A nest hesiolo)l)' -17:455-4ti5, 1977

Medical Intelligence JOHN D. MICHENFELDER, M.D., Editor

A Critique of Flow-directed Pulmonary Arterial Catheterization

Nathan Leon Pace, M.D. •

IN I 9:13, Lategola and Rahn reported the use in clogs of a hand-fashioned, balloon-tipped, self'..guiding catheter for cardiac and pulmonary arterial cathe­terization and occlusion.• During the following 15 years, several self'..guiding right-heart catheters were developed for human use, but none was balloon­guicled, and none became well known. 2- 5 In 1970, Swan ,•t al. 0 reported I heir initial ex pcriencc with a 111ultih1111en, balloon-Lipped, radiopaquc, extruded pol}'\'inyl chloride catheter (with adequate frequency response) that met three criteria: I) reliable, prompt passage to the pulmonary artery, 2) minimal ar­rhythmias, and 3) passage without fluoroscopy. The catheter may be introduced either by cutdown or percutaneously in one of several veins (femoral, antecubital, axillary, subclavian, external jugular, proximal basilic or internal jugular). 1

1-1 11 Placement is optimally performed by continuous pressure moni­toring with electronic transduction and oscilloscopic display. 11- 13 After the catheter tip is advanced into the thorax (detected by respiratory fluctuations in the pressure trace), the balloon is inflated and the catheter is further advanced, relying on blood flow lo direct the catheter Lip through the tricuspid and pulmonic valves into the pulmonary artery. Details of tech­niques of cat hctcr passage and of care of the catheter arc straightforward and widely reprinted. 0,H-IH Since the initial report, a family of balloon-tipped catheters has been developed to allow: I) in-vivo oximetry, tu

2) pulmonary angiography,211 3) pediatric cardiac catheterization, 21 4) transvenous cardiac pacing, 22 5) His-bu ml le elcctrocardiogra ph y, 23 6) thermocl ii ution cardiac output dctcrmination,2' 1 and 7) artifact-free cardiac monitoring. 25

The catheter has been used in enormously diverse clinical situations. 7•11•14•211-:m In general, the indications

* Assistalll Professor, Department of Anesthesiology, Uni\'ersity of Utah College of i\leclidne, Salt Lake Cily, Utah tH 132.

Accepted for publication June 23, 1977.

455

for its use appear to be: I) continuous hcmoclynamic monitoring following complicated acute myocardial infarction, 2) managemclll of fluid balance in non­canliogenic pulmonary edema, in non-canliogenic shock, and following cardiopulmonary bypass, and 3) evaluation of therapeutic interventions with mechan­ical ventilation, vasoactive drugs, hemodialysis and assisted circulation. Swan has recommernled that a pulmonary-artery catheter should be used when one thinks that a central venous pressure (CVP) measure­ment is needcd. 37 Several review articles detailing Swan Ganz (S-G) catheter use are available. 17·a8-~ 2

This article critically examines certain limitations inherent in pulmonary arterial moniroring and dis­cusses its use in clinical anesthesia.

Pulmonary "Capillary" Pressure

Pulmonary "capillary" pressure refers to the pres­sure measured through a cardiac catheter impacted into a branch of the pulmonary artery in such a fashion that there is a free communication between the catheter tip and the capillary-venous compart­ment of the lung. This pressure has been called pulmonary wedge pressure (PWP), pulmonary-artery wedge pressure (PA WP), pulmonary capillary pres­sure (PCP), and more recently, pulmonary-artery occlusion pressure (PAOP). Three criteria ha\'e been thought necessary for a true wedge prcssure:~a I) blood withdrawn from wedge position should be fully saLUrated with oxygen, 2) the pulmonary-artery phasic contour should change Lo a left atrial trace on wedging, and 3) mean wedge pressme should be less than mean pulmonary arterial pressure; it has been observed that a wedged catheter blood sam pie may or may not be I 00 per cent oxygen-saturated in patients who have pulmonary shunts and during positive end-expiratory pressure (PEEP). 0•44·~5 Thus, only the latter two criteria now apply. 44 Initial studies in both animal and man confirmed the

456 NATIIAN L. !'ACF. AneMhf'!\h,1,,~­V •17, No !'i, N,w IH77

validity or the pulmonary-artery wedge pressure as an index or pulmonary venous pressure and left atrial pressure (LAP).43

