Pulmonary Oedema: a Review

PULMONARY OEDEMA: A REVIEW

WILLIAM H. NOBLE

ABSTRACT Pulmonary oedema results from derangement of a normal physiological process which is continuously producing and removing extravascular lung water according to principles stated by Starling's equation of fluid flow across semipermeable membranes. The parameters in Starling's equation cannot all be measured. However, experiments have suggested that increased pulmonary capillary hydrostatic pressure forces fluid extravascularly, diluting the colloid osmotic pressure of tissue fluids and increasing the hydrostatic pressure of lung tissue fluids. Once these reserves and the ability of puhnonary lymphatics to remove lung water are overcome, pulmonary oedema results. This oedema can also result from reduced colloid osmotic pressure in the pulmonary capillaries and increased capillary permeability, even at low pulmonary capillary hydrostatic l~ressure. Perhaps because of the reserve created by colloid osmotic pressure of tissue fluids, hydrostatic pressure of lung tissue fluids and lymphatic drainage, pulmonary oedema accumulates at a slow rate initially, and at a much more rapid rate in later stages of oedema development. The rate of oedema formation may also relate to damage to the lung created by interstitial oedema, which opens the barrier to a later stage of alveolar oedema. While lung compliance is reduced with each successive increase in oedema formation, increased shunting and hypoxaemia do not result until alveolar oedema is present, in normal lung. The diagnosis of pulmonary oedema is best made by searching for causes of oedema and by chest radiographs. The management of pulmonary oedema must begin with maintenance of oxygenation of blood. This can best be achieved by applying continuous positive pressure ventilation (CPPV). CPPV does not remove lung water (in fact it may slightly increase it), but it does improve oxygenation by ventilating alveoli that were previously filled with fluid. The improved oxygenation buys time, so that therapy directed at the cause of pulmonary oedema (Starling's law) can be applied. Since current knowledge is inadequate we do not know how to reverse an increased capillary permeability, other than by removing its cause; or how to reduce tissue colloid osmotic pressure, or to increase the hydrostatic pressure of lung tissue fluids or the intracapillary colloid osmotic pressure or the lymphatic flow of fluid. This leaves only increasing intracapillary colloid osmotic pressure or decreasing pulmonary capillary hydrostatic pressure as the means available to reduce pulmonary oedema. In the face of a non-compliant left ventricle colloid infusions may be dangerous, as the attendant increase in blood volume may increase pulmonary capillary hydrostatic pressure and worsen pulmonary oedema. If increased capillary permeability is the cause of pulmonary oedema, colloids might leak ex- travasculady and draw fluid with them. Therefore the most important therapy in pulmonary oedema, regardless of cause, is to reduce pulmonary capillary hydrostatic pressure. Depend- ing on the cause of pulmonary oedema and the associated cardiac output, pulmonary capillary hydrostalic pressure may be decreased by reducing left ventricular preload, increasing myocardial contractility, reducing left ventricular after-load or some combination of these. The anaesthetic implications are that Starling reserves are large and pulmonary oedema should not occur in the normal patient. In the patient with pulmonary oedema or reduced cardio-pulmonary reserve preoperatively, every effort must be made to optimize Starling's forces before undertaking an anaesthetic in these life threatening situations.

I Introduction Pathology II Pathophysiology Effects of pulmonary oedema Starling's Equation III Clinical Correlates of Pathophysiology normal values COP-r interaction of values Pmv Time course of pulmonary oedema P'r COPmv William H. Noble, M.D., F.R.C.P.(C), Associate Lymphatic removal of oedema Professor, University of Toronto; Department of Anaesthesia, St. Michael's Hospital, 30 Bond Street, Capillary permeability Toronto, Ontario, M5B 1W8. Cardiopulmonary bypass

286 Canad. Anaesth. Soc. J., vol. 27, no. 3, May 1980 NOBLE:PULMONARYOEDEMA 287

1V Diagnosis Gas Exchange history and physical examination Pao2 arterial partial pressure of oxygen CVP versus pulmonary artery Qs/Qt shunt fraction occluded pressure FRC functional residual capacity blood gases CPPV continuous positive pressure venti- lung compliance lation chest radiograph V/Q ventilation perfusion ratio V Management Pvoz mixed venous partial pressure of 1. MaintainOxygenation oxygen Flo z CPPV I INTRODUCTION 2. Lower Pmv lower ventricular preload PULMONARY OEDEMA may be defined as an ab- increase myocardial preload normal collection of fluid in the extravascular reduce ventricular afterload tissues and spaces of the lung. It is important to (improve ventricular compliance) realise that the lungs have a dynamic and not a 3. Remove the cause of increased static water content. Water and proteins do move capillary permeability into the interstitial space and are returned to the 4. Increase COPmv (cautiously) venous circulation by an extensive network of VI Implications of Pulmonary Oedema for lymphatics. Once the capacity of the lymphatics the Anaesthetist: to remove excess fluids is exceeded, fluid ac- normal patients cumulates in the interstitial space and, if un- patients with pulmonary oed- checked, will lead to alveolar flooding. ema preoperatively Theoretically it should be possible to distin- patients with decreased cardio- guish between interstitial and alveolar oedema. pulmonary reserves However, an easy technique to detect small increases in extravascular water is not currently GLOSSARY OF TERMS available. Consequently little is known about the early interstitial phase of pulmonary oedema. In Haemodynamics animal experiments, determinations of volume and protein concentration of the lymphatic fluid Pmv pulmonary capillary hydrostatic from the lung or double indicator dilution tech- pressure niques to quantitate lung water are shedding PAO pulmonary artery occluded (wedge) some light on the process of extravascular lung pressure water formation in normal conditions and in dis- PPA pulmonary artery pressure ease. Since techniques to quantify lung water in LVEDP left ventricular end diastolic pressure patients are invasive, most of the patient data is LVEDV left ventricular end diastolic volume gathered in cardiac surgery settings. It is assumed CVP central venous pressure the principles learned there will apply to other Q cardiac output patients as well. Other clinical information usu- Lung Liquid Flow ally begins at the late alveolar oedema stage and Qf net transvascular flow of fluid makes assumptions about its cause. Kf fluid filtration coefficient In this review I will stress basic physiology and PT tissue fluid interstitial hydrostatic recent advances in knowledge of pulmonary pressure oedema. Gf reflection coefficient COPmv colloid osmotic pressure of plasma II PATHOPHYStOLOGY proteins COPr colloid osmotic pressure of tissue To understand the pathophysiology of pulmo- proteins nary oedema we should start by studying the ETV ~ extravascular thermal volume of lung physical forces and permeability properties that (a double indicator dilution mea- produce shifts in water from one compartment to sure of lung water) another. In 1896 Starling ~ stated the general 288 CANADIAN ANAESTHETISTS ~ SOCIETY JOURNAL

