preload, afterload and contractility Flashcards
what affects the amount of blood pumped by the heart for each cardiac cycle
stroke volume
what affects the amount of blood delivered to the tissues
- stroke volume
- heart rate
- vasculare tone
what is cardiac output
the amount of blood pumped in 1 minute
- usually close to blood volume (blood usually circulates every minute)
- at rest, tissue oxygen delivery exceeds oxygen consumption (2:1)
cardiac output = heart rate x stroke volume
what happens if the cardiac output from the left and right ventricles arent matched
normal heart automatically pumps our whatever blooc volume is put into it
stroke volume must be matched (volume entering lungs = volume entering systemic circulation otherwise:
- increase in pressure on venous side
- leading to oedema (pulmonary or peripheral hence:
- tightly regulated by a range of mechanisms
how is stroke volume regulated
by preload (end diastolic volume), afterload (resistance to ventricular ejection) and contractility (end systolic colume)
stroke volume = end diastolic volume - end systolic volume
what is preload
dependent of venous return of blood
- if low: ventricular filling is reduced thus stroke volume is reduced (ex. hemorrahge)
- if high: ventricular filling is increased hence stroke volume increases (ex. exercise)
is stretch of cardiac muscle prior to contraction
descrieb the frank-starling mechanism
- generally, a linear relationship between preload and stroke volume
- ventricular muscle stretching leads to stronger contractile force
describe the length-tension relationship
increased preload leads to increased exposure of myosin to actin leading to increased cross bridge formation leading to increased force of contraction
what are the limits to 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
clinically: 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 (=> DCM, because bigger has to work harder to maintain pressure)
what factors 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
how does the skeletal muscle pump increase venous return
contraction of skeletal muscle leads to compression of veins leading to the blood being forced toward heart. this increases preload (more blood to stretch cardiac muscles)
describe how the respiratory pump increases venous return
inspiration: diaphragm moves caudally, increasing abdominal pressure and reducing thorax pressure increasing abdominal return of blood. this increases preload
how does sympathetic control of venous return increase preload
- venous system acts as reservoir for blood
- sympathetic stimulation of the venous system causes venous vasoconstriction, increases venous pressure. this leads to increased preload
how does the SNS influence stoke volume
increases contractility thus increases strength of contraction at any given preload
how does contractility effect stroke volume
increased contractility = greater force of contraction = increases amount of blood being pushed out = increase stroke volume = increased cardiac output
what does increased contractility enable the heart to do
- empty more completely and thus there is reduced end systolic volume
- handle a greater pre-load and thus creates a 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
involves activation of beta 1 adrenoreceptors (when activated by adrenaline causes increased contractility
how does the PSNS influence contractility
- decreased force of contraction
- inhibition of noradrenaline release from sympathetic NS
- also decreases HR
- this involves activation of M2 muscarinic receptors
what is afterload
the amount of pressure that the heart needs to exert to eject the blood during ventricular contraction
limiting factor in stroke volume
how does afterload effect stroke volume
- creates resistance against which ventricle pumps
- increased stroke volume leads to increased cardiac output and thus increased afterload
- also influenced by pressure of blood in circulation
describe the effects on stroke volume if afterload is normal, increased and decreased
normal: the ejection pressure is greater than afterload hence blood is ejected out of the heart
reduced afterload: more blood can be ejected because the afterload is much less
increased afterload: reduced stroke volume, heart has to work harder to maintain cardiac output (because afterload pressure is too high)
what are intrinsic mechanisms for stroke volume
mechanisms of maintenance that are turned on all the time regardless of ANS –> the normal heart pumps venous return each cycle
what are extrinsic mechanisms of stroke volume
sympathetic nervous system activation which increases contractility (inotropy) of the heart and consequently there is an increased contraction at any given preload
how is the heart rate (and thus cardiac output) controlled
- intrinsic activity from SA node (has external influences by PSNS and SNS)
- controlled by SNS and PSNS to enable rapid response (increase or decrease), and is tightly regulated to maintin blood pressure)
how does blood pressure influence heart rate and thus cardiac output
if blood pressure is elevated: PSNS activated to slow HR, reduce CO and return BP to normal
if blood pressure low: activation of SNS to increase HR, increase vascular tone, increase CO and resotre BP
how is blood pressure controlled
blood pressure (MAP) = cardiac output x total peripheral resistance (vasoconstriction)
1. caridac output = intrinsic control (starlings law;preload) and SNS (contractility)
2. TPR is in effect arterial vascular resistance (tone) and is influenced by:
- SNS (alpha and beta adrenoreceptors) in the vasculature
- renin-angiotensin aldosterone system
- local endothelial derived factors
- also by arterial blood volume and compliance
how to you calculate blood flow
blood flow = pressure difference/resistance
resistance is proportional to length/radius^4
decreased radius - less blood flow
what is pulse pressure
pulse pressure = Psystolic-Pdiastolic
influenced by:
- arterial compliance (ability to increase in pulse pressure, decreases with age)
- stroke volume
- ejection rate
- consistent high pulse pressure will age the heart quicker
what will result in increased cardiac output
increased preload
SNS stimulation will increase HR by acting on which receptor
beta 1 adrenoreceptor
what is the effect of arterial vasodilation on BP
will decrease it
