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2. Cardiovascular System > 24. ACS & AMI (acute coronary syndrome + acute myocardial infarction) > Flashcards

24. ACS & AMI (acute coronary syndrome + acute myocardial infarction) Flashcards

1
Q

What are the main presentations of coronary heart disease in community from most popular to least. (4)

A
  1. new exertional angina
  2. acute MI
  3. unstable angina
  4. sudden cardiac death
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2
Q

What is the difference between stable and unstable angina?

A
  • Stable angina, chest pain will adhere to a specific pattern and symptoms usually disappear after a few minutes of rest (can be brought about my stress, alcohol, temperatures, overexertion, smoking etc)
  • Unstable angina, symptoms are more unpredictable and serious and discomfort can last 20 minutes or more even during sleep or rest
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3
Q

When does stable angina occur?

A

If myocardial blood flow is reduced and when there is increased demand ischaemia

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4
Q

What are the symptoms in terms of chest pain in stable angina?

A

central chest tightness, often radiation to neck and/or arms

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5
Q

What is stable angina aggravated by? (stimulated/ brought about) (2)

A

by

  • exertion
  • stress
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6
Q

What brings about relied to stable angina? (2)

A
  • stopping activity

- sublingual nitrate

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7
Q

Describe atherosclerosis steps in a progressive process that lead to stable angina. (4)

A
  1. normal
  2. fatty streak
  3. non-obstructive plaque (fibrous plaque)
  4. obstructive plaque; atherosclerotic plaque (>70% lumen) = stable angina
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8
Q

What is another name for acute coronary syndrome?

A

unstable angina

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9
Q

When does acute coronary syndrome (unstable angina) develop?

A

spontaneous plaque rupture and disruption and local thrombosis with degrees of occlusion

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10
Q

What 3 things can plaque rupture lead to?

A
  1. unstable angina
  2. NSTEMI
  3. STEMI
    Which all ultimately lead to acute coronary syndrome (ACS)
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11
Q

What type of process is atherotrombosis?

A

an unpredictable process caused by unstable plaques

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12
Q

What are different types of ACS (acute coronary syndromes) caused by plaque rupture and thrombosis which lead to unstable angina? (4)

A
  1. unstable angina
  2. non ST elevation myocardial infarction (NSTEMI)
  3. ST elevation myocardial infarction (STEMI)
  4. sudden cardiac death
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13
Q

Why do plaques rupture?

A
  • inflammation is important determinant in plaque stability along with other mechanisms including shear stress
  • aggregated platelets build up on fibrin, fibrous cap and lipid rich core with macrophages
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14
Q

How to distinguish ACS symptoms (unstable angina) from stable angina?

A

ACS symptoms will almost always give symptoms AT REST compared to stable angina which is only on exertion

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15
Q

What factors are important o get from patient when making diagnosis about acute coronary syndromes? (unstable angina) (4)

A
  1. CHARACTER of patient’s pain to differentiate from other causes of pain; often tight band/ pressure/heaviness
  2. SITE of pain; watch for gestures; retrosternal
  3. RADIATON; neck and/or jaw, down arms
  4. AGGRAVATING; with exertion, stress, or relieving facotrs e.g. incomplete improvement with GTN or physical rest and/or ongoing
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16
Q

What are non-modifiable risk factors for coronary artery disease? (5)

A
  • age
  • gender
  • creed/ faith
  • family history+ genetic factors
  • previous angina, cardiac events or interventions
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17
Q

What are modifiable risk factors for coronary artery disease? (5)

A
  • smoking
  • diabetes mellitus
  • hyperlipidaemia
  • hypertension
  • lifestyle; diet and exercise
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18
Q

How does unstable angina present?

A
  • Unstable angina pectoris (UAP) presents as angina on effort but also of progressive increasing frequency and severity often provoked by LESS exertion and/or then at rest
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19
Q

How does NSTEMI elevation MI present?

A

Will start with myocardiac ischaemic symptoms occurring at rest

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20
Q

What is seen on examination when diagnosing unstable angina and NSTEMI elevation MI? (4)

A
  1. patient may look unwell or fine
  2. often no specific features found
  3. check BP and heart rate
  4. listen for murmurs and crackles in chest
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21
Q

What is seen on ECG in unstable angina and NSTEMI?

