2. Mechanical Properties of the Heart 1 Flashcards
What shape are ventricular cells and what influences their contraction?
- Rod shaped
- Electrical event
- Calcium transient - amount of calcium increasing (changing) in the sarcoplasmic reticulum for a short period of time
- Contractile event - shows sequence of AP => [Ca] => contraction
How does the heart muscle differ to the skeletal muscle in terms of the need for external calcium?
- The heart will not beat without external calcium (reliance on calcium channels)
- The skeletal muscle can contract without external muscle (AP=>DHPR=>internal calcium)
Structure of a heart muscle cell
- Length: 100µm
- Width: 15µm
- T-tubule diameter - 200nm
- T-tubule spacing - 2µm apart (lie on each Z-line of every myofibril)
- Sarcoplasmic reticulum (junctional in T-tubules - terminal part) - stores calcium (very low concentration inside the cell under normal conditions)
What 2 components make up most of the ventricular myocyte?
- Myofibrils (46%)
* Mitochondria (36%) - energy heavy
Excitation-Contraction Coupling in the Heart
- Depolarisation sensed by L-type calcium channel
- Ca2+ from outside enters through LTCC
- Some of this calcium directly causes contraction
- The rest binds to RyR - release of more calcium from SR
- Some calcium taken back up into SR by Ca ATPase channels (SERCA - sarco/endoplasmic reticulum calcium ATPase)
- Calcium enters = calcium leaves (leaving via sodium-calcium exchanger - not energy needed, concentration gradient from sodium used)
What is the relationship between intracellular calcium concentration and force production?
- Sigmoidal (force on y axis)
- Logarithmic [Ca] scale
- around 10 micromolar [Ca] sufficient to produce maximum force (100%)
What is active force production?
- Force of (ISOMETRIC) contraction
- Muscle doesn’t shorten but pulls on the force transducer
- Get to a point where further stretching => no force (not enough overlap between filaments)
What is passive force?
- Due to the elasticity of muscle when stretching - resistance to the stretch
- Linear relationship - Hooke’s law
What is the overall relationship between muscle length and force production?
- As muscle length increases, active and passive force increase (active above passive)
- At greater lengths, active force starts to decrease but passive force keeps increasing
How does the force-muscle length relationship compare in skeletal muscle?
- Overstretch skeletal muscle - decrease in force (pulling a muscle)
- Skeletal - much less passive force, still bell-shaped active/total curve
- Cardiac - much more resilient to stretch - much more passive force - less compliant
- Resilient due to the properties of its extracellular matrix and cytoskeleton
Which limb of the cardiac length tension curve is important and why?
- Ascending limb
- Descending limb doesn’t happen in physiological conditions
- Pericardium restricts stretching
What happens during the isometric contraction of the heart?
- Muscle fibres don’t change in length
- Occurs when heart fills up and contracts initially
- Change in tone but not length as contraction resists the high pressure
- This increases the blood pressure in the ventricles
What happens during the isotonic contraction of the heart?
- Shortening of fibres
- Blood ejected from ventricles
- Happens once the heart is full - enough pressure to eject blood (ventricular pressure > arterial pressure)
What is preload and afterload?
• Preload - weight that stretched the muscle before it is stimulated to contract i.e. ventricles filling with blood makes it stretch before stimulation
- governs the amount of force the muscle is capable of producing
• Afterload - weight that is not apparent to the muscle in the resting state, only during contraction e.g. back pressure of aortic valves in left ventricle
- the weight that the muscle is trying to overcome
What is the relationship between preload and force?
- More preload = more force
- More stretch
- Up to a certain point
What is the relationship between afterload and force?
- More afterload = less shortening
- Same afterload - larger preload => more shortening + force
- More afterload = lower velocity of shortening
What happens in the ventricles during preload with reference to pressure/volume?
• Blood fills the ventricles during diastole - stretching the resting walls
• Stretching/filling determines preload - dependent upon venous return to the heart
• Measures of preload:
- End-diastolic volume (EDV)
- End-diastolic pressure (EDP)
- Right atrial pressure
What happens in the heart during afterload and how is it measured?
- The load against which the left ventricle ejects blood after opening of the aortic valve
- Hypertension - heart has to work harder against a greater pressure
- Simple measure - diastolic arterial blood pressure
- Increase in aortic pressure => increased afterload => less shorterning
- Same aortic pressure + more ventricular filling => increase in shortening
What is the Frank-Starling relationship?
- aka Starling’s Law
- Increased diastolic fibre length increases ventricular contraction
- in other words, increase in stretching/preload leads to an increase in shortening and speed of shortening
- Consequence - ventricles pump a greater stroke volume - cardiac output exactly balances augmented venous return
- Strength and volume of output determined by blood coming into ventricles
- Independent of nervous input
What are the 2 factors (in myocytes) affecting The Frank-Starling Relationship and explain how?
• Changes in the number of myofilament cross bridges that interact
- at shorter lengths than optimal, actin filaments overlap each other - reduced number of myosin cross bridges
- more stretch - more optimum interdigitation of actin and myosin
- overstretch - actin too far from myosin, less cross-bridges
• Changes in the calcium sensitivity of the myofilaments
- calcium sensitivity increases when myofilaments are stretched
Why does the calcium sensitivity increase when myofilaments are stretched?
• Unknown but 2 possibilities
1) • Troponin C binds to calcium and regulates the formation of cross-bridges between actin and myosin
• At longer sarcomere lengths - affinity of troponin C for calcium increases due to a conformational change
• Less calcium needed for same amount of force at greater lengths
2) • Space between myosin and actin decreases when stretched (lattice spacing)
• Decreasing myofilament lattice spacing => probability of forming strong binding cross bridges increases
• More force for the same amount of calcium (less linked to the sensitivity of calcium)
What is stroke work?
- Work done by the heart to eject blood under pressure into the aorta and pulmonary artery (in one contraction)
- stroke volume x pressure
- Preload and afterload influence SV
- Structure influences pressure at which blood is ejected
What is The Law of Laplace?
- Constant pressure within cylinder
- Increase radius = increase tension on walls
- Tension/force around the side = pressure x radius
What is the physiological relevance of The Law of Laplace (comparing different scenarios)?
- Radius of curvature of LV is less than RV (LV is round, RV is like a crescent)
- LV can generate high pressures but have similar wall stress (tension) to the right ventricle
- Giraffe - long, narrow, thick-walled ventricle => small radius => high pressure
- Frog - almost spherical ventricles => large radius => low pressure
- Failing hearts (dilated myopathy) - dilated heart => increases radius => increases wall stress => heart needs to work harder to maintain same pressure, but CO decrease when unable
