How Preload and Afterload govern Cardiac Output

Question 1

What is cardiac output?

Answer 1

CO = SV x HR. Cardiac output is therefore the volume of blood ejected from each ventricle per minute. The CO of the right and left side of the heart are equal.

Question 2

What is blood pressure?

Answer 2

BP = CO x TPR

Question 3

What is blood flow?

Answer 3

Blood flow (CO) = BP / TPR

Question 4

Which 3 factors control stroke volume?

Answer 4

Contractility, preload, afterload.

Question 5

What is energy of contraction?

Answer 5

Energy of contraction is the amount of work required to generate the stroke volume.

Question 6

What 2 functions does stroke work carry out?

Answer 6

Stroke work is the product of pressure and volume changes in the left ventricle. Stroke work causes 1) isovolumetric contraction (generation of pressure gradient to open aortic valve) and 2) ejection.

Question 7

What does Starling’s Law state?

Answer 7

Energy of contraction of cardiac muscle is proportional to the muscle fibre length at rest, within physiological ranges of stretch.

Question 8

Stroke volume decreases when the central venous pressure (CVP) exceeds approximately 15 mmHg. explain why.

Answer 8

At CVP of above 15 mmHg, excess ventricular filling means very high EDV, leading to overstretched muscle fibres.

Question 9

Define preload.

Answer 9

Preload is the intrinsic stretch of ventricular cardiomyocytes immediately prior to contraction.

Question 10

Explain why increased preload leads to a greater stroke volume.

Answer 10

Increasing the pre-contraction length of cardiomyocytes facilitates increased cross-bridge formation between actin and myosin filaments. This is because there is less overlap of actin and myosin in stretched myocytes and less mechanical interference. Stretched myocytes also have increased sensitivity to Ca2+. Increased cross-bridge formation and Ca2+ sensitivity leads to greater energy of contraction.

Question 11

Explain the roles of Starling’s law in the CVS.

Answer 11

1. Balances the output of the right and left ventricles.
2. Responsible for fall in CO during drop in blood volume.
3. Restores CO in response to intravenous fluid transfusions.
4. Responsible for fall in CO during orthostasis - standing.
5. Contributes to increased SV during upright exercise.

Question 12

What is Laplace’s law?

Answer 12

P = 2T / r. Wall tension (T) = wall stress (S) x wall thickness (w). Thus, P = 2Sw / r. “2T” because chamber has 2 directions of curvature.

Question 13

Define afterload.

Answer 13

Afterload is the wall stress of the ventricle that opposes the ejection of blood. The greater the afterload, the greater the energy of contraction required to overcome this stress and cause ejection.

Question 14

Describe the factors the influence afterload.

Answer 14

Wall stress - S = (P x r) / 2w (from Laplace’s law). Thus, increasing pressure and radius increase afterload. Increasing wall thickness reduces afterload.

Question 15

Why does ventricle radius affect afterload?

Answer 15

Larger ventricle radius > less wall curvature > more wall stress directed through heart wall instead of through centre of chamber > more afterload > less ejection.

Question 16

Explain how Laplace’s law opposes Starling’s law at rest.

Answer 16

Increasing preload also increases afterload due to increased ventricle radius. In healthy heart Starling’s law overcomes Laplace’s.

Question 17

Explain how Laplace’s law contributes to a failing heart at rest and during contraction.

Answer 17

In failing heart, chambers are often dilated - increased radius > increased afterload > less ejection.

Question 18

Explain how Laplace’s law facilitates ejection during contraction.

Answer 18

Ventricular contraction decreases radius and increases curvature, leading to reduced afterload during “emptying”. This aids expulsion and increases SV during the ejection phase.

Question 19

How does the body offset acute rises in blood pressure?

Answer 19

1. Starling’s law - increased stretch > increased SV.
2. Intrinsic increase in contractility due to local positive inotropes.
3. Baroreflex - decreased sympathetic stimulation.

Question 20

What is the consequence of chronic hypertension on the heart?

Answer 20

Increased energy expenditure needed to maintain SV - SV decreases over time. For this reason BP needs to be kept constant during exercise.

Question 21

Explain how ventricular hypertrophy initially helps to maintain SV but may lead to heart failure in the long-term.

Answer 21

Ventricular hypertrophy = greater myocyte size > increased wall thickness (w) > decreased afterload > increased ejection. However, requires more energy and more O2 use, ultimately leading to reduced contractility and potentially heart failure. This is the “vicious cycle of heart failure”.

Question 22

How does Starling’s law affect the ventricular pressure-volume loop?

Answer 22

Increased venous return > increased EDV > increased SV.

Question 23

How does increased arterial blood pressure affect the ventricular pressure-volume loop?

Answer 23

Increased arterial blood pressure - i.e. increased aortic pressure > greater isovolumetric contraction needed to generate pressure gradient > greater pressure in ventricle > greater afterload > decreased SV - increased ESV. More energy used to eject less blood.

Question 24

What is the distinction between preload and contractility?

Answer 24

Preload describes the intrinsic stretch of ventricular cardiomyocytes prior to contraction. Increased preload means increased force of contraction. Contractility describes the strength of contraction at any given muscle fibre length - i.e. altering the preload does not alter contractility, which is under the extrinsic control of the sympathetic NS and circulating adrenaline.