transport equation for fluid flow across capillary ducts must return this fluid to the systemic ven- membranes: ous circulation or pulmonary oedema will result. If one variable in Starling's equation is Qf= Kf[(Pmv - P'r) - Gf(COPmv - COPT)] (I) changed, other variables will change. If an increase in hydrostatic pressure (Pmv) occurs fluid where Qfis the net transvascnlar flow of fluid, Kf will immediately move into the extravascular is the fluid filtration coefficient, Pray is the micro- lung and dilute the proteins (lymph proteins are vascular hydrostatic pressure, P,r is the tissue reduced in the presence of an increased Pray). 4 P~ interstitial fluid hydrostatic pressure, Gf is the changes have not been measured in pulmonary reflection coefficient describing the "effective" oedema, but data from Parker, et ol. 7 suggest an transvascular protein osmotic pressure differ- increase, lfwe assume these changes we obtain ence, COPmv is the colloid osmotic pressure of Qfof 3.6 as follows: plasma proteins, and COPy is the tissue fluid colloid osmotic' pressure. Together Kt" and Gf de- Elevated Pray scribe pulmonary capillary permeability. Capillary Pray = 22 mm Hg COPmv = 25 mm Hg Examples of normal values and changes which lnterstitium P'r = 0 mm Hg COP.r = 2 mm Hg can occur in Starling's equation will clarify how oedema formation is affected. In the normal these Substituting in (1) results might apply. Kf is assumed to be 1 ml Qf= 1[(22 - o) - 0.8(25 - 2)] = 3.6 H20/mmHg. min -~ and is a property of the system that expresses how much water will flow This represents a small rise in the force,, across the membrane per unit change in pressure. favoring pulmonary oedema (3.6 versus 1.6 in th~ Gf is assumed to be 0.8, indicating that protein normal). The lung lymphatics should be able t~ can cross the pulmonary capillary membrane; but offset the development of pulmonary oedema bl the membrane is normally about 80 per ccnt ef- increasing lymph flow. But now the available t~s fective as a barrier to protein crossing. Pray is a sue "reserves" have been reduced. P,r can not b~ calculated value which has not been directly increased and COPr can not be effectively dilute( measured. Since pulmonary capillary pressure further, so that any fall in COPmv below 25 mn (Pray) is between pulmonary a~tery and left atrial Hg (3.33 kPa) or rise in Pray above 22 mm HI pressure, Garr-" has described an equation to (2.93 kPa) should lead to pulmonary oederna onc~ define Pray where: lymphatic removal is overwhelmed. This same argument could be applied to th~ Pmv = PAO + (P~- PAO) (2) patient with low serum protein concentrations o and PAO is the pulmonary artery occluded pres- increased capillary permeability. Once tissue hy sure (wedge pressure) and P~- is the mean pul- drostatic and colloid osmotic pressure "re monary artery pressure. serves" have been used and lymphatic ability t~ COPT has been derived by measuring the pro- remove lung water overwhelmed, pulmonar~ tein concentration of lymph from the lung and oedema will result. In the case of pulmonarl assuming that it relates to interstitial protein con- capillary permeability and low serum proteil cent ration)'5 P'r can not be measured directly concentrations, pulmonary oedema will result with present techniques and it is the least well much lower levels of Pmv than 22ram H understood parameter in Starling's equation; but (2.93 kPa). Pmv levels as low as 5 mm H it may relate to pleural pressure and seems to be a (0.67kPa) have been associated with clinic~ negative number. 6'7 Assuming normal values we pulmonary oedema severe enough to allow col obtain aQfof 1.6 as follows: lection of oedema fluid through a tracheal tube ~ pulmonary wedge pressures of 11 4- 4.5 mm H Normal (1.46 +_ 0.6 kPa) were found in 10 patients wit sepsis and pulmonary oedema. 9 Capillary Pray = 5 mm Hg COPmv = 25 mm Hg Interstitium Pv=-7mmHg COP,r = 12mmHg Time Course of Puhnonary Oedema Substituting in (I) The amount of water present in the extrava: cular compartment of the lung represents the n Qf= 1[(5 - (-7)) - 0.8(25 - 12)] = 1.6 sultant of the amount filtered (Starling's lay Since Qf is normally a positive number fluid is minus the amount removed (lymph flow). Who continuously moving extravascularly. Lymph the left heart is overloaded in a dog by infusion c NOBLE: PULMONARY OEDEMA 289

30- 25- .DEXTRAN / ~. 2o-

10-

v m 5-

I I I o 3 4 5 FIGURE 2 Normal dog lung exhibiting characteris!ic HOURS features, Note that one portion of the alveolar capillary FIGURE I When dextran 40 in normal saline is in- membrane is very thin and should serve as an excellent fused into dogs to increase and hold pulmonary artery gas exchanging surface~ (A: alveolar lumen, C: capil- pressure at 5.32-5.99kPa (40-45 mm Hg), lung water lary, arrow: tightly joined collagen fibres in in- (ETVL) accumulates slowly at first and much more terstitium, x 22,600) (Reprinted by permision of Can, rapidly later. Anaes. Soc, J.)

