exam 8
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| what general receptor type stimulates heart activity | B1 receptors. sympathetic
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| what general receptor type inhibits heart activity | M2 receptors. parasympathetic
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| skin, renal, and splanchnic smooth muscle constricts via activation of what receptor (sympathetic) | a1
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| skeletal muscle dilates via activation of what receptor (sympathetic) | B2
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| skeletal muscle constricts via activation of what receptor (sympathetic) | a1
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| amount of Ca released during an AP is based on what | 1. previous stored Ca
2. size of inward Ca current during phase 2
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| how long does cross bridging during an AP last | as long as intracellular [Ca] high enough to bind troponin C
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| when does relaxation occur during AP | When Ca is reaccumulated in SR via Ca-ATPase
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| magnitude of muscle tension during AP is related to what | amount of intracellular [Ca]
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| how can the tension amount during an AP be altered | use of hormones, NT, and drugs that:
1. alter inward Ca current during AP
2.Alter SR Ca stores
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| Preload | pressure in aorta
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| afterload | pressure in ventricle. ideally matched
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| Homeometric regulation | hearts ability to increase contractility and restore stroke volume when afterload is increased.
Independent of cardiomyocyte fiber length
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| hetermetric regulation | Frank-Starling relationship. dependent on fiber length
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| stroke volume | volume of blood ejected by ventricle on each beat
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| stroke volume equation | End diastolic volume- end systolic volume
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| ejection fraction | fraction of the end diastolic volume ejected in each stroke volume. ventricular efficiency
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| ejection fraction equation | stroke volume/end diastolic volume
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| Cardiac output | total volume ejected by ventricle per unit time
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| cardiac output equation | stroke volume x HR
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| voltage effect | increase HR, increase intracellular Ca, increase force of contraction, increase velocity
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| extrasystole effects | premature depolarization. increase Ca. when next beat comes along more Ca than normal. Results in more forceful beat (Postestrasystole)
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| positive inotropic effect of cardiac cycosides | 1.poisons Na/K pump
2.used to increase cardiac force of contraction.
Tension directly proportional to intracellular Ca
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| starlings law of heart | Increase length, increase force of contraction
1.increase muscle length, increase Ca sensitivity to troponin C
2. increase muscle length, increase Ca release in SR
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| ideal sarcomere length for cardiac muscle | 2.2u
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| ideal sarcomere length in skeletal muscle | 1.6u
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| Ventricular pressure volume loop: 1-2 | isovolumetric contraction
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| Ventricular pressure volume loop: 2-3 | ejection phase
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| Ventricular pressure volume loop:3-4 | isovolumetric relaxation
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| Ventricular pressure volume loop:4-1 | refilling phase. relaxed
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| P-V loop: increased preload | end diastolic volume. increase venous return. Increased stroke volume. Afterload and contractility constant. increase stretch on ventricle, more blood pumped out.
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| P-V loop: increased afterload | increased aortic pressure. decrease stroke volume. increase end systolic volume
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| P-V loop: increased contractility | increased stroke volume, increase ejection fraction, decrease end systolic volume
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| myocardial O2 consumption. | increase O2 consumption. increase wall thickness (protection) therefore decrease overall tension. maintain normal O2 consumption and prevent O2 deficiency
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| 4th heart sound associated with | Atrial systole. atria contract. final phase of ventricular filling
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| 1st heart sound associated with | isovolumetic ventricular contraction. mitral valve closes
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| 2nd heart sound associated with | isovolumetic ventricular relaxation. aortic valve closes
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| 3rd heart sound associated with | rapid ventricular filling. mitral valve heart opens
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| chemoreceptors | respond to specific chemical changes in CO2, O2, and pH
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| Baroreceptors | high pressure sensors.
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| components of baroreceptor reflex arch | 1.sensors of BP
2.afferent neurons. info to brainstem
3.brain stem centers
4.efferent neurons. direct change in heart and blood vessels
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| ADH V1 receptor | vascular smooth muscle. vasocontriction of arterioles. increase TPR
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| ADH V2 receptor | principal cells of renal collecting ducts. water reabsorption in collecting ducts. maintain body fluid osmolarity
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| ADH secretion stim when | 1. increase serum osmolarity
2. decrease BV and BP
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| Low pressure baroreceptors | located in veins, atria, pulmonary arteries. sense change in blood volume
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| Low pressure baroreceptor response to increased BV | 1.secretion of ANP
2.decrease ADH
3.increase renal vasodilation
4.increase HR
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| How does ANP work | secreted by atria. binds ANP receptors on vasculature smooth muscle. promotes relaxation, vasodilation, and decrease TPR
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| outcome of general sympathetic regulation | 1.increase HR
2. increase contractility
3.increase vasoconstriction
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| outcome of general baroreceptor relflex | 1. decreased HR
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| outcome of Aldosterone | Na and H2O reabsorption
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| outcome of ADH | increased H2O reabsorption in kidney
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| outcome of ANP | Increase Na, and H2O excretion (increase vascular permeability)
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| starling law of capillar | fluid pushed out entire length of capillary. never reabsorbed
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| Kf | hydraulic conductance. water permeability of capillary wall. increase this increase fluid movement
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| what is kf influenced by | capillary injury
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| what does not influence kf | 1.change in arteriolar resistance
2.hypoxia
3.build up of metabolites
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| Pc | capillary hydrostatic pressure. force favoring filtration out of capillary.
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| what determines Pc | arterial and venous pressure. more affected by change in venous pressure
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| Pi | interstitial hydrostatic pressure. force opposing filtration. normal is zero
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| PiC | Capillary oncotic pressure. force opposing filtration. determined by [protein]
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| PiI | interstitial oncotic pressure. force favoring filtration. near zero
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| What factors cause a change in starling force in capillaries | 1.increase filtration
2.increase Pc. increase in arterial pressure or venous pressure
3.decrease PiC. dilution of plasma [protein]
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| special circulations controlled via local metabolites only | 1.coronary
2.cerebral
3.pulmonary
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| special circulations controlled via sympathetics only | 1.renal
2.skin
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| coronary circulation regulation sp. metabolites | hypoxia, and adenosine
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| cerebral circulation regulation sp. metabolites | CO2
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| pulomary circulation regulation sp. metabolites | O2
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| Skeletal muscle circulation regulation during rest | sympathetic. a1 receptors increase
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| Skeletal muscle circulation regulation during exercise | local metabolites. changes in O2 demand
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| hemorrhage: baroreceptor reflex | increase sympathetic outflow
1.increase HR (increase cardiac output)
2.Increase contractility
3.constriction of arterioles
4.constriction of veins
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| hemorrhage: renin system | increase angiotenin II
1.increase TPR
2.increase aldosterone
3.increase Na reabsorption
4.increase BV
5.increase stress volume
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| hemorrage: capillaries | change in starling.
Decrease Pc
1.increase fluid absorption
2. increase blood volume
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