174 I X . C h a p t e r 5
General discussion and conclusions, including clinical implications.
For convenience, the investigations reported in Chapter 3 will be referred to as experiment 1 or the first experiment, and those in Chapter 4 as experiment 2 or the second experiment.
5.1. In the clinical setting one heavily relies on arterial pressure measurement for the hemodynamic management of the patients either during anesthesia or intensive care.
This is because pressure measurement is technically easy to perform, either non- invasive or invasive, and as a consequence of medical education one is focused on arterial pressure measurement. Most probably the measurement of arterial pressure, along with heart rate, is the most often performed measurement by medical students and by a large number of physicians.
On the basis of the arterial pressure measurement one decides of the patient is
normotensive, hypertensive or hypotensive. Accordingly no treatment, a vasodilator or a vasoconstrictor is started. In the anesthetic setting, one also can alter the level of
anesthesia.
This approach assumes that arterial pressure is an index of left ventricular afterload, afterload being the forces opposing ventricular ejection (cfr. section 2.1.). In first instance calculated systemic vascular resistance is considered to be a quantitative index of afterload. However, equation 2.9 demonstrates that the relation between arterial pressure and (calculated) systemic vascular resistance in not equivocal. As a consequence cardiac output should be measured and systemic vascular resistance calculated according equation 2.7.
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5.2. A technical consideration: cardiac output and aortic flow measurements.
Cardiac output was measured by the thermodilution method. To this purpose a thermistor-tipped pulmonary artery catheter was introduced via a central vein and a right heart catheterization was performed (cfr. Methods sections 3.2 and 4.2). Therefore the flows and cardiac outputs reported in table 3.1 and table 4.1 respectively are right ventricular outputs (assuming no intracardiac shunt) and the values reported represent the mean of least three CO determinations. Right ventricular output is approximately 2% less than left ventricular output because of the bronchial circulation [90].
Instantaneous aortic blood flow was measured by an ultrasonic flow positioned around the aortic root and as consequence measures left ventricular output minus coronary blood flow. The resting coronary blood flow amounts to approximately 5% of total left ventricular output [90, 200].
Ewalenko reported that ultrasonic flow measurement of pulmonary blood flow underestimated thermodilution right ventricular output by an average of 15% [68].
During our experiments we observed an underestimation of the thermodilution cardiac output by ultrasonic aortic flow measurements between 10 and 25 %, a value that is far greater than coronary blood flow. In addition we observed an electronic drift of the ultrasonic flow signal over time, eventually leading to negative flow values.
We therefore decided to scale the ultrasonic flow signal to the thermodilution cardiac output. This scaling does not affect our conclusions, because the ultrasonic flow signal was essentially used to determine vascular properties.
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5.3 Generation of pressure-flow plots : stepwise versus rapid caval occlusions.
In the first experiment P/Q plots were generated by reduction of venous return through stepwise inflation of the inferior vena cava balloon, and at each flow value
hemodynamic equilibration was allowed (sections 2.3.1.2 and 3.2.4). This resulted in
“slow” P/Q plots that were well characterized by second-degree polynomials (figure 3.1).
In the second experiment the preload reduction was generated by rapid inflation of the inferior vena cava balloon (section 4.2.3). This resulted in ‘fast” P/Q plots which were essentially linear over the range of flows studied (figure 4.1).
It is important to realize that slow P/Q plots and fast P/Q plots do not provide identical information [26]:
- A slow P/Q plot represents the integrated neurohumoral responses to changes in flow.
- A fast P/Q plot represents the direct mechanical effects of an intervention upon the arterial tree.
As already alluded to in section 3.4.2, the difference in the slow P/Q plots in figure 3.1 probably represents a different effect of isoflurane (1.4 % end-tidal) and propofol (18 mg • kg-1 • h-1) upon the autonomic nervous system.
