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Misled by the Wedge?* The Swan-Ganz Catheter and Left Ventricular Preload R. Raper, M.B., B.S.;t and William]. Sibbald, M.D.,
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assessment of left ventricular preload by the PAoE WHAT IS THE PAoP?
*From the Critical Care/'Ii'auma Unit, Victoria Hospital, London, Canada. tChief Resident. *Coordinator, Critical Careffiauma Unit;. Ass~iate Professo! of Medicine and Coordinator of the Program m Cntical Care, UnIversity of Western Ontario, London, Canada. This work was supported by a grant from the Ontario Heart Association (No. 310). Reprint requests: Dr. Sibbald, Victoria Hospital Corporation, PO 85375, London, Ontano, Canada N6A-4G5
The clinical use of a Hotation device for right heart catheterization was first reported by Swan et aP in 1970. This group described the safe introduction of a Hexible, balloon-tipped, How-directed catheter into the pulmonary artery, the measurement of the downstream pressure in the balloon-occluded pulmonary artery segment, and the correlation between this pressure, the PAoE and the pulmonary wedge pressure (PWP) measured with the more rigid, traditional right heart catheter formally wedged into a small pulmonary vessel. Subsequently, direct correlations between the PAoP and the fWE and b~tween the PAoP and the LAP have been confirmed. 4•5 Since the mean LAP correlates well with the LVEDJ>6 in the healthy heart, the PAoP has become a common measure of left ventricular filling for both clinical and research purposes. In fact, alterations in left ventricular contractility have been inferred by analysis of changes in the Frank-Starling relationship in which the PAoP was used as the measure of left ventricular preload. 7-9 Recently, however, important limitations ofpressure measurements obtained using right heart catheters have become apparent. For a variety of technical and pathophysiologic reasons, the PAoP may not adequately reflect the LVEDE and the LVEDP may bear little relationship to the LVED\z In early studies, Lozman et allO demonstrated a good correlation tween the mean PAoP and the LAP in postoperative surgical patients, although this correlation was lost at higher levels of positive end-expiratory pressure (PEEP) in ventilated patients. Subsequently, Horton et alll found that the LVEDP did not adequately reflect changes in the LVEDV in a model of hemorrhagic hypotension in dogs. ~rom clinical studies, we also have reported significant discrepancies between the LVEDP and the LVED~ 12 To emphasize this point, we have compared tlle PAoP with the LVEDV in patients with acute respiratory insufficiency and varying de(Fig 1). 12 The PAoP in grees ofpulmonary hypertensio~ these patients was measured with a Swan-Ganz catheter, while the LVEDV was calculated from a simultaneously measured thermodilution cardiac output and a radionuclide LV ejection fraction (LVEDVI = stroke
flotation pul?:~nary artery quantum leap In the physiologic information available fo~ the management of critically-ill patients. Pre-existing suppositions that the central venous pressure (CVP) provided a reliable indication of left ventricular preload, and that changes in .the CVP would reflect parallel changes in left ventricular filling pressures, were quickly dispelled. 1 Clinical studies identified wide disparities between the CVP and the pulmonary artery occlusion pressure (PAoP), both in terms of the absolute magnitude of these pressures, as well as in their direction of change with acute hemodynamic intervention. The SwanGanz catheter was considered to provide, at last, the clinical means for a frequent and reliable assessment of the left ventricular preload. As we will define, however, this may not always be the case. Although the PAoP obtained with the Swan-Ganz catheter generally provides a reliable index of the mean left atrial (LAP), and hence, of the left ventricular end-diastolic (LVEDP) pressures, for a variety oftechnical and physiologic reasons, it does not always do so. More importantly, this extrapolated measurement of the LVEDP does not provide a reliable index of either the left ventricular end-diastolic volume (LVEDV) or the left ventricular end-diastolic dimension (LVEDD), both of which are more reliable clinical measures of the left ventricular preload than is the LVEDE 2 Several factors combine to negate any relationship between the LVEDP and the LVED\z These include the inherent stiffness properties of the myocardial fibers, the thickness of the myocardium, and the effect of changes in the pressure surrounding the cardiac chambers. In this review, we will briefly in examine some of the common pitfalls encoun~ered the measurement of the PAoP and in the extrapolation of the measured PAoP to an assessment of left ventricular preload. We will particularly emphasize the effect of altered left ventricular compliance on the ~,e
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volume index/ejection fraction). In Figure 2, we have also plotted the LVEDV against the PAoP for three patients at various stages of an acute illnesss. From these two figures, it is apparent that the PAoP must be regarded as ap unreliable clinical index of the LVED~ both in large patient groups as well as in individual patients sequentially assessed over time. For the LVEDV to be inferred from the measured PAo~ several assumptions are inherent: the PAoP must be accurately measured, the PAoP must reflect the LA~' the LAP must reflect the LVEDP and the LVEDP must relate directly to the LVEDV: In clinical p~ctice, errors may be encountered at each step ofthis progression, thus invalidating the primary inference. MEASUREMENT OF THE
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The Swan-Ganz catheter is a relatively simple device consisting of a Hqid-filled central lumen with an inHatable balloon proximal to its tip. Recent modifications involving the addition of proximal ports for buusion apd pressure measurement, electrodes for cardi~c pacing, and thermistors for measurement of the cardiac output and the right ventricular ejection ~tion have not altered the basic concept of the original cathetet: Since the frequency and rate of pressure change within the pulmonary artery is too great to be reliably reproduced by water column manometry, as was originally employed for CVP monitoring, the Swan-Ganz catheter must be coupled to an electronic measuring system by a transducer. While it is beyqnd the scope of this article to provide a detailed review of the limitations of the electronic assessment of dynamic pressures, these cannot be dismissed lightly. The inherent underdamping of even a well-functioning system13
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FIGURE 2. LVEDVI in mllm2 BSA plotted against PAoP for three patients at various stages of their illnesses. Changes in LVEDVI are not well reflected by changes in PAoP in individual patients.
