The Heart: Pressure-Propulsion Pump or Organ of Impedance?
2015; Elsevier BV; Volume: 29; Issue: 6 Linguagem: Inglês
10.1053/j.jvca.2015.02.022
ISSN1532-8422
Autores Tópico(s)Heart Failure Treatment and Management
ResumoHEMODYNAMIC MONITORING and support of circulation are at the center of acute intervention-based specialties such as anesthesiology and critical care. In spite of the general assumption that the understanding of basic and clinical hemodynamics is relatively complete, clinicians often invoke a number of reasons to explain away the discrepancies between the commonly used mental model of circulation and various pathophysiologic states. A cursory review of the literature on treatment modalities of various hemodynamic states over the past several decades suggests that this mental model has undergone a steady revision. For example, contrary to expectations, the results of a 2012 intra-aortic balloon pump (IABP)-Shock II randomized, open-label multicenter trial found no difference in 30-day mortality (40%) in patients with acute myocardial infarction associated with cardiogenic shock and treated with combined pharmacologic therapy, percutaneous intervention and IABP, or with pharmacologic therapy and percutaneous intervention only.1Thiele H. Zeymer U. Neumann F.-J. et al.Intraaortic balloon support for myocardial infarction with cardiogenic shock.N Engl J Med. 2012; 367: 1287-1296Crossref PubMed Scopus (1597) Google Scholar Results of the recently published follow-up study confirmed the original outcomes.2Thiele H. Zeymer U. Neumann F.-J. et al.Intra-aortic balloon counterpulsation in acute myocardial infarction complicated by cardiogenic shock (IABP-SHOCK II): Final 12 month results of a randomised, open-label trial.Lancet. 2013; 382: 1638-1645Abstract Full Text Full Text PDF PubMed Scopus (634) Google Scholar On the basis of previously reported meta-analyses and conflicting evidence from data registries, joint American College of Cardiology and American Heart Association, together with the European Society of Cardiology, downgraded the class of recommendation for IABP use from class IB (should be used) to IIbB (may/can be used).3Sjauw K.D. Piek J.J. Is the intra-aortic balloon pump leaking?.Lancet. 2013; 382: 1616-1617Abstract Full Text Full Text PDF PubMed Scopus (6) Google Scholar In the wake of these findings, some have questioned the recommendations of potentially harmful adjunct therapies, namely, the use of intra-aortic balloon pumps, in this high-risk group of patients based on "pathophysiologic assumptions and expert opinions" rather than on randomized clinical trials.4Khashan M.Y. Pinsky M.R. Does intra-aortic balloon support for myocardial infarction with cardiogenic shock improve outcome?.Crit Care. 2013; 17: 307Crossref PubMed Scopus (10) Google Scholar Moreover, in the editorial to this landmark study, O'Connor and Rogers submitted that "the results of the IABP-SHOCK II trial parallel those from many recent outcome trials that have challenged the understanding of the management of acute and chronic heart failure, including those regarding the use of pulmonary artery catheters and the role of revascularization in ischemic cardiomyopathy."5O'Connor C.M. Rogers J.G. Evidence for overturning the guidelines in cardiogenic shock.N Engl J Med. 2012; 367: 1349-1350Crossref PubMed Scopus (30) Google Scholar Similarly, the emerging modalities in pharmacologic therapy of acute and chronic heart failure further question the fundamental understanding of the circulation. Most notable is a shift from the use of potent sympathomimetic amines (epinephrine, isoproterenol, and dopamine) in the 1960s and 1970s,6Goldberg L.I. Use of sympathomimetic amines in heart failure.Am J Cardiol. 1968; 22: 177-182Abstract Full Text PDF PubMed Scopus (42) Google Scholar, 7Elliott W.C. Gorlin R. Isoproterenol in treatment of heart disease hemodynamic effects in circulatory failure.JAMA. 1966; 197: 315-320Crossref PubMed Scopus (24) Google Scholar to a widespread use of vasodilators. On the contrary, the use of inotropes (dobutamine and milrinone) currently is reserved for the treatment of a minority of patients with severe systolic dysfunction who do not tolerate vasodilators due to hypotension.8Bayram M. De Luca L. Massie M.B. et al.Reassessment of dobutamine, dopamine, and milrinone in the management of acute heart failure syndromes.Am J Cardiol. 2005; 96: 47-58Abstract Full Text Full Text PDF PubMed Scopus (194) Google Scholar Data from the ADHERE registry showed that fewer than 3% of acute heart failure patients (from a group of 150,000) had a systolic BP of<90 mmHg,9Fonarow G. The Acute Decompensated Heart Failure National Registry (ADHERE): Opportunities to improve care of patients hospitalized with acute decompensated heart failure.Rev Cardiovasc Med. 2003; 4: S21PubMed Google Scholar and of approximately 14% of those who were treated with inotropes, 19% had higher mortality compared with non-inotrope-treated patients (14%).10Abraham W.T. Adams K.F. Fonarow G.C. et al.In-hospital mortality in patients with acute decompensated heart failure requiring intravenous vasoactive medications: An analysis from the Acute Decompensated Heart Failure National Registry (ADHERE).J Am Coll Cardiol. 