dextran, lung water accumulates slowly at first and much more rapidly later, I~ in spite of a con- stant pulmonary artery pressure of 40-45 mm Hg (5,32-5.99 kPa) (Figure 1). This suggests that lymph flow can remove excess fluid initially when Pa, and COPT "reserves" are not exhausted. Once PT has increased to 0 mm Hg and COPr has fallen to 2 mm Hg the lymphatics will be overwhelmed and lung water accumulation will be time dependent, This is supported by Parker, et a[. 7 who found an increase in lung water of 1 per cent per mm Hg rise in PT below 0 mm Hg. When P'r was just above or at 0ram Hg, lung water increased by 15 per cent per mm Hg rise in PT. A FIGURE 3 Alterations in the same dog lung in inter- second suggestion might be that as the lung be- stith~ pulmonary oedema, Interstitial fluid has sepa- comes oedematous, capillary endothelium and]or rated the capillary endothelium from the basement membrane and slightly increased the diffusion distance alveolar epithelium become more permeable to from alveolus to red cell (top and middle of photo- fluid or plasma..1 The clinical implications of this graph). Most of the interstitial fluid, however, is not in are Ihat pulmonary oedema on an overload basis the thin, gas exchanging surface between alveolus and will probably not occur immediately. Pmv is in- capillary. (A: alveolar lumen, arow: fluid in interstidum creased, but only after extravascular fluid move- separating collagen fibres, x 16.000) (Reprinted by permission of Can. Anaes. Soc. J,) ment has had time to reduce tissue "'reserves" and removal of fluid by lymphatics has been overwhelmed will pulmonary oedema accumu- oedema and alveolar oedema, This is valuable in late at a rapid rate This also suggests treatment terms of ultramicroscopic changes, ability to designed to remove pulmonary oedema may not diagnose and effects of the fluid on gas exchange. be immediately effective and that time will be Figure 2 (ETVL6.5 ml/kg, Pad2 13.3 kPa [ 100 mm necessary to clear the lung water. This should be Hg]) is an electron microphotograph of a normal especially true if the late rapid rise in pulmonary dog lung, II In dogs, lung interstitial oedema oedema is a result of an increased membrane without alveolar fluid is present when lung water permeability, increases are less than 60 per cent above control values (Figure 3. ETV L7.5 ml/kg, Pad2 11.84 kPa Pathology [89 mm Hg]). ~ This represents a 100 ml increase Pathologically, pulmonary oedema accumula- in lung water in a large dog. In spite of this lung tion can be divided into two stages: interstitial water increase, oxygen exchange is not impeded. 290 CANADIAN ANAESTHE[ISTS' SOCIETY JOURNAL oedema. A fall in dynamic compliance consis- tently occurs with an elevated lung water, but the relationship is variable so that the amount of lung water cannot be predicted from compliance values. t2 FRC changes are variable, either rising if airway closure predominates or falling if com- pression or filling of alveoli predominates. Peripheral airway resistance increases with congestion t4 but it is not until alveolar oedema is present that a marked increase in total pulmonary resistance occurs, t2 The surface lining layer might be changed in pulmonary oedema, but Cook. et al. ~s found that the elastic behaviour of FIGURE 4 Alevolar pulmonary oedema in the same oedematous lungs was not significantly different dog lung. The alveoli (A) are filled with a proteinaceus from that of normal lungs when these excised material (possibly plasma), cellular debris and fibrin lungs had surface forces minimized by ventilating deposits. Oxygenation of blood cannot occur since with liquid. oxygen cannot get into the alveolus, tTA:alveolar lumen, C: capillary, x 11,300.) (Reprinted by permission of An important effect of early pulmonary Can. Anaes. Soc. J.) oedema is the reduction of tissue "'reserves" of Starling forces. Small changes in Starling forces This is so because, although the fluid has entered that would not have led to pulmonary oedema in and thickened the interstitium and lifted the normal lungs may now do so (Figure 1). capillary endothelium away from the basement Work is now being done to determine how membrane, the oedema has not thickened the gas these effects might apply in patients with other exchanging surface markedly and fluid has not lung disease, such as chronic obstructive lung crossed the alveolar epithelium to fill the alveolus disease. ~6. ~7 and prevent gas from entering the alveolus) t In- terstitial oedema may create a gas exchange III CLINICAL CORRELATESOF PATHO- problem in patients with lung disease when PHYSIOLOGY oedema may alter the relationship between the airway closure and FRC, so that closing lung COPT volumes exceed FRC, creating low V/Q ratios COPT is being estimated clinically by measur- and hypoxaemia) 2 However, as long as gas can ing the protein concentration of fluid suctioned enter the alveolus the slightly greater diffusion from the airways 8.~s Airway fluid is even further distance created by interstitial oedema does not removed than lymph fluid from lung interstitial seem to impede gas exchange) t Once oedema fluid, both temporally and spatially. This creates fluid enters the alveoli (tung water more than 85 problems with the assumption that COPT can be per cent above control values) shunting develops derived from COP of airway fluid and must ac- and hypoxaemia results, j~ (Figure 4, ETV,. count for COP of airway fluid > plasma COP in 40 12 ml/kg, Pap2 6.25 kPa [47 mm Hg].) per cent ~a and 25 per cent s of patients reported to have an increased capillary permeability type of Effects oJPulmona~ Oedema pulmonary oedema. Nevertheless, airway fluid As stated earlier, interstitial pulmonary proteins may be helpful clinically in defining a oedema does not appear to create a diffusion pulmonary capillary permeability problem. barrier for oxygen, t~ While considerable lung damage seems to take place with interstitial emv oedema, most of the fluid is not in the thin gas Since the advent of the Swan Ganz catheter ~9 exchanging membrane between alveolus and we can estimate Pmv in a c|inical setting (equa- capillary (Figure 3). Once alveolar oedema de- tion 2), Pmv and COPmv remain the only factors velops, shunting increases leading to hypoxaemia in the Starling equation which are measurable in (Figure 4), This stimulates respiration, but in the patients, but they appear to be important factors presence of a slow circulation may lead to periods in the pathogenesis of pulmonary oedema, of apnoea. ~3 At a late stage hypercapnoea may also Pmv is elevated in many forms of heart disease occur, although this is not usual, and may result from either an elevated PeA or Lung mechanics are influenced by pulmonary PAP pressure (equation 2). In most cases, NOBLE:PULMONARYOEDEMA 291