The slope of a slow P/Q plot, i.e. the ratio ΔPin/ΔQ (or the derivative dPin/dQ), has units of resistance, but is not a measure of hydraulic (or vascular) resistance. In section 2.3.1.1, one states that vascular resistance is used to assess the geometric and physical properties of a vasculature (equation 2.4); it measures how much of gradient is required to drive a given flow. The ratio ΔPin/ΔQ is a measure of how the inflow pressure
changes in response to small changes in flow to the vascular bed. In analogy to the theory of stability analysis of nonlinear electrical circuits, the ratio ΔPin/ΔQ can be referred as the incremental resistance, but it should always be kept in mind that this
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variable does not necessarily reflect the geometric and physical changes across a vascular bed [158]. Consequently one can state that a slow P/Q plot represents the stability, or autoregulatory capacity, of the (arterial) cardiovascular system [222].
Comparing slow and fast P/Q plots with a particular anesthetic at different dosages, and manipulating autonomic nervous system and/or endothelial function, should allow to elucidate the effects of the particular anesthetic upon the different components of homeostatic control mechanisms.
5.4. In the first experiment one investigated the systemic vascular effects of isoflurane and propofol anesthesia in dogs. In the second experiment one investigated the cardiac and vascular effects of sevoflurane and propofol anesthesia in dogs.
In experiment 1, at baseline (i.e. at high or unrestricted flow) there was no difference in cardiac output, heart rate, stroke volume and total hydraulic power (tables 3.1 and 3.3) during isoflurane and propofol anesthesia, indicating an equivalent cardiac performance and indirectly suggesting a similar anesthetic state. However, despite similar flow conditions, aortic pressure was lower during isoflurane anesthesia than during propofol anesthesia (table 3.1). Nonetheless, there was no difference in (calculated) systemic vascular resistance during both anesthetic regimens (table 3.1). Moreover, pressure- flow curves demonstrated that systemic vascular tone was higher during propofol anesthesia at all levels of flow except at the lowest level of flow (figure 3.1).
Notwithstanding the aortic pressure was higher during propofol anesthesia the characteristic impedance ZC, the first impedance harmonic modulus Z1 and the Wosc/Wtot ratio‡ was lower with propofol than with isoflurane (tables 3.2 and 3.3).
These findings indicate a different elastic behavior of the large conduit arteries and less energy loss in pulsations during propofol anesthesia.
‡ In textbooks, power is usually denoted as
!
W• (cfr. section 2.5.1). In this chapter the dot is omitted [131, 143].
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Similar findings were observed during experiment 2. During sevoflurane anesthesia calculated systemic vascular resistance SVR did not change when increasing the sevoflurane doses (table 4.1), but the pressure-flow curves demonstrate a two-step phenomenon for the systemic arteriolar tone (figure 4.1 and section 4.4.2). Also, when increasing the sevoflurane concentration, the characteristic impedance ZC and the first impedance harmonic modulus Z1 increased although aortic pressure decreased and SVR remained unchanged. In contrast, when increasing the propofol dose the characteristic impedance ZC and the first impedance harmonic modulus Z1 essentially remained unchanged, notwithstanding that aortic pressure was higher than during sevoflurane.
Conclusion I : Arterial pressure measurement is an inappropriate surrogate measure for the evaluation of ventricular afterload, meaning the forces opposing ventricular ejection. Calculated systemic vascular resistance is an inadequate index of ventricular afterload and arteriolar tone. Pressure-flow plots are necessary for detecting changes in arteriolar tone. Impedance data demonstrates a different effect of volatile anesthetics and propofol on the elastic properties of large conduit arteries.
5.5. In both experiments aortic pressure was reduced. Although the reduction was induced by different means, some unexpected findings are common to both
experiments. In the first experiment, aortic pressure was decreased by reduction of venous return (i.e. a preload reduction) during a particular anesthetic state, either during isoflurane 1.4% end-tidal or propofol 18 mg • kg-1 • h-1. In the second experiment, hypotension was caused by deepening the anesthetic level by increasing the anesthetic concentration.
5.5.1. In both experiments total arterial compliance Ca did not increase when reducing aortic pressure. In the first experiment Ca was significantly decreased (i.e.
minus 50%) at low flow, and as consequence at low pressure, during both anesthetic regimens (table 3.2). In the second experiment Ca was significantly decreased when increasing sevoflurane concentration, while increasing the propofol concentration did
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not change Ca although aortic pressure was reduced (table 4.2). These findings are counter-intuitive with the idea of increasing compliance while decreasing pressure [155]
and are in contrast with the results of Hettrick and Lowe [100, 142, 143]. As already alluded to in section 4.4.5, vasodilators , such as phenoxy-benzamine and hydralazine, do decrease aortic pressure without increasing arterial compliance [30, 233, 281]. A bell-shaped compliance-pressure relation is also predicted by the arctangent model of Langewouters (figure 5.1) [133].