renders measurement of systolic and diastolic pressures unreliable. The use of variable resistors within the circuit apparently permits optimization of the damping characteristics of the system, and hence, more accurate pressure measurement;14 at this time, however, these are not in common clinical use. The unselective nature of time-based electrical sampling and averaging may render digital displays unreliable; graphic displays are mandatory if any respiratory artifact is to be excluded. Figure 3 demonstrates the limitations of digital display units and time-based averaging. Although more sophisticated electronic algorithms are available, the tachypneic patient on an intermittent mandatory ventilation circuit may well confound even these. When Does the PAoP not Reflect the LAP? The problems of electronic pressure measurement, inherent to all systems, have been reviewed elsewhere. 15 Even when such problems are minimized, the measured PAoP may not adequately reflect the LA~ and hence, the LVEDE The potential difficulties involved in estimating the LVEDP and the left ventricular preload from the measured PAoP are as follows: incorrect catheter placement; incorrect transducer placement; incorrect transducer calibration; pressure overdamping or underdamping; respiratory pressure artifact; eccentric balloon occlusion and overwedging; nonzone III balloon occlusion; pulmonary venous obstruction; valvular heart disease; increased pericardial pressure; and altered left ventricular compliance. Accurate measurement of the PAoP depends on correct positioning of the catheter within the pulmonary artery, careful placement of the transducer such that its fluid column is at the level of the left atrium, and accurate calibration of the transducer at that level Misled by the VVedge? (Raper, Si/;JbaJd)
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FIGURE 3. Graphic display of PAoP over time with the respiratory artifact imposed by intermittent mandatory ventilation. The end-expiratory PAoP is 20 mm Hg. The time-based average PAoP which would be displayed on a digital recorder (represented by the broken line) at no time provides a true reflection of end-expiratory PAoE
so that it reliably assesses pressures within the anticipated range. the traditional reference point for the left atrium is the fourth intercostal space in the midaxillary line; the proper position of the catheter within the pulmonary vasculature should be confirmed by pressure wave monitoring and chest roentgenography. IS The system must be fully purged ofair to prevent overdamping, and as previously mentioned, a graphic display is preferred to allow measurement ofpressures at end-expiration when the effects of superimposed respiratory variations on intrathoracic pressures are minimized. 16 With these prerequisites fulfilled, the measured PAoP may still not reliably reBect the LAE Eccentric balloon inBation and "over-wedging" have been described. 17 Both complications are easily recognized by the steady rise in pressure observed as a consequence of the continuous Bush devices employed to maintain catheter patency; repositioning of the catheter is mandatory in this situation. More difficult to appreciate is the occlusion of the pulmonary artery in a segment oflung where the pulmonary venous pressure does not exceed the alveolar pressure (West's non-zone III). 18 With catheter placement above the level of the left atrium, animal studies have demonstrated that the PAoP reBects changes in alveolar pressure rather than in the LAP;19 the same is likely true in humans. 10 Since Swan-Ganz catheters are Bow-directed, they should migrate to regions of greatest blood Ho~ specifically West's zone III. This is usually, but not universally, true. iO Non-zone III catheter migration may be recognized by observing the effects ofsudden increments or decrements of PEEP on the measured PAoP: if the PAoP changes by more than 50 percent ofthe change in applied PEE~ it is likely that the catheter tip is in a non-zone III position. If this is so, the catheter should then be repositioned. IS The incidence of non-zone III placement of the catheter can be expected to be
greatest when the LAP is low, when alveolar pressure is elevated by the use of PEE~ or in the presence of airways obstruction. Another potential source of disparity between the PAoP and the LAP is the presence of pulmonary venous obstruction. Apart from functional obstruction within the pulmonary microcirculation in non-zone III regions of the lung, this is probably a rare occurrence; it may be seen with fixed lesions such as tumours, atrial myxomas, mediastinal fibrosis and pulmonary venous thrombosis. IS Compression of the pulmonary venous system in low Bow states or as a consequence of increased intrathoracic or pericardial pressures has also been suggested,18.21 although the clinical significance of this remains uncertain. When Does the LAP Not Reflect the LVEDPP
Even when the measured PAoP accurately assesses the LA~ it may not provide a reliable measure of the LVEDP. Discrepancy between the LAP and the LVEDP is, for example, characteristic of mitral valve disease. Mitral stenosis results in a diastolic pressure gradient between the left atrium and the left ventricle, while mitral regurgitation allows the back transmission of ventricular systolic pressures. This back-transmission of the systolic pressure elevates the mean LAP above the diastolic LA~ and hence above the LVEDE This may be recognized from a graphic pressure display by identification of exaggerated CCV" waves; when present, the "a" wave on the LAP or PAoP trace may be used to estimate the LVEDE Conversely, aortic regurgitation may cause the LVEDP to exceed the LAP and hence the PAoP; premature mitral valve closure and continued left ventricular filling from the aorta may result in an end-diastolic pres"' sure gradient between the left ventricie and the left atrium. Disparity between the LAP and the LVEDP is, CHEST I 89 I 3 I MARCH, 1986
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perhaps, more commonly observed in the presence of impaired left ventricular compliance. The enddiastolic atrial "kick" is exaggerated when the left ventricle is abnormally stiff and atrial contraction may then substantially increase both the LVEDV and the LVED~ while having a significantly lesser effect on the mean LAE In such a situation, the "a" wave of the PAoP tracing will again provide a more reliable assessment of the LVEDP than will the mean PAoE2l.22 RELATIONSHIP BElWEEN THE LVEDP AND THE LVEDV Despite the difficulties and potential inaccuracies previously described, in most clinical circumstances, the PAoP does provide a reliable measure of the It does not, howevet; reflect intracavitary LVED~4.5 the left ventricular preload. As preload is the enddiastolic distending force of the ventricle, i3 and as this correlates better with the LVEDV or the LVEDD than with the LVED~2 to reliably reflect left ventricular preload, the PAoP must reliably correlate with the LVEDV or the LVEDD. Since no such correlation exists in both animalll and human studies (Fig 1 and 2), J4 the PAoP cannot be considered an acceptable clinical measure of the left ventricular preload. Several factors combine to distort the previously assumed direct relationship between the LVEDP and the LVED\z Those include variations in the stiffness properties of the left ventricular myocardium, the pressure surrounding the cardiac chambers, and the diastolic volume of the right ventricle. Clinically, where only the intracavitary LVEDP is commonly assessed, increased juxtacardiac pressure will result in an increase in the measured LVEDP for any given chamber volume without any change in the characteristics of the myocardium. When ventricular volumes are also assessed, this may result in a false assumption
of increased myocardial stiffness. Myocardial stiffness is ideally assessed by relating the measurement of the chamber volume to the simultaneous transmyocardial filling pressure, rather than to the intracavitary filling pressure.
Left Ventricular Compliance In a steady state, the relationship between the enddiastolic transmyocardial filling pressure and the enddiastolic volume of the left ventricle is curvilinear (Fig 4 and 5). Ventricular compliance is defined by the instantaneous relationship between the ventricular end-diastolic volume and pressure, and is mathematically expressed as the slope of the tangent to the diastolic pressure-volume curve (dv/dp). Ventricular compliance is the inverse of chamber stiffness. Changes in left ventricular compliance may result from changes in the level ofleft ventricular filling, involving a shift along a single diastolic pressure-volume curve. Changes in left ventricular compliance may also result from changes in the inherent stiffness properties ofthe myocardium, represented by a shift of the pressurevolume curve and defined by a change in the modulus of chamber stiffness. Figure 4 demonstrates the effect of altered left ventricular filling on left ventricular compliance. Since the pressure-volume curve is non-linear, an equivalent increase in volume (4V) will produce a greater increase in pressure when the ventricle is relatively distended {4PJ than when it is relatively empty {4PJ. This change in left ventricular compliance does not imply any alteration in the inherent stiffness properties ofthe ventricle since the modulus of chamber stiffness remains unchanged. By contrast, Figure 5 depicts a hypothetical family of compliance curves and demonstrates the second mechanism responsible for an alteration of left
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FIGURE 5. A family of diastolic pressure-volume curves for the left ventricle. A measure ofLVEDP may represent quite different states ofleft ventricular filling depending on compliance (AI' At, AJ. Also, an increase in PAoP may indicate either a change in left ventricular compliance without any change in left ventricular filling (At-+ BJ or may indicate a true increase in left ventricular filling (At-+ BJ.
