chemical change that creates and action potential that leads to contraction
- located in the walls of aorta & internal carotid
- detect changes in BP & cardiac center responds through stimulation
increased heart rate
decreased heart rate
relaxation phase of cardiac activity
CO = HR x CV
volume of blood ejected by a ventricle in 1 minute
the amount of blood ejected from each ventricle with each contraction
The number of contractions of the ventricles each minute
amount of blood delivered to the heart by venous return
the force required to eject blood from the ventricles
the force opposing blow flow; the amount of friction with the vessel walls encountered by blood
Increased afterload ->
Normal CO & SV in each ventrical
L<3 is bigger than R<3
BP = CO x PR
increased = vasoconstriction
decreased = vasodilation
build up of plaques (atheromas) in the arteries (large, coronary, carotid)
Choleserol, Foam Cells, CT cells (fibroblasts), Fibrin, Cell debris
steroid used as a precursor our steroid hormones; some is needed for our body
cholesterol from tissues to liver (excretion in bile)
cholesterol from liver to tissues
1. damage to endothelial cells
2. inflamation -> leukocytes and lipids accumulate (Fat Streak)
3. Thrombus/ calcification or necrosis
clot that has broken & lodged in a downstream vessel
chest pain caused by myocardial ischemia; not permanent
-caused by increased HR
-relieved by rest and vasodilators
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