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PHASE 2 cardio conditions > acute coronary syndrome > Flashcards

acute coronary syndrome Flashcards

1
Q

what does acute coronary syndrome include

A

Umbrella term that includes:

  1. ST-elevation myocardial infarction
  2. Unstable angina
  3. Non-ST-elevation myocardia infarction
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2
Q

what is normal troponin an indication of

A

unstable angina

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3
Q

what is high troponin an indication of

A

NSTEMI

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4
Q

define unstable angina

A

A new onset of angina or deterioration in previously diagnosed stable angina.

Chest pain that occurs at rest, is not relieved by GTN and occurs more frequently and lasts for longer.

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5
Q

what does unstable angina require

A

usually requires immediate admission or referral to hospital

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6
Q

what is STEMI

A

Complete occlusion of a MAJOR coronary artery

This leads to full thickness damage of heart muscle

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7
Q

how is STEMI diagnosed

A

Diagnosed on ECG at presentation

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8
Q

what is NSTEMI

A

Partial occlusion of a MAJOR coronary artery or complete occlusion of a MINOR coronary artery
Causes partial thickness damage of the heart

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9
Q

how is NSTEMI diagnosed

A

Diagnosis made on troponin results

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10
Q

what may NSTEMI ECG show

A

ECG may show ST-depression and/or T wave inversion

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11
Q

pathology of acute coronary syndromes

A
  1. Rupture or erosion of the fibrous cap of a coronary artery atheromatous plaque
  2. Subsequent formation of a platelet-rich clot (thrombosis), inflammation and vasoconstriction produced by platelet release of serotonin and thromboxane A2
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12
Q

how does unstable angina differ to NSTEMI

A

in NSTEMIs the occluding thrombus is sufficient to cause myocardial damage and an elevation in serum markers of myocardial injury (troponin and creatine kinase)

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13
Q

do acute coronary syndromes always present with ST elevation

A

NO

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14
Q

ECG changes in unstable angina

A

normal or T wave depression

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15
Q

ECG changes in STEMI

A
  1. ST elevation and tall T waves
  2. Will produce pathological Q waves sometime after an MI
  3. There may be a new LBBB in larger MIs (WiLLiaM)
    V1 – W shape
    V6 – M shape
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16
Q

ECG changes in NSTEMI

A

A retrospective diagnosis

Will see ST depression and/or T wave inversion

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17
Q

ECG changes in infarction

A

ST depression

T wave flattening or inversion

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18
Q

what are Q waves evidence of

A

previous infarction

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19
Q

how do pathological Q waves differ to normal ones

A

are deeper and wider than normal (>35% QRS height and wider than one small square)

The larger the infarction is, the more likely it will result in pathological Q waves

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20
Q

what would a posterior STEMI ECG show

A

will show ST depression in V1 to V4 as the view of the heart on the ECG is inverted.

V7-V9 are additional leads that can be placed on someone’s back to check for a posterior MI

21
Q

main cause of acute coronary syndrome

A

Rupture of atherosclerotic plaque and consequent arterial thrombosis

22
Q

other causes of acute coronary syndromes

A
  1. coronary vasospasm without plaque rupture
  2. drug abuse (amphetamines, cocaine)
  3. dissection of the coronary artery related to defects of the vessel connective tissue
  4. thoracic aortic dissection
23
Q

investigations for acute coronary syndromes

A
  1. ECG
  2. Bloods
  3. cardiac enzymes
  4. CT angiography
24
Q

which blood tests to do for ACS (4)

A

FBC
U&E
Glucose
Lipids

25
Q

what do cardiac enzymes do

A

released into blood stream when cardiac muscle is damaged

26
Q

3 examples of cardiac enzymes

A
  1. Troponin T and I
  2. creatine kinase
  3. myoglobin
27
Q

describe troponin T and I

A

highly sensitive and specific markers of cardiac muscle injury but not diagnostic