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ventricular compliance, a change in the stiffness properties of the left ventricle. From this figure, two observations are important. First, a measure of the LVEDP may represent quite different states of left ventricular filling, and hence, of left ventricular preload (points Ab At, A3). Second, an increase in the LVEDP (points A-+B) may indicate an increase in when the modulus of chamber preload (points ~-+BJ stiffness is unchanged, or may reflect a change in the modulus of chamber stiffness without any concurrent change in the LVED~ and hence, in the left ventricular preload (points At-+BJ. the principle determinants of left ventricular compliance are left ventricular preload, left ventricular mass, myocardial fiber stiffness, and right ventricular end-diastolic volume. Left ventricular compliance may also be affected by temperature,25 osmolality,26 and heart rate;27 within the usually en,countered range in clinical practice, the effect of ~ese variables is sufficiently minute to be discounted. The diastolic myocardial perfusion gradient may also alter ventricular compliance;27 unless myocardial ischemia results, howeve!; this mechanism seems also to be of minimal clinical significance. Increased systolic pressure is associated with a right-shift of the end-diastolic pressure-volume curve.9:1 This may explain the observed effect of exogenous catecholamines on left: ventricular compliance,28 an effect not seen with catecholamines when the blood pressure is controlled. Neither the mechanism nor the clinical significance of this effect is known. The effect of left ventricular preload on left ventricular compliance is evident from Figure 4, as well as from the previous discussion. This is clinically apparent when administration of a small volume of fluid is accompanied by a significant increase in the measured PAo~ all other variables remaining normal. Regardless of the absolute left-ventricular preload in this clinical situation, the instantaneous end-diastolic pressure-volume (compliance) curve must reflect a poorly compliant ventricle. This is an important clinical observation since further fluid administration will have little effect on ventricular preload, and hence, by the Frank-Starling mechanism, on left ventricular output. Instead, continued fluid infusion may dramatically increase the LVED~ and hence, the propensity for the development of pulmonary edema on a hydrostatic basis. H augmentation of cardiac output remains desirable in such a clinical situation, it would be more appropriate to administer agents designed to either increase the inotropic state of the myocardium or to reduce the modulus of chamber stiffness. Alterations in the modulus of chamber stiffness are seen in both acute and chronic disease states as well as with acute hemodynamic interventions. For instance,
left ventricular hypertrophy may result in a decrease in left ventricular co.mpliance due to an increase in the modulus of chamber stiffness. 29 Conversely, chronic left ventricular dilatation results in enhanced left ventricular compliance. 29 These effects are largely mediated by changes in the end-diastolic volume to mass ratio and probably do not reflect changes in individual myocardial fiber stiffness. Acute myocardial ischemia,30 myocardial fibrosis, and infiltrative processes such as amyliodosis, may aiso effect an increase in the moduhis of chamber stiffness; this appears mediated by changes in individual myocardial fiber stiffness rather than by any increase in myocardial mass. The clinical implication of such alterations in compliance is apparent from studies of the hemodynamic management of acute myocardial infarction where optimal left ventricular filling usually requires a higher LVEDP than would be considered necessary in the normal heart. 31 Many of the factors which may potentially influence left ventricuiar compliance can often be anticipated froin the clinical history, physical examination, and standard investigative procedures such as electrocardiography and chest roentgenography. However, alterations in left ventricular compliance may also result from a variety of hemodynamic interventions commonly employed in the management of the criticallyill. These are more difficult to anticipate and to consider when attempting to estimate left ventricular preload from a measure of the LVEDE Vasoactive drugs such as nitroprusside and nitroglycerini4 •32 induce apparent shifts in left ventricular diastolic compliance curves. Vasopressor; inotropic,J4·28 and p-blocking agents33 may also alter left ventricular compliance. The mechanisms of the effect of these agents on left ventricular compliance has not been fully elucidated. For instance, nitroglycerin has been alternately shown to change compliance by producing a shift of the pressure-volume curve (ie, a change in the modulus of chamber stiffness)32 or by producing movement along a single pressure-volume curve. 29 In different patients, therefore, equivalent changes in a measure of LVEDP following administration of nitroglycerin may be associated with quite different changes in left ventricular end-diastolic filling and hence preload. Ventricular Interdependence
The left ventricular pressure-volume curve is affected not only by the intrinsic state ofthe myocardium and by acute pharmacologic interventions, but also by the state of right ventricular filling. Since the two ventricles are physically coupled by the interventricular septum and by the constraining pericardium, the end-diastolic pressure-volume curve of either ventricle is dependent upon the diastolic volume of the othe!: 23 Any factor which increases right CHEST I 89 I 3 I MARCH, 1986
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ventricular filling results in a leftward shift of the left ventricular end-diastolic pressure-volume curve. Thus, disease states associated with abnormally increased right ventricular preload (eg, acute pulmonary hypertension) have also been associated with evidence for impaired left ventricular compliance. 12 Further; as right ventricular preload is directly related to right ventricular afterload,12 agents which alter right ventricular afterload may thereby affect left ventricular compliance. Indeed, the effect of a variety of pharmacologic agents on the left ventricular pressure-volu~e relationship may be mediated by this phenomenon of ventricular interdependence. For instance, nitroglycerin,31 angiotensin, and nitroprussidei4 have been reported to alter left ventricular compliance by their effect on right ventricular preload. The clinical implication of this relationship between the left and right ventricles is that the administration of vasoactive drugs may alter the LVEDP without parallel changes in the LVEDV: Under such circumstances, changes in the PAoP may not reflect parallel changes in the left ventricular preload. Alterations in the measured PAoP may reflect a shift in the left ventricular pressure-volume relationship rather than a change in the LVEDV (Fig 5). Jurtacardiac Pressure and Left Ventricular Filling The distending pressure resulting in left ventricular diastolic filling is the difference between the simultaneous intracavitary pressure and the pericardial or juxtacardiac pressure. Figure 6 demonstrates that a true increase in left ventricular preload may not be apparent from a measured change in the LVEDP if the pericardia! pressure is not held constant. The pericardial pressure is directly related to the right atrial pressure (RAP). In fact, a linear relationship exists between the RA~ or the RVED~ and the pericardial pressure.lI.3t This relationship accounts, in part at 432
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FIGURE 6. The increase in left ventricular filling represented by points A-+B is not apparent from the measured intracavitary LVEDP which has actually de...... 0-0--_--J creased from A to B. The discrepancy is a function ofthe change in pericardial pressure (PP) between the two points.
