The functional significance of the Frank-Starling mechanism under physiological and pathophysiological conditions is discussed, based mainly on animal experiment results (in the dog, pig and rat). The dependence of individual stroke volume on end-diastolic volume can be described adequately using Frank's diagram. This can be illustrated by varying filling pressure (respiratory cycle, vascular tone in the capacitance system, body position, circulating blood volume) and by alterations in the duration of the filling period (heart rate and rhythm, rate of relaxation) and in ventricular compliance (wall thickness, fibrosis; contracture, rigor). The functional importance of the Frank-Starling mechanism lies mainly in adapting left to right ventricular output. During upright physical exercise an increase in end-diastolic volume due to the action of the peripheral muscle pump and increased venous tone can assist in enhancing stroke volume. Reduced contractility leads to a shift of the operating point to the right in the pressure-volume diagram, thus tending to prevent a decrease in stroke volume. However, the consequences of increased circulating blood volume in chronic heart failure are, as a rule, mainly detrimental (congestive symptoms; myocardial component of coronary resistance; cardiac energetics). Reduced contractility results in a flattening of the relation between stroke volume (or stroke work) and end-diastolic volume. Furthermore, the Starling mechanism is prevented from becoming effective if the sarcomere-length reserve is exhausted, or in the presence of inadequate sarcomere extension due to impaired relaxation or reduced distensibility of the ventricular wall. The latter is illustrated using the example of a dilated fibrotic left ventricle from a rat with experimental supravalvular aortic stenosis.

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The validity of the thermal dilution technique for the measurement of cardiac output was verified in experiments on a circulation model and on anesthetized rats under open- and closed-chest conditions. In the circulation model thermal dilution was compared with direct (Fdir) and electromagnetic (F(elm)) flowmetry. Flow values measured in the circulation model with the thermal dilution (Fth) technique correspond well with direct flowmetry (Fth = 0.92 Fdir + 7.0; r = 0.888) and with electromagnetic flowmetry (Fth = 0.95 F(elm) + 1.2; r = 0.990). In the anesthetized rat cardiac output was determined with thermal dilution and simultaneously with Fick's method and/or with electromagnetic flowmetry. Fick's method and electromagnetic flowmetry resulted in identical cardiac output values (COFick = 0.95 COelm; r = 0.865), whereas the thermal dilution technique yielded unequivocally higher values. The extent of overestimation is much more pronounced at low cardiac output than at a high output. The study clearly demonstrates that this overestimation is due to heat diffusion, which is obviously of greater significance in small animals than in large animals or humans. Therefore, the thermal dilution technique is not appropriate for the measurement of cardiac output in the rat.

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Considering ventricular function from the vantage point of the pressure-volume (P-V) diagram permits not only quantification of ventricular working capacity under normal and pathophysiological conditions but also promotes understanding of cardiac dynamics including prediction of the effects of mechanical and pharmacological interventions. Therefore it seems appropriate, at least intellectually, to classify all measured volume and pressure data into the scheme of the P-V diagram. The use of so-called contractility indices and also the restriction to the end-systolic P-V relation alone means deliberate renunciation of important information. In principle, Frank's original concept can be confirmed which, under afterloaded conditions, implies the existence of distinct end-systolic P-V curves each related to a particular end-diastolic volume. As an approximation, however, the assumption of one common end-systolic P-V relation seems tolerable. Based on Frank's diagram, a concept for assessment of ventricular and myocardial function is presented following a discussion of the determinants of the diastolic and end-systolic P-V relations, as well as the methodological difficulties and different notions with regard to the end-systolic P-V curve. The P-V area between the curves of systolic maxima and diastolic minima, up to a defined end-diastolic pressure, is recommended as a measure for quantitative evaluation of ventricular working capacity. Transformation into stress-length (sigma-l) relations is indispensable for assessment of myocardial function under the conditions of changed ventricular geometry. The normalized sigma-l area yields a measure for interindividual evaluation of myocardial working capacity. This concept of evaluation does not mean acknowledgement of the visco-elastic theory of muscle contraction nor of the Emax concept. The P-V and sigma-l relations must, however, be complemented by time related parameters in order to estimate ventricular and myocardial power capacity. After a long-lasting search through international literature for "contractility indices" of general applicability and significance it seems appropriate to return to Frank's diagram as the primary basis for evaluating cardiac mechanics.