A

May appear normal but can have:

commonly ST segment depression, transient/ short time ST segment elevation and/or T wave inversion

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22
Q

What do changes in ECG look like in

  • unstable angina
  • NSTEMI
A
  • in unstable angina, changes occur AFTER pain

- in NSTEMI, changes persist (but not always)

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23
Q

What type of ECG is needed to detect delayed changes during an MI?

A

SERIAL ECG: two or more successive recordings from same patient made and compared to detect MI

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24
Q

Which groups of people have atypical ACS/unstable angina presentation? Why? (3)

A
  • women
  • elderly
  • diabetics
    Due to reduced pain sensation
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25
Q

What are common symptoms for acute coronary syndrome (ACS)? (3)

A
  1. breathlessness alone +/- signs of heart failure
  2. nausea and vomiting +/- other autonomic symptoms
  3. epigastric pain +/- recent onset indigestion
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26
Q

What are important cardiac biomarkers for diagnosing unstable angina and NSTEMI elevation MI (acute coronary syndromes)? (2)

A

cardiac troponin (cTn) I &T

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27
Q

What are cardiac biomarkers such as cardiac troponin, helpful in while diagnosing? (2)

A
  • determining risk stratification
  • elevated levels suggest high risk of adverse events
    (helpful in diagnosis)
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28
Q

Are all troponin elevations ACS related and caused by atherothrombosis?

A

No

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29
Q

What is cardiac troponin (cTn)?

A
  • part of contractile apparatus of myocytes’ thin filament
  • normally undetectable
  • elevated with compromise of myocyte integrity (when myocytes don’t communicate)
  • sensitive and specific marker of cardiac myocyte damage
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30
Q

When is cardiac troponin elevated?

A
  • during ischaemic damage

- when there is no compromise of myocyte integrity (when myocytes don’t communicate)

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31
Q

What is the immediate treatment for unstable angina and NSTEMI elevated MI? (acute coronary syndromes) step by step? (2)

A
  1. ABCDE approach
  2. MONA:
    - morphine (or diamorphine)
    - oxygen
    - nitroglycerine (GTN spray or tablet)
    - Aspirin 300mg orally (crush or chew)
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32
Q

What 2 things should ALL ACS patients receive when acute coronary syndrome symptoms appear as part of anti-platelet therapy?

A

They should receive BOTH;

  • aspirin
  • ADP receptor blocker, either:
    1. Clopidogrel
    2. Prasugrel
    3. Ticagrelor
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33
Q

What is the dosage for Clopidogrel (ADP receptor blocker) for ACS patients?

A

Clopidogrel: bolus 200mg and 75mg daily

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34
Q

What is the dosage for Prasugrel (ADP receptor blocker) for ACS patients?

A

Prasugrel; Bolus 60mg and 10mg daily

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35
Q

What is the dosage for Ticagrelor (ADP receptor blocker) for ACS patients?

A

Ticagrelor: Bolus 180mg and 90mg BD daily

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36
Q

What is the treatment called that uses both aspirin and an ADP receptor blocker?

A

anti-platelet therapy

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37
Q

For how long is the dual anti-platelet therapy used for following an ACS event?

A

for one year following the ACS event

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38
Q

What are common anti-platelet agents used in drugs to prevent clotting? (8)

A
  • terutroban
  • sulotroban
  • daltroban
  • ifetroban
  • ramatroban
  • linotroban
  • ridogrel
  • terbogrel
    (“troban” and “grel”)
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39
Q

What are common thrombin receptor antagonists which prevent clotting? (6) (anti-thrombotic therapy)

A
  • ticlopidine
  • clopidogrel
  • prasugrel
  • ticagrelor
  • cangrelor
  • elinogrel
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40
Q

What are 2 most common anti-thrombotic treatments for acute coronary syndromes e.g. unstbale angina or NSTEMI MI.

A
  1. intravenous unfractionated heparin (UFH)

2. low molecular weight heparin

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41
Q

What are the benefits of low molecular heparin? (4)

A
  1. improved clinical outcome
  2. easier to administer
  3. given subcutaneously and not needed to be monitored
  4. safe to give to pregnant women
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42
Q

What is low molecular heparin now largely replaced by?

