Coronary Artery Disease 1 Flashcards Preview

Term 5 - PathoPhysio > Coronary Artery Disease 1 > Flashcards

Flashcards in Coronary Artery Disease 1 Deck (19):

Etiology of CAD

  • Atherosclerotic obstruction of the large epicardial vessels – the most common cause
  • Spasm of the coronary arteries
  • Emboli
  • Congenital abnormalities – rare cause


  • In Left coronary dominant individuals
  • The LCX supplies:

  • Major part of Inferior wall
  • Posterior wall of LV
  • Apex

The remaining perfusion is same as that in RCA dominance

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The coronary blood flow is mainly controlled by

  • The coronary blood flow is mainly controlled by local metabolic autoregulation
  • Sympathetic stimulation does not produce significant vasoconstriction in coronary vessels


  • At rest the heart produces 70% of its ATP from oxidation of fatty acids and 30% from oxidation of carbohydrates
  • During exercise, lactate becomes an important substrate for the myocardial metabolism


Chest Pain

  • The actual trigger for nerve stimulation is 

  • The actual trigger for nerve stimulation is adenosine. Blocking adenosine receptor (P1) with aminophylline leads to reduced anginal pain
  • Chest pain is mediated by sympathetic afferent fibers: T1-T5
  • In the spinal cord, the pain impulses converge with impulses from other somatic structures and hence radiated to the chest wall, back, and arm


Cellular ischemia occurs by

  1. Increased O2 demand: Eg: Thyrotoxicosis, Hypertrophy, High afterload, High heart rate.
  2. Absolute reduction in O2 supply: Eg: atherosclerosis and spasm.
  3. Combination of i & ii (eg:cocaine abuse)


  • ECG changes during an attack:

  • T wave (invesion) discordant to the QRS complex
  • ST-segment depression
  • Decreased R-wave height


  • The ECG between attacks:
  • At rest is normal (30%)
  • In the remaining 70%, the ECG shows evidence of previous infarction, or hypertrophy

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Location of lesion (ischemia/MI) by observing changes in 12 lead ECG:

  • Inferior (diaphragmatic) wall:
  • Anterior wall/Anteroseptal: 
  • Lateral wall: 
  • Right Ventricle: 
  • Septal wall : 

  • Inferior (diaphragmatic) wall: Lead II, III & aVF
  • Anterior wall/Anteroseptal: V1-V4
  • Lateral wall: Lead I, aVL, V5, V6
  • Right Ventricle: V1, V2 & V3
  • Septal wall : V1, V2


Pathophysiology of Unstable Angina

  • Plaque disruption & fissuring
  • Platelet activation: adhesion, aggregation & secretion
  • Thrombotic occlusion
  • Platelet release of vasoconstrictors such as thromboxane A2 or serotonin that contribute to further decrease in flow

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Diagnosis of unstable angina

  • Characteristic chest pain
  • ECG: during episodes of chest pain:
    • Transient ST-segment elevation
    • Transient ST-segment depression
    • Symmetric T-wave inversion

A normal ECG does not exclude the possibility that chest pain is ischemic in origin


  • Diagnosis:

  • A form of acute coronary syndrome caused by coronary spasm
  • Patients are usually younger, female, smokers, and without other significant risk factors for coronary artery disease
  • Transient ST-segment elevation during chest pain
  • Intermittent chest pain: often repetitive; usually at rest; typically in the early morning hours & rapidly relieved by nitroglycerine
  • Patients often have manifestations of other vasospastic disorders such as migraine headaches and Raynaud’s phenomenon
  • Most attacks resolve without progression to MI
  • Angiography shows no obstructions in vessels at rest


  • Pathophysiology

  • Within 60 sec after coronary artery occlusion → Myocardial oxygen tension in the affected cells falls to zero →  Rapid shift to anaerobic metabolism in myocytes →  Lactic acid production →  Dysfunction in myocardial contraction and relaxation.
  • If re-perfusion is not done, an irreversible injury occurs.



  • Most common in inferior wall myocardial infarction (due to occlusion of RCA)
  • Reasons for bradycardia
    • Ischemia of AV node and conduction defects and/or
    • Vagus nerve stimulation and conduction defects
  • Dysfunction of the SA node is rare because of dual blood supply from both the right and the left coronary arteries


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  • In Left coronary dominant individuals (15%):
  • The LCX supplies:
  • Major part of Inferior wall
  • Posterior wall of LV
  • Apex
  • The remaining perfusion is same as that in RCA dominance

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