which is the case for a strip of muscle connected to a force transducer.If one records the force of a contraction, and then measures it again at a longer length, the force is found to be higher. If by making other interventions, such as increasing the calcium ion (Ca 2+ ) concentration of the extracellular fluid, and the force is higher, it is called increased contractility, or lower contractility if the force is lower if the contractility is lower in all the fibres in a heart, could that be called heart failure?Therefore, can you measure contractility in heart failure?
Cardiac Muscle MechanicsThe fundamental mechanism of cardiac muscle was identified in strips of heart muscle from which the cell membrane had been removed in a solution where intracellular Ca 2+ was simulated, so the length-force curve could be measured at different Ca 2+ concentrations, i.e. complete lengthforce curves at different levels of contractility via Ca 2+ .1 The purpose of muscle contraction is to create movement, so one also needed to characterise the way cardiac muscle shortened. Early attempts involved the assumption of a model of muscle that had a contractile unit in series with an elastic element, but this was found to be incorrect 2 and a complete characterisation had to wait for the development of the laser diffraction technique for measuring sarcomere length (SL). 3 Sarcomere shortening velocity has an inverse hyperbolic relationship to force (load).Increasing SL increased velocity at any given load except in the absence of any load (maximum velocity V 0 ). With an increased contractility (increased Ca 2+ ), velocity increased at all levels of load. An attempt was made to apply the series elastic model to assessing contractility in patients by measuring V max as dP/dt/P, where dP/dt is the rate of rise of left ventricular pressure (LVP) and P is the LVP. Not only was the model wrong, but which P do you take? If one takes the developed pressure above diastolic, V max starts at zero and dP/dt/P is infinity, which is absurd. If you take the total pressure, dP/dt/P can be anything you like (according to your zero pressure reference value) and V max is not of use. 4 A simpler and quite useful index is dP/dt max , the maximum rate of rise of LVP, which, by chance, is not affected much by end-diastolic volume (EDV) in the intact human, but does reflect changes in contractility. 5 However, one can use this method to assess changes in contractility in a given patient, in response to an intervention, but not compare contractility in a patient with heart failure with a normal person because the rate of pressure rise also depends on synchronicity of contraction of the whole left ventricle.
Frank and StarlingOtto Frank (1865-1944) 6 and Ernest Henry Starling (1866-1927) 7 were contemporary physiologists who both studied the mechanical function of the heart. They both correctly realised that a strip of heart muscle, as with skeletal muscle, developed more force if you increased its length.Starling expressed this as the energy of contraction ...