopraphy

64
Q

When would you give GIIb/IIIa inhibitors in an ACS?

A

NSTEMI/UA - High risk patients only

65
Q

What LMWH can be used in treating someone with an NSTEMI/UA?

A
  • Dalteparin
  • Enoxaparin
66
Q

When would you want to start giving ACEi in a STEMI?

A

Within the first 24 hours

67
Q

In someone with NSTEMI/UA who has had all initial and hospital management they require, what long term management would you continue them on?

A
  • Continue B-blockers - 12 months
  • Add/Continue ACEi
  • GTN spray PRN
  • CVS risk reduction regime
    • Dual antiplatelet - aspirin + clopidogrel
    • Statin
    • BP control
    • Lifestyle modification
    • Cardiac rehab
68
Q

What is the critical time period for transfer of a patient with an ACS to a PCI centre (after which thrombolysis should be used)?

A

90 minutes

69
Q

How long should patients be on bed rest for after an ACS?

A

48hrs with cardiac monitoring

70
Q

What are complications of myocardial infarction?

A
  • Cardiac death
  • Heart failure
  • Pericarditis
  • Arrhythmias
  • Myocardial rupture
  • Ventricular aneurysm
  • Embolism
  • DVT + PE
  • Tamponade
  • Dressler’s syndrome
  • Valve problems - papillary muscle rupture
71
Q

What is dressler’s syndrome?

A

A secondary form of pericarditis that occurs in the setting of injury to the heart or the pericardium (the outer lining of the heart). It consists of fever, pleuritic pain, pericarditis and/or a pericardial effusion.

72
Q

When would you give someone unfractionated heparin in an ACS scenario?

A

If they were going for PCI in next 24 hrs, otherwise give LMWH

73
Q

What lifestyle advise would you give someone post-MI?

A
  • Stop smoking
  • Diet: oily fish, fruit, veg, ↓sat fats
  • Weight Loss
  • Exercise: 30min OD
  • Work: return in 2mo
  • Sex: avoid for 1mo
  • Driving :avoid for 1mo
74
Q

If using ticagrelor as part of you initial management of ACS, what dose would you use?

A

180mg loading dose, then 90 mg twice daily

75
Q

If someone had UA/NSTEMI, and there were no facilities to perform PCI or CABG within 24 hrs from initial presentation, what would you treat them with?

A

Fondaparinux

76
Q

What are features of dressler’s syndrome?

A
  • Mild fever
  • Pleuritic chest pain - positional - relived sitting forward
  • Friction rub
77
Q

What mnemonic could you use for remembering how to manage someone with a STEMI once you’ve initially treated someone with MONACT?

A
  • ACEi
  • B-Blocker
  • Cholesterol lowering drugs
  • Dual antiplatelet therapy
  • ECHO to assess left ventricle
78
Q

What do q waves on an ECG imply?

A

Full thickness infarct

79
Q

Why would you perform FBC in suspected ACS?

A

Anaemia could be causing cardiac ischaemia

80
Q

Why would you perform U+E’s in ACS?

A
  • Impaired renal function can cause false positive elevations in troponin
  • Baseline levels required prior to ACEi use
  • Hypo/hyperkalaemia associated with arrhythmias
81
Q

Why would you perform LFTS in someone with ACS?

A
  • Baseline prior to statin use
  • Hepatic impairment is a contra to ticagrelor use
82
Q

Why wou perform blood glucose in someone with suspected ACS?

A

Check for diabetes - aim for 4-11 mmol/L

83
Q

What mnemonic could you use to remember the complications of an MI?

A
  • Pump failure
  • Rupture of papillary muscle/septum
  • Aneurysm/arrhythmias
  • Embolism
  • Dressler’s Syndrome

Cardiology (29 decks)

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