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Cardiology 2023 1MB > MI and Ischaemic Heart Disease > Flashcards

MI and Ischaemic Heart Disease Flashcards

1
Q

What is chronic stable angina?

A

Demand led ischaemia of the heart muscle due to a fixed stenosis

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2
Q

What is the recommendation for patients who have an angina attack and have stable angina?

A

Stop, sit and use GTN spray

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3
Q

When may angina commonly be felt?

A
  • After a meal
  • In cold air
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4
Q

Where does pain for angina commonly radiate?

A
  • Jaw
  • Back
  • Epigastrium
  • Left (and right) arm
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5
Q

What type of pain is felt with angina?

A

Heavy crushing pain with tightness

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6
Q

What are the two types of acute MI?

A
  1. STEMI
  2. NON-STEMI (NSTEMI)
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7
Q

Why does acute cornonary syndrome occur?

A

Development of an atheromatous plaque that develops a thrombosis and ruptures

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8
Q

Which steps lead to thrombosis occuring?

A
  • Normal
  • Fatty streak
  • Atherosclerotic plaque
  • Fibrous plaque
  • Rupture/thrombosis
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9
Q

In what ways is chronic stable angina different to an acute coronary syndrome such as unstable angina?

A
  • It has a fixed stenosis (not comple occulsion)
  • Demand led ischaemia (not supply led)
  • Predictable
  • Safe
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10
Q

What are the three sub-stages of thrombosis formation?

A
  1. Initiation
  2. Adhesion
  3. Activation
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11
Q

Describe the initiation stage of thrombosis formation

A

There is vascular damage exposing the sub-endothelium, collagen and von Willebrand factor

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12
Q

Describe the adhesion stage of thrombosis formation ( two thinks platelets bound to)spells as v instead of w

A

Platelets recruit to the area and bind to the exposed collagen and von Willebrand factor forming a monolayer

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13
Q

Describe the activation stage of thrombosis formation

A
  • Platelets become activated after adhesion and change shape from discs to star-like shapes
  • Platelets release ADP and thromboxane A2 (generated by cyclooxygenase)
  • ADP bind to receptors on circulating platelets allowing more activation to occur
  • Activated platelets express adhesion sites for leukocytes (P-selectin and CD40 ligand)
  • These processes contribute to the platelet cascade which causes acceleration of platelets activation and coagulation
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14
Q

What is the consequence of intraluminal coagulation?

A

Vascular blockage

Hence MI, stroke and death are all possible

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15
Q

What are key synptoms of MI?

A
  • Severe crushing (10/10) pain not relieved by GTN and lasting a long time
  • Pain occurs at rest
  • Pain radiates to jaw, left (and right) arm, back and epigastric region
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16
Q

For a MI, where will the changes be seen on an ECG?

A
  • ST elevation
  • T wave inversion
  • Q waves
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17
Q

How is a STEMI seen on an ECG?

A
  • >/= 1mm ST elevation in 2 adjacent limb leads
  • >/= 2mm ST elevation in at least 2 continous precordial leads
  • New onset bundle branch block
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18
Q

How does the ECG change after an MI?

A
  1. Initially an ST elevation is present (a few hours)
  2. Q wave formation and T wave inversion follow (within a day)
  3. Finally, Q waves are present with or without T waves
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19
Q

In an inferior MI, which limb leads will be affected?

A

II, III, aVF

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20
Q

In an aterior MI which limb leads can be affected?

A

V1-6

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21
Q

In an anteroseptal MI, which limb leads are affected?

A

V1-4

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22
Q

In an anterolateral MI, which limb leads are affected?

A

I, aVL, V1-6

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23
Q

Which two urine tests can help in the diagnosis of MI?

A
  1. Creatinine kinase
  2. Troponin C
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24
Q

At what time will creatinine kinase levels peak in the urine after MI and what does this signify?

A

Within 24 hours

Creatinine kinase found in muscle and brain cells

Suggests muscle damage

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25
Q

What does the presence of troponin C in urine suggest?

