Cardiovascular Mechanics Flashcards
What is the length and width of ventricular cells?
100um long
15 um wide
What are T-tubules?
- transverse tubules
- finger-like invaginations from the cell surface
- 200nm diameter
- carry surface depolarisation deep into the cell
How are T-tubules spaced?
-spaced (approx 2um apart) so that a T-tubule lies alongside each Z-line of every myofibril
What are the main component of heart cells?
- myofibrils (46%)
- mitochondria (36%)
- sarcoplasmic reticulum (4%)
What is the process of excitation-contraction coupling in the heart (calcium induced calcium release) ?
- L-type Ca channels open in response to AP and Ca moves into the cell down its concentration gradient
- some of the Ca goes to activate myofilaments
- most of the Ca binds to SR Ca release channel, undergoes conformational change which opens the channel
- Ca goes from stores in SR into cytosol to bind to myofilaments for contraction
Relaxation:
-Ca pumped into SR via Ca ATPase- restored to be released at next excitation
Na/Ca exchange system:
- the same amount of Ca that enters the cell to trigger SR release is removed via Na/Ca exchanger
- no ATP, uses downhill gradient of Na to remove Ca
Where are the L-type Ca channels found?
-in the T-tubules
What is the SR Ca release channel also known as?
-ryanodine receptor
What is the relationship between cytoplasm Ca concentration and force (% max) ?
- sigmoidal relationship
- force increases as more myofilaments are activated
What is the length-tension relation in cardiac muscle?-
- as the length of the cardiac muscle increases, there is more passive and active force produced
- like elastic band, it stretches
- isometric contraction
-only ascending limb of the relation between length and force is important is important for cardiac muscle
Is cardiac or skeletal muscle more resistant to stretch, and why?
-cardiac muscle is more resistant to stretch
-due to properties of the extracellular matrix and cytoskeleton
-
Is cardiac or skeletal muscle more complaint, and why?
- skeletal muscle is more complaint
- due to properties of the extracellular matrix and cytoskeleton
What is isometric contraction?
-muscle fibres do not change length but pressures increase in both ventricles
What is isotonic contraction?
-shortening of fibres and blood is ejected from ventricles
Why can’t you overstretch cardiac tissue?
-because the heart is contained in the pericardium sac (membrane), prevents overstretching
What is the preload?
-weight that stretches muscle before it is stimulated to contract
What is afterload?
-weight not apparent to muscle in resting state; only encountered when muscle has started to contract
What happens to the amount of shortening as the after load is increased (in isotonic contraction)?
-shortening decreases
What effect do longer muscle lengths have on the the amount of stretch?
-at longer muscle lengths, there is more stretch and shortening for the same amount of load
What are the in vivo correlated of preload?
- as blood fills during diastole, it stretched the resting ventricular walls
- this stretch (filling) determines the preload on the ventricles before ejection
- measures of preload include end-diastolic volume, end-diastolic pressure and right atrial pressure
-important as then heart pumps exactly how much blood is coming back
What is preload in the heart dependent on?
-venous return
How can preload in the heart be measured?
- end-diastloic volume
- end-diastolic pressure
- right atrial pressure
What are the in vivo correlates of afterload?
- afterload is the load against which the left ventricle ejects blood after opening of the aortic valve
- any increase in afterload decreases the amount of isotonic shortening that occurs and decreases the velocity of shortening
How can afterload in the heart be measured?
-diastolic blood pressure
What affects isometric contraction of the heart?
-ventricular filling
What affects isotonic contraction of the heart?
-pressure in the aorta
What is Frank-Starling relationship?
- as filling of the heart increases, the force of contraction also increases
- increased diastolic fibre length increases ventricular contraction
Consequence: ventricles pump greater stroke volume so that (at equilibrium), cardiac output exactly balances the augmented venous return
What are the two factors causing the Franklin-Starling relationship?
- Changes in the number of myofilament cross bridges that interact
- at shorter lengths than optimal the actin filaments overlap on themselves so reducing the number the number of myosin cross bridges that can be made - Changes in the Ca sensitivity of the myofilaments
-hypothesis 1:
At longer sarcomere lengths, the affinity of TnC for Ca is increased due to conformational change in protein (since less Ca required for same amount of force)
-hypothesis 2:
With decreasing myofilament lattice spacing, the probability of forming strong binding cross-bridges increases (produced more force of the same amount of activating Ca)
What is troponin C (TnC) ?
- thin filament protein that binds Ca
- regulates formation of cross-bridges between acting and myosin
What is lattice spacing?
- the spacing between myosin and actin filaments
- decreases with stretch
What is stroke work?
-work done by the 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 the blood is ejected (P)
SW = SV x P
What greatly influences stroke volume?
- preload:
- more stretch in ventricles produces larger SV - after load:
- if after load is larger, the SV is smaller as it is having to push blood out against a higher pressure
What greatly affects the pressure at which the blood is ejected (P) ?
-cardiac structure
What is the stroke volume?
-the volume of blood ejected during each stroke
What is Law of LaPlace?
-when the pressure within a cylinder is held constant, the tension on its walls increases with increasing radius
What is the wall tension?
wall tension = pressure in vessel x radius of vessel
T = P x R
incorporating wall thickness (h):
T= (PxR)/h
Link the Law of LaPlace with the heart.
-the radius of curvature of walls of LV less than that of RV allowing LV to generate higher pressure with similar wall stresses.
What happens as muscle length increases to passive force?
-passive forces increases continuously (unlike active force)
What often happens to failing hearts?
-failing hearts often become dilated, increasing the radius and os the tension (wall stress) increases
Does increased adrenaline secretion during fight or flight response affect the preload, and why?
-expect more blood to be coming back to the heart, increased venous return
Arrange the following events into the correct order.
A. Ca enters cell B. Ca binds to TnC C. AP travels down T-tubules D. Muscle fibres shorten E. Ca enters cytoplasm from sarcoplasmic reticulum F. The sinoatrial node depolarises G. Myosin heads bind to actin H. Ca binds to ryanodine receptor
F C A H E B G D
lecture slides
https://d3c33hcgiwev3.cloudfront.net/vWzHzxW1SkCsx88VtapAfg_a1a5d45165ce4b50b567f74c2c248805_Final_SV_CVR_LE02Cardiovascular_mechanics.pdf?Expires=1582070400&Signature=cGop8-DVZ7rRZ9xp-y0~NDbtsqmU~wmLWcWpxeZrG1-E49mw-13gGsxnXojNeEC2YZ1ev~Jl7mwnSep54xDXMIhuz3OD-9WreSFDB63ioVlsnA9i9nUCj~GU6CE3Bb~8ZtnQxtA4PTIGlZ0A~JA-hH-93Yq3hev1o2dA6Wt~RiE&Key-Pair-Id=APKAJLTNE6QMUY6HBC5A
