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31 Cards in this Set
- Front
- Back
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Cardiac Output
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changes in HR or SV will change Co
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Factors Affecting HR
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1.) Symp. + parasymp. fibers innervate SA + AV nodes and cardiac m. cells
2.)Cardiac center-in medulla sends out simultaneous symp. and parasymp. impulses (homeostasis) 3.) Baro and Chemoreceptors 4.)Nicotine stimulates symp. nerves |
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2.) Cardiac Center in medulla sends out simultaneous symp. and parasymp. impulses (homeostasis)
(Factors Affecting HR) |
a.)Symp.- increases HR; Norepinephrine (NE)
b.)Parasymp.- decreases HR; Ach |
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3.)Baro + chemoreceptors
(Factors Affecting HR) |
-->adjustments made if necessary
baro-->BP cehmoreceptors--> H+, CO2, and O2 |
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Factors Affecting SV
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Preload
Contractility Afterload Autonomic activity |
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Preload
(Factors Affecting SV) |
-the degree of stretch on ventricular cells due to filling(diastole)
a.)sacromerer need to be stretched somewhat to contract efficiently, therefore more filling causes greater stretch followed by a stronger contraction-"more in=more out"- Frank-Starling principle |
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Contractility
(Factors Affecting SV) |
-the force of the contraction
-stronger contraction-->greater SV |
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Afterload
(Factors Affecting SV) |
-amount of tension needed during contraction to force the semilunar valves open-->eject blood
a.) increases due to any factor that restricts blood flow through aa.; e.g. blockage or constriction of peripheral aa. |
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Coronary Artery Disease (CAD)
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Definition
Treatments |
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Definition
Coronary Artery Disease |
-areas of partial or complete blockage of coronary circulation
1.) caused by thrombus, or fatty deposits-plaque 2.) a symptom can include angina pectoris-sensation of pressure/pain in chest and can radiate into shoulder and left arm -women-indigestion, dizziness, nausea, can't catch breath, sweaty and clammy |
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Treatments
Coronary Artery Disease |
Cathetar-to remove plaque
Balloon angioplasty Stent Coronary artery bypass graft (CABG) |
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Stent
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placed in vessel to hold vessel open
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Coronary artery bypass graft (CABG)
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(take a section of another vessel and attach it and loop over the blockage and attach again. "bypassing" the blockage)
-great saphenous v. or internal thoracic a. |
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Heart Attack (M.I.)
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Process and Treatmen
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Process of a Heart Attack (M.I.)
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1-Coronary circulation becomes blocked-->infaret
-the more proximal the blockage, the greater the symptoms (more damage) 2-Scar tissue forms and heartbeat may b/c irregular 3-Damaged/dying cells release certain enzymes into blood |
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Treatment of a Heart Attack (M.I.)
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1-Vasodilators-improve circulation
2-Additional O2 3-Reduce workload 4-Anti-coagulents--eliminate blockages (and prevent formation of blockages) |
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Differences btw vessels
Arterioles + Arteries |
1-Thicker tunics
2-Vasomotor center 3-Parasympathetic is typically NOT involved *4-REMOVAL of sympathetic stimulation does opposite *5-Overall, there is more vasoconstriction |
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Capillaries
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1-Thin walled (endothelium)
2-Blood flows through the capillaries slowly--so exchange can occur 3-Some are "fenestrated" (holes found in some capillaries) (allows more and larger things to move in or out). Pores=fenestrations 4-CAPILLARY BEDS (network of capillaries that connect arteries to veins) (this is where exchange is taking place) |
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Veins + Venules
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1-In extremities, they contain valves. If these b/c weak (incompetent) and blood can "pool" and walls can weaken and stretch=VARICOSE VV.
2-Have high CAPACITANCE-expand easily w/ little pressure--allows for large vol. changes if necessary aa. have LOW capacitance |
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Cardiocascular Physion
General |
*1-vessels function to maintain adequate blood flow to tissues and organs-perfusion
2-normally blood flow=CO therefore changes in CO will change blood flow 3-continually adjusting to maintain homeostasis 4-HYDROSTATIC PRESSURE--force exerted on a liquid-always moves to lower pressure |
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Cardiovascular Physion
Resistance |
Resistance--any force that opposes blood flow
1-If R increases, blood flow decreases 2-TOTAL PERIPHERAL RESISTANCE--the R of entire CU system 3-PERIPHERAL RESISTANCE--R of arteriole system 4-Sources include: |
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Sources include:
Resistance |
1-VASCULAR RESISTANCE--friction b/w blood and vessel walls
a-vessel length *b-vessel diameter (greater effect than the length) 2-VISCOSITY-(thickness) 3-TURBULENCE--upset of smooth blood flow-swirls + eddies-can increase R (scar tissue or plaque) |
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Cardiovascular Pressures
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1-The COMBINED cross-sectional area of vessels determines BP and flow rates. Capillaries have largest x-sectional area-->slowest rate of blood flow
2-Arterioles offer the most TOTAL R (small diameter + great length) 3-Systolic-highest pressure in aa. (top number) Diastolic-lowest pressure in aa. (bottom number) 4-HYPERTENSION-abnormally high BP, usually >150/90 mm Hg a--ventricular hypertorphy b/c increase workload-->therefore increase O2 demand b--increase stress on arterial walls too |
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Capillary Exchange-3 actions
1 |
1-Diffusion-thru capillary PM or thru channels or fenestrations
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Capillary Exchange
2 |
2-FILTRATION-H2O is forced out of capillary due to CAPILLARY HYDROSTATIC PRESSURE (CHP)-->small solutes move out w/ H2O thru fenestrations or b/w endothelial cells. Larger molecules remain in capillary
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Capillary Exchage
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3-REABOSORPTION-by BLOOD COLLAIDAL OSMOTIC PRESSURE (BCOP)-force of osmotic water movement, i.e. solutions w/ high solute concentrations (like blood) "pull" H2O in
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Capillary Exchange
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4-Hydrostatic pressure forces water out. Osmotic pressure PULLS H2O in
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Capillary Exchange
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NET FILTRATION PRESSURE (NFP)-different b/w CHP and BCOP (normally is POSITIVE) therefore net movement of H2O is OUT--> excess is carried away by lymphatic vessels-->back into bloodstream
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Capillary Exchange
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If CHP increases-too much H2O moves into tissues-->tissues swell=edema
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Capillary Exchange
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If CHP decreases- too much H2O moves into tissues-->tissues swell=edema
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Capillary Exchange
7 cont |
a-BRUISING--capillaries are damaged-->leak proteins (plasma proteins) into surrounding tissues-->edema (H2O follows the solutes)
b-high BP (edema) c-kidney disease--H2O NOT excreted (edema) |