A

even more specific anti-thrombotic Fondaparinux

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43
Q

What other medical therapies are used for acute coronary syndromes that don’t include anti-platelet or anti-trombotic therapies? (3)

A
  • Beta blockers (in the absence of contrindications; asthma, acute left ventricular dysfunction, impaired AV nodal conduction), target heart rate should be between 50-60
  • Statins (both acutely and chronically reduced further events)
  • ACEIs; always in left ventricular dysfunction; controversial in normal function
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44
Q

What are ALL treatment options available for acute coronary syndromes? (5)

A
  1. Immediate treatment (ABCDE and MONA)
  2. anti-platelet therapy (both aspirin and ADP receptor blocker)
  3. anti-thrombotic therapy (intravenous unfractioned heparin or low molecular weight heparin)
  4. Medical therapy (e.g. Beta blockers, statins and ACEIs)
  5. coronary revascularisation
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45
Q

Which patients should be offered coronary revascularisation?

A
  • high risk patients with unstable angina or NSTEMI MI who will benefit from early invasive strategy compared to medical therapy alone
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46
Q

What are common coronary revascularisation methods? (2)

A
  • coronary angiography + revascularisation (PCI: percutaneous coronary intervention)
  • CABG (coronary artery bypass graft) within 3 months since it’s highest risk period for recurrent events
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47
Q

Describe steps for heart catherisation. (7)

A
  1. needle introduced into brachial or femoral artery
  2. guide wire passed through needle across stenotic atherosclerotic plaque
  3. needle withdrawn and cathether introduced over wire which travels into aorta and l.side of heart through arteries
  4. double-lumen cathether with a balloon is slid over the guide wire, the balloon inflated to compress the plaque and open obstruction
  5. balloon cathether containing the stent is placed in the dilated area
  6. balloon is inflated and expanded, deploying the stnet
  7. once stent is deployed/put in place, the balloon and guide wire are removed
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48
Q

How long do patients stay in hospital for usually following an ACS event?

A

2-7 days (not all will have angiography and not all will have revascularisation)

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49
Q

Which group of people will have to be thoroughly examined for the right treatment path for more difficult decisions? (2)

A
  • elderly

- people with co-morbidities

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50
Q

What are 3 main types of acute coronary syndromes?

A
  1. unstable angina
  2. NSTEMI MI (non-ST segment elevation)
  3. STEMI MI (ST segment elevation)
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51
Q

What occurs during a STEMI MI?

A
  • plaque rupture leads to more complete or complete thrombotic occlusion of coronary lumen and infarction of distal myocardium
  • proximal occlusion of main artery causes greater damage
  • occlusion of a distal branch vessel can cause big problems
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52
Q

Occlusion in which part of the artery causes a greater damage?

A

in the proximal part of artery (proximal occlusion)

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53
Q

What problems can occlusion in distal branches cause? (2)

A
  • rupture of papillary muscle leading to acute mitral regurgitation
  • occlusion of AV nodal artery leading to complete heart block
54
Q

What occurs straight after coronary occlusion to the heart tissue?

A
  • necrosis of myocardial tissue
  • sooner, the occlusive thrombus is then dissolved/removed and vessel opened (the sooner, the more myocardium will be salvaged)
55
Q

To which part of the heart does damage need to be monitored which has a direct link to survival chances?

A

L. ventricular damage ( the less damage to l. ventricle, the better the survival)

56
Q

What are 2 options to open infarcted artery in a STEMI MI treatment?

A
  1. fibrinolysis

2. primary PCI; percutaneous coronary intervention (cardiac catherisation)

57
Q

During which hours following a STEMI MI, is the critical period for myocardial salvage using medication for example? (time dependent)

A

hours 0-3

58
Q

During which hours following a STEMI MI, is the critical period for opening an infarct related artery?

A

hours 7- 12

59
Q

Which method; fibronolysis or primary PCI shows better evidence for improving mortality?

A

primary PCI

60
Q

Why is primary PCI (cardiac catherisation) a better treatment option that fibrinolysis for STEMI MI? (3)

A
  • less chance of reinfarction (recurrent MI)
  • less chance of haemorrhagic stroke
  • less chance of total stroke
61
Q

When is PCI most effective following a STEMI MI?

A

if delivered within 120-150 minutes of patient’s call for help

62
Q

What does primary PCI do?