30 I I I I I I INOPERATIVE EN0-OLASTOI.IC OIAMIE~A ~ FILLING PRESSURE - HUMAN LEFT VENTRICLE ES - 13 AVn C.S. 53 l :ol 25- CONTROL . o -rN =ol "-. 20-

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I oolNo oN flYP.t.ss o COUlN~ ORe BYPASS // J 10- i io 0 +,o LV EN~-DIA.STOLIC DIAMETER - I~

5- FIGURE 6 Left ventricular end - diastolic pressure (LAP) - left ventricular end-diastolic diameter data before and after 60 minutes of ischaemic arrest for I I I I aortic valve replacement. (From Spotnitz, H., Breg- 0 1 2 3 4 5 6 man, D. et al; 2~ reprinted by permission of The Ameri- MM C.,NGE 'N MYOC,,..,, can Heart Association, Inc.) SEGMENT LENGTH +4- FIGURE 5 The X-axis is the mm change in segment length of the left ventricular muscle as it is increased in size which is plotted against the left ventricular end- +3- diastolic pressures (LVEDP) at the same times. (From Sardoff, S.J. & Mitchell, J.H.; :~ reprinted by permis- ~- +2- sion of American Journal of Medicine.) ,l- excluding mitral valve disease, acute aortic regurgitation with preclosure of the mitral valve, i O- pulmonary veno-occlusive disease, and high S -1- pulmonary vascular resistance (PVR), PAO pres- y=0.52 + 0.23x sure elevations reflect left atrial pressures and left -2- r= 0.75 ventricular end-diastolic pressure (LVEDP) which relates to the size of the left ventricle just -3 -6 before it contracts. A PMV mm Hg The compliance curve of the normal left ventricle (Figure 5) :~ indicates that as the ventricle is FtCURE 7 The change in Pmv (APmv) from filled to pressures beyond 20 cm H20 (15 mm Hg, preoperatively to the day following aorto-coronary or 2 kPa) very small volume increases will result bypass surgery is plotted against the change in lung in very large pressure increases that should be water (AETVt,) over the same time. (Reprinted by permission of Can. Anaes. Soc. J.) transmitted to the pulmonary vessels as an increased Pmv and an increased tendency to pulmonary oedema, The non-compliant ventricle nary bypass for aortocoronary bypass proce- would worsen this tendency. An example of a dures we found an increase in lung water the day non-compliant ventricle in a patient is presented after operation which relates to an increased in Figure 6, and was created by 60 minutes of Pmv 2" (Figure 7). ischaemic arrest for aortic valve replacement. 2~ In the cases where PAO does not reflect After coming off bypass this patient has a smaller LVEDP, as in mitral valve disease, aortic regur- left ventricular end diastolic diameter and a gitation, pulmonary venous constriction (post- higher left atrial pressure, indicating a tendency ulated to occur in shock :3) and high PVR, the to a low cardiac output and high Pray. result will still be an increased Pmv and tendency Regardless of why the left ventricle fails, in- to oedema formation. It is difficult in patients creased preload or afterload, reduced myocardial with mitral valve disease to explain why they do contractility or heart rate and rhythm problems, not have pulmonary oedema more often. Several left ventricular failure will increase Pmv and may explanations have been proposed: The wall of lead to pulmonary oedema. After cardiopulmo- dependent arterioles hypertrophy, reducing flow 292 CANADIAN ANAESTHETISTS' SOCIETY JOURNAL to the lower lung and so tending to ,educe the 23- effect of a high Pmv in capillaries at the lung 21- bases. 24 The dependent arterioles are surrounded by oedema fluid, increasing perfusion to the top of the lung. 25 Lymphatics may hypertrophy and increase the capacity for removal of fluid from the lung. An alternate explanation for the apparent lack of pulmonary oedema in patients with milral " 13- ~, valve disease is that the fluid is present in the o. 9,e*..3 interstitium of the lung and our techniques for o 11- diagnosing small increases in lung water are not adequate. F--4 Pmv may also be elevated with an increase in 7- P~(equation 2) without increases in PAO, when 5 I i i pulmonary vascular resistance (PVR) is elevated. CONTROL 0 30 60 90 120180POST*OPAI~1 PM1 AM2 The classic lesion creating this disturbance is ON PUMP (rain) TIME OF MEASUREMENT pulmonary embolus. Pulmonary emboli may be FIGURE 8 Colloidosmotic pressure before, during large (fibrin clot), or small (platelet micro- and after cardiopulmonary bypass (on pump). (Re- aggregates). After haemorrhagic shock and blood printed by permission of Can. Anaes. Soc. J.). reinfusion in dogs we have shown an immediate increase in lung water associated with increased COPmv PVR. 26 Staub has shown that various forms of The normal value quoted in most textbooks for emboli (glass beads, fibrin or fat) sufficient to colloid osmotic pressure is 3.33 - 3.72 kPa (25 - increase pulmonary vascular resistance are as- 28 mm I--lg).27 This is true in the normal mobile sociated with increased lymphatic flow from individual. However, in patients undergoing sheep lungs and, presumably, increased lung aorto-coronary bypass surgery we found control water. 5 The increased lung water of these studies values of 2.51 _ 0.09 kPa (18.9 + 0.7mm Hg) zz can be explained either by high Pmv in capillaries (Figure 8). This agrees with data on supine sub- that remain open, pulmonary arteriolar fluid jects when COPmv fell 0.8 + 0.33kPa (6 + leakage when P~ is elevated, or increased capil- 2.5 mm Hg) from their control mobile values. ~s lary permeability,s This implies that patients in the operating room, recovery room or Intensive Care Unit will have PT COPmv at or below 2.53 kPa (19 mm Hg), de- Of the factors in Starling's equation, we know pending on their fluid and nutritional status. least about Pr. Many attempts have been made to If fiaemodilution is used during cardiopulmo- measure Pr, with only partial success because to nary bypass, COPmv is further reduced while on dale there is no direct method to enter the inter- bypass. We studied two groups of patients under- stitial space without altering it. Several tech- going cardiopulmonary bypass procedures. ~2 niques ,6,7 each with their own assumptions, have One group (Ringer's) had the pump primed with now suggested that P~ is normally a negative lactated Ringer's solution (2,000 ml), the second number in animal experiments (-0.67 to -0.93 group (plasma) with lactated Ringer's solution kPa [-5 to -7 mm Hg]). Parker, et al. 7 have also and 2 units of plasma. Figure 8 indicates that the found that Pr increases as pulmonary oedema plasma group has a slightly higher COPmv (I.3(] increases and above PT = 0 mm Hg the rate of 4- 0.04 kPa [9.8 4- 0.3 mm Hg]) than the Ringer's oedema formation increases. The upper limit of group ( 1.17 4- 0.04 kPa [8.8 4- 0.3 mm Hg]) while PT has not been defined, but the highest levels on cardiopulmonary bypass. Within one hour ol reported by Parker, et al. 7 of +5ram Hg surgery COPmv was the same in both groups al (+0.67 kPa) P'r were associated with a doubling of 1.89 4- 0.11 kPa (14.2 4- 0.8mm Hg) and con- lung water. Since very little is known about Pr in tinued to rise over the next two days although il highly invasive animal experiments, it is not sur- remained significantly lower than control values prising that clinical data are not available. What Lung water was measured in these patients pre. there is suggests that pleural pressure may relate and postoperatively with a double indicator dilu. to Pr. If this is so, we may be able to alter PT by lion technique (ETVL), There were no significanl changing ventilation patterns. increases in lung water immediately after opera. NOBLE: PULMONARY OEDEMA 293