2005; 46: 57-64Abstract Full Text Full Text PDF PubMed Scopus (580) Google Scholar Practice guidelines of the Heart Failure Society of America (HFSA), the American College of Cardiology Foundation/American Heart Association (ACCF/AHA), as well as the European Society of Cardiology (ESA) therefore recommend the use of vasodilators and deemphasize the use of inotropes in the management of acute heart failure syndromes.11Coons J.C. McGraw M. Murali S. Pharmacotherapy for acute heart failure syndromes.Am J Health Syst Pharm. 2011; 68: 21-35Crossref PubMed Scopus (34) Google Scholar It is of note that, from the range of available inotropes, dobutamine and milrinone are chosen for their significant vasodilatory effect. In addition, the use of ß-blockers is recommended universally in all patients with stable mild, moderate, and severe heart failure with ischemic or non-ischemic cardiomyopathy and reduced LV ejection fraction.12Swedberg K. Cleland J. Dargie H. et al.Guidelines for the diagnosis and treatment of chronic heart failure: Executive summary (update 2005) The Task Force for the Diagnosis and Treatment of Chronic Heart Failure of the European Society of Cardiology.Eur Heart J. 2005; 26: 1115-1140Crossref PubMed Scopus (247) Google Scholar The question naturally arises as to whether or not the above-mentioned treatment modalities and recommendations arose from poorly designed trials or whether or not the understanding of pathophysiologic mechanisms involved is in need of "renewed growth and development."5O'Connor C.M. Rogers J.G. Evidence for overturning the guidelines in cardiogenic shock.N Engl J Med. 2012; 367: 1349-1350Crossref PubMed Scopus (30) Google Scholar A number of other examples challenge the understanding of the basic tenets of circulation, such as the curious phenomenon of increase in cardiac output during aortic cross-clamp by up to 25% in a controlled experimental setting13Stene J.K. Burns B. Permutt S. et al.Increased cardiac output following occlusion of the descending thoracic aorta in dogs.Am J Physiol Regul Integr Comp Physiol. 1982; 243: R152-R158PubMed Google Scholar and, in some patients, during aortic surgery.14Gelman S. The pathophysiology of aortic cross-clamping and unclamping.Anesthesiol. 1995; 82: 1026-1057Crossref PubMed Scopus (371) Google Scholar The Fontan repair used for surgical correction of various hypoplastic right and left heart syndromes (HLHS) presents a yet-to-be explained hemodynamic paradox which, in the absence of the right heart complex, the single, often weakened, ventricle supposedly pumps the blood through systemic and pulmonary circulations.15Gewillig M. Brown S.C. Eyskens B. et al.The Fontan circulation: Who controls cardiac output?.Interact Cardiovasc Thorac Surg. 2010; 10: 428-433Crossref PubMed Scopus (208) Google Scholar There are a large amount of conflicting data from exercise physiology in which the concept of a muscle pump has been evoked in order to explain the greatly increased systemic blood flows that exceed theoretical limits of the heart's pumping capacity. Review of literature suggests that increased cardiac outputs can neither be ascribed to the heart (on account of a greatly shortened diastole that precludes adequate filling) nor to contracting muscles.16Furst B. Cardiovascular response during exercise: The Heart and Circulation - An Integrative Model. Springer-Verlag, London2014Crossref Google Scholar From the physiologic perspective, the heart is considered to be a dual pump, driving the blood through pulmonary and systemic circuits arranged in series. In the course of an average life span of 75 years, the heart, weighing around 350 grams, pumps 400 million liters of blood (the amount that fills a lake 1 km long, 40 m wide and 10 m deep)17Boulpaep E. Organization of the cardiovasuclar system.in: Boron W.F. Boulpaep E.L. Medical physiology: A cellular and molecular approach. Saunders, Philadelphia2003: 423-462Google Scholar through a system of conduits with the total length of about 100,000 km. Considering the fact that the diameter of the red blood cells frequently exceeds the width of the capillary beds, the heart as a pump truly performs a prodigious task. The idea that the heart is a pump providing the total mechanical energy for blood's propulsion has dominated the field of cardiovascular physiology for well over a century. A detailed discussion of the history of the propulsion pressure circulation model is beyond the scope of this article,18Fuchs T. Grene M. The mechanization of the heart: Harvey and Descartes. University of Rochester Press, Rochester, NY2001Google Scholar but even a cursory look at the leading medical journals in the 1850's showed that there was a lively debate among the proponents of the heart-centered circulation model who supported the view that the heart is the "motor" of the circulation, and those who maintained that the "capillary power," or the force from behind (vis á tergo), played a principal role in blood's propulsion.19Thudichum I. On the Cause of the Emptiness of the Arteries after Death.Association Medical Journal. 