A

Highly specific for cardiac muscle

It is a good indicator for myocardial necrosis

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26
Q

How is a STEMI immediately treated?

A

Clopidogrel - 300mg

Aspirin - 300mg

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27
Q

What is clopidogrel?

A

An inhibitor of ADP binding sites (P2Y12 receptor) which prevents activation of glycoprotein IIb/IIIa (fibrinogen receptors) on platelets

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28
Q

How does aspirin work?

A

Aspirin prevent cyclooxygenase (COX-1) activation in platelets

This prevents production of thromboxane A2

(it also blocks COX in endothelial cells blocking production of anti-thrombotic prostaglandin I2 is inhibited - this is not useful)

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29
Q

What is thrombolysis?

A

A way of unblockign arteries by breaking down clots using thrombolytic drugs such as streptokinase

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30
Q

When should thrombolysis be administered?

A
  1. Chest pain is suggestive of acute MI (more than 20 minutes and less than 12 hours)
  2. ECG changes - acute ST elevation, new LBBB
  3. No contraindications

It is NOT administered if PCI will be available

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31
Q

What is the downside to thrombolysis?

A

It can lead to severe intracranial haemorrhage

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32
Q

What is primary angioplasty?

A

A procedure also termed percutaneous coronary intervention (PCI) or coronary angioplasty, which involves inserting a wire through the coronary artery and opening it up again by inserting a balloon

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33
Q

What type of pain relief is given for MI?

A

Analgesic - Diamorphine (IV)

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34
Q

What is the full list of treatment given to a patient with a STEMI?

A
  • Analgesia - diamorphine (IV)
  • Antiemetic - IV
  • Aspirin - 300mg
  • Clopidogrel - 300mg
  • GTN - when BP >90mmHg
  • Oxygen - if hypoxic
  • Primary angioplasty (PCI)
  • Thrombolysis - when angioplasty is not available within 90 minutes
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35
Q

Infarction of myocytes most likey causes which type of arrhythmia?

A

Ventricular fibrillation

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36
Q

What is the KILLIP classification?

A

A system used in individuals with acute MI taking into account examination and the development of heart failure in order to predict the risk of mortality

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37
Q

Describe stages 1 to 4 in the KILLIP classification

A
  • I - No signs of heart failure
  • II - Crepitation < 50% of lung fields
  • III - Crepitations > 50% of lung fields
  • IV - Cardiogenic shock
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38
Q

How may an NSTEMI be diagnosed?

A
  • ECG may show ST ↓ + TWI
  • Pain is present in normal areas - left/right arm, jaw, back and epiastrium
  • Troponin/creatinine kinase levels in urine
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39
Q

Troponin is a proetin exclusive to which cells?

A

Cardiac cells

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40
Q

Why is troponin a good test and relevant to MI?

A

When mycotyes undergo necrosis after MI, troponin is released and can be present in the urine

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41
Q

What are the three types of troponin?

A

Troponin C - binds to calcium and is identicle in heart and muscle cells

Troponin I - in absence of calcium it binds to actin and inhibits actin-myosin ATPase induced contraction, it is specific to the heart

Troponin T - links troponin complex to tropomyosin faciliating contraction, it is also specific to the heart

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42
Q

Which two out of the three troponin types have a higher likelihood of pointing towards MI?

A

TnT and TnI - they are specific to the heart muscle

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43
Q

Troponin may be detected in the urine in which other conditions?

A
  • PE
  • Post arrhythmia
  • Renal failure
  • Hypertensive crisis
44
Q

What is a class I MI?

A

Spontaneous MI related to ischaemia due to a primary coronary event such as plaque erosion and or rupture

45
Q

What is a class 2 MI?

A

MI secondary to ischaemia due to imbalance of oxygen supply and demand from cornary spasm, embolism, anaemia, arrhythmias etc.

46
Q

What is a class 3 MI?

A

Sudden unexpected cardiac death including cardiac arrest often with symptoms suggestive of ischaemia

With new ST segment elevation, new LBBB, or pathological or angiographic evidence of fresh coronary thrombus

47
Q

What is a class 4a MI?

