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Cardiovascular (Annie) > Heart Attack > Flashcards

Heart Attack Flashcards

1
Q

What characterises chronic stable angina? (4)

A
  • fixed stenosis
  • demand led ischaemia
  • predictable
  • safe
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2
Q

what advice can be given when pain arises from chronic stable angina?

A
  • stop
  • site
  • GTN spray
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3
Q

whats is ACS?

What disease do ACS comprise?

A

= Acute Coronary Syndrome

= any acute presentation of coronary artery disease;

  • unstable angina
  • acute NSTEMI
  • STEMI

(covers a spectrum of diseases)

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4
Q

what are the 2 types of acute myocardial infarction?

A

1) ST elevation MI
(STEMI)
2) Non-ST elevation MI (NSTEMI)

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5
Q

what are the 5 pathogenetic stages of acute coronary syndrome?

A

1) normal
2) fatty streaks
3) atherosclerotic plaques
4) fibrous plaque
5) plaque rupture/fissure & thrombosis

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6
Q

what are the characteristics of acute coronary syndrome? (4)

- unstable angina/MI

A
  • dynamic stenosis
  • supply led ischaemia
  • unpredictable
  • dangerous
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7
Q

what is the main pathogenetic factor that occurs in ACS?

A

= spontaneous plaque rupturing

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8
Q

what factors affect plaque rupture/fissure?

A
  • lipid content of plaque
  • thickness of fibrous cap
  • sudden changes in intra-luminal pressure or tone
  • bending & twisting of an artery during each heart contraction
  • plaque shape
  • mechanical injury
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9
Q

what does vascular damage expose?

A
  • exposes tissue elements, e.g. sub-endothelial collagen.
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10
Q

what happens in response to vascular injury?

A

= PLATELET recruitment and adhesion at site of injury forming a monolayer.

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11
Q

when platelets undergo degranulation what do they release and generate?

A

Release = ADP & other activators

Generate = thromboxane A2 via cycloxyganse

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12
Q

what binds to platelet receptors which consequently results in platelet activation and hence platelet aggregation?

what do these activated platelets express and trigger?

A

ADH binds to platelet receptors.

express = adhesion receptors for leukocytes.

trigger = inflammatory cascade

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13
Q

what is platelet aggregation?

A

= the clumping together of platelets in the blood which eventually leads to the formation of a thrombus.

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14
Q

what 4 things in a history is indicative of a ST elevation MI?

A

1) severe crushing central chest pain
2) radiating to jaws, arms, especially left
3) similar to angina but more severe, prolonger & NOT received by GTN
4) associated with sweating nausea & vomiting

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15
Q

describe the differences between angina and MI in terms of duration, onset, severity, GTN and associate symptoms.

A

ANGINA;

  • 10mins duration
  • onset on exertion
  • usual severity
  • relived by GTN
  • no associated symptoms

MI;

  • 30min or longer duration
  • onset at rest
  • severe
  • not relived by GTNN
  • sweating, nausea and vomiting.
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16
Q

what changes would be seen in an ECG during an acute STEMI?

A

1) ST elevation
- more than 1mm elevation in 2adjacent limb leads
or
- more than 2mm elevation in 2 continuous pre-cordial leads

3) new onset bundle branch block (BBB)
3) T wave inversion
4) Q wave

17
Q

where is ST elevation seen in INFERIOR MI?

A

Leads II, III, aVF

18
Q

where is ST elevation seen in anterior MI?

A

V1-V6

19
Q

specifically, where is ST elevation seen in anteroSEPTAL MI?

A

V1-V4

20
Q

specifically, where is ST elevation seen in anteroLATERAL MI?

A

Leads I, aVL, V1-6

21
Q

what 2 cardiac enzymes could be used to diagnose an STEMI?

A

1) CK (creatinine kinase)
- peaks in 24hours but is non-specific

2) Tn (troponin)
- highly specific for cardiac muscle damage
- detecting tiny amounts of MI necrosis

22
Q

what 2 anti-platelet drugs should be given to treat STEMI?

A

1) aspirin, 300mg

2) clopidogrel, 300mg

23
Q

what are 3 indications for repercussion therapy (thrombolysis or PCI)?

A

1) chest pain suggestive of acute MI
- more than 20minutes less than 12hours

2) ECG changes
- acute ST elevation
- new LBBB

3) no contraindications

24
Q

what are 3 risks for thrombolytic therapy?

A

1) failure to re-perfuse
2) haemorrhage
- minor
- major
- intra-cranial haemorrhage
3) hyper-sensitivity

25
Q

why is it useless to undergo thrombolysis after 12hours?

A

because after 12hours, clot formation is hardened and won’t be able to be dissolved.

26
Q

what happens in PCI?

A
  • catheter with balloon at end is inserted through an artery
  • balloon is directed to blockage, where it is inflated, thereby pushing fatty tissue in narrow artery out of way to improve blood supply
  • a stent is inserted and balloon removed
27
Q

what 7 things are given as part of the early treatment fo STEMI.

A

1) analgesia = diamorphine IV
2) anti-emetic, IV = nausea & vomiting
3) aspirin 300mg & clopidogrel 300mg
4) GTN - if BP > 90mmHg
5) oxygen = if hypoxic
6) primary angioplasty (surgical repair or unblocking of blood vessel)
7) thrombolysis (if angioplasty is not available within 90 minutes)

28
Q

what are the 4 complications of acute STEMI?

A

1) death
2) arrhythmic complications
3) structural complications
4) functional complications

29
Q

what are arrhythmic complications associated with in an acute MI?

A

= ventricular fibrillation

30
Q

what is ventricular fibrillation?

A

= a rapid and disorder electrical ‘storm’ within the heart.

31
Q

what are the 8 structural complications associated with an acute MI?

A

1) cardiac rupture
2) ventricular septal defect
3) mitral valve regurgitation
4) left ventricular aneurysm formation
5) mural thrombus +/- systemic emboli
6) inflammation
7) acute pericarditis
8) dressler’s syndrome

32
Q

what are 4 functional complications associate with an acute MI?

A

1) ventricular dysfunction (left, right, both)
2) acute ventricular failure (left, right, both)
3) chronic cardiac failure
4) cardiogenic shock

33
Q

what are the 4 parts to the KILLIP classification?

A

1) no signs of heart failure
2) crepitations <50% of lung fields 17%
3) crepitations >50% of lung fields 38%
4) cardiogenic shock 81%

34
Q

what effect does NSTEMI have on artery occlusion and ST elevation?

A

= does NOT cause an acute occlusion

= and as a result has NO ST ELEVATION.

35
Q

what might an ECG show in a NSTEMI?

A

IT MAY BE NORMAL

36
Q

what does troponin mark?

A

1) embolization
2) microvascular circulation
3) myonecrosis
- preferable TnT or TnI

37
Q

what other conditions cause an elevated TnT?

A

1) CCF
2) hypertensive crisis
3) renal failure
4) pulmonary embolism
5) sepsis
6) stroke/TIA
7) pericarditis/myocarditis
8) post arrhythmias

38
Q

what receptor is expressed that allows for platelet aggregation?

A

= GP IIB/IIIa which fibrinogen will bind to

GP = glycoprotein

39
Q

what 3 things could be done to treat NSTEMI?

A

1) early coronary angiography & re-vascularisation
2) stents
3) people with stents use clopidogrel

Cardiovascular (Annie) (36 decks)

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