Rise within 3-12 hours
Peak at 24-48 hours
Return to baseline by 5-14 days

28
Q

diagnostic criteria for troponin T and I

A

<14g/l normal = no MI

14-30 ng/l = possible MI

> 30ng/l = definite MI

29
Q

what does creatine kinase do

A

catalyses conversion of creatine and utilises ATP to create phosphocreatine (PCr) and ADP

30
Q

3 types of creatine kinase

A
  1. CK-MM
  2. CK-BB
  3. CK-MB
31
Q

where is CK-MM found

A

mainly in skeletal muscle

32
Q

where is CK-BB found

A

predominantly in the brain

33
Q

where is CK-MB found

A

predominantly in the heart

highly specific and sensitive, will peak earlier if reperfusion occurs

34
Q

how is CK-MB used to determine infarction

A

CK-MB rise within 3-12 hours of onset of pain and can be used to determine re-infarction as levels drop back to normal after 36-72 hours

35
Q

what do myoglobins do

A

Rises within 1-4 hours of onset of pain

Highly sensitive but not specific

36
Q

2 types of causes for raised troponin

A
  1. cardiac causes
  2. non cardiac causes
37
Q

5 cardiac causes for raised troponin

A
  1. Congestive heart failure
  2. Acute or chronic stable coronary artery disease
  3. Myocarditis (and endocarditis and pericarditis)
  4. Tachy/bradyarrhythmia’s
  5. Heart block
38
Q

8 non cardiac causes for raised tropnin

A
  1. PE
  2. Gram negative sepsis
  3. Severe pulmonary hypertension
  4. Renal failure
  5. COPD
  6. Diabetes
  7. Drugs
  8. Acute neurological events
39
Q

3 things to classify unstable angina

A
  1. cardiac chest pain at rest
  2. May have crescendo pattern (it gets worse and worse more readily)
  3. New onset angina
40
Q

what happens to untreated unstable angina

A

50% of patients with unstable angina will get an infarction within 30 days if left untreated

41
Q

diagnosis and investigations for unstable angina

A

History

FBC – anaemia aggravates it

Cardiac enzymes (troponin normal) – excludes infarction

ECG – ST depression when patient is in pain

CT Coronary angiography

Risk assessment (QRISK2) – if low risk do an elective stress test

42
Q

management options for unstable angina

A
  1. risk factor modification
  2. PCI & CABG
  3. anti platelet therapy
  4. anti coagulants
  5. nitrates
  6. beta blockers
  7. statins
  8. ACE inhibitors
  9. calcium channel blockers
43
Q

4 risk factor modifications for unstable angina

A

Stop smoking
Lose weight
Healthy diet
Exercise

44
Q

3 examples of anti coagulants

A
  1. heparin
  2. enoxaparin - LMWH
  3. Fondaparinux
45
Q

what does heparin do

A

interferes with thrombus formation at site of plaque rupture by inhibiting factors II (prothrombin), VII, IX and X and reduces risk of ischaemic events and death

46
Q

why is enoxaparin better than heparin

A

enoxaparin has better efficacy than unfractionated heparin

47
Q

what does Fondaparinux do

A

synthetic polysaccharide) inhibits factor Xa of the coagulation cascade and has a lower risk of bleeding than heparin

48
Q

differences between the 3 conditions

A

NSTEMI and unstable angina have similar management,

only difference is that an NSTEMI is an acute infarction and will not involve the whole of the heart wall like a STEMI.

Both are due to a narrowing of the coronary artery lumen rather than a total occlusion like a STEMI

49
Q

complications of CS (DARTH VADER)

A

Death
Arrhythmias
Ruptured septum
Tamponade
HF
Valve disease
Aneurysm of ventricle
Dressler’s syndrome – pericarditis and pericardial effusion after 2-12 weeks
Embolism
Reoccurrence of ACS

PHASE 2 cardio conditions (20 decks)

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