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Flashcards in Acute coronary syndromes. Deck (101):
1

What do we tell someone with angina to do to keep themselves safe?

Stop, sit and spray.

2

What is an acute coronary syndrome? What does it cause?

Acute presentation of any coronary artery disease including unstable angina and evolving MI. Both have a common underlying pathology.
It is a dynamic stenosis causing either subtotal or complete occlusion.
Causes demand led ischaemia.
Also includes sudden death.

3

What is angina brought on by?

Exercise, cold, emotions, heavy meals.

4

What is angina relieved by?

Rest and GTN.

5

What are the symptoms of angina?

Chest pain that may radiate.

6

What two types of angina do we have and what are they?

Stable - exercise exacerbated, relieved by rest.
Unstable - increasing severity and frequency. Happens at exercise or at rest and gives a great,y increased chance of MI.

7

What two types of MI are there and what are the differences on ECG?

STEMI - ST elevation. QRS doesn't come back to baseline.
NSTEMI - without ST elevation. May have no electrical disturbance and so a normal ECG. Could also have a depressed or Inverted ST.

8

What treatment does a STEMI require and what is the time scale?

PCI - door to needle time 90 mins.

9

What symptoms do we get with a fatty streak?

Clinically silent.

10

What syndromes do we get with atherosclerosis plaques and fibrous plaques of the coronary arteries?

Angina.

11

What symptoms do we get with plaque rupture fissure and thrombi of coronary arteries?

Acute coronary syndromes.

12

What factors can affect coronary plaque rupture and fissuring?

Sudden changes in intraluminal pressure of tone.
Bending and twisting of an artery during each heart contraction.
Lipid content of plaque.
Thickening of fibrous cap.
Plaque shape.
Mechanical injury.

13

What is the central pathway of platelet activation?

Initiation --> Activation --> activator release, aggregation and inflammation --> vascular blockage --> acute MI, stroke or death.

14

How can the platelet cascade activation be stopped?

By effective management of platelet activation over time.

15

What can an MI lead to in 25% of people?

Heart failure.

16

Where does an MI radiate in a lot of patients?

Especially the left arm. Also jaw and right arm.

17

What type of pain do we get with cardiac chest pain?

Gripping, squeezing, heavy and crushing.

18

What are the steps in management of angina?

Modify risk factors.
Aspirin.
Beta blockers.
Nitrates.
Possibly long acting calcium antagonist, especially if there is a contraindication to beta blockers.
Potassium channel activator if it's still not controlled.

19

What are the duration differences between MI and angina?

Angina 10 mins vs MI 30 mins or longer.

20

What are the onset differences between MI and angina?

Angina at exertion and MI at rest.

21

What are the severity differences between MI and angina?

Angina - usual pain.
MI - more severe.

22

What are the associated symptom differences between MI and angina?

Angina - usually none.
MI - nausea vomiting and sweating.

23

What do we see on an ECG for angina?

May be normal or may show ST depression or inverted T waves from a past MI.

24

What else can we do if an angina ECG is normal?

Consider an exercise ECG.

25

At what time in an MI do we see ST elevation?

First few hours.

26

At what time in an MI do we see Q wave formation and T wave inversion?

The first day.

27

At what time in an MI do we see Q waves +\- inverted T waves?

With an old MI.

28

What must we see on an ECG in order to diagnose a STEMI?

Greater or equal to 1mm ST elevation in 2 adjacent limb leads. Or at least 2mm in at least 2 contiguous precordial leads. Or new onset bundle branch block.

29

What blood tests do we do for MI?

FBC, U and E, glucose and lipids.
Cardiac enzymes.
Myoglobin.

30

When do we see myoglobin in blood tests for MI, what does it mean?

Rise within 1-4 hours of onset of chest pain.
It is sensitive but not specific.

31

What is our differential for an MI?

Angina, myocarditis, aortic dissection, PE and oesophageal reflux/spasm.

32

What might cardiac enzymes be like on presentation and what does this mean for our diagnosis?

May be normal initially and we may not have time to wait for them and must diagnose before this.

33

What two cardiac enzymes are we interested in?

CK - creatinine Kinase.
TnT- troponin T.

34

Where do we find creatinine kinase and what times do we find it in blood post MI?

Heart, skeletal muscle and brain.
Peaks within 24 hours.

35

Why do we use at TnT as a marker for MI?

It is highly specific for cardiac muscle damage. Can detect tiny amounts of myocardial necrosis. It is a marker for cardiac damage.

36

What else can TnT be raised in other than MI?

PE, sepsis, renal failure, CCF, hypertensive crisis, stroke TIA, pericarditis, myocarditis or post arrhythmia.

37

What do patients with chest pain and a raised troponin get?

ECG.

38

What early treatment of an MI do we give?

