Cardiovascular Mechanics Flashcards
(23 cards)
What is excitation contraction coupling
Electrical event/AP leads to calcium influx and release (calcium transient) , which is followed by the contractile event.
The electrical event and the contractile event are coupled
What external ion is cardiac muscle depend on for contraction
Calcium
__ __________ are the finger like invaginations on ventricular cells that lie alongside each __ line of every myofibril. ________ __________ is the lace like structure that lies above the myofilaments
T(ransverse) tubules
z
Sarcoplasmic reticulum
What channels are found in T tubules
LTC CC ( L type calcium channel) Close to RyR (Ryanidine receptors/ SR calcium release channel)
How is muscle contraction brought about
L type Ca channel opens in response to change in voltage
Ca enters cytosol
Binds to SR Ca release channels(ryanodine recep) (ligand operated)
Calcium stored in SR released into cytosol
Ca binds to troponin in myofilaments and causes contraction
How is muscle relaxation brought about
Ca pumped back up against conc grad by SR Ca ATPase
Active transport back into SR for release at next beat
Ca that entered cell effluxed via Na Ca exchanger during diastole
What happens during the diastolic period
Same amount of calcium that entered cell to trigger contraction is effluxed via the Na Ca exchanger in the T tubule membrane.
Uses downhill energy gradient of sodium moving into cell to supply necessary energy to expel calcium from cell
Cardiac muscle is in calcium balance
Describe the length tension relation in cardiac muscles
As we increase muscle length, we increase the force of production
Both baseline force and max force increase (passive and active force)
Relates to ISOMETRIC FORCE
What is active force vs passive force
Active force caused by cross bridges
Passive force caused by elasticity of cardiac cells; when stretched, they recoil a bit
Compare the elasticity of skeletal and cardiac muscle, and the consequences of this in terms of length tension relation
Cardiac muscle is more resistant to stretch and less compliant than skeletal, due to properties of extra cellular matrix and cytoskeleton
Therefore can generate more passive force as muscle length increases
If you keep stretching cardiac tissue, will force keep increasing? Why?
No
Force falls when length passes optimum
Cardiac cells only work on ascending limb of length tension graph; cannot overstretch cardiac tissue
Heart contained in pericardial sac, can only stretch a certain amount
Where and when do isometric and isotonic contraction occur in the heart
Isometric- muscle fibres don’t change length but pressures increase in both ventricles
Isotonic- shortening of fibres and blood is ejected from ventricles
When pressure in ventricles overcomes back pressure in aorta, blood expelled, ventricular cells shorten, eject blood out of ventricles
What is preload vs afterload
Weight that stretches muscle before it is stimulated to contract
Weight not apparent to muscle in resting state, only encountered when muscle has started to contract
What happens to force (isometric)/shortening(isotonic) as preload and afterload increases
How do you change the steepness of the relationship between shortening and afterload
As preload increases, force increases (until optimum is passed)
As afterload increases, shortening is reduced
Increase preload (longer muscle length) to produce more fore and more shortenings
What are the in Vivo correlates of preload in the heart, what is it dependent on and what measures are there of it
Blood fills heart during diastole, stretching resting ventricular walls, which determines preload on ventricles before ejection
Preload dependent of venous return
Measures include end diastolic volume, end diastolic pressure, right atrial pressure
What are the in Vivo correlates of afterload in the heart, what is it dependent on and what measures are there of it
Afterload is the load against which the left ventricle ejects blood after opening of the aortic valve
Any increase in afterload decreases amount of isotonic shortening, decreases velocity of shortening
Measures include diastolic blood pressure
What is the frank- starling relationship
As filling of the heart increased, force of contraction increased
Increased diastolic fibre length increases ventricular contraction
Ventricles pump greater stroke volume so that at equilibrium, cardiac output exactly balances the augmented venous return
Eg more venous return= more stretch on vm = more forceful contraction
Why does force of contraction increase as you stretch muscle?
As you stretch muscle, increase num of myofilaments cross bridges that interact with each other
Increase in Ca sensitivity
What is stroke work
Work done by heart to eject blood under pressure in aorta and pulmonary artery
Stroke volume x pressure ejected at (SV x P)
What factors affect stroke work
SV- preload and afterload
P- cardiac structure
What is the law of LaPlace
When pressure within a cylinder is held constant, the tension on its walls increases with increasing radius
Wall tension = pressure x radius (T= P x R)
Including wall thickness, T= (PxR)/h
What is the physiological relevance of the law of Laplace
Need same amount of wall tension in surrounding muscle around left and right ventricle, right heart working at lower pressure than left heart
radius of curvature of walls of LV less than RV so T stays constant
What happens to failing hearts in regards to their ventricles and what does this do to wall stress
Become dilated and spherical, Which increases wall stress, adds to difficulty that failing hears have in producing contraction
