PBL 3- Chest pain Flashcards

1
Q

Describe the cardiovascular changes during exercise.

A
Increased Heart Rate 
Increased myocardial contractility and stroke Volume 
Increased Cardiac Output 
Increased Blood Flow 
Increased Blood Pressure
Total peripheral resistance is decreased
Increased venous return
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2
Q

What role does the ANS play to cardiovascular changes during exercise

A
  • Increased Sympathetic action, decreased Parasympathetic activity
  • Increases the rate of spontaneous firing from the SA node, thus increasing heart rate.
  • Redistribution of blood flow to skeletal muscles instead of visceral organs. The sympathetic innervation to the following muscles is decreased: Stomach, Liver, Kidneys, Small Intestines etc.
  • Release of catecholamines (noradrenaline & adrenaline). This increases myocardial contractility
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3
Q

What are the risk factors for coronary artery disease?

A
  • older age
  • sex (men)
  • family history
  • smoking
  • high blood pressure
  • high cholesterol levels
  • diabetes
  • overweight or obese
  • physical inactivity
  • high stress
  • unhealthy diet
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4
Q

Describe the mechanisms which lead to atherosclerosis.

A

Endothelial cell injury:
• (LDLs) can deposit in the tunica intima due to chronic endothelial injury (smoking, stress, diabetes)
• Increased adhesion and transmigration of leukocytes- create oxidant stress
• Establishes a focus of inflammation

Migration of inflammatory cells:
• Monocytes enter the tunica intima, becoming macrophages
• Macrophages engulf oxidised LDLs and become foam cells

Smooth muscle cells proliferation and migration from tunica media to tunica intima:
• Activated macrophages produce growth factors which contribute to the migration of SMCs
• Proliferation leads to production of collagen and the elaboration of the ECM (hardening of the plaque)
• Lipid is released from dying foam cells, contributing to the extracellular free lipid pools

Plaque formation:
• Formation of fibrous cap
• Below the fibrous cap is a central core of lipid laden foam cells and fatty debris (necrotic core)
• Rupture, ulceration or erosion of an unstable fibrous cap may lead to Intraplaque haemorrhage
or Vessel occlusion. Hence, leading to myocardial infarction.

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5
Q

What is the definition of atherosclerosis.

A

hardening or narrowing of the arteries, putting blood flow to the heart at risk.

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6
Q

What is coronary artery stenosis?

A

narrowing of the coronary arteries that supplies the myocardium with oxygen needed for its normal function.

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7
Q

How does coronary artery stenosis lead to myocardial ischaemia.

A

There is reduced blood flow to the myocardium and a reduced oxygen delivery. When the myocardium is deprived of oxygen, it dies and becomes ischeamic.

Myocardial ischaemia is also due to the increased oxygen demand of the myocardium e.g. due to cardiac hypertrophy.

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8
Q

Describe the distribution of chest pain due to myocardial ischaemia.

A
  • Tight pressure on the middle of the chest
  • Pain that radiates to arms, neck, jaw, shoulder or back, accompanying the chest pain
  • Nausea
  • Fatigue
  • Shortness of breath
  • Sweating
  • Dizziness
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9
Q

What is the difference between NSTEMI and STEMI

A

Non-ST elevated MI- partial occlusion

ST-elevated MI- complete occlusion

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10
Q

What is Angina Pectoris?

A

chest pain due to myocardial ischaemia

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11
Q

Describe the investigations carried out for Angina Pectoris

A

ECG- Looks for abnormalities of rhythm, conduction, repolarisation.

Bruce protocol- treadmill exercise stress test, During the exercise, blood pressure is monitored, and a 12 lead ECG reading is monitored.

Chest X-ray- pulmonary oedema

Coronary angiography- gold standard for imaging coronary artery

Blood tests

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12
Q

What is the main target for Angina treatment

A

To reduce myocardial O2 demand

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