MONAC.
DiaMorphine etc. with antiemetic. IV.
Oxygen if hypoxic.
Nitrates if BP over 90 mmHg.
Aspirin 300mg chewable or oral dispersible.
Clopidogrel 300mg.

Thrombolysis if PCI is not available in 90 mins.

39

What are side effects of GTN?

1 in 10 get a headache.
Drops BP.
GTN syncope.

40

How long can aspirin and clopidogrel be continued in patients ST elevation acute coronary syndromes?

Up to 4 weeks.

41

What is reperfusion therapy?

Thrombolysis or PCI.

42

What are the indication for reperfusion therapy?

Chest pain suggestive of MI for more than 20 mins, less than 12 hours.
Acute ST elevation or new bundle branch block.
No contraindications.

43

What are the early risk of thrombolysic therapy?

Failure to reperfuse.
Haemorrhage.
Hypersensitivity.

44

What are the complications of MI?

Death.
Arrhythmias.
Structural complications.
Functional complications.
Ischaemia, angina, reinfarction, infarct extension, embolism

45

What are arrhythmic complications following MI?

Atrial or ventricular from damage of either node.

46

What are structural complications following MI?

Cardiac rupture, ventricular septal defect mitral regurg.
Aneurysms, mural thrombus, inflammation, acute pericarditis, Dressler's syndrome.

47

What is Dressler's syndrome?

Secondary form of pericarditis that occurs in the setting of injury to the heart or pericardium.

48

What are functional complications following MI?

Ventricular dysfunction.
Acute HF.
Chronic cardiac failure.
Cardiogenic shock.
Valvular dysfunction from papillary muscle rupture.

49

What are the killip classifications? Which are the most common?

Describes in hospital mortality.
1. no signs of HF.
2. Crepitations under half of lung fields.
3. Crepitations over half.
4. Cardiogenic stock.

4 most common by far and get less with lower number.

50

What routine observations do we do post MI?

Cardiac monitor. Pulse, BP, heart sounds, murmurs, crepitations, fluid balance and urine output. Speak to patient, see if they feel well.

51

What is the TIMI risk factor assessment for ACS?

Score 1 point for each.
Over 65 years old.
3 risk factors.
Prior stenosis of 50% or more.
ST segment deviation on presenting ECG.
At least 2 anginal events in last 24 hours.
Use of aspirin in last 7 days.
Elevated TNT CK etc.

52

What are troponins?

Tiny repeating protein units in heart fibres.
TnT
TnI
tnC.

53

What are other names for minimal cardiac damage?

Infarctlet or necrosette.

54

What are we measuring with troponins?

Embolisation, micro vascular circulation and myonecrosis.
Increases as embloli amount increases.

55

What are the different levels of cardiac enzymes with:
1. ACS with unstable angina?
2. ACS with myocyte necrosis?
3. ACS with clinical MI?

1 troponins and CKmb undetectable.
2. Troponins elevated, TnT under 1.0 ng/ml
3. TnT over 1. +/- raised CK or accuTn 1 over 0.5 ng/Ml.

56

What are the differences in ventricular function between unstable angina and clinical MI?

Angina - no measurable LV dysfunction.
MI - systolic dysfunction and LV dilatation.

57

What should any troponin rise be classified as?

An MI.

58

What are the new clinical classifications of MI?

1. Spontaneous MI related to ischaemia from a primary coronary event e.g. Plaque rupture.
2. MI secondary to O2 imbalance in supply and demand.
3. Sudden unexpected cardiac death.
4a. MI associated with PCI.
4b. MI associated with documented in stent thrombosis.
5. MI associated with CABG surgery.

59

When should patients with non ST elevation acute coronary syndromes undergo early coronary angiography and reVascularisation?

When they have a medium or high risk of early recurrent CVS events.

60

What should patients with STEMIs that have had thrombolysis be considered for?

Early coronary angiography and revascularisation.

61

What four categories of anti platelet drugs do we have?

ADP antagonists.
COX inhibitors.
Phosphodiesterase inhibitors.
GP IIb/IIIa inhibitors.

62

What three ADP antagonist drugs do we use?

Triclopidine.
Clopidogrel.
Prasugrel

63

What COX inhibitor drugs do we use?

Aspirin.

64

What Phosphodiesterease inhibitor drugs do we use?

Dipyridamole

65

What GP IIb/IIIa inhibitor drugs do we use?

Tirofiban.
Eptifibatide.
Abciximab

66

What other things do we use clopidogrel for in Tayside and for how long?

Any drug eluding stent - 1 year.
ACS medical treatment - 3 months.
ACS bare metal stent - 3 months.
Elective PCI - 3 months.
STEMI and no PCI - 4 weeks.
Aspirin intolerant - indefinitely.

67

How long are MI's normally discharged after?

4-6 days.

