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
