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ESA 2 CVS > Ischaemic Heart Disease (11) > Flashcards

Ischaemic Heart Disease (11) Flashcards

0
Q

What is pre load and after load?

A
  • Preload: end diastolic pressure

- Afterload: pressure of the wall of left ventricle during ejection

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1
Q

What is the definition of heart failure?

A
  • The chronic inability of the heart to perfuse tissues of the body despite adequate filling pressure
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2
Q

What is coronary blood flow affected by?

A
  • Perfusion pressure

- Coronary artery resistance

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3
Q

What is meant by supply?

A
  • O2 carrying capacity of the blood
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4
Q

What myocardial causes are there for IHD?

A
  • Increase in myocardial demand: tachycardia, thyrotoxicosis, aortic stenosis increasing afterload
  • Decrease in myocardial O2 supply: decreased coronary blood flow, severe hypotension, leads to severe anaemia, strictures
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5
Q

What are the risks of having unstable plaques?

A
  • Fibrous cap undergoes erosion/fissuring -> exposing blood to thrombotic material in necrotic core -> platelet clot can then lead to fibrin thrombus
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6
Q

Outline how plaque fissuring may lead to myocyte injury.

A
  • Sudden decrease in artery lumen
  • Acute severe decrease in blood flow
  • Ischaemia
  • Cause myocyte injury/necrosis
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7
Q

What is meant by stable angina pectoris?

A
  • Brief episodes from exertion or stress
  • Presence of risk factors
  • Relieved after 5 mins
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8
Q

What is a stable plaque?

A
  • Moderate decrease in blood flow
  • Flow is sufficient at rest
  • Exercise -> transient ischaemia
  • No necrosis or myocyte injury
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9
Q

Where are collaterals found?

A
  • Smaller arteries

- Absent in major arteries

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10
Q

What are the treatments available for IHD?

A
  • B blockers: decrease hr and contractility strength
  • Statins: increases stability of plaques, decreases progress of atherosclerosis
  • Aspirin: anti-platelet aggregation, decreases thrombus formation
  • Ca channel blockers: decreases afterload by peripheral vasodilation
  • Organic nitrates: venodilators -> decreases preload
  • Revascularisation
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11
Q

What is revascularisation?

A
  • Percutaneous coronary intervention and stenting
  • Internal mammary artery grafts
  • Saphenous and radial grafts
  • Coronary artery bypass grafting (CABG)
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12
Q

What is a STEMI?

A
  • ST elevation MI: due to randomly depolarising myocytes
  • 90% occlusion
  • Lots of necrosis
  • Biomarkers present (Tropanin & Creatin kinase)
  • PCI needed
  • Thrombolysis
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13
Q

What is a NSTEMI?

A
  • No ST elevation MI
  • Positive to Biomarkers
  • Necrosis
  • Adequate collateral circulation to keep alive
  • Not full thickness myocyte death
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14
Q

What is unstable angina?

A
  • No ST elevation
  • No necrosis
  • Partial/brief occlusion
  • Adequate collateral circulation
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15
Q

What is the treatment for STEMI?

A
  • Re-establish perfusion: PCI/stenting, Thrombolysis
  • Anti platelet agents: aspirin
  • Anti ischaemic therapy
16
Q

What is the treatment for long term MI?

A
  • Risk factor management
  • ACE inhibitors
  • Statins
  • B blockers
  • Aspirin
17
Q

What is the treatment for unstable angina/NSTEMI?

A
  • Prevent MI/muscle loss
  • Risk assessment
  • Prevent progression of thrombus: anti platelet, anticoagulant
18
Q

What are the signs and symptoms of acute MI?

A
  • Tachycardia
  • Arrhythmias
  • Low bp
  • S3/S4 crackles
  • Sweating
19
Q

What is the history for an Acute MI?

A
  • Central, crushing chest pain and radiation
  • Distressed
  • Persistent, severe pain
  • Pallor
  • Sweating
  • Nausea
  • Vomiting
  • Not relieved by rest
20
Q

What are the possible complications of acute MI?

A
  • Arrhythmias
  • Heart block
  • Atrial fibrillation
  • Heart failure: loss of myocardium, decrease myocardial contractility
  • Cardiogenic shock
  • Ventricular fibrillation, tachycardia
21
Q

What are the two main biomarkers for IHD?

A
  • Tropanin: cardiac tropanin 1/tropanin T

- Creatin kinase

22
Q

Where is creatin kinase released from and when does it first show, peak and disappear?

A
  • Skeletal muscle
  • Brain
  • HEART
  • 3-8hrs first shows
  • Peak: 24hrs
  • Normal 48-72hrs
23
Q

What is tropanin and when does it first show, peak and disappear?

A
  • Cardiac tropanin 1: cTn1
  • Tropanin T: cTnT
  • 3-4hrs after onset of pain
  • Peak: 18-36hrs
  • Slow decline 10-14 days

ESA 2 CVS (16 decks)

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