A
  • opens blocked coronary artery and restored blood flow

- stent is put in place to open artery and prevent angina, MI and death

63
Q

When should fibrinolysis be performed in patients with STEMI MI?

A
  • when PCI cannot be performed
  • within 90 minutes of patient calling for help
    OR
  • within 30 minutes of hospital arrival
64
Q

Which form of fibrinolysis is most effective at reducing early mortality by 15-20%?

A
  • pre-hospital fibrinolysis (compared to in-hospital fibrinolysis)
65
Q

What is fibrinolysis?

A
  • fibrinolytic drugs are given that break down fibrin clots following an MI to dissolve the thrombus blocking the coronary artery (thrombolytic drugs also given)
66
Q

Out of; primary PCI,in-hospital thrombolysis and prehospital thrombolysis, which have the best survival rates? (from best to worst)

A
  1. primary PCI
  2. prehospital thrombolysis
  3. in-hospital thrombolysis
67
Q

What are the main risks associated with fibrinolytic therapy? (1)

A

bleeding and intra-cranial haemorrhage in some patients

68
Q

What patients are at risk of intra-cranial haemorrhage or further bleeding after fibrinonolyic therapy? (7)

A
  • people aged >75
  • females
  • patients with previous stroke
  • low body weight patients (<65kg for females and <70kg for males)
  • BP>160mmHg
  • International normalised ratio (blood coagulation) >4
  • chronic kidney disease and elevated creatine (recycles ATP)
69
Q

What is a normal INR (international normalized ratio) in a healthy individual?

A

1.1 or less

70
Q

What is an INR (international normalised ratio) in patients considered for anticoagulant therapy e.g. warfarin?

A

2-3 (effective therapeutic range e.g. for atrial fibrillation with clots patients)

71
Q

When is thrombolysis best option for a STEMI MI? (2)

A
  • door-balloon >90 mins

- <3 hours symptom onset

72
Q

What is primary PCI best option for a STEMI MI? (5)

A
  • door balloon <90 mins
  • > 3 hours symptom onset
  • cardiogenic shock/ heart failure
  • high bleeding risk
  • diagnosis uncertain e.g. coronary dissection
73
Q

What general and modifiable measures can be taken to treat STEMI MI as a secondary prevention? (4)

A
  • stop smoking
  • change diet and exercise
  • control BP
  • control glycemic levels
74
Q

What medical treatment is given as a SECONDARY intervention for a STEMI MI? (4)

A
  • aspirin and clopidrogel (for 1 year only)
  • Beta blockers (target heart rate <60bpm)
  • Statins (to LDL cholesterol <3.2 mmol)
  • ACEIs
75
Q

When are ACEIs ALWAYS given in a STEMI MI?

A

always if l. ventricular dysfunction (and probably if normal function too)

76
Q

What other drug is given on prescription along with ACEIs?

A

Ramipril 5mg

77
Q

What are important in-patient investigations for STEMI MI that determine myocardial function and survival? (3)

A
  1. echocardiogram
  2. age
  3. left ventricular ejection fraction
78
Q

What do we look for in an echocardiogram for myocardial dysfunction? (4)

A
  1. size of wall motion abnormality (whether hypokinetic or akinetic)
  2. overall heart contractiliy
  3. presence and degree of mitral regurgitation (inferiors)
  4. presence of mural thrombus (antero-aprical MIs)
79
Q

What percent of patient are resuscitated and survive a sudden cardiac death?

A

only ~2%

80
Q

In resuscitated patients, what 2 conditions did 80% have?

A
  1. ventricular tachycardia

2. ventricular fibrillation

81
Q

What occurs during a sudden cardiac death that leads to ventricular arrhythmia?

A
  • atherothrombotic event causes acute myocardial ischaemia

- this leads to subsequent sufficient electrical disturbance which causes ventricular arrhythmia

82
Q

Where do most proximal occlusions happen in younger patients?

A

in LAD (left anterior descending coronary artery)

83
Q

Are all sudden cardiac deaths ACS events?

A

No, not all of them

84
Q

What is ventricular fibrillations?