1855; 3: 122-127Google Scholar It should be noted parenthetically that the classic concept, vis á tergo, goes back to antique medicine when it played only a secondary role to vis á fronte, or "force from the front," which referred to suction forces (vacuum) working locally, (eg, ventricular diastolic suction) and at a distance, akin to gravity.20Prioreschi P. A History of Medicine: Roman Medicine, Galen (book section). Horatius Press, Omaha, NE1998: 419-420Google Scholar By the 1950s, these concepts still were mentioned in physiologic texts for historic interests 21Wiggers C.J. The ciruclation and ciruclation research in perspective.in: Handbook of Physiology. Vol I. American Physiological Society, Washington, DC.1962: 1-9Google Scholar, 22Guyton AC, Jones CE, Coleman TG: Circulatory Physiology: Cardiac output and its regulation. Philadelphia, London, W.B. Saunders, 1973, pp 175-180Google Scholar, 23Brecher G.A. Critical review of recent work on ventricular diastolic suction.Circulation Research. 1958; 6: 554-566Crossref PubMed Scopus (59) Google Scholar but, largely bereft of their original meaning, slowly acquired a new identity. The force from behind now assumes the dominant role as pressure generated by ventricular contraction, pushing the blood through the capillary beds back to the atria. A portion of this force is stored in vessel walls as elastic energy and is represented in the concept of the mean systemic pressure (Pms). The force from the front, on the other hand, became a generic term for a host of phenomena ranging from ventricular diastolic suction and/or respiratory pump, which facilitate filling of the heart, to a range of factors that impede venous return.22Guyton AC, Jones CE, Coleman TG: Circulatory Physiology: Cardiac output and its regulation. Philadelphia, London, W.B. Saunders, 1973, pp 175-180Google Scholar The latter became the mainstay of Guyton's venous return model of circulation discussed in the following section. Over time, the pressure-propulsion (PP) model has become deeply engrained in the collective subconscious and, with few exceptions, virtually has remained unchallenged. It is suggested that in the light of rapidly accumulating growth of information obtained with the help of in-vivo experimental and clinical imaging modalities, the number of discrepancies between the observed phenomena and the constraints imposed by the existent circulation model is likely to increase. It is the purpose of this article to present some of the recently collected evidence against the commonly accepted PP model of circulation and to propose the conceptual framework for a new, more complete understanding of the circulatory phenomena. In the first part of the article a brief historic outline and the salient features of Guyton's venous return (VR) model of circulation are discussed as well as the reason for its incongruence with the left ventricular (LV) model of circulation. Attention then is turned to the heart and to ways in which its mechano-energetic function compares to a standard hydraulic pump. Work on isolated heart preparations demonstrates that the heart is unable to maintain constant pressures or flow in face of the changing loading conditions and suggests that it is a rather inefficient pressure-propulsion pump. It is proposed that the heart functions by interrupting the flow of blood already in motion; that is, as an impedance pump, whose mechanical action can be compared to a hydraulic ram. It is further suggested that in place of the mechanistic PP model, the biologic model of circulation be adopted in which the blood is a self-moving agent driven by the metabolic demands of the tissues. The evidence in support of this model comes from observations of the embryonic circulation, through comparative anatomy and from phenomenology of the mature circulation. It is then shown that the conceptual framework for the PP model is rooted in the principles of a thermodynamically closed system, which, according to current understanding, no longer adequately describes the biologic phenomena in general and, as proposed in this article, the circulatory system in particular. Finally, the phenomenon of autonomous blood movement is discussed in the context of open-systems biology. In spite of the general assumption that the heart provides the total mechanical energy for blood propulsion, the experimental observations have polarized basic scientists and clinicians into 2 opposing views concerning the control of cardiac output (CO). While proponents of Guyton's VR model contend that the peripheral circulation plays the dominant role in control of CO, adherents of the LV model ascribe this role, by default, to the heart.24Magder S. The classical Guyton view that mean systemic pressure, right atrial pressure, and venous resistance govern venous return is/is not correct.J Appl Physiol. 