least, for the reported effect of vasoactive drugs on the left ventricular end-diastolic pressure-volume curve. For instance, the venodilating effect of nitroglycerin reduces the RVED~ and hence, the pericardial pressure. With this reduced constraining pressure, the intracavitary LVEDP-LVEDV curve will be rightshifted without any change in the inherent stiffness properties of the left ventricle. 32 Pericardial tamponacJe is associated with an increase in the pericardial pressure, and hence, an alteration of the intracavitary LVEDP to LVEDV relationship.34 Perhaps of greater clinical significance, however; is the effect of an elevated intrathoracic pressure (particularly in association with positive pressure ventilation and PEEP) on juxtacardiac pressure, and hence, upon the intracavitary pressure-volume relationship of the left ventricle. Although it is beyond the scope of this paper to discuss the effects of positive pressure ventilation and the use of PEEP on the clinical assessment of left ventricular filling in any detail, several observations are pertinent. First, the assessment of left ventricular filling is best performed at end-expiration at which point the effect of alterations in respiration-induced intrathoracic pressure are minimized. 16 Secondly, a variable proportion ofapplied PEEP will be transmitted to the pericardium, depending upon pulmonary compliance;35 this variable, therefore, needs to be considered when trying to extrapolate an index of left ventricular preload from a measured PAoE This concern is especially relevant at higher levels of PEEE Although an assessment of juxtacardiac pressure is available from a measured pleural pressure36 or from a measured esophageal pressure in the lateral position, 37 each of these has its limitations and neither is utilized with frequency. Momentary discontinuation of the PEEP has been advocated38 to exclude its effect on the LVED~ but this maneuver is hazardous since it may precipitate profound hypoxia. Moreover, it may not Misled by the wedge? (Raper, S1bbald)
provide any useful information concerning the actual hemodynamic events operative when the PEEP is being applied. A more approximate, but potentially less dangerous, estimate of juxtacardiac pressure can be obtained by considering airway pressure and pulmonary compliance;15 the greater the pulmonary compliance, the greater is the effect of applied PEEP on the juxtacardiac pressure. Finally, a simple estimate of the juxtacardiac pressure as approximately 50 percent of the applied PEEP has also been suggested. 39 CUNICAL IMPLICATIONS
It is apparent from the preceding discussion that the measured PAoP may not provide a reliable guide to the state of left ventricular preload. How, then, can the Swan-Ganz catheter be used to guide and monitor therapy in the critically-ill patient? In general, this requires the development of therapeutic goals in individual patients based upon an appreciation of the expected physiologic response of the cardiovascular system to the specific disease process, and the careful assessment of therapeutic interventions with a view to such goals. The management ofthe critically-ill patient most commonly involves the optimization of oxygen transport to match concurrent systemic oxygen demand, at the minimum physiologic cost to the patient. The Swan-Ganz catheter provides a measure of the LVED~ a major determinant of fluid flux across the pulmonary microvascular bed. It also enables the convenient measurement of cardiac output, the major clinical determinant ofoxygen transport, and by enabling the sampling of mixed venous blood for the assessment of oxygen saturation, provides an index of the balance between total body oxygen supply and demand. Having decided that oxygen transport is not adequate and that cardiac output should be augmented to improve oxygen transport, an appropriate therapeutic plan can be instituted and its effect on the pretreatment goals assessed. In this context, preload augmentation, either by fluid administration or by the use of vasoactive drugs which might improve left ventricular compliance may be appropriate. For instance, if the measured PAoP is low and if pulmonary edema is not a major concern, then fluid administration to increase stroke volume by the Frank-Starling mechanism may be an appropriate first step; if noncardiac pulmonary edema is of clinical relevance, the level of the PAoP accepted is usually lower than in the setting of cardiaG pulmonary edema. Alternatively, if the PAoP is elevated and further fluid infusion might simply result in an increase in the PAoP without any significant increase in the preload, therapeutic manipulation of the compliance characteristics of the ventricle might be considered; vasodilating agents such as nitroglycerin, for instance, may improve left ventricular compliance
potentially resulting in a larger left ventricular preload at a lower LVEDE In neither situation is the effect of such intervention on left ventricular preload entirely predictable; the net effect can, however, usually be surmized from resultant changes in the measured stroke volume. The optimal left ventricular preload is that which results in adequate oxygen transport with a reasonable heart rate and the lowest possible PAoE Clinical situations in which a higher PAoP will be required to subserve adequate oxygen transport (eg, left ventricular hypertrophy or ischemia) can often be suspected from the medical workup. Nevertheless, the level of PAoP which corresponds to optimal left ventricular preload can only be determined by sequentially assessing the effects of acute hemodynamic interventions on the determinants of systemic oxygen transport, and may in fact vary over time in any particular patient. Finally, organ imaging using radionuclide angiography or two-dimensional echocardiography, in conjunction with hemodynamic assessment using the Swan-Ganz cathetet; enables a considerably more detailed assessment of biventricular function. Apart from its research value, such assessment may provide a useful guide to therapeutic intervention, especially in more difficult patients. It does not, however, negate the need to assess the effects of hemodynamic interventions with regard to the prestated therapeutic goals. CONCLUSION
The Swan-Ganz catheter is, then, a relatively simple device which, with careful attention to the mechanics of pressure measurement, will reliably and reproducibly measure pressure. In that sense, the device cannot be said "not to work." The clinical challenge lies in interpreting the measurement so obtained, and in extrapolating from it to an assessment of left ventricular preload. Many artifacts may be introduced into the system, negating the relationship between the PAoP and the intracavitary LVEDE Even when these artifacts are removed, however, and a reliable measure ofthe LVEDP is thus obtained, extrapolation ofa PAoP to the LVEDV is clinically unreliable. The proper use of the Swan-Ganz catheter demands a knowledge of the assumptions involved, a careful consideration of the variables previously discussed, particularly the effects of altered left ventricular transmural pressure and left ventricular compliance, and careful monitoring of hemodynamic interventions with a view to welldefined therapeutic goals. REFERENCES
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RM, Sperelakis N, Geiger SR, eds. Handbook ofphysiology: the cardiovascular system. Bethesda, MD: American Physiological Society, 1979: 533-80 Swan HJC, Ganz W, Forrester J, Marcus H, Diamond G, Chonette D. Catheterization of the heart in man with use of a flowdirected balloon-tipped catheter. N Eng) J Med 1970; 283:447-51 Fitzpatrick GF, Hampson LG, Burgess JH. Bedside determination of left atrial pressure. CMAJ 1972; 106:1293-98 Batson GA, Chandrasekhar Payas Y, Rikards DF: Measurement of pulmonary wedge pressure by the How-directed SwanGanz catheter. Cire Res 1972; 6:748-52 Parmley ww, 1ll1bot L. Heart as a pump. In: Berne RM, Sperelakis N, Geiger SR, eds. Handbook of Physiology. The Cardiovascular System. Bethesda, MD: American Physiological Society, 1979: ~ Cann M, Stevenson 'I: Fiallos E, ThaI ~ Depressed cardiac performance in sepsis. Surg Gynecol Obstet. 1972; 134:759-63 Weisel RD, Vito L, Dennis RC, Valeri R, Hechtman HB. Myocardial depression during sepsis. Am J Surg 1977; 133: 512-21 Manny J, Grindlinger GA, Dennis RC, Weisel RD, Hechtman RB. Myocardial performance curves as guide to volume therapy. Surg Gynecol Obstet 1979; 149:863-73 1.Dzman}; Powers SR, Older 1: Dutton RE, Roy RJ, English N, et ale Correlation ofpulmoriary wedge and left atrial pressures: a study in the patient receiving positive end-expiratory pressure ventilation. Arch Surg 1974; 109:270-76 Horton ~ Coin D, Mitchell JH. Left ventricular volumes and contractility during hemorrhagic hypOtension: dimensional analysis and biplane cineHuorography. Cire Shock 1983; 11:73-83 Sibbald WJ, Driedger AA, Myers ML, Short AIK, Wells GA. Biventricular function in the adult respiratory distress syndrome: hemodynamic and radionuclide assessment, with special emphasis on right ventricular function. Chest 1983; 84:126-34 Gardner RM. Direct blood pressure measurement: dynamic response requirements. Anesthesiology 1981; 227-36 Abrams JH, Olson ML, Marino]A, Cerra FB. Use of a needle valve variable resistor to improve invasive blood pressure monitoring. Crit Care Med 1984; 12:978-82 O'Quin R, Marini JJ. Pulmonary artery occlusion pressure: clinical physiology, measurement and interpretation. Am Rev Respir Dis 1983; 128:319-26 Berryhill RE, Benumoff JL, Rauscher LA. Pulmonary venous pressure reading at the end of exhalation. Anesthesiology 1978; 49:365-68 Shin B, McAslan TC, Ayella RJ. Problems with measurement using the Swan-Ganz catheter. Anesthesiology 1975; 43:474-76 West JB, Dollery Cl: Naimark A. Distribution of blood How in isolated lung; relation to vascular and alveolar pressures. J Appl Physioll964; 19:713-24 Tooker J, Huseby J, Butler J. The effect of Swan-Ganz catheter height on the wedge pressure-left abial pressure relationship in edema during positive-pressure ventilation. Am Rev Respir Dis 1978; 117:721-25 Kronberg GM, Quan SF, Schlobohm RM, Lindauer JM, Goodman PC. Anatomic location of the tips of pulmonary-artery
