w3- cardiac function Flashcards
which valves are open during diastole
AV valves
diastole is ventricular filling
AV valves open to allow filling then during the last 3rd the atria contract to fill the remaining 20% and the valves shuts after the contraction
which valves are open during systole
semilunar valves
systole contraction
the semilunar valve is open and closes at the end due to the high pressure
define preload and afterload
Preload
degree of tension on the muscle when it begins to contract
the end-diastolic pressure when the ventricle has become filled
Afterload
the load against which the muscle exerts its contractile force
The pressure in the aorta leading from the ventricle
which cell type does not have a stable membrane potential and why
SA node due to the Na/ Ca channels open (naturally leaky)
what leads to the depolarization and repolarization in conduction cells
Depolarization –> (slow) open L Ca channels
Repolarization –> L type channels close and the K channels open
what leads to the depolarization, plataeu and repolarization in contractile cells
- Depolarization = rapid Na influx
- Plateau= L type Ca( which are Na/Ca channels, slower to open and stay open for longer) and K channel have decreased permeability
- Repolarization= Ca channels closed but the K are open
what protects the cardiac cells from tetany
inactivated Na channels during ARP
also the long platae from the Na/ca channel
what differs from skeletal and cardiac muscle in contraction
extracellular calcium
Ca2+ influx causes conformational change in ryanodine receptors (RyR) on sarcoplasmic reticulum (SR), initiating Ca2+release from SR (calcium-induced calcium release).
Phospholamban(PLB) inhibits SERCA activity. Also, extrusion of Ca2+ into extracellular space via Na+-Ca2+ antiporter and sarcolemmalCa2+ pump.
function of the Phospholamban (PLB)
Phospholamban (PLB) inhibits SERCA activity. Also, extrusion of Ca2+into extracellular space via Na+-Ca2+ antiporter and sarcolemmal Ca2+ pump
what are the two factors contribute to contractility of the heart
determined at a fixed muscle length by:
- amount of Ca2+ available to myofilaments
- myofilament sensitivity to Ca2+
what impact would increased atrial stretching have
increased atrial stretching could be from increased venous return. This would increase contraction (not contractility)
name 3 things that can influence contractility
receptors
cardiac glycosides
contraction frequency
how do cardiac glycosides increase contractility
by inactivating the Na/K pump causing more Na to stay in the cells. This inactivates the Na/Ca antipoter allowing it to build up intracellularly
what is the impact of the sympathetic nervous center on contractility
activate B adrenergic receptors to increase contractility and relaxation
increased adenyl cyclase and cAMP
activation of PKA and also phophorylates PLB to stop its inactivation of SERCA allowing the faster reuptake
what impact do parasympathetics have on cardiac contractility
decrease contractility by activate muscarinic AcH
inhibits adenyl cyclase to decrease cAMP also Phosphorylation of Troponin I –> accelerates the dissociation of calcium from troponin-C, accelerating relaxation