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CVS Pathology > Acute Coronary Syndrome and Acute MI > Flashcards

Acute Coronary Syndrome and Acute MI Flashcards

1
Q

Definition of acute coronary syndrome

A

Any sudden cardiac event suspected or proven to be related to a problem with the coronary arteries

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2
Q

How do the problems of an ACS arise?

A

Due to myocardial ischaemia

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3
Q

Definition of myocardial ischaemia

A

Reduction of blood supply of heart muscle

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4
Q

Definition of MI

A

Cell death due to ischaemia

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5
Q

Major vs minor MI

A

Major - complete coronary artery occlusion

Minor - partial (or transient complete) coronary artery occlusion

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6
Q

ECG initially then at 3 days in a complete coronary artery occlusion

A

Initially - ST elevation

3 days - Q waves

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7
Q

ECG initially then at 3 days in a partial coronary artery occlusion

A

Initially - No ST elevation

3 days - no Q waves

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8
Q

What are the ACS?

A

Unstable angina
MI (STEMI / NSTEMI)
Sudden cardiac death

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9
Q

What part of the heart is affected in a STEMI?

A

Q wave MI

Transmural MI

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10
Q

What part of the heart is affected in NSTEMI?

A

Non Q wave MI

Subendocardial MI

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11
Q

What does STEMI stand for?

A

ST elevation MI

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12
Q

What does NSTEMI stand for?

A

Non ST elevation MI

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13
Q

What does a completely occluded artery cause?

A

Ongoing myocyte death

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14
Q

Non cardiac causes of troponin rise

A

Pulmonary embolism
Sepsis
Renal failure
SAH

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15
Q

What is troponin?

A

A group of proteins that help regulate the contractions of the heart and the skeletal muscles

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16
Q

When does the heart release troponin into the blood?

A

Heart injury e.g. MI

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17
Q

Causes of MI

A

Coronary atherosclerosis
Coronary vasospasm
Coronary dissection
Embolism of material down coronary artery
Vasculitis of coronary arteries
Radiotherapy to chest causing fibrosis and stenosis of coronary arteries

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18
Q

Who often gets coronary dissection?

A

Younger, healthier females

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19
Q

Causes of coronary vasospasm

A

Cocaine
Triptans
5-FU (chemo)

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20
Q

Cardiac risk factors

A 
Male
Age
Known heart disease
High BP
High cholesterol 
DM
Smoker
FH of premature heart disease
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21
Q

Diagnostic criteria for MI

A
  1. Detection of cardiac cell death by +ve cardiac biomarkers
  2. AND ONE OF
    - symptoms of ischaemia
    - new ECG changes
    - evidence of coronary problem on coronary angioplasm or autopsy
    - evidence of new cardiac damage on another test
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22
Q

Presentation of MI

A 
Chest pain 
- radiating to neck / arm / jaw
- may be described as a discomfort 
- severe pain 
Nausea
Sweating
SOB
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23
Q

Causes of chest pain

A 
Cardiac
- coronary artery disease 
- aortic valvular disease
- pulmonary HTN
- mitral valve prolapse
- Pericarditis
- idiopathic hypertrophic subaortic stenosis
Pulmonary 
- PE
- Pneumonia
- Pleuritis
- Pneumothorax
Emotional 
- Anxiety
- depression 
Vascular 
- aortic dissection 
Neural 
- herpes zoster
MSK
- costochondritis 
- Arthritis
- muscular spasm 
- bone tumour
GI 
- ulcer 
- bowel disease
- hiatus hernia
- pancreatitis 
- cholecystitis
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24
Q

How long do the symptoms of typical angina last of an ACS?

A

> 20 mins

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25
Q

What would you do if someone presented with ACS chest pain?

A
  1. ECG
    - ST elevation = STEMI
    - No ST elevation…….
  2. After 3 - 4 hours
    - Troponin
    - if NO - unstable angina, if YES - NSETMI
  3. After 1 - 2 days
    - From NSTEMI if Q waves - Qw MI, if no Q waves the NQMI
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26
Q

Treatment for STEMI

A 
Reperfusion 
- Primary PCI
- Pharmacological
Angioplasty 
Thrombolysis
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27
Q

How does angioplasty work?

A

Expanded balloon in between plaque and the artery

Stent is deployed compressing the plaque

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28
Q

How does thrombolysis work?

A

Tenecteplase (TNK) given as a bolus

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29
Q

What is the risks of thrombolysis?

A

Bleeding

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30
Q

Who should thrombolysis not be given to?