n
catheters in supine patients. Anesthesiology 1979; 51:467-69 21 Smith HC, Butler J. Pulmonary venous waterfall and perivenous pressure in the living dog. J Appl Physioll975; 38:304-08 22 Rahimtoola SHe Left ventricular end-diastolic and filling pressure in assessment ofventricular function. Chest 1973; 63:858-60 23 Weber n Janicki JS, ShroffS, Fishman AE Contractile mechanics and interaction of the right and left ventricles. Am J Cardiol 1981; 47:686-95 . 24 Alderman EL, Glantz SA. Acute hemodynamic interventions shift the diastolic pressure-volume curve in man. Circulation 1976; 65:662-71 25 Templeton GH, Wildenthal K, Willerson JR, Reardon WC. Influence oftemperature on the mechanical properties of cardiac muscle. Circ Res 1974; 34:624-34 26 Templeton GH, Mitchell JH, Wildenthal K. Influence of hyperosmolality on left ventricular stiffness. Am J Physiol 1972; 222:1406-11 27 Janicki JS, Weber lIT Factors influencing the diastolic pressure-volume relation of the cardiac ventricles. Fed Proc 1980; 39:133-40 28 Sonnenblink EH, Ross J Jr, Covell IN, Braunwald E. Alterations in resting length-tension relations of cardiac muscle induced by changes in contractile force. Circ Res 1966; 19:980-88 29 Gaasch WH, Levine HJ, Quinones MA, Alexander JK. Left ventricular compliance: mechanisms and clinical implications. Am J Cardiol 1976; 38:645-53 30 Barry WH, Brooker JZ, Alderman EL, Harrison DC. Changes in diastolic stiffness and tone of the left ventricle during angina pectoris. Circulation 1974; 49:255-63 31 Crexells C, Chatterjee K, Forrester JS. Optimal level of filling pressure in the left side of the heart in acute myocardial infarction. N Eng} J Med 1973; 289:1263-66 32 Smith ER, Smiseth OA, Kingma I, Manyari D, Belenkie I, 1Yberg ~ Mechanism of action of nitrates: role of changes in venous capacitance and in the left ventricular diastolic pressurevolume relation. Am J Med 1984; 76:14-21 33 Coltart DJ, Alderman EL, Robison SC, Harrison DC. Effect of propranolol on left ventricular function, segmental wall motion and diastolic pressure-volume relation in man. Br Heart J 1975; 37:357-64 34 Reddy PS, Curtiss EL, Oloole JD, Shaver JA. Cardiac tamponade: Hemodynamic observations in man. Circulation 1978; 58:265-72 35 Wallis ~ Robotham JL, Compean R, Kindred MK. Mechanical heart-lung interaction with positive end-expiratory pressure. J Appl Physioll983; 54:1039-47 36 Downs JB. A technique for direct measurement of intrapleural pressure. Crit Care Med 1976; 4:207-10 37 Jardin F, Farcot JC, Boisante L, Curien N, Margairaz A, BoUl'darias J-E Influence of positive end-expiratory pressure on left ventricular performance. N Eng} J Med 1981; 304:387-92 38 Archer G, Cobb A. Long term pulmonary artery pressure monitoring in the management of the critically ill. Ann Surg 1974; 180:747-52 39 Boysen PG. Hemodynamic monitoring in the adult respiratory distress syndrome. Coo Chest Med 1982; 3:157-69
Misled by the Wedge? (Raper, SibbaJd)
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Misled by the Wedge?* The Swan-Ganz Catheter and Left Ventricular Preload R. Raper, M.B., B.S.;t and William]. Sibbald, M.D.,
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assessment of left ventricular preload by the PAoE WHAT IS THE PAoP?
*From the Critical Care/'Ii'auma Unit, Victoria Hospital, London, Canada. tChief Resident. *Coordinator, Critical Careffiauma Unit;. Ass~iate Professo! of Medicine and Coordinator of the Program m Cntical Care, UnIversity of Western Ontario, London, Canada. This work was supported by a grant from the Ontario Heart Association (No. 310). Reprint requests: Dr. Sibbald, Victoria Hospital Corporation, PO 85375, London, Ontano, Canada N6A-4G5
The clinical use of a Hotation device for right heart catheterization was first reported by Swan et aP in 1970. This group described the safe introduction of a Hexible, balloon-tipped, How-directed catheter into the pulmonary artery, the measurement of the downstream pressure in the balloon-occluded pulmonary artery segment, and the correlation between this pressure, the PAoE and the pulmonary wedge pressure (PWP) measured with the more rigid, traditional right heart catheter formally wedged into a small pulmonary vessel. Subsequently, direct correlations between the PAoP and the fWE and b~tween the PAoP and the LAP have been confirmed. 4•5 Since the mean LAP correlates well with the LVEDJ>6 in the healthy heart, the PAoP has become a common measure of left ventricular filling for both clinical and research purposes. In fact, alterations in left ventricular contractility have been inferred by analysis of changes in the Frank-Starling relationship in which the PAoP was used as the measure of left ventricular preload. 7-9 Recently, however, important limitations ofpressure measurements obtained using right heart catheters have become apparent. For a variety of technical and pathophysiologic reasons, the PAoP may not adequately reflect the LVEDE and the LVEDP may bear little relationship to the LVED\z In early studies, Lozman et allO demonstrated a good correlation tween the mean PAoP and the LAP in postoperative surgical patients, although this correlation was lost at higher levels of positive end-expiratory pressure (PEEP) in ventilated patients. Subsequently, Horton et alll found that the LVEDP did not adequately reflect changes in the LVEDV in a model of hemorrhagic hypotension in dogs. ~rom clinical studies, we also have reported significant discrepancies between the LVEDP and the LVED~ 12 To emphasize this point, we have compared tlle PAoP with the LVEDV in patients with acute respiratory insufficiency and varying de(Fig 1). 12 The PAoP in grees ofpulmonary hypertensio~ these patients was measured with a Swan-Ganz catheter, while the LVEDV was calculated from a simultaneously measured thermodilution cardiac output and a radionuclide LV ejection fraction (LVEDVI = stroke
flotation pul?:~nary artery quantum leap In the physiologic information available fo~ the management of critically-ill patients. Pre-existing suppositions that the central venous pressure (CVP) provided a reliable indication of left ventricular preload, and that changes in .the CVP would reflect parallel changes in left ventricular filling pressures, were quickly dispelled. 1 Clinical studies identified wide disparities between the CVP and the pulmonary artery occlusion pressure (PAoP), both in terms of the absolute magnitude of these pressures, as well as in their direction of change with acute hemodynamic intervention. The SwanGanz catheter was considered to provide, at last, the clinical means for a frequent and reliable assessment of the left ventricular preload. As we will define, however, this may not always be the case. Although the PAoP obtained with the Swan-Ganz catheter generally provides a reliable index of the mean left atrial (LAP), and hence, of the left ventricular end-diastolic (LVEDP) pressures, for a variety oftechnical and physiologic reasons, it does not always do so. More importantly, this extrapolated measurement of the LVEDP does not provide a reliable index of either the left ventricular end-diastolic volume (LVEDV) or the left ventricular end-diastolic dimension (LVEDD), both of which are more reliable clinical measures of the left ventricular preload than is the LVEDE 2 Several factors combine to negate any relationship between the LVEDP and the LVED\z These include the inherent stiffness properties of the myocardial fibers, the thickness of the myocardium, and the effect of changes in the pressure surrounding the cardiac chambers. In this review, we will briefly in examine some of the common pitfalls encoun~ered the measurement of the PAoP and in the extrapolation of the measured PAoP to an assessment of left ventricular preload. We will particularly emphasize the effect of altered left ventricular compliance on the ~,e
