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PHYS201 · Study guide

Cardiac output and what sets it

  • 27 min lecture
  • 5 key ideas
  • 2 review sheets
  • 8 questions
  • 9 flashcards

Made by StreamSnag with AI from the transcript of this lecture. Every part points to the minute it comes from: check anything important against the lecture itself.

Big picture

This lecture asks how much blood the heart pumps each minute and what sets that amount. It starts from cardiac output as heart rate times stroke volume, then takes the three determinants of stroke volume in turn: preload and the Frank-Starling law, afterload and the law of Laplace, and contractility driven by calcium. The pressure-volume loop then shows all three on one diagram, and exercise and heart failure show them working together.

After this lecture you should be able to

  • Calculate cardiac output, stroke volume and ejection fraction from heart rate, end-diastolic volume and end-systolic volume, and decide whether an ejection fraction is normal or reduced.
  • Explain the Frank-Starling law, its two cellular mechanisms and why it keeps the outputs of the right and left ventricles matched.
  • Predict how a rise in afterload changes end-systolic volume and stroke volume, and explain with the law of Laplace why hypertrophy compensates for chronic high afterload.
  • Compare a change in preload with a change in contractility in terms of calcium, the Frank-Starling curve and end-systolic volume.
  • Sketch the left ventricular pressure-volume loop and predict how it changes when preload, afterload or contractility increases.
  • Explain how heart rate, preload, afterload and contractility account for cardiac output in hard exercise and in heart failure with reduced ejection fraction.

Key ideas

1

Why can a normal 5 L/min cardiac output hide a badly failing ventricle?Core

01:18 · slide 2also at01:2702:5203:1103:2704:18

A normal cardiac output can hide a failing ventricle because output is a product of two things, and a fast heart rate can make up for a poor stroke volume. Cardiac output is the volume one ventricle (not both) pumps per minute: heart rate times stroke volume. Stroke volume is end-diastolic volume minus end-systolic volume, 120 mL minus 50 mL giving 70 mL. Ejection fraction is stroke volume divided by end-diastolic volume, so 70 over 120 is about 58 percent. Below about 40 percent it is called reduced, and this is how heart failure is classified. So you have to look at how the output is being achieved, not just at the total.

In the lecturer's words“Cardiac output is the volume of blood one ventricle pumps per minute”
Example

A patient with heart rate 100, end-diastolic volume 150 mL and end-systolic volume 100 mL has a stroke volume of 50 mL and a cardiac output of 5 litres a minute, which looks normal. But the ejection fraction is 50 over 150, 33 percent: a big ventricle that empties poorly and keeps its output up only by beating faster.

Ask yourself

Why does the ejection fraction reveal a problem in the patient with a heart rate of 100 that the cardiac output of 5 litres a minute does not?

2

How does a larger end-diastolic volume give a larger stroke volume without extra calcium?Core

07:53 · slide 4also at08:3110:2111:5712:1212:28

A fuller ventricle ejects more because stretch makes the filaments respond better to the same calcium. Preload is the stretch on the ventricular muscle cells at the end of diastole, just before contraction. By the Frank-Starling law, raising end-diastolic volume raises stroke volume; within limits, the heart pumps out whatever is returned. Two things cause this. Resting sarcomeres are about 1.8 micrometres, shorter than optimum, and stretching towards about 2.2 micrometres improves actin-myosin overlap so more cross-bridges form. The bigger effect is length-dependent activation: stretch makes troponin C more sensitive to calcium. No nerves or hormones are needed, so it is called intrinsic regulation. Its most important job is keeping the two ventricles, which are in series, matched.

In the lecturer's words“Preload is the stretch on the ventricular muscle cells at the end of diastole, just before contraction”
Example

If end-diastolic volume goes from 120 to 140 millilitres and end-systolic volume stays at about 50, stroke volume goes from 70 to 90 millilitres on the very next beats. And if the right ventricle pumped even one millilitre more per beat than the left, at 70 beats a minute that would be 70 millilitres every minute piling up.