A

MI associated with PCI

48
Q

What is a class 4B MI?

A

MI associated with documented in-stent thrombosis

49
Q

What is a class 5 MI?

A

MI associated with coronary artery bypass graft surgery

50
Q

Which drugs can act as ADP antagonists?

A
  • Ticegralor
  • Ticlopidine
  • Clopidogrel
  • Prasugrel
51
Q

Which drugs can act as COX inhibitors?

A

Aspirin

52
Q

Which drugs are phosphodiesterase inhibitors?

A

Dipyridamole

53
Q

Whcih drugs are GP IIb/IIIa inhibitors?

A
  • Tirofiban
  • Eptifibatide
  • Abciximab

(block platelet aggregation)

54
Q

What may be used to identify stenosis?

A

Coronary angiography

55
Q

Describe coronary revascularisation

A

A balloon catheter can stretch out a vessel and push down the plaque to keep the vessel open

or

An intracoronary stent can be administered via balloon to keep the vessel open

56
Q

What is a transient ischaemic attack (TIA)?

A

This occurs due to an unstable plaque

The blockage will last only for a short time

57
Q

Acute MI involves what extent of vessel occulusion?

A

Complete

58
Q

What is ischaemic cardiomyopathy?

A

The negative effects of remodelling and scar tissue from a previous MI

59
Q

Is angina a symptom?

A

No

It is a clinical diagnosis

60
Q

Does pain from angina last a long time?

A

No, usually a short period

61
Q

What type of pain is angina?

A

Visceral pain

Feels like squeezing, heaviness and is similar to a weight on the chest

62
Q

Where does pain from angina often radiate?

A
  • Arms
  • Back
  • Jaw
  • Teeth
  • Shoulder
63
Q

How can anginal pain be brought on?

A
  • Exertion
  • Stress
  • Cold wind
  • After meal
64
Q

Which drug is commonly used to relieve anginal pain?

A

GTN spray

65
Q

What is the differential diagnosis of chest pain?

A
  • GI - acid reflux, peptic ulcer, oesophageal spasm, biliary colic
  • MSK - Hurts during movement, lasts longer, nerve root pain
  • Pericarditis - central and posture related
  • Pleuritic pain - exacerbated by breathing, sharp
66
Q

Is it true that morphine can relieve the pain from an MI?

A

Not always

The pain from an MI is very severe

67
Q

What type of pain is felt with a PE in comparision to an MI?

A

Dull pain

68
Q

How can angina be tested for?

A

Exercise testing - shows characteristic changes on ECG

Perfusion scanning - can identify areas of the heart with decreased blood flow

CT angiography - non invasive, but less precise than angiography when calcium is present

Angiography - a sheath is instered into the artery (radial/femoral), x-ray contrast is injectedto outline arteries. This test is the gold standard

69
Q

How can the risk factors be reduced for angina?

A
  • Drugs - aspirin, B blockers, statins, ACEI
  • Lifestyle - smoking cessation and diet
  • Revascularisation - CABG, PCI
70
Q

Which two veins may be targeted for coronary revascularisation?

A
  1. The left internal thoracic artery
  2. A great saphenous vein
71
Q

Describe how the left thoracic artery can be used in coronary artery bypass grafts

A

The left thoracic artery is diverted to the left anterior descending branch of the left coronary artery, bypassing the occulusion

72
Q

Describe how a great saphenous vein is used for coronary revascularisation

A

The vein is removed from a leg

One end is attched to the aorta or one of the major branches

The other end is attched to the obstructed artery immediately after the occulsion

This will restore blood flow

73
Q

What is cardioplegia?

A

The intentional cessation of cardiac activity

This is often done for surgical purposes

74
Q

For a STEMI what is the gold standard treatment?

A

PCI

75
Q

Where can Q waves be considered normal?

