Flashcards in Cardiac 8: Cardiac Function Deck (63):
What two effects does HR have?
# beats per minute - increases cardiac output
frequency relationship - (positive staircase), increases myocardial contractility.
Why is the shape of the ejection phase of the P-V loop segment not flat as in skeletal muscle?
bc the afterload is not constant. It changes throughout ejection because blood flow into the aorta raises the pressure (afterload) into the aorta.
During ejection phase describe the contraction and afterload of the heart.
during ejection phase the heart generates an isotonic contraction with a changing (rather than constant) afterload
Draw a pressure-volume diagram. (Left ventricle)
Describe the left ventricular volume in the P-V loop.
Where is end-diastolic, end-systolic mark?
its ventricular volume- not end-diastolic volume specifically... volume changes, maxes out at end-diastolic volume but the minimum volume at end of systole is end-systolic volume. its continuous- diff between the two is stroke volume.
bottom line, same diastolic line as in L-tension relationship, its filling of heart, as heart fills the passive pressure in the heart goes up, can see doesn't go up v much.. end diastolic pressure at end is less than 10 mmHg. usually around 6 or 8 mmHg.
Describe what happens after the L ventricle has filled with blood until the aortic valve closes(cardiac cycle). Integrate when the cardiac muscle is shortening/effect that has.
QRS comes and activates heart to contract when valves still closed. so thats isovolumic contraction. then aortic valve opens and have isotonic like contraction bc have ejection of blood from ventricle, pressure goes up, length of muscle shortening bc volume going down, heart shortening and thats what causes it to eject volume. so heart goes up, rapid ejection then reduced ejection… heart is shortening so getting weaker bc length getting shorter and after load increasing and that will reduce shortening as well. eventually pressure in ventricle falls below in arterial system and aortic valve closes right there
Describe what happens in the cardiac cycle after the aortic valve closes. What is happening with the contractility line in the L-tension relationship?
contractility line there in L-tension rel. and will keep shortening till it gets to shortest length at which it can generate force, then heart relaxes, t wave comes along and you have isovolumic relaxation. then once pressure in ventricle falls below pressure in atrium, mitral valve opens and you have rapid filling then reduced filling then atrial kick right at end. (mitral valve opening till when it closes those are the 3 phases)
Describe how the isotonic contraction during ejection in the cardiac muscle differs from an isotonic contraction in skeletal muscle.
classic isotonic contraction like in skeletal muscle (lift weight and force constant,
in skeletal muscle that ejection phase of PV loop would be flat, no change in afterload)
but after load changes in heart bc blood flow into aorta raising the pressure, raises the after load that the heart has to pump against. really referred to as isotonic-like contraction. after load not constant, ever changing
What are 3 variables that determine the O consumption of the heart?
HR, contractility, afterload
not just pressure when aortic valve opens (thats just beginning, after load is entire arterial pressure change, when changes the O consumption of heart changes and ability of heart to generate force changes) … heart generates its own afterload.
How do you determine stroke volume looking at the P-V loop?
look at end-diastolic volume and end-systolic volume. 130-60 - this difference is stroke volume
(P-V loop lets us look at how preload, afterload, and contractility affect SV specifically)
What is the ejection fraction of the ventricle?
EF = (EDV-ESV)/EDV x 100
The ejection fraction is the fraction of blood ejected during one stroke of the heart in relation to the total left ventricular end-diastolic volume. In other words, stroke volume divided by end-diastolic volume. The ejection fraction is a clinical index of left ventricular contractility. Normal ejection fraction is approximately 60%.
A normal ejection fraction is about 60 percent. What would it be in congestive heart failure? What does this indicate.
congestive heart failure-ejection fraction 10 percent or 15 percent. when ejection fraction is depressed its considered a depression of contractility specifically ..not related to preload, not to afterload.
How are preload, afterload, and contractility related to ejection fraction?
when ejection fraction is depressed its considered a depression of contractility specifically ..not related to preload, not to afterload. ejection fraction is clinical indicator of contractility of heart. we know that depression of ejection fraction always related to depression of contractility.