This is one example of how the difference between Pmv and COPmv is a major determinant of r pulmonary oedema. In 12 patients undergoing aortocoronary bypass surgery, the most Patient ] o significant relationship emerged when we plotted ~25. Patient 2 x the change in pre-operative to post-operative [Pmv - COPmv] against the change in lung water over the same time (Figure 10). Therefore the !--22 x relationship between Pray and COPmv is important in the formation of pulmonary oedema.

Lymphatic Removal of Oedema Once fluids and proteins pass into the ex- ,d-oP ~ ' go' ,'o ' ]~o' iLo' 2~,o' do Pd~.oP min, On CPB travascular compartment of the lung, lymphatics TIME OF MEASUREMENT must remove them. Since the lymphatics are not FIGURE 9 Polmonary artery and colloid osmotic thought to be muscular vessels~~ movement of (COP) pressure in two patients preoperatively fluid is considered passive along pressure gra- (PRE-OP). while on cardiopulmonary bypass (CPB) dients created by respiratory movements. The and postoperatively (POST-OP). Patient one developed lung lymph fluid finally empties into the central a 57 per cent increase in lung water and 143 per cent increase in shunt fi'action because the left ventricular venous system. There is evidence3~ that a high vent was inadequate, while patient two had no increase central venous pressure may impede lymphatic in either lung water or shunt with a well functioning left drainage from the lung. The reserve within the ventricular vent. The brief increases in pulmonary ar- lymphatic drainage system of the lung seems to tery pressure in patient two relate to episodes of lifting the heart. (Reprinted by permission of Anesthesiology.) be very large. In sheep a tenfold increase above normal lung lymph flow has been measured at tion in either the Ringer's or plasma group of Pmv levels of 3.99 kPa (30 mm Hg). 4 patients despite their low COPmv. This would suggest COPmv is not very important in the Capillary Permeabilio, production of pulmonary oedema. However it is Evaluation of membrane permeability to water more likely that interstitial tissue "reserves" of and proteins remains a problem because we have P'r and COP.r had been used up by the low no method to measure this parameter. Indirect COPmv, for, with time and a slight rise in Pray evidence indicates that increased capillary per- from 1.68 to 2.0kPa (12.6 to 15ram Hg) a meability does occur. 3'3z'33 Brigham, et al. 3 fol- significant increase in lung water occurred. lowed lymph flow from the lungs as an indicator Figure 9 illustrates pressure in the pulmonary of lung water while they increased Pray (Figure artery (P~-A)and COPmv values from two patients 1 l). In normal sheep there was a slight rise in undergoing aortocoronary bypass surgery. 29 lymph flow; but in the same sheep, after COPmv is low while on cardiopulmonary bypass pseudomonas bacteria were infused, smaller in- in both patients. When the left ventricular vent creases in Pmv created very large increases in was placed in patient number two blood was lung lymph flow. This indicated a new increased drained from the left ventricle and P~ fell to capillary permeability so that fluid and proteins below COPmv values. There were temporary moved into extravascuIar lung at a low Pray. rises in P~ associated with lifting the heart, but There is a long list of causes of increased on the whole P~- COPmv was a negative capillary permeability. Table 1 is not exhaustive, number. This patient did not develop pulmonary but it indicates the kinds of clinical cases which oedema or increased shunting. For various rea- may be associated with an increased pulmonary sons (aortic regurgitation and technical) the left capillary permeability. A large number of dis- ventricular vent was inadequate in patient eases in this list are well known to be associated number one and P~ was high throughout the with a high Pmv. For example: shock, pulmonary pump run and well above COPmv values. This emboli, uraemia, massive blood transfusion, post patient developed radiologically visible pulmo- cardiopulmonary bypass, neurogenic and high nary oedema immediately after operation, a 57 altitude pulmonary oedema may all be associated per cent increase in lung water and a 143 per cent with a high Pray. This will compound any capil- increase in shunt fraction. lary permeability problem and should be consid- 294 CANADIAN ANAESTHETISTS' SOCIETY JOURNAL