2006; 101: 1533Crossref PubMed Scopus (21) Google Scholar, 25Magder S. Point:Counterpoint: The classical Guyton view that mean systemic pressure, right atrial pressure, and venous resistance govern venous return is/is not correct.J Appl Physiol. 2006; 101: 1523-1525Crossref PubMed Scopus (46) Google Scholar, 26Brengelmann G. Counterpoint: The classical Guyton view that mean systemic pressure, right atrial pressure, and venous resistance govern venous return is not correct.J Appl Physiol. 2006; 101: 1525-1526Crossref PubMed Scopus (41) Google Scholar, 27Pinsky M.R. The classical Guyton view that mean systemic pressure, right atrial pressure, and venous resistance govern venous return is/is not correct.J Appl Physiol. 2006; 101: 1528-1530Crossref PubMed Scopus (1) Google Scholar Since the ultimate source for blood propulsion in both models can be traced to the hydrodynamic equivalent of Ohm's law (where the power source for the circulating blood clearly originates in the pump, ie, the heart), those seemingly opposing views differ only on the surface but not in essence. It is apparent that this central issue in cardiovascular physiology will not be resolved until the fundamental question ("What makes the blood go around?")25Magder S. Point:Counterpoint: The classical Guyton view that mean systemic pressure, right atrial pressure, and venous resistance govern venous return is/is not correct.J Appl Physiol. 2006; 101: 1523-1525Crossref PubMed Scopus (46) Google Scholar is considered not only in the light of the conventional model but also from the observed circulatory phenomena themselves. Between the 1950s and 1970s, Arthur Guyton and coworkers developed a circulation model that has, in due course, become almost universally accepted. At the core of the model is the idea that venous circulation plays a central role in control of CO. The starting point for the VR model was a number of observations that convinced Guyton and his collaborators that cardiac output largely was unaffected by the activity of the heart.28Guyton A.C. Jones C.E. Coleman T.G. Circulatory physiology: Cardiac output and its regulation. W.B. Saunders, Philadelphia, PA1973: 137-146Google Scholar For example, artificial pacing of the heart at rates up to 4 times above baseline in animals29Cowley Jr, A.W. Guyton A.C. Heart rate as a determinant of cardiac output in dogs with arteriovenous fistula.Am J Cardiol. 1971; 28: 321-325Abstract Full Text PDF PubMed Scopus (26) Google Scholar and humans30Stein E. Damato A. Kosowsky B. et al.The relation of heart rate to cardiovascular dynamics pacing by atrial electrodes.Circulation. 1966; 33: 925-932Crossref PubMed Scopus (54) Google Scholar, 31Ross Jr, J. Linhart J.W. Braunwald E. Effects of changing heart rate in man by electrical stimulation of the right atrium: Studies at rest, during exercise, and with isoproterenol.Circulation. 1965; 32: 549-558Crossref PubMed Scopus (154) Google Scholar did not cause an increase in CO. Similarly, experiments on dogs, in which the right heart was replaced by a bypass pump, showed that CO could be maintained at the baseline level only when the pump output matched the autonomous rate of venous return. The increase in pump flows above the baseline would result in collapse of the great veins without change in CO.32Permutt S. Caldini P. Regulation of cardiac output by the circuit: Venous return..in: Boan J. Noordegraff A. Raines J. Cardiovasuclar System Dynamics. MIT Press, Cambrige, MA1987: 465-479Google Scholar Significant to Guyton's model is the division of the circulatory system into 2 parts. The first consists of the heart and lung and the second of the entire systemic circulation. Both parts were, in turn, investigated separately. The heart-lung segment was examined on the isolated heart preparation and in an intact animal under a variety of experimental settings. The isolated systemic circulation, on the other hand, was studied by replacing the heart with a bypass pump, and on intact animals by measuring pressure and flow at different points while stressing the circulation.33Guyton A. Venous return. Handbook of Physiology. Edited by Hamilton WF.Circulation. American Physiological Society, Washington, DC1963: 1099-1133Google Scholar The other key component of the model is the role of elastic recoil pressure within the vessels that supplies potential energy to the circulating blood. This pseudostatic pressure, technically known as Pms, is defined as the equilibrium pressure generated by the elastic recoil of the vessels during no-flow state. Its value represents the filling of the vessels and is, according to the theory, the principal force for driving the circulation.34Guyton A.C. Lindsey A.W. Kaufmann B.N. Effect of mean circulatory filling pressure and other peripheral circulatory factors on cardiac output.Am J Physiol–Legacy Content. 