If ejection fraction goes down, how will this affect cardiac output?
The ejection fraction is the fraction of blood ejected during one stroke of the heart in relation to the total left ventricular end-diastolic volume.
ejection fraction is not same as cardiac output…one can go up while other doesn’t or one can go up and one can go down. can have increase in HR and decrease in SV (look at equation CO = SV x HR) could have increase in HR and decrease in SV and that could have no effect on cardiac output (but SV depressed so ejection fraction is depressed)
If you had a larger end diastolic volume, how would this affect ejection fraction, stroke volume, and cardiac output ?
larger end diastolic volume you’d eject more blood but fraction of blood is same bc increased end-diastolic volume which is on bottom of fraction so by increasing that, even if you increase absolute SV, the percent could remain constant but cardiac output could go up if you increased the absolute amount of blood being ejected w each stroke, CO goes up but fraction doesn't change.
don't get fraction and total amount of blood confused w e/o. not the same.
What is contractility? How would it be changed after an MI?
contractility scientifically due to intracellular Ca. more Ca, more cross bridges, stronger contraction.
clinically can change contractility, if someone has MI and chunk of heart damaged or not contracting and not contributing to SV anymore its said clinically that total heart has lower contractility. clinically the term used to indicate if not using all cells in heart to contribute to contraction anymore your ejection fraction will go down and if ejection fraction goes down thats a decrease in contractility.
clinically its anything that interferes w amount of blood ejected w each stroke. after MI contractility depressed bc lost some of his muscle.
Describe how the changes in preload below affect the L-Tension graph. Draw.
How does an increase in preload affect...?
-max. tension developed
increased preload – increased resting tension
increased preload – no change in max. tension developed
increased preload – more shortening (L1 to L4 is greater than L3 to L4)
Describe how changes in preload affect the P-V loop.
How does an increase in preload affect...?
increased preload – increased EDP
increased preload – increased stroke volume (EDV3 – ESV1 is greater than EDV1 – ESV1)
On the L/Tension graph describe what happens at a given muscle length.
What happens if you increase preload?
start w L 3 as control, stretch or preload on muscle so muscle length increased to L3, stimulate, get isometric contraction bc length not changing but tension is, eventually meets after load and moves it so get isotonic contraction (force is constant, all you have to do is generate force to meet the load) then it shortens. and it’ll shorten until gets to point of Peak isometric tension (max. amt. of force muscle can generate at this length so diff between 2 is amount of shortening
if increase preload and start at longer length, stimulate and get more shortening. increasing preload increases amount of shortening
Analyze the P-V loop at a given preload.
analysis of heart- preload, isometric contraction, aortic valve opens, ejection. then it'll shorten and shorten until it gets to line defined by ventricular contractility (the amount of Ca in the heart) ..at that length can't shorten any further, relaxes when t wave comes along and that's end-systolic volume (ESV1) this is max. amount of force heart can generate at any given length.
How does increasing preload affect cardiac output?
Does the ejection fraction go up?
increase preload, get to same afterload, get ejection, get end-systolic volume, relax. showing same thing as in top figure. getting more shortening when you increase preload and therefore getting a greater stroke volume . diff between end systolic volume and end diastolic volume gets larger as preload gets larger and therefore you’ve increased cardiac output by using what is called diastolic reserve…
heart is able to generate greater cardiac output by increasing preload.
stroke volume went up but did fraction of blood ejection in relationship to end diastolic volume go up? no. end diastolic volume has gone up but heart prob. ejecting same percentage of blood. so absolute amount of blood increased, SV increased but fraction of blood ejected is probably still 60 percent of total end diastolic volume.
Describe how an increase in afterload affects the L-Tension graph. Draw.
increased afterload –
increased tension development
increased afterload – less shortening (L1 to L3 is less than L1 to L2)
end diastolic volume, (in this case its a preload, just a stretch on the muscle. get isometric contraction, meets after load and shortens then relaxes (thats total amount of shortening) here is increase in afterload, increase after load get to greater tension but when you shorten you shorten less (amt of shortening defined by peak isometric tension line) shortens less then relaxes (increase after load then amount and velocity of shortening is reduced)
Describe how an increase in afterload affects the P-V loop. Draw.