Figure 5.1
Aortic cross-sectional area A(p) and aortic compliance C(p) over the pressure range 0-200 mmHg.
The solid line in the left hand panel is the graphical representation of the arctangent function.
From : Langewouters, G. J., Wesseling, K. H., & Goedhard, W. J. (1984). The static elastic properties of 45 human thoracic and 20 abdominal aortas in vitro and the parameters of a new model. J Biomech, 17(6), 425-435.
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Hettrick and Lowe did found a consistent increase in total arterial compliance for halothane, isoflurane, sevoflurane and propofol but not for desflurane [100, 142, 143].
There are, however, substantial differences between their experiments and ours:
a. Hettrick and Lowe performed their experiments in chronically
instrumented dogs trained to stand quietly in an animal sling. It means that their experiments were performed with the dogs in upright
(standing) position. We performed our experiments in acutely instrumented dogs in supine, recumbent, position.
b. Hettrick and Lowe measured aortic pressure with fluid-filled catheters, with the tip positioned in the proximal descending aorta. We measured aortic pressure with high-fidelity manometer-tipped Millar® catheters with the tip positioned at the aortic root (sections 3.2.1 and 4.2.1).
c. The dosage of the anesthetics are different:
a. Halothane and isoflurane: 1.25, 1.5 and 1.75 MAC;
b. Propofol: 25, 50 and 100 mg • kg-1 • h-1;
c. Sevoflurane (and desflurane): 0.6, 0.9 and 1.2 MAC.
d Hettrick and Lowe calculated total arterial compliance by the area method of Liu [141].We estimated total arterial compliance as the ratio of stroke volume to pulse pressure.
Because we estimated total arterial compliance as SV/PP one might argue that our results represent a mathematical artifact. The arterial system is not an completely closed system since part of the stroke volume leaves the arterial system through the periphery (“diastolic leak”) (cfr. figure 2.19) and as a result the SV/PP ratio overestimates the total arterial compliance [272]. We therefore calculated total arterial compliance with the data of the second experiment by the pulse pressure method (PPM) [220]. Although
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the absolute values of CPPM are lower than the absolute values of CSV/PP, the conclusions are similar: sevoflurane anesthesia decreases total arterial compliance, while during propofol anesthesia total arterial compliance remains unchanged (CPPM : Ca calculated by the PPM, CSV/PP : Ca calculated by the SV/PP ratio). It has been demonstrated that the pulse pressure method is superior to the SV/PP and the area method for estimating total arterial compliance [220, 272].
One might speculate concerning the mechanisms of our findings. We already alluded to the arctangent model of Langewouters, but it is unclear how the max-C-pressure P0
relates to mean arterial pressure in an “in vivo” system (figure 5.1) [133]. It is generally stated that total arterial compliance is reduced in hypertension [210], but Hayoz et al.
reported that conduit artery compliance and distensibility are not necessarily reduced in hypertension [94].
General anesthetics exert their vascular actions partly through an effect upon the vascular smooth muscle cells (cfr. Chapter 1: Introduction) [2]. In first instance general anesthetic induce a smooth muscle relaxation, and as consequence general anesthesia should increase arterial compliance. However, Cholley et al. reported that diltiazem induced smooth muscle relaxation (with concomitant reduction in arterial pressure) does not necessarily yielled the desired reduction in arterial compliance and local hydraulic impedance [41].
Inhibition of vasorelaxation by volatile anesthetics has been described in vascular in vitro models (e.g. aortic strips) [162, 235-237]. The significance of the phenomenon in the intact circulation has never been investigated, but it might partially explain our observations. It may also explain the limited vasodilating properties of sevoflurane as seen in figure 4.1 (cfr. section 4.4.2).
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Other explanations of the decrease in total arterial compliance in the face of a decreased aortic pressure might be:
- a de-recruitment of certain vascular beds : when arterial pressure decreases below the critical closing pressure of a vascular bed (cfr. section 2.3.1.2), this vascular bed is excluded from the circulation (i.e. a reduced diastolic leak).
