Coronary Artery Disease 1 Flashcards Preview

Term 5 - PathoPhysio > Coronary Artery Disease 1 > Flashcards

Flashcards in Coronary Artery Disease 1 Deck (19):
1

Etiology of CAD

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

2

  • 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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3

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

4

  • 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

5

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

6

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)

7

  • 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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8

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

9

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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10

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

11

  • PRINZMETAL’S or VARIANT ANGINA
  • 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

12

  • MYOCARDIAL INFARCTION
  • 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.

13

BRADYCARDIA in acute MI

  • 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

14

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18

  • 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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19

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