-pressure development before ejection?
increased afterload – increased pressure development before ejection; increased energy consumption
increased afterload – decreased stroke volume
hypertension…afterload is elevated about 100, 110, much higher than before, now heart has to generate a lot more isometric contraction (isovolumic phase), tremendous O involved trying to bring heart up to much higher level to open the aortic valve …in addition to additional O consumption used, when heart does try to shorten against higher after load can’t shorten as much bc defined by ventricular contractility and relaxes after t wave and see end systolic volume is larger than it was under controlled conditions so you left more blood behind.
What will happen if you raise diastolic pressure up to 120mmHg?
have to appreciate that heart does not generate its max. force, never does under normal conditions which allows it to have all this reserve… can go to 160 mmHg if it had to to overcome an afterload… pathology- if raise arterial pressure/diastolic pressure up to 120 it can still meet that but the amount and velocity of shortening will be reduced. lots more O consumption. right here during isometric contraction phase. cross bridges making and breaking latches and every time they do that they use ATP. after load is increase in diastolic arterial pressure…
What is a valve abnormality? How does heart respond? How will it respond to hypertension over years?
presented to heart as increase in after load =aortic stenosis… open to v small cross sectional area..heart generate huge force to shove blood thru openings.
how does heart respond? can meet that afterload, lost some CO.
how will respond to hypertension or aortic stenosis over years? it hypertrophies, gets thicker, compensation.. pathological response. (pathological hypertrophy - not using O normally, cells not normal, heart less efficient, actually uses more O and heart gets sicker and sicker) thats why you have to repair aortic valve or bring down afterload, so heart using less ATP, less O consumption and able to generate greater SV. whole point in giving person w hypertension diaretics or Ace inhibitors, things that lower bp
When does the heart generate its max. force?
heart does not generate maximum force- only time it generates max. force is during premature beat that is unable to open up the aortic valve and under those circumstances wouldn't have contractility line up there, know that during premature beat contractility is depressed…heart would cause isometric contraction and max. force can generate at that line. increase pressure up to that point. never get to point where can open aortic valve…then will relax. squeezing against high afterload, unable to open aortic valve bc contractility is depressed and contractility is defined by that line.
What happens in heart failure in regards to contractility?
depressed too, cant generate as much force but can open aortic valve.. SV down, ejection fraction down bc contractility depressed, cant shorten v much, therefore total SV is depressed, and heart congested w blood… end systolic volume- left enormous amount behind and heart getting congested w blood bc end systolic volume is abnormally large.. (will ask how drugs affect this. this analysis is widely used.)
How will an increase in contractility change the L-Tension graph? Where does the curve shift? Draw.
preload & afterload unchanged
increased contractility – shifts curve upward & left
increased contractility – more shortening
increase contractility-shift curve up and to L and now can get greater change in preload, greater change in afterload, can still shorten to a greater extent and you’ve gained all of this amount of shortening
How does an increase in contractility affect the P-V loop? Draw.
increased contractility – increased stroke volume
increased contractility – increased ejection velocity
systolic reserve- during systole, heart can shorten more
How does preload affect stroke volume?
it increases end diastolic volume and therefore there's a greater amount of shortening
How does contractility affect SV?
it shortens or reduces end systolic volume
(increase in contractility does not affect preload/afterload - it affects end-systolic volume)
How does afterload affect SV? Increase/decrease
reduces SV by increasing end-systolic volume.
reducing afterload would do opposite- would allow more shortening and would reduce end-systolic volume.
What 3 things must be done to maximize shortening in muscle or stroke volume in the heart?
factors that would affect SV clinically
decrease afterload (max. shortening and SV)
increase contractility (max. shortening)
What is heart failure? What is the difference between systolic heart failure and diastolic heart failure? Graph.
heart failure = A condition in which the heart fails to provide cardiac output sufficient to meet the needs of the body.
