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T year CVS > Acute Coronary Syndrome / MI > Flashcards

Acute Coronary Syndrome / MI Flashcards

1
Q

what is the definition of ACS

A

a clinical syndrome of acute ischaemia chest pain either at rest or with a crescendo pattern of pain on minimal exertion, associated with ECG change of ischaemia.

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2
Q

what does ACS include (3)

A

STEMI
NSTEMI
unstable angina

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3
Q

how is STEMI distinguished

A

presence of persistant ST elevation

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4
Q

what is different in NSTEMI compared to angina

A

rise in troponin or creatinine kinase (serum markers of myocardial injury)

(negative serum troponin at 6-12 hours after onset of chest pain suggests unstable angina rather than NSTEMI).

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5
Q

what is the difference between stable angina and unstable angina?

A

occurs at lower level of exertion. if occurs at rest its more severe.

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6
Q

what is ACS caused by?

A

atherescloertoic narrowing of the coronary arteries.

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7
Q

what is mechanism of all ACS?

A

rupture or erosin of fibrous cap of a coronary artery plaque
with subsequent formation of a platelet rich clot and vasoconstriction produced by platelet release of seratonin and thromboxane A2.

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8
Q

what is a myocardial infarction due to?

A

rupture of an atheresclerotic plaque, followedy by thromobosis and inflammation.

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9
Q

what are the two types of acute MI?

A

1) Transmural (Q waves) area of ischaemia necrosis extends throughout the whole thickness of the heart muscle from endocardium -> myocardium -> epicardium. leaves permanent Q waves on ECG.

usually result of complete occlusion of area’s blood supply. associated with atheresclerosis involving major coronary artery and can be subdivided into anterior, posterior and inferior

2) non transmural ( non Q waves) - area of ischemic necrosis that does not extend through the full thickness of myocardial wall segment. it is the endocardial and subendocardial zoens of hte myocaridal wall segment that are the least perfused regions of the heart and most vulnerable to condiition of ischameia.

occurs as the occluded artery is a relatively small branch or becuase there is good collatoeral flow around the occluded vessel

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10
Q

what do you see on an ECG for NSTEMI?

A

T wave invresion
ST depression
no new pathalogical Q waves

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11
Q

symtpoms of acute MI (8)

A
  1. acute central chest pain (more severe than angina and lasts for hours and occurs at rest)
  2. pain which radiates to arms, neck, jaw, back and epigastrium
    3, dysopnea
  3. nausea / vomiting
  4. sweating (diaphoresis)
  5. restlessness
  6. palpitations
  7. 20% have no pain (silent infarctions) e.g. elderly, diabetic or post tranpsnat pateints. may present with hypotension, syncope, arrhythmias, pulmonary oedema, epigastric pain, acute confusion state or stroke.
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12
Q

sigsn of acute STEMI

A

may present with no physical signs unless ocmplciations

  1. anxious,
  2. pale
  3. grey
  4. increased BP
  5. Signs of heart fialure.
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13
Q

what blood investigaitons would you do?

A

FBC
U&E
Glucose
Lipids

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14
Q

what doy ou see in an ECG for STEMI?

A

ST segment elevation (1mm in limb leads and 2mm in 2 contingous chest leads

New LBBB is also and indicator of acute MI

T wave flattening or inversion

Pathological Q waves (broad > 1mm) and deep (> 2mm or >25% of r wave) which are aseen once full-thickness infarction has occured.

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15
Q

where is the infarct if ECG changes are seen in leads II, III or AvF?

A

inferior MI

RCA

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16
Q

where is the infarct if ECG cahgnes are seen in V2 - V4?

A

anterior septal MI

LAD

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17
Q

where is the infarct if ECG changes are seen in v5 - v6?

A

lateral wall MI

LCX

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18
Q

where is the infarct if R waves in V1 and V2, ST depression in V1- V3

A

posterior MI

RCA

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19
Q

what is indiciative of a posteiror MI + RBBB

A

RSR in V1 instead of an rSR

20
Q

when are cardiac markers done after admission?

A

0h
6h
12hrs after admission

21
Q

what are the levels of increase of troponin T and I?

A

increase within 3-12 hours from onset of chest pain.
peak at 24-48 hours
returns to baseline over 5-14 days.

22
Q

what are the levels of CK?

A

creatine kinase produced by skeletal muslce and brain. less sensitive than troponin.

CK-MB is specific for heart muslce damage. and is proportional to infarct size.

serum levels increase iwthin 3-12 hours from onset
reaches peak within 24 hours
and then retursn to baseline in 3-4 days.

USEFUL for new episode > 3 days after first.
CK-MB would have fallen to baseline after first episode and hence show a sharp rise during the second episode.

23
Q

when is AST and LDH used?

A

rarely used because serum levels remain elevated for upt o 10 days after an infarct. but can be used after presenting days after episode of chest pain.

24
Q

what do you see in a CXR?

