Mechanical Properties 1 Flashcards
List the 3 steps for the contraction of a ventricular cell
A single ventricular cell
CALCIUM IS NEEDED FOR CONTRACTION
They are rod shaped - they can be stimulated to contract
Process:
Electrical event
Calcium Transient (the amount of calcium in the sarcoplasm has increased for a short period of time)
Contractile event
IMPORTANT: THE HEART WILL NOT BEAT WITHOUT EXTERNAL CALCIUM
This is DIFFERENT to skeletal muscle which can contract without external calcium
What is the important ion channel in a cardiomyocyte?
Important ion channel in a cardiomyocyte is the L-type calcium channel
Describe the process of Excitation-Contraction Coupling in the Heart ?
Important ion channel in a cardiomyocyte is the L-type calcium channel
Depolarisation is sensed by the L-type calcium channel and calcium from outside enters the cell
Some of this calcium can directly cause contraction
The rest of the calcium binds to Ryanodine Receptors (also called Sarcoplasmic Reticulum Calcium Release Channel) which causes release of calcium from the sarcoplasmic reticulum
After it has had its effect, some of the calcium is taken back up into the SR by Ca ATPase channels (also called SERCA - SARCO/ENDOPLASMIC RETICULUM CALCIUM ATPase)
Same amount of calcium that came into the cell is effluxed by a Sodium-Calcium Exchanger
This does NOT need energy - it uses energy from the concentration gradient of sodium to expel calcium form the cell
SR Ca release channel= ryanodine receptor
What shape is the graph showing the relationship between force production and intracellular {Ca}
The force-calcium relationship is SIGMOIDAL
Around a 10 micromolar intracellular concentration of calcium is sufficient to produce maximum force
An increase in muscle length causes an ……………. in force
An increase in muscle length causes an increase in force
As you keep stretching the muscle, you get to a point where further stretching DOES NOT generate more force?
Why does this happen?
As you keep stretching the muscle, you get to a point where further stretching DOES NOT generate more force - this is because there is not enough overlap between the filaments to produce force
This is ISOMETRIC CONTRACTION so the muscle doesn’t shorten - it is just pulling on the force transducer
An increase in muscle length causes an increase in force
As you keep stretching the muscle, you get to a point where further stretching DOES NOT generate more force - this is because there is not enough overlap between the filaments to produce force
Passive force- Think of the muscle as Stretching an elastic band. It is the recoil after stretching. Also increase as muscle length increases
Active force- caused by the cross bridges forming and …..
What is more resilient to stretch and why?
Cardiac muscle or Skeletal muscle
Cardiac muscle is more resilient to stretch
Due to properties of the extracellular matrix and cytoskeleton
Which part of the graph is important in physiological circumstances in cardiac muscle?
ONLY THE ASCENDING LIMB OF THE LENGTH-TENSION CURVE IS IMPORTANT IN PHYSIOLOGICAL CIRCUMSTANCES IN CARDIAC MUSCLE
The descending limb doesn’t happen in physiological conditions because the pericardium restricts the stretching
What two forms of contraction does the heart use and explain each one?
What is preload?
PRELOAD - the weight that stretched the muscle BEFORE it is stimulated to contract (i.e. the filling of the ventricles with blood makes it stretch before it is stimulated to contract)
Why can’t you overstretch the heart muscle?
The descending limb doesn’t happen in physiological conditions because the pericardium restricts the stretching
What is afterload?
AFTERLOAD - weight that is NOT APPARENT to the muscle in the resting state - only encountered ONCE MUSCLE HAS STARTED TO CONTRACT
Explain the graph below?
The preload causes the stretching of the cardiac muscle. Because the cardiac muscle is now longer, it can generate more force when it contracts.
If you have a large load you have less shortening- think of a heavy weight- you won’t be able to lift it all the way up
What is preload dependant on?
•Preload is dependent upon venous return to the heart
What determines the preload on the ventricles before ejection?
•The stretch or filling determines the preload on the ventricles before ejection
Describe preload inside the heart
•As blood fills the ventricles during the relaxation phase of the cardiac cycle (diastole) it stretches the resting ventricular wall
List some measures of preload?
•Measures of preload: end-diastolic volume, end diastolic pressure, right atrial pressure
Name a simple measure of afterload?
Define afterload in the context of the heart?
- The load against which the left ventricle ejects blood after opening of the aortic valve
- A simple measure of afterload is the diastolic arterial blood pressure
•Any increase in afterload ………………….. the amount of isotonic shortening that occurs and ………………….. the velocity of shortening
•Any increase in afterload decreases the amount of isotonic shortening that occurs and decreases the velocity of shortening
More afterload= ……….. shortening
MORE AFTERLOAD = LESS SHORTENING
MORE PRELOAD = …………. FORCE (up to a certain point)
MORE PRELOAD = MORE FORCE (up to a certain point)
MORE AFTERLOAD = ………….. VELOCITY OF SHORTENING
MORE AFTERLOAD = LOWER VELOCITY OF SHORTENING
Preload will govern 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 - it only becomes apparent after contraction has been stimulated
So, for the same afterload if you stretch the muscle prior to excitation it will generate more force
What is the sequence of events linking cardiac muscle excitation with contraction, then relaxation?
Use the terms below and put them in order
T-Tubule
Ca2+ influx
L-type Ca channel activation
SR Ca channel (RyR) activation
SR Ca Release
Myofilament Activation
Ca binds to troponin
Action potential
SERCA (sarco/endoplasmic reticulum Ca²⁺-ATPase) and Na/Ca2+ exchange
Relaxation
Action potential
T-Tubule
L-type Ca channel activation
Ca2+ influx
SR Ca channel (RyR) activation
SR Ca Release
Ca binds to troponin
Myofilament Activation
SERCA (sarco/endoplasmic reticulum Ca²⁺-ATPase) and Na/Ca2+ exchange
Relaxation
What is the Frank-Starling relationship?
Definition: Increased diastolic fibre length increases ventricular contraction
The Frank–Starling law of the heart (also known as Starling’s law and the Frank–Starling mechanism) represents the relationship between stroke volume and end diastolic volume.[1] The law states that the stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles, before contraction (the end diastolic volume), when all other factors remain constant.
What is the consequence of the Frank-Starling Relationship?
Consequence: Ventricles pump greater stroke volume so that, at equilibrium, cardiac output exactly balances the augmented venous return
In other words: the amount of blood coming in to the ventricles determines the strength of the ventricular contraction and hence determines the amount of blood leaving the ventricles
Definition: Increased diastolic fibre length increases ventricular contraction
What 2 factors cause the Frank-Starling relationship
•Due to two factors:
–Changes in the number of myofilament cross bridges that interact
–Changes in the Ca sensitivity of the myofilaments
The mechanism(s) responsible for the increase in calcium sensitivity with increased length remain(s) elusive
Name 2 possible mechanism
•At longer sarcomere lengths the affinity of troponin C for Ca is increased due to conformational change in protein
With decreasing myofilament lattice spacing, the probability of forming strong binding cross- bridges increases
What is stroke work and how is it calculated?
What is the law of laplace?
•This Law states that: when the pressure within a cylinder is held constant, the tension on its walls increases with increasing radius
What is the Physiological relevance of Laplace’s Law?
