Cardiac Function Flashcards
(43 cards)
What are some factors that can change cardiac muscle contraction through a change in cardiac contractility?
- catecholamines (NE & Epi)
- Cardiac glycosides (digitalis)
- Ca channel blockers
- force-frequency relationship
How do catecholamines affect contractility?
bind the b1 receptors on membrane
activate Gs protein which activates adenylate cyclase to increase cAMP
it activates PKA
-phosphorylates
1. Ca channels: incr Ca influx
2. phospholamban: incr SR Ca uptake (enhance relaxation)
*increase strength of contraction and relaxation (HR)
How does digitalis work?
inhibits Na-K pump the Na stays in so decreases gradient that messes the Ca-Na exchanger increases intracell [Ca] increase SR Ca content: greater release
*Increase rate of contraction + decr HR (less O2 consumption!)
How do Ca channel blockers work?
smooth muscle:
block Ca influx -> decrease Ca SR release/content
= less contraction (vasodilator)
heart:
inhibit slow inward Ca current: inhibit conduction of AV node AP (block SVT)
side effect: negative inotropic
*used to bock arrhythmia!
How does cycle length influence cardiac contraction amplitude?
it alters contractility!
- alter time available for Ca handling
e. g. AFib: diff strength of beats cuz diff intervals
Positive & Neg staircase
Explain PVC and PESP strength
heart beating normally
when get a premature beat and then stimulated at higher HR it is gonna be a weaker contraction cuz less time for Ca to recover
u get less time between beats so readjusts to new cycle by faster everything, more Ca going in so keep increasing till reach a new steady state
when slow down the heart the next beat is extra strong cuz was still getting Ca in fast but had extra time
then keeps decreasing till gets used to new rate again
What is the mechanism for positive staircase?
Increase HR, increase contraction strength
greater Ca influx per time and less time for efflux via exchange
increased SR Ca content and release
=greater contraction strength
What is the mech for negative staircase?
Decr HR, decr strength
less Ca coming in and more time to get out
less SR contact, smaller CICR
=smaller contraction strength
Explain post-extrasystolic potentiation
stronger contraction of beat following premature beat
more time for recovery of Ca current
more time for recovery of SR Ca release channels
more time for recovering Ca stores in SR cistern
=larger induced CICR = larger contraction strength
What are the 4 factors that determine cardiac output?
- HR
- Contractility
- Preload
- Afterload
How does HR affect Cardiac Output?
HR x SV = CO
if increase HR get + staircase
interval determines amount of Ca available and thus contraction strength
What is contractility?
the inherent ability of actin and myosin to form cross bridges and generate contractile force
determined by intracell [Ca]
incr Ca = incr contractility
What is preload?
load on the muscle before the contraction is initiated
it stretches the muscle length: generates passive tension
dependent on ventricular filling (end diastolic volume)
What is afterload?
load on the muscle after contraction is initiated
ANY FORCE THAT RESISTS MUSCLE SHORTENING
normally: arterial pressure resists LV shortening
What is a contraction?
process by which muscle generates tension or force
MUSCLE CONTRACTION NOT ALWAYS ASSOCIATED WITH MUSCLE SHORTENING
*can be changed by changing preload or afterload
What is an isometric contraction?
contraction without shortening
is muscle is unable to generate enough force to meet the after load, then the contraction is isometric
What is an isotonic contraction?
contraction with shortening and constant force
if muscle can generate enough force to meet the asteroid then contraction is isotonic
What is the length tension relationship?
Preload stretches the muscle length: generates passive tension
-> the more you stretch, the bigger the strength of the contraction
What is resting (diastolic) tension?
amount of tension that develops passively by stretching the muscle
e.g. the more you increase the preload aka end-diastolic volume, the more tension you generated
slope of resting tension curve is determined by muscle compliance
(the more compliant, faster it can stretch)
What is active (systolic) tension?
amount of isometric tension that can be developed at a particular length (preload) aka Stroke Volume
e.g. the higher the length/EDV, the higher the force of the contraction
slope determined by contractility
(the higher the contractility, the more isometric tension is gonna build)
What is compliance?
determines slope of cardiac resting tension
volume/pressure or length/tension
decrease in compliance increases the slope: higher pressure for a given filing volume
What is the compliance of cardiac muscle?
low! pretty stiff compared to skeletal
doesn’t allow the heart to overfill and create bunch of pressure
What is inotropy?
contractility! determined by intracellular [Ca]
the more Ca, the more bridges formed = stronger contraction!
increase contractility (+ inotropic effect): shift slope of active tension curve up and to the left aka can develop more force at a given length/EDS
How does an increase in preload cause an increase in tension development?
creates more optimal overlap b/w thin an thick filaments
increases Ca sensitivity of myofilaments
