L25 – Control of the Heart Flashcards Preview

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Flashcards in L25 – Control of the Heart Deck (52):

How is cardiac output calculated?

Stroke volume x Heart rate = cardiac output


Modify which two parameters can change cardiac output?

Stroke volume
Heart rate


What is the one parameter that must increase for cardiac output to increase? Why?

Venous return must also increase
Because heart is closed system, can only output the input


What is stroke volume a function of?

Filling and force of contraction


How does contractility and rate of force development related?

rate of force development =contractility


What are the 2 ways that the force of contraction can be increased?

1) Prolong time of contraction at same rate of force development
2) Increase rate of force development but keeping same time of contraction


What ion does contractility depend on?

Intracellular Ca2+ concentration (relating to number of actin- myosin crossbridges formed)


Total force of contraction of ventricles is influenced by intracellular Ca2+ concentration, how?

Increase intracellular Ca2+ conc. > more excitation-contraction coupling > Increase number of actin-myosin crossbridges form > Increase force of contraction


What are the two mechanisms for controlling Force of Contraction in heart?



What is the difference between homeometric and heterometric control of force of contraction in heart ventricles?

Homeometric = change in rate of force development, no change in muscle length, same duration of contraction

Heterometric = change in muscle length, same rate of force development, prolong duration of contraction


What causes change in ventricular muscle length (heterometric control)?

When ventricle walls are more stretched
e.g. increase venous return fills and stretches ventricular wall


What is the main role of heterometric control of contractility?

Protective, prevent overfilling


Which of 2 controls of contractility is intrinsic, which is extrinsic?

Heterometric always INtrinsic - arise from within muscle itself/ autoregulation

Homeometric= INtrinsic OR EXtrinsic - induce by external agent on ventricular muscle


Which mechanism is autoregulatory of venous return volume?

Heterometric control (intrinsic)


Heterometric control changes contractility or not?

No, doesnt change rate of force development
Only prolongs duration of contraction


Does homeometric control change contractility or not?

Yes- Change rate of force development
Same duration of contraction


What do inotrophic and chronotropic refer to ?

Inotrophic = change in contractility
Chronotrophic = change in HR


Explain Inotrophic mechanism/cardiac excitation-contraction coupling, starting with cardiac AP, channels, ion movements... to contraction.

Cardiac AP > Open L-type channels in cell membrane and T-tubule during plateau of AP > Entry of extracellular Ca2+ through Ryanodine receptor by diffusion

> Induce Ca2+ release from sarcoplasmic reticulum > Ca2+ diffuses to contractile protein > Bind to troponin to expose tropomyosin for actin binding/ crossbridge > contraction


Explain how Ca2+ moves out of cardiac cell in diastole.

Removal of AP > Uptake of Ca2+ back to SR by Sarcoplasmic Reticulum Ca-ATPase (SERCA) > detach cross bridge > Ca2+ pumped from SR to extracellular space


Why is it necessary that Ca2+ exits cardiac cell in diastole?

Balances initial Ca2+ entry in AP


What is the main channel used to pump Ca2+ to extracellular space during diastole apart from SERCA?

Ca2+ movement mostly by Na/Ca exchanger

(Na+ moves down through concentration gradient)


How does inotropic mechanism depend on Ca2+ conc. intracellular?

Increased intracellular Ca = increased Ca in SR
More Ca released from SR for excitation- contraction coupling
Increase no. of actin-myosin cross bridges form
Increases force of contraction


How is homeometric mechanism different from sympathetic nerve control on force of contraction?

Homeometric = Increase rate of force development but NO CHANGE in duration of contraction

Whereas Sympathetic nerve DECREASES the time of contraction

Not the same***


How is cAMP important to the sympathetic nerve control of contractility of ventricles?

(think what causes release of cAMP, what channels, receptors and proteins are involved)

Sympathetic nerve release noradrenaline > bind to B1-receptor on ventricular cell membrane

> activate adenyl cyclase > convert intracellular ATP to cAMP > cAMP activates Protein Kinase A > Phosporylate Ca2+ channel in cell membrane

> Increased time in open-state > increased calcium permeability during AP plateau > increase extracellular Ca2+ enter cell > increase contractility


What channels does Protein Kinase A phosphorylate after being activated by cAMP?

SERCA and L-type Ca2+ channels in cell membrane


Sympathetic control of contractility is different from homeometric control because it decreases duration of contraction. How?

Increased rate of Ca uptake into SR because of Protein Kinase A phosphrylating SERCA > more Ca pump from SR to extracellular space during diastole

allows faster relaxation, shortening overall duration of contraction


Sympathetic nerves also produces a minor effect in addition to changing contractility and duration. What is it?

