Cardio - ACS Flashcards

1
Q

what is the difference in pathophysiology in NSTEMI vs STEMI?

A

NSTEMI = incomplete occlusion of artery causing partial thickness death of myocardium

STEMI = complete occlusion of artery causing full-thickness death of myocardium

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2
Q

suggest modifiable and non-modifiable risk factors for MI

A

Non-modifiable:

  • increasing age
  • male gender
  • FHx of premature CHD
  • premature menopause

Modifiable:

  • smoking
  • HTN
  • hyperlipidaemia
  • DM
  • obesity/metabolic syndrome
  • physical inactivity
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3
Q

describe the typical presentation of MI

A

Symptoms:

  • dull retrosternal/epigastric chest pain (pressure/ aching/ burning/ squeezing)
  • pain is severe, occurs at rest and is ongoing >15 min
  • can radiate to L arm, shoulder neck or jaw
  • dyspnoea
  • nausea

Signs:

  • low-grade fever, pale and cool, clammy skin
  • hypo- or hypertension depending on extent of MI
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4
Q

in which pt group do MIs tend to present atypically?

A

diabetics

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5
Q

which investigations would you request in a pt with suspected MI?

A
  1. ECG
  2. Bloods:
    - troponin I & T: differentiate from stable angina
    - FBC: ?anaemia, leucocytosis common
    - CRP: inflammation
    - UandE: K+ and Mg+ can cause arrhythmias
    - eGFR: should be measured prior to starting ACEi
    - lipid profile: should be obtained at presentation as levels can change after 12-24hrs of acute illness
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6
Q

which ECG features are suggestive of acute MI?

A
  1. ST segment elevation or depression
  2. new Q waves
  3. T wave inversion
  4. new conduction defect
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7
Q

an ECG shows ST elevation in leads V3 and V4. What type of MI is this and which artery is likely affected? What is V1 and V2 also showed changes?

A

Anterior MI: LAD

If V1 and V2 affected, suggests proximal LAD occlusion also involving septum.

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8
Q

an ECG shows ST elevation in leads II, III and aVF. What type of MI is this and which artery is likely affected?

A

Inferior MI: 90% right coronary artery, 10% left circumflex artery

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9
Q

an ECG shows ST elevation in leads I and aVL. What type of MI is this and which artery is likely affected?

A

Lateral MI: left circumflex artery

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10
Q

an ECG shows ST elevation in leads V5 and V6. What type of MI is this and which artery is likely affected?

A

Lateral/apical MI: left circumflex artery or distal LAD

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11
Q

what is Wellen’s syndrome? what are the criteria?

A

Critical stenosis of proximal LAD artery, often progresses to devastating anterior wall MI. Usually require invasive therapy.

Criteria:

  • deeply inverted or biphasic T waves in leads V2-V3
  • Hx of anginal chest pain
  • normal or minimally elevated cardiac enzyme levels
  • ECG without Q waves or sig. ST elevation and with normal precordial R wave progression
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12
Q

describe your initial management of a pt with suspected MI

A
  1. A-E assessment
  2. cannulate and take bloods
  3. ECG
  4. O2 therapy and analgesia
  5. offer aspirin 300mg
  6. continue close clinical monitoring, inc. symptoms, pulse, BP, heart rhythm and O2 sats
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13
Q

what are the 2 main mechanisms for restoring patency of an occluded artery? when is each indicated?

A
  1. PERCUTANEOUS CORONARY INTERVENTION
    - MOA: immediate antiplatelet therapy (clopidogrel, prasgruel or ticagrelor)… insert balloon catheter through femoral or radial artery, inflate balloon at site of occlusion (balloon angioplasty) and insert stent… offer LMWH/UFH or bivalirudin
    - Preferred method if presentation within 12 hrs of Sx onset and can be delivered within 2 hrs of time when fibrinolysis could be given. Also used in pts with failed fibrinolysis (residual ST segment elevation on ECG 60-90 min after administration).
  2. FIBRINOLYSIS using THROMBOLYTIC DRUG
    - MOA: administration of thrombolytic drug + UFH/ LMWH (e.g. enoxaparin)/ fondaparinux.
    - For pts presenting within 12hrs of Sx onset if PCI cannot be delivered within 2 hrs of time when fibrinolysis could be delivered
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14
Q

how should pts with acute STEMI presenting >12 hr after Sx onset be managed?

A

Consider coronary angiography, with view to coronary revascularisation if indicated.

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15
Q

How should pts who have had an MI be managed in the long-term?

A
  1. Medications
    i) Anti-platelet agent: long-term low-dose aspirin (75 mg)
    ii) Beta-blockers (usually started IV within hrs of infarction to decrease mortality, cardiac arrest and re-infarction, then continued orally)
    iii) ACEi
    iv) statins
  2. Cardiac rehabilitation program, e.g. screen for depression, structured exercise and rehabilitation, long-term follow-up/review
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16
Q

suggest possible complications post-MI

A
  1. Arrythmias and cardiac arrest (most common cause of death post-MI) - Vfib or Vtach may be caused by infarction, reperfusion, K+ imbalance, etc.
  2. Re-occlusion of vessel (esp. following fibrinolysis) or recurrent infarction in separate territory
  3. LV dysfunction and HF - usually due to myocardial damage
  4. L ventricular aneurysm - wall stress and infarct expansion
  5. ventricular septal rupture or free wall rupture - uncommon but can be lethal
  6. Pericarditis