Preload, Afterload, & Contractility Flashcards
Outline cardiac function
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
What are the two components to the cardiac cycle?
Systole: Contraction of the heart
Diastole: Filling of the heart (active and passive)
Define stroke volume. Outline its calculation
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)
What affects the amount of blood delivered to the tissues?
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
What is the matching of stroke volume and what are the reasons for this?
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
Define and describe cardiac output. Outline its calculation
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
Define and describe the three components of stroke volume
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
Explain the principles of preload under normal, high and low blood pressure
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
State the Starling law of the heart
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.
Explain the intracellular mechanisms underlying the Frank-Starling effect (length-tension curve)
Increased preload means
Increased exposure of myosin to actin, meaning
Increased cross-bridge formation, so
Increased force of contraction
The limits of the Frank-Starling mechanism
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
Outline the clinical consequences of Laplace’s law
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
List and describe the factors that influence preload
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
Outline the skeletal muscle pump
Contraction of skeletal muscle
Veins compressed
Blood forced to heart
Increased pre-load
Outline the respiritory pump
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
Outline how sympathetic control influences of venous return
Sympathetic stimulation of venous system:
Causes venous vasoconstriction which increases venous pressure that leads to increased preload
Define and explain the principles of ‘contractility’
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)
Describe how increasing contractility influences the heart function
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)
Explain the manipulation of contractility by pharmacology
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)
How does parasympathetic stimulation influence ventricular contractility
activation of M2 muscarinic receptors decrease contractility
Decreased force of contraction
Inhibition of noradrenaline release from sympathetic NS
Also decreases heart rate
Define and explain the principles afterload
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
Explain the principles behind normal, high and low afterload
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
Outline some disease process which affect afterload and describe how they occur
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
Draw a graph showing how a rise in contractility affects the Starling curve
Explain Heart rate in terms of its relation to cardiac output
Directly increase cardiac output, it can also influence preload
Describe how heart rate is controlled
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)
Describe how blood pressure influences heart rate
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
Define and describe the relationship between blood pressure, cardiac output and total peripheral resistance
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
- Cardiac Output
Intrinsic control (Starlings law; preload)
Sympathetic nervous system (contractility) - Arterial vascular resistance (tone) influenced by:
Sympathetic nervous system (α and -adrenoceptors) in the vasculature
Renin-Angiotensin Aldosterone System (RAAS)
Local Endothelial-derived factors - Also by arterial blood volume and compliance
Blood flow and blood pressure calculations
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
Define pulse pressure and arterial compliance
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
