cardiac physiology Flashcards
what is the purpose of the cardiovascular system?
to deliver nutrients, oxygen, immune cells etc. to tissues and the rapid removal of metabolic waste products2t
what can be used to see the coronary arteries in a patient
coronary angiogram
when is coronary blood flow greatest and why
during diastole as the vessels a compressed by the contracting myocardium during systole
what is the significance of the coronary arteries being end arteries
they don’t form anastomoses and so if there is a blockage in one artery, ischaemia occurs in all areas downstream
structural adaptation of the heart to meet the high O2 requirement
very high myocardial capillary density - more blood per mm^2 of muscle fibre allowing for great O2 deliver
functional adaptations the heart to meet the high O2 requirement (3)
high basal flow/O2 extraction; metabolic hyperaemia (myocardial cell release vasodilating factors which cause the coronary vessels to dilate when more O2 is needed due to increasing work being done); autoregulation (blood flow to the heart is maintained even if BP is low)
what is cardiac output + typical value at rest
the volume of blood ejected by 1 ventricle in 1 minute; 5L/min
what is stroke volume + typical value at rest
the volume of blood ejected from the ventricle in sytole; 75ml
cardiac output equation
CO = HR x SV
where is the majority of the blood found in the body and why is this important
in the veins (2/3 of the blood found here); acts as a blood reservoir so if HR increases then blood is moved small veins -> large veins -> heart to increase cardiac output, this is essential in topping up the heart/arteries after a haemorrhage
why is there a disparity between kidney CO and O2 consumption
they filter the blood and so require more blood flowing through them than O2 they carry
what is the significance of the myocardium receiving a small proportion of the CO but requiring a high O2 conc (2)
coronary blood has little spare reserve O2; cardiac pain due to O2 drop (angina) can be triggered by just a modest fall in blood flow
what factors affect stroke volume (3)
preload (↑SV) ; contractility (↑SV) ; afterload (↓SV)
what is preload
the stretch on ventricular fibres before contracting; the greater the stretch, the greater the contraction
what can be used as a surrogate marker of preload and why/how
end diastolic volume/pressure; pressure is exerted on the walls of the heart as it stretched (stretch on ventricular fibres) which can be detected using a specialised catheter
what is the relationship between central venous pressure and right ventricular preload?
CVP = vena cava pressure at the entrance to the RA => CVP can be used to estimate RA pressure; in diatole RA pressure = RV pressure => CVP can be used to estimate RV end diastolic pressure (which = preload)
what is end diastolic pressure/volume
the volume/pressure of blood in the ventricle at the end of ventricular filling
what is the frank-starling mechanism (law of the heart)
the greater the preload the greater the force of contraction (frank), the greater the stroke volume (starling)
what is starling’s law (from frank-starling)
the more the ventricle is stretched in diastole (preload), the greater the stroke volume; the energy of contraction is proportional to muscle fibre length at rest
what is the starling curve (ventricular function curve) - draw it out
stroke volume/CO on the y-axis, and central venous pressure/end diastolic volume on the x-axis; A shift along the same line indicates a change in preload, while shifts from one line to another indicate a change in afterload or contractility; A blood volume increase would cause a shift along the line to the right, which increases left ventricular end diastolic volume (x axis), and therefore also increases stroke volume (y axis)
what factors influence central venous pressure?
volume of blood in circulation; distribution of blood between central and peripheral veins
what could affect the volume of blood in circulation?
