Not immediately obvious CVS physiology Flashcards
what are the phases of the cardiac cycle
isovolumetric ventricular relaxation, ventricular filling, atrial systole, isovolumetric contraction, ventricular ejection
of the phases of the cardiac cycle, whats first and how many fit in to diastole vs systole
we have diastole first in the cardiac cycle.
in diastole is isovolumetric ventricular relaxation, passive ventricular filling, atrial systole.
systole follows and it has isovolumetric ventricular contraction followed by ventricular ejection.
hypertrophy increases the thickness of the cardiac muscle which means it demands more O2 leading to angina on exertion, what other physiology also leads to this exertional angina
with the increased pressures of the ventricles we get hypertrophy eventually. with the hypertrophy the heart cannot fully relax during diastole. this decreases cardiac perfusion as diastole is the main time this occurs. with the under perfusion angina is experienced.
what are the supposed three waves of atrial pressure
A, C, and V waves
A waves occurs when the atria are contracting
C wave occurs when the atria is being compressed by the contractile activity of the ventricles
V wave is the increase in pressure in the atria due to their filling
why do we get the jugular venous pressure
because the internal jugular vein has no valves, so the pressure waves in the atria are seen in the ventricles. especially seen when we lay down as we see the waves of JVP. the height is used to assess the Right atrial pressures
what type of calcium channels are on the cardiac muscle
these are the L type calcium channels that are involved in the excitation contraction coupling of the heart muscle
what do the L type calcium channels do in the cardiac muscle
these will open when the cell is depolarised, allowing calcium into the cell. this activates the RYR channel in the SERCA pump, thereby causing calcium induced calcium release to create strong contractions in the cardiac muscle.
how does reuptake of Ca2+ work via SERCA in the cardiac muscle cell
ATP is needed to make the contractions occur via the cross bridge cycle. this ATP will also phosphorylate the PLN. when dephosphorylated PLN has an inhibitory function on SERCA. hence now with PLN phosphorylated the SERCA pump is opened up and the Ca2+ is taken back up into the sarcoplasmic reticulum. and contraction stops
what effects does noradrenaline binding to the beta-1 receptors on the heart have
Na to the B1 increases cAMP concentrations as the B1s are GPCRs. thus with high cAMP we get higher PKA activity. increased PKA leads to increased phosphorylation or the L type Ca2+ channels and RYR leading to increased Ca2+ influx.
also get the same process happening to phosphorylate the Ca2+ L type channels involved in the pacemaker cell depolarisation - hence faster influx of Ca2+ ions increasing the upstroke.
also get increased phosphorylation of PLN which increases SERCA activity resulting in faster pacemaker cell depolarisation. both of these last two acting to increase heart rate.
also also increased PLN phosporylation in muscle cell means faster Ca2+ reuptake and hence faster relaxation of the msucle cells.
what is starlings law
if left ventricular end diastolic volume increases the left ventricle responds by doing more work.
hence an increased venous return increases our stroke volume.
what makes the spontaneous depolarisation of the cardiac pacemaker cells
the inward flow of Na+ ions through the funny sodium channels
why are they funny sodium channels
because they are open at low negative voltages, they are open by cell polarisation. whereas the normal voltage gated sodium channels in the skeletal muscle for example will be opened by depolarisation
what happens in the phase 4 pacemaker potential during pacemaker cell action potentials
initial RMP is about -60mV. it will naturally depolarise due to the funny Na+ channels brining Na+ inwards. once the influx of Na+ through these channels changes RMP to about -45mV, the Ca2+ (t) channels open to finish the last part of the pacemaker potential until threshold is reached
in pacemaker cell action potentials what happens in phase 0
this is the upstroke phase. this is when we have threshold reached and we get slow depolarisation due to Ca2+ influx through L type channels. the action potential is slow in cardiac pacemaker cells due to the lack of fast Na+ cells.
once the cell depolarises to a certain extent the Ca2+ channels close and K+ channels begin to open
what happens in phase 3 of cardiac pacemaker cell action potentials
the cell is in late repolarisation. this is due to the opening of K+ channels, resulting in K+ efflux and cell repolarisation. this happens untol a point where the funny Na+ then reopen, and the K+ close so that we can have the cyclical nature of the pacemaker cell action potentials
how do we shorten the pacemaker action potential
SNS innervation on the Beta1, does the normal thing resulting in phosphorylation of inward flowing Na+ and Ca2+ channels decreasing depolarisation time.
what also happens is that outward K+ channels are phosphorylated decreasing time for repolarisation, thereby speeding up the pacemaker cell action potentials
how does the PNS affect the pacemaker potential cells
it slows it.
