Ischaemic Heart Disease Flashcards

1
Q

Aetiology

A

Genetic infection
Alcohol
Cocaine

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2
Q

Cause of Ischaemic heart disease

A

Decreased O2 supply- blocked coronary artery- also, lack of blood flow allows a build up of waste products (lactic acid) or accumulation of electrolytes causing injury to tissue.

Increased O2 demand- stress, exercise

Most common causes are:
atherosclerosis
thrombosis- thrombus is built/ fixed.

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3
Q

Pathogenesis

A

Atheroma and thrombus

  • vasospasm of coronary artery: loss of vasodilators, platelet aggregation eg micro-thrombus forms on the artery wall, platelets release TXA2, causing vasoconstriction and activation of more platelets. Vasospasm can occur on arteries with or without significant atheroma.
  • blood flow is constricted during an artery spasm- found most obstructions were in proximal parts of RIght coronary artery, LEft ascending d and circumflex arteries. Left hand arteries most common.
  • thrombus is fixed, it is built into the wall of the artery, not travelling (embolus)
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4
Q

Clinical effects of IHD: angina

A

Angina- pain.

  • stable- typical, predictable, bought on by exercise, stress and is relieved by decreased exercise
  • unstable- unpredictable, progressive increases in frequency, intensity, caused by thrombosis or vasospasm in a coronary artery.
  • variant
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5
Q

Type of heart disease

A
Congenital heart disease 
Rheumatic heart disease 
Endocarditis
Cardiomyopathy 
Myocarditis
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6
Q

Clinical effects of IHD: Myocardial Infarct

A

If somebody doesn’t survive myocardial Infarct it’s called sudden cardiac death.
Assume they survived, complication:
- rupture of ventricular wall. Generally occurs in first two weeks. Loss of blood in the pericardial sac, leads to a decrease in cardiac output and a drop in blood pressure.
- rupture leads to blood in pericardial sac- pressure against heart, reducing cardiac output (cardiac tamponade: when there is fluid in pericardial sac). Pressure against venous return.
- mitral incompetence: infarction may cause damage to papillary muscles causing failure of AV valves to close properly.
- thrombosis formation. Fine until it travels (thrombosis embolism).
- ventricular aneurysm: decreased cardiac output. Thrombosis/ embolism formation.
- arrhythmia-

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7
Q

Clinical effects of IHD: Sudden cardiac death

A

Death within 24 hours of the CV event- most die in first 6 hours.
Causes:
- congenital malformations- hypertrophic cardiomyopathy
- commotio cordis (myocardial concussion), chest trauma
- coronary (Ischaemic) artery disease
speed and location of obstruction- history of obstruction may allow people to quickly form new blood vessels
location and extent of infarction- effects range from subclinical, to AMI, to fatal arrhythmia (ventricular fibrillation- quivering of ventricles)

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8
Q

Acute coronary syndrome

A
  • unstable angina
  • acute myocardial Infarct
  • sudden cardiac death
    Caused by erosion or rupture of the plaque, followed by thrombosis or vasospasm of the artery
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9
Q

Clinical effects of IHD: chronic ischaemic heart disease

A

Leads to left or right heart failure.
Left heart failure:
-Left ventricular Hypertrophy- from hypertension, or from Hypertrophy of surviving fibres
-Left ventricular dilatation- decreased contraction force, heart failure
- congestive heart failure- decrease in cardiac output m, congestion, oedema
Right heart failure:
- pulmonary hypertension
- ischaemic heart disease
- valve disease
- right ventricular failure- Hypertrophy then dilatation. Congestion and oedema.

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10
Q

Risk factors for IHD

A

Disease development:

  • risk factors for atherosclerosis (long term factors) - fatty streak, occurs at bends and bifurcations, and increased inflammatory mediators in the plasma
  • risk factors for thrombosis (short term risks)

Sudden events
- risk factors for unstable angina, AMI, and sudden cardiac death. Usually caused by rupture of an atheroma, and thrombosis

Unchangeable:

  • age
  • gender
  • genetic factors

Modifiable:

  • hypertension, risk factors for hypertension all risk factors for CVD-damage to arterial wall, high sodium intake, binge drinking, genetics
  • high blood cholesterol
  • diabetes
  • smoking - stable angina, unstable angina, AMI, stroke, peripheral vascular disease, chemical injury to vessel wall, inflammation in vascular endothelial cells, increases platelet aggregation and adhesion
  • binge drinking
  • stress - leads to AMI, sudden death, stroke
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