Balloon-tipped and ordinary pulmonary-arterr catheters have been shown to give identical PAOP reaclings. 11 Whereas pulmonary-artery catheters without a balloon tip must be manually advanced to measure PAOP and then withdrawn, the S-G catheter requires onl)' intermittent inflation or the balloon to let blood flow pull the catheter tip out into a wedge position; tlrns, catheter manipulation is avoided and long-term monitoring becomes more feasible. Artifactual PAOP readings can be produced by an overinflated balloon occluding the catheter tip or an eccentrically inflated balloon not producing complete occlusion or the vessel lumen; inflating the balloon with the minimum volume of air sufficient to yield a PAOP trace and maintaining a central position or the catheter tip will avoid these prob­lcms:12,·1t1-4K Analysis of PAOP (by S-G) as a measure of' LAP has shown very good correlation in most st11clics.41H 1 LAP has also been estimated from meas­urements of' pulmonary arterial encl-diastolic pressure (PAEDP). PAEIW is usually only 1-2 torr higher than PAOP ancl LAP; however, in critically ill pa­tients, the correlation between PAEDP and PAOP is unreliable because of either pre-existing pulmonary hypertension or increased pulmonary vascular re­sistance secondary to acute cardiopulmonary failure. 1uo- 54 Normal hemoclynamic values in the pulmonary artery are 20/12 (torr), with a mean of 13 torr and a mean PAOP of 6-12 torr. Caution must always be used in interpreting a single reading; sequential readings are thus necessary. The frequency of readings will, of course, depend on the instability of the patient, and might be as often as every 30 seconds, but certainly no less often than every 15 minutes.

The widespread availability of S-G catheters prom pt eel a re-evaluation of central venous pressure measurements. Previously accepted as an adequate guideline for managing shock and hypovolemia, 5~-su poor or absent correlation was found in comparing PAOI>, PAEDP, or LAP with CVP in seriously ill patients. 0•211- 3 i. 51 •57-u 3 In the absence of cardiopul­monary dysfunction, CVP remains a reliable assess­ment of right and left heart filling,3 '·

58 but in serious illness right ventricular function and left ventricular function are so disparate that not only the absolute CVP but even CVP changes are unreliable and mis­leading estimates of left heart filling.57·60

Some controversy does remain. First, a recent large series showed a good correlation of PAOP and LAP al pressures of' IO torr or less, but as PAOP increased

the prediction of LAP from PAOP was su~ject to considerable error 64; at PAO P's greater than 15 torr the 95 per cent confidence interval for predicting LAP was at least ±5 torr. This was auributed to a change in the ratio of pulmonary arterial Lo pul­monary venous compliance. Second, evidence has been found for a pulmonary venous waterfall effect at the exit of the large pulmonary veins from the surface of the lung. 65 A pulmonary vascular water­fall effect is said Lo occur in a collapsible vascular segment when the intra vascular downstream pressure is less than the pressure surrounding the collapsible section. 66 Under these conditions the vessels exposed to the surrounding pressure partially collapse and blood flow becomes independent of the more negative downstream pressure. Under no-flow conditions, a wedged upstream pressure will fall lo the level of the pressure around the collapsible segment and not to the more negative downstream pressure. With a waterfall effect in the pulmonary veins and al very low LAP's, PAOP will be higher than LAP. This work65 was clone in the clog with an open thorax; the conditions under which it might apply to man arc unknown.

Whether PAOP reflects LAP during mechanical ventilation with PEEP is in doubt; PEEP raises alveolar pressure and creates a waterfall effect al the alveolar level, thus keeping PAOP higher than LAP.45·67•68 The presence or absence of a PAOP-to­LAP discrepancy during PEEP will depend on the complex relationship of: l) the height of the S-G catheter tip above the left atrium during wedging, 2) the lel'L atrial pressure, and 3) the level of PEEP; if the catheter tip wedges in a region of hmg where alveolar pressure excedes pulmonary venous pres­sure, PAOP will reflect alveolar pressure and not LAP.45·66 (The recent suggestion of Benumof el al. m, that a PAOP-to-LAP discrepancy will arise only when alveolar pressure excedes pulmonary arterial pressure appears in error. 611) Since the S-G catheter tip can distribute to peripheral regions of lung, 69 it is easily conceivable that a change in patient position (supine LO sitting or lateral decubilus) would produce a sud­den, unexpected error in PAOP estimates of LAP. Equally, a change in the level of PEEP or LAP or a random migration of the S-G catheter tip during wedging would produce or eliminate an alveolar waterfall effect without a change in patient position. Unfortunately, the presence or absence of an alveolar waterfall effect during PEEP is not discernible with only an S-G catheter.