1. Decreased ventricular contractility (A); systolic heart failure
2. Decreased ventricular compliance (B); diastolic heart failure
What is responsible for systolic heart failure?
decrease in ventricular contractility.
contractility line depressed in heart failure, less shortening, higher end -systolic volume. when little more filling, heart fills to larger extent but not enough to offset the loss in stroke volume bc of decrease in contractility bc you can’t overfill the heart.. can't get much more end-diastolic volume than you normally do.
What happens over time with heart failure? What are some signs/symptoms in regards to the graph.
what happens is over time contractility gets more and more depressed, end systolic volume goes up and up and up and you you’re basically in congestive heart failure - SV gets smaller, end-diastolic volume goes up, end-diastolic pressure goes up bc heart being congested w blood - all signs/symptoms of congestive heart failure- higher end diastolic pressure, higher end-systolic volume, lower contractility, lower SV.
Describe diastolic heart failure.
this is due to decrease in ventricular compliance (heart getting stiffer or not relaxing normally) relaxation of heart, if goes to 0mmHg at the end of isovolumic relaxation, that's a nice relaxed heart and has high compliance, but if heart doesn't relax, then something still wrong w ability of heart to remove actin/myosin interactions. heart stiff, lower compliance of heart.
low compliance (curve shifted upward bc stiffer heart, cant fill normally bc at end of filling, this pressure is so much higher than was before. volume that normally comes back creates this much larger pressure, can’t even fill as much bc gradient for filling has been reduced. heart not going back down at end of cardiac cycle to 0 mm of Hg. when fills, fills to much higher pressure and that pressure is preventing further filling can see end diastolic volume being prevented from getting where it was, therefore preload goes down. positive feedback as well. this is diastolic heart failure.
In relation to preload, what changes to the following factors will decrease ventricular filling?
a) pressure gradient between atria and ventricles
b) time for ventricular filling (HR)
c) ventricular compliance
d) atrial function (atrial kick)
Pressure gradient between atria and ventricles
- an increase in end-diastolic pressure decreases ventricular filling.
Time for ventricular filling (heart rate)
- an increase in heart rate decrease ventricular filling time.
- a decrease in ventricular compliance decreases ventricular filling.
Atrial function (atrial kick)
- loss of atrial function (atrial fibrillation) decreases ventricular filling.
How do pressure gradients involved in diastolic filling affect ventricular filling?
preload is diastolic filling -have to go back to cardiac cycle- think about pressure gradients involved in diastolic filling (in ventricular filling, the ventricle pressure down to 0, atrial pressure going up bc of atrial systole, atrial diastole, when those pressures cross e/o mitral valve opens and ventricle begins to fill w blood so theres pressure gradient between atria and ventricle and that drives blood in passively. that pressure gradient between atria and ventricle really det. to large extent the preload, the filling of ventricle
How will an increase in end diastolic pressure affect preload?
reduces preload/ventricular filling
Why is time for ventricular filling important in determining preload?
How is a decrease for ventricular filling time compensated during exercise?
as HR goes up theres a decrease for ventricular filling time but that is compensated under normal conditions by other factors. one of them is breathing. when you take deep breath during exercise suck blood back to heart as a result of greater gradient for blood flow back to heart. during VT there is no compensation and you only have shortened cycle length (don’t have these sympathetic responses that will push blood back to heart- which is what happens during exercise) so there’s no compensation for this.
What happens during VT in regards to preload? What will this lead to?
during VT decrease in filling decreases preload and decreases SV and that causes heart to be less ischemic bc CO less, heart depolarizing more, conduction worse, eventually goes into VF as result of preload and abnormal wall pattern…abnormal conduction during VT -not conducting efficiently
What happens as the heart becomes stiffer?
ventricular compliance- heart becomes stiffer. (shown in previous diagram- generally results from MI that becomes scarred. thats why MI people have severed impairment of ventricular function and of diastolic compliance which leads to congestive heart failure. decrease in ventricular compliance (even cardiac hypertrophy can decrease ventricular compliance bc muscle getting thicker…doesn’t relax or stretch normally and this raises end diastolic pressure which reduced gradient for blood flow to come in)
What happens in a-fib if ventricular compliance is decreased.
loss of atrial function in a-fib decreases atrial filling. normal heart can deal with but if you’re in congestive heart failure and heart not filling normally, problems w compliance, etc..then that atrial kick is v important and if you’re in heart failure then go into a-fib you've lost more preload and can now go into serious decrease in CO. in pathological conditions this atrial kick can be important for survival. under normal conditions this atrial kick v important in exercise …max exercise tolerance impaired if a fib. cant do it to same extent.
