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Cardiovascular MBCHB2 > Lecture 23: Acute chest pain > Flashcards

Lecture 23: Acute chest pain Flashcards

1
Q

What are the symptoms of acute chest pain?

A

Chest pain +/- Shortness of Breath

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2
Q

What are some of the chest pain differentials?

A

Cardiac
- MI, Myocarditis, Pericarditis, HF

Vascular
- Aortic stenosis

Respiratory
- PE, Infection; Pneumonia, Bronchitis, COPD, Asthma, Pneumothorax

Vascular
- Aortic dissection

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3
Q

What are the investigations to make for diagnosis of acute chest pain?

A
  • History and examination
  • Blood tests; Full blood count, blood gases, troponin, D dimer
  • ECG
  • Radiology (CXR, CTPA)
  • Coronary angiogram
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4
Q

What are the two types of acute MI?

A

ST elevation MI (STEMI)

Non-ST elevation MI (Non-stemi)

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5
Q

What triggers a STEMI?

A

Full occlusion of CA

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6
Q

What triggers a non-stemi?

A

Very dynamic situation, can open, vasospasm, closed, clot

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7
Q

What is the pathophysiology of vascular occlusion?

A
  • Plaque fissure
  • Platelet adhesion
  • Platelet activation
  • Platelet aggregation

(Anti-platelet medications)

  • Thrombotic occlusion (LMWH + Thrombolytics)
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8
Q

What does non-STEMI lead to on ECG?

A

ST depression

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9
Q

What is non-STEMI initial management?

A
  • Pain relief (morphine, anti-emetic)
  • Nitrate (Coronary vasodilator)
  • Aspirin (+/- other platelets)
  • Beta-blockers
  • Low Molecular Weight Herapin (LMWH)
  • Stent
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10
Q

What is the initial treatment of STEMI MI?

A
  • Pain relief (morphine, anti-emetic)
  • Nitrate (Coronary vasodilator)
  • Aspirin (+/- other platelets)
  • Beta-blockers
  • Thrombolytic + LMWH
  • NB Stent (Urgent) (Current standard)
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11
Q

What was found when streptokinase and aspirin were given together?

A

Synergistic effect

i.e thrombolysis and aspirin

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12
Q

What are some thrombolytics?

A
  • Streptokinase
  • Alteplase (human t-PA)
  • Tenecteplase (t-PA variant) (More specific human types)
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13
Q

Describe the action of thrombolytics;

A

Plasminogen in blood (endogenous thrombolytic)
(Streptokinase activates)
Plasminogen binds to fibrin
(alteplase, reteplase - activates plasminogen on fibrin)
Plasmin produced on fibrin. Fibrin broken down.

Fibrin degredation products

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14
Q

When are thrombolytics given? and how are they given

A

Within 12 hrs of chest pain

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15
Q

Describe streptokinase;

A

Streptokinase

  • Streptococci-synthesised protein
  • Streptokinase-plasminogen complex
  • Renal excretion
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16
Q

Describe tenecteplase:

A

Tenecteplase

  • Bolus
  • Liver metabolised
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17
Q

What are the thromoblysis risks?

A

All:
- Bleeding
+ Local (To lure site)
+ Intracerebral

Streptokinase

  • Allergy / anaphylaxis
  • Hypotension
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18
Q

What are contraindications for thrombolysis?

A

Surgery
Bleeding

and many more

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19
Q

What are the anti-platelet agents?

A

Aspirin
Clopidogrel
Ticagrelor

20
Q

What is the action of aspirin?

A
  • Inhibits platelet aggregation
  • Anti-inflammatory
  • Analgesic
  • Anti-pyretic
21
Q

What is the mechanism of action for aspirin?

A

Inhibits platelet COX 1 (Irreversible)

  • Acetylates serine residue at active site
  • Arachidonic acid unable to access active site
  • Prostaglandin / thromboxane production inhibited (decreased bioavailability)

Aspirin metabolised to salicylic acid

22
Q

What is the secondary prevention of aspirin?

A

Secondary prevention

  • Vascular events
  • Mortality
23
Q

What vascular events does aspirin prevent?

A

CAD

  • MI
  • Chronic Angina

Stroke
Peripheral vascular disease

24
Q

What are aspirin side effects?

A

Upper GI effects

  • Reduced production of protective prostaglandin E2 (bicarb and mucous)
  • Dyspepsia, upper GI ulcers

Asthma (sensitive people)

25
What is the action of clopidogrel?
- Antithrombotic / antiplatelet drug (irreversible) - Absorbed -> CYP P450 metabolism -> active metabolite. - > Inhibits P2Y platelet receptor
26
What are the limits of clopidogrel?
Ceiling effect (50-60% platelet aggregation inhibition) Time and dose dependant
27
What are the side effects of clopidogrel?
- GI bleeding - Upper GI symptoms - Rash - Beware if concurrently on warfarin
28
When should you use clopidogrel?
- Acute coronary syndromes - Aspirin allergy - Vascular stening (b.c foreign material)
29
Write some notes on ticagrelor?
Efficacy > Clopidogrel - Reversible antagonist
30
Whats the risk of ticagrelor?
Dyspnoea | Bleeding
31
What are LMWH?
Take naturally occuring herapins which have varying KDA, and take the specific subset with LMW
32
How do LMWH do?
Inhibit factor Xa
33
When do you use LMWH?
Indications: - Non-STEMI - STEMI
34
What are the adverse effects of LMWH?
Bruising/bleeding sites - Intra-cranial - Injection sites - Gastro-intestinal loss - Epistasis Thrombocytopenia (Next year, autoimmune phenomenon)
35
What really increases the risk of bleeding?
``` Post MI - Fibrinolysis + - LMWH + - Antiplatelet agent ```
36
When do you use nitrates?
- Acute coronary disease | - Chronic angina
37
What are the potential mechanisms of nitrate administration?
Rapidly absorbed; - Oral - Intravenous - Sublingual - Transdermal
38
What are the pharmacodynamics of nitrates?
- Uncertain mechanism + Biotransformation + Denitration + Increased bioavailability/activity Nitric Oxide
39
What do nitrates do?
Vascular smooth muscle relaxation - Arterial Dilation (Coronary and Peripheral) - Veno dilation (decreased cardiac work)
40
What is nitrate tolerance?
Loss of haemodynamic and anti-anginal efficacy during sustained therapy
41
How can nitrate tolerance be prevented?
- Nitrate dosing | - Nitrate-free period
42
What are the mechanisms of action for beta blockers?
- Antagonise b adrenoreceptors - Reduced cardiac work - Negatively inotropic (acutely) - Negatively chronotropic
43
Whats the relative selectivity of metoprolol / atenolol?
B1 >>>> B2
44
Whats the differences of the various Beta blockers?
- Selectivity (B1 or B2) - Elimination (Renal vs Liver) - Half life - Solubility (water vs fat) - Additional properties / mechanisms
45
What beta blockers are used in an acute MI?
Metoprolol | Carvedilol
46
What are the potential adverse effects of beta blockers?
Resp. - Asthma exacerbation CVS - Hypotension - Bradycardia - CCF exacerbation - Vasospasm

Cardiovascular MBCHB2 (31 decks)

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