cardiovascular mechanics Flashcards
What ion is required extracellularly for cardiomyocyte excitation-contraction?
Calcium
Describe the main carduimyocyte cell structures
Cells are around 100um long and 15um wide
The membrane is invaginated-t tubules
Near the t-tubules, which invaginate around each z lines-Sacroplasmic reticulum that surround the myofibrils 4%
The t tubules are full of mitochondrias-for energy
The rest is myofibris 46%
Describe the sequence of events leading from excitation to contraction
Action potential comes in-open up t tubules voltage gated Ca channels-Ca comes in
Ca inside is little-open up SR Ryanodine receptors-open Ca channels on SR-release Ca inside.
Thats a massive increase-Ca go to tubulin-opens tubumyosin etc…
Once that happens-Ca ATPase on SR start pumping it back in
The ca that came in the cell is also taken out with Na/Ca exhanger, using Na energy
Describe the relation between force and intraceullar Ca conc
As log of Ca conc goes up, force increase in sigmoidal fashion-complex
What is the length tension relation in cardiac muscle?
A unstretched cardio will provide a certain (x) force
If you stretch it, it will provide passive force (resistance to stretch), but it will also have increased active force peak (y>x)
The more you stretch, the more the passive force increase, (linear) and the more active force increase (linear) -UNTIL A CERTAIN LIMIT
What is the difference between cardiac and skeletal muscle in terms of length tension relation?
Skeletal force does not increase much with length increase-passive a bit and active a bit but overall not much
Cardiac muscle increases passive beteen 0 and 100% length well, but not much after 100% (limit)-BUT increase much more
Cardiac are more resistant and less compliant-due to ECM and cytoskeleton differences.
In cardiac-only relay see ascending forces (up to 100% length increase)
What is the difference between isometric and isotonic, with exemples?
Isometric-muscle fiber provide tension and strength WITHOUT change in length-doing planque abs/ increase pressure in both ventricules
Isotonic-tnesion and strength with shortening of muscle-pulling weights/ ejecting blood out of ventricules
What is Preload and afterload in cardiac muscle?
Preload-like a weight stretching the muscle before it contracts-like stretching-force increases with increased preload (till a point)
Afterload-the weight apparent to muscle that it needs to fight to pull-only encountered once muscle contracts-as preload increase, more shortning and faster
What are the in vivo correlations of preload and afterload, and how do they correlate?
Preload-when blood comes in, stretches the resting ventricular walls-and the more blood comes in, the more stretches (depends on venous return)
Afterload is the blood pressure outside the aotric and pulmonary arteries that the outcoming blood has to push
Preload increases the strength needed to fight afterload-means that autoregulates, as more/less blood comes in, more/less strength will push it out of the ventricules
But as Blood pressure increase, harder and harder to push against (increase of afterload with no preload increase)-heart failure
What is the Frank-Starling relationship, and what are the consequences ?
FS relation-as diastolic fibre length increase, so does ventricular contraction strength (preload after laod relation)
Means that as ventriculres are more full, the cardiac output always balances the augmented/reduced venous return
What are the 2 factors (second one has 2 theories) explaining why muscle strength increase as its strecthed?
1st factor says that as you stretche, the number of myofilaments cross birdge increase, and they can form more ideals one
Factor 2 says that the stretch increases the affinity forCa,
Theory one says taht its toponin that has increased affinity for Ca same amount of Ca for more strength
Another theory for factor 2 is that with decreasing lattice spacing (thins as spacing), the porbabilitiy of forming strong cross bridge increases
What is aotra stroke work, how do you calculate it and why?
Stroke work is defined by work done by the heart to eject blood under pressure
Stroke Works=volme of blood ejected (SV) multiplied by pressure of ejected blood (P)
SW=SVxP
SV-influenced by pre/afterlaod, while P is affected by heart strcuture
What is the law of LaPlace? What relation does it have with veins and circulation? What are the consequences?
