CVS Lecture 2/3 - Mechanical Properties of the Heart 1 and 2 Flashcards
What is the difference between skeletal and cardiac muscle contraction?
Cardiac needs external Ca2+ to contract, skeletal does not
How are the cardiac cells structured?
Ventricular cells -> T-tubules in the cells surface, which are spaced so that a T-tubule lies alongside each Z-line ( of every myofibril)
What is the purpose of the T-tubule?
To carry surface depolarisation deep into the cell
What is the sarcoplasmic reticulum used for?
Stores Ca2+ in the cardiac cell (doesn’t occupy much volume c.f. mitochondria)
Which transport proteins lie on the T-tubule membrane?
How does E-C coupling in the heart occur?
On excitation, depolarisation sensed by L-type Ca channel, allowing Ca2+ to enter the cell, with some binding to the myofilament and most binding to the RyR (ligand binding channel), which opens, allowing Ca2+ (70% of Ca needed) out into cytoplasm so it can bind to myofilaments. Then CaATPase is used to pump Ca back into the SR -> to keep a steady state, Na/Ca exchanger maintains Ca2+ balance
What is the relationship between force production and intracellular [Ca2+]?
Sigmoidal -> with a logarithmic scale about cytoplasmic Ca2+ concentration
What is the length-tension relation in cardiac muscle?
Active force production (isometric contraction) -> cross-bridges forming and moving along/overlapping. Passive force due to recoil of the muscle.
How do cardiac and skeletal muscle length-tension relationships differ?
Cardiac tissue produces more passive force as it is stretched, so is more resistant to stretch (less compliant than skeletal muscle) -> due to properties of ECM and cytoskeleton NB: Cardiac muscle only works on ascending limb of graph
Why does the cardiac muscle only work on the ascending limb of the length-tension relationship graph?
Pulling a skeletal muscle is the rupturing of the myofilaments -> Doesn’t occur in cardiac muscle because: more resistant to stretch and retained within the pericardium which doesn’t allow it to over-stretch
What is isometric contraction?
Muscle fibres do not change length but pressures in both ventricles increase
What is isotonic contraction?
Shortening of fibres and blood is ejected from ventricles
When does isometric and isotonic contraction occur in the cardiac cycle?
What is the preload?
Weight that stretches the muscle before it is stimulated to contract
What is the afterload?
Weight not apparent to muscle in resting state, only encountered when muscle has started to contract
What is the in vivo correlation of preload?
As blood fills the ventricles during diastole it stretches the resting ventricular walls, which determines the preload on the ventricles before filling
What is preload dependent on in the heart?
Venous return to the heart
How is preload measured in the heart?
EDV, Diastolic pressure, right atrial pressure
What is the in vivo correlation of afterload in the heart?
Load against which the LV ejects blood after opening of the aortic valve -> pressure in aorta (too much is a bad thing)
How is afterload measured in the heart?
Diastolic arterial BP
What happens when afterload is increased?
Decreases the amount of isotonic shortening that occurs and decreases the velocity of shortening
What is the sequence of events linking cardiac muscle excitation with contraction and relaxation?
What is the Frank-Starling relationship?
Increased diastolic fibre length, increases ventricular contraction -> consequence: Ventricles pump greater SV so that at equilibrium CO exactly balances the augmented venous return
What 2 factors is the F-S relationship due to?
Changes in number of myofilament cross bridges that interact and changes in Ca sensitivity of the myofilaments
How does changing the number of myofilament cross bridges affect the F-S relationship?
At shorter lengths than optimal, the actin filaments overlap on themselves so reducing the number of myosin cross bridges formed (NOT DESCENDING)
What are the 2 reasonings for the increased Ca sensitivity with increased length in the heart?
1) At longer sarcomere lengths Troponin C affinity for Ca is increased due to conformational change in the protein, so less Ca needed for the same amount of force. 2) With stretch, space between actin and myosin decreases, so the probability of forming strong cross bridges increases, producing more force for the same amount of activating calcium.
What is stroke work?
The work done by heart to eject blood under pressure into aorta and pulmonary artery -> SW= SV x P (pressure at which blood is ejected)
What is the Law of Laplace?
When the pressure within a cylinder is held constant, tension on its walls increases with increasing radius -> T=P*r/H
What is a cardiac cycle?
Description of mechanical and electrical events, volume changes and sounds associated with heart beat
What is the end diastolic volume?
