Preload, Afterload, & Contractility

Question 1

Outline cardiac function

Answer 1

key function of the heart is to pump blood around the body leading to the perfusion of the tissues providing necessary nutrients and oxygens, whilst also to remove waste products to allow optimum function

Question 2

What are the two components to the cardiac cycle?

Answer 2

Systole: Contraction of the heart
Diastole: Filling of the heart (active and passive)

Question 3

Define stroke volume. Outline its calculation

Answer 3

The volume of blood pumped out of the left ventricle of the heart during each systolic cardiac contraction

Stroke volume = EDV (end diastolic volume) – ESV (end systolic volume)

Question 4

What affects the amount of blood delivered to the tissues?

Answer 4

Stoke volume
Heart rate
Vascular tone

Stroke volume and heart rate together affect cardiac output, whihc in turn affects blood pressure. Vascular tone influence blood pressure directly.

Blood pressure is important as it will will ensure the tissue receive sufficient nutrients, oxygen and removal of waste

Question 5

What is the matching of stroke volume and what are the reasons for this?

Answer 5

Volume entering lungs is equal to volume entering systemic circulation, otherwise:

Otherwise:
-Increases in pressure in venous side

-Leading to oedema (pulmonary or peripheral), hence

-Tightly regulated by a range of mechanisms

Question 6

Define and describe cardiac output. Outline its calculation

Answer 6

The amount of blood pumped in 1 minute

Cardiac output(ml/beat) = Heart rate(ml/min) x Stroke volume(beats/min)

Usually close to total blood volume
i.e. Blood usually circulates every minute

At rest, tissue oxygen delivery exceeds oxygen consumption (20:1). So Spare capacity in the system means we are able to increase cardiac output

Question 7

Define and describe the three components of stroke volume

Answer 7

Preload - The amount of stretch the heart has at the end of diastole. Ventricular end-diastolic volume (EDV). Intrinsic regulation (automatic response)

After Load - Resistance to ventricular ejection

Contractility- End systolic volume (ESV). Sympathetic NS activity. Extrinsic regulation of stroke volume

Question 8

Explain the principles of preload under normal, high and low blood pressure

Answer 8

Dependant on venous return of blood (i.e. central venous pressure)

If low venous return then ventricular filling is reduced, thus stroke volume reduced

If high venous return then ventricular filling is increased, hence Stroke volume increases

Question 9

State the Starling law of the heart

Answer 9

Defines the normal relationship between the length and tension of the myocardium.

A decrease in preload diminishes the force of ventricular contraction and therefore decreases stroke volume. As a result, preload reduction generally results in a decrease in cardiac output.

Question 10

Explain the intracellular mechanisms underlying the Frank-Starling effect (length-tension curve)

Answer 10

Increased preload means

Increased exposure of myosin to actin, meaning

Increased cross-bridge formation, so

Increased force of contraction

Question 11

The limits of the Frank-Starling mechanism

Answer 11

Excessive stretching causes a decrease in cross-bridge formation

Laplace’s law
In a large sphere more wall tension is required to generate the same internal as it does in a small sphere as governed by:

pressure= tension/radius

Question 12

Outline the clinical consequences of Laplace’s law

Answer 12

As the heart fills up with more blood, then the muscle will find itself at an increasing mechanical disadvantage.

Thus, the chambers will become more difficult to empty

Clinical implication:
Dilated cardiomyopathy, a common cardiac disease in dogs

Question 13

List and describe the factors that influence preload

Answer 13

Filling time of the heart
-Low heart rates > longer period for ventricular filling
- Greater distension of the ventricle

Venous return
i.e. Pressure difference between venous system and –atrium
-The skeletal muscle pump
-The respiratory pump
-Sympathetic nervous system activity
-Blood volume

Question 14

Outline the skeletal muscle pump

Answer 14

Contraction of skeletal muscle

Veins compressed

Blood forced to heart

Increased pre-load

Question 15

Outline the respiritory pump

Answer 15

Inspiration
Diaphragm moves caudally which increases abdominal pressure and thorax pressure reduced

Increased abdominal return of blood. Inspiration increases return of blood to heart forces due to greater pressure difference between abdomen and thorax

Increases preload

Question 16

Outline how sympathetic control influences of venous return

Answer 16

Sympathetic stimulation of venous system:
Causes venous vasoconstriction which increases venous pressure that leads to increased preload

Question 17

Define and explain the principles of ‘contractility’

Answer 17

Refers to the force of contraction of the heart muscle, which contributes to SV, and the ESV. The more forceful the contraction is, the greater the SV and the smaller the ESV are.