In addition, PEEP increases intrathoracic pressure and thus all imravascular and intracarcliac pressures. The true distending pressure of a vessel or of a

A11t.·~1 ht.·~ic,lc1M) \' ·17. :-.:or,, Nm· IH77 PULMONARY ARTERIAL MONITORING 457

cardiac chamber under these conditions is the intra­luminal pressure minus the surrounding pressure. Calculation of' transmural pressures (PAOP - intra­pleural or esophageal pressure) has been recom­mended to preserve the accuracy of PAOP in estimating distending pressures charing PEEP. Sur­rounding pressures have been taken with an esoph­ageal balloon 711 and with a fluid-filled intrapleural cat hcter.7 1 The laller technique has been criticized by Craig 72 as measuring pleural liquid pressure, which can be quite clifferelll from pleural surface pressure. It is pleural surface pressure that determines ex­pansion of the lung and is transmitted to intra­I horacic extra pulmonary structures. Use of an esoph­ageal balloon pressure must be taken with reserva­tion owing to the possible artifacts introduced by the esophagus and surrounding structures. 73 Even if pleural surface pressure is measured accurately, calculation of transmural filling pressures is poten­tially in error, as the pressure around the heart is more negative than pleural surface pressure and varies with hmg volume. 73

Some have ol~jected that in patients with chronic ohst ructivc pulmonary disease (COPD) an elevated PAOP may be an artifact of the pulmonary abnor­mality and docs not necessarily indicate left ventric­ular l'ailure (LVF).74 In general, however, elevated PAOP's in COPD have been shown to reflect true LVF.15

- 77 In patients who have severe obstructive pulmonary disease, the wide swings in intrathoracic pressure during "active expiration" can influence PAOP interpretation; ideally, in this circumstance transmural PAOP should again be used 78 ; however, this technique is not routinely employed as it re­quires an esophageal balloon.

How, then, should PAOP be measured during elevated or rapidly changing intrathoracic pressure? The following suggestions might be useful. Pul­monary arterial pressures should be taken as the average over several heart beats at end-expiration with the transducer at the mid-axillary line and referenced to atmospheric pressure. For the mechan­ically ventilated patient who has a respiratory rate so rapid that a stable end-expiratory trace cannot be seen, the ventilator should be momentarily dis­connected during the measurement. During vigorous spontaneous respiration, the patient with COPD or severe respiratory distress should be instructed to hold his breath at encl-expiration; if this is not possible, transmural pressures must be taken or apnea induced.

Positive end-expiratory pressure of modest amounts (perhaps to as high as 10-12 cm H20) ap­pears to induce clinically unimportant errors in end­expiratory PAOP estimates of LAP.67•68 Temporary

withdrawal of PEEP during wedging would also ap­pear valid. 14•30 During higher levels of PEEP (> 10-12 cm H20) no consistently reliable measurement protocol exists; it is possible that further experience comparing PAOP with LAP or LVEDP in patients with severe acute respiratory failure will confirm one report showing no PAOP to LVEDP discrepancy charing PEEP to as high as 30 cm H20. 79

Left Ventricular Filling

It is widely accepted that the Frank-Starling law applies to the intact human heart; i.e., at any given functional state the force of ventricular contraction is dependent upon its end-diastolic volume or end­diastolic wall tension. For want of a technique for routine ventricular volume determination, investi­gators and clinicians have relied on ventricular end­diastolic pressure as an index of' end-diastolic volume and tension. Two questions arise: I) how re­liable is left ventricular end-diastolic pressure (LVEDP) in assessing left ventricular end-diastolic volume (LVEDV), and 2) how reliable is PA WP in estimating LVEDP.

During diastole the left ventricle fills passively and the pressure developed is exponentially related lo the volume. An elevated LVEDP is commonly taken to signify the presence of LVF: a normal LVEDP is assumed to be evidence against its presence. In fact, apparent left ventricular (LV) function as reflected by LVEDP can change in many ways.80 Among them arc a true change in the LV contractile state, a change in the diastolic properties of the L V, and hypervolemia. 57

•81

•82 Particularly following acute myo­

cardial infarction (AMI) or acute hemodynamic inter-

ABBREVIATIONS

AMI = acute myocardial infarction C(a - v)0, = arterial-venous oxygen content difference

COPD = chronic obstructive pulmonary disease CVP = central venous pressure LAP = left atrial pressure

L V = left ventricle L VEDP = left ventricular end-diastolic pressure LVEDV = left ventricular end-diastolic volume

L VF = left ventricular failure L VSWI = left venaricular stroke work index PAEDP = pulmonary arterial end-diastolic pressure

PAOP = pulmonary-artery occlusion pressure PA WP = pulmonary-artery wedge pressure