Ask yourself

Why does the fact that the amount of calcium does not change in the Frank-Starling mechanism separate it from a change in contractility?

3

Why does stroke volume fall when afterload rises, and how does hypertrophy compensate?Core

14:04 · slide 6also at14:5915:1115:2315:3716:36

Stroke volume falls when afterload rises because the ventricle cannot empty as well against the higher pressure, so more blood is left behind. Afterload is the load the ventricle must overcome to eject blood; for the left ventricle the simplest picture is the pressure in the aorta. With preload and contractility unchanged, afterload up means stroke volume down and end-systolic volume up. Strictly, afterload is not the pressure itself but the stress in the ventricular wall during ejection. The law of Laplace gives wall stress as pressure times radius, divided by two times the wall thickness. So a thicker wall brings wall stress back towards normal, which is why hypertrophy is a compensation for high afterload.

In the lecturer's words“Afterload is the load the ventricle has to overcome in order to eject blood.”
Example

In a patient with long-standing high blood pressure or a narrowed aortic valve (aortic stenosis), the left ventricle faces a high afterload for years and its wall gets thicker: left ventricular hypertrophy. The price is that a thick ventricle is stiff and fills badly.

Ask yourself

How does the law of Laplace explain why a thicker ventricular wall compensates for a high aortic pressure?

4

How does a contractility change differ from moving along the Frank-Starling curve?Core

17:59 · slide 7also at07:3618:3318:5420:1220:20

A contractility change gives you a whole new curve, while a preload change moves you along the same one. Contractility, or inotropy, is the strength of contraction at a given preload and a given afterload. If the ventricle pumps more because it was filled more, that is Frank-Starling, not contractility. A contractility change means a bigger stroke volume for the same end-diastolic volume, and the mechanism differs: more calcium is made available to the filaments inside the cell. The new curve is shifted upwards and to the left, the ventricle empties more completely, end-systolic volume falls and ejection fraction rises. About a third of students mix up preload and contractility in the exam every year.

In the lecturer's words“Contractility is the strength of contraction at a given preload and a given afterload.”
Example

Noradrenaline binds to beta-1 receptors on ventricular muscle cells, raising cyclic AMP, which activates protein kinase A; this phosphorylates the L-type calcium channels so more calcium comes in with each action potential. In the throwing analogy, contractility is how strong your arm is: you can throw further by pulling back more, by picking a lighter ball, or by going to the gym.

Ask yourself

How would you tell from a graph of stroke volume against end-diastolic volume whether preload or contractility has changed, and why are the mechanisms behind the two different?

5

How does the pressure-volume loop change with preload, afterload and contractility, and in heart failure?Core

22:29 · slide 8also at23:0623:3523:4323:5825:41

Each determinant changes the loop in its own way. The width of the pressure-volume loop is the stroke volume, here 120 minus 50. More preload fills the ventricle more, so the bottom right corner moves right and the loop widens: stroke volume up. More afterload makes the aortic valve open later, at a higher pressure, so the loop is taller and narrower, end-systolic volume is higher and stroke volume is down. More contractility empties the ventricle further, so the left side moves left, end-systolic volume falls and the loop widens. The straight line through the end-systolic points of several loops has a slope that measures contractility; steeper means a more strongly contracting ventricle.

In the lecturer's words“The width of the loop is the stroke volume, a hundred and twenty minus fifty”
Example

In heart failure with reduced ejection fraction, contractility is down, for example after a heart attack, so the patient is on a lower, flatter curve with less stroke volume at any filling volume. The kidneys hold on to salt and water, blood volume and preload go up, but because the curve is flat this gains only a bit of stroke volume.

Ask yourself

Why does raising preload help a patient with reduced-ejection-fraction heart failure only a little, and how does that connect to the difference between moving along a curve and being on a different curve?