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volume index/ejection fraction). In Figure 2, we have also plotted the LVEDV against the PAoP for three patients at various stages of an acute illnesss. From these two figures, it is apparent that the PAoP must be regarded as ap unreliable clinical index of the LVED~ both in large patient groups as well as in individual patients sequentially assessed over time. For the LVEDV to be inferred from the measured PAo~ several assumptions are inherent: the PAoP must be accurately measured, the PAoP must reflect the LA~' the LAP must reflect the LVEDP and the LVEDP must relate directly to the LVEDV: In clinical p~ctice, errors may be encountered at each step ofthis progression, thus invalidating the primary inference. MEASUREMENT OF THE
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The Swan-Ganz catheter is a relatively simple device consisting of a Hqid-filled central lumen with an inHatable balloon proximal to its tip. Recent modifications involving the addition of proximal ports for buusion apd pressure measurement, electrodes for cardi~c pacing, and thermistors for measurement of the cardiac output and the right ventricular ejection ~tion have not altered the basic concept of the original cathetet: Since the frequency and rate of pressure change within the pulmonary artery is too great to be reliably reproduced by water column manometry, as was originally employed for CVP monitoring, the Swan-Ganz catheter must be coupled to an electronic measuring system by a transducer. While it is beyqnd the scope of this article to provide a detailed review of the limitations of the electronic assessment of dynamic pressures, these cannot be dismissed lightly. The inherent underdamping of even a well-functioning system13
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renders measurement of systolic and diastolic pressures unreliable. The use of variable resistors within the circuit apparently permits optimization of the damping characteristics of the system, and hence, more accurate pressure measurement;14 at this time, however, these are not in common clinical use. The unselective nature of time-based electrical sampling and averaging may render digital displays unreliable; graphic displays are mandatory if any respiratory artifact is to be excluded. Figure 3 demonstrates the limitations of digital display units and time-based averaging. Although more sophisticated electronic algorithms are available, the tachypneic patient on an intermittent mandatory ventilation circuit may well confound even these. When Does the PAoP not Reflect the LAP? The problems of electronic pressure measurement, inherent to all systems, have been reviewed elsewhere. 15 Even when such problems are minimized, the measured PAoP may not adequately reflect the LA~ and hence, the LVEDE The potential difficulties involved in estimating the LVEDP and the left ventricular preload from the measured PAoP are as follows: incorrect catheter placement; incorrect transducer placement; incorrect transducer calibration; pressure overdamping or underdamping; respiratory pressure artifact; eccentric balloon occlusion and overwedging; nonzone III balloon occlusion; pulmonary venous obstruction; valvular heart disease; increased pericardial pressure; and altered left ventricular compliance. Accurate measurement of the PAoP depends on correct positioning of the catheter within the pulmonary artery, careful placement of the transducer such that its fluid column is at the level of the left atrium, and accurate calibration of the transducer at that level Misled by the VVedge? (Raper, Si/;JbaJd)
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so that it reliably assesses pressures within the anticipated range. the traditional reference point for the left atrium is the fourth intercostal space in the midaxillary line; the proper position of the catheter within the pulmonary vasculature should be confirmed by pressure wave monitoring and chest roentgenography. IS The system must be fully purged ofair to prevent overdamping, and as previously mentioned, a graphic display is preferred to allow measurement ofpressures at end-expiration when the effects of superimposed respiratory variations on intrathoracic pressures are minimized. 16 With these prerequisites fulfilled, the measured PAoP may still not reliably reBect the LAE Eccentric balloon inBation and "over-wedging" have been described. 17 Both complications are easily recognized by the steady rise in pressure observed as a consequence of the continuous Bush devices employed to maintain catheter patency; repositioning of the catheter is mandatory in this situation. More difficult to appreciate is the occlusion of the pulmonary artery in a segment oflung where the pulmonary venous pressure does not exceed the alveolar pressure (West's non-zone III). 18 With catheter placement above the level of the left atrium, animal studies have demonstrated that the PAoP reBects changes in alveolar pressure rather than in the LAP;19 the same is likely true in humans. 10 Since Swan-Ganz catheters are Bow-directed, they should migrate to regions of greatest blood Ho~ specifically West's zone III. This is usually, but not universally, true. iO Non-zone III catheter migration may be recognized by observing the effects ofsudden increments or decrements of PEEP on the measured PAoP: if the PAoP changes by more than 50 percent ofthe change in applied PEE~ it is likely that the catheter tip is in a non-zone III position. If this is so, the catheter should then be repositioned. IS The incidence of non-zone III placement of the catheter can be expected to be
greatest when the LAP is low, when alveolar pressure is elevated by the use of PEE~ or in the presence of airways obstruction. Another potential source of disparity between the PAoP and the LAP is the presence of pulmonary venous obstruction. Apart from functional obstruction within the pulmonary microcirculation in non-zone III regions of the lung, this is probably a rare occurrence; it may be seen with fixed lesions such as tumours, atrial myxomas, mediastinal fibrosis and pulmonary venous thrombosis. IS Compression of the pulmonary venous system in low Bow states or as a consequence of increased intrathoracic or pericardial pressures has also been suggested,18.21 although the clinical significance of this remains uncertain. When Does the LAP Not Reflect the LVEDPP
Even when the measured PAoP accurately assesses the LA~ it may not provide a reliable measure of the LVEDP. Discrepancy between the LAP and the LVEDP is, for example, characteristic of mitral valve disease. Mitral stenosis results in a diastolic pressure gradient between the left atrium and the left ventricle, while mitral regurgitation allows the back transmission of ventricular systolic pressures. This back-transmission of the systolic pressure elevates the mean LAP above the diastolic LA~ and hence above the LVEDE This may be recognized from a graphic pressure display by identification of exaggerated CCV" waves; when present, the "a" wave on the LAP or PAoP trace may be used to estimate the LVEDE Conversely, aortic regurgitation may cause the LVEDP to exceed the LAP and hence the PAoP; premature mitral valve closure and continued left ventricular filling from the aorta may result in an end-diastolic pres"' sure gradient between the left ventricie and the left atrium. Disparity between the LAP and the LVEDP is, CHEST I 89 I 3 I MARCH, 1986
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perhaps, more commonly observed in the presence of impaired left ventricular compliance. The enddiastolic atrial "kick" is exaggerated when the left ventricle is abnormally stiff and atrial contraction may then substantially increase both the LVEDV and the LVED~ while having a significantly lesser effect on the mean LAE In such a situation, the "a" wave of the PAoP tracing will again provide a more reliable assessment of the LVEDP than will the mean PAoE2l.22 RELATIONSHIP BElWEEN THE LVEDP AND THE LVEDV Despite the difficulties and potential inaccuracies previously described, in most clinical circumstances, the PAoP does provide a reliable measure of the It does not, howevet; reflect intracavitary LVED~4.5 the left ventricular preload. As preload is the enddiastolic distending force of the ventricle, i3 and as this correlates better with the LVEDV or the LVEDD than with the LVED~2 to reliably reflect left ventricular preload, the PAoP must reliably correlate with the LVEDV or the LVEDD. Since no such correlation exists in both animalll and human studies (Fig 1 and 2), J4 the PAoP cannot be considered an acceptable clinical measure of the left ventricular preload. Several factors combine to distort the previously assumed direct relationship between the LVEDP and the LVED\z Those include variations in the stiffness properties of the left ventricular myocardium, the pressure surrounding the cardiac chambers, and the diastolic volume of the right ventricle. Clinically, where only the intracavitary LVEDP is commonly assessed, increased juxtacardiac pressure will result in an increase in the measured LVEDP for any given chamber volume without any change in the characteristics of the myocardium. When ventricular volumes are also assessed, this may result in a false assumption
of increased myocardial stiffness. Myocardial stiffness is ideally assessed by relating the measurement of the chamber volume to the simultaneous transmyocardial filling pressure, rather than to the intracavitary filling pressure.