PCP = pulmonary capillary pressure PEEP = positive end-expira1ory pressure

Pv0 , = mixed venous oxygen tension PWP = pulmonary wedge pressure S-G = Swan-Ganz Sv0 , = mixed venous oxygen saturation

458 NATHAN L. PACE Anr:sthcsi«tlngy V 47, !'.o 5, il:m· 1!177

ventions (vasopressor and vasodilator infusions), impaired ventricular relaxation and decreased di­astolic ventricular compliance may account in part for an elevation in LVEDP without any change in L VEDV. "2

·" 3 Under these conditions it may be incor­rect to assume that an elevated LVEDP represents an impairment of myocardial contractility.Ht.H3 A systematic study of the relationships of LVEDV, LVEDP. ventricular relaxation and ventricular dia­stolic compliance in many forms of cardiovascular dysfunction (anesthesia, trauma, sepsis, burns) is not available.

Second, the relationship between PAOP and LVEDP is complex . In subjects who have normal cardiovascular systems, PAOP, LAP and LVEDP arc essentially interchangeable. Following myocardial in­farction, atrial contraction makes a greater con­tribution to left ventricular filling (probably clue to changes in ventricular compliance) and raises LVEDP 1nuch higher than mean PAOP 17·" 4-

86; LVEDPisoften

10 torr or more greater than LAP or PAOP. One study ol' anesthetized patients with coronary-artery disease also showed LVEDP greater than PAOP." 7

PAOP 11m,· reflects the left ventricular diastolic pres­sure prior to atrial contraction and is a poor estimate ol' left ventricular filling, but still provides reliable information about pulmonary venous hypertension and pulmonary edema. The lower the cardiac output, the more important is atrial contraction for ventric­ular filling and the less reliable is mean PAOP for estimating L V EDP. 115 During severe respiratory f'ail­u re, PAOP has been shown in a few patients both to equal LVEDP 711 and to underestimate LVEDP. 1111

But the relationship of PAOP and LVEDP during cardiopulmonary failure has not been systematically investigated.

A11empts to get a better estimate of LVEDP than that given by PAOP have been madc," 4•80-ot and the pulmonary-artery occlusion "a" wave appears most valid. The wedge pressure trncc is a reflection ol' the lefr at rial phasic events and can show prominent "a" and "v" waves. 1\·lcasurcment of the "a" wave pressure ol' the wedged pressure trace (rather than mean PAOP) seems to correlate very well with LVEDP.112 Unfortunately, the "a" wave is rarely dis­tinctly seen in the wedge trace, and the "a" wave pres­sure has not been widely used.

Ventricular Function

An early modification of the S-G catheter was a multiple-lumen, thermistor-tipped S-G unit that

permitted thermodilution determination of cardiac output. 24

•93 The principles of measurement are as

follows: If a known quantity of cold solution is introduced into the circulation and adequately mixed, recording of the resulting cooling curve at a down­stream site allows calculation of net blood flow. In practice 10 ml ol' 5 per cent dextrose at O C or room temperature arc injected into the superior vcna cava or right atrium via the proximal lumen of the S-G. The thermistor allows recording of the baseline pulmonary-artery blood temperature and the sub­sequent temperature change. The resulting curve may be analyzed manually by simple planimelric methods or by computer.

Validation studies of the thcrmodihnion technique using S-G catheters show both good reproducibility and good correlation with the dye dilution methods of measuring cardiac output. 24 •114•95 However, large variations in baseline pulmonary-artery temperature related to cardiac and respiratory cycling may occur, especially in mechanically ventilated critically ill patients, which lessens precision and accuracy 94 ·1lf1; such errors may be minimized by repeating the cold i1~jcctions during the same point in the respiratory cyclc.911 Only a modest correlation between thermo­dilution and Fick oxygen methods has been found in one study. 117

Perhaps this is not too surprising, as patients in the operating room or intensive care unit are rarely in a steady hcmodynamic stale and the thermodilution method is an average over 4-10 heart beats, while the Fick method averages over 2-3 minutes. In addi­tion, there arc other potential errors in both meth­()(ls. Ultimately, there is no standard by which to compare accuracy. Each method must be consiclcrecl an estimate, but the lhermodilution methods appear particularly simple and efficicnt. 98

With lhc easy availability of frequent cardiac output determinations in critically ill patients, con­struction of ventricular function curves has been recommcnded.114

•1111 Left ventricular stroke work indcxt is plotted versus left ventricular filling pressure; filling pressure is altered by such maneuvers as administering fluid challenges, diuretics and vasoprcs­sors, or by varying mechanical ventilation, PEEP and assisted circulation; Starling curves may then be con­structed. Because of the previously mentioned dis­parity between PAOP and LVEDP, Starling curves so constructed from PAOP must be considered critically. It is easily seen that since trnc left ventricular filling pressure may be 8-10 torr greater than

cardiac output in I/min X (mean arterial pressure in torr - occlusion pressure in torr) t LVSWI (in gram-meters/1112 ) = _________ ...,_ ____ --'------ x 13.6.