Review sheets

Preload versus contractility: Frank-Starling and calcium

This topic separates two determinants of stroke volume that the lecturer says about a third of students mix up in the exam every year: preload, which works through the Frank-Starling law, and contractility, which works through the amount of calcium available. The rest of the lecture needs the distinction because a rise in preload moves the ventricle along the same curve, while a rise in contractility puts it on a new, higher curve.

Step by step

  1. Start with the definition: preload is the stretch on the ventricular muscle cells at the end of diastole, just before contraction. That stretch cannot be measured in a patient, so end-diastolic volume, or sometimes end-diastolic pressure, is used as a stand-in. 07:53
  2. With end-diastolic volume standing in for preload, the key relationship follows: if end-diastolic volume increases, the ventricle ejects a bigger stroke volume. This is the Frank-Starling law of the heart; within limits, the heart pumps out whatever volume is returned to it. 08:31
  3. Why does stretch give more force? The first reason is filament overlap: resting cardiac sarcomeres are about 1.8 micrometres, shorter than the optimum, and stretching them towards about 2.2 micrometres makes actin and myosin overlap better, so more cross-bridges can form. 11:57
  4. The bigger reason is length-dependent activation: when the sarcomere is stretched, troponin C becomes more sensitive to calcium, so the same amount of calcium released produces more force. In the Frank-Starling mechanism the amount of calcium does not change, only the filaments' sensitivity to it. 12:12
  5. Contractility, or inotropy, is the strength of contraction at a given preload and a given afterload. If the ventricle pumps more because it was filled more, that is Frank-Starling, not contractility. Contractility goes up when more calcium is made available to the filaments inside the cell. 17:59
  6. The classic example is the sympathetic nervous system: noradrenaline binds to beta-1 receptors, which raises cyclic AMP, which activates protein kinase A, which phosphorylates the L-type calcium channels so more calcium comes in with each action potential. Anything that does this is called a positive inotropic agent. 18:54
  7. On the graph, more preload moves you along the same curve, while more contractility moves you onto a higher curve, shifted upwards and to the left. On that higher curve the ventricle empties more completely, so end-systolic volume falls and ejection fraction goes up. 20:20

How it connects

This sheet joins two other key ideas of the lecture: how a larger end-diastolic volume gives a larger stroke volume without extra calcium, and how a contractility change differs from moving along the Frank-Starling curve. The definition of contractility also relies on afterload, since it is the strength of contraction at a given preload and a given afterload.

Common mistakes

  • MistakeTreating preload and contractility as the same thing.InsteadThey are different determinants of stroke volume; the lecturer says about a third of students mix them up in the exam every year.
  • MistakeCalling a bigger stroke volume after more filling a rise in contractility.InsteadPumping more because of more filling is Frank-Starling; contractility is the strength of contraction at a given preload and afterload.
  • MistakeThinking Frank-Starling works by releasing more calcium.InsteadIn Frank-Starling the amount of calcium does not change; only the filaments' sensitivity changes. More calcium available is contractility.
  • MistakeDrawing a rise in contractility as a move along the same curve.InsteadMore preload moves along the same curve; more contractility gives a higher curve, shifted upwards and to the left.

Go back to

Reading the pressure-volume loop

The left ventricular pressure-volume loop is a diagram of one heartbeat whose corners mark valve events and whose width, area and end-systolic line can be read as stroke volume, stroke work and contractility. The lecture uses it to show on one picture what happens when preload, afterload or contractility is increased, and the lecturer says that if you can draw those three loops you understand the lecture.

