Chapter 19 A V F

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Chapter 19 A







In the intact organism the Ventricular Function Curve is usually presented as the relation between Stroke Volume (or Cardiac Output or stroke work) and ventricular filling. If we make a graph between filling volume and Cardiac Output, we can derive the Ventricular Function Curve from the pressure- volume relation as follows. If the aortic pressure and thus ventricular pressure in systole is kept constant (Starling experiment), Cardiac Output is proportional to end-diastolic volume. In the intact organism, however, the pressure increases with increasing Cardiac Output, and this increase in pressure depends on the neural and humoral regulatory mechanisms. If changes are performed so rapidly that regulation cannot set in, we follow a family of curves: for larger filling Cardiac Output increases but the higher pressure counteracts this increase in part (see figure on next page). Thus an increase in filling volume results in a smaller increase in Cardiac Output than


THE RELATION BETWEEN LEFT VENTRICULAR filling pressure and cardiac output depends on the pressure in systole, or simpler, aortic pressure. The family of curves, dotted lines, can be derived from Starling’s experiments at constant aortic pressure.

When the actual arterial load is present increased filling results in increased output and increased pressure, i.e., a lower Starling curve.

under the assumption of a constant arterial pressure, as in Starlings’ experiment. We thus see that the Ventricular Function Curve depends on the heart in combination with the arterial load, and therefore characterizes ventriculo-arterial coupling and not the heart alone. The relation between diastolic filling and Cardiac Output is therefore more difficult to interpret than the original experiments by Frank and Starling.

Before the cardiac Echo technique became available, ventricular filling pressure or diastolic ventricular pressure was easier to determine than end-diastolic volume and the Ventricular Function Graph was therefore often presented in the form of filling pressure and Cardiac Output. The graph is, in general, more linear when volume is used as independent variable than when filling pressure is used, because of the nonlinear diastolic pressure-volume relation. When circumferential strain is determined together with myocardial stroke work (Chapter 14), the so-called Preload Recruitable Stroke Work can be calculated and plotted as a function of end-diastolic strain and an almost perfectly linear relationship is found [3].

Global left ventricular contractile function compared between patients Indices of contractile function or contractility are dominated by the contribution of left ventricular (LV) cavity volume because arterial pressures are usually similar between patients. When end-systolic volume (ESV) and end-diastolic volume (EDV) are increased, while Stroke Volume, SV, is not changed, Ejection Fraction (EF) is decreased because EF = SV/EDV. MUGA, Multiple Gated Acquisitions, is the best method of assessment, at least in theory, because the radioactive counts from the LV cavity, when the blood is labeled, are proportional to volume. Other methods such as echocardiography (Echo) and magnetic resonance imaging (MRI) depend on assumptions about geometry. There is nothing to be gained in this assessment from invasive measurements.

Invasive assessment of global ventricular function in the patient

The maximum rate of rise of left ventricular pressure, can be determined by measuring left ventricular pressure (LVP) with a catheter-tip manometer and passing the signal through an electronic differentiator. The signal has a prominent positive maximum, an index of global LV contractile function and contractility. There is also a prominent negative maximum,

which is a load dependent variable, and cannot be used as a measure of ventricular relaxation.


To be a measure of muscle function should be related to wall stress, This can be done using LaPlace’s law (Chapter 9).

with a geometry factor accounting for the (local) radius of curvature and myocardial wall thickness. By the chain rule, differentiating with respect to time, we obtain:

This shows that it is important to determine during isovolumic conditions so that may be assumed constant, i.e.,


TIME DERIVATIVE OF LEFT VENT- RICULAR PRESSURE, as a measure of global function. Increased filling, resulting in an increase in end- diastolic pressure (dashed lines) does not affect but this index is sensitive to inotropic interventions.

Adapted from [2], used by permission.

With changes in filling the geometric factor will change. At low volumes, such as during cardiac surgery with open chest, a change in may result both from changes in muscle function and filling. In the closed chest, and in the catheter laboratory the geometric factor does, in general, not change so that gives

useful information on global muscle function. At very large ventricular volumes an increase in the factor may even result in a decrease in Thus

can be used only as a convenient volume independent index for changes in cardiac contractility in the catheter laboratory. In the figure above the record on the left was obtained with the patient in head-up tilt and the record on the right with the patient in head-down tilt.

It can be seen that the left ventricular end- diastolic pressure is higher in the right hand record due to the increase in ventricular volume, but is unchanged [2].

END-SYSTOLIC PRESSURE- VOLUME RELATION as a measure of global ventricular function. Several pressure- volume loops, preferably obtained with changes in cardiac filling, are required to determine this relation. Approximations by assuming a straight relation, with slope stippled line, or measuring a single loop and assuming linearity and zero may lead to unacceptable errors.