heart rme in bemsJmin x body surface area in 1112

At1t•Ml1r,inl••)O: \' ·17, So !",, So,· I !l77 l'Ul.MONARY ARTERIAL MONITORING 459

PAOP in certain patient groups, all points clerivecl using PAOP may be eri·oncously plouccl leftward and upward, thus creating a left-shif"tecl Starling curve and suggesting left ventricular function better rhan in f"acl.

Crexclls 1•t al.911 constructed Starling curves for the left vent ride with volume cfo,llcnges i11 patients fol­lowing A l\H and found maximum LVSWI at PAOP 14-18 torr: this, then, was considered t.o be the optimal filling pressure for adequate cardiac perform­ance without risk of pulmonary congestion. 1111-rn2

However, since it is well demonstrated that pul­monary edema can develop in association with low colloid oncotic pressure or increased pulmonary capillary permeability at normal PAOP's, 27·2K,in3-rn5

PAOP's of 14-18 torr may not be tolerable for adequate gas exchange in all patients. Whether sur­vival following AM I is enhanced by manipulating PAOP to 14-18 torr is not proven. Others have not found an optimal left ventricular filling pressure following AMl. 11111

Swan and co-workers, using hemodynamic data ob­tained by S-G catheter, divided patients with AM I into subsets and suggested specific therapies. 107 The ther­apies arc clepcnclent on continual reassessment of hcmodynamics with pulmonary-artery catheters. Al­though classificalion of patients within these groups is of prognostic value, little evidence that overall morbidity or mortality may be changed by the sug­gested manipulations is yet available. 1117

Rapid diagnosis of certain complicatioi1s of AM I and open-heart surgery (ruptured inierventricular septum, acute mitral insufficiency, and cardiac tamponade) 1°K-III and serial hemodynamics during intra-aortic balloon pumping 112·113 have been facili­tated by pulmonary-artery monitoring. However, it was recently found that cardiac tamponade is probably better detected by CVP monitoring. 114

Analysis of Mixed Venous Blood

As a simpler method of assessing effective tissue perfusion or oxygenation in seriously ill patients, serial sampling for determination of blood oxygen saturation in the right atrium, right ventricle, or pulmonary artery has been used, since mixed venous blood oxygen saturation is directly proportional to cardiac output when arterial oxygen content and oxygen consumption remain constan1.m-llK Normal mixed venous blood 0 2 saturation is 70- 75 per cent: values less than 60 per cent have been associated with heart failure and values less than 40 per cent with shock. 118 Only true mixed venous blood from the right ventricle or pulmonary artery can be used in seri­ously ill patients, as right atrial samples are poorly

mixed and may give falsely elevated whole-body \'enous oxygen saturat ions. 115·118·119 Fiberopt ic S-G catheter oximeters have been developed to monitor mixed venous blood oxygen saturation (S,•0 ,) contin­uously. rn,120-122 Also, serial measurements of mixed venous blood oxygen tension (Pv02 ) have been used to assess circulation a11d oxygen therapy (normal 38-42 torr), 123- 125 and the arterial-venous oxygen content difference [C(a-v)02 ] (normal 3.5-5 vol per cent .) has been used to detect and differentiate co-existent cardiac failure and respiratory failure. 128

Clinical decisions based on C(a-v)02 • P,•02 , and S,•02

must . be made cautiously. It is important to remem­ber that a single C(a-v)0 ,, Sv02 , or P,1

02 is, strictly speaking, uninterpretable without a simultaneous car­diac output determination,' 27 but a very low P,•0 ,

( <20 t.oiT) or s,,02 ( <40 per cent) or a very high C(a-v)02 (>9 vol per cent) by itself docs confirm a very severe derangement of oxygen transport. There is another possible error. As contamination of de­saturated mixed venous blood by saturated pul­mhnary capillary blood is possible during aspiration through the non-wedged S-G, withdrawal of blood should be slow and abnormally high values sus­pect. •2K-120

Other Uses

Measurement of PAOP has proved essential to cliscriniinate LVF in tile presence of acute respir­atory failure as traditional signs of L VF (tachy­cardia, engorged jugular veins, hepatomegaly, gal­lop rhythm) become nonspecific and insensitive. 136•131