A 
Recent stroke
Previous intracranial bleeding
Caution if
- recent surgery 
- on warfarin 
- severe HTN
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31
Q

In STEMI, what should be done if can get to cath lab in 2 hours and what if not?

A

Within 2 hours - Primary PCI

After 2 hours - Thrombolysis then transfer for PCI

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32
Q

Compared to STEMI, NSTEMI patients tend to be…..

A

Older
More likely to have had previous MI
More likely to have had previous CABG/PCI
May not have clear obvious coronary presentation

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33
Q

Investigations of suspected ACS

A

Serial ECGs

Bloods

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34
Q

What should be given if admitted with suspected ACS?

A

GTN

Opiates (e.g. morphine)

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35
Q

What are the antithrombotic drugs?

A

Heparin
LWMH
Fondaparinux

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36
Q

Example of ACEI

A

Ramipril

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37
Q

Risks of coronary angiography/angioplasty/stenting

A 
Bleeding
Blood vessel damage 
MI
Coronary perforation 
Stroke
Contrast nephropathy
38
Q

What does CABG stand for?

A

Coronary artery bypass graft

39
Q

Who gets CABG?

A

Three vessel disease
Left main stem disease
Disease not amendable to PCI

40
Q

Complications of MI

A 
Arrhythmia 
Cardiogenic shock 
Myocardial rupture
Valve dysfunction due to papillary muscle dysfunction / rupture 
Acute VSD
Death
41
Q

Types of MI

A

Type 1 - 6

42
Q

Type 1 MI

A

Spontaneous MI associated with ischaemia and due to a primary coronary event such as plaque erosion, rupture, fissuring or dissection

43
Q

Type 2 MI

A

Imbalance of supply and demand of oxygen. Result of ischaemia

44
Q

Type 3 MI

A

Sudden cardiac death including cardiac arrest, with symptoms of ischaemia, accompanied by new ST elevation or LBBB

45
Q

Type 4a MI

A

Assosiated with PCI

46
Q

Type 4b MI

A

Assosiated with verified stent thrombosis via angiography or autopsy

47
Q

Type 5 MI

A

Assosiated with CABG

48
Q

What would occlusion of R coronary artery cause?

A

Inferior MI

49
Q

What would occlusion of left anterior descending coronary artery cause?

A

Anterior MI

50
Q

What would occlusion of circumflex coronary artery cause?

A

Lateral MI

51
Q

How do thrombolytic agents work?

A

Covert plasminogen to plasmin which lyses the clot by breaking down the fibrinogen and fibrin contained in the clot

52
Q

Two categories of thrombolytic agents

A

Fibrin specific agents

Non fibrin specific agents

53
Q

Examples of fibrin specific agents

A

Alteplase
Reteplase
Tenecteplase

54
Q

Example of non fibrin specific agents

A

Streptokinase

55
Q

Contraindications to thrombolytic agents

A

Prior ICH
Known structural cerebral vascular lesion
Known malignant intracranial neoplasm
Ischaemic stroke within 3 months
Suspected aortic dissection
Active bleeding or bleeding diathesis (excluding menses)
Significant closed head trauma or facial trauma within 3 months

56
Q

If no evidence of STEMI, use the ACS treatment protocol, which involves….

A 
Aspirin 
Ticagrelor/clopidogrel 
Fondaparinux/LWMH
IV nitrate
Analgesia
BBs
57
Q

Management to reduce the risk from NSTEMI

A 
PCI 
CABG
Aspirin 
Clopidogrel etc
LWMH 
Fondaparinux
Gllb/IIIa receptor blockers
Statins
BBs
58
Q

How does clopidogrel work?

A

Inhibits ADP receptor activated platelet activation (ADP receptor antagonists)
Blocks activation of GP IIb/IIIa pathway
This complex is a receptor for fibrinogen, fibronectin and von WF. Activation of this is a final combination pathway for platelet aggregation and cross linking of platelets by fibrin

59
Q

What is clopidogrel / ticagrelor always used in combination with?

60
Q

What does LWMH stand for?

A

Low weight molecular heparin

61
Q

Examples of LWMH

A

Enoxaparin
Dalteparin
Tinzeparin
Fondaparinux

62
Q

How do glycoprotein IIb/IIIa receptor inhibitors work?

A

Integrin complex found on platelets
Receptor for fibrinogen aids in platelet activation
Platelet activation by ADP (blocked by clopidogrel) leads to a conformational change in platelet GPIIb/IIIa receptor that induces binding to fibrinogen

63
Q

SIGN guidelines for treatment of ACS

A
  1. Immediately aspirin (300mg loading dose) and ticagrelor (180mg loading dose)
  2. Maintained on long term aspirin therapy
  3. Started on long term statin
  4. Maintained on long term beta blocker therapy
64
Q

What should patients with unstable angina be started on?

