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Cardiovascular > MI 1 + 2 > Flashcards

MI 1 + 2 Flashcards

1
Q

Risk factors for MI? (10)

A
  • Smoking
  • Alcohol
  • Drug abuse
  • Age
  • Gender - male
  • Stress
  • Hypertension
  • High cholesterol
  • Obesity
  • Family history
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2
Q

Features of chronic stable angina? (4) Treatment? (3)

A
  • fixed stenosis
  • demand led ischaemia
  • predictable
  • safe

Treatment

  • Stop
  • Sit
  • Spray - GTN
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3
Q

Common descriptions of cardiac chest pain? What is acute coronary syndrome? What conditions does acute coronary syndrome include?

A
  • Heavy feeling, weight on chest, pressure, tightness
  • Any acute presentation of coronary artery disease - only a provisional diagnosis that covers a spectrum of conditions
  • Unstable angina, acute NSTEMI, STEMI
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4
Q

Types of acute MI? (2)

A
  • STEMI and NSTEMI
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5
Q

Pathogenesis of acute coronary syndromes?

A

Key pathogenic process that leads to ACS is spontaneous plaque rupture

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6
Q

Features of acute coronary syndrome? Examples?

A 
* dynamic stenosis
(subtotal or complete occlusion)
* supply led ischaemia
* unpredictable
* dangerous
  • e.g. unstable angina, MI
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7
Q

Process of ACS development? (8)

A
  • Vascular damage (e.g. by percutaneous coronary interventions) exposing collagen and VWF
  • Platelet adhesion and activation
  • Release of ADP (degranulation) and TXA2 via cycloxygenase
  • ADP and TXA2 bind to receptors resulting in further aggregation
  • Leukocyte recruitment
  • Collagen and smooth muscle deposition
  • Spontaneous plaque rupture
  • Fibrin-rich thrombus
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8
Q

Factors affecting plaque rupture/fissure? (6)

A
  • Lipid content of plaque
  • Thickness of fibrous cap
  • Sudden changes in intraluminal pressure or tone
  • Bending and twisting of an artery during each heart contraction
  • Plaque shape
  • Mechanical injury
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9
Q

Does heart have collaterals? What does this mean? What does ST elevation indicate?

A
  • No, end arteries
  • If artery blocked, territory starved of oxygen causing MI
  • Tells us coronary artery has been blocked and downstream heart muscle is dying
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10
Q

Will patient completely recover from infarct? Symptoms of LVF? (5)

A
  • If survive, dead tissue is replaced with scar tissue which will not contract properly leading to left ventricular failure

Symptoms

  • Fatigue
  • Breathlessness
  • Orthopnoea
  • Paroxysmal nocturnal dyspnoea
  • Ankle oedema
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11
Q

5 year survival rate of heart failure? Prognosis compared to carcinoma in males/females and lung cancer? (3)

A
  • 25% 5 year survival rate
  • HF poorer outcome than large bowel, prostate and bladder cancer in men
  • HF poorer outcome than breast, large bowel and ovary cancer in women
  • Only lung cancer has worse prognosis than HF
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12
Q

History of MI includes? (4)

A
  • Severe crushing central chest pain
  • Radiating to jaw and arms, especially the left
  • Similar to angina but more severe, prolonged and not relieved by GTN
  • Associated with sweating nausea and often vomiting
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13
Q

Differentiation of attack of angina from acute MI? (5)

A
  • Duration: angina - 10 mins, MI - >30 mins
  • Onset: angina - on exertion, MI - at rest
  • Severity: angina - usual pain, MI - more severe
  • GTN: angina - relief, MI - no relief
  • Associated symptoms: angina - none, MI - sweating, nausea, vomiting
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14
Q

Other causes of chest pain other than MI? (4)

A
  • Pneumothroax (sudden onset pain, SOB)
  • Bronchopneumonia (pleuritic pain to one side)
  • Musculoskeletal pain (worse on movement)
  • Heartburn (important mimic of heart pain – often central)
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15
Q

