Heart 7: Cardiac Muscle Mechanics Flashcards Preview

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Flashcards in Heart 7: Cardiac Muscle Mechanics Deck (46):

Why is verapamil used to block tachycardias?

in WPW when impulse goes through AV node (slow conducing pathway) and bc of delay gives accessory pathway to recover excitability and impulse goes into ventricle then goes retrograde through accessory pathway back to atria and have supra ventricular re-entering arrhythmia. give slow channel blocking agents like verapamil to slow conduction further…

verapamil -many anti a drugs (class 1 and 3s) have characteristic of state-dependent. means these drugs bind to diff states of Na or Ca channel. verapamil binds more effectively to Ca channel when its in activated or inactivated state and not so much as when in resting state. means that these drugs bind more when channel activate and they actually unbind from channel when goes into another state and rebind when in active or inactivated state- so use- dependent… so bind more effectively when being used so in tachycardia will bind more. under resting conditions verapamil doesn't have much use on conduction but in tachycardia the channel is going through active/inactivated state more frequently and therefore verapamil binds more effectively and breaks arrhythmia. back to sinus rhythm not effecting sinus rhythm at all- just when its in tachycardia. use-dependent so will only block the channel when its going into rapid rhythm like tachycardia -good characteristic. thats why verapamil used to block tachycardias.


What are the four factors that determine cardiac output?

Cardiac factors: HR, myocardial contractility
coupling factors: preload, afterload

cardiac output- HR x SV (SV is how much blood squirted out with each beat)

HR times SV =Cardiac output. if HR up or down will modulate cardiac output. force frequency rel- as HR goes up get positive staircase, freq of HR will determine how much Ca gets into cell which det. the contractility of the heart.


What is myocardial contractility?

How hard the muscle is contracting ...directly related to Ca in the cell
-more Ca, more cross bridges, stronger contraction strength


If you saw a patient with low ejection fraction (around 10 or 15 or 20) what would this indicate?

ejection fraction is percentage of blood ejected with one stroke of heart-usually around 60 percent of volume of L ventricle.
low ejection fractions around 15 indicate congestive heart failure bc not handling Ca efficiently.

-could be lots of steps in the EC coupling mechanism involved.

congestive heart failure tho is considered a decrease in myocardial contractility...


Describe preload.

preload is the filling of heart - amount of blood in the heart at the beginning of contraction

more blood in the heart- greater preload, greater force of contraction.

The load on the muscle BEFORE contraction is initiated. The preload stretches the muscle length and therefore generates passive tension on the muscle. In the heart, preload is dependent on ventricular filling (end-diastolic volume=volume in ventricles at end of diastole. in normal heart each chamber holds about 150 mL of blood).


Describe how constant blood flow out of different sides of the heart is maintained.

length tension relationship.
every time you breathe you get a little bit more blood back to one side of heart and less blood back to other side. constantly changing. need length- tension relationship to maintain constant blood flow out of different sides of heart. not pumping exactly same amount of blood out with each beat. over a minute each will both pump out 5 L but on a beat to beat basis not exactly the same …L and R ventricle change ejection fraction with each beat. when important? in hemorrhage.


What is happening if someone is hemorrhaging?

if someone hemorrhaging less blood in heart, preload is low, contraction strength of heart reduced as result of length-tension relationship and nothing to do with contractility. if person bleeding to death
cardiac output quite low… preload problem and need to give more volume.


How might you treat congestive heart failure?

congestive heart failure-congested with blood..can’t pump it out. length tension relationship depressed in pt. with congestive heart failure even tho they have large volume, don't generate a large amount of tension in heart

if give more fluid would make it worse. … sometimes avoid giving volume. give patients with congestive heart failure diaretics to reduce volume - have to understand whats causing decrease in cardiac output


Describe afterload.
Give a clinical example.

high downstream pressure- its pressure that prevents the heart from ejecting its volume. afterload prevents the heart from shortening and muscle from shortening.
-The load on the muscle AFTER contraction is initiated. Afterload is any force that resists muscle shortening. Normally, arterial pressure is the force that resists left ventricle contraction (muscle shortening).

hypertension. arterial pressure on other side of aortic valve..prevents heart from ejecting its volume from aortic valve (normally and w hypertension) but if elevated its more work for heart and more difficult to eject volume. spends more O. not ejecting normal cardiac output…


Would you give digitalis to a person with hypertension?

no creates more O consumption…no, need to lower afterload. give Ace inhibitors…


What effect does HR have on cardiac output?

freq of HR will determine how much Ca gets into cell which det. the contractility of the heart. HR has 2 effects on cardiac output- beats per minute (more beats more cardiac output) brings in more Ca and you get stronger contraction and that will boost myocardial contractility a little bit.