What will sympathetic nerve activity, drugs (digitalis) affect?
What are some physiological changes that affect afterload?
aortic pressure- hypertension (must generate much larger isometric contraction. much larger isovolumic contraction during cardiac cycle..tremendous amount of ATP consumption. over period of years heart will fail over this. silent disease bc no symptoms of hypertension…btu heart straining to keep up w larger afterload. O consumption.)
ventricular outflow tract resistance -vavular stenosis or subaortic stenosis (constriction)
ventricular size (wall tension)
dilated hearts- higher wall tension, larger afterload
In what situation would you want to decrease contractility? How would you do it?
(How will this affect exercise?)
a lack in sympathetic nerve activity will decrease contractility … give beta blockers to reduce contractility of ventricle. reduce symp. nerve activity to heart bc (increasing contractility costs O…ATP=O) w patients w coronary disease want to reduce demand for O and so give beta blockers… to try to conserve O/the demand for O. want to try to keep HR down, beta blockers even when try to exercise will keep HR under 100 beats per min. wont be able to exercise to same extent but thats ok
What does loss of myocardium/dysfunctional myocardium lead to? What is lost?
contractility can also be considered loss or disfunction of myocardium. not just matter of Ca clinically when someone lost a chunk of heart or damaged L ventricle has considered to have a lowered contractility bc total number of oars pulling in water has been reduced so total amount of force heart can generate is reduced. not due to preload or afterload..its due to ability of heart to generate force and thats referred to as a decrease in contractility
How are aortic or pulmonary artery stenosis related to afterload?
rep tremendous afterload on heart. aortic stenosis-constrictions of aorta that also occur after valve..congenital abnormalities where L ventricle and septum hypertrophy and squeeze the aorta opening. diseases that affect outflow tract resistance (anything that impairs that reduces heart ability to shorten)
The heart doesn't overfill easily? How might it dilate over time? What will this impede?
dilated heart. not heart w simply more volume (dont overload w volume easily. pericardium prevents overfilling of heart) over time, if you do overfill heart, over time heart will remodel as result of volume overload .
if have aortic insufficiency and it wasn't repaired, during diastole blood would be flowing in through the mitral valve into ventricle and some blood would be ejected back forcefully…aortic constricting during diastole, cardiac notch, and that increase in pressure is pushing blood back through insufficient valve that forceful ejection of blood will remodel or stretch ventricle. stretch cells and slips them past each other so heart physically bigger than it was… dilated. its remodeled. this causes much higher wall tension (force pulling heart apart) this force opposes shortening during systole and its tremendous after load on heart. dilated cardio-myopathy. general def of afterload-anything that prevents shortening of the heart. and when the heart is stretched out physically.. it will impede shortening, prevent shortening of the heart.
What are the 2 effects of increasing absolute heart rate?
increase in HR increases contractility (force-freq relationship, positive staircase) -contributes to CO
increase in HR decreases time for ventricular filling
How does arrhythmic activity and abnormal sequence of activation affect heart?
affects efficiency of ventricular filling and ejection
What are 4 factors thatt influence HR?
-normal sinus rhythm
-shifts in pacemaker location change rate
-enhanced or depressed pacemaker function
What causes the positive staircase with increases HR? What will this look like in patients with congestive heart failure?
people in congestive heart failure don't have positive staircase bc its a Ca-handling process. increase HR more Ca comes in beat per minute over time bc more channels being activated over time so have this positive staircase. well, congestive heart failure patients don't have positive staircase bc their contractility is depressed and they don't respond normally to Ca.