1955; 180: 463-468PubMed Google Scholar As the heart begins to pump, it transfers the blood from the highly compliant venous into the poorly compliant arterial limb of the circuit where the pressure increases with each increment in pump flow. Concomitantly, on the venous side, the right atrial pressure (Pra) begins to decrease until it reaches zero when the veins collapse and the flow ceases (Fig 1). According to the model, the right atrial pressure plays a dual role; viewed from the heart, Pra determines the degree of filling of the right heart and regulates its output according to the degree of its filling (Starling's law). In respect to the blood returning to the heart (ie, venous return), the positive value of Pra acts as an impedance to venous return by exerting back pressure. Therefore, any value of Pra smaller than Pms allows for the flow of venous blood in accordance with the pressure gradient. In a simple analogy, the model has been compared to the flow of water from a bathtub (venous compartment) in which the rate of emptying is determined by the height of water in the tub (Pms) and the physical characteristics of the drain pipe, (ie, its resistance and downstream pressure [pressure difference between the Pms and Pra]). Importantly, the outflow from the tub does not depend on the force of stream issuing from the tap filling the tub, as represented by the action of the heart in generating arterial pressure.25Magder S. Point:Counterpoint: The classical Guyton view that mean systemic pressure, right atrial pressure, and venous resistance govern venous return is/is not correct.J Appl Physiol. 2006; 101: 1523-1525Crossref PubMed Scopus (46) Google Scholar Guyton skillfully demonstrated the dual role of Pra in control of cardiac output by a composite diagram in which cardiac function and venous return curves are shown on the same coordinates. Guyton, moreover, maintained that venous return and cardiac function curves are complementary to each other and that the crossing of the 2 in the equilibrium point represents their solutions (Fig 2). The value of Guyton's emphasis on the role of peripheral circulation in the overall approach to studying the cardiovascular system has undoubtedly set the stage for progressive growth in knowledge about control of cardiac output. His unique graphic representations of dividing the circulation into systemic and cardiac segments (comprising of the heart and pulmonary circulations) has made it possible to visualize changes in hemodynamic variables in normal and pathologic conditions. They became a valuable tool in the hands of clinicians and educators and have been reproduced in virtually every text of basic and clinical hemodynamics. However, for reasons mentioned below, this model remains incomplete. Critics of the VR circulation model contend that the pivotal role played by the right atrium as back pressure in Guyton's analysis is exactly its most controversial point.35Henderson W.R. Griesdale D.E.G. Walley K.R. et al.Clinical review: Guyton - the role of mean circulatory filling pressure and right atrial pressure in controlling cardiac output.Crit Care. 2010; 14: 243Crossref PubMed Scopus (64) Google Scholar At the core of the argument is the fact that simultaneous depiction of "cardiac function" and "venous return" curves on the same diagram presupposes that the 2 sets of experiments were performed on the same preparation, whereas they were obtained in two different sets of experiments.36Brengelmann G.L. A critical analysis of the view that right atrial pressure determines venous return.J Appl Physiol. 2003; 94: 849-859Crossref PubMed Scopus (83) Google Scholar Levy repeated the above-mentioned Guyton's right-heart bypass experiment on a dog with arrested circulation in which the heart had been replaced by a bypass pump. He showed that over the range of pump flows from zero to maximal, the Pra progressively declined with a concomitant rise in arterial pressure, thus demonstrating a reciprocal relation between the two.37Levy M.N. The cardiac and vascular factors that determine systemic blood flow.Circulation Research. 1979; 44: 739-747Crossref PubMed Scopus (111) Google Scholar In the graphic representation of the experiment, Levy expressly stated that under conditions of this experiment, the venous return is clearly the dependent variable (Fig 3). He further argued that in a plot with joint representation of cardiac and vascular function curves, one of the curves necessarily is depicted backwards, giving the erroneous impression that Pra controls CO as back pressure rather than the bypass pump. It has, moreover, been pointed out that Guyton and coworkers recorded venous return curves and cardiac function curves at steady states where, for each point on the graph, the flow of the pump was adjusted manually (Fig 1). As such, the relationships do not record venous return in dynamic states, blur distinction between dependent and independent variables, and confuse mathematic abstraction with reality.36Brengelmann G.L. A critical analysis of the view that right atrial pressure determines venous return.J Appl Physiol. 