Volume of blood in the ventricles at the end of diastole
What is the end-systolic volume?
Achieved just after complete ventricular ejection of blood ->
What happens during atrial systole to the ventricles and atria?
Just before, blood flows passively through open AV valves, atria contract, ‘topping off’ volume of blood in ventricle -> atrial contraction complete before ventricle starts
What occurs to the pressures in atrial systole?
‘A’ wave occurs as atria contract -> blood pushed up jugular vein causing first discernible wave in jugular venous pulse
What changes can be seen on an ECG and heart sounds can be heard during atrial systole?
SAN activation, depolarises atria, P wave is atrial depolarisation -> 4th heart sound is abnormal and occurs with congestive HF, PE or tricuspid incompetence
What happens during isovolumic contraction to the ventricles and atria?
Interval between AV valves and SL valvs opening -> contraction of ventricles with no change in volumes
What occurs to the pressures in isovolumic contraction?
AVV close as ventricular pressure exceeds atrial pressure -> pressure in ventricles increases without a volume change and approaches aortic pressure
What changes can be seen on an ECG and heart sounds can be heard during isovolumic contraction?
QRS complex marks ventricular depolaristion -> 1st heart sound ‘lub’ due to closure of AVV and associated vibrations
What happens during rapid ejection to the ventricles and atria?
Aortic and pulmonary valves open and mar the start of this phase
What occurs to the pressures in rapid ejection?
As ventricles contract, pressure within them exceeds pressure in aorta and pulmonary arteries -> SLV open, blood pumped out and volumes of ventricles decreases. C wave caused by RV contraction pushing tricuspid valve into atrium so creating small wave into jugular vein
What changes can be seen on an ECG and heart sounds can be heard during rapid ejection?
Valves open, so no heart sounds and electrically silent
What happens during reduced ejection to the ventricles and atria?
Phase marks end os systole -> Aortic and pulmonary valves begin to close
What occurs to the pressures in reduced ejection?
Blood flow from ventricles decrease and ventricular volume decreases more slowly -> as pressures in ventricles fall below that in arteries, blood begins to flow back, causing SL valves to close
What changes can be seen on an ECG and heart sounds can be heard during reduced ejection?
The T wave is due to ventricular repolarisation marking the end of ventricular systole
What happens during isovolumic relaxation to the ventricles and atria?
Beginning of diastole, SLV have now just shut and AVV are still closed until the end of the phase
What occurs to the pressures in isovolumic relaxation?
Atria have now filled with blood but AVV shut hence atrial pressure rises, blood pushing tricuspid valve gives second jugular pulse - v wave. Dichrotic notch due to rebound pressure wave against aortic valve as distended aortic wall relaxes
What changes can be seen on an ECG and heart sounds can be heard during isovolumic relaxation?
2nd heart sound (dub) occurs when SLV shut
What happens during rapid ventricular filling to the ventricles and atria?
Once AVV open blood in atria flows to ventricles
What occurs to the pressures in rapid ventricular filling?
Ventricular volumes increases and arial pressures fall
What changes can be seen on an ECG and heart sounds can be heard during rapid ventricular filling?
Prescence of 3rd heart sound is usually abnormal and can signify turbulent ventricular filling -> due to severe hypertension to severe hypertension or mitral incompetence. Electrically silent
What happens during reduced ventricular filling to the ventricles and atria?
Often called diastasis
What occurs to the pressures in reduced ventricular filling?
Ventricular volume increases more slowly
What changes can be seen on an ECG and heart sounds can be heard during reduced ventricular filling?
Silent heart sounds and electrically silent
What is the Wiggers diagram’s information?
What are pressure-volume loops?
EDV -> Aortic pressure increases -> ESV -> no ventricular pressure
How does preload and afterload appear on the pressure-volume loops?
Where does the pressure-volume loop fit in the active and passive force graph (FSR)?
What happens to the pressure volume loop if preload is increased?
Increase EDV, so SV increases as stronger force can be enacted
What happens to the pressure volume loop if afterload is increased?
Greater pressure is needed to open the valve, which produces less shortening, so can’t expel as much blood, so SV decreases
What happens if there is a change in contractility?
What happens during exercise to the heart?
Contractility is increased, due to increased sympathetic activity; EDV is increased due to changes in peripheral circulation (venoconstriction and muscle pump)
