Cardiac Physiology - in brief!

Muscle Mechanics

Isolated strips of cardiac muscle (or, papillary muscles, for example) provide a good starting point for understanding how the heart works. One must realise that investigation of such muscle chunks provides only an initial approximation, an idea that is reinforced when one considers the following definitions: It can be seen that using experiments based on the above definitions, one can construct function curves that characterise some aspects of heart muscle behaviour. Isometric contraction is perhaps analogous to the contraction of say the left ventricle during the brief period when all the valves are closed, and isotonic contraction is a poor approximation of contraction of the ventricle as it forces blood into the aorta, against pressure.

Passive muscle properties

Diagram of resting muscle tension vs length: tension increases exponentially As resting muscle is stretched, the tension increases exponentially. The resting tension is also affected by a variety of influences, including time-dependent factors (stress relaxation), creep and myocardial lusiotropy.

Active properties - isometric length versus tension

Diagram of muscle tension vs length for ISOMETRIC stimulation is nearly linear

In examining the above curve, note that the curve reflects the sum of the tension generated due to muscle contraction and the resting tension. The basic idea is simple - as the resting length increases, so does the tension generated, as noted above. This is the basis for Starling's law of the heart: increasing venous return to the heart stretches the ventricle, which in turn results in more forceful ejection of blood at the very next heartbeat!

This brings us to a very important point: the isometric length-tension curve helps us greatly when we examine isotonic shortening. If we examine the length of the muscle after an isotonic contraction, and the corresponding tension, we find this tension to be the same as the tension we would have obtained had we performed an isometric contraction at this final length!! In other words, the isometric curve provides a limit for the isotonic performance of the muscle.

The effect of inotropy

Inotropy is the term applied to changes in heart muscle performance independent of alterations in preload and afterload. This implies that any one of the active function curves that we plot will alter once the inotropic state of the myocardium changes. The curve commonly used to assess inotropy is the isometric length-tension curve - a positive inotropic stimulus shifts the curve up and to the left, and a negative stimulus down and right.

Diagram of effects of inotropy on isometric length-tension curve: POSITIVE inotropy shifts the curve up and to the left

Inotropy varies with a variety of factors, including increases associated with increased frequency of contraction and the effect of post-extrasystolic potentiation, as well as catecholamines, glucagon, and inotropic drugs; and decreases with myocardial ischaemia, heart failure, and depressant agents (including almost all anaesthetics).

The Cardiac Cycle.

Wiggers diagram relates ECG, pressures, flows and other cardiac events on a common TIME axis

It is convenient to plot against time, various cardiac events on the same set of axes (commonly termed "Wiggers' diagram"). We will not consider all the events here, but concentrate on the relationship between pressure and volume in the left ventricle. You can see that this forms a closed loop:

 We can create an LV pressure/volume loop which fits nicely within the passive and active length-tension curves

Work around the loop: passive filling of the ventricle occurs from point "4" to point "1", there is an isovolumetric increase in pressure between 1 and 2, blood is ejected between 2 and 3, and then isovolumetric relaxation occurs back down to point 4.

The utility of our simplistic curves for isolated muscle now becomes apparent. Because passive filling occurs between 4 and 1, this curve approximates that seen with passive stretch of cardiac muscle, the so-called "passive pressure-volume curve". The slope of this curve (delta P/delta V) represents the stiffness of the LV wall, more frequently expressed by the compliance, which is the reciprocal (delta V/delta P).

Also note that if we were to completely obstruct left ventricular outflow, then we would create a situation similar to our "isometric length-tension curve". If we indeed do this, then we get an "isovolumetric pressure-volume curve", with remarkably similar characteristics. There is then an almost linear relationship between the ventricular end-diastolic volume and the maximum pressure developed. And surprise, surprise, the end systolic pressure-volume point on our left-ventricular pressure-volume curve (point 3 in our diagram) falls on this curve . Just as with the isolated muscle, the isovolumetric pressure-volume curve represents a limiting curve for the pressure-volume loop!

Factors affecting ventricular performance

As indicated in West, there are four major players in determining ventricular systolic performance:

Ventricular relaxation

This is a complex topic. Quite apart from the overall passive filling properties of the ventricle, the rate of relaxation of the ventricles can have a marked effect on early ventricular filling. Ventricular relaxation is influenced by:

An integrated approach

The integration of cardiac performance and peripheral demand is the topic of another lecture.


  1. West JB, ed. 1990, 12ed.
    Best & Taylor's Physiological Basis of Medical Practice. Williams & Wilkins, ISBN 0-683-08947-1.
    The best cover of cardiac physiology that we have found in a general physiology book! Worth a read.
  2. Guyton AC, Jones CE & Coleman TG. 1973, 2ed.
    Circulatory Physiology: Cardiac output and its regulation. WB Saunders. ISBN 0-7216-4360-4
    A superb book. If you have the time, read it from cover to cover. At the very least, skim through it.