Step by step

  1. Start at the bottom left corner: the mitral valve has just opened and the ventricle holds 50 mL. It fills along the bottom of the loop to 120 mL while pressure stays low. The bottom right corner is the end-diastolic volume, which is the preload. 21:21
  2. From the end-diastolic volume the ventricle starts to contract and the mitral valve closes, so both valves are closed. Pressure shoots straight up with no change in volume, drawn as a vertical line: this is isovolumetric contraction. 21:39
  3. When ventricular pressure reaches aortic pressure, about 80 mmHg, the aortic valve opens at the top right corner and ejection begins. Pressure keeps rising to a peak of about 120 mmHg while volume falls across the top of the loop back to 50 mL. 21:48
  4. At the top left corner the aortic valve closes and pressure drops straight down with both valves closed again: isovolumetric relaxation, which brings you back to the start. Two readings follow: the width is the stroke volume, 120 minus 50 mL, and the area inside is the stroke work for one beat. 22:15
  5. Take the top left corner, the end-systolic point, from several loops at different filling volumes: the points fall on a straight line, the end-systolic pressure-volume relationship. Its slope measures contractility; a steeper line means a more strongly contracting ventricle, and a positive inotropic agent makes it steeper. 23:06
  6. Now turn the knobs. Increasing preload fills the ventricle more, so the bottom right corner moves right, the loop widens and stroke volume goes up. Increasing afterload opens the aortic valve later at a higher pressure, so the loop is taller and narrower, end-systolic volume is higher and stroke volume goes down. 23:35
  7. Increasing contractility makes the ventricle empty further, so the left side of the loop moves to the left. End-systolic volume is lower, the loop is wider and stroke volume goes up. 23:58

How it connects

The loop is where the lecture's ideas of preload, afterload and contractility meet: the bottom right corner is the preload, the slope of the end-systolic line is contractility, and the taller, narrower loop shows stroke volume falling when afterload rises. The lecturer then turns each knob in turn, which is the key idea of how the loop changes with preload, afterload and contractility.

Common mistakes

  • MistakeThinking that both changes which widen the loop move the same side of it.InsteadIncreased preload moves the bottom right corner to the right; increased contractility moves the left side to the left, lowering end-systolic volume.
  • MistakeAssuming a taller loop under increased afterload means more stroke volume.InsteadThe loop is taller but narrower: ejection stops sooner, end-systolic volume is higher and stroke volume goes down.
  • MistakeMixing up what the width and the area of the loop stand for.InsteadThe width is the stroke volume, 120 minus 50 mL; the area inside is the stroke work, the work done in one beat.
  • MistakeDrawing volume changing during the two isovolumetric phases.InsteadBoth valves are closed in both phases, so pressure goes straight up or straight down with no change in volume.

Go back to

Key figures

Slide 4: Frank-Starling curve: stroke volume against end-diastolic volume

Frank-Starling curve: stroke volume against end-diastolic volume

What it shows. A Frank-Starling curve with end-diastolic volume (mL) on the x axis and stroke volume (mL) on the y axis, rising steeply and then flattening.

What the lecturer said. The graph shows the Frank-Starling law: if you increase the end-diastolic volume, the ventricle ejects a bigger stroke volume. The curve flattens at high volumes because you cannot stretch the muscle indefinitely and keep getting more force. More preload moves you along the same curve, whereas more contractility moves you onto a higher curve.

07:51 · slide 4

Slide 8: Left ventricular pressure-volume loop

Left ventricular pressure-volume loop

What it shows. A left ventricular pressure-volume loop with volume (mL, 50 to 120) on the x axis and pressure (mmHg, up to 120) on the y axis, showing the phases filling, isovolumetric contraction, ejection and isovolumetric relaxation, plus the ESPVR line.

What the lecturer said. One heartbeat is one trip anticlockwise round the loop: filling along the bottom to the end-diastolic volume at the bottom right corner (the preload), a vertical line up for isovolumetric contraction, ejection from the top right corner once the aortic valve opens at about 80, then pressure dropping straight down in isovolumetric relaxation. The width of the loop is the stroke volume, 120 minus 50, and the area inside the loop is the stroke work, the work the ventricle does in one beat.