ECG changes in acute STEMI? (4)

A
  • ST elevation (>1mm in 2 adjacent limb leads and >2mm in at least 2 contiguous precordial leads)
  • T wave inversion
  • Q waves
  • New onset bundle branch block
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16
Q

Evolving ECG changes of acute MI? (3)

A
  • ST elevation - first few hours
  • Q wave formation and T wave inversion – first day
  • “Old MI” – Q waves +/-
    inverted T waves
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17
Q

How can you tell anatomical site of myocardial infarction? Examples? (4)

A
  • Inferior - II, III, AVF
  • Anterior - V1 - V6
  • Anteroseptal - V1-V4
  • Anterolateral - I, AvL, V1-V6
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18
Q

Features of left bundle branch block on ECG? What causes left bundle branch block?

A
  • QRS much broader
  • Loss of Q waves
  • Critical part of heart conducting system has been affected by the infarct
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19
Q

What can also be used in diagnosis of MI other than ECG and history? Examples? (2)
Why are cardiac enzymes and protein markers not as useful as ECG in MI?

A
  • Cardiac enzymes and protein markers
  • Enzyme - creatine kinase
  • Protein marker - troponin
  • Levels may be normal at presentation
  • May not have time to wait for results in STEMI
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20
Q

Features of creatine kinase? (2)

Features of troponin? (2)

A

CK

  • peaks in 24 hrs
  • also in skeletal muscle and brain (non-specific)

Troponin

  • Troponin I and T (not C) highly specific for cardiac muscle damage
  • can detect tiny amounts of myocardial necrosis
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21
Q

What does early treatment of STEMI include? Modes of action? (2)

A
  • Antiplatelet drugs like aspirin and clopidogrel
  • Aspirin - switches off production of TXA2 by blocking COX1
  • Clopidogrel - blocks ADP receptors on platelets so prevents activation
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22
Q

Treatment for patients with acute coronary syndrome? Treatment for patients with cute coronary syndrome with ischaemic ECG changes or elevation of cardiac markers?

A
  • 300 mg aspirin

* 300 mg aspirin and 300 mg clopidogrel (nowadays 180 mg ticagrelor)

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23
Q

Will treatment with aspirin and clopidogrel/ticagrelor alone unblock artery in STEMI? What agents are used for this? Examples? (2)

A
  • Very unlikely

* Thrombolytic agents e.g. streptokinase, t-PA

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24
Q

When does thrombolysis have a greater outcome?

A

When administered early

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25
Q

What is reperfusion therapy? What are indications for reperfusion therapy? What do contraindications for reperfusion therapy include? (3)

A
  • Includes thrombolysis and PCI

Indications

  • Chest pain suggestive of acute MI (more than 30 mins, less than 12 hours)
  • ECG changes - acute ST elevation, new bundle branch block (BBB)
  • No contraindications

Contraindications

  • bleeding ulcer
  • haemorrhagic stroke
  • surgery
26
Q

Is thrombolysis only given in hospital?

A

No, paramedics can administer pre-hospital

27
Q

Risks of thrombolytic therapy? (3)

A
  • Failure to re-perfuse
  • Haemorrhage - Intracranial haemorrhage (2%)
  • Hypersensitivity
28
Q

Probability of an open artery after thrombolysis e.g. SK? What happens to patient with failed thrombolysis or acute reocclusion?

A
  • 50%

* Doubled long term mortality risk

29
Q

Benefit of PCI over being thrombolysed? What is PCI? Process? (2)

A
  • Decreased risk of CVD events
  • PCI - percutaneous coronary intervention i.e. primary angioplasty (GOLD STANDARD)
  • Artery opened with wire, ruptured plaque fixed to wall of artery with stent
30
Q

What is optimal re-perfusion therapy?

