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Cardiovascular Block > L11 - Acute Coronary Syndrome > Flashcards

L11 - Acute Coronary Syndrome Flashcards

1
Q

Hypoxemia

A
  • aerobic metabolism and oxidative phosphorylation inhibited
  • ATP cannot be regenerated
  • ADP & AMP accumulate and are subsequently degraded into adenosine
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2
Q

Effect of accumulation of adenosine (5)

A
  • potent vasodilator
  • binds to receptors on VSM
  • decrease calcium entry into cell
  • hence relaxation
  • increased coronary BF
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3
Q

Examples of other chemicals resulting in vasodilation (4)

A
  • CO2
  • Lactate
  • acetate
  • H+
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4
Q

Describe endothelial cell dysfunction

A
  • inappropriate vasoconstriction of coronary arteries

- loss of normal antithrombotic properties

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5
Q

Describe interaction between platelets and endothelial cells

A

Normal endothelium , aggregating platelets
Serotonin 5HT, Thromboxane TXA2
- contraction of VSM
- vasoconstriction

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6
Q

Describe the appearance of STEMI vs NSTEMI

A

NSTEMI - platelet rich, partially occlusive

STEMI - red thrombus, fibrin rich when clot is aspirated, totally occlusive

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7
Q

Symptoms of myocardial infarction

A
  • acute central chest pain, crushing, gripping, tight
  • chest pain radiates to arms, neck, jaw or epigastrium
  • associated nausea, sweatiness, breathlessness, palpitations
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8
Q

3 main manifestations of atherosclerosis

A
  • coronary
  • cerebrovascular
  • peripheral
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9
Q

Patient consequences of Coronary atherosclerosis

short and sweet, literally 3 words

A

MI
Angina
sudden death

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10
Q

Cerebrovascular atherosclerosis

TIA?
CVA?

A

TIA - Transient Ishcaemic attack

CVA - cerebrovascular attack (stroke)

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11
Q

Peripheral atherosclerosis may lead to.. (2)

A

Intermittent claudication (muscle pain on mild exertion)

Gangrene

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12
Q

Angina

A
  • Ischaemic pain due to reduced blood supply to the heart muscle
  • due to blocked coronary arteries,
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13
Q

Why does cocaine use increase the risk of heart attack?

A

Cocaine causes intense vasospasm in artery causing ishcaemia.

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14
Q

Silent infarct common in

A

Diabetics

Elderly

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15
Q

What do silent MI presentations include

notes

A
  • Syncope (temp loss of consciousness) (rare)
  • pulmonary oedema
  • epigastric pain
  • chundering
  • post operative hypotension
  • oliguria
  • acute confusional state
  • diabetic hyperglycaemic states
  • stroke
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16
Q

Signs of STEMI in patients

e.g. how may they present?

A

Pallor
Sweatiness
Pulse - BP increased (pain, symp drive)
Pulse - BP decreased (hypotension, SA or AV node ischaemia)

17
Q

What are the criteria needed to define Acute coronary syndrome ?

3 main points

A
  1. unstable, ischaemic, chest pain (history)
  2. ischaemic ECG changes
  3. raised cardiac biomarkers
18
Q

Persistence of Q waves indicates

A

Manifestation of previous MI

19
Q

Describe coronary artery anatomy

A
  1. Right coronary artery
  2. Left main coronary artery
    - circumflex
    - left anterior descending
20
Q

Infarction in left main coronary artery may present with (3)

A
  1. Widespread ST depression
  2. ST elevation in AVR
  3. Cardiogenic shock
21
Q

Infarction of circumflex coronary artery would come up where on ECG?

A

Silent?
Posterior
Lateral V5-V6, I, aVL
Inferior II, III, aVF

22
Q

Infarction in left anterior descending coronary artery would come up where on ECG?

A

Anterior V1-V4
Septal
Lateral V5-6
aVL

23
Q

What is the worst type of infarct & why?

A

LAD

- supplies LV

24
Q

Describe classic anterior STEMI ECG?

A

Tombstoning

  • ST elevation V1-V6
  • reciprocal changes in II, III, AVF
25
How can troponin help differentiate between unstable angina & NSTEMI
Unstable angina - troponin negative, chest pain | NSTEMI - raised trop, not full ST elevation
26
What cardiac enzymes are used as markers of myocardial necrosis ? When do the levels peak
Troponin - produced by ventricular myocytes in response to stretch - peak at 24-48hrs
27
Describe a suitable test for identifying re-infarction?
CKMB - creatine kinase MB - enzyme found in heart muscle - correlates well with amount of myocardial death
28
WHO classification of different types of MI *read*
NEED TO KNOW TYPE 1: - spontaneous MI related to ischaemia due to a primary coronary event TYPE 2: - MI secondary to ischaemia due to either increased oxygen demand or decreased supply e.g. coronary artery ``` TYPE 3: - Sudden unexpected cardiac death - cardiac arrest - symptoms suggestive of myocardial ischaemia TYPE 4a - MI associated with PCI TYPE 4b - MI associated with stent thrombosis ``` Type 5 - Myocardial infarction associated with CABG
29
Acute management of ACS - pre hospital - in hospital
Pre hospital - aspirin. GTN spray In hospital - morphine & metoclopramide - oxygen if low sats - GTN spray or IV - antiplatelet agents
30
Metoclopramide
Symptomatic treatment of nausea and vomiting.
31
Chronic management of ACS (4)
- Dual antiplatelet therapy (DAPT) - Statins (lower cholesterol) - ACE I (left ventricle remodelling) - Betablockers
32
Mechanism of action of aspirin
1. Aspirin blocks production of Thromboxane A2 receptor. Enables aspirin to be sticky and aggregate. 2. Action of aspirin on platelet COX-1 is permanent, lasting for the life of the platelet. - thus preventing platelets sticking together.
33
Role of the P2Y12 receptor (3)
- recruitment of platelets - potentiation of procoagulant activity - potentiation of aggregation
34
Mechanism of clopidogrel
- irreversible inhibitor of the P2Y12 receptor - pro-drug with slow onset of action - superior to aspirin at secondary prevention of CV events.
35
Describe why there are differences on how patients will react to clopidogrel
- capacity of clopidogrel to inhibit ADP-induced platelet aggregation varies among subjects. - variability due to genetic polymorphisms in the CYP isoenzymes involved in the metabolic activation of clopidogrel.
36
Prasugrel
- pro-drug, quicker onset | - greater, more predictable inhibition of ADP-induced platelet aggregation
37
Why is Ticagrelor now seen as a better anti-platelet therapy?
- different class of anti-platelet - direct acting - reversibly binds to P2Y12 receptor - more rapid onset of action - greater anti-platelet effect than clopidogrel
38
What is the effect that nitrates have?
- relaxes VSM by donation of NO, activating gyanylate cyclase, producing cGMP. - dilation of coronary vessels improves oxygen supply to the myocardium - dilation of peripheral veins, and in higher doses peripheral arteries. - reduces preload and afterload - thereby lowers myocardial oxygen consumption
39
Describe how nitrates are introduced into the body?
- sublingual or IV for rapid effect | - develop tolerance

Cardiovascular Block (16 decks)

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