TABLE I +4- RINGER'S PLASMA CAUSES OF NON - CARDIOGENIC PULMONARY OtCDEMA +3- Shock - any aetiology

"- +2- Infection - pneumonias Trauma - fat embolism

+1- - lung contusion I,'- M,I - pneumothorax - post re-expansion ~ O- - radiation pneumonitis Aspiration - liquid - gastric contents

-1" , r=0.78 - near drowning - gas - 02 - smoke

- NO2, C12, NHa - phosgene ,,', [~, -c,o.e.,.] Metabolic - pancreatitis - uraemia FIGURE l0 Preoperative to postoperative changes Drug related -allergic reaction in [Pmv-COPmv] in mm Hg after A-C bypass surgery -overdose - heroin relate well to changes in lung water (ETVO over the - barbiturates same time. (Reprinted by permission of Can. Anaes. - methadone Soc. J.) - acetylsalicylic acid

- dextran 80 - alloxan

- oleic acid Hematologic - diffuse intravaseular coagulation - massive blood transfusion 6O - post cardio-pulmonary bypass - pulmonary embolism Others - neurogenic Lunq Lymph - high altitude pulmonary oedema Flow 4C (ml/h) concept that Starling's law is still operative 3'34'35 and the effectiveness of lowering Pmv in treating 2( pulmonary oedema due to increased capillary permeability.

-/7 40 Puhnonary Oedema while on Cardiopubnonary Pulmonory Microvosculor Pressure {cm H20) Bypass Since there is very little lung peffusion during FIGURE 11 Open symbols represent increases in cardiopulmonary bypass (CPB), pulmonary lung lymph flow seen when Pmv is increased in normal oedema during CPB would seem an unlikely sheep. Closed symbols represent changes in lung lymph flow with increased Pmv after pseudornonas bacteria. event. What blood there is comes from the (From Brigham, K.L., Woolverton, W.C., eta/., 3 re- bronchial circulation and back flow of blood printed by permission ofJ. Clin. Invest.) through incompetent aortic and mitral valves, lfa left ventricular vent is used Pray is kept below ered in patient management, for we know of no COPmv and pulmonary oedema is not formed. 29 specific therapy to reduce pulmonary capillary However, ifa left ventricular vent is not used, or permeability. Steroids are not of proven benefit. if the vent is not functioning properly, Pray is Obviously we should remove any cause of in- elevated and pulmonary oedema may accumulate creased capillary permeability. If we re-examine in spite of low blood flows through the lungs while Starling's equation (1), we do not know how to on CPB. 29 influence Kf, Gf, Pr or COPr. We are left with The type of oxygenator used may also play a either reducing Pmv or increasing COPmv. One role as PVR was found to be elevated 100 per cent of the problems with infusing colloids is their immediately after bubble oxygenation, but not tendency to leak into the extravascular lung, after membrane oxygenation? 6 In the bubble worsening pulmonary oedema. The only alterna- oxygenator group of patients PVR had returned tive left is to reduce Pmv even when it is not to control levels by the morning after operation. elevated. There is evidence to support both the Presumably these results indicate that substances NOBLE: PULMONARY OEDEMA 295 have been released from platelets or cells dam- resulting in incorrect treatment; and if initial aged in the bubble oxygenator, since platelet and therapy based on CVP information has not im- cell survival is better after membrane oxygena- proved the patient, a pulmonary artery catheter tion ?6 Lung water was elevated the morning after should be placed at least in those patients where operation in patients with bubble oxygenation pulmonary oedema is suspected. An additional and was not elevated in patients with membrane benefit of this catheter would be the determina- oxygenation. 36 Lack of lung peffusion apparently tion of cardiac output using a thermodilution did not create an increase in capillary permeabil- technique. 3~ ity as lung water was not increased immediately Blood gas and hlng compliance changes ~2 after operation when left ventricular venting was should be measured in pulmonary oedema, but adequate. 29 and lung water was not related to the they are not very helpful in diagnosing pulmonary length of CP bypass. oedema as they occur for many other reasons. The best non-invasive method for recognition IV DIAGNOSIS of early pulmonary oedema appears to be the chest radiograph.+~ In order to achieve diagnostic The history and physical examination of the accuracy, films should be taken with the patient patient are valuable, looking for features which in the upright position, with fixed distances be- could lead to pulmonary oedema. Several points tween machine and patient to allow sequential concerning this examination should be stressed. comparisons and with short exposures of less First, tales or rhonchi may occur only in the late than 0.033see (producing 200MA) to minimize stages of alveolar oedema and be absent in the artifacts due to respiratory and cardiac motion. 4~ interstitial phase. Second, the left and right ven- Using these techniques the haziness of pulmo- tricles can each fail independently of the other. nary vessel and bronchial borders are a valuable Several papers have indicated there is no re- early sign of interstitial pulmonary oedema. At lationship between CVP and PAO or between least in the intensive care unit (I.C.U.) these changes in CVP and PAO after volume infu- standards are difficult to meet, so that methods to sion. 37as We have noted patients after aorto- quantify lung water may be needed. In I.C.U. coronary bypass surgery with high CVP and low patients, when both pulmonary artery and sys- PAO and, on the other hand, with high PAO and temic arterial lines are needed, double indicator low CVP. The potential problems in attempting dilution techniques using thermal (ETVL) 4t'42 or to relate CVP to PAO are the function of the radioactive isotopes (tritiated water) 43 can be pulmonary vessels and the different diastolic employed to quantify lung water. pressure volume curves of the two ventricles. If the pulmonary vascular resistance (PVR) were V MANAGEMENT high, CVP might reasonably be expected not to relate to PAO. If the right ventricle were either Management of patients should be directed to failing or hypertrophied, CVP might not relate to preventing the causes of pulmonary oedema. If PAO. It is also possible that differences in left and this fails, an early diagnosis may prevent the vi- right ventricular compliance will remove any cious cycle of: CVP to PAO relationship, or that pulmonary vas- Pulmonary Oedema cular responses will remove a relationship between changes in CVP and changes in PAO. Left Ventricular < Hypoxaemia While CVP and PAO sometimes parallel each Failure other, we could not predict when this relationship would hold. An example of a situation that might and the late rapid rise in pulmonary oedema. be expected to lead to a low CVP and a high PAO Once alveolar oedema is present, hypoxaemia would be the patient after closure of an atrial will rapidly follow. This requires that oxygen septal defect who is given large volumes of fluid therapy be instituted. This may be by nasal can- to raise the CVP and keep the filling pressure nula, mask or positive pressure ventilation, de- high. The right ventricle is hypertrophied due to pending on the severity. If positive pressure ven- chronic volume overload and unlikely to fail. The tilation is to be undertaken, continuous positive previously protected left ventricle can only eject pressure ventilation (CPPV) should be consid- at the expense of a much higher filling pressure. ered. Many investigators have shown ~~ This could lead to a high PAO while the CVP is that CPPV increases FRC and Pao~, but it does low. This implies that CVP can be misleading, not remove lung water. 296 CANADIAN ANAESTHETISTS' SOCIETY JOURNAL

