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46 Cards in this Set
- Front
- Back
Cardiac output |
quantity of blood pumped into the aorta each minute by the heart
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What are some main factors that affect CO
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1) basic body metabolism 2) whether person is exercising 3) age 4) size of body
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resting CO for young healthy male and female
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5.6 L/min and 4.9 L/min
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cardiac index
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CO per square meter of body surface area
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normal average cardiac index
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3L/min/m^2; with 70 kg person, SA 1.7 m^2, CO 5 L/min
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primary controller of CO
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venous return
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Frank-starling law of the heart
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heart pumps automatically the amount of blood that flows into the right atrium
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what effect does stretching of the heart have on contractions
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causes heart to pump faster; stretching SA node has effect on rhymicity to increase 10-15%
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Bainbridge reflex
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stretching R atrium initiates a nervous reflex passing to vasomotor center of brain back to heart via sympathetics and vagi to increase heart rate
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when does the heart become the limiting factor in CO
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returning blood becomes more than heart can pump
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long term CO level varies reciprically with
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changes in total peripheral resistance
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equation for CO
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(arterial P)/(total peripheral resistance)
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what can CO increase to without special stimulation
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2.5 times normal
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what can cause a hypereffective heart
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1) nervous stimulation 2) hypertrophy of heart muscle
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dinitrophenol
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increases metabolism of virtually all tissues of the body 4-fold
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what occurs with dinitrophenol administration with and without nervous stimulation
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with-CO increased, no change in arterial P; without-CO same, arterial P falls
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what can cause high CO
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1) beriberi 2) AV shunt 3) hyperthyroidism 4) anemia
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what is the source of high CO in all these causes
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chronically reduced total peripheral resistance
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beriberi
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insufficient vit B
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how does anemia cause increased CO
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reduced viscosity of blood, diminished O2 delivery
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two categories that cause CO to be decreased
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1) pumping effectiveness of heart to fall to low 2) venous return is too low
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cardiac shock
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CO falls so low that tissues throughout body begin to suffer nutritional deficiency
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non-heart causes for low CO
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1) decreased blood V 2) acute venous dilation 3) obstruction of large veins 4) decreased tissue mass
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what can cause acute venous dilation
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sympathetic system suddenly becomes inactive (fainting)
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normal external P outside the heart
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equal to normal intrapleural P = -4 mmHg
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what direction does a rise in intrapleural P cause the CO curve to shift
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to the right; extra P must be exerted to overcome
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What can alter external P on the heart
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1) cyclical changes during respiration (+/-2 mmHg normal breathing and +/-50 mmHg strenuous breathing) 2) breathing against neg P 3) positive P breathing 4) opening thoracic cage 5) cardiac tamponade
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3 factors that affect venous return to the heart from systemic circulation
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1) right atrial P 2) mean systemic filling P 3) resistance to blood flow
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mean systemic filling P
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P measured everywhere in the systemic circulation when all flow of blood is stopped; generally ~7 mmHg
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why does venous filling stop at negative Ps
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collapse of veins entering chest (sucks walls of veins together)
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what occurs to mean systemic filling P with extra blood V
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increases due to stretch of walls of vasculature
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how does sympathetic nervous stimulation affect mean systemic filling P
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increases it; constricts vessels making lower capacity of vasculature
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mean circulatory fillng P
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excludes lung when calculating P, otherwise same as mean systemic filling P
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pulmonary circulation vs systemic circulation
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less than 1/8 capacitance and 1/10 the amount of blood as systemic
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pressure gradiant for venous return
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difference btwn R atrial P and mean systemic filling P
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what occurs when resistance in veins increases
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blood begins to be damned up mainly in the veins, but little change in P since veins highly distensible
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formula for caculating venous return
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equals (Psf-PRA)/RVR; Psf is mean systemic fillng P, PRA is right atrial P, RVR is resistance to venous return
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values for calculating venous return in healthy adult
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Psf= 7 mmHg, RVR = 1.4 mmHg, PRA= 0 mmHg
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highest level R atrial P can rise and still have venous blood flow
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mean systemic filling P
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how does homeostatis occur after infusing extra V of blood
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1) increased CO increases capillary P causing fluid to go into tissues 2) veins distend (stres-relaxation) 3) autoregulatory increase in peripheral resistance increasing resistance to venous return
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how does sympathetic stimulation affect CO
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1) makes heart stronger pump 2) increases mean systemic filling P-peripheral vessel contration, increased resistance to venous return
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how can sympathetic nervous system be blocked
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total spinal anesthesia, hexamethonium (block transmission through autonomic ganglia)
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what occurs to CO during total synpathetic inhibition
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1) mean systemic filling P falls to 4 mmHg 2) heart pumping effectiveness decreases 80% 3) CO falls about 60%
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what occurs immediately after opening of large AV fistula
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1) large decrease in resistance to venous return 2) slight increase in CO curve
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Fick principle eqn for CO
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(O2 absorbed per minute by lungs)/(arteriovenous O2 difference)
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what artery and vein are used in fick principle
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brachial vein through system and intopulmonary artery; any systemic artery
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