What is contractility?

The inherent ability of actin and myosin to form cross-bridges and generate contractile force. Contractility is INDEPENDENT of preload and afterload. Contractility is primarily determined by intracellular [Ca2+]. In cardiac muscle, the active tension curve (determined by contractility) rises steeply in relation to changes in muscle length.


What is end diastolic volume?
What is the end diastolic volume if patient is hemorrhaging?

end diastolic volume- volume in ventricles at end of diastole. in normal heart each chamber holds about 150 mL of blood.
amount of blood at end of diastole just before heart contracts.

if hemorrhaging then end-diastolic volume is low.


Can you overfill the heart?

can’t overfill heart. if want strong contraction can you overfill heart a little bit? can only fill a little bit more than normal conditions but not much bc heart has v still fibrous pericardium around it and really cant overfill v much, can’t expand volume much more than normal,

but can reduce it- anything that prevents venous return, or bleeding will reduce preload. preload sets stage for contraction. same mech. as in skeletal. creates overlap between actin and myosin, optimal overlap so good line up of cross bridges to get strongest contraction as stretch heart


Describe the Frank Sterling mechanism.

length tension relationship. heart fills with blood during diastole. then AP then contraction and heart shortens on that volume of blood and tries to eject out. ability to eject out is dep. on after load which is any force that resists muscle shortening. normally arterial blood pressure is always resisting, preventing heart from ejecting blood, if goes too high arterial pressure elevated… then that resists ability of heart to shorten and eject volume.


What is the problem with afterload? What can it lead to?

if heart has to generate more force to eject its volume, uses more ATP and ATP comes from O… O consumption going up if arterial bp goes up and get O from coronary arteries in heart and people with hypertension usually have arterial sclerosis as well so have coronary disease … increase work on heart but not increasing supply of O. formula for ischemia and heart attack.


How is contractility related to preload and afterload?

contractility- doesn’t make diff of volume in heart. doesn’t make diff after load. if u increase Ca you’ll increase contraction. this is only under normal conditions. congestive heart failure it doesn't work v well. but under normal conditions contractility is independent of preload and after load. more cross bridges, more contraction strength.


Describe contraction and the two types of muscle contraction.

Contraction - Process by which muscle generates tension or force.

Note: muscle contraction is not always associated with muscle shortening.

Two types of muscle contraction:

1. Isometric contraction - Contraction without shortening (no change in length). If a muscle is unable to generate enough force to meet the afterload, then the contraction is isometric (no muscle shortening).

2. Isotonic contraction - Contraction with shortening and constant force (no change in force). If a muscle is able to generate enough force to meet the afterload, then the contraction is isotonic (muscle shortens).

During a normal cardiac cycle, cardiac muscle initially generates isometric tension and then isotonic contractions.


Describe the diff between contraction and contractility.

contraction is NOT synonymous with contractility (change in force specially related to Ca) so can get a change in force in heart by either changing preload or after load- which is not contractility.

contractility= The inherent ability of actin and myosin to form cross-bridges and generate tension. Contractility is primarily determined by intracellular [Ca2+]. More intracellular [Ca2+] leads to more cross-bridge formation and thereby stronger contraction. Contractility also is referred to as inotropy, i.e. positive and negative inotropic effects.


What type of muscle contraction would it be if you were generating a lot of force to lift a weight you couldn't lift.

isometric- generating lots of force to lift weight you cannot lift, not shortening the muscle but generating force.