A

Long term ACEIs

65
Q

Patients with MI should be commenced on what within the first 36 hours?

A

Long term ACEI

66
Q

Patients with MI complicated by LV dysfunction (ejection fraction < 40%) in the presence of either clinical features of HF or DM should be commenced on what?

A

Long term eplerenone therapy

67
Q

What can happen to the lungs after an MI?

A

Flash pulmonary oedema can occur - after acute mitral valve regurg due to MI

68
Q

Complete heart block following an MI indicates damage to which artery and why?

A

Right coronary artery
The AV node is supplied by the posterior interventricular artery which is a branch of the right coronary artery (in the majority). In the minority it is a branch of the left circumflex artery

69
Q

What does persistent ST elevation after an MI indicate and what are the consequences of this?

A

Left ventricular aneurysm
Blood stagnates around the left ventricular aneurysm, thereby promoting platelet adherence and thrombus formation
Embolization of left ventricular thrombi can lead to embolic stroke or other systemic embolis

70
Q

MI and driving regulations

A

If private vehicle - does NOT need to notify DVLA following PCI and can resume driving after 4 WEEKS

If group 2 license (bus or lorry) - MUST notify DVLA. May not drive for at least 6 weeks. Then DVLA can do further assessment after this time scale.

71
Q

ECG changes for thrombolysis or PCI

A

ST elevation of > 2mm (2 small squares) in 2 or more consecutive anterior leads (V1 - V6)
OR
ST elevation of > 1mm (1 small square) in greater than 2 consecutive inferior leads (II, III, aVF, aVL)
OR
New LBBB

72
Q

Reversible causes of MI

A 
Hypoxia
Hypovolaemia
Hyperkalaemia
Hypokalaemia
Hypoglycaemia
Hypocalcaemia
Acidaemia
Other metabolic disorders
Hypothermia
Thrombosis (coronary or pulmonary)
Tension pneumothorax
Cardiac tamponade
Toxins
73
Q

Management of a VT/VF cardiac arrest

A

A single shock followed by
1 mins of chest compressions
Adrenaline 1mg once they have restarted after the third shock and then every 3 - 5 mins (during alternative cycles of CPR)

74
Q

Management of cardiac arrest if it was witnessed

A

Up to 3 quick successive shocks (stacked) rather than 1 shock followed by CPR

75
Q

What should be given asap in asystole / pulseless electrical activity?

A

Adrenaline 1mg

76
Q

What is the Framingham risk score?

A

Used to estimate the 10 year risk of a heart attack

77
Q

Where would ECG changes occur in an anteroseptal MI? Which coronary artery would be involved?

A

V1 - V4

LAD

78
Q

Where would ECG changes occur in an inferior MI? Which coronary artery would be involved?

A

II, III, and aVF

Right coronary

79
Q

Where would ECG changes occur in an anterolateral MI? Which coronary artery would be involved?

A

V4-V6, I, aVL

LAD or left circumflex

80
Q

Where would ECG changes occur in a lateral MI? Which coronary artery would be involved

A

I, aVL +/- V5 + V6

Left circumflex

81
Q

Where would ECG changes occur in a posterior MI? Which coronary artery would be involved?

A

Tall R waves V1 - V2
Usually left circumflex
Also right coronary

82
Q

What may also point to the diagnosis of an ACS on ECG?

83
Q

What are the only shockable rhythms?

84
Q

What does a posterior MI cause on a 12 lead ECG?

A

ST depression NOT elevation

85
Q

What does an inferior MI on ECG and a AR murmur raise suspicions of?

A

Ascending aortic dissection

86
Q

How long does troponin stay raised for after an MI?

87
Q

How long does creatine kinase stay raised for after an MI?

A

3 - 4 days

88
Q

Which is best to measure if suspect a re-infarction a few days after the initial MI, creatine kinase or troponin?

A

Creatine kinase better for 4 - 10 days post original insult

89
Q

Poor prognostic factors in ACS

A 
Age
Development (or history) of HF
PVD
Reduced systolic BP
Killip class
Initial serum creatinine conc.
Elevated initial cardiac markers
Cardiac arrest on admission 
ST segment deviation
90
Q

What is the killip class?

A

System used to stratify risk post MI

91
Q

Most common cause of death in a patient following an MI

A

Ventricular fibrillation

92
Q

What can beta blockers reduce awareness of?

A

Hypoglycaemic episodes

CVS Pathology (19 decks)

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