A
  • most serious cardiac rhythm disturbance
  • ventricles contract in a rapid, irregular,unsynchronised way
  • create multiple wavelets of electrical activity and ventricles “quiver”
  • heart pumps little or no blood
85
Q

What are the causes for ventricular fibrillation? (5)

A
  • lack of proper blood flow to heart muscle or damage due to previous MI
  • cardiomypathy (disease of muscle fibres)
  • problems with aorta
  • drug toxicity
  • sepsis (severe blood infection)
86
Q

What is the only effective treatment for ventricular fibrillation arrest?

A

defibrillation

87
Q

What does ventricular fibrillation tend to rapidly deteriorate into?

A

Into asystole (no electricla activity on ECG monitor)-flat line; which makes it more difficult to restore cardiac output

88
Q

In sudden cardiac death, by how much are chances of reduced with each minute?

A

chances of success reduced by 7-10% each minute (resuscitation vs time)

89
Q

When are best chances of success during sudden cardiac arrest?

A

within 3-4 minutes

90
Q

What is ventricular tachycardia?

A
  • very fast heart rhythm which begins in ventricles
  • refers to more than 120 bpm and 3 or more irregular beats in a row
  • broad complex, regular but v.fast heart rate (uniform)
  • initiated by ventricular premature beat and sustained by re-entry loop
91
Q

What are some causes of ventricular tachycardia? (5)

A
  • late phase myocardial infarction (such as l. ventricular aneurysm)
  • cardiomyopathy (e.g. hypertrophic or alcohol)
  • r. ventricular dysplasia (genetic defect with desmosomes linking myocytes together)
  • myocarditis
    -drug toxicity
    (mainly due to ischaemia and/or myocardial damage)
92
Q

What are the 2 groups of IMMEDIATELY life threatening complications of acute MI (esp. in STEMI)?

A
  1. mechanical complications
  2. ventricular arrhythmic complications
    (both need urgent intervention, proper diagnosis and early management)
93
Q

What is a LATER complication of acute MI (esp. STEMI)?

A

l. ventricular thrombus

94
Q

What is the most dramatic complication of an MI? Why?

A
  • mechanical complications
  • tearing or rupture of infarcted myocardium
  • 15% of all acute MI deaths
95
Q

What are 3 main complications of mechanical complication associated with MI?

A
  1. free wall rupture (10-12%)
  2. papillary muscle rupture (1-2%)
  3. rupture of inter-ventricular septum (ventricular-septal defect)
96
Q

What percent does free wall rupture compose of in acute MI deaths?

A

10-12% of all AMI deaths

97
Q

When do free wall ruptures mainly occur following an acute MI? (2)

A
  • 85% occur in first week

- 1/3 in first 24 hours

98
Q

What territory of the heart is most susceptible to free wall rupture (mechanical complication of MI)?

A
  • LAD territory (left anterior descending coronary artery)

- occurs at edge of infarcted area

99
Q

What can free wall rupture as a mechanical complication of MI lead to?

A

leads to hamopericardium and acute tamponade (compression of heart by accumulation of fluid in pericardial sac)

100
Q

Free wall rupture in heart leads to immediate cardiac death unless adhesions and false aneurysms contain what?

A

pericardial effusion

101
Q

In which groups of people is free wall rupture more common in? (4)

A
  • elderly
  • females
  • high BP patients
  • anterior MI patients
102
Q

What is the main course of action for a free wall rupture as a result of MI complication? (3)

A
  • urgent echo
  • pericardiocentesis (aspiration of fluid from pericardial space surrounding the heart)
  • drainage with pigtail cathether
    (and if patient survives inital episode then surgery is needed; but it’s rare)
103
Q

What percent of MI patients have septal wall rupture as an MI complication?

A

2%

104
Q

What groups of people are more likely to get septal wall rupture? (4)

A
  1. elderly
  2. females
  3. high BP patients
  4. patients not thrombolysed
105
Q

What do anterior and inferior MIs lead to in terms of septal wall ruptures?

A
  • anterior MI (60%): leads to apical ventricular-septal defect
  • inferior MI (40%): leads to basal ventricular- septal defect (most patients have multiple vessel coronary artery disease)
106
Q

What type of papillary muscle rupture does inferior MI and anterior/lateral MI lead to?

A
  1. Inferior MI; leads to posterior/medial muscle rupture

2. Anterior/ lateral MI; anteriro/ lateral muscle (LAD coronary artery)

107
Q

Can papillary muscle rupture occur with small or large infarcts?