A

should be requested but should not delay treatment/
1. cardiomegaly
2. pulmonary oedema
3, widended mediastinum (aortic rupture)

25
Q

what do you need for the diagnosis of an acute MI?

A

rise and fall in troponin and CK-MB
accompaniend iwth at least one of the following:
1) symtposm of ischameia
2) ECG changes of new ischeamia (new LBBB or ST/T changes)
3) development of pathological Q waves
4) coronary artery intervention (e.g. coronary angiopalsty)
5) imaging evidence of new loss of viable myocardium

26
Q

DDXs for ST elevation?

A

1) saddle shaped ST in pericarditis
2) high take-off
3) ventricular aneurysm

27
Q

acute management of ST elevation.

A

1) Oxygen 2-4L aim for Sao2 > 95% (caution if CODP)
2) brief history and examinatino (12-lead ECG, BP, bloods (cardiac enzymes and FBC)
3) aspirin 300mg PO unesls already given followed by 75 mg daily OR clopidogrel 300mg PO (followed by 75mg daily)
4) morphine 5-10 mg IV + metoclorproime 10mg IV
5) GTN sublingualy 2 puffs or 1 tablet PRN
6) primary PCI or thromoblysic with daleparin
beta blockers e.g. Atenalol 5mg IV (unless asthma or LVF)

28
Q

what should the time be for door to needle thrombolyic adminstration
and door-to-balloon?

A

30 minutes

door to balloon is 90 minutes.

29
Q

what are the aboslute contraindications for thromobolysis?

A

any active bleeding from any site in the body
pregnancy
any recent history of heamorrhagic stroke
taking warfarin

30
Q

what are the relative risks of thrombolysis

A

acute liver disease

peptic ulcer disease

31
Q

where are ACEi in ht eline of treatment

A

reduce mortality and prevent development of heart fialure and should be started on the first day after MI.

32
Q

what do you consider in diabetic patients?

A

sliding scale of insluin partilculy if blood glucose is elevated.

33
Q

MONA in hospital

A

morphine
oxygen
nitrates
asprin

34
Q

what do you do in a STEMI?

A

1) primary angioplasty or thrombolysis if no contraindications
2) beta blockers (atenolol 5mg unless contraindications)
3) CXR
4) ACEi
5) clopidogrel 300mg

35
Q

what do you do in an NSTEMI?

A

beta blockers (atenlol unless contraindications - No PCI or thormoblyiss)
LMWH
IV nitrates
asses for low risk of high risk and treat appropriately.

36
Q

how do you assess ofr low risk in NSTEMI and what do you do?

A

no further pain
flat or inverted T
normal ECG
negative troponin

discharge if repeat troponin is negative (<0.2) after 12 hours.

37
Q

how do you assess high risk in NSTEMI and what do you do?

A

persistatn or recurrent ischaemia
ST depression
diabetes
increased troponin

infusion of glycoprotein 2b/3a antagonis
add clopidogrel.

38
Q

what should pateints with NSTEMI be considered for?

A

PCI or coronary angiography unless contraindicated.

39
Q

what do you give after a PCI?

A

bare metal stent = clopidogrel for 1 month

drug eluting stent = clopidogrel for 1 year due to risk of in-stent thrombosis.

40
Q

what does post MI primary care involve?

A

smoking habits
blood pressure
full lipid profile (cholestorl will be lower than usual for 6 weeks post MI)

41
Q

what interventiosn can you do?

A

cardiac rehabilitaiton
stop smoking
dietary advice with weight control if indicated
control BP - treatment threshold is 140/90

42
Q

wehn should beta blockers be given?

A

in apteints with preserved left ventricular function who are asymptomatic should not be routeinely offered treamtent with beta blockes.

43
Q

what are complciatoisn of MI?

A

1) pericarditis - 2-3 days after transmural MI. (fibrin on surface of pericardium manifests as pain and fever, rubbing of inflammed pericardium manifests as rub
2) ventricular aneurysms (LV if anteiror MI) acute presentation after MI with persisting ST elevation, shock hand a PSM suggestive of acute MR if LV. warrants an eco
3) Dressler’s syndrome - fever, pleurtic pain, pericardial effusion) - occurs weeks to onths aften an MI. give NSAIDs corticosteroids.
4) Arrhytmias - presents with syncope and palpiatations. a 24 hour/72 hour tape must

44
Q

how would you manage complications?

A 
Aiwrays 
Breathing - high flow O2 NRBM 
circulation - give fluids cautiosly since cardiogenic shock, give inoptropes 
offload with diuretics (frusemide IV) 
strict input/output 
fluid restriction 
intra aortic blaoon pump 
urgent cardiothoracic referral
45
Q

how does aspirin work?

A

antiplatelt action by inhibitin the production of thromboxane A2. it irreversibly inactivates COX1 & COX2 by acetylation.

46
Q

what are the side effects of oxygen

A

dry mucosa.

T year CVS (5 decks)

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