Describe isometric/isotonic contractions in the heart.

in heart it goes through isometric contraction before it actually ejects volume. isotonic - with shortening and has constant force. tonic=force, iso=same.

if muscle able to generate enough force to meet after load then contraction is isotonic… if trying to lift weight you can lift, can meet load and biceps will generate 10 pounds of force, doesn't need to generate more. heart will do that too, meet after load and generate that pressure. thats isotonic- actual ejection of blood from heart.

volume of blood in ventricle, activate electrically and tries to eject its volume but isometric bc can’t overcome the after load (pressure on other side of aortic valve) until it exceeds pressure on other side of aortic valve so know diastolic pressure about 80 mm of Hg. so heart has to generate 80 mm of Hg isometrically before aortic valve pops open, when it opens thats the isotonic phase and heart can shorten. both phases important bc both use ATP and O.


Describe preload: length-tension relationship (Frank-Starling).
Define resting (diastolic) tension and active (systolic) tension.

An increase in resting cardiac muscle length will increase contraction strength.

Resting (Diastolic) Tension: amount of tension that develops passively by stretching the muscle, i.e. increasing preload. In the heart, the preload is the ventricular filling volume, i.e. end-diastolic volume. The slope of the resting tension curve is primarily determined by muscle compliance.

Active (Systolic) Tension: amount of isometric tension that is developed by muscle contraction at a particular muscle length (preload). In the heart, the systolic tension curve represents stroke volume. The slope of the active tension curve is primarily determined by contractility.


Draw the graph for length-tension relationship. Explain it.

strength of contraction does depend on what load is. no time in this graph. x axis- length of fibers or sarcomeres or volume, all same idea. as volume increasing sarcomeres being stretched… as heart filling w blood sarcomeres having to get longer, sarcomere length det. strength of contraction. so volume det. strength of contraction. y axis- developed force. related to ventricular pressure. 2 lines. 1 line for when muscle activated when Ca high. other line is diastole when muscle not activated, filling phase. start with low volume and low pressure then heart starts filling with blood, as volume increasing sarco-length increasing and stretching cells, as fill up balloon is elasticity, tendency to rebound to natural length, as build up, building up some passive force. so takes some pressure to fill ventricle up. when push on something.. going counter clockwise, fill up w blood, squirt out, pressure high during systole and rel. low during diastole. one thing regulated and other is not- compliance is not really regulated, main thing is regulated is contractility. isometric contraction- developing force but not filling up so perfect vertical line from end of diastolic line. developing pressure but not changing volume.

length meaning sarcomere length. can think of as volume. chamber- think about volume, individual cell- talking about sarcomere
fluid goes back to heart, increases end diastolic volume, stretches the sarcomere and bc of length tension relationship heart contracts stronger and it increases bp. thats what happens… this curve describes length-tension relationship. diastolic filling causing passive increase in force actual contraction with actin and myosin causing contractility causing slope of this line. saying can talk about single fiber and sarcomere length, whole heart talk about end diastolic volume, same thing. developed force (individual fiber) ventricular pressure-whole chamber but same idea
isometric contraction. not talking about skeletal muscle summation…talking about individual cardiac twitch, one contraction. relationship showing you if you increase end diastolic volume can get larger contraction, lower volume you get lower contraction strength.


How does the infusion of fluid into venous system (saline solution into venous system) increase cardiac output in patient? how does infusion of volume (IV) cause increase in cardiac output?

it increases sarcomere length of cardiac muscle cell


Describe the passive pressure in the heart. What is a normal end diastolic pressure? What is it in congestive heart failure? Why?

say fill heart to particular volume. say 150 mL of blood. passive tension generated. stretching rubber band, stretching heart, heart has resistance, component of actin/ myosin called titin. believed to be component inside cell thats being stretched when you stretch cell and that generates a force, resistance - trying to pull apart when stretch and thats passive force generated in heart. its v low in heart, less than 10 mm of Hg- v important. that pressure is called ventricular end diastolic pressure. at end of diastole when heart filled with blood. if heart congested and overfilled they have end diastolic pressure of 25 and 30 mm Hg. usually normal is less than 10 and its passive. at that particular volume you stimulate electrically and thats maximum amount of force it can develop at top


Why is the heart a very stiff muscle?

has low compliance … compliance is directly related to slope of lower line. (on length-tension graph)


What is compliance? Describe its relation to the graph. (What would an increase in compliance do to the curve?)