The use of S-G catheters in severe acute respiratory failure has also revealed the almost universal pres­ence of pulmonary hypertension and elevated pul­monary vascular resistance. 711 Calculation of right ventricular stroke work index shows a threefold elevation over normal values: but afterload re­duction to prevent right heart failure docs not appear jmssible. Pulmonary angiography has been facilitated in critically ill patients by use of an indwelling S-G catheter. 132

Complications

Initial reports of S-G catheter use mentioned fre­quent minor problems 6

•211

•133; these included: transient

arrhythmias during passage, balloon rupture, catheter thrombosis, catheter coiling in the right ventricle, and local infection at the cutaneous insertion site. More serious complications have also been reported (table I); some of these arc preventable or treat­able. Rhythm disturbances may usually be terminated by withdrawal of the catheter, 134,t:15 but deaths have resulted. 136 Pulmonary infarction can probably

460 NATIIAN I.. PACE Am·~• ht·~ioluh~· \' ·17, !'\o !i, :'\n\ · 1Hi7

TAnu: I. Swan-C:;mz Ca1hc1cr Complica1ions

Type

·- --,\rrh1 ·1h111ias

V1'.i11rirnlar 1achycardia Ill' lihrillation :\1rial arrhy1h111ias Rii:111 hundle -hrand1 hlm:k Cn111ple1t• hearl hlock

- - - -- · E111h11lis111, I hromhosis

1'11lm1111an· embolism 1'11lm1111,ir)' infarction l'nlmonary l'ascnlar 1hrn111bosis

.

En,J,,rnrdi1is As1•p1k 1hrn111ho1ic endocardial l'ege1a1ion E111locardial mural 1hromhosis llac1erial cndocarcli1is

--- -~lisrellaneous

l'nln111nary-ar1cry perforntion ln 1rarnrd iac knolling of ca1he1er(s) Ca1he1er s11111recl lo rigl11 airial wall 1'1·1Tn1aneous placemen! of ca1he1cr into carotid artery :\hsrl'SS at 1·cnous cutclown silc Rup111red d10rclae of tricuspicl ,·ah-c

··-~- ·

he averted if the pulmonary artery tmcc is con­ti1111ously monitored so as to permit immediate nxog-11it ion and withdrawal of the catheter should inad\'ertelll wedging occur. t:17 Fatal pulmonary ar­terial rnp1urc has occurred; keeping the S-G catheter as close as possible to the pulmonic valve (while still able Lo obtain PAOP) and slow balloon inflation ha\'c been recommended to avoid this complication. 111

Other complications, such as aseptic thrombotic c11cloca n I ial vegetations, sub;1cute bacterial cmlo­carcl it is. and cndocardial mural thrombosis, appear unarniclahlc if a catheter must remain in the central l'irc11latio11 for prolonged pcriods. •:iH-i.tt

Considering the wide use, remarkably little serious morbidity or mortality has been reported . Perhaps this 1cd111iquc is i11hcrc111ly safe ; however, without a larg-e-scalc, nHtlti-ccntcr, prnspcctivc study (such as the Cooperative Study on Cardiac Cathclcriza­t ion ,..2), 1111cler-rcport.ing of the true complication rate must be suspected.

Use during Anesthesia

The availability of pulmonary-artery cathetcrizatio11 has been a boon to the study of pulmonar) ' and systemic he mod ynamics during diverse anesthetic circumstances ; for example, halothane and enllurane anesthesia , tr.K pentolinium hypmension, 159 large-close morphine,1 1111 nitrous oxide with morphinc,K 7 and in­duction of anesthesia." 11 Some of the limitations in using PAOP to evaluate left ventricular function, previously described, must be kept in mind when interpreting such studies. S~rensen and Jacobsenlll 1

Numhcl'ol' Number of l'a1ic11t!I llea1h, Rcl'erc11l'l'!i

Iii I 7, 1-1, 110, HO , 1·1:\ 2 (I I :\.I :1 () J.1-1 I I t:lti

I 0 Ii J.I 0 113, 1:1:1. 1:n. 1-1r, I I 146

7 () 139, 140 2 () 138 I I 141

5 2 28 , 147-1:,0 5 () till, 151- 15,f I (I 155 I () 15ti I () 14 I I 157

found large transient increases in PAOP for a few minutes immediately following endotrachcal int uba­t ion with a barbiturate and succinylcholine induction; this was associated with large increases in pulmonary arterial and systemic blood pressures . While these increases in PAOP might rellect left ,·e111ricular failure, changes in left ventricular re­laxation or compliance might also be involved.

