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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
Q

How can troponin help differentiate between unstable angina & NSTEMI

A

Unstable angina - troponin negative, chest pain

NSTEMI - raised trop, not full ST elevation

26
Q

What cardiac enzymes are used as markers of myocardial necrosis ?

When do the levels peak

A

Troponin

  • produced by ventricular myocytes in response to stretch
  • peak at 24-48hrs
27
Q

Describe a suitable test for identifying re-infarction?

A

CKMB - creatine kinase MB

  • enzyme found in heart muscle
  • correlates well with amount of myocardial death
28
Q

WHO classification of different types of MI

read

A

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
Q

Acute management of ACS

  • pre hospital
  • in hospital
A

Pre hospital
- aspirin. GTN spray

In hospital

  • morphine & metoclopramide
  • oxygen if low sats
  • GTN spray or IV
  • antiplatelet agents
30
Q

Metoclopramide

A

Symptomatic treatment of nausea and vomiting.

31
Q

Chronic management of ACS (4)

A
  • Dual antiplatelet therapy (DAPT)
  • Statins (lower cholesterol)
  • ACE I (left ventricle remodelling)
  • Betablockers
32
Q

Mechanism of action of aspirin

A
  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
Q

Role of the P2Y12 receptor (3)

A
  • recruitment of platelets
  • potentiation of procoagulant activity
  • potentiation of aggregation
34
Q

Mechanism of clopidogrel

A
  • irreversible inhibitor of the P2Y12 receptor
  • pro-drug with slow onset of action
  • superior to aspirin at secondary prevention of CV events.
35
Q

Describe why there are differences on how patients will react to clopidogrel

A
  • 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
Q

Prasugrel

A
  • pro-drug, quicker onset

- greater, more predictable inhibition of ADP-induced platelet aggregation

37
Q

Why is Ticagrelor now seen as a better anti-platelet therapy?

A
  • different class of anti-platelet
  • direct acting
  • reversibly binds to P2Y12 receptor
  • more rapid onset of action
  • greater anti-platelet effect than clopidogrel
38
Q

What is the effect that nitrates have?

A
  • 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
Q

Describe how nitrates are introduced into the body?

A
  • sublingual or IV for rapid effect

- develop tolerance

Cardiovascular Block (16 decks)

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