Your SlideShare is downloading. ×
Atherosclerosis Mi 2010
Upcoming SlideShare
Loading in...5
×

Thanks for flagging this SlideShare!

Oops! An error has occurred.

×
Saving this for later? Get the SlideShare app to save on your phone or tablet. Read anywhere, anytime – even offline.
Text the download link to your phone
Standard text messaging rates apply

Atherosclerosis Mi 2010

83

Published on

pathophysiology

pathophysiology

Published in: Health & Medicine
0 Comments
1 Like
Statistics
Notes
  • Be the first to comment

No Downloads
Views
Total Views
83
On Slideshare
0
From Embeds
0
Number of Embeds
1
Actions
Shares
0
Downloads
11
Comments
0
Likes
1
Embeds 0
No embeds

Report content
Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
No notes for slide

Transcript

  • 1. Coronary Artery Disease and Myocardial Infarction
  • 2. Coronary Artery Disease
    • Cardiovascular diseases are the major cause of death in NZ (40% of all deaths)
    • Heart attacks are still the leading cause of all cardiovascular deaths and deaths in general
    • Maori are disproportionately at risk
    • Male deaths twice that of females
  • 3. Atherosclerosis
    • Major cause of CAD
    • Begins as soft deposits of fat that harden with age
    • Referred to as the “hardening of the arteries”
    • Abnormal accumulation of lipid, or fatty, substances and fibrous tissue in the vessel wall
    • Can occur in any artery of the body
    • Atheromas (fatty deposits) have a preference for the coronary arteries
    • Substances create blockages or narrow the vessel in a way that reduces blood flow
  • 4. 3 Types of Lesions Associated with Atherosclerosis
    • Fatty streaks
    • Fibrous atheromatous plaque – basic lesion
    • Characterised by accumulation of lipids, proliferation of smooth muscle cells & formation of scar tissue
    • 3. Complicated lesion – characterised by haemorrhage, ulceration & scar tissue formation
  • 5. Pathophysiology
    • Endothelial lining altered as a result of injuries – hyperlipidaemia & hypertension
    • Platelets are activated
    • Smooth muscle cell proliferation entraps lipids, which are calcified over time & form an irritant to the endothelium on which platelets adhere & aggregate
    • Fibrin formation & thrombi occur
  • 6.  
  • 7. Atherosclerosis
  • 8. Atherosclerosis
  • 9. Collateral Circulation
    • Normally some arterial branching, termed collateral circulation exists within the coronary circulation
    • Growth of collateral circulation is attributed to 2 factors
    • - The inherited predisposition to develop new vessels
    • -The presence of chronic ischaemia
  • 10. Collateral Circulation
    • When atherosclerotic plaque occludes the normal flow of blood through a coronary artery & ischaemia is chronic, increased collateral circulation develops
  • 11.  
  • 12. Coronary Artery Disease (CAD)
    • Other causes of heart disease include:
    • Vasospasm (sudden constriction or narrowing) of coronary artery
    • Myocardial trauma
    • Structural disease
    • Congenital abnormalities
    • Decreased oxygen supply (acute blood loss)
    • Increased demand for oxygen (e.g.. rapid heart rate)
  • 13. Non-modifiable Risk Factors
      • Increasing age
      • Gender (more common in men than premenopausal women)
      • Genetic predisposition & family history of heart didease
      • Ethnicity (Maori)
  • 14. Modifiable Risk Factors
    • Major
      • Elevated serum lipid levels (serum cholesterol of more than 5.2mmol/L)
      • Hypertension
      • Cigarette smoking
      • Physical activity
      • Obesity
      • Contributing
      • Diabetes mellitus
      • Stressful lifestyle
      • Lack of oestrogen in women
  • 15. NHF – Risk Tables
    • http://www.nhf.org.nz/index.asp?print=true&PageID=2145828662
  • 16. Clinical Manifestations of CAD
    • Angina pectoris
    • Acute coronary syndrome
    • Sudden cardiac death
    • They all result from ischaemia (lack of oxygen supply to the heart)
  • 17.  
  • 18. Angina Pectoris
    • Episodes or paroxysms of pain or pressure in anterior chest
