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CP3 @ UoN - Medicine & Surgery > Acute Coronary Syndromes > Flashcards

Acute Coronary Syndromes Flashcards

1
Q

What are the risk factors for ACS?

A 
Male
Family history
Smoking
Hypertension
DM
Hyperlipidaemia
Obesity
Sedentary lifestyle
Cocaine use
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2
Q

Define ACS

A

Acute Coronary Syndromes

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3
Q

What are the three different ACS’?

A

Unstable Angina
ST segment elevation myocardial infarction (STEMI)
Non-ST segment elevation myocardial infarction (nonSTEMI)

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4
Q

What are the common underlying pathology of all ACS’?

A

Plaque formation in coronary arteries
Plaque rupture and platelet aggregation
Thrombosis, vasoconstriction, thromboembolism
ISCHAEMIA

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5
Q

What is Unstable Angina?

A

Angina occurring at rest OR sudden increased frequency/severity

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6
Q

What is the cause of Unstable Angina?

A

Plaque rupture and platelet aggregation

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7
Q

What are the two types of Acute Myocardial Infarction?

A

STEMI

NSTEMI

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8
Q

What are the three patterns of AMI?

A 
Regional Myocardial (90%)
Regional Subendocardial
Circumferential Subendocardial (10%)
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9
Q

Define a Regional Myocardial AMI

A

Infarct of one segment of ventricular wall

Usually due to thrombus formation

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10
Q

Define a Regional Subendocardial AMI

A

Infarct limited to subendocardial zone

Associated w/ thrombus lysis

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11
Q

Define a Circumferential Subendocardial Infarction

A

General hypoperfusion of all coronary arteries

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12
Q

What is required for a diagnosis of AMI?

A

Elevated troponin + 1 of:

  • ST elevation/new LBBB (STEMI)
  • No ST elevation/LBBB (NSTEMI)
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13
Q

What are the key coronary arteries?

A

Right Coronary
Left Coronary
Circumflex
Left Anterior Descending

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14
Q

What area does the RCA supply?

A

RA, RV, post septum
AVN/SAN
Gives post/inf MI –> Leads II, III, aVF

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15
Q

What area does the LCA supply?

A

Antero-Lateral –> Splits into circumflex and LAD

Gives antero-lateral MI –> Leads I, aVL, V1-V6

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16
Q

What area does the circumflex supply?

A

LA, LV

Gives a lateral MI –> Leads I, aVL, V5/6

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17
Q

What area does the LAD supply?

A

LV, ant septum

Gives antero-septal MI –> Leads V1-V4

18
Q

What is the end result of MI, with regards to cardiac tissue?

A

Replacement of necrotic area w/ collagenous scar

10 days-several months

19
Q

What are the absolute contraindications to thrombolysis?

A 
Previous intracranial haemmorhage
Ischaemic stroke <6/12
Cerebral malignancy
Recent major trauma
GI bleeding <1/12
Known bleeding disorder
Aortic dissection
Non-compressible punctures
20
Q

What are the relative contraindications to thrombolysis?

A 
TIA <6/12
Oral anticoagulant therapy
Pregnancy/<1/12 post partum
Refractory hypertension
Advanced liver disease
Infective endocarditis
Peptic ulcer
Prolonged/traumatic resuscitation
21
Q

What are the 1st line thrombolytic agents in ACS?

A

Tissue plasminogen activators (alteplase)

22
Q

What are the causes of ACS?

A 
Atherosclerosis
Thrombosis
Inflammation
Less commonly
-emboli
-coronary artery spasm
-vasculitis
23
Q

What is the mortality of STEMI ACS?

A

7% before discharge

- 50% of deaths w/i 2 hours,

24
Q

What is the mortality of non-STEMI ACS?

A

1-2%

15% for refractory angina

25
Q

What is the immediate pathway of care w/i the hospital for STEMI?

A

Record ECG
Get i.v. access
Assessment of CVD, examination, identify CIs
Give Aspirin 300mg
Give Morphine 5-10mg i.v. + 10mg metoclopramide
GTN spray
Either PCI or Fibrinolysis

26
Q

What is the immediate pathway of care w/i the hospital for NSTEMI/UA?

A 
Give low flow O2 if SaO2 <90%/SOB
Analgesia (Morphine 5-10mv i.v. + anti emetic)
Nitrates
Aspirin (300mg)
Fondaparinux/Clopidogrel
Elective PCI
27
Q

What are the TIMI/GRACE scores?

A

TIMI - categorises risk of death/ischaemia/basis of therapeutic decision making
GRACE - helps assessment of future risk of death due to MI in patients w/ ACS

28
Q

What are the symptoms of ACS?

A

Severe crushing, gripping, heavy chest pain
>20 minutes
Radiates to L.arm, neck, jaw
Associated dyspnoea, nausea, fatigue, sweatiness, palpitations

29
Q

What are the signs of ACS?

A

Sympathetic Activation –> Tachycardia, HTN, pallor, sweating
Vagal Stimulation –> Bradycardia, vomiting
Myocardial Impairment –> Hypotension, narrow pulse pressure, raised JVP, basal creps, 3rd heart sound

30
Q

What are the ST changes in a non-reperfused STEMI?

A

5 mins –> Tall, pointed T waves
30 mins –> ST elevation
>2hrs –> T wave inversion, Q waves develop (pathognomic)
Days –> ST normalises
Weeks –> T wave may normalise, Q wave remains

31
Q

What is the long term management of ACS?

A 
Aspirin 75mg OD (for life)
Bisoprolol (for life, titrate to 60bpm)
Clopidgorel 75mg OD (1yr)
Atorvostatin 80mg ON
Ramipril 2.5mg BD
32
Q

What are the immediate complications of AMI?

A

Arrhythmias (VT/VF/AF)

Bradycardia/AV block

33
Q

Whar are the short term complications of AMI?

A 
Pulmonary oedema
Cardiogenic shock
Thromboembolism
VSD
Ruptured chordae tendinae
Rupture of ventricular wall (2-10/7)
34
Q

How does pulmonary oedema present?

A

Extreme dyspnoea, sweating, anxiety, frothy cough w/ blood stained sputum)
PO2/PCO2 fall (PCO2 later rises)

35
Q

What is VSD associated with?

A

Development of severe LVF

36
Q

What is a ruptured chordae tendinae associated with?

A

Mitral valve incompetence

37
Q

What is a ruptured ventricular wall associated with?

A

Haemopericardium
Cardiac tamponade
Death

38
Q

What are the long term complications of AMI?

A

Heart failure
Dressler’s syndrome
Ventricular aneurysm formation

39
Q

What is Dressler’s syndrome?

A

Immune mediated pericarditis

40
Q

What is the treatment for Dressler’s syndrome?

A

High dose aspirin/NSAIDs

CP3 @ UoN - Medicine & Surgery (135 decks)

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