PNS via vagus nerve sees ACh bind to M2 receptors. this leads to a fall in cAMP. thereby undoing SNS effects. this means slower Na+ and Ca2+ influx, decreasing speed of depolarisation.
ACh on the M2 also causes activation of ACh sensitive K+ channels. activating these increases K+ permeability resulting in hyperpolarisation of the cell, meaning the pacemaker potential will take longer to reach threshold.
what is the escape pacemaker phenomema
the fact that the SA node and AV nodes propogate their own AP at their own rate. its just the SA node does it faster so the SA node will always propogate the action potential throughout the heart. but if SA node doesn’t work then the AVs slower depolarisations can take over resulting in life saving action potentials still propogating, just slower.
why can we not get summation of the cardiac muscle
the refractory period of the cardiac muscle is a similar duration to the development of tension in the muscle, so a second action potential can not be fired while tension is being developed hence no summation possible
also controlled firing of the cardiac pacemaker cells make it so that no summation can occur as the action potential rate is fixed
what speed do action potentials travel through each part of the heart, muscle and conduction system
atrial muscle 0.5m^-1
av node 0.05ms^-1
bundle of his, bundle branches and purkinjie fibres 5ms^-1
ventricular myocardium 0.5ms^-1
explain the physics of laminar flow
this is the blood flow pattern we see in the blood vessels. shear stress acting on the blood creates layers of flow that slide ontop of each other creating a parabolic blood flow profile.
the sliding of one layer of fluid over top of another is called shear.
what are the determinants of venous pressure
sympathetic innervation, blood volume, respiratory pump - this is the blood moving action of the diaphragm pumping, skeletal muscle pump.
what is encapsulated within myogenic response of changes in blood pressure
there is autoregulation - constriction in response to alterations in pressure
metabolic (active) hyperaemia - when an organ is more metabolically active it increases in metabolites released, this causes arteriolar dilation thereby increasing blood flow to an organ
reactive hyperaemia: this is vasodilation of arterioles in response to some kind of blockage causing a lack of flow, so when obstruction is cleared more blood comes in to make up for what happened. the organ still metabolises while blockage is present hence theres the vasodilatory effect
what prevents excessive myogenic constriction
when the vessels narrow due to myogenic reponse there is an increase in endothelial shear stress, this stimulates endothelium to produce NO. NO is a potent vasodilator.
when myogenic response doesnt work what do we go to
the paracrine factors or some physical factors like skin temperature or pressure
example of paracrine factors
vasoconstrictors: endothelin, angiotensin 2. O2
vasodilators: NO, PGI2, adenosine, CO2
why do we have extrinsic control
to regulate overall TPR, also to allow the brain to alter blood flow selectively to individual organs when needed
what are the three capillary types
continuous continuous epithelia and basement membrane, fenestrated perforated eptithelium and continuous basement membrane, sinusoidal leaky epithelium and basement membrane
what types of molecule transport are there across the capillaries
continuous - diffusion, vesicular, paracellular transport - all continuous can do
fenestrated and sinusoidal can do the above plus transport via the large fenestrations and intracellular clefts
what is O2 extraction
how much O2 content a tissue will withdraw from the blood at a pressure
talk about O2 extraction in terms of skeletal muscle and cardiac
skeletal muscle extracts like 25% at base rate, so when it needs more for metabolism it is easily able to extract more as the more it uses the partial pressure in the tissue goes down so more extracted. as the skeletal muscle will recruit more capillaries. cardiac tissue cant do this as it takes 75% at base rate, the heart extracts most O2 supplied by coronary vessels. so we increase O2 supply through myogenic control, as we vasodilate the arteries so that more blood flows through, this is active hyperaemia.