A

with small infarcts (50%)

108
Q

What are the mortality statistics for papillary muscle rupture complications with medical prescriptions? (3)

A
  • 33% die immediately
  • 50% die within 24 hours
  • only 6% live >2 months
109
Q

When do both papillary muscle rupture and ventricular-septal defects occur following an MI?

A

generally within the 1st week of MI

110
Q

What are main symptoms for papillary muscle rupture or ventricular septal defect following an MI? (3)

A
  • sudden severe breathlessness

- autuonomic activation e.g. sweating, nausea and vomiting - chest pain

111
Q

What are the signs for papillary muscle rupture and ventricular-septal defect? (7)

A
  1. shock
  2. tachycardia
  3. pulmonary oedema
  4. new harsh systolic murmur (ventral septal always defect on right chest
  5. right parasternal heave
  6. palpable thrill
  7. elevated JVP
112
Q

How can you differentiate from clinical signs between papillary muscle rupture (mitral valve rupture) and ventricular-septal defect?

A
  • mitral valve rupture (papillary muscle rupture) causes more shortness of breath and oedema
  • ventricular-septal defect causes more elevated JVP
113
Q

What does inferior MI lead to?

A

mitral regurgitation ( papillary muscle rupture)

114
Q

What does anterior MI lead to?

A

ventricular-septal defect

115
Q

What diagnosing method determines whether MI is inferior or anterior?

A

echocardiography

116
Q

What are main investigations done for diagnosing mechanical complications of MI? (2)

A
  1. echocardiogram

2. cath lab

117
Q

What do we look for when using echocardiogram for mechanical complication from MI?

A
  • prolapsing mitral leaflet +/- chunks of muscle
  • broad mitral regurgitation jest into normal sized l.atrium
  • ventricular-septal defect easily missed
  • r. ventricle size; function and pressure is a strong predictor of outcome of ventricular-septal defect
118
Q

How does right heart cath help with mechanical complication diagnosis following MI? (3)

A
  • step up in O2 saturations with ventricular-septal defect
  • confirms diagnosis and quantifies shunt
  • large v waves on wedge with acute mitral regurgitation
119
Q

How does left heart cath help with mechanical complication diagnosis following MI? (2)

A
  • establishes coronary anatomy

- better localisation of pathology

120
Q

What is the temporary medical management for papillary muscle rupture and ventricular-septal defect? (3)

A
  1. IV nitrates if systolic BP>90mmHg
  2. Inotropes if systolic BP <90mmHg
  3. IABP (intra-aortic balloon pump); reduces afterload, increases diastolic BP)
121
Q

What can surgery do for papillary muscle rupture or ventricular septal defect as a result of mechanical complications from an MI?

A
  1. mitral valves usually replaced rather than repaired
  2. VSD; ventricular-septal defect repair with pericardial or synthetic patch
  3. coronary artery bypass if needed
122
Q

When is longterm prognosis for papillary muscle rupture or VSD good?

A

if patient survives acute episode

123
Q

What does ECG look like in a ventricular tachycardia patient?

A
  • P waves usually not visible (PR interval not measurable)
  • QRS complex are rapid wide and regular
  • T waves are large with deflections opposite to QRS complexes
124
Q

When can ventricular tachycardia occur following an MI?

A

any time after an MI

125
Q

What is needed if sustained ventricular tachycardia occurs for a period of time?

A
  • urgent cardioversion required usually electrically

- amiodarone (antiarrythmic medication) or pacing intervention

126
Q

What does an ECG look like in ventricular fibrillation?

A
  • P waves not present
  • QRS complexes not present (heart rate cannot be defined without QRS complexes)
  • highly irregular heart rhythm
127
Q

What types of MI can commonly present with LV thrombus?

A

seen typically in apical/ antero-apical MI resulting in significant l. ventricle dysfunction

128
Q

When is l.ventricular thrombus seen and identified following an MI?

A

seen after 48 hours

129
Q

What is the treatment for l. ventricular thrombus? (2)

A
  • anticoagulation with warfarin

- repeat echo

130
Q

Overall, what are the main threatening MI complications? (3)

A
  • mechanical complications
  • ventricular arrhythmic complications (ventricular fibrillations and ventricular tachycardia)
  • l. ventricular thrombus

2. Cardiovascular System (42 decks)

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