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Y2S1 CARDIO. > Ischaemic Heart Disease and its Consequences > Flashcards

Ischaemic Heart Disease and its Consequences Flashcards

1
Q

Epicardial

A

outer surface of heart

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2
Q

Endocardial

A

inner surface of heart

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3
Q

Subendocardial region

A

water-shed area of perfusion and first to become ischaemic

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4
Q

Coronary Artery Imaging in humans in life

A
  • Coronary Angiography • CT

* MR imaging

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5
Q

Causes:

A

Chronic coronary insufficiency:
Angina

Unstable coronary disease:
Myocardial infarction
Sudden ischaemic coronary death

Heart Failure

Arrhythmia:
acute Ischaemia
Scar related

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6
Q

Atherosclerotic Coronary Artery Disease risk factors

A 
Age
Hypertension Hypercholesterolaemia Smoking
Diabetes
Obesity
Physical inactivity
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7
Q

Atherosclerotic Coronary Artery Disease

Pathology- the three components

A
  • fatty streak
  • fibro-fatty plaque
  • plaque disruption (plaque rupture or erosion)
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8
Q

symptoms of angina

A

– Gripping central chest pain
– Radiation to arm and jaw
– Clear and precise relationship to exercise
– Goes off in 2-10 mins after discontinuation of exercise – Worse after food. Worse in cold
– No autonomic features
– Flat of hand/fist to describe pain

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9
Q

cause of angina

A

– Sub-Endocardial ischaemia

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10
Q

how does angina present on an ECG

A

ST depression

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11
Q

angina mechanism

A

MISMATCH OF BLOOD SUPPLY TO DEMAND BECAUSE OF EPICARDIAL STENOSIS:
Supply = Coronary Blood Flow
Demand = Myocardial Oxygen Consumption
(MVO2 )

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12
Q

• Two regulatory systems with two control mechanisms

A

– Autoregulation (myogenic control)

– Metabolic regulation

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13
Q

determinants of myocardial oxygen consumption

A 
- variable per unit mass of tissue:
tension development – LV pressure and LV volume Contractility
Heart rate
- fixed per unit mass of tissue:
basal activity (10-20%)
- Mass of tissue
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14
Q

Identification of Coronary Disease as the cause: anatomical assessment

A

– CT coronary angiography

– Invasive angiography

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15
Q

Identification of Coronary Disease as the cause: Test of Inducible ischaemia

A

– Exercise stress test
– Dobutamine stress echo
– Myocardial perfusion imaging with either exercise or phamacological stress
– Cardiac magnetic resonance imaging (cMR)

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16
Q

Identification of Coronary Disease as the cause: anatomic and functional

A

– Invasive angiography and fractional flow reserve (FFR)
– cMR
– Novel CT

17
Q

Angina Treatment - Reduce Myocardial Oxygen consumption.

A

drugs

18
Q

Angina Treatment - improve coronary flow reserve

A

– Percutaneous Coronary Intervention (stents and balloons)

– Coronary Artery Bypass Grafting (CABG) – Drugs - Vasodilators

19
Q

Drug treatment and Angina

A
  1. Reduction in myocardial oxygen consumption

2. Reduction in the variability of coronary flow reserve

20
Q

Beta Adrenoceptor Blockers

A

– Reduce Heart Rate, Reduce Blood Pressure

– i.e. Reduce work of heart

21
Q

• Nitrates(GTN)

A

– Venodilation → Reduced LV size → Wall tension. (reduces work) Small effect on epicardial stenosis dilation (improved supply)

22
Q

• Calcium Channel blockers

A

– Reduce HR, some reduce Heart rate, small effect on from epicardial dilatation (mixed)

23
Q

• Ikf Channel Inhibitors

A

– Selective heart rate reduction by inhibiting channels in SA node - Ivabridine

24
Q

MYOCARDIAL INFARCTION – Clinical Presentation

A
  • chest pain, severe, crushing radiating to jaw and arm
  • associated ‘autonomic’ symptoms (nausea, sweating, terror)
  • breathlessness
25
Q

events modifying presentation of AMI

A
  • time of day
  • inflammatory activity
  • infection esp. respiratory
  • elevation of BP
  • catecholamines
26
Q

Classifications of Myocardial Infarction - by site of infarction, pathology

A

– Full thickness, transmural

– Sub endocardial

27
Q

Classifications of Myocardial Infarction - By ECG - Clinical

A

– ST Elevation myocardial infarction (STEMI)

– Non-ST elevation myocardial infarction (non- STEMI)

28
Q

Classifications of Myocardial Infarction - By cause

A

– Type 1-4

29
Q

Relation between anatomy and ECG

A
  • STEMI implies transmural myocardial infraction

* NSTEMI will include subendocardial infraction but does not exclude transmural infraction in regions remote from ECG

30
Q

• A Clinical History with:

– ECGChanges,definingsub-classificationof:

A
  • STEMI

* NSTEMI

31
Q

ECG Changes, defining sub-classification of: And raised cardiomyocyte markers in blood

A
  • Troponin T or I
  • Creatine kinase MB isoform (CKMB)
  • Creatine Phosphokinase (CPK)
  • AST
  • Myoglobin
32
Q

STEMI Management

A

Antiplatelet agents:
Aspirin + Clopidogrel or other antiplatelet (P2Y12 inbibitor)

Immediate revascularisation:
Primary PCI
(Thrombolysis – clot busting)

33
Q

Adjunctive Therapy for STEMI: • After anti-platelets agents and revascularisation

A

– Statin drugs (reduce cholesterol – plaque passivation)
– ACE inhibitors (usually a couple of days later to inhibit dilation of the left ventricle)
– Beta blockers (reduce myocardial infarction)

34
Q

Complications of STEMI - immediate

A

– Ventricular Arrhythmia and death

– Acute Left Heart Failure

35
Q

Complications of STEMI - Early (Day 2-7)

A

– Myocardial Rupture
– Mitral valve insufficiency
– Ventricular Septal defect
– Mural thrombus and emobolisation

36
Q

Complications of STEMI Late (beyond day 7)

A

– LV dilatation and heart failure
– Arrhythmia
– Recurrent myocardial infarction

37
Q

NSTEMI

A

• Getting more frequent (STEMI less common)
• More common in elderly
• Implies sub-endocardial ischaemia
• Caused by:
– Threatened STEMI
– Small branch occlusion
– Occlusion of well collateralised vessel
– Lateral STEMI in territory not well seen by ECG

38
Q

Treatment of non-STEMI

A

• Anti platelet therapy (Aspirin and clopidogrel)
• Anti-ischaemics(beta blockers and nitrates)
• Statin drugs
• ACE inhibitors
• Coronary angiography and revascularisation
– Early if symptoms continue
– Early if Troponin raised
– Risk score (eg GRACE)

Y2S1 CARDIO. (47 decks)

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