When a pressure within a cylinder is constant, tension on its walls increase with increasing radious
Wall tension (T)= Pressure in vessel x Radius of vessel0
T=PxR
(Wall thickness can be incoroporated as T=(PxR)/h°
This means that as walls of RV curvature of walls and LV being smaller allows LV to generate larger pressure with similar wall stress
Also why gifarffe have thick muscle and long/narrow
Also failing hearts become dilated-often cause of failure as tension increases
What are the 2 main phases of heart beats?
Diastole-2/3 of the beat-ventricular relaxation while ventriclules fill with blood-4 phases
Systole-1/3 of beat-ventricular contration where blood is expelled-3 phases
What is end diastolic volume?
End diastolic volume is the volume of blood in the heart just before contraction. Maybe around 100ml
What is end systolic volume?
End systolic volume is the volume of blood in the ventricule after contraction. Around 30ml
What is stroke volume and how do you calculate it?
Stroke volume is how much the heart has expelled in one beat-calculated and end diastolic volume- end systolic volume. Around 70ml in healthy
What is the heart ejection fraction?
How much (in %) of the end diastolic volume was ejected in a stroke
calculated as 100 x stroke volume / End-diastolic volume
Around 70% is healthy
Measure of unhealthy heart (40% with failure)
Explain and describe Atrial systole in the heart cycle
Start of systole 1st step
Atrial systole is the initial contraction of the atriole-atria is almost full and ventricule too
Atrial contraction “tops up” the ventricules
Correspond top-wave on the ECG (atrial cell depolarisation)
Atrium and ventricule pressure and volume up a bit
Abnormal-4th heart sound if valves arent closing properly
Explain and describe Isovolumetric contraction in the heart cycle
2nd step
All the valves (AV and semi lunar) are closed. Ventricules full of blood contract but no shortening or volume change-but drastic increase in pressure
Corresponds to QRS complex on ECG (ventricule cell depolarising)
Correspond to 1st heart sound (lub in Lub dub)-as AV valves close
Explain and describe Rapid ejection in the heart cycle
3rd step
After the pressure in ventricule increases from isovolumetric contraction and reaches aortic pressure (and pulmonary)-opening of aotric and pulmonary valve and rapid ejection as ventricule isotonic contractings
no heart sound-pressure continues increasing but ventricular volume drops as blood enters arteries
Explain and describe reduced ejection in the heart cycle
End of systole-4th step
As blood ejects in rapid ejection, volume decrease and pressure lower-blood comes out at a lower rate (reduced pressure gradiant)-aortic and pulmonary valve start closing (and slow down the volume decrease)
At the end of this phase, valves are nearly closed, volume is low and ventricule pressure is dropping. depolarised cells start repolarising (T on ECG)
Explain and describe Isovolumetric relaxation in the heart cycle
5th steo (diastole)
Aortic and pulmonary valves closed by AV valves not yet open-remain closed until ventricular pressure drops UNDER atrial pressure
Atrial pressure rises because of dochrotic notch caused by rebound pressure and relaxation of distended walls
Closing of the semi-lunar valves cause 2nd heart sound
Explain and describe Rapid passive filling in the heart cycle
6th step
AV opens and blood rapidly floods in from atrium and veins-happens natrually down pressure gradient (and just down in general)
3rd heart sound abnormal-tubrbulant filling
Explain and describe reduced filling in the heart cycle
7th step
As ventricule fills and pressure rises slowly-ventricular volume rises slower
Still fills in considerably without atria contraction
also called diastasis
Followed up by restart-atriole systole
What is the pressure change relations between the right and left heart ventricule?
The patterns of change are identical between both sides, even if the ABSOLUTE pressure of the right is much lower (25mmHg)
Thats because the same volume of blood
What is a pressure volume loop? Try and describe what point corresponds to what
Graphing ventricular pressure vs ventriuclar volume (x)
point A-end diastolic volume is high volume (near left) and low pressure
Point B-encountering aotric pressure-same volume but higher pressure-directly above point A
Point C-end systolic volume-same pressure as B but a lower volume (more right)
Point D-pressure drop but with same volume (relaxation)-directly under point C
Then back from D to A-forms a closed loop
How do pre-load and afterload fit on a pressure volume loop?
