Cardiac Function Flashcards
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
What is the effect of changing preload on isotonic contractions?
as you increase the preload, you increase the amount of shortening
higher stroke volume!
What is the effect of changing afterload on isotonic contractions?
as you increase the afterload, the tension is greater but the amount of shortening decreases
*remember afterload resists shortening
How does sympathetic nerve stimulation affect contractility?
it increases it!!
it increases peak isometric tension plus enhances rate of relaxation!
(normal contractility just changes peak…)
-decrease in contractility would decrease peak plus slow rate of relaxation
What is the effect of changing contractility on isotonic contraction?
- increase in contractility increases amount of muscle shortening
- allow muscle to reach shorter length: contract more! - increase velocity of shortening
- increase rate of relaxation
What is the force-velocity relationship?
the force (afterload) generated by the muscle determines the velocity of shortening
*increasing afterload decreases the velocity of shortening + amount
(heavier weight takes longer to lift)
*increasing preload increased the velocity
*increasing contractility increases the velocity
What is ejection fraction?
the fraction of the blood ejected in relation to the total LV end diastolic volume
SV/EDV
*index of LV contractility- normal ~60%
What happens to the pressure volume loop if you change preload?
if you increase it, you gonna extend the graph to the right
aka increased EDP and overall greater SV cuz was able to shorten more
What happens to the pressure volume loop if you change afterload?
Now it needs more pressure to open the aortic valve (more O2/energy)
it tries to shorten but can do it less (less contractility at the higher tension)
overall decreased SV :(
e.g. HTN or aortic stenosis
What is diastolic reserve?
heart has some reserve so if you increase the preload it is able to generate more force
-doesnt use max force under normal conditions -> only needs enough to open the aortic valve
What happens to the pressure volume loop if you change contractility?
the heart is now able to shorten more! so eject more volume (systolic reserve)
if increase contractility -> incr SV plus ejection velocity
How would you maximize the shortness of a muscle or store volume in the heart?
increase preload
decrease afterload
increase contractility
What happens to the pressure volume loop of patients suffering from systolic heart failure?
decreased contractility!!!
u get less shortening
heart tries to compensate by filling up a lil more (incr ESV)- bring more venous return
*overall still lose stroke volume
What happens to the pressure volume loop of patients suffering form diastolic heart pressure?
decreased compliance!!! stiffer :/ get smaller everything! lower preload less shortening *overall lose stroke volume
How do you determine cardiac output?
SV x HR
What factors affect Stroke Volume?
- preload
- contractility
- afterload
What determines preload?
aka diastolic filling?
- pressure gradient from the atria to the ventricle
e. g. if u increase EDP, u will decrease ventricular filling - HR: time for ventricular filling
e. g. higher HR decreases filling time - ventricular compliance
e. g. stiffer heart decreases amount of filling - atrial kick
e. g. if u lose it (AFib), u decrease filling
What determines contractility?
- sympathetic nerve activity?
- drugs e.g. digitalis
- disease (damaged myocardium): reduce # of oars…
What determines afterload?
- aortic pressure e.g. HTN
- ventricular outflow tract resistance e.g. valve stenosis, subaortic stenosis
- ventricular size e.g. dilated hearts have higher tension so larger afterload
What determines HR?
- absolute rate: incr HR incr contractility (+ staircase) but decr filling time
- sequence of activation: arrhythmic activity and abnormal seq of activation affects efficient of filling and ejection
- factors affecting ventricular rate
- pacemaker function: normal SA node function, shift in pacemaker, enhanced or depressed pacemaker function (brady or tachy)
- AV nodal conduction: 2nd and 3rd degree blocks, AFibt and atrial flutter
- ventricular arrhythmias