Relates to length-tension relationship. Defined as change in volume (length) in relation to change in pressure (tension). change in V/change in P = change in Length/change in tension (passive)

Cardiac muscle exhibits a significantly lower compliance (is stiffer) than skeletal muscle. Therefore, cardiac muscle develops significant resting tension at much shorter muscle lengths compared to skeletal muscle. Compliance primarily determines the slope of the resting tension curve. A decrease in compliance increases the slope of the resting tension curve. Because of its relatively low compliance, cardiac muscle works on the ascending limb of the length-tension curve.

compliance- how much does something move when put force on it.


How would volume increasing but pressure staying mostly the same affect compliance?

What if you increase volume slightly and pressure significantly?

1) compliance would be high, stretch v easily

2) if increase volume some and pressure a lot then compliance would be v low and heart v stiff


How does compliance relate to the diastolic filling curve?

ability of the heart to fill with blood is dependent on compliance characteristics of muscle.. pressure going up, increasing volume and look at increase in passive pressure.
-slope of this line, relationship between volume and pressure is compliance characteristics of heart.


What would a steeper diastolic filling curve indicate?

less compliant the heart, the steeper the relationship… if compliance characteristics get lower, that same volume causes much higher pressure. v fundamental to heart.


After infarct, what happens to that tissue? How will this affect compliance? What kind of pressure will the heart then generate?

how stiff heart is… after infarct, chunk of muscle dead, what happens to that tissue? gets stiff bc inflammatory reaction and heals over with fibrosis, scars… scar is stiff, that tissue cant expand passively when heart fills with volume. makes compliance of heart less. as that heart tries to fill with blood during venous return pressure goes up abnormally inside ventricle and that prevents normally filling bc compliance is too stiff.

very stiff tissue develops low pressures (about 6 mmHg)


What determines the systolic curve slope?
What happens to the slope if you increase sympathetic nerve activity?

contractility- amount of Ca in the cell.
in heart systolic curve rep. stroke volume- how much you can actually eject and slope of active curve is det. by contractility or Ca. amount of active pressure can develop for given volume, if you increase sympathetic nerve activity it would shift curve up so can get more pressure at a given volume, increase in contractility.


Where would heart failure be on the curve?



How would an increase in contractility shift the slope of the active tension curve? Decrease in contractility?

An increase in contractility (positive inotropic effect) will shift the slope of the active tension curve up and to the left. A decrease in contractility (negative inotropic effect) will shift the slope of the active tension curve down and to the right.


How does an increase in preload cause an increase in tension development?

Stretching cardiac muscle:
a) creates more optimal overlap between thin and thick filaments.
b) increases Ca2+ sensitivity of myofilaments.

if increase volume in heart, more optical overlap of thin and thick filaments. some evidence also that by stretching muscle can increase sensitivity of myofibrils to Ca and get stronger contraction.


Describe the effects of changing preload on isotonic contractions. (Draw the graph)

What do vertical lines represent?

Increase in preload increases the amount of muscle shortening (1-2-3)
Decrease in preload decreases the amount of muscle shortening (3-2-1)
Slide 9.
graph showing effects of changing preload on actual ejection of blood from heart (isotonic contraction)

length of muscle or volume, tension developed by L ventricle
(vertical line) length of muscle not changing- so isometric contraction) not changing bc valves on both sides are closed…
isotonic phase of contraction (horizontal line)

if you increase preload to 2 get isometric contraction and shorten. 3- isometric contraction, shorten and get greater amount of shortening

plot change in muscle from 1-2-3 and percent change in amount of shortening. greater amount of shortening with greater amount of preload, the more the preload, the more shortening you’ll get. shortening in heart will translate to SV essentially.


What is contractility and how is it related to preload and afterload?

The inherent ability of actin and myosin to form cross-bridges and generate tension. Contractility is primarily determined by intracellular [Ca2+]. More intracellular [Ca2+] leads to more cross-bridge formation and thereby stronger contraction. Contractility is INDEPENDENT of changes in preload or afterload.


Draw a graph showing isometric contraction with preload held constant. Draw normal contractility and then increased contractility and decreased contractility. (Tension- y, time-x)

Provide a clinical example of what would cause and increase or decrease in contractility.

Slide 11.