A
  • If <2 hrs, PCI (angioplasty) in hospital

* If >2 hrs, thrombolysis in community and taken to PCI clinic

31
Q

Early treatment of STEMI? (7)

A
  • Analgesia - diamorphine iv
  • Anti-emetic - iv (as morphine can induce vomiting)
  • Aspirin - 300 mg and clopidogrel 300 mg (now ticagrelor 180 mg)
  • GTN - if BP > 90 mmHg
  • Oxygen - ONLY if hypoxic (SaO2 <92%)
  • Primary angioplasty
  • Thrombolysis – if angioplasty not available within 90 minutes
32
Q

Complications of acute MI? (4)

A
  • Death
  • Arrhythmic complications
  • Structural complications
  • Functional complications
33
Q

What do arryhmic complications of acute MI include? Treatment?

A
  • Ventricular fibrillation

* Defibrillation (easily treatable)

34
Q

What do structural complications of acute MI include? (8)

A
  • Cardiac rupture – usually fatal
  • Ventricular septal defect
  • Mitral valve regurgitation
  • Left ventricular aneurysm formation
  • Mural thrombus + systemic emboli (can cause stroke)
  • Inflammation
  • Pericarditis
  • Dressler’s syndrome
35
Q

How is ventricular septal defect treated? Mitral regurgitation?

A
  • Occluding devices inserted to prevent fluid travelling across septum
  • Offload the heart with diuretics and then emergency valve replacement surgery
36
Q

Functional complications of acute MI? (3)

A
  • Acute ventricular failure (left, right, biventricular failure)
  • Chronic cardiac failure
  • Cardiogenic shock
37
Q

What is KILLIP classification used for? Explain? (4)

A
  • To predict in-hopsital mortality of heart disease

KILLIP

  • I - No signs of heart failure 6%
  • II - Crepitations < 50% of lung fields 17%
  • III- Crepitations > 50% of lung fields 38%
  • IV- Cardiogenic shock 81%
38
Q

Routine observation of cardiac patients includes? (6)

A
  • Cardiac monitor
  • Pulse and blood pressure
  • Heart sounds (esp added sounds)
  • Murmurs
  • Pulmonary crepitations
  • Fluid balance (urine output)
39
Q

What is key trigger for NSTEMI? Why would there be a plaque rupture but no STEMI? Treatment for NSTEMI? (3)

A
  • Atherosclerotic plaque rupture
  • Endothelium can produce t-PA – so potential for body to prevent build up of thrombus and occlusion of vessel
  • Aspirin, clopigrogrel/ticagrelol, GP IIb, IIIa and PCI
40
Q

Features of NSTEMI on ECG? STEMI?

A
  • ST depression - sign of cardiac ischaemia

* ST elevation - sign of cardiac injury or infarction

41
Q

Complications of ACS treatments?

A
  • Minor bleed
  • Major bleed
  • Allergic reactions
  • Acute MI
  • Death – bleed out
42
Q

What is important to remeber about ECG in acute NSTEMI?

A

ECG MAY BE NORMAL (unlike STEMI, ECG may not tell you there is a problem)

43
Q

What is used instead of ECG to diagnose NSTEMI? Preferred biomarkers?

A
  • Troponin marker

* TnT or TnI

44
Q

What does troponin maker tell us in NSTEMI? (2) When is condition labelled as MI?

