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Semester 1 Year 2 > Ischaemic heart disease > Flashcards

Ischaemic heart disease Flashcards

1
Q

So, heart disease is bad yeah?

A

Yeah, leading cause of death bro

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2
Q

What are some causes of atherosclerotic coronary diseases?

A

Chronic coronary insufficiency
Angina

Unstable coronary disease

Myocardial infarction

Sudden ischaemic coronary death

Heart Failure

Arrhythmia
Acute ischaemic
Scar related

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3
Q

Describe the layers used when discussing the anatomy of the coronary artery

A
  • Epicardial–outer surface of heart
  • Endocardial–inner surface of heart
  • Subendocardialregion is water-shed area of perfusion and first to become ischaemic
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4
Q

Name the epicardial coronary arteries

A

Circumflex coronary

Left anterior descending

Posterior descending artery

Right ventricular branch

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5
Q

What can be used to image coronary arteries

A

Coronary angiography

CT

MRI

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6
Q

Discuss what factors increase risk for atherosclerotic coronary artery disease

A 
Age
Hypertension Hypercholesterolaemia Smoking
Diabetes
Obesity
Physical inactivity
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7
Q

Discuss the pathology found in atherosclerotic coronary artery disease

A

 Fatty streak

 Fibro-fatty palque

 Plaque disruption Plaque rupture Plaque erosion

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8
Q

What will occur in the coronary arteries in response to total occlusion of the left anterior descending artery?

A

The supply will be filled by collaterals from the RCA

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9
Q

Discuss the symptoms, cause and ECG indications of angina

A 
• SYMPTOMS
– 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

• CAUSE
– Sub-Endocardial ischaemia

• ECG
– ST depression

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10
Q

What mechanisms are at play in angina in relation to basic physiology?

A

MISMATCH OF BLOOD SUPPLY TO DEMAND BECAUSE OF EPICARDIAL STENOSIS

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11
Q

Discuss the cause of angina pectoris

A

Mismatch of supply and demand

Supply = Coronary Blood Flow

Demand = Myocardial Oxygen Consumption
(MVO2 )

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12
Q

What are the two regulatory systems of the normal control of the coronary circulation?

A

– Autoregulation (myogenic control) – Metabolic regulation

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13
Q

Discuss exercise and myocardial blood flow

A

 CBF can rise up to five fold (400 ml/min/100g) to accommodate a 20 fold increase in total body O2 consumption.

 Little change in a near maximal O2 extraction.

 A rise in heart rate where per beat CBF is constant can account for 1/3 of the increase seen.

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14
Q

What are the 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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15
Q

Discuss investigation of chest pain to identify CAD as the cause

A

• Anatomical assessment
– CT coronary angiography
– Invasive angiography

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

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

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16
Q

Discuss angina treatment

A

• Reduce Myocardial Oxygen consumption. – Drugs

• Improve coronary flow reserve.
– Percutaneous Coronary Intervention (stents and balloons)
– Coronary Artery Bypass Grafting (CABG) – Drugs - Vasodilators

17
Q

CABG bitches

A

Coronary artery bypass graft is bae, great saphenous vein grafted to RCA and left internal mammary artery grafted to LAD

18
Q

What are the principles of drug treatment and angina

A
  1. Reduction in myocardial oxygen consumption

2. Reduction in the variability of coronary flow reserve

19
Q

Discuss the action of drugs in angina

A

• Beta Adrenoceptor Blockers
– Reduce Heart Rate, Reduce Blood Pressure
– i.e. Reduce work of heart

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

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

• Ikf Channel Inhibitors
– Selective heart rate reduction by inhibiting channels in SA node - Ivabridine

20
Q

What are the stats on myocardial infarction (heart attack)

A

• 15-20 % do not make it to hospital • In hospital Mortality ~ 6 -15%

21
Q

What is the clinical presentation of a myocardial infarction

A
  • Chest Pain – severe – crushing radiating to jaw and arm
  • Associated “Autonomic􏰀 symptoms (nausea, sweating, terror)
  • Breathlessness
22
Q

What are the causes of a myocardial infarction

A
  1. Plaque rupture – 70 – 75%
  2. Plaque erosion – 25 – 30%
  3. Coronary embolism
  4. Coronary artery spasm / drugs
  5. Coronary anomaly
  6. Spontaneous coronary dissection
23
Q

What events modify the presentation of AMI?

A

Time of day

Inflammatory activity

Infection esp. Respiratory

Elevation of blood pressure

Catacholamines

24
Q

How do we classify myocardial infarctions

A

• By site of infarction - pathology
– Full thickness, transmural
– Sub endocardial

• By ECG - Clinical
– ST Elevation myocardial infarction (STEMI)
– Non-ST elevation myocardial infarction (non- STEMI)

• By cause
– Type 1-4

25
Q

Discuss the relation between anatomy and ECG in AMI

A
  • STEMI implies transmural myocardial infraction

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

26
Q

What are the type categories of myocardial infarction

A

Type 1 - spontaneous MI related to schema due to primary coronary event like plaque erosion +/or rupture, fissuring or dissection

Type 2 - MI secondary to ischaemia due to either increased O2 demand or decreased supply

Type 3 - Sudden unexpected cardiac death often with symptoms suggestive of myocardial ischaemia

Type 4 - MI associated with percutaneous coronary intervention (4a) or stent thrombosis (4b)

Type 5 - Myocardial infarction associated w cardiac surgery

27
Q

How does one diagnose myocardial infarction

A

• A Clinical History with:
– ECG Changes, defining sub-classification of:
• STEMI
• NSTEMI

  • And raised cardiomyocyte markers in blood
  • Troponin T or I
  • Creatine kinase MB isoform (CKMB)
  • Creatine Phosphokinase (CPK)
  • AST
  • Myoglobin
28
Q

Discuss STEMI management

A

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

Immediate revascularisation
Primary PCI (percutaneous coronary intervention)
(Thrombolysis – clot busting)

29
Q

What is adjunctive therapy for STEMI

A

• After anti-platelets agents and revascularisation
– 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)

30
Q

What are the complications of a STEMI

A

• Immediate
Complications of STEMI
– Ventricular Arrhythmia and death
– Acute Left Heart Failure

• Early (Day 2-7)
– Myocardial Rupture
– Mitral valve insufficiency
– Ventricular Septal defect
– Mural thrombus and emobolisation

• Late (beyond day 7)
– LV dilatation and heart failure
– Arrhythmia
– Recurrent myocardial infarction

31
Q

Discuss the causes of NSTEMI

A

• 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

32
Q

Discuss treatment of non-STEMI

A
  • Antiplatelet 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)

Semester 1 Year 2 (69 decks)

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