Q.M

A

They are normal in most leads. Should not be seen in leads V1-V3

76
Q

What are the ECG changes associated with a posterior MI? Q.M

A
  1. ST elevation, Q waves in leads V7-V9
  2. Horizontal ST depression
  3. Tall, dominant R waves with R wave/S wave ratio >1 in lead V2
    1. Upright T wave
77
Q

Inferior STEMI is seen in which ECG leads?- Q.M

A
  1. ST elevation in II, III, aVF
  2. Reciprocal ST depression in aVL
78
Q

Which type of muscle(s) is Troponin found in?

A

Cardiac and skeletal muscle

79
Q

Which heart failure medications have evidence to support a reduction in mortality rates? Q.M

A

Beta blockers, ACE inhibitors, Aldosterone antagonists, hydralazine/nitrates

80
Q

What are the causes of Left axis deviation? Q.M

A

Normal variant. Inferior myocardial infarction. Hyperkalaemia. Congenital heart disease. LBBB. Left ventricular hypertrophy (rare cause)

81
Q

Which lead on an ECG specifically looks at the right ventricle?

Q.M

A

V1 - as the most anterior of the chest leads

82
Q

What percentage of patients develop post infarction pericarditis?

Q.M

A

5-10%

83
Q

Which vessel is most likely to be occluded in an inferior STEMI? Q.M

A

RCA

84
Q

Which scoring system can be used to estimate the probability of a patient having a PE?

Q.M

A

Wells score

85
Q

What coronary territory is involved in an anterior MI? Q.M

A

Left anterior descending artery

86
Q

What are some of the complications of anterior STEMI?

A

Ventricular arrhythmia

Recurrent ischaemia/infarction

Acute mitral regurgitation

Congestive heart failure

2nd, 3rd degree heart block

Cardiogenic shock

Cardiac tamponade

Ventricular septal defects

Left ventricular thrombus/aneurysm

87
Q

What are some of the characteristic murmurs that may be heard in a patient with hypertrophic cardiomyopathy? Q.M

A
  1. Ejection systolic murmur, loudest between lower left sternal edge and apex, louder with exercise/standing, quieter when supine/squatting/valsalva.
  2. Pansystolic murmur - loudest at the apex and radiating to the axilla (mitral regurgitation) due to systolic anterior motion (SAM) of the mitral valve.
  3. Rarely, diastolic murmur from aortic regurgitation.
88
Q

What coronary territory is involved in a lateral MI?

Q.M

A

Left circumflex

89
Q

What are the causes of right axis deviation?

  • Q.M
A
  • Right ventricular hypertrophy
  • Right bundle branch block
  • Dextrocardia
  • Ventricular ectopic rhythms
  • Lateral wall infarction
  • Right ventricular load
  • WPW
90
Q

Diagnostic features of different ACS subtypes

Diagnosis depends on a combination of clinical, ECG and biochemical findings which helps distinguish between the various types of ACS.

  • Q.M
A
  • Unstable angina - Cardiac chest pain + abnormal/normal ECG + normal troponin
  • NSTEMI - Cardiac chest pain + abnormal/normal ECG (but not ST-elevation) + raised troponin
    • STEMI - Cardiac chest pain + Persistent ST-elevation/new LBBB (note that there is no need for a troponin in this case)
91
Q

What are the leads involved in an anterior MI?

Q.M

A

V1-V4

92
Q

When is septal rupture post-MI more likely to happen? Q.M

A

Without reperfusion, septal rupture typically occurs within the first week after the infarction.

93
Q

What are the leads involved in an anterolateral MI?

Q.M

A

I, aVL, V1-V6

94
Q

Myocardial infarction and Acute Coronary Syndrome (ACS) Question: Management of STEMI

  1. Q.M
A
  1. Targeted oxygen therapy (aiming for sats >90%)
  2. Loading dose of PO aspirin 300mg
    • Note that some hospital protocols will also call for a loading dose of a second anti-platelet agent such as clopidogrel (300mg) or ticagrelor (180mg)
    • For those going on to have PCI, NICE guidance suggests adding Prasugrel (if not on anti-coagulation) or clopidogrel (if on anti-coagulation)
  3. Sublingual GTN spray - for symptom relief
  4. IV morphine/diamorphine - in addition this causes vasodilation reducing preload on the heart
  5. Primary percutaneous coronary intervention (PPCI) for those who:
    • Present within 12 hours of onset of pain AND
    • Are <2 hours since first medical contact

Remember that (particularly in STEMI) time is heart therefore urgent treatment, escalation and delivery of PPCI is critical to good outcomes.