- a reversible interaction of the anesthetic with the components of the arterial wall other than the vascular smooth muscle cell (e.g. collagen or elastin).
Of course, these explanations are entirely speculative.
Our experiments were conducted in acutely instrumented dogs with periods of profound hypotension. As a consequence, large fluid shifts may happened towards the
interstitium, with concomitant changes in transmural pressure thereby altering the arterial compliance. This approach does not invalidate our findings, on the contrary, it probably better mimics the situation of a patient either during and after surgery, or either during shock states at the intensive care unit [40].
This reduced total arterial compliance in hypotensive states, whether due to preload reduction or deep levels of anesthesia, leads to a therapuetic question : what’s the
optimal way to restore aortic pressure ? A vasoconstrictor, or an inotrope or (more) fluid resuscitation ?
Conclusion II : Total arterial compliance Ca did not increase when aortic pressure was reduced, whether this hypotension was due to preload reduction or whether due to deepening the level of anesthesia. Sevoflurane and propofol affects total arterial compliance in a different way : sevoflurane anestheia decreased total arterial
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compliance but during propofol anesthesia total arterial compliance remained unchanged. These findings suggest that volatile anesthetics and propofol do have a different effect on the mechanical properties of the arterial wall.
5.5.2. In both experiments total and steady hydraulic power decreased in every instance of pressure and flow reduction (tables 3.3 and 4.3). Reduced pressure and flow also resulted in a decrease of left ventricular oxygen consumption as estimated by the pressure work index (PWI, equation 2.41) (tables 3.3 and 4.3). In both experiments and for all anesthetic regimens the net result was a reduction in cardiac mechanical
efficiency (CME), calculated as the Wst/PVI ratio (section 2.5.4.2). These findings are in line with the results of Hoeft [104]. These results were obtained in a clinical study assessing the influence of several anesthetic regimes on myocardial oxygen utilization efficiency in patients undergoing coronary bypass surgery. In patients with heart failure it was demonstrated that mechanical preload unloading had a detrimental effect on CME, but that pharmacological afterload unloading had a limited beneficial effect on CME [113].
In Experiment 2, propofol caused less reduction in CME than sevoflurane, probably because propofol does have more favorable effects on the resistive and reactive components of ventricular afterload.
Conclusion III : Anesthesia and (mechanical) preload reduction does decrease cardiac mechanical efficiency. Propofol anesthesia is to prefer when CME is of concern for hemodynamic optimization of the patient, e.g. the patient with heart failure.
5.6. In the second experiment the effects on left ventricular (LV) performance, left ventricular contractility and left ventricular afterload of escalating doses of either sevoflurane or either propofol were investigated, without the intention to compare the effects of individual doses of sevoflurane and propofol.
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Sevoflurane caused a dose-related decrease in cardiac output and end-systolic elastance Ees, indicating that both performance and contractility are impaired (table 4.1 and 4.3).
There was decrease in arterial tone between 0.5 and 1 MAC, but arterial tone remained unchanged between 1 and 1.5 MAC (table 4.1 and figure 4.1). Sevoflurane increased the characteristic impedance ZC and the first impedance harmonic modulus Z1 and
decreased total arterial compliance Ca, indicating an increased pulsatile load (table 4.2).
It also increased the effective arterial elastance Ea, meaning the left ventricle is facing an increased global afterload (table 4.3). An increased Ea taken together with a
decreased Ees, leads to a decreased Ees/Ea ratio, indicating an impaired left ventricular- arterial coupling.
During propofol anesthesia there was a nonsignificant decrease in cardiac output and Ees
remained unchanged (table 4.1 and 4.3). Propofol decreased significantly the arteriolar tone (table 4.1 and figure 4.1), confirming that propofol is an “actual” arteriolar dilator, but did not increase the pulsatile components of left ventricular afterload (table 4.2).
Because propofol did not affect Ea, the Ees/Ea ratio remained unchanged, implicating that LVA coupling is preserved (table 4.3).