Another question remains. What is the proper clinical use of pulmonary-artery cathetcrization in the operating room? To visitors orlarge hospital cen­ters (especially those doing open-heart surgery), there appears to be no widely accepted common cri­teria for S-G use.i In some centers very l'cw pa­tienls arc catheterized; in others, the anesthesiologists seem to follow the dictum of' Swan 37 that if a CV P line is considered, a S-G should be used. Yet pul­monary-artery cathetcrization is expensive and has dclinitc risks.

Bedside S-G cathctcrization for preoperative evalu­ation of the elective surgical patient docs not seem to be generally indicated. Although this has been rccom mended prior to vascular su rgcry, rn2 the history, ph ysical examination and laboratory data arc usually adequate to reveal evidence of' myocardial ischemia, myocardial failure , and p11lmonar}' edema, and to allow selection of therapy. This, of course, excludes patients for open-hcarL surgery , who usually require formal cardiac cathcterizat ion.

Routine S-G monitoring for open-heart surgery 1s

:I: Wong KC, Stanley TJ-1: Personal rnmm1111icatio11.

A1u·Mlwsi1,l1•KY \' •17, ~u !i, !\:o\ ' 1!177

l'UI.MONAlff ARTERIAi. :\IONITORING 461

probably an unnecessary expense, hazard, and in­convenience for 111ost patients, with the exception ol" those with very severely impaired left atrial or lcli ventricular !'unction. Anesthesia may be induced and maintained with arterial and central venous pres­sure monitoring; after cardiopul111onary bypass, di­rect LAP is easily and frequently used lo a<Uust lcli heart lilting. It is possible that certain patients who have coronary-artcr)' disease will bcnclit by pharmacologic unloading or I.he left ventricle during hypertensive episodes 111

=1 prior to cardiopulmonary

bypass to alleviate myocardial ischcmia, 1114 and that this will be facilitated by S-G monitoring. This ap 'proach needs validation.

One situation where S-G 111onitoring should be routinely employed has been identiliecl. lnfrarcnal aortic cross-cla111ping during repair of abdominal aortic a11eurys111s or during aortofcmoral bypass surgery in patients with severe coronary artery disease frequently produces severe hemodynamic disturham:cs and myocardial ischemia. 1115•

11111 Observa­tion ol" PAOP and ECG seems necessary to detect and ameliorate these changes.

Early detection or venous air embolism during si11i111,{ intracranial surgery was rcportcd 1117

; however, I real IIICIII of such embolism by withdrawal of air through I he S-G docs not appear superior to use ol" com•c111ional right atrial lincs. 111K Since other sensitive met hods for detecting air e111bolism exist (prccordial Doppler monitoring and end-tidal CO 2 sa111pling), the rout inc use or pulmonarr-artery catheterization for siu ing craniotomies docs not appear warranted.

Certainly, the critically ill patient (in partirnlar, I hose with cardiogenic and septic shock and acute respiratory failure) whose care is dependent 011 pulmonary-artery catheterization will also benefit by its use during emergency surgical procedures. The anesthesiologist should be prepared to initiate S-G cathcterization in these patients (by himself or by others) ii" the need has not been perceived.

Swan-Ganz catheters have been placed during many 01 her types or surgical procedures but except for the operations mentioned above, it is the cardio­pul111011ary status or the patient that should deter­mine cathcterization. Overall, pulmonary-artery cath­ctcrization should never become a m11ti11e technique for most anesthesia care .

Conclusion

Pulmonary arterial monitoring with Swan-Ganz catheters must be considered one or the most im­portant advances in the care of the critically ill. As I have detailed, a more critical attitude should be adopted in evaluating data derived from the

catheter because or the inherent limitations in pulmonary arterial monitoring and unresolved de­tails of cardiovascular dysfunction. Fault' tf,, 111i1•11x, its use should be encouraged in appropriate patient groups.

References

I. l.:11egola M, Rahn 1-1: A sell~g11idi11g ca1he1er for cardiac and pulmonary ar!erial ca1he1erization and occlusion . l'rnc Soc Exp l\iol Med 84 :titi7-lili8, 1!15:l

2. 1'radley RD: piagnos1ic righ1-hear1 catheterizatim1 with miniature catheters in sc\'crcly ill patients. Lancet 2:!M I -!142, l!lli4

:I. Fife WP, Lee BS: Construction and use of sell~guiding right heart ;md pulmonar)' artery catheter. J A1>pl Physiol :!II: 1-18-14!1, l!lli5

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84. Rahimtoola SH: Left \'entricular end-diastolic and filling pres­sures in assessment of \'entricular function. Chest 63:858-860, 1973

85. Rahimtoola SH, Ehsani A, Si11110 MZ, et al: Left atrial trans­port function in myocardial infarction: Importance of its booster pump function. Am J Med 59:686-694, 1975