2003; 94: 849-859Crossref PubMed Scopus (83) Google Scholar It also should be mentioned that the method by which these experiments were performed by Guyton and Levy, namely, on animal preparations with arrested hearts and abolished vasomotor reflexes, is essentially not compatible with life.38Guyton A.C. Satterfield J.H. Harris J.W. Dynamics of central venous resistance with observations on static blood pressure.Am J Physiol. 1952; 169: 691-699PubMed Google Scholar In this sense, the circulatory system of a nearly deceased experimental animal does approach a mechanical system subject to pressures and flows as demonstrated in Levy's experiment, and it is superfluous to talk of Pms as the driving force for venous return. For methodologic difficulties with stopping the circulation and the measurement of mean systemic pressure, the reader is referred to reference 39Furst B. Circulatory and respiratory function of the blood: The Heart and Circulation - An Integrative Model. Springer-Verlag, London2014Crossref Google Scholar. In conclusion, it can be argued that for all its inconsistencies with the pressure-propulsion model, Guyton's concept of right atrial pressure as an impedance to venous return finds its validation in numerous experimental and clinical studies. The intersection point of the cardiac and vascular function curves in his graphic analysis (Fig 2) is an ingenious attempt to represent dependence of the pulmonary and systemic circulations on right atrial pressure. However, by considering the heart and the pulmonary circulation as a single unit, rather than, in analogy with the systemic venous return, treating it independently as pulmonary arterial return, the real function of the pulmonary circulation and of the left heart complex had been obscured.40Furst B. Increased pulmonary flows: The Heart and Circulation - An Integrative Model. Springer-Verlag, London2014Crossref Google Scholar Implicit in the LV circulation model is the idea that, in addition to impelling the blood, the heart is also the chief regulator of cardiac output. The model further assumes that the circulation is a closed system of vessels in which the pressure gradient between the aorta and the right atrium determines the flow and where, during a steady state, the outputs of the left and right hearts are closely matched in accordance with the law of conservation of energy and matter. The understanding of the physical laws governing the flow of fluids through hydraulic systems as described by Hagen-Poiseuille in the 19th century was the starting point for quantification of flow-related phenomena in biologic systems. The law describes the relation between pressure drop and volume flow in a rigid tube under steady conditions with laminar flow,ΔP=8µLQπr4(Eq. 1) where: ΔP is the pressure gradient along the tube, L is the length of tube, μ is the dynamic viscosity, Q is the volume flow rate, r is the radius, and π is the mathematic constant. However, since the physical dimensions of the circulatory system are not known, a simplified relation of variables in the form of Ohm's law for fluids has been adopted:41Nichols W.W. O'Rourke M.F. McDonald's blood flow in arteries: Theoretic, experimental, and clinical principles. Lea & Fabiger, Philadelphia, London1990: 12-53Google ScholarPao−Pra=CO×Rp(Eq. 2) where the pressure gradient (Pao-Pra) is the difference between the mean aortic and right atrial pressures, the flow is cardiac output (CO), and (Rp) is the peripheral resistance.41Nichols W.W. O'Rourke M.F. McDonald's blood flow in arteries: Theoretic, experimental, and clinical principles. Lea & Fabiger, Philadelphia, London1990: 12-53Google Scholar Assuming a zero value for right atrial pressure the equation can be re-written as:Rp=Pao/CO(Eq. 3) By analogy, the pressure difference between the right ventricle and left atrium is used to calculate resistance of the pulmonary circulation. It should be noted that pulmonary capillary wedge pressure (PCWP) is used as a surrogate for left atrial pressure. The integration of the above concepts with the emerging technology of pulmonary artery pressure measurement in the 1970s ushered in a new era in the understanding of normal hemodynamics and of various pathophysiologic states. Simultaneous measurement of CO and right and left ventricular filling pressures with the use of Swan-Ganz catheters became an essential tool in the hands of sapient practitioners to observe trends and manipulate CO in terms of preload, afterload, and contractility. The presence of such a relationship may undoubtedly be applicable in a laboratory setting where the heart of an experimental animal has been replaced by a bypass pump and vascular reflexes have been abolished, as demonstrated in Levy's experiment cited above.37Levy M.N. The cardiac and v
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