    • Caused by insufficient coronary blood flow
    • Insufficient flow results in decreased oxygen supply to meet an increased myocardial demand for oxygen in response to physical exertion or emotional stress
    • Usually associated with significant obstruction of a major coronary artery
  • 19. Types of Angina
    • Stable Angina Pectoris
    • Pain usually lasts 3-5 minutes
    • Subsides when precipitating factor is relieved
    • Pain at rest unusual
    • 2. Unstable Angina Pectoris
    • Occurs at rest
    • Has a worsening pattern
    • Unpredictable
    • Considered to be an acute coronary syndrome
  • 20. Anginal Pain
    • Chest pain or discomfort
    • Sometimes referred to as a vague sensation, strange feeling, pressure or ache in chest
    • Unpleasant feeling – constrictive, squeezing, heavy, choking, or suffocating sensation
    • Usually not sharp or stabbing
    • Does not change with position or breathing
    • Pain usually located substernally but may occur in neck or radiate to jaw, shoulders & down arms
  • 21. Factors associated with Anginal Pain
    • Physical exertion (  myocardial oxygen demand)
    • Exposure to cold (vasoconstriction &  BP, with  oxygen demand)
    • Eating a heavy meal (  blood flow for digestion, therefore reducing blood supply to heart muscle)
    • Stress or any emotion-provoking situation (causes release of adrenaline &  BP, increases heart rate & myocardial workload)
  • 22.  
  • 23. Clinical Manifestations of Angina
    • Feeling of anxiety or impending doom
    • Shortness of breath
    • Cold sweat
    • Weakness
    • Paraesthesia of one or both arms
    • Usually relieved by rest
    • Doesn’t usually wake pt from rest
  • 24. Myocardial Infarction (MI)
    • Death of heart tissue caused by lack of oxygenated blood flow
    • Reduced blood flow in coronary artery usually due to atherosclerosis & occlusion of an artery by an embolus or thrombus
    • Area of infarction takes time to develop
    • As cells are deprived of oxygen, ischaemia develops, cellular injury occurs, then lack of oxygen results in death of tissue
    • Most infarcts involve left ventricle
    • Location & area of infarct correlate with part of coronary circulation involved
  • 25.  
  • 26. Myocardial Infarction
    • Contractile function of the heart stops in the area of myocardial necrosis
    • Transmural MI
    • Involves the entire thickness of the myocardium
    • Subendocardial MI
    • The damage has not penetrated through the entire thickness
  • 27. Healing Process
    • Body’s response to cell death is inflammation. Within 24 hrs, leucocytes infiltrate the area
    • Enzymes are released from dead cardiac cells (important indicators of MI)
    • Proteolytic enzymes of neutrophils & macrophages remove all necrotic tissue by 2 nd or 3 rd day
    • Development of collateral circulation improves area of poor perfusion
    • By 6 weeks after MI, scar tissue has replaced necrotic tissue & area is healed
  • 28. Clinical Manifestations of MI
    • Sudden chest pain, unrelieved by rest & medication
    • May have no previous symptoms (sudden death)
    • Increased or decreased BP
    • ECG may show tachycardia, bradycardia & dysrhythmias
    • Dyspnoea, tachypnoea
    • Nausea & vomiting
    • Cool clammy skin
    • Anxiety, restlessness, feeling of impending doom
  • 29. Pain of MI
    • Severe & immobilizing
    • Described as a heaviness, pressure, tightness, burning, constriction or crushing
    • Common locations are substernal, retrosternal or epigastric
    • May radiate to neck, jaw, arms or back
    • Occurs while active or at rest, or asleep or awake
    • Commonly occurs in early morning hrs
    • Lasts for 20 mins or more & more severe than anginal pain
    • Some may not experience pain but may have ‘discomfort’, weakness or shortness of breath
  • 30. Complications of MI
    • Arrhythmias
    • - present in 80% of MI pts
    • - common cause of death in pre-hospital period
    • Congestive Heart Failure
    • - pumping power of heart has diminished
    • Cardiogenic Shock

×