A
  • Presence of myocardial ischaemia
  • Microscopic zones of myocyte necrosis
  • Any amount of myocardial ischaemia
45
Q

What are troponin levels actually measuring? (3)

A
  • Embolisation
  • Microvascular circulation
  • Myonecrosis
46
Q

Treatment for all ACS patients (unstable angina, STEMI, NSTEMI)? (3)

A
  • LMWH, Fondaparinux (inhibit coagulation cascade by blocking activation of X)
  • B - blockers
  • ACEI
47
Q

What other conditions is TnT elevated in? (8)

A
  • CCF
  • Hypertensive crisis
  • Renal failure
  • Pulmonary embolism
  • Sepsis
  • Stroke/TIA
  • Pericaditis / Myocarditis
  • Post arrhythmia
48
Q

What are classifications of MI? (3)

A
  • 1 - spontaneous MI due to ischaemia from primary coronary event e.g. plaque rupture, dissection
  • 2 - MI due to ischaemia from imbalance of O2 supply and demand e.g. coronary embolism, anaemia, arrhythmia, hyper/hypotension
  • 3 - sudden unexpected cardiac death with symptoms suggesting ischaemia e.g. ST-segment elevation, new loeft bundle branch block, fresh coronary thrombus
49
Q

What does type 2 MI occur due to? Is it classed as an MI? What causes ischaemic imbalance?

A
  • Ischaemic imbalance
  • Not ACS but MI as troponin is released
  • Increased O2 demand due to tachycardia (arrythmia), hyper/hypotension, embolism
50
Q

Difference beween type 1 and type 2 MI? (3)

A
  • Type 1 - sudden symptoms, major ECG changes, no other obvious cause
  • Type 2 - more gradual symptoms, minor ECG changes, secondary causes
51
Q

What is non-ischaemic myocardial injury with necrosis (NIMI)? MINOCA?

A
  • Not technically type 2 MI but classed as such

* Myocardial infarction with non-obstructive coronary arteries

52
Q

Conditions associated with NIMI? (3)

A
  • Arrhythmia
  • Myocarditis
  • Chemotherapy
53
Q

Benefits of adding clopidogrel/ticagrelor to standard treatment? What is ticagrelor?

A
  • Fewer patients on clopidrogrel/ticagrelor have ischaemia, recurent angina or pulmonary oedema
  • ADP antagonist (liek clopidogrel)
54
Q

What is used to estimate the risk of death from MI in hospital?

A

GRACE score

55
Q

What is another drug other than clopidogrel/ticagrelor that blocks platelet aggregation in NSTEMI?

A

Glycoprotein IIb, IIIa inhibitors e.g. tirofiban

56
Q

What patients should have angiography (not angioplasty) and revascularisation? (2)
What are 2 revascularisation techniques?

A
  • Patients with NSTEMI at mod/high risk of recurrent cardiovascular events
  • Patients with STEMI treated with thrombolytic therapy
  • PCI
  • Coronary bypass
57
Q

Types of PCI? (2)

A
  • Percutaneous balloon angioplasty

* Stent placement

58
Q

Types of stenting? (2)

A
  • Drug-eluting stent

* Bare metal stent

59
Q

What is troponin-itis? When can you diagnose MI? (4)

A
  • Misdiagnosis of NSTEMI due to raised troponin - other conditions lead to raised troponin
  • Only when troponin levels are raised AND one of the following:
  • Ischaemia symptoms
  • ST changes
  • Imaging showing ischaemic changes to heart
  • Identification of intracoronary thrombus by angiography
60
Q

Secondary prevention of MI? (9)

A
  • Smoking cessation
  • Control of BP
  • Control diabetes
  • Control cholesterol (statins)
  • Aspirin + clopidogrel
  • B-blockers (atenolol/bisoprolol)
  • ACEI (ramipril/perinopril)
  • Simvastatin/atervastatin
  • GTN spray
61
Q

Cardiac rehabilitation post-MI?

A
  • Cardiac rehabilitation nurses
  • Physiotherapy exercise classes
  • Smoking cessation specialists
  • Pharmacists, nutritionists, clinical psychologists
  • Cardiologists
62
Q

Targets for cholesterol in secondary prevention? BP? (2)

A
  • Cholesterol <4 mmol/l
  • BP <140/85 mmHg
  • Diabetes, renal disease, target organ damage <130/80 mmHg

Cardiovascular (28 decks)

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