Left Ventricular Compliance In a steady state, the relationship between the enddiastolic transmyocardial filling pressure and the enddiastolic volume of the left ventricle is curvilinear (Fig 4 and 5). Ventricular compliance is defined by the instantaneous relationship between the ventricular end-diastolic volume and pressure, and is mathematically expressed as the slope of the tangent to the diastolic pressure-volume curve (dv/dp). Ventricular compliance is the inverse of chamber stiffness. Changes in left ventricular compliance may result from changes in the level ofleft ventricular filling, involving a shift along a single diastolic pressure-volume curve. Changes in left ventricular compliance may also result from changes in the inherent stiffness properties ofthe myocardium, represented by a shift of the pressurevolume curve and defined by a change in the modulus of chamber stiffness. Figure 4 demonstrates the effect of altered left ventricular filling on left ventricular compliance. Since the pressure-volume curve is non-linear, an equivalent increase in volume (4V) will produce a greater increase in pressure when the ventricle is relatively distended {4PJ than when it is relatively empty {4PJ. This change in left ventricular compliance does not imply any alteration in the inherent stiffness properties ofthe ventricle since the modulus of chamber stiffness remains unchanged. By contrast, Figure 5 depicts a hypothetical family of compliance curves and demonstrates the second mechanism responsible for an alteration of left
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FIGURE 5. A family of diastolic pressure-volume curves for the left ventricle. A measure ofLVEDP may represent quite different states ofleft ventricular filling depending on compliance (AI' At, AJ. Also, an increase in PAoP may indicate either a change in left ventricular compliance without any change in left ventricular filling (At-+ BJ or may indicate a true increase in left ventricular filling (At-+ BJ.
Misled by the VVedge? (Raper, SlbbaJd)
ventricular compliance, a change in the stiffness properties of the left ventricle. From this figure, two observations are important. First, a measure of the LVEDP may represent quite different states of left ventricular filling, and hence, of left ventricular preload (points Ab At, A3). Second, an increase in the LVEDP (points A-+B) may indicate an increase in when the modulus of chamber preload (points ~-+BJ stiffness is unchanged, or may reflect a change in the modulus of chamber stiffness without any concurrent change in the LVED~ and hence, in the left ventricular preload (points At-+BJ. the principle determinants of left ventricular compliance are left ventricular preload, left ventricular mass, myocardial fiber stiffness, and right ventricular end-diastolic volume. Left ventricular compliance may also be affected by temperature,25 osmolality,26 and heart rate;27 within the usually en,countered range in clinical practice, the effect of ~ese variables is sufficiently minute to be discounted. The diastolic myocardial perfusion gradient may also alter ventricular compliance;27 unless myocardial ischemia results, howeve!; this mechanism seems also to be of minimal clinical significance. Increased systolic pressure is associated with a right-shift of the end-diastolic pressure-volume curve.9:1 This may explain the observed effect of exogenous catecholamines on left: ventricular compliance,28 an effect not seen with catecholamines when the blood pressure is controlled. Neither the mechanism nor the clinical significance of this effect is known. The effect of left ventricular preload on left ventricular compliance is evident from Figure 4, as well as from the previous discussion. This is clinically apparent when administration of a small volume of fluid is accompanied by a significant increase in the measured PAo~ all other variables remaining normal. Regardless of the absolute left-ventricular preload in this clinical situation, the instantaneous end-diastolic pressure-volume (compliance) curve must reflect a poorly compliant ventricle. This is an important clinical observation since further fluid administration will have little effect on ventricular preload, and hence, by the Frank-Starling mechanism, on left ventricular output. Instead, continued fluid infusion may dramatically increase the LVED~ and hence, the propensity for the development of pulmonary edema on a hydrostatic basis. H augmentation of cardiac output remains desirable in such a clinical situation, it would be more appropriate to administer agents designed to either increase the inotropic state of the myocardium or to reduce the modulus of chamber stiffness. Alterations in the modulus of chamber stiffness are seen in both acute and chronic disease states as well as with acute hemodynamic interventions. For instance,
left ventricular hypertrophy may result in a decrease in left ventricular co.mpliance due to an increase in the modulus of chamber stiffness. 29 Conversely, chronic left ventricular dilatation results in enhanced left ventricular compliance. 29 These effects are largely mediated by changes in the end-diastolic volume to mass ratio and probably do not reflect changes in individual myocardial fiber stiffness. Acute myocardial ischemia,30 myocardial fibrosis, and infiltrative processes such as amyliodosis, may aiso effect an increase in the moduhis of chamber stiffness; this appears mediated by changes in individual myocardial fiber stiffness rather than by any increase in myocardial mass. The clinical implication of such alterations in compliance is apparent from studies of the hemodynamic management of acute myocardial infarction where optimal left ventricular filling usually requires a higher LVEDP than would be considered necessary in the normal heart. 31 Many of the factors which may potentially influence left ventricuiar compliance can often be anticipated froin the clinical history, physical examination, and standard investigative procedures such as electrocardiography and chest roentgenography. However, alterations in left ventricular compliance may also result from a variety of hemodynamic interventions commonly employed in the management of the criticallyill. These are more difficult to anticipate and to consider when attempting to estimate left ventricular preload from a measure of the LVEDE Vasoactive drugs such as nitroprusside and nitroglycerini4 •32 induce apparent shifts in left ventricular diastolic compliance curves. Vasopressor; inotropic,J4·28 and p-blocking agents33 may also alter left ventricular compliance. The mechanisms of the effect of these agents on left ventricular compliance has not been fully elucidated. For instance, nitroglycerin has been alternately shown to change compliance by producing a shift of the pressure-volume curve (ie, a change in the modulus of chamber stiffness)32 or by producing movement along a single pressure-volume curve. 29 In different patients, therefore, equivalent changes in a measure of LVEDP following administration of nitroglycerin may be associated with quite different changes in left ventricular end-diastolic filling and hence preload. Ventricular Interdependence
The left ventricular pressure-volume curve is affected not only by the intrinsic state ofthe myocardium and by acute pharmacologic interventions, but also by the state of right ventricular filling. Since the two ventricles are physically coupled by the interventricular septum and by the constraining pericardium, the end-diastolic pressure-volume curve of either ventricle is dependent upon the diastolic volume of the othe!: 23 Any factor which increases right CHEST I 89 I 3 I MARCH, 1986
