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.
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AIH!slhcsic,loK)' V ·17, No !i, Nu\' 1977 l'ULi\lONARY ARTERIAL MONITORING 465
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lll2. St,\rcnscn MB: Pulmonary artery pressure measurements in surgical patients. Scand J Thorne Cardiuvasc Surg 9:2ti4-270, 1975
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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.)
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