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124. Stanley TH, Iscrn-Amaral J: Periodic analysis of mixed vcuous oxygen tcusion to monitor the adequacy of per­fusion during and afrer cardiopulmonary bypass. Can Anaesth Soc.J 21:454-460, 1974

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134. Geha DG, Davis NJ, Lappas DG: Persistent atrial arrhyth­mias associated with placement or a Swan-Ganz cat hctcr. ANESTHESIOLOGY 39:651-653, I 973

135. Voukydis PC, Cohen SI: Cathctcr-imlucccl anhythmias. Am Heart J 88:588-592, I 974

131i. Abernathy WS: Complete heart block caused hy the Swan­Ganz catheter. Chest 65:349, I !174

137. Foote GA, Schabel SI, Hodges M: Pulmonary complications of the flow-directed balloon-tipped catheter. N Engl J ~led 290:927-931, 1974

138. Goodman DJ, Rider AK, Billingham ME, cl al: Thrombo­cmbolic complications with the indwelling balloon-tipped pulmonary arterial catheter. N Engl .J Med 2!11 :777, 1!174

139. Greene .JF Jr, Cummings KC: Aseptic thrombotic c111lo­canlial vegetations. A complication of indwelling pul­monary artery catheters. JAMA 225: 1525-152li, l!l7:I

140. Pace NL, Horton W: lnclwclling pulmonary artery cathe­ters: Their relationship to aseptic thrombotic cmlocanlial vegetations. JAMA 233:893-894, 1!175

141. Greene JF Jr, Fitzwater JE, Clemmer Tl': Septic t•ndo­carditis and indwelling pulmonary artery catheters. JAMA 233:891-892, 1975

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AIH!slhcsic,loK)' V ·17, No !i, Nu\' 1977 l'ULi\lONARY ARTERIAL MONITORING 465

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15ti. McNabb TG, Green LH, Parker FL: A potentially serious complication with Swan-Ganz catheter placement by the percutaneous internal jugular route. Br J Anacsth 4 7:895-897, 1!175

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158. Filncr BE, Karlincr JS: Alterations of normal left ventricular performance b)' general anesthesia. ANESTHESIOLOGY 45: (ii 0-(i2 J, H17ti

l!'i!I. Fahmy N R, Selwyn AS, Patel D, ct al: Pulmonary vasomotor lone during general anesthesia and deliberate hyputcnsiun in man. ANESTtu:SIOLOGY 45:3-13, 197tl

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161. St,\rcnsun MB, Jacobsen E: Pulmonary hcmodynamics during induction of anesthesia. ANESTHESIOLOGY 4ti:24tl-25 J, 1977

lll2. St,\rcnscn MB: Pulmonary artery pressure measurements in surgical patients. Scand J Thorne Cardiuvasc Surg 9:2ti4-270, 1975

Hi3. Kaplan JA, Dunbar RW, Jones EL: Nitroglycerin infusion during coronary-artery surgery. ANESTHESIOLOGY 45: 14-21, 1976

Jti4. Hillis LD, Braunwuld E: Myocardial ischcmia. N Engl J Med 296:971-978, 1034-1041, 1093-1096, I !177

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Obstetric Anesthesia

CLOSING VOLUME AND PREGNANCY New pul­monary function tests (e.g., flow-volume loops and closing volume), as well as standard pulmonary function tests, were performed on 19 healthy pregnant patients in the third trimester and after delivery. It was found that the flow characteristics manifested in the flow-volume loops and the closing volume remained unaltered during pregnancy. With regard to the standard pulmonary function tests, no sta­tistically significant change was found except for a decrease in the expiratory reserve volume and in the functional residual capacity dming pregnancy. (/Jaldwiu GR, aud othe,:~: Nt'll' luug Ji111ctio11s aud prt'g11a11cy, Am J Obstl'I Gy11t'l'11! l2i:235-239, /9i7.)

ROLL-OVER TEST The supine pressor test was per­formed on 207 nulliparous young women between the twenty-eight and thirty-second weeks of gestation. The supine pressor test predicted pregnancy-induced hyper­tension in 78 per cent of those women in whom the condition subsequently developed. Ninety-six per cent of the women who failed to demonstrate a rise in diastolic pressure on position change remained normotensive throughout the remainder of the pregnancy. (Plwla11 JP, aucl otlwrs: ls the supine pressor It's/ ,111 mlequa/1' llll'tllls of' predicting acute hyper/1!11sio11 in pregnancy? A III J Ohs/I'/ Gy,wcol /28:173-176, 1977.)