Cardiovascular mechanics 1 Flashcards
What are the characteristics of cardiac myocytes?
They are rod shaped. They are able to contract and have calcium ion support to allow a contractile event to occur.
ventricular cells are 100micrometers long and 15micrometers wide.
The cell surfaces are invaginated by t-tubules. They are small up to 200nm in diameter. Spaced at every z line of the myofibril. They carry the surface depolarisation deep into the cell.
Cardiac myocytes are mostly made up of myofibrils (46%) and mitochondria (36%). There is also the sarcoplasmic reticulum and the nucleus.
What does a t-tuble look like?
What is important to note is that there are numerous protein transporters on the surface.
External calcium is required for the heart to contract ( experiment done by ringer- worked with saline solution made with tap water- the cells contracted but did not when it was made with distilled water)
Describe excitation-coupling in the heart
Depolarisation sensed by L type calcium channel on the surface of the t tubule, it opens up and allows ca from outside the cell to move in down it’s concentration gradient.
Ca binds to the ryr so ca stored in the sarcoplasmic reticulum is released. This is CICR- calcium induced calcium released. This can lead to muscle contraction.
Cardiac muscle needs extracellular ca to function.
Skeletal does not because there is a mechanical linkage between the the SR and the Ca channel. (conformational changes).
Calcium released from the SR into the cytoplasm can be taken back by the SR with enzyme Ca ATPase.
There is an Na/Ca exchanger on the surface of the t-tubule which lets ca out of the cell and Na in (it is an antiporter). ATP is not required because the downhill gradient of Na is enough for it to influx and for the Ca to efflux
What is the relationship between the force production and the intracellular Ca 2+ stores?
It is a sigmoidal relationship.
around 10 micromolar ca concentration is required to produce maximum % force.
What is the length-tension relation in cardiac cell?
Induce excitation and contraction on cardiac myocytes.
Measure the contraction and plot on graph. Muscle length vs force.
Stretch tissue (same piece)- stimulate again but produces more force in the same time. Baseline increases slightly.
The more you stretch, the more force you produce. The passive force is the recoil force (like elastic)
This is for isometric contraction- the muscle cells do not shorten- it is just pulling on the transducer.
An increase in muscle length causes an increase in force
As you keep stretching the muscle, you get to the point where you no longer have an increased force. This is because there is not enough overlap between the filaments to produce a force.
Length-tension theory skeletal vs cardiac muscle?
If you overstretch the muscle, there will be a decrease in force- and this happens in skeletal muscle when you ‘pull’ a muscle. Passive force is based on the resistance to stretch of the muscle.
You can see from the graphs that skeletal muscle has much less passive force compared to cardiac muscle, even though it still produces a bell shaped curve.
Cardiac muscle is more resistant to stretching and less compliant than skeletal muscle. This is why it produces more passive force. It is more resistant to stretching because of the composition of its extracellular matrix and cytoskeleton.
Only the ascending limb of the relation is important for the cardiac muscle- the descending limb (stretching) can’t really happen with the pericardium.
What are the two forms of contraction?
Isometric- muscle fibres do not change length but pressures increase in both ventricles
Isotonic- shortening of fibres and blood is ejected from ventricles.
Changing muscle length before stimulation
Preload- weight that stretches muscle before it is stimulated to contract
Afterload- weight is not apparent to muscle in resting state- only encountered when muscle has started to contract.
Preload causes stretching so the force-preload graph is the SAME as the force length graph. The more preload, the more stretched the muscle is and so more force is produced. More preload= more force (until a certain point)
Afterload is the back pressure on the aortic valves. The more afterload, the less shortening you get. But if you have a large pre-load, you can shorten the muscle more.
NB: more afterload= lower velocity of shortening
Preload- governs the amount of force the muscle is capable of producing
Afterload- is the weight or mass or pressure that the muscle is trying to overcome- only becomes apparent after the muscle has contracted.
So for the same afterload, a greater pre-load prior to excitation will produce a greater force.
In vivo correlates of preload?
- As blood fills the heart during diastole, it stretches the resting ventricular walls
- This stretch (filling) determines the preload on the ventricles before ejection
- Preload is dependent on venous return (ie the amount of blood returning to the heart)
- Measures of preload are end-diastolic volume, end-diastolic pressure and right atrial pressure
in vivo correlates of afterload
Afterload is the load against which the left ventricle ejects blood after the opening of the aortic valve.
Any increase in the afterload decrease the amount of isotonic shortening that occurs and decreases the velocity of shortening.
Measures of preload include diastolic blood pressure.
The pressure that the ventricle has to work against to send blood into the aorta. Higher bp (diastolic in particular), means that the heart has to work harder.
Factors that affect the contraction of heart
- isometric contraction- ventricular filling
- isotonic contraction- pressure in aorta
The same aortic pressure with more ventricular filling will give an increased shortening- more force
Increase in aortic pressure (increased afterload) will lead to a decrease in shortening
What is the Frank-Starling relationship?
Frank and starling found that as the filling of the heart increased, so did the force of contraction.
I.e. increased diastolic fibre length increases ventricular contraction
This means that ventricles pump greater stroke volume so that, at equilibrium, cardiac output exactly balances the augmented venous return.
The frank- starling relationship is caused by 2 factors. what are they?
- Changes in the number of myofilament cross bridges that interact. At shorter lengths than normal, the actin filaments overlap, reducing the number of myosin cross bridges that can be made. The more you stretch, there is greater interaction between myosin and actin
- Changes in the Ca sensitivity of the myofilaments. Ca sensitivity increases when the myofilaments are stretched. there are two possibilities for this:
- 1) Troponin C is a thin filament protein that binds to calcium and it regulates the formation of actin and myosin cross-bridge formation. At longer sarcomere lengths, the affinity for troponin C to Calcium is increased due to a conformational change in the protein. Therefore less calcium is required to produce the same force.
- 2) When stretched, the space between myosin and actin filaments (the lattic space) decreases. therefore the probability of forming strong binding crossbridges increases. This produces more force for the same amount of calcium.
What is 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 the pressure at which blood is ejected
What is the Law of LaPlace?
when the pressure within a cylinder is held constant, the tension on its walls increases with increasing radius.
Wall tension= pressure in vessel x radius of vessel
What is the physiological relevance of the Law of LaPlace ?
Radius of curvature of the walls of LV is less than RV. Allowing LV to generate higher pressure with similar wall stress.
Giraffe wall stress is kept low as it has a long, narrow, thick walled ventricle. Small radius
Frog pressures are low so the ventricles are almost spherical large radius so low pressure
Failing Hearts (Dilated Cardiomyopathy)- dilated which increases the wall stress.