Conclusion IV : Sevoflurane and propofol does have different effects on LV
performance, LV contractility and LV afterload. Sevoflurane decreases cardiac output and LV contractility, and demonstrates a limited arterial dilatation, but does increase the pulsatile and total load on the left ventricle. As a consequence sevoflurane impairs LVA coupling. In contrast, propofol maintains LVA coupling, as a result of a minimal decrease in left ventricular performance combined with arterial dilatation, and without affecting the pulsatile components of LV afterload. If these findings from animal
research can be confirmed in humans, then propofol may considered as a better anesthetic in patients with LVA coupling disease.
185 X . C o d a
A couple of personal notes on my experiences and perspectives concerning anesthesia related cardiovascular research.
In November 1987, I started my career as a cardiothoracic anesthesiologist at the Thorax Center Rotterdam, Academisch Hospital Dijkzigt Rotterdam (present name:
Erasmus Medical Centre Rotterdam). At the same time Professor Mark M. Mitchell from UC San Diego started a sabbatical at the Thorax Center. His main focus was transoesophageal echocardiography related research during cardiac surgery.
At the Thorax Center it was standard practice for routine perioperative monitoring of arterial pressure to insert a long catheter (C.V.P. Intrafusor® System, a Sorenson Research 18-gauge radiopaque catheter, list number 41008-01) via the radial artery, with the distal end positioned in the subclavian artery [209]. During the period of time 1985-1987 a number of reports appeared, questioning the accuracy of radial artery pressure measurement after discontinuation of cardiopulmonary bypass [78, 159, 194, 230]. Subsequently Mark Mitchell became the driving force for an investigation comparing arterial pressure measurement at the subclavian artery and the radial artery.
To be honest, I was rather reluctant to be instrumental for the study, because one had to insert two large bore arterial catheters in the patients and at that time I wasn’t really proficient in arterial catheterization.
However, given my education in biomedical engineering (School of Engineering Sciences, Vrije Universiteit Brussel), I soon became intrigued by this phenomenon of the “reversal of the aorta-to-radial artery pressure gradient” (figure 2.18). Especially through the classes of professor’s emeriti Alain Barel (‘Electrical Measurement Techniques’) and Charles Hirsch (‘Fluid Mechanics in Living Systems’), I became aware of the potential of frequency domain analysis for investigating this phenomenon.
A paper of Michael O’Rourke, in which he introduced implicitly the concept of transfer function, confirmed my intuition:
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O'Rourke, M. F. (1970). Influence of ventricular ejection on the relationship between central aortic and brachial pressure pulse in man. Cardiovascular Research, 4(3), 291-300.
Early 1990’s, back in Belgium and working at the Ghent University Hospital, I had an appointment with Robert Naeije to invite him for a lecture at “Update in Cardiac Surgery, Anesthesia and Intensive Care 1993 – 2nd International Symposium”. Talking about my research interests, he suggested me to perform research in his laboratory. This thesis is the result of his generous offer.
The “Journées d’Enseignement Post-Universitaire d’Anesthésie et de Réanimation 1991” (JEPU, Paris) resulted in a monograph entitled La Pression Artérielle en Anesthésie (Arnette, Paris, 1991), which undoubtedly attracted my attention. The first presentation “The arterial pressure waveform: a driving force for blood flow”, written by Björn Biber, had and still has a significant influence on my research endeavors and clinical practice. Although written in 1991, this presentation is still of outmost current value. In this context I cannot resist to iterate Björn Biber’s conclusions:
Recent data have clarified many aspects of the driving force for the circulation - the central and the peripheral arterial pressure wave. We have reason to
underscore the differences between pressures recorded in either central vessels or from the peripheral vasculature. This has implications for our understanding of peripheral organ perfusion and for the evaluation of cardiac work load. The importance of pulse pressure wave reflection for the features of the pulse profile have been explored. This seems to imply differential central and peripheral pressure effects of vasodilators. Together, this represents an exciting background in our efforts to increase our knowledge in cardiovascular physiology.
187 Research relating to these issues will include:
1) studies on differences between systolic pressures in central and peripheral arteries,
2) studies of arterial stiffness with aging and the subsequent effects on arterial pressure waves,
3) studies of the impact of cardiovascular disease on arterial stiffness and vascular impedance,
4) studies on the effects of drugs on stiffness of large and small arteries, 5) studies of wave reflection and its alteration by pharmacological treatment,
and
6) studies on the differential effects of drugs on the caliber of arteries and arterioles.
