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CVS Pathology > Acute Coronary Syndrome and Acute MI > Flashcards

Acute Coronary Syndrome and Acute MI Flashcards

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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
What would you do if someone presented with ACS chest pain?
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
26
Treatment for STEMI
``` Reperfusion - Primary PCI - Pharmacological Angioplasty Thrombolysis ```
27
How does angioplasty work?
Expanded balloon in between plaque and the artery | Stent is deployed compressing the plaque
28
How does thrombolysis work?
Tenecteplase (TNK) given as a bolus
29
What is the risks of thrombolysis?
Bleeding
30
Who should thrombolysis not be given to?
``` Recent stroke Previous intracranial bleeding Caution if - recent surgery - on warfarin - severe HTN ```
31
In STEMI, what should be done if can get to cath lab in 2 hours and what if not?
Within 2 hours - Primary PCI | After 2 hours - Thrombolysis then transfer for PCI
32
Compared to STEMI, NSTEMI patients tend to be.....
Older More likely to have had previous MI More likely to have had previous CABG/PCI May not have clear obvious coronary presentation
33
Investigations of suspected ACS
Serial ECGs | Bloods
34
What should be given if admitted with suspected ACS?
GTN | Opiates (e.g. morphine)
35
What are the antithrombotic drugs?
Heparin LWMH Fondaparinux
36
Example of ACEI
Ramipril
37
Risks of coronary angiography/angioplasty/stenting
``` Bleeding Blood vessel damage MI Coronary perforation Stroke Contrast nephropathy ```
38
What does CABG stand for?
Coronary artery bypass graft
39
Who gets CABG?
Three vessel disease Left main stem disease Disease not amendable to PCI
40
Complications of MI
``` Arrhythmia Cardiogenic shock Myocardial rupture Valve dysfunction due to papillary muscle dysfunction / rupture Acute VSD Death ```
41
Types of MI
Type 1 - 6
42
Type 1 MI
Spontaneous MI associated with ischaemia and due to a primary coronary event such as plaque erosion, rupture, fissuring or dissection
43
Type 2 MI
Imbalance of supply and demand of oxygen. Result of ischaemia
44
Type 3 MI
Sudden cardiac death including cardiac arrest, with symptoms of ischaemia, accompanied by new ST elevation or LBBB
45
Type 4a MI
Assosiated with PCI
46
Type 4b MI
Assosiated with verified stent thrombosis via angiography or autopsy
47
Type 5 MI
Assosiated with CABG
48
What would occlusion of R coronary artery cause?
Inferior MI
49
What would occlusion of left anterior descending coronary artery cause?
Anterior MI
50
What would occlusion of circumflex coronary artery cause?
Lateral MI
51
How do thrombolytic agents work?
Covert plasminogen to plasmin which lyses the clot by breaking down the fibrinogen and fibrin contained in the clot
52
Two categories of thrombolytic agents
Fibrin specific agents | Non fibrin specific agents
53
Examples of fibrin specific agents
Alteplase Reteplase Tenecteplase
54
Example of non fibrin specific agents
Streptokinase
55
Contraindications to thrombolytic agents
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
If no evidence of STEMI, use the ACS treatment protocol, which involves....
``` Aspirin Ticagrelor/clopidogrel Fondaparinux/LWMH IV nitrate Analgesia BBs ```
57
Management to reduce the risk from NSTEMI
``` PCI CABG Aspirin Clopidogrel etc LWMH Fondaparinux Gllb/IIIa receptor blockers Statins BBs ```
58
How does clopidogrel work?
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
What is clopidogrel / ticagrelor always used in combination with?
Aspirin
60
What does LWMH stand for?
Low weight molecular heparin
61
Examples of LWMH
Enoxaparin Dalteparin Tinzeparin Fondaparinux
62
How do glycoprotein IIb/IIIa receptor inhibitors work?
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
SIGN guidelines for treatment of ACS
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
What should patients with unstable angina be started on?
Long term ACEIs
65
Patients with MI should be commenced on what within the first 36 hours?
Long term ACEI
66
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?
Long term eplerenone therapy
67
What can happen to the lungs after an MI?
Flash pulmonary oedema can occur - after acute mitral valve regurg due to MI
68
Complete heart block following an MI indicates damage to which artery and why?
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
What does persistent ST elevation after an MI indicate and what are the consequences of this?
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
MI and driving regulations
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
ECG changes for thrombolysis or PCI
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
Reversible causes of MI
``` Hypoxia Hypovolaemia Hyperkalaemia Hypokalaemia Hypoglycaemia Hypocalcaemia Acidaemia Other metabolic disorders Hypothermia Thrombosis (coronary or pulmonary) Tension pneumothorax Cardiac tamponade Toxins ```
73
Management of a VT/VF cardiac arrest
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
Management of cardiac arrest if it was witnessed
Up to 3 quick successive shocks (stacked) rather than 1 shock followed by CPR
75
What should be given asap in asystole / pulseless electrical activity?
Adrenaline 1mg
76
What is the Framingham risk score?
Used to estimate the 10 year risk of a heart attack
77
Where would ECG changes occur in an anteroseptal MI? Which coronary artery would be involved?
V1 - V4 | LAD
78
Where would ECG changes occur in an inferior MI? Which coronary artery would be involved?
II, III, and aVF | Right coronary
79
Where would ECG changes occur in an anterolateral MI? Which coronary artery would be involved?
V4-V6, I, aVL | LAD or left circumflex
80
Where would ECG changes occur in a lateral MI? Which coronary artery would be involved
I, aVL +/- V5 + V6 | Left circumflex
81
Where would ECG changes occur in a posterior MI? Which coronary artery would be involved?
Tall R waves V1 - V2 Usually left circumflex Also right coronary
82
What may also point to the diagnosis of an ACS on ECG?
LBBB
83
What are the only shockable rhythms?
VF | VT
84
What does a posterior MI cause on a 12 lead ECG?
ST depression NOT elevation
85
What does an inferior MI on ECG and a AR murmur raise suspicions of?
Ascending aortic dissection
86
How long does troponin stay raised for after an MI?
10 days
87
How long does creatine kinase stay raised for after an MI?
3 - 4 days
88
Which is best to measure if suspect a re-infarction a few days after the initial MI, creatine kinase or troponin?
Creatine kinase better for 4 - 10 days post original insult
89
Poor prognostic factors in ACS
``` 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
What is the killip class?
System used to stratify risk post MI
91
Most common cause of death in a patient following an MI
Ventricular fibrillation
92
What can beta blockers reduce awareness of?
Hypoglycaemic episodes

CVS Pathology (19 decks)

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