Week 4- Cardiac Output Flashcards
Define Cardiac Output
What is the average cardiac output and how much of it is in the heart and lungs?
Cardiac output= Volume of blood ejected from each side of the heart each minute, units L/min
Average CO = 5/L min, of which 1.5 L is in the heart and lungs.
Define End diastolic volume
What is the normal EDV?
EDV= Volume of blood in the ventricles at the end of filling/ diastole or before systole.
Normally 140 mls
Define End Systolic Volume
What is the normal ESV?
ESV= the volume of blood left in the ventricle after systole/ before diastolic filling occurs
Normally 50 mls
Define Stroke volume
what is the equation for SV?
What is the average SV?
Stroke volume = volume of blood ejected from the ventricles with each ventricular contraction
SV = EDV -ESV
Normally: SV= 140 - 50 SV= 90 mls
Define Ejection fraction
What equation would be used to work out the ejection fraction?
What is the normal ejection fraction?
Ejection fraction is the proportion of blood ejected from the ventricle with each ventricular contraction.
EDV= 140 mls ESV = 50 mls SV= 90 mls
EF= SV/ EDV x 100
EF= 90/ 140 x 100 = 64%
Normally Ejection fraction 50 -70%
Define preload
Preload= End diastolic volume that stretches the ventricle prior to contraction
Define after load
Afterload= pressure against which heart must work to eject blood during systole
Describe the influences of different factors on Left ventricular Stroke volume
Stroke volume= EDV - ESV and will be affected by both the preload and afterload.
Preload:
1) Systemic venous return- amount of blood returning to the heart
2) The functionality of the Right ventricle- dictates how much blood will enter the pulmonary system
3) Pulmonary vascular resistance- again determines flow and how much blood will return to the LA.
4) Mitral valve function-if narrowed or stenosed forms obstruction to flow and therefore ↓ LVEDV.
Afterload:
1) Aortic valve function- again if narrowed or stenosed increases the amount of force that needs to be generated by LV
2) Systemic Blood pressure - dictates how much force needs to be overcome to direct blow into systemic circulation
3) systemic vascular resistance/ arteriolar tone - again dictates amount of force needed to be generated.
What is the equation for cardiac output
CO (L/ min) = HR (beats per min) x SV (mls/min - convert to L/min).
Describe the factors that influence cardiac output
CO = HR x SV therefore any factor that affects HR or SV will affect CO.
HR:
1) Autonomic NS - Symp NS ↑ HR and Para symp ↓ HR
2) Hormones- Adrenaline/ Noradrenaline , RAAS
3) Atrial reflex - where ↑ in central venous pressure leads to ↑ atrial stretch, firing to medulla to inhibit paraSNS and stimulate SNS output to ↑HR. Reduces atrial pressure and allows for more filling from central veins.
SV= EDV- ESV therefore anything that can affect EDV or ESV.
EDV:
1) Venous return determines EDV and therefore preload 2) Heart rate itself controls EDV as ↑HR less time for diastole and therefore filling, ↓EDV
ESV:
1) Afterload - Affected by arteriolar tone, either constricted or dilated
2) Contractility- affected by the ANS, hormones, drugs
State three factors which will reduce preload:
1) valve stenosis
2 ) atrial fibrillation
3) ↑HR reducing diastolic filling time
What is the frank starling mechanism?
What is directly measured by?
What is it usually measured by?
Frank starling mechanism describes the relationship between sarcomere length and the force of contraction. The more cardiac myocytes are stretched by filling, the more force they generate during contraction. Therefore the heart can increase its stroke volume in response to diastolic filling. ↑ CO when ↑ preload.
Directly measured by sarcomere length.
Usually measured by End Diastolic volume.
Describe the factors that affect cardiac preload of the ventricles:
Factors that increase it : (6)
1) Increased Central venous pressure due to:
* ↑ total blood volume, respiration rate, muscular contraction, gravity, venous return (reduced venous compliance)
2) Increased atrial contractility (SNS or frank starling mechanism)
3) Increased filling time by either:
- Reduced HR
- Increased arterial BP which ↑afterload which ↓SV but increases ESV which increases EDV secondarily. ↑Arterial BP also activates central baroreceptor reflex which ↓SNS.
4) Increased ventricular compliance
5) Pathology - stenosis of outflow valves or regurgitation
Describe the factors that affect cardiac preload:
Factors which decrease cardiac preload:
(6)
1) Increased HR and ↓ Filling time
2) ↓ Venous return
3) ↓ Atrial contraction/ arrhythmia
4) ↓Afterload leading to ↑SV and ↓ ESV therefore reduces preload
5) ↓ Ventricular compliance or relaxation
6) Pathology: AV valve stenosis or regurgitation
Describe the effect of preload on the frank starling curve
- There is no single frank starling curve, but a set of curves defined by particular level of inotropy and afterload for a set preload.
- Effect of preload: ↑ preload, ↑ myocyte stretch ↑ sarcomere length ↑ velocity of fibre shortening and therefore ↑ force of contration ↑ Stroke volume.
- This is up to a point however- myofibrils can become overstretched at which point the heart is overloaded.
Describe the effects of afterload and inotropy on the frank starling curve
Inotropy:
↑ inotropy shift frank starling curve up and towards the left, for each LVEDP the stroke volume is increased by increased contractility.
↓ inotropy has the opposite effect.
Afterload:
↓ afterload reduces the pressure which needs to be overcome by the ventricle, meaning that for each EDP the stroke volume will be higher. (Shift F/S curve up and to the left).
