MI/ACS Flashcards

1
Q

Fixed RFs for ACS

A

Age
Gender
FMx (genetics)

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2
Q

Most common cause of stable angina

A

Atheroma

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3
Q

What is stable angina?

A

Clinical manifestation of ischaemia due to obstructed blood flow. Pain is relieved after <5mins when resting

‘Induced by effort and relieved by rest’

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4
Q

What else, besides exercise, can bring on symptoms of angina?

A
Mental and emotional stress
Sexual activity
Tachycardia from any source
Anxiety
Fever
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5
Q

Primary prevention of angina

A

Reduce any RFs related to IHD

Maintain an idea blood pressure (<140/80)

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6
Q

Secondary prevention of angina

A

Patient education RE healthy lifestyle

Antiplatelet therapy indefinitely

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7
Q

Investigations to consider in Angina with rationale

A

ECG - may be normal between attacks but may show ST depression during an attack. This is indicative of ischaemia

Hb - anaemia means the heart has to work harder which may exacerbate angina or cause it without coronary obstruction

Fasting lipid profile - Elevated LDL = increased risk

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8
Q

Typical angina symptoms

A

Pain brought on by exercise or stress
Relived by rest or GTN
Anterior chest ‘squeezing’

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9
Q

Pt with diagnosis of angina is not able to tolerate her B-blocker. What can you prescribe?

A

Calcium Channel Blocker

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10
Q

When would a long acting nitrate be prescribed in angina?

A

When the pt cannot tolerate BB or CCB

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11
Q

What should be done if the pt is still symptomatic after LAN, BB and CCB?

A

Consider revasc. w/ PCI or CABG depending on pt

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12
Q

Differentiating factor between angina and unstable angina

A

UA involves prolonged (>20mins) pain at rest, angina of increasing freq. or that occurs after a recent MI

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13
Q

Most common cause of UA

A

Coronary artery narrowing due to thrombus development on a disrupted atherosclerotic plaque

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14
Q

Difference between NSTEMI and UA

A

NSTEMI involves occluding thrombus which leads to myocardial necrosis and increase in cardiac enzymes

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15
Q

Primary prevention of CAD

A

Lifestyle changes
Statin therapy
Antiplatelet therapy

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16
Q

Presentation of unstable angina

A
Positive RFs in history
Increasing severity of CP
Increasing freq. of CP
Dyspnoea
S4 heard (indicates reduced myocardial relaxation due to ischemia)
17
Q

Investigations to order in UA plus rationale

A

ECG - obtained and analysed within 10 mins of CP presentation. May be normal or have transient ST depression or T wave inversion. If the ECG is not diagnostic but the pt remains symptomatic then think ACS

Troponin assay - Excludes MI if not elevated

FBC (Hb) - Check for anaemia

BM - Should be normal but if elevated then an assessment for diabetes is reqd.

U+Es - Should be normal. Reqd to establish predictor for mortality

Lipid profile - recommended for risk stratification

Coagulation profile - to establish baseline results as some treatment may affect the coag

CXR - to exclude mediastinal changes

18
Q

UA DDx

A

Stable Angina
STEMI
NSTEMI
Heart Failure

19
Q

Management of Unstable Angina

A

Low risk:
Aspirin + Clopidogrel + Analgesia + B-Blocker + lifestyle changes

Stabilised high risk:
Manage with angiography + lifestyle changes + anti platelet therapy + ACEi +

20
Q

Clinical presentation of an MI

A
Severe crushing CP > 20 mins
No relief w/ GTN or rest
CP radiate to neck, jaw and arm
Dyspnoea, fatigue, syncope
Px is pale and clammy
Thready pulse
Vomiting
21
Q

Which group of patients must be closely monitored in MI history taking?

A

Diabetics due to silent MIs

22
Q

Which other conditions can cause ST elevation?

A

ELAVATION

Electrolyte abnormalities
Left bundle branch block
Aneurysm of left ventricle
Ventricular hypertrophy
Arrhythmia disease (Brugada syndrome, ventricular tachycardia)
Takotsubo/Treatment (iatrogenic pericarditis)
Injury (myocardial infarction or cardiac contusion)
Osborne waves (hypothermia or hypocalcemia)
Non-atherosclerotic (vasospasm or Prinzmetal’s angina)

23
Q

ECG findings weeks after an MI

A

Presence of Q wave
T wave inversion sometimes
T wave flattening

24
Q

Bloods to order in MI

A

Serum lipids
Glucose
UEs
Cariac Biomarkers

25
Q

DDx in MI

A
UA
NSTEMI
AAA
PE
Pneumothorax
Pneumonia
GORD
Anxiety
26
Q

Management in suspected MI

A

Aspirin + O2
Analgesia
GTN

27
Q

Management of unstable MI

A
Emergency revasc. 
Anticoagulation (abciximab + enox./hep)
Aspirin
Analgesia
O2
Glucose control
Inotrope
28
Q

Subsequent management of stable post MI pt

A
Aspirin
Beta Blocker
ACEi
Statin
Lifestyle changes
29
Q

Which vessel and aspect of the heart is affected if there are ST elevations in leads II,III and aVF?

A

Right Coronary Artery and Inferior aspect

30
Q

Which vessel and aspect of the heart is affected if there are ST elevations in leads I, aVL, V5+6?

A

Left circumflex and anterolateral aspect

31
Q

Which leads represent the LAD and anteroseptal aspect of the heart?

A

V2-4

32
Q

Which leads and aspect do V2-6 represent?

A

Anterior aspect and left main stem

33
Q

Which leads represent the posterior aspect + RCA

A

V1/2/3

34
Q

Lead placement in ECG

A
V1: 4th ICS RSE
2: 4TH ICS LSE
3: Midway V2-4
4: 5th ICS MCL
5: Midway V4-6
6: 5th ICS MAL
R: R WRIST
Y: L WRIST
G: L ANKLE
B: R ANKLE
35
Q

Indication of absent P waves

A

AF

SAN block

36
Q

Indication of biphasic P waves / peaked P waves

A

Left Atrial Hypertrophy / Right atrium Hypertrophy

37
Q

What is the indication of deep ST waves in leads 1-3

A

True Posterior MI

Rememebr the posterior leads are on the back so the ECG is inverted but it’s still an ST rise