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Chapter 18: Cardiovascular Disorders

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Depolarization
chemical change that creates and action potential that leads to contraction
Baroreceptor
- located in the walls of aorta & internal carotid
- detect changes in BP & cardiac center responds through stimulation
Tachycardia
increased heart rate
Bradycardia
decreased heart rate
Diastole
relaxation phase of cardiac activity
systole
cardiac contraction
Cardiac Output
CO = HR x CV
volume of blood ejected by a ventricle in 1 minute
Stroke Volume
the amount of blood ejected from each ventricle with each contraction
Heart Rate
The number of contractions of the ventricles each minute
Preload
amount of blood delivered to the heart by venous return
Afterload
the force required to eject blood from the ventricles
Peripheral Resistance
the force opposing blow flow; the amount of friction with the vessel walls encountered by blood
Sympathetic System
increases HR
Parasympathetic System
decreases HR
Increased afterload ->
DECREASES CO
Blood Flow
Pulmonary
R<3 L<3
Systemic
Normal CO & SV in each ventrical
is EQUAL
Normal Pressure
L<3 is bigger than R<3
Blood Pressure
BP = CO x PR
PR
increased = vasoconstriction
decreased = vasodilation
Atherosclerosis
build up of plaques (atheromas) in the arteries (large, coronary, carotid)
Ateromas
Choleserol, Foam Cells, CT cells (fibroblasts), Fibrin, Cell debris
Foam Cells
cholesterol-loaded macrophages
Cholesterol
steroid used as a precursor our steroid hormones; some is needed for our body
HDL
BAD
cholesterol from tissues to liver (excretion in bile)
More protein
Less cholesterol
LDL
GOOD
cholesterol from liver to tissues
Less protein
More cholesterol
Atheroma Formation
1. damage to endothelial cells
2. inflamation -> leukocytes and lipids accumulate (Fat Streak)
3. Thrombus/ calcification or necrosis
Embolus
clot that has broken & lodged in a downstream vessel
Angina Pectoris
chest pain caused by myocardial ischemia; not permanent
-caused by increased HR
-relieved by rest and vasodilators