Despite the efforts of Michael O’Rourke (Sydney) and the duo Laurent – Safar (Paris) [179, 210], the medical community (including anesthesiologists) paid little attention to the research topics mentioned before. It was not until Stanley Franklin [74], on the basis of a population-based cohort study from the original Framingham Heart Study, pointed out the importance of large artery stiffness in systolic hypertension of the elderly that cardiovascular physicians became interested in arterial stiffness, arterial wave
reflections and central aortic blood pressure. Since then, a multitude of research reports concerning the impact of alteration in these hemodynamic factors on clinical outcome appeared in the cardiovascular literature, the report on the CAFE study being perhaps the most prominent one (CAFE: Conduit Artery Function Evaluation, a spin-off of the ASCOT study) [276]. Reports concerning these topics in the perioperative setting are sparse and exclusively related to coronary artery bypass graft surgery [6, 72, 173, 174].
Basic science research related to the effects of general anesthetics upon the pulsatile components of ventricular afterload is also limited. Concerning the pulmonary
circulation the laboratory of Robert Naeije was and is a key player in the field [68, 126].
Concerning the systemic circulation it was essentially the ”power team from
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Milwaukee”, under the direction of David Warltier and Paul Pagel (Medical College of Wisconsin), who made several contributions concerning the effects of general
anesthetics on aortic input impedance and left ventricular-arterial coupling [98-101, 142, 143]. A number of findings presented in this thesis diverge from theirs. These divergences should not to be a problem; instead it is the stimulus for a subsequent investigation [216]. It is my opinion that “divergence in findings and opinions is the core business of research”. It is imperative to test our laboratory findings in the clinical perioperative setting (including the critical care setting). Taking into account of Björn Biber’s suggestions for research, one should develop methods for assessing vascular impedance, arterial mechanics and wave reflections in the perioperative setting. This will need a collaborative effort of anesthesiologists, cardiovascular physicians and biomedical engineers.
Most of the theoretical basis of this thesis relies upon the following four books:
McDonald, D. A. (1974). Blood Flow in Arteries (Second ed.).
Milnor, W. R. (1982). Hemodynamics.
Sagawa, K., Maughan, L., Suga, H., & Sunagawa, K. (1988). Cardiac Contraction and the Pressure-Volume Relationship.
Nichols, W. W., & O'Rourke, M. F. (1990). McDonald's Blood Flow in Arteries : theoretical, experimental and clinical principles (Third Edition).
I mention Blood Flow in Arteries, written by Donald A. McDonald and McDonald's Blood Flow in Arteries: theoretical, experimental and clinical principles, written by Wilmer Nichols and Michael O’Rourke, as two different books : they are ! Although Nichols and O’Rourke’s book, now in its Sixth edition, contains up to date information and is essential reading for all of those involved in cardiovascular research, one should
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read the book written by Donald McDonald: this is the only way “to get access to the mind of this brilliant biophysicist”. Unfortunately, the book is unavailable for purchase, even through Amazon®, but “in tempore non suspecto” I made a photocopy of the book when studying biomedical engineering.
The monograph written by Sagawa, Maughan, Suga and Sunagawa, was one of my indispensable companions during my research for this thesis (and still will be a companion in the future !). Every time I needed to check my knowledge concerning cardiac mechanics and cardiovascular interactions (and it did happen many times), I did put an eye on their preface and every time I was struck by the humbleness of “these giants of cardiac biophysics”. Therefore I conclude this thesis with the pre-final paragraph of their preface:
To some historians, even textbooks of medical sciences are nothing but a
collection of misconceptions and deficient – or at best immature – understandings of life and disease processes. No reader of a scientific monograph like this should be naïve enough to believe every statement in it as an absolute and eternal truth.
Usually the immediate aim of such reference books is to compile and tramsmit the best available and most up-to-date pieces of information and to present basic concepts emerging in the field. The ultimate purpose of these books is to
stimulate and challenge the minds of researchers, both young and established. We will be the first to admit that our book contains many biases, and the last to claim authoritative value for it. We simply wish to open the eyes of young trainees in cardiological sciences to the potentials of the pressure-volume approach and to help senior researchers of cardiac pathophysiology to review the state of knowledge in this field.
190 X I . B i b l i o g r a p h y
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