95
Q

Classification of MI

Q.M

A

MI is generally categorised into two types:

  • ST-elevation MI (STEMI) - Caused by complete occlusion of a coronary artery
  • Non-ST-elevation MI (NSTEMI) - Caused by severe but incomplete stenosis/occlusion of a coronary artery

It is important to remember that some patients can have NSTEMIs due to lack of cardiac oxygenation for other reasons (e.g. severe sepsis, hypotension, hypovolaemia, coronary artery spasm). These cases might not respond to (or need) conventional treatment.

96
Q

: Post-MI management

*

A
  • ALL patients post-MI patients should be started on the following 5 drugs:
    1. Aspirin 75mg OM + second anti-platelet (clopidogrel 75mg OD or ticagrelor 90mg OD)
    2. Beta blocker (normally bisoprolol)
    3. ACE-inhibitor (normally ramipril)
    4. High dose statin (e.g. Atorvastatin 80mg ON)
  • All patients should have an ECHO performed to assess systolic function and any evidence of heart failure should be treated.
  • All patients should be referred to cardiac rehabilitation.
    • Patients who have been treated without angiography should be considered for ischaemia testing to assess for inducible ischaemia.
97
Q

ECG features of acute pericarditis?

  1. Q.M
A
  1. Widespread concave ST elevation
  2. PR depression
  3. ST depression and PR elevation in aVR +/- V1

https://www.youtube.com/watch?v=zC3kGghQFLA

98
Q

Which leads are involved in an inferior infarct?

A

II, III and AVF

99
Q

Management of NSTEMI

1.

A
  1. Targeted oxygen therapy (aiming for sats >90%)
  2. Loading dose of PO aspirin 300mg and fondaparinux
    • Patients should have their 6 month mortality score (often the GRACE score) calculated as early as possible - all those who are anything other than lowest risk should also be given prasugrel or ticagrelor unless they have a high risk of bleeding where PO clopidogrel 300mg is more appropriate.
  3. Sublingual GTN spray - for symptom relief
  4. IV morphine/diamorphine - in addition this causes vasodilation reducing preload on the heart
  5. Start antithrombin therapy such as treatment dose low molecular weight heparin or fondaparinux if they are for an immediate angiogram
  6. Patients with high 6 month risk of mortality should be offered an angiogram within 96 hours of symptom onset.

Note that management of unstable angina is similar to that of NSTEMI with aspirin for all patients and fondaparinux and early angiography for those at high risk.

100
Q

What ECG changes point towards Right ventricular infarction?

  • Q.M
A
  • ST elevation in lead V1 and V1>V2
  • ST depression in V2
  • ST elevation lead III>II
101
Q

What are the complications associated with inferior myocardial infarction? Q.M

A

Papillary muscle rupture, bradycardia and AV block. Concurrent right ventricular infarction

102
Q

What are the examination findings in patients with ventricular septal defect post-MI? Q.M

A

On examination patients will have a harsh, loud pansystolic murmur along the left sternal border.

Patients also often have a palpable parasternal thrill.

There may be features associated with low output cardiac failure.

103
Q

Which is the best way to visualise a posterior MI on an ECG Q.M

A

By using a 15-lead ECG

104
Q

What is the coronary territory affected in posterior MI?

A

posterior coronary circulation becomes disrupted. PAD

105
Q

What is the appearance of the ECG leads in Left axis deviation?

Q.M

A

Positive in lead I and negative in lead II and III

106
Q

What ECG features are associated with third-degree heart block? Q.M

A

Bradycardia, no association between P waves and QRS complexes

107
Q

Which arteries supply the lateral wall of the left ventricle?

Q.M

A

Branches of the LAD and left circumflex arteries

Cardiology 2023 1MB (28 decks)

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