Merits and drawbacks of ESPVR and as assessments of global contractility The theoretical gold standard for assessment of cardiac contractility is the End-Systolic Pressure-Volume Relation (ESPVR, figure on the left), but in practice this ESPVR is usually only obtainable invasively, as during cardiac surgery. Volume changes are required and they can be obtained by, partial, occlusion and release of the vena cavae. An increase in


contractility corresponds to an upward and leftward movement of the ESPVR. The slope of the relation, is only an acceptable index of contractility if the relation is straight. For a curved relation the slope depends on the chosen pressure. The straight-line extrapolation often suggests a negative, physically impossible, and thus virtual, intercept with the volume axis. Thus in open thorax experiments, where volume and pressure can be measured, the ESPVR should be reported because it gives much more accurate information than the

The is unsuitable for

comparing the contractility of patients because it is also an index of the synchronicity of contraction. This figure shows, as an example, that during conduction defects, e.g., bundle branch block or inappropriate pacing

sites, is different. In

general, the is highest during sinus rhythm (extreme right hand point). The End-Systolic Pressure-Volume Relation, ESPVR, has the same shortcoming. In other words, the two quantities do not quantify muscle contractility but overall pump function.


During ventricular pacing from various sites is compared with its value during sinus rhythm (SR). RVA = Right Ventricular Apex; LVFW = Left Ventricular Free Wall; LVA = Left Ventricular Apex;

2xLV = LV free wall and apex. Redrawn from [4], used by permission.

Non-invasive assessment of global ventricular function in the patient

By definition, non-invasive assessment rules out methods such as catheter-tip manometry and conductance catheter volume measurement. One approach that gained some popularity is calculating by dividing peak aortic pressure, as an index of end-systolic left ventricular pressure, by end-systolic volume, obtained by Echo or MRI. In addition to the assumption of linearity of the ESPVR, the intercept volume is assumed to be negligible. These non- invasive approaches are subject to errors.

The assessment of contractility may be complicated by the nonlinearity, i.e., the pressure dependence of the ESPVR. Of course, if during an intervention mean arterial pressure does not change the nonlinearity of the ESPVR does not play a role and does not affect the results. If arterial pressure changes it is recommended that the changes in mean arterial pressure are accounted for. If there are no changes in mean pressure, it may be because the intervention does not affect the periphery, or that mean arterial pressure has been clamped by the baroreflex [1]. In either case end- systolic volume can be used as an inverse index of contractility. If the intervention of interest causes an increase in mean arterial pressure, a control run should be compared in which the mean arterial pressure changes are reproduced with a pure vasoconstrictor. The end-systolic volume can then be compared at similar mean arterial pressures between the two runs to deduce whether the unknown intervention included an inotropic response. If the intervention of interest causes a decrease in mean arterial pressure, a control run should be compared in which the mean arterial pressure changes are reproduced with a pure vasodilator. The end-systolic volume can then be


compared at similar mean arterial pressures between the two runs to deduce whether the unknown intervention included an inotropic response.

Assessment of change in regional left ventricular function

Global contractile function can be affected both by contractility and by regional dysfunction, e.g. myocardial infarction. In the latter case, regional contractile function is of clinical importance, but cannot be studied in absolute terms as is the case with global function indices such as the ESPVR and The pragmatic approach therefore is to study local wall movement to see whether it is impaired or, in some cases such as hypertrophic cardiomyopathy, enhanced. Dysfunctional myocardium may respond to a positive inotropic intervention, e.g. post-extra-systolic potentiation or dobutamine infusion. This indicates that the tissue is viable and may improve with reperfusion. This approach is followed in Stress-Echo and Stress-MRI investigations.

Physiological and clinical relevance

The Ventricular Function Curve is very regularly used to demonstrate the effects of therapy on Cardiac Output.

An example is given in this figure where the Ventricular Function Curve is shown in control and heart failure. Again, one should be aware of the fact that the graphs do not reflect the differences in the heart alone but also contain what is changed in the arterial load.

VENTRICULAR FUNCTION curves under normal conditions, and in heart failure. The characterization pertains to ventriculo-arterial interaction and not to the heart alone.

References 1.




Brooks CIO, White PA, Staples M, Oldershaw PJ, Redington AN, Collins PD, Noble MIM. Myocardial contractility is not constant during spontaneous atrial fibrillation in patients. Circulation 1998;98:1762-1768.

Drake-Holland AJ, Mills CJ, Noble MIM, Pugh S. The response to changes in filling and contractility of various indices of human left ventricular mechanical performance. J Physiol (Lond) 1990;422:29-39.

Glower DD, Spratt JA, Snow ND, Kabas JS, Davis JW, Olson CO, Tyson GS, Sabiston DC Jr, Rankin JS. Linearity of the Frank-Starling relationship in the intact heart: the concept of preload recruitable stroke work. Circulation 1984;


Prinzen, F.W, and Peschar, M. Relation between the pacing induced sequence of activation and left ventricular pump function in animals. Journal of Pacing and Clinical Electrophysiology 2002;25:484-498.


Part C

Arterial Hemodynamics




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