20:41 · slide 8

Easily confused

Preload (Frank-Starling)Contractility (inotropy)
What it isPumping more because the ventricle was filled moreStrength of contraction at a given preload and a given afterload
On the curveMoves you along the same curveMoves you onto a higher curve, shifted upwards and to the left
07:36 · slide 3
Venous returnPreload
What it isA flow: volume of blood coming back to the heart per minuteThe stretch that results in the ventricle at the end of filling
How they relateOne of the things that determines preloadDetermined by venous return among other things; not the same
Very fast heart rateHasn't changedFalls, because there is less time to fill
10:47 · slide 4

Formulas and numbers

As given in this lecture. Where a value matters beyond the exam, check it against a current source.

  • Cardiac output is calculated by multiplying heart rate by stroke volume. 01:27 · slide 2
  • A typical resting adult, with heart rate about 70 beats per minute and stroke volume about 70 mL, has a cardiac output of roughly 5 litres per minute. 01:49 · slide 2
  • Stroke volume equals end-diastolic volume minus end-systolic volume: 120 mL minus 50 mL gives 70 mL. 02:52 · slide 2
  • Ejection fraction is stroke volume divided by end-diastolic volume; 70 mL over 120 mL is about 58 percent. 03:11 · slide 2
  • A normal ejection fraction is somewhere above 55 percent. 03:23 · slide 2
  • An ejection fraction below about 40 percent is called reduced, and ejection fraction is how heart failure is classified. 03:27 · slide 2
  • By the law of Laplace, ventricular wall stress equals pressure times radius divided by two times the wall thickness (P × r / 2h). 15:37 · slide 6

Self-test

Answer each one from memory, out loud or on paper, before you open the answer. Then mark yourself honestly.

  1. Apply

    A patient at rest has a heart rate of 90 beats per minute, an end-diastolic volume of 180 mL and an end-systolic volume of 125 mL. Calculate the cardiac output and the ejection fraction, and say what the two numbers together tell you about this ventricle.

    Show answer

    Stroke volume is 180 − 125 = 55 mL, so cardiac output is 90 × 55 = 4950 mL/min, about 5 L/min, which looks normal. Ejection fraction is 55 / 180, about 31 percent, which is below the roughly 40 percent threshold and counts as reduced. A normal resting cardiac output therefore does not mean a normal heart: this ventricle is failing and maintains output through a higher heart rate and a larger filling volume.

    A good answer includes
    • Stroke volume 55 mL; cardiac output about 5 L/min
    • Ejection fraction about 31 percent, below 40 percent, so reduced
    • Normal resting output does not mean a normal heart

    Review this part01:27 · slide 2

    How did you do?
  2. Explain

    Explain the difference between venous return and preload, and describe a situation in which preload falls even though venous return has not changed.

    Show answer

    Venous return is a flow: the volume of blood coming back to the heart per minute. Preload is the stretch on the ventricular muscle cells at the end of diastole, and venous return is only one of the things that determines it. At a very fast heart rate there is less time for the ventricle to fill, so preload falls even though venous return is unchanged.

    A good answer includes
    • Venous return is a flow, volume returning per minute
    • Preload is ventricular stretch at the end of diastole
    • Fast heart rate shortens filling time, so preload falls

    Review this part10:47 · slide 4

    How did you do?
  3. Go further

    Suppose the right ventricle ejected 2 mL more per beat than the left at a heart rate of 60 beats per minute. How much extra blood would be in the pulmonary circulation after 10 minutes, and how does the Frank-Starling mechanism normally prevent this from happening?

    Show answer

    2 mL × 60 beats × 10 minutes gives 1200 mL, about 1.2 litres of extra blood in the pulmonary circulation. Normally the extra blood pumped by the right ventricle returns to the left ventricle and raises its end-diastolic volume, and by the Frank-Starling law the left ventricle responds with a bigger stroke volume. This keeps the outputs of the two ventricles, which are in series, matched, without any nerves or hormones.

    A good answer includes
    • About 1200 mL (1.2 L) accumulates in the pulmonary circulation
    • Higher left ventricular end-diastolic volume gives a bigger stroke volume
    • Frank-Starling keeps the two ventricles' outputs matched

    Review this part08:31 · slide 4

    How did you do?
  4. Go further

    A left ventricle dilates so that its radius becomes 1.5 times larger, while ejection pressure and wall thickness stay the same. Using the law of Laplace, what happens to its afterload, and what does that do to stroke volume if preload and contractility are held constant?