haemorrhage
what factors affect the distribution of blood? (5)
- gravity - when standing up blood flow to the heart reduces by around 0.5L by pooling in the lower limbs
- skeletal muscle pump - when active it pushes more blood back to the heart which increases preload and therefore stroke volume
- sympathetic nerves - constrict peripheral veins which can cause increased central venous return, increasing central venous pressure
- respiratory pump - when breath in, chest pressure becomes -ve which increases flow of blood to R side of heart, increasing R stroke volume
- pumping ability of the heart - heart pumps blood from venous to arterial system, if damaged it becomes less efficient and CVP rises
why might someone faint if standing for too long
standing upright and still means that gravity is decreasing blood flow to the heart and the calf muscle pump is not working (bc not exercising) meaning that CVP decreases as less blood is returning to the heart; this means that there is less filling of the LV which reduces Cardiac Output, dropping BP and leading to decreased brain perfusion, resulting in loss of consciousness; vasodilation from wearing hot clothes can also aid this
why is starling’s law important? (5)
- balances output of the RV and LV - if the RV pumps more blood than the LV can handle then it would end up in the lungs causing a pulmonary oedema
- contributes to increased SV during upright exercise
- causes a fall in CO during standing (postural hypotension)
- causes a fall in CO during haemorrhage & shock
- helps to restore CO in response to IV fluid
what factors affect contractility (3)
sympathetic nerves; circulating hormones/drugs (NA, adrenaline); intracellular Ca2+ level
what is contractility
a change in the force of contraction INDEPENDENT of fibre length
affect of increased/decreased contractility on starling curves
increased - shifts curve up (increased SV), so increased stroke volume for the same CVP
decreased - shift curve down e.g. in heart faliure
what is afterload
the resistance the heart must overcome to eject its contents
what pressure corresponds to the LV afterload?
aortic pressure during diastole - LV has to generate the same pressure before the aortic valve can open; the more energy required to reach aortic pressure, the less there is for contraction and so SV falls => ↑ BP causes ↓SV
what is the ‘pump function curve’
mean arterial pressure on the x-axis and SV on the y-axis; higher MAP = ↓SV
what controls heart rate
sympathetic and parasympathetic activity -> innervate the SAN and AVN
what does the autonomic system and adrenaline affect (3)
HR; energy of contraction (contractility); venous tone
what affects preload (CCP - 6)
venous tone; gravity; muscle pump; respiratory pump; pumping ability of the heart; blood volume
what affects the energy of contraction (2)
contractility; preload (starling’s law)
what affects stroke volume (2)
energy of contraction; aortic pressure (afterload)
what affects cardiac output
heart rate; stroke volume
what does the cardiovascular system need to do during exercise
supply tissues that have an increased demand of O2; stabilise BP as it could swing wildly
how does cardiac output change with exercise
CO increased 4-6x; due to changes in HR and SV
what contributes to increase SV in exercise (3)
preload: smale increase in EDV activated starling’s law (increased contractive force), caused by skeletal muscle pump, peripheral venoconstirction
contractility: leads to faster ejection- due to increased sympathetic activation of β1 receptors (adrenogenic)
decreased end-systolic volume: results in increased stroke volume
what contributes to increased heart rate in exercise (2)
decreased parasympathetic activity; increased sympathetic activity
what affects BP and how is this changed in exercise
BP = CO (increased bc blood diverted from non-essential organs - hyperaemia) x SVR (systemic vascular resistance, vasodilation causes a drop in this)
max heart rate?
max HR = 220 - age n years
how is SAN and AVN stimulation increased
by decreased vagal parasympathetic activity; increased cardiac sympathetic fibre activity
how does hyperaemia occur (blood flow to active muscles)
active muscles release metabolites that cause dilation of the local resistance vessels, increasing blood flow; blood flow can increase by 40x in active muscles
what is a danger of metabolic hyperaemia during exercise
hypotension (SVR decreases so much)
how is hypotension avoided in exercise
compensatory vasoconstriction in non-active tissues
why can heat stroke occur in exercise
due to the body having to chose to preserve CO or decrease body temp - CO is preserved which results in bv constriction leading to increasing body temp
what contributes to CO rise in swimming?
rise in HR, supine position means that SV is already high at rest
what contributes to preload increase in cycling
skeletal muscle pump (explosive bursts)
why is isometric exercise associated with BP increase?
total peripheral resistance increases due to compression of intra-muscular bvs
how do heat transplant patients increase CO with exercise as the heart is denervated
circulating catecholamines increase the heart rate; skeletal muscle pump incites the frank-starling mech by increasing preload
