Busy. Please wait.
or

show password
Forgot Password?

Don't have an account?  Sign up 
or

Username is available taken
show password

why


Make sure to remember your password. If you forget it there is no way for StudyStack to send you a reset link. You would need to create a new account.
We do not share your email address with others. It is only used to allow you to reset your password. For details read our Privacy Policy and Terms of Service.


Already a StudyStack user? Log In

Reset Password
Enter the associated with your account, and we'll email you a link to reset your password.
Don't know
Know
remaining cards
Save
0:01
To flip the current card, click it or press the Spacebar key.  To move the current card to one of the three colored boxes, click on the box.  You may also press the UP ARROW key to move the card to the "Know" box, the DOWN ARROW key to move the card to the "Don't know" box, or the RIGHT ARROW key to move the card to the Remaining box.  You may also click on the card displayed in any of the three boxes to bring that card back to the center.

Pass complete!

"Know" box contains:
Time elapsed:
Retries:
restart all cards
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.

  Normal Size     Small Size show me how

physiology 8

exam 8

QuestionAnswer
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
Created by: ejohnson17