Preload in the heart was determined by the volume of blood filling in the ventricule during diastole-so its point A/affected by point A (bottom right)
Afterlaod is the pressure of the aorta-which is what point B corresponds too-same value
What happens to a pressure volume loop if you increase preload?
Increasing preload means increasing diastolic blood volume AND increasing force from muscle
Therefore point A moves right (towards more volume) and B (as its just above A)
Point B and C also move slightly down as the increased force reduces the pressure needed
RESULTS IN INCREASE STOKE VOLUME
What happens to a pressure volume loop if you increase afterload?
Increase of afterload means more pressure for the heart to fight againts
Greater pressure needed to open the valve means point B and C move up towards high pressure
But high afterload also means less shortening of muscle-less blood expulsed. So point C and D move right (closer to A) as stroke volume goes down
What are 3 factors that impact stroke volume?
Preload, afterload and contractility (contractile capabilities of heart (such as sympathetic stimulation by adrenaline in exercise)-measured with ejection fraction)
How does contractlity affect the frank-starling relation?
Increase in contractility is linear and just corresponds to higher ventricular pressure per volume)
less contractility is the opposite (lower gradient of pressure vs volume
How many different circulation circuits are there in the human body? Which ones?
Pulmonary circuit-from pulmonary valve, arterie to lungs and into right atrium (and mitrial valce)
Aterial/body crculation-vena cava, bicuspid, pulmo, pulmo, mitrial, aortic, aorta
What are the 3 layers of blood vessel lining? hwo do their size vary between types of vessels
Intima (epithelia), media and advantitia
Intima is always small, but arteies have large media and avdentitia-wwhile veins have thinner media and adventitia
Why does blood flow? How do you calculate blood flow? and resistance?
Blood flows due to a difference in pressure between heart/arteies/veins Blood flow (Q)=Pressurechange/resistance Or pressure difference= flow * Resistance This means mean arterial pressure = cardiac output * total resistance Resistance= 8*length*visocity/pi+radius^4 as viscosity and length stays the same-main control is radius-and a 1/2 radius is 1/16 change in flow
How does pressure vary across circulation?
Pressure is highest in LV and arteies (where it goes up and down with heart beats) and then drops in cappilaries. raises slightly in RV, then back up in LV
What is the approximate blood flow to organs? And during exercise?
about 5L/min at rest-1L to gut and kindey, 0.25 heart and skin, 0.75 brain and muscle
in exercise, 20L/min-main increase is 16L to muscle
What are the two ways the blood can flow within a vein? Why does it matter?
Blood flow can be laminar (velocity and direction constant)-fastest at center
Or turbulent-erratic, prone to pooling, nothing specific-random =pathophysiological
Laminar flow promotes endothelial quiescence, with aligned cells-vasodilation and anticoagulation
Tubrulant promotes proliferation, apoptosis, shape chane, vasoconstriction, coagulation, platelet agreegation
How do you calculate shear rate and shear stress?
Shear rate is the gradient of the velocityprodil at any point = deltav/deltar
Shear stress is that * viscosity
how does arteral and aortic pressures differ? why?
ventricular pressure falls fast-erratic, while aortic pressure falls slowly
the difference is that the aorta is like a balloon-and will blow up when blood comes in (compliant) and reduce slowly after-makes flow regular -Windkessel effect
Recall the law of Laplace, and its role in aneurysm
Law of laplace is that Transmural force= Pressure x radius
and circumferance stress is T/thickness of vessel
This means that as vessels dilate and expand-wall tension increases, which increases dilation. If SMC cant keep up-keep expanding until death (surgery adds mesh to keep it together)
Explain the compliance difference between veins and arteries, what it means in terms of blood storage and effects of gravity. What mechanisms exist to counteract that?
Veins are much more compliant than arteies-they will increase their volume as pressure increases
This means that most of the blood is stored in veins-they increase size with the BP
With gravity-increase of hydrostatic force that means blood flows out
Increase compliance of veins pools, which decreases venous return to heart-less blood to then pump out-fainting
Skeletal muscle pumps around vessels and the diaphragm pressure change of the thorax help balance that-but not enough-cause DVT or/and oedama