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ventricular filling results in a leftward shift of the left ventricular end-diastolic pressure-volume curve. Thus, disease states associated with abnormally increased right ventricular preload (eg, acute pulmonary hypertension) have also been associated with evidence for impaired left ventricular compliance. 12 Further; as right ventricular preload is directly related to right ventricular afterload,12 agents which alter right ventricular afterload may thereby affect left ventricular compliance. Indeed, the effect of a variety of pharmacologic agents on the left ventricular pressure-volu~e relationship may be mediated by this phenomenon of ventricular interdependence. For instance, nitroglycerin,31 angiotensin, and nitroprussidei4 have been reported to alter left ventricular compliance by their effect on right ventricular preload. The clinical implication of this relationship between the left and right ventricles is that the administration of vasoactive drugs may alter the LVEDP without parallel changes in the LVEDV: Under such circumstances, changes in the PAoP may not reflect parallel changes in the left ventricular preload. Alterations in the measured PAoP may reflect a shift in the left ventricular pressure-volume relationship rather than a change in the LVEDV (Fig 5). Jurtacardiac Pressure and Left Ventricular Filling The distending pressure resulting in left ventricular diastolic filling is the difference between the simultaneous intracavitary pressure and the pericardial or juxtacardiac pressure. Figure 6 demonstrates that a true increase in left ventricular preload may not be apparent from a measured change in the LVEDP if the pericardia! pressure is not held constant. The pericardial pressure is directly related to the right atrial pressure (RAP). In fact, a linear relationship exists between the RA~ or the RVED~ and the pericardial pressure.lI.3t This relationship accounts, in part at 432
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least, for the reported effect of vasoactive drugs on the left ventricular end-diastolic pressure-volume curve. For instance, the venodilating effect of nitroglycerin reduces the RVED~ and hence, the pericardial pressure. With this reduced constraining pressure, the intracavitary LVEDP-LVEDV curve will be rightshifted without any change in the inherent stiffness properties of the left ventricle. 32 Pericardial tamponacJe is associated with an increase in the pericardial pressure, and hence, an alteration of the intracavitary LVEDP to LVEDV relationship.34 Perhaps of greater clinical significance, however; is the effect of an elevated intrathoracic pressure (particularly in association with positive pressure ventilation and PEEP) on juxtacardiac pressure, and hence, upon the intracavitary pressure-volume relationship of the left ventricle. Although it is beyond the scope of this paper to discuss the effects of positive pressure ventilation and the use of PEEP on the clinical assessment of left ventricular filling in any detail, several observations are pertinent. First, the assessment of left ventricular filling is best performed at end-expiration at which point the effect of alterations in respiration-induced intrathoracic pressure are minimized. 16 Secondly, a variable proportion ofapplied PEEP will be transmitted to the pericardium, depending upon pulmonary compliance;35 this variable, therefore, needs to be considered when trying to extrapolate an index of left ventricular preload from a measured PAoE This concern is especially relevant at higher levels of PEEE Although an assessment of juxtacardiac pressure is available from a measured pleural pressure36 or from a measured esophageal pressure in the lateral position, 37 each of these has its limitations and neither is utilized with frequency. Momentary discontinuation of the PEEP has been advocated38 to exclude its effect on the LVED~ but this maneuver is hazardous since it may precipitate profound hypoxia. Moreover, it may not Misled by the wedge? (Raper, S1bbald)
provide any useful information concerning the actual hemodynamic events operative when the PEEP is being applied. A more approximate, but potentially less dangerous, estimate of juxtacardiac pressure can be obtained by considering airway pressure and pulmonary compliance;15 the greater the pulmonary compliance, the greater is the effect of applied PEEP on the juxtacardiac pressure. Finally, a simple estimate of the juxtacardiac pressure as approximately 50 percent of the applied PEEP has also been suggested. 39 CUNICAL IMPLICATIONS
It is apparent from the preceding discussion that the measured PAoP may not provide a reliable guide to the state of left ventricular preload. How, then, can the Swan-Ganz catheter be used to guide and monitor therapy in the critically-ill patient? In general, this requires the development of therapeutic goals in individual patients based upon an appreciation of the expected physiologic response of the cardiovascular system to the specific disease process, and the careful assessment of therapeutic interventions with a view to such goals. The management ofthe critically-ill patient most commonly involves the optimization of oxygen transport to match concurrent systemic oxygen demand, at the minimum physiologic cost to the patient. The Swan-Ganz catheter provides a measure of the LVED~ a major determinant of fluid flux across the pulmonary microvascular bed. It also enables the convenient measurement of cardiac output, the major clinical determinant ofoxygen transport, and by enabling the sampling of mixed venous blood for the assessment of oxygen saturation, provides an index of the balance between total body oxygen supply and demand. Having decided that oxygen transport is not adequate and that cardiac output should be augmented to improve oxygen transport, an appropriate therapeutic plan can be instituted and its effect on the pretreatment goals assessed. In this context, preload augmentation, either by fluid administration or by the use of vasoactive drugs which might improve left ventricular compliance may be appropriate. For instance, if the measured PAoP is low and if pulmonary edema is not a major concern, then fluid administration to increase stroke volume by the Frank-Starling mechanism may be an appropriate first step; if noncardiac pulmonary edema is of clinical relevance, the level of the PAoP accepted is usually lower than in the setting of cardiaG pulmonary edema. Alternatively, if the PAoP is elevated and further fluid infusion might simply result in an increase in the PAoP without any significant increase in the preload, therapeutic manipulation of the compliance characteristics of the ventricle might be considered; vasodilating agents such as nitroglycerin, for instance, may improve left ventricular compliance
potentially resulting in a larger left ventricular preload at a lower LVEDE In neither situation is the effect of such intervention on left ventricular preload entirely predictable; the net effect can, however, usually be surmized from resultant changes in the measured stroke volume. The optimal left ventricular preload is that which results in adequate oxygen transport with a reasonable heart rate and the lowest possible PAoE Clinical situations in which a higher PAoP will be required to subserve adequate oxygen transport (eg, left ventricular hypertrophy or ischemia) can often be suspected from the medical workup. Nevertheless, the level of PAoP which corresponds to optimal left ventricular preload can only be determined by sequentially assessing the effects of acute hemodynamic interventions on the determinants of systemic oxygen transport, and may in fact vary over time in any particular patient. Finally, organ imaging using radionuclide angiography or two-dimensional echocardiography, in conjunction with hemodynamic assessment using the Swan-Ganz cathetet; enables a considerably more detailed assessment of biventricular function. Apart from its research value, such assessment may provide a useful guide to therapeutic intervention, especially in more difficult patients. It does not, however, negate the need to assess the effects of hemodynamic interventions with regard to the prestated therapeutic goals. CONCLUSION
The Swan-Ganz catheter is, then, a relatively simple device which, with careful attention to the mechanics of pressure measurement, will reliably and reproducibly measure pressure. In that sense, the device cannot be said "not to work." The clinical challenge lies in interpreting the measurement so obtained, and in extrapolating from it to an assessment of left ventricular preload. Many artifacts may be introduced into the system, negating the relationship between the PAoP and the intracavitary LVEDE Even when these artifacts are removed, however, and a reliable measure ofthe LVEDP is thus obtained, extrapolation ofa PAoP to the LVEDV is clinically unreliable. The proper use of the Swan-Ganz catheter demands a knowledge of the assumptions involved, a careful consideration of the variables previously discussed, particularly the effects of altered left ventricular transmural pressure and left ventricular compliance, and careful monitoring of hemodynamic interventions with a view to welldefined therapeutic goals. REFERENCES
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Misled by the Wedge? (Raper, SibbaJd)