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
what do cardiac enzymes do
released into blood stream when cardiac muscle is damaged
26
3 examples of cardiac enzymes
1. Troponin T and I 2. creatine kinase 3. myoglobin
27
describe troponin T and I
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
diagnostic criteria for troponin T and I
<14g/l normal = no MI 14-30 ng/l = possible MI >30ng/l = definite MI
29
what does creatine kinase do
catalyses conversion of creatine and utilises ATP to create phosphocreatine (PCr) and ADP
30
3 types of creatine kinase
1. CK-MM 2. CK-BB 3. CK-MB
31
where is CK-MM found
mainly in skeletal muscle
32
where is CK-BB found
predominantly in the brain
33
where is CK-MB found
predominantly in the heart highly specific and sensitive, will peak earlier if reperfusion occurs
34
how is CK-MB used to determine infarction
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
what do myoglobins do
Rises within 1-4 hours of onset of pain Highly sensitive but not specific
36
2 types of causes for raised troponin
1. cardiac causes 2. non cardiac causes
37
5 cardiac causes for raised troponin
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
8 non cardiac causes for raised tropnin
1. PE 2. Gram negative sepsis 3. Severe pulmonary hypertension 4. Renal failure 5. COPD 6. Diabetes 7. Drugs 8. Acute neurological events
39
3 things to classify unstable angina
1. cardiac chest pain at rest 2. May have crescendo pattern (it gets worse and worse more readily) 3. New onset angina
40
what happens to untreated unstable angina
50% of patients with unstable angina will get an infarction within 30 days if left untreated
41
diagnosis and investigations for unstable angina
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
management options for unstable angina
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
4 risk factor modifications for unstable angina
Stop smoking Lose weight Healthy diet Exercise
44
3 examples of anti coagulants
1. heparin 2. enoxaparin - LMWH 3. Fondaparinux
45
what does heparin do
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
why is enoxaparin better than heparin
enoxaparin has better efficacy than unfractionated heparin
47
what does Fondaparinux do
synthetic polysaccharide) inhibits factor Xa of the coagulation cascade and has a lower risk of bleeding than heparin
48
differences between the 3 conditions
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
complications of CS (DARTH VADER)
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