100-

80- ' ? 9 "-- 20 NORMAL 15 ~_~ 'E VASODILATIUN ! g - g. 40- 0 TAILING i VENTRICLE i

20- M lION

l 1 ~ 1 ; '6 L vt.op m~,, TIME (HOURS) FIGURE 14 Normal and failing Frank-Starling FIGure 12 The time course of lung water (ETVL) curves. Left ventricular end-diastolic pressure and Pao~ before and after the rapid infusion of dextran (LVEDP) is plotted against cardiac index (C.I.). Once a 40 to increase and hold PPA to 5.32kPa (40mm Hg). patient has both pulmonary congestion and a low car- Once alveolar oedema was present CPPV was applied. diac index the effect of three pharmacologic interventions are plotted.

Why CPPV does not reduce pulmonary oedema has been clarified by Bo, et al. 45 In isolated perfused rabbit lungs they found divergent effects of CPPV on fluid filtration in the lungs, depending on experimental conditions. When alveolar pressure was increased without increasing alveolar volume, fluid filtration decreased. This was thought to be due to an increased PT. When alveolar volume was increased, fluid filtration increased. The effect of CPPV in the clinical situation should then depend on the balance between an increased alveolar volume (more oedema) and increased alveolar pressure (less oedema), since FIGURE 13 The same lung shown in Figure 11 but these are both applied with CPPV. This equation now with CPPV applied, There is still debris in the will also be influenced by the effects of CPPV on alveolus (A) but now air is forced in. Blisters (B) of vascular pressures (both Pmv and central venous interstitial fluid are still present and collagen fibres are still widely separated (arrow) • 10,200. (Reprinted by pressure 31'46) and hormonal influences47 in the permission of Can. Anaes, Soc. J.) intact patient. In summary, CPPV improves Pap2, probably Figure 12 illustrates results from a dog when by increasing FRC, but it does not remove pul- pulmonary oedema was induced by increasing monary oedema. The improved Pap2 gained with Pmv with an infusion of dextran 40. The amount CPPV will provide lime so that therapy directed of pulmonary oedema (ETVL) shows the typical at Starling's forces can be started. The difficulty time course associated with a falling Pap2. When with CPPV is that Q may be reduced and hence CPPV is applied the rate of rise of ETVt, is not worsen oxygen transport t2 to tissues. This may changed while there is a sudden increase in Pan2. reduce Pvo~ and magnify the effect of any existing Figure 13 (ETVL 19.7 ml kg, Pap29.18 kPa [69 mm pulmonary shunt, This is best handled by Hg]) is an electron microscopic section taken monitoringQ to determine the best CPPV level to from the same dog illustrated earlier(Figures 2, 3, apply, and whether vasoactive drugs are needed and 4), but now with CPPV applied following to support the circulation. alveolar oedema. ~~ The lungs have more pulmo- Obviously oxygenation must be maintained nary oedema than in Figure 4, but now CPPV has and either an increased inspired oxygen concen- opened alveoli so that in spite of a slight increase tration or CPPV should do this. But to actually in alveolar capillary distance oxygenation can remove or prevent pulmonary oedema we must occur. do one of three things: reduce Pmv, increase NOBLE: PULMONARY OEDEMA 297

c.,~1,~ B J l z'~ 04 ZD w coml,a~' 0.41 ec 15 NiIrOplv~u41ej~ 14 Z5~ '~o 7/. |. O~ /0~ I~II IMa I i I I I I , , , , : , lO |0 UO 130 1SO 170 o ~ 70 w 11o lao 120 t tO lO0 VOLUME VOLUME~Ni VOLUME I~) FIGURE 15 Left ventricular pressure volume curves of patients exhibiting shifts following haemodynamic interventions are shown. The left panel shows continuity of curves with nitroprusside, but a marked shift with angiotensin. The middle panel shows a similar result following nitroprusside and angiotensin. The right panel shows a marked downward shift of the pressure volume curve with nitroprusside. (From Alderman, E.L. & Glantz, S.A. ;4~ reprinted by permission of The American Heart Assoc. Inc.)