Rate-induced regulation called Treppe effect
Increase in HR causes increase in Force of contraction


Explain Treppe effect as a result of sympathetic nerve control of contractility.

Minor effect of raising HR > less time for diastole > less time for Ca to be pumped from SR to extracellular space > more intracellular Ca > increase force of contraction


Does sympathetic or parasympathetic DIRECTLY affect heart contractility?

ONLY sympathetic can DIRECTLY affect contractility

Parasympathetic can INdirectly affect


How can parasympathetic innervation indirectly change contractility?

only innervates atria and nodal tissues (not ventricles) > cannot influence force but can change heart rate

> change force indirectly by rate-induced regulation, Treppe effect


What does heterometric autoregulation of heart/ Starling's law of the heart concern?

Effect of venous return on force of contraction of the ventricles


How does venous return and contraction of ventricles relate?

Increase venous return = increase preload = increase ventricle filling = increase force of contraction (same contractility/ rate of force development)


What two parameters can cause force of contraction to increase whilst keeping same contractility?

Increase venous return/ preload
Increase arterial pressure/ afterload


How can increase in afterload increase force of contraction but maintain same contractility?

Increase arterial pressure/ afterload > Increase pressure to pump against (higher peripheral resistance > initial drop in stroke volume > increase end-systolic/ residue volume > increase end-diastolic volume > Increase force of contraction


Why is there an optimum length to striated muscle? Remember that force of contraction depends on number of crossbridges formed.

Too long= reduce actin-myosin overlap
Too short = distort filaments, reduce actin- myosin overlap

Optimum = maximum actin- myosin overlap


What length is cardiac muscle usually at in relation to its optimum length? Why?

Slightly shorter than optimum length

Any stretching of cardiac muscle > closer to optimum length > more crossbridges form > Increase force


How is congestive heart failure a result of cardiac muscle fiber property?

Overstretch of cardiac muscle > stretch beyond optimum length > reduce actin- myosin overlap > less force generated > cannot pump out over-filled ventricles > congestive heart failure


Optimum length of muscle and its mechanism is related to which control mechanism?

Heterometric- since there is change in muscle length


What is Cardiac function curve a graphical representation of?

graphical representation of cardiac force of contraction against length of ventricular muscle for the intact heart


What can the cardiac function curve have on its x -axis? (3)

1) Ventricular muscle fiber length

Since length increases with pressure and volume:
2)Left ventricular end-diastolic volume/ pressure
3)Right atrial pressure (indirectly measure ventricular muscle fibre length) (common)


What can the cardiac function curve have on its y-axis? (4)

1)Force of contraction
2)Stroke work
2)Stroke volume
3)Cardiac output (proportional to force) (common)


How can right atrial pressure be measured to produce cardiac function curve?

Right heart catheterization


How does homeometric increase in force compare to heterometric increase in force on cardiac function graph?

Homeometric has steeper and higher curve


Why does homeometric increase in force have higher and steeper curve in cardiac function graph? (remember properties of homeometric - extrinsic or intrinsic, and no filling)

Homeometric = same duration of contraction, increase rate of force development/ contractility, no change in muscle length

Increase intracellular Ca2+ > change contractility > change slope of cardiac function curve (steeper, higher) > increase force


Explain heterometric increase in force on cardiac function graph. (Heteormetric is always intrinsic)

Not higher and steeper curve like homeometric

Increase muscle length due to more filling > reach optimal muscle length > increase force of contraction


How does the heterometric and homeometric curve compare to normal ?

Heterotrometric : Position of cardiac function curve does not change, but shifted to the right due to higher right atrial pressure, same cardiac output

Homeometric: same right atrial pressure associated with DIFFERENT cardiac output, steeper and higher curve than normal due to increased contractility


Why do both homeometric and heterometric curves dip at high muscle length on the cardiac function graph?

Over-stretch = reduce actin-myosin overlap = reduce cross bridge formation = decrease force


What heart structure resists overstretching of heart to prevent congestive heart failure?

Tough Fibrous pericardium is indistendable


What is the position of the cardiac function curve for a congestive heart failure patient vs normal?

Curve shift to right, higher right atrial pressure


What happens to cardiac function curve if patient has poor contractility e.g. ischaemic scar tissue?

Curve slope becomes shallower


What pathological conditions can likely lead to congestive heart failure?

Heart unable to compensate heart failure by enabling heterometric effect and increasing force of contraction

In hearts with poor contractility e.g. ischaemic scar tissue from MI


What is the difference between compensated heart failure and decompensated?

Compensated = kick in heterometric effect, stretching > operate at maximal force to maintain normal stroke volume (a function of force and filling)

Decompensated means over-stretching beyond optimum length and cannot recover, right atrial pressure at peak, heart gives up, congestive heart failure

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