↑ afterload increases the pressure against which the ventricle has to contract, ↓ the velocity of muscle fibre shortening, which therefore reduces the SV per EDV. (Shifts F/S curve down and to right). Leads to increase in ESV.
What is the relationship between afterload and ESV?
- ↑ afterload leads to ↓ SV and therefore ↑ ESV.
- This leads to an ↑ in EDV (as ESV partially makes up EDV).
- In this way the frank- starling mechansim can partly compensate for decreased CO when there is increased afterload.
- ↓ Afterload leads to ↑ SV which ↓ ESV which reduces EDV.
- However, reducing arterial BP in consecutive HB’s increases stroke volume in each beat as the reduction in ESV is more than the reduction in EDV, ejection fraction still increased.
Describe the innervation of the heart and blood vessels by the sympathetic NS
- Medulla contains cell bodies for sympathetic NS
- Sympathetic fibres travel out medulla down spinal cord and synapse with short preganglionic fibres.
- These short preganglionic fibres travel to and synapse with post ganglionic fibres.
- These long post ganglionic fibres travel to the heart and vessels.
- Post ganglionic fibres release NA (remember noradrenaline = neurotransmitter, adrenaline = hormone released by adrenal medulla.)
- In the HEART: NA binds to beta 1 and beta 2 adrenoreceptors -> increases inotropy, chronotropy, conduction velocity.
- In BLOOD VESSELS: NA binds alpha 1 and alpha 2 adrenoreceptors. Causes smooth muscle contraction and vasoconstriction.
Describe the innervation of the heart and blood vessels by the parasympathetic NS
- Parasympathetic cell bodies contained within medulla
- These long pre ganglionic fibres project out the medulla to the post ganglionic cell bodies within the tissue
- These short postganglionic cell bodies are within the heart and vasculature itself and project short post ganglionic fibres that innervate the tissue.
- For the heart parasympathetic innervation is via the Vagus nerve. (CN X).
- In the heart: Ach binds to M2 MUSCARINIC AchR in cardiac muscle, especially at SA and AV node, negative chronotropy, inotropy and conduction velocity.
- In the blood vessels: Ach binds to M3 muscarinic AchR on endothelial cell promoting NO synthesis. NO diffuses into VSM cell which promotes vasodilation.
What regions of the heart is innervated by the Sympathetic NS?
What is released and acts on what receptor?
what is the effect on the cardiac AP?
Sympathetic fibres innervate:
- SA node, AV node, Conducting system, Atria and ventricles.
- Noradrenaline
- Bind to B2 adrenergic receptors (most important) and B1 adrenergic receptors
Effect on cardiac AP:
- Reduces repolarisation and K+ efflux
- Increases slow Ca2+ influx and fast Na+ influx.
- Therefore cell remains closer to threshold
- Increased speed of depolarisation, increased slope of AP
- Reaches threshold of AP more rapidly.
What regions of the heart are innervated by the Parasympathetic NS?
What is released and what receptors does it act on within the heart?
what is the effect on the cardiac AP?
Parasympathetic NS innervates:
- SA node, AV node, atria
- Releases ACh
- Binds to muscarinic Ach receptors within heart tissue
Effect on cardiac AP:
- Increases K+ efflux hyperpolarising the cell
- Reduces Ca2+ influx and Na+ influx
- Decreases slope of depolarisation
- Takes longer to reach threshold
Describe the Bainbridge reflex
(atrial stretch receptor reflex)
- ↑ atrial filling due to ↑ central venous pressure (CVP)
- Stretches atrial stretch receptors (low pressure baroreceptors) which signal via the Vagus nerve (CNX) to the medulla
- Synapses with cardiovascular centre and vasomotor centre medulla
1) Increase heart rate:
- ↑ sympathetic outflow to ↑ HR and atrial contraction into ventricles - ↓ CVP
2) Reducing fluid volume:
- Renal vasodilation by ↓ symp outflow. ↑ renal blood flow, ↑ GFP, ↑ fluid clearance by kidney, diuresis
- Stretch of atrial myocytes releases ANP (atrial natriuretic peptide) leads to ↑ Na+/ H2O clearance which also ↓ Fluid volume
- ANP also induces Vasodilation
- Afferent fibres of atrial stretch receptors also synapse with the hypothalamus (synthesises and transports ADH to post. pituitary).
- Inhibits release of ADH from post pit
- Prevents H2O uptake from collecting duct
- ↓ fluid volume.
Describe how peripheral and central chemoreceptors affect the heart and blood vessels (instead of the resp system which it primarily functions to regulate).
Peripheral chemoreceptors respond primarily to ↓ pO2 but ↑ pCO2 and ↓pH enhance response.
1) aortic body (less important signal via CNX) 2) Carotid body (CNIX)
When hypoxia occurs, stimulates peripheral chemoreceptor to signal to respiratory centre in medulla- increases rate and depth of breathing.
Stretches pulm stretch R’s which signal to inhibit cardioinhibitory centre –> tachycardia
Central Chemoreceptor detects ↑ pCO2 via ↓pH of CSF.
CSF pH depends entirely on HCO3- from choroid plexus and H+ from diffusion of CO2 across BBB.
↓pH detected, signals to medulla to inhibit cardioinhibitory centre –> tachycardia
↓pH detected, signals to medulla to inhibit vasomotor centre –> induces vasoconstriction.
Hypoxia induces: tachycardia
Hypercapnia induces: tachycardia and vasoconstriction
