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