Determines end-systolic volume (ESV) and provides extrinsic regulation of stroke volume

It is influenced by the sympathetic NS. When this is activated there are increases in strength of contraction in the heart known as inotropy. Which increase the stroke volume

Intrinsic contractility is dependent on the levels of intracellular calcium (can be increased by SNS)

Question 18

Describe how increasing contractility influences the heart function

Answer 18

Activation of beta1-adenoreceptors :

Empty more completely (i.e. reduces end systolic volume)

Handle a greater pre-load (i.e. greater filling volume)

Deliver an increased stroke volume (even when increased HR reduces time for ventricular filling)

To do all this against, if afterload is increased (increased aortic pressure)

Question 19

Explain the manipulation of contractility by pharmacology

Answer 19

Positive inotropes lead to:
-Phosphorylation of Ca2+ channels1
-Faster calcium re-uptake (more calcium in cytoplasmic -reticulum)
-Sensitisation of Troponin C to calcium
-Increased contractility

Clinical drug examples
-Cardiac glycoside (e.g. digoxin)
-Beta1-adrenoceptor agonists (e.g dobutamine)

Question 20

How does parasympathetic stimulation influence ventricular contractility

Answer 20

activation of M2 muscarinic receptors decrease contractility

Decreased force of contraction
Inhibition of noradrenaline release from sympathetic NS
Also decreases heart rate

Question 21

Define and explain the principles afterload

Answer 21

Increased stroke volume means increase in cardiac output thus higher afterload

Is influenced by resistance to ventricular ejection, which will reduce cardiac output

It relates to resistance of blood in the vessels (predominantly affected in the arterioles)

Also influenced by pressure of blood in circulation
Principally affected by vasomotor tone
Primarily arteriolar tone1

Take note: Venous tone controls preload

Question 22

Explain the principles behind normal, high and low afterload

Answer 22

In normal circumstance the ejection pressure is greater than afterload hence blood is ejected out of heart

Reduced afterload:
More blood can be ejected

Increased afterload: Reduced stroke volume
Heart has to work harder to maintain CO

Question 23

Outline some disease process which affect afterload and describe how they occur

Answer 23

Disease processes that affect after-load:
-increased blood pressure
-aortic valve disease.

Increased blood pressure means increased after-load
Heart has to work harder to eject blood into the aorta.
Tension produced by a chamber of the heart in order to contract
Aortic valves

Question 24

Draw a graph showing how a rise in contractility affects the Starling curve

Question 25

Explain Heart rate in terms of its relation to cardiac output

Answer 25

Directly increase cardiac output, it can also influence preload

Question 26

Describe how heart rate is controlled

Answer 26

Intrinsic activity from SA (sino-atrial) node

Controlled by sympathetic and parasympathetic NS that enables
-Rapid response (increased or decreased)
-Tightly regulated to maintain blood pressure
-Heart rate linked to baroreceptor activity in carotid artery

Can be influenced by adrenaline, stimulation of either PNS (increasing vagal tone) or SNS (increasing sympathetic tone)

Question 27

Describe how blood pressure influences heart rate

Answer 27

If blood pressure is elevated (transient), then there is
Parasympathetic activation1 that
-Heart rate slows
-Reducing cardiac output
-BP returns to normal

If blood pressure is low, then there is
Sympathetic nervous system activation2 that
-Increases heart rate
-Increases vascular tone
-Increasing cardiac output
-Restores blood pressure

Question 28

Define and describe the relationship between blood pressure, cardiac output and total peripheral resistance

Answer 28

Blood pressure (MAP) = Cardiac Output x Total Peripheral Resistance

It is regulated by these factors.
Increased vascular resistance increases blood pressure. Increased cardiac output also increase blood pressure

1. Cardiac Output
   Intrinsic control (Starlings law; preload)
   Sympathetic nervous system (contractility)
2. Arterial vascular resistance (tone) influenced by:
   Sympathetic nervous system (α and -adrenoceptors) in the vasculature
   Renin-Angiotensin Aldosterone System (RAAS)
   Local Endothelial-derived factors
3. Also by arterial blood volume and compliance

Question 29

Blood flow and blood pressure calculations

Answer 29

Blood flow += pressure difference/resistance

Resistance is proportional to length/radius^4
-Radius can be changed, the power to 4 takes this into account
-If radius reduce the pump is increased – heart will pump harder to compensate

Question 30

Define pulse pressure and arterial compliance

Answer 30

Pulse pressure = Pressure at Systolic – Pressure at Diastolic

Influenced by:
Arterial compliance (particular in aorta) (expand to an extent & will contract to dampen pulse pressure and push through system)
-“ability to accommodate the increase in pulse pressure”
-Decreases with age (elasticity of tissues will reduce)
Stroke volume
Ejection rate (ventricular inotropy)
Consistent high pulse pressure will “age” the heart quicker