S1W2 L2- Circulatory Physiology- Regulation of Cardiac Function-Ruth Norman Flashcards
cardiac output=
heart rate x stroke vol
stroke volume=
end diastolic vol- end systolic vol
end diastolic volume:
volume of blood in ventricle before contraction
end systolic vol:
vol of blood in ventricle after contraction
ejection fraction:
SV/EDV
what is a normal ejection fraction?
55-75%
what can the ejection fraction reach during exercise
90%
4 factors that effect HR
autonomic innervation
hormones
fitness levels
age
7 factors affecting SV
heart size
gender
fitness
contractility
contraction duration
preload (EDV)
afterload (resistance)
what is preload
degree of filling of a ventricle and how much ventricular muscle is being stretched by during filling
what is afterload
pressure ventricles need to overcome in arteries to eject blood during systole
contractility
how well the ventricles contract
what does EDV determine
preload (preload directly affects amount of stretch experienced by ventricular muscle fibres at the end of diastole)
what is EDV determined by
filling pressure (from venous return)
filling time
relationship between filling pressure and edv
higher filling pressure (due to high venous return and atrial pressure) = higher edv
relationship between filling time and HR
filling time: time ventricles are in systole and are filling with blood
HR increases, filling time decreases
can lead to lower edv if heart doesnt compensate by increasing
what is the effect on SV and CO when preload increases
both increase
what is the frank starling law
as degree of stretch increases, force of contraction increases
why does the frank starling mechanism help the heart
maintains efficient circulation levels by helping heart adjust its output to accommodate varying levels of blood return
what is the afterload on the left ventricle
diastolic aortic pressure
4 consequences of afterload increasing
less blood ejected from ventircle,
increased ESV,
SV and CO decrease,
heart muscle hypertrophies (left v wall)
what is a positive ionotropic influence
factor which increases contractility of heart muscle therefore enhances strength and force of contraction
leads to increased SV
how are sympathetic fibres an example of an extrinsic factor regulating CO
terminate throughout the heart, outside of the heard muscle
what do sympathetic fibres release
noradrenaline
how does sympathetic stimulation increase contraction force?- 5 steps
1.) norepinepherine binds to B1 receptoes in membrane
2.) alpha subunit of Gs protein activates adenylate cyclase
3.) increases cAMP production from ATP
4.) cAMP activates PKA
5.) PKA phosphorylates protein targets to affect functions
why does epinephrine have a similar effect to norepinephrine
both bind to B1 receptors
PKA phosphorylates:
L type calcium channel
Ryanodine receptor
Phopsholamban
troponin
how does parasympathetic stimulation decrease contraction force?
Ach binds to muscarinic M2 receptors
activates Gi protein
inhib effecgt on adenylate cyclase
opposes effects of symp stim
effects on symp NS stim
rise in cAMP
increases If, pacemaker potential rate accelerated
threshold reached faster
reduction to k permeability
max diastolic potnetial becomes more +
threshold easier to reach
increased L-type Ca 2+ current
upstroke faster
more APs per unit time
increased speed of contraction
effect of parasymp NS stim
Ach decreases If by reducing cAMP
threshold potential takes longer to reach
increase K permeability of SA node cells, hyperpolarises MDP
fewer APs per unit time
If
funny current
helps innitiate and regulate heart’s rythmic contractions