How will latent pacemakers affect HR?
change HR if pacemaker shifts to different location.
latent pacemakers have lower rates but they can also change wall motion dep. on location. premature beat- VT generated from v abnormal location, going to have high rate but also abnormal wall function and wall motion depressed and that will impact CO.
What are AV nodal conduction abnormalities?
Describe how AV nodal conduction abnormalities and ventricular arrhythmias affect HR.
AV nodal conduction
- 2nd and 3rd degree AV nodal block.
- atrial fibrillation and atrial flutter
conduction is a main problem w arrhythmias. heart blocks- will change CO dramatically dep. on severity. esp. 3rd degree heart block. this is arrhythmia- when in 3rd degree or 2nd degree heart block thats a arrhythmia also - strictly conduction abnormality. a fib and a flutter are conduction abnormality through re-entry. that will change your ventricular function. a flutter is v rapid rate. regular. a fib is irregular. regular rate is not transmitted to ventricle in regular pattern very arrhythmic.
If someone is hemorrhaging what is the immediate problem?
fix problem of low blood volume which leads to low bp. immed. after hemmorrhage have decrease in preload- less blood overall in system, less blood in venous side which means less return to heart, heart fills less well, bc of that its at shorter sarcomere lengths, neg. impact on contraction strength,
decrease in after load (this is low bp) not bad thing in sense of cardiac function- easier to pump. thats sorta good but need certain bp, need to perfuse all tissues
What will lead to compensation mechanisms when someone is hemorrhaging?
low bp sensed by baroreceptors and that’ll lead to compensation.
bp falling, baroreceptors sense, increase sympathetic tone, so sympathetics fire both in terms of cardiac function and also in vascular function, will also release lots of adrenaline from adrenals. increase in catecholamines circulating will cause on arterial side vasoconstriction. constriction of resistance vessels on arterial side, increase total peripheral resistance, bp will be improved (will fix problem in blood drive...)
What effect will circulating catecholamines have?
as a result of circulating catecholamines and result of direct sympathetic stimulation of heart, will be change in contractility- the activation state of heart. how heart is it working? heart contracting much more forcibly and so whatever blood in heart, improved ability to squirt out w/e blood in heart w more force, improve CO and pressure of vessel squirting blood into.
In addition to arterial constriction, what other compensatory mechanisms will occur when someone hemorrhages?
in addition to arterial constriction, also get constriction on venous side as sitting there lots of blood hanging in reserve. this woman laying on ground… not running… so her blood supply would be adequate but has lost a lot. but everyone has a reserve, so all blood sitting in great veins and vena cava in reserve but can be called upon in venoconstriction- veins smaller, capacity of venous system decreased so that blood gets sent to heart improving transiently venous return and in long term shifting blood from reserve side (venous side) to arterial side where it can do some good.
How is pressure, preload, contractility improved when someone hemorrhages?
improving pressure by vasoconstriction, improving preload by veno-constriction, improving contractility by circulating catecholamines.. and all those things together should help improve function. she’s getting some compensation but not off hook prob needs blood transfusion
What is a negative side effect of massive vasoconstriction when someone hemorrhages?
massive vasoconstriction everywhere, may not affect core functions, brains lung heart get adequate perfusion but things like kidneys, gut liver at risk.. sometimes person in car accident goes into kidney failure bc ischemic to kidneys bc vasoconstriction so strong.
get ischemia as consequence
as consequence of high level of vasoconstriction..
other systems that are v at risk are all of portal systems of body. in portal system have capillary bed that partially depletes bed then pools into portal vein then goes to 2nd capillary bed which is at risk for all adverse effects of hemorrhage. syndrome where pregnant woman infarcts pituitary bc of hemorrhage during childbirth and increased hyperplasia of pituitary gland during pregnancy, -increased metabolic demand, yet during hemorrhage exposed to ischemia. and she infarcts pituitary gland.
but really all portal systems at risk and many organ systems at risk as consequence of this. skeletal muscle usually ok.