Note that compared to normal contractility (NML) an increase in contractility achieved by sympathetic nerve stimulation (A) not only increases peak isometric tension but also enhances the rate of relaxation. Conversely, a decrease in contractility (B) decreases peak isometric tension and also slows the rate of relaxation of the heart.

increase in contractility -greater rate of rise, greater peak, and sympathetic nerve stimulation get more rapid relaxation … decrease in contractility…is heart failure. B is congestive heart failure. much slow development of force, smaller peak force, smaller relaxation- doesn't relax normally.


What causes sympathetic nerve stimulation?

what causes sympathetic nerve stimulation? SR Ca pump and decrease of affinity of Ca for troponin C due to phosphorylation


Draw a isotonic contraction graph with muscle tension on the y axis, muscle length on the x axis.

At constant afterload (2g) and preload, an increase in contractility will have what effect on shortening? (how can you tell?)

How will an increase in contractility affect muscle shortening?

Graph slide 12.

At constant afterload (2 g) and preload (LPL), an increase in contractility increases the amount of shortening (LB is shorter than LA).

-shorten going R to L under same constant force, under normal conditions you’d shorten to the length that you can’t shorten any further (defined by this line) then muscle relaxes. if you increase contractility preload and after load doesn't change but can get to shorter length so therefore you have greater amount of total shortening, ejected more blood.

An increase in contractility increases the amount of muscle shortening by allowing the muscle to reach a shorter length.

A decrease in contractility decreases the amount of muscle shortening by not allowing the muscle to reach a shorter length.


How will contractility affect the isometric portion of contraction?

What happens if you increase afterload?

contractility won't affect isometric portion of contraction

if you increase after load then you increase amount of isometric contraction you have to generate (and thats by def. the increase in after load) and that means more O consumption, so if your arterial pressure goes up or or something prevents you from shortening, your isometric phase of contraction is going to go up and you’ll use more O.


Describe how an increase and decrease in contractility will affect:
-muscle shortening
-velocity of shortening
-rate of relaxation

increase contractility and muscle shortening, velocity and rate of relaxation increase
(rate of relaxation- sympathetic stimulation)

all factors decrease with decrease in contractility
decreasing rate of relaxation (inhibit sympathetic stimulation)


Describe the force-velocity relationship. Draw a graph with vmax, and maximal isometric force marked. x axis- afterload (force), y axis- shortening velocity.

velocity is speed with which heart can actually shorten, related to force of heart. heart generates more force with greater velocity of shortening

Fig. 1- Increasing afterload decreases the velocity of isotonic muscle shortening.

Vmax represents the maximal velocity of shortening with “no load”. It is used as an index of contractility.

Maximal isometric force is when the muscle is unable to meet the afterload, i.e. zero velocity of shortening (isometric contraction).
Slide 15

here’s afterload, and here’s shortening velocity of actin and myosin filaments. as after load goes up L to R, velocity of shortening goes down (if try to lift heavy weight cant lift rapidly… if after load is high then velocity of shortening is low and can get to after load which is maximum and have isometric contraction and velocity of shortening is zero.


Draw the effects of increasing preload on the force-velocity relationship graph.

increasing preload (a-c) shifts the force-velocity curve to the right without changing Vmax. In other words, at any given afterload, increasing preload increases the velocity of shortening.

increase preload a to b to c at any given afterload, same after load-if increase preload get greater velocity of shortening, at same after load if increase preload, get greater velocity of shorting. increasing preload increases velocity and amount of shortening


Draw the effects of increasing ionotropy on the force-velocity relationship graph.

increasing contractility (positive inotropy) shifts the force-velocity curve to the right and increases Vmax. In other words, at any given afterload, increased contractility increases the velocity of shortening.

ionotropoy is contractility- at any given after load get certain amount of velocity of shortening and if you increase contractility you’d get greater amount of velocity of shortening at same after load and up to c get higher velocity of shortening. preload and contractility enhance velocity and amount of shortening at any given afterload. getting greater force development with increase in preload or after load w velocity of shortening and amount of shortening.


How will increasing ionotropy or preload affect vmax and maximum isometric force?

increasing preload- no effect on vmax, increase max. isometric force

increasing iontropy- increase vmax and max. isometric force