Cardiovascular (Annie) > Heart Attack > Flashcards

Heart Attack Flashcards

(39 cards)

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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?

Study These Flashcards
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?

Study These Flashcards
A

Leads II, III, aVF

18
Q

where is ST elevation seen in anterior MI?

19
Q

specifically, where is ST elevation seen in anteroSEPTAL MI?

20
Q

specifically, where is ST elevation seen in anteroLATERAL MI?

Study These Flashcards
A

Leads I, aVL, V1-6

21
Q

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

Study These Flashcards
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?

Study These Flashcards
A

1) aspirin, 300mg

2) clopidogrel, 300mg

23
Q

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

Study These Flashcards
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?

Study These Flashcards
A

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

25
why is it useless to undergo thrombolysis after 12hours?
because after 12hours, clot formation is hardened and won't be able to be dissolved.
26
what happens in PCI?
- 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
what 7 things are given as part of the early treatment fo STEMI.
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
what are the 4 complications of acute STEMI?
1) death 2) arrhythmic complications 3) structural complications 4) functional complications
29
what are arrhythmic complications associated with in an acute MI?
= ventricular fibrillation
30
what is ventricular fibrillation?
= a rapid and disorder electrical 'storm' within the heart.
31
what are the 8 structural complications associated with an acute MI?
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
what are 4 functional complications associate with an acute MI?
1) ventricular dysfunction (left, right, both) 2) acute ventricular failure (left, right, both) 3) chronic cardiac failure 4) cardiogenic shock
33
what are the 4 parts to the KILLIP classification?
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
what effect does NSTEMI have on artery occlusion and ST elevation?
= does NOT cause an acute occlusion | = and as a result has NO ST ELEVATION.
35
what might an ECG show in a NSTEMI?
IT MAY BE NORMAL
36
what does troponin mark?
1) embolization 2) microvascular circulation 3) myonecrosis - preferable TnT or TnI
37
what other conditions cause an elevated TnT?
1) CCF 2) hypertensive crisis 3) renal failure 4) pulmonary embolism 5) sepsis 6) stroke/TIA 7) pericarditis/myocarditis 8) post arrhythmias
38
what receptor is expressed that allows for platelet aggregation?
= GP IIB/IIIa which fibrinogen will bind to GP = glycoprotein
39
what 3 things could be done to treat NSTEMI?
1) early coronary angiography & re-vascularisation 2) stents 3) people with stents use clopidogrel
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