Ischaemic Heart Disease Flashcards
Aetiology
Genetic infection
Alcohol
Cocaine
Cause of Ischaemic heart disease
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.
Pathogenesis
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)
Clinical effects of IHD: angina
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
Type of heart disease
Congenital heart disease Rheumatic heart disease Endocarditis Cardiomyopathy Myocarditis
Clinical effects of IHD: Myocardial Infarct
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-
Clinical effects of IHD: Sudden cardiac death
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)
Acute coronary syndrome
- unstable angina
- acute myocardial Infarct
- sudden cardiac death
Caused by erosion or rupture of the plaque, followed by thrombosis or vasospasm of the artery
Clinical effects of IHD: chronic ischaemic heart disease
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.
Risk factors for IHD
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