Cardiac contractility in fish depends on extracellular calcium concentrations, reflecting the general importance of transsarkolemmatic calcium movements for the availability of activating calcium for excitation-contraction coupling (see Chapter 6). In several types of elasmobranchia and teleosts, including bonit oxen, the maximum isometric strength increases several times with the increase in extracellular calcium (1 to 9 mM) (Driedzic and Gesser, 1985; Driedzic and Gesser, 1988; Keen et al., 1992). One of the consequences of the positive inotropic effect of extracellular calcium is to shift the relationship between the maximum isometric voltage and the frequency of contraction to the right (Driedzic and Gesser, 1988). Despite pronounced in vitro effects on extracellular calcium contractility, in vivo effects may be quite limited, as a reasonably good homeostatic mechanism keeps extracellular calcium levels above the threshold of severe cardiac effects. An increase of 1 mM to 2 mM of extracellular calcium significantly increased and pressure development in isolated infused Atlantic cod cores (Driedzic and Gesser, 1985). However, an increase in extracellular calcium above the threshold of approximately 1.5 mM resulted in a very modest increase in the maximum cardiac output volume of cardiac preparations in situ (Farrell et al., 1986a). Obviously, contractility is not so simple, and this parameter has its drawbacks. Loaned to Mason (1969): Moderate hypothermia (32-38°C) affects contractility, and there is a known decrease proportional to the temperature of cardiac output. One might think that this has something to do with the loss of affinity of catecholamine receptors (and to be fair, they do), but there are other factors that also play a role. In particular, hypothermia results in decreased sensitivity of cardiac myofilaments to calcium (Han et al., 2010) and cardiac actin-activated myosin ATPase activity decreases (de Tombe et al., 1990). This reasoning is somewhat suspicious.
First of all, diastolic pressure of the aorta is certainly a factor affecting dP/dT, and it is certainly related to post-load. It should also be taken into account that dP/dTmax (i.e. the maximum slope of the curve, the steepest tangent) can be observed some time after the opening of the aortic valve. So what is the experimental evidence? To test these ideas, Quiñones et al. (1976), because it was 1976, managed to convince elective outpatients to have a huge bolus of angiotensin. The peak tension of the wall was increased by 44%, but the dP/dT barely moved (the change was 2.5%). Similarly, Kass et al. (1987) found that dP/dT did not vary much over a range of high postload values and only became dependent on postload when postload was extremely low (i.e., when the diastolic pressure of the aorta was so low that the maximum value of dP/dT was observed long after the aortic valve was opened). In summary, dP/dT should be relatively independent of postload within a normal range of postload values. This will be a problem for its quality as a measure of contractility, since contractility is clearly affected by post-load.
And you know it`s an official definition because it appears in the original textbook in screaming capital letters. Although Berne & Levy is not on the official reading list of the first part of the CICM, the contractility entry in Pappano & Weir (p.78 of the 10th edition) is identical, a direct copy and paste. So either this definition is particularly good, or the editors are particularly lazy. In both cases, it seems that trainees need to memorize this specific definition of primary school. The net systolic contractility of the left ventricle is of high prognostic value and powerfully defines the rates of cardiac events in hypertensive patients. The development of hypertensive heart disease from the state of hypertrophic changes (with systolic contractility usually well preserved) is a complex process (see other chapters), with a gradual change to a phase of ventricular dilation and systolic insufficiency. These patients tend to have undetected, untreated, or persistent uncontrolled hypertension, and progression to systolic deficiency of the heart is often not recognized, except that acute pulmonary edema occurs. The highly cited but poorly analyzed association of high blood pressure with systolic left ventricular failure indicates the presence of such a gradual change, regardless of the definition or recognition of intermediate coronary occlusion and ventricular infarction.
The positive inotropic effect of β-adrenergic stimulation is the result of an increase in the rate of contraction and duration of contraction in Crucian carp and rainbow trout (Vornanen, 1989). Again, positive chronotropy also caused by β-adrenergic stimulation compensates, but does not overcome positive inotropic effects (Ask, 1983). In contrast, adrenaline increased the maximum voltage regardless of the frequency in the skipjack ear bands; the duration of contraction increased without change in contraction and relaxation rates (Keen et al., 1992). Post-loading affects contractility. This is a well-known thing. Gleb von Anrep discovered it in 1912 after pinching a dog`s aorta, although he had no idea what he was seeing. The heart, with a sharp increase in post-load, significantly and immediately increased its contraction force – and then gradually, even more, in the following minutes. Here`s a recording of what it looks like, made by Cingolani et al (2013) of a rat papillary muscle they tortured: Not discouraged by the lack of scientific consensus on the issue, the researchers seem to give their own definition of contractility in the surprisingly comprehensive commentary on question 4 of the second 2012 paper: Its central role in excitation-contraction coupling makes intracellular calcium the last common pathway for the activity of most inotropic drugs and physiological factors that affect contractility. It`s basically the leverage you pull when you want to change contractility in some way.
The basis of its central role in this process is discussed elsewhere; for an immediate overview, you can be redirected to Eisener et al (2017). In short, important authors have also called this the pedal phenomenon, the staircase phenomenon (staircase is the German word for staircase) and frequency-dependent activation.. .