    Show answer

    Wall stress equals pressure times radius divided by twice the wall thickness, so a radius 1.5 times larger gives a wall stress 1.5 times larger. Strictly, afterload is the wall stress during ejection and not the pressure itself, so afterload rises although the pressure is unchanged. With preload and contractility constant, a higher afterload means the ventricle empties less well and stroke volume falls.

    A good answer includes
    • Wall stress = P × r / 2h, so it rises 1.5-fold
    • Afterload is wall stress, so afterload rises at unchanged pressure
    • Stroke volume falls when afterload rises alone

    Review this part14:59 · slide 6

    How did you do?
  5. Explain

    In heart failure with reduced ejection fraction, the kidneys retain salt and water. Explain why this gains the patient only a little stroke volume, and why diuretics are given even though they do not strengthen the heart.

    Show answer

    Contractility is reduced, so the patient is on a lower, flatter Frank-Starling curve where stroke volume is less than normal at any filling volume. Salt and water retention raises blood volume and preload, but because the curve is flat the extra filling regains only a little stroke volume. The high filling pressure backs fluid up into the lungs and causes breathlessness, so diuretics are given to bring preload back down, not to make the heart stronger.

    A good answer includes
    • Reduced contractility puts the patient on a lower, flatter curve
    • Raising preload on a flat curve adds little stroke volume
    • High filling pressure backs fluid into the lungs, causing breathlessness
    • Diuretics lower preload; they do not strengthen the heart

    Review this part25:41 · slide 9

    How did you do?
  6. Go further

    During hard exercise the arterioles in working muscle normally dilate. Suppose they failed to dilate while the heart still tried to pump much more blood. What would you expect to happen to afterload, end-systolic volume and stroke volume, and why?

    Show answer

    Normally the arterioles dilate, the resistance the heart pumps against falls, and this stops afterload rising much even though more blood is pumped. Without that dilation the resistance would not fall, so afterload would rise as output increased. Against a higher afterload the ventricle empties less well, so end-systolic volume rises and stroke volume is lower than it would otherwise be.

    A good answer includes
    • Arteriolar dilation normally lowers resistance and limits the rise in afterload
    • Without dilation, afterload rises
    • End-systolic volume rises and stroke volume falls

    Review this part14:59 · slide 6

    How did you do?

Practice quiz

New cases to try the lecture's ideas on. Pick an answer to see why each option is right or wrong.

  1. Apply

    A drug is given that makes more calcium enter the cardiac muscle cell with each action potential. End-diastolic volume and aortic pressure are unchanged, yet stroke volume rises. How is this change best described?

    Show answer
    • AConfuses contractility with preload: Frank-Starling needs a higher end-diastolic volume and involves no change in the amount of calcium.
    • BCorrect. A stronger contraction at the same preload and afterload, due to more calcium, is contractility; it shifts the ventricle to a higher curve.
    • CLength-dependent activation changes calcium sensitivity through stretch, but here the filling volume is unchanged and the calcium amount itself rises.
    • DA lower afterload would raise stroke volume, but aortic pressure is unchanged; the cause here is more calcium.

    Review this part12:28 · slide 5

  2. Apply

    A second left ventricular pressure-volume loop is recorded. Compared with the first, its bottom right corner is in the same place, the aortic valve opens at a higher pressure, and the loop is taller and narrower. What changed between the two recordings?

    Show answer
    • ACorrect. Higher afterload makes the aortic valve open later at a higher pressure, giving a taller, narrower loop with a higher end-systolic volume.
    • BMore preload would move the bottom right corner to the right and widen the loop; here that corner has not moved.
    • CMore contractility moves the left side of the loop leftwards and widens it; this loop is narrower.
    • DDirection reversed: a lower afterload would not make the valve open at a higher pressure or narrow the loop.

