Cardiovascular Mechanics Flashcards
What does a ventricular cell require for contraction?
Calcium and excitation of cell
Outline the basic process leading up to the contraction of a ventricular cell
Excitatory event (AP) at myocyte leads to influx of Ca2+ and then Ca2+ release which causes contraction
The contraction is very dependent on the influx of external Ca2+ → heart cell won’t contract unless this happens
What is the length and width of myocytes?
100μm long and 15μm wide
T tubules
Invaginations of sarcolemma
Are 200nm
Carry depolarization deep into cell
What are myocytes made of
46% myofibrils, 36% mitochondria (high energy requirement), 4% sarcoplasmic reticulum, 2% nucleus and 12% other
Describe the mechanism of excitation-contraction coupling/calcium induced calcium release, starting from an AP (remember to detail how the myocyte relaxes/stops contraction)
1) AP produced along cell surface membrane (sarcolemma)
2) Depolarisation carried deep into cell down T-tubule and sensed by L-type Ca2+ channels in T-tubules
3) LTCC opens so extracellular Ca2+ flows down its conc. grad into cytosol
4) This Ca2+ binds to ryanodine receptors on sarcoplasmic reticulum, (which are Ca2+ release channels on SR), that then open
5) Ca2+ stored in SR released into cytosol- this Ca2+ binds to troponin C in myofilaments and activates contraction
6) To relax, Ca2+ is actively pumped against conc grad by SR Ca2+ ATPase into SR where it’s ready to be released by next wave of depolarisation
7) The Ca2+ that came into cell to trigger release of Ca2+ is removed from cell during diastolic interval by Na+/Ca2+ exchanger in T-tubule which uses downhill movement energy of Na+ into cell to pump Ca2+ out of cell
8) Myocyte now in Ca2+ balance
- Can the hearts contractility be sustained by saline solution with bicarbonate of soda and potassium chloride?
No; the addition of lime or a calcium salt will restore good contractility.
Does skeletal muscle need external calcium for contraction?
No
Explain the length-tension relation (LTR) in muscle
- As you increase muscle length and stimulate it, active force production increases due to cross bridge formation happening in response to Ca2+ being released from SR
- Cardiac cells also have some elasticity so have a tendency to recoil as they are stretched- meaning as you increase muscle length, base force produced increases too (called passive force)
- Passive force increases continuously
What are active and passive force due to?
Active - Dependent on sarcomere shortening, forces act in the direction of point of muscular attachment towards centre
Passive - Based on the resistance to stretch of the muscle
Total force
Passive force +active force
Why does cardiac muscle produce more passive force than skeletal muscle?
Cardiac muscle is more resistant to stretch and less compliant than skeletal muscle
What does it mean that the cardiac muscle only works on the ascending limb of the length-tension relationship?
You can’t overstretch cardiac muscle- you can with skeletal muscle (where you pull a muscle)
Heart is contained in pericardial sac so can only stretch a certain amount
Why is there a descending limb
force increases with length, but after a certain length force decreases in both
In actzive force when the distance is so long that the myosin and actin filaments are far they can’t form cross bridge so no sarcomere shortening
Isometric contraction
Muscle fibres don’t change length but pressure increases in both ventricles
When ventricles fill with blood we get isometric contraction and valves are closed so blood doesn’t go anywhere- builds up ventricular pressure
e.g. plank
What is isotonic contraction of the heart?
Shortening of fibres and blood is ejected from ventricles
When pressure in ventricles from isometric contraction overcomes backpressure in aorta, blood is expelled from ventricle, ventricular cells shorten and blood pushed out
E.g. Bicep curls, bench press etc.
Preload
Degree to which cardiac muscle cells are stretched from filling of the ventricles, prior to contraction (during diastole)
What is preload dependent on
Venous return
What are the (3) measures of preload?
End-diastolic volume (EDV)
End-diastolic pressure (EDP)
Right atrial pressure
What is afterload
Pressure (in the aorta) that ventricles must overcome, to pump blood out of heart
Afterload is the load against which the left ventricle ejects after opening of aortic valve
As afterload increases, the amount of muscle shortening decreases and the velocity of shortening decreases
How do we measure after load
Diastolic blood pressure (the one in the aorta)
aortic pressure
Define the Frank-Starling relationship and what the consequence is in terms of cardiac output
Definition - Increased diastolic fibre length increases ventricular contraction
(As filling of the heart increased, force of contraction of ventricular muscle also increased)
Consequence - Ventricles pump greater stroke volume so that, at equilibrium, cardiac output exactly balances the augmented venous return
Diastolic fibre length^ → Ventricular stretching^ → Greater SV → Increased cardiac output
What are the 2 factors that are thought to cause the Frank-Starling relationship and then explain each one?
- Change in number of myofilament cross bridges that interact- what does this mean?As you stretch muscle, you increase number of myofilament cross bridges so more myosin and actin interactionsAt shorter lengths than optimal the actin filaments overlap on themselves so reducing the number of myosin cross bridges that can be made!https://s3-us-west-2.amazonaws.com/secure.notion-static.com/46123b47-7266-47f6-a72b-1af39d732e4a/Untitled.png
- Changes in Ca2+ sensitivity of myofilaments- meaning?
Calcium is needed for myofilament activation
At longer sarcomere lengths the affinity for troponin c for calcium increases due to conformational change in protein so less calcium is needed for same amount of force
Stroke work
Work done by heart to eject blood under pressure into aorta and pulmonary artery
Stroke work = volume of blood ejected during each stroke (SV) x pressure at which blood is ejected (P)
Stroke work = Stroke Volume x Pressure
Affected by preload and afterload
What is the law of LaPlace
When the pressure in a cylinder is held constant, the tension on its walls increases with increasing radius
Wall tension = pressure in vessel x radius of vessel
T = P x R
Incorporating wall thickness (h) amends this to: T = (P x R)/h
Which ventricle of the heart generates greater pressure and why?
Radius of walls of left ventricle lower than that of right ventricle hence it can generate higher pressures but the tension/stress in the walls remains roughly the same.
LV: Lower R therefore greater P; T is constant.
- What happens to the structure a failing heart?
Becomes dilated and spherical which increases wall stress