68

What pre discharge checks must we do with the patients post MI?

Feeling well? know what happened? Know what to expect? Understand their drug therapy?

69

What are the 4 phases of cardiac rehab?

1- in patient.
2- early post discharge period.
3- structured exercise prog.
4- long term maintenance.

70

What is heartatab?

Combo of drugs e.g. Aspirin/clopidogrel, beta blocker, ace inhibitor and a statin.

71

When are troponins usually raised?

4-6 hours after MI.

72

What are the biochemical events in the first few seconds of MI?

Reduced available oxygen and reduced ATP production.

73

What are the biochemical events in the first few minutes of MI?

ST segment changes and intracellular acidosis.
Depletion of energy stores, cell swelling, inhibition of glycolysis, severe reduction of ATP and mitochondrial swelling.

74

What are the biochemical events in the onset of irreversible damage in the first few minutes of MI?

Loss of metabolic control and loss of mitochondria.

75

What are the biochemical events in the onset of irreversible damage in the first few hours of MI?

Disintegration of myofibrils, disruption of cell membranes, cell auto lysis, cell death, tissue necrosis and leakage of enzymes and other macromolecules.

76

What is the difference between CK and CKMB?

CK in all the different places.
CKMB in cardiac muscle alone.

77

How do use CK to diagnose MI's?

Increased total CK and increased percentage of CKMB.
The diagnostic threshold is only 6%.

78

When is there a detected rise in CKMB?

8-12 hours post MI.

79

When should we initiate beta blockers and what patients should we exclude?

First 24 hours after event.
Exclude:
HF
Low output state
Those at increased risk of cardiogenic shock

Contraindications: 1st deg AV block (over 0.24 seconds) 2nd or 3rd heart block and reactive airway disease.

80

What two drugs do we use for thrombolysis?
Which is more common and why?

Streptokinase and TPA (alteplase).
TPA as there are less allergy problems, better results and lower risk of cerebral haemorrhage.

81

If a patient has an MI more than 90 mins from the hospital?

Start thrombolysis within 30 mins.

82

How long do cardiac troponins stay elevated for?

At least 7 days.

83

What are the levels of troponins like in healthy blood?

Negligible making it very easy to spot an increase even if it's small.

84

What is the relationship of troponin level to damage level?

The higher the troponin level the greater the damage.

85

What are the contraindications for thrombolysis?

Trauma or haemorrhage.
Recent surgery within the last 2 weeks.
Recent strokes 6 months.
Sever hypertension over 200/120
Known active peptic ulcer.
Traumatic CPR.
Streptokinase more than 5 days ago but less than 2 years.
Proliferation retinopathy.
On anticoags already.
Cardiogenic shock.

86

What increases the risk of VT after MI and what kinds of HR do we see?

Higher risk with more LV damage and also generally in first two days post MI.
May only have HR of 140.

87

When can a ventricular septal perforation happen post MI and what will we find with the patient?

In the first few days.
Patient initially well, then has a drop in BP and a new murmur. Deteriorates rapidly after this.

88

What do we see with mitral regurg and papillary wall rupture post MI?

Very uncommon. Very unwell very quickly.
Will have sudden flash oedema.

89

What is the second or third most common complication?

Ventricular free wall rupture. Usually deadly.

90

How is morphine related to pulmonary oedema?

It can help as it vasodilates but we need to watch with already saggy BP.

91

What does a intra-aortic balloon pump do?
Where is it inserted?

Helps with afterload and preload. Helps push blood to the head, preserving cerebral function.
In femoral and around to descending aorta. Sized on height so they aren't concluding other vessels.

92

What are side effects of streptokinase?

Nausea, hypotension, allergy, bleeding, reperfusion arrhythmias.

93

What are the side effects of TPA?

Bleeding and reperfusion arrhythmias.

94

What are side effects of opiates?

Sedation, hypoventilation and nausea.

95

What are the side effects of beta blockers?

Bradycardia, cardiac failure, bronchospasm in asthma and chronic bronchitis. Hypotension.

96

What drug treatment should all patients who have had an MI be given?

ACEi
Aspirin
Betablockers
Statin.

97

When should the combination of aspirin and clopidogrel be prescribed?

After an NSTEMI.
After PCI and stents.
Duration dependent on type of stent.

98

What should people with signs or symptoms of heart failure be offered?
What should the time scale be?

Licensed aldosterone antagonist within 3-14 days.

99

What symptoms do we get with an MI?

Associated autonomic upset.
Angor animi - an overwhelming sense of impending doom.
Chest pain, radiating.
Nausea, vomiting and sweating.

100

What is chronic stable angina?

Fixed stenosis causing demand led ischaemia.

101

What other use does morphine have in MI other than just pain relief?

It is a venodilator and so reduces preload, decreasing pain and strain on the heart.