    Review this part23:35 · slide 8

Check this

Terms the transcription may have misheard
  • The transcript says “Frank Sterling”; the lecturer most likely said Frank-Starling, as on slide 4. 08:44 (5 times in all)
  • The transcript says “ionotropic”; the lecturer most likely said inotropic, as on slide 3. 06:56 (5 times in all)
Parts that could not be heard

16:56

Not from the lecture

The boxes marked “Beyond the lecture (not from your lecturer)” were added by the AI to help. Your lecturer did not say what is in them. They are under:

  • Key idea 1: Why can a normal 5 L/min cardiac output hide a badly failing ventricle?
  • Key idea 2: How does a larger end-diastolic volume give a larger stroke volume without extra calcium?
  • Key idea 3: Why does stroke volume fall when afterload rises, and how does hypertrophy compensate?
  • Key idea 4: How does a contractility change differ from moving along the Frank-Starling curve?
  • Key idea 5: How does the pressure-volume loop change with preload, afterload and contractility, and in heart failure?

Glossary

Afterload 14:04 · slide 6
Afterload is the load the ventricle must overcome to eject blood; for the left ventricle it is most simply thought of as the pressure in the aorta.
Cardiac output 01:18 · slide 2
Cardiac output is the volume of blood that one ventricle (not both) pumps per minute.
Contractility (inotropy) 17:59 · slide 7
Contractility (inotropy) is the strength of contraction at a given preload and a given afterload; pumping more because of greater filling is Frank-Starling, not a contractility change.
Ejection fraction 03:11 · slide 2
Ejection fraction is stroke volume divided by end-diastolic volume; 70 mL over 120 mL is about 58 percent.
End-diastolic volume (EDV) 02:24 · slide 2
End-diastolic volume (EDV) is the volume in the left ventricle at the end of filling, about 120 mL.
End-systolic volume (ESV) 02:35 · slide 2
End-systolic volume (ESV) is the roughly 50 mL left in the ventricle after contraction; the heart never empties completely.
Frank-Starling law of the heart 08:31 · slide 4
The Frank-Starling law of the heart states that increasing end-diastolic volume makes the ventricle eject a bigger stroke volume; within limits, the heart pumps out whatever is returned.
Preload 07:53 · slide 4
Preload is the stretch on the ventricular muscle cells at the end of diastole, just before contraction.
Stroke volume 01:36 · slide 2
Stroke volume is the volume of blood ejected in a single beat.
Stroke work 22:37 · slide 8
The area inside the pressure-volume loop is the stroke work, the work the ventricle does in one beat.
Venous return 10:47 · slide 4
Venous return is a flow: the volume of blood coming back to the heart per minute.

Flashcards

9 cards from this lecture are in your flashcard file and in StreamSnag's review. Each one shows the minute it comes from.

Look through the cards
Cardiac output: through which two variables must any change in cardiac output act?Heart rate or stroke volume05:52 · slide 2
Stroke volume: set by three things, namely preload, afterload and contractility.06:23 · slide 3
Frank-Starling law: what happens to stroke volume when end-diastolic volume increases?Stroke volume increases08:31 · slide 4
Frank-Starling mechanism: what changes about calcium in the filaments, given that the amount of calcium stays the same?The filaments' sensitivity to calcium12:28 · slide 5
Afterload: what happens to stroke volume when afterload rises with preload and contractility unchanged?Stroke volume falls14:59 · slide 6
Frank-Starling curve: how does more contractility move the ventricle, compared with more preload?Onto a higher curve20:20 · slide 7
Pressure-volume loop: which way does the bottom right corner move when preload increases?To the right23:35 · slide 8
Pressure-volume loop: how does the loop's shape change when afterload increases?Taller and narrower23:43 · slide 8
Pressure-volume loop: what happens to end-systolic volume when contractility increases?End-systolic volume falls23:58 · slide 8