COPmv or remove the cause of the increased diastolic volume (LVEDV), for this relates to the capillary permeability. Of these, the one we seem stretch of the myocardial fibres before contrac- to have most influence over is Pmv. Left ven- tion. But LVEDV is difficult to measure, so we tricular preload can be reduced with phlebotomy, assume there is a relationship between LVEDP increased venous capacity (eg. morphine or ni- and LVEDV. There is a compliance relationship troglycerine), diuretics, valve repair, or de- but it is alinear; and the right and left ventricles creased volume loading with appropriate in- are different. Figure 15 is taken from Alderman travenous therapy. Myocardial contractility can and Glantz 48 who have demonstrated shifts in the be increased by correcting acid base or electro- left ventricular pressure volume relationship de- lyte disturbances or adding digoxin, isuprel, pending on whether afterload was increased (less dopamine, dobutamine or adrenaline. Afterload compliant) or decreased (more compliant). They may be reduced with vasodilators such as phen- suggest that the steep compliance curve created tolamine or nitroprusside, intra-aortic balloon by increasing afterload with angiotension may be counterpulsation support, or by repairing a a result of increased right ventricular volume stenosed valve. Arrythmias must be controlled. pushing the interventricular septum to the left. Patients with pulmonary oedema may also Reduction of afterload with nitroprusside would have a low cardiac output (Figure 14). This will decrease right ventricular volume, shift the sep- determine whether one reduces Pmv by manipu- turn to the right and increase left ventricular com- lation of preload, myocardial contractility or af- pliance. Bemis, et al. 49 used an isolated perfused terload. A diuretic may reduce Pmv but may de- dog heart with an intact pericardium to show that crease Q. Dopamine or catecholamines may re- increases in right ventricular filling pressure in- duce Pmv and increase Q, but may also increase creased left ventricular filling pressure. Elzinga, myocardial oxygen consumption and, in the et aL so found the same thing in an isolated cat presence of a coronary artery stenosis, may heart. In addition they showed that removing the create an imbalance between oxygen supply and pericardium makes the left ventricular pressure demand in the myocardium. A vasodilator may less sensitive to right ventricular pressure improve both Pmv andQ, but in the patient with a changes. External forces acting on the left ventri- very low blood pressure might decrease coronary cle, including those that arise from pleural pres- peffusion. All three therapeutic interventions re- sure, right ventricular pressure and the pericar- duce Pmv, and therefore the tendency to pulmo- dium must be considered when interpreting nary oedema, but which is the best? LVEDP and LVEDV. Increases in pericardial Re-examining Figure 14, the abscissa should and right ventricular pressures should create a not be left ventricular end-diastolic pressure steep compliance curve. Then, small increases in (LVEDP). It should be left ventricular end- LVEDV (one of the determinants of stroke vol- 298 CANADIAN ANAESTHETISTS' SOCIETY JOURNAL ume) will create large increases in LVEDP and, after aorto-coronary bypass operations we found therefore, the flat failing Starling curve of Figure that PAP pressures of less than 2 kPa ( 15 mm Hg) 14. The data of Alderman and Glantz48 would did not lead to pulmonary oedema. :2 If the patient suggest treatment of the patient with a steep left has an adequate O to maintain wakefulness, a ventricular compliance curve (and therefore the good urine putput and warm extremities with a failing Starling curve of Figure 14) with afterload PAP pressure of 1.33kPa (10ram Hg) there reduction. This should create both an inereasedQ would seem little point in raising that pressure and a reduced LVEDP, which will lower Pmv and with further fluid infusions. On the other hand, an decrease the tendency to pulmonary oedema. inadequate O at PAP pressures of 2 kPa ( 15 mm Following cardiac surgery, patients present Hg) may dictate further fluid infusions to raise with several of these problems. They are likely to PAP pressures to 2.39kPa (18ram Hg) or even be well volume loaded and, therefore, to have higher. Finally, the patient with an increased high right ventricular volumes; to be on a ven- capillary permeability should have the lowest tilator, increasing pleural pressure; and they may PAP compatible with wakefulness, an adequate have some degree of pericardial tamponade. For Q and renal function. This may mean reducing these reasons Intensive Care Unit patients are PAP well below pressures that are considered also likely to have poor compliance of the left normal and may involve manipulations of pre- ventricle. Reduction of aflerload may be benefi- load, contractility or afterload that would other- cial in some of these patients. wise not be necessary. There is a long list of vasodilating drugs avail- Attempts to reverse Starling's forces by in- able. The choice depends on the patient's predo- creasing COPmv must be used cautiously. Col- minant problem. If mitral regurgitation predomi- loid infusions will increase blood volume. If this nates, arterial vasodilation with hydralazine or volume increase occurs in the rapidly rising por- phentolamine should be useful. If the worse tion of the ventricular compliance curve (Figures problem is pulmonary congestion, nitroglycerine 5, 6 & 15) a large increase in LVEDP will result should reduce preload, lfQ is reduced and pul- and pulmonary oedema may be worsened. If any monary congestion is present, nitroprusside or portion of the oedema accumulation is due to an prazosin should be helpful. Miller, et al. ~ have increased capillary permeability, colloids may shown that while reduction of afterload with ni- leak into the extravascular compartment and in- troprusside improvesQ while lowering Pmv, and crease COP,v, thereby increasing the tendency to improving myocardial contractility with dopa- oedema formation. With these considerations in mine does the same. the largest increase inQ and mind, slow infusions of colloid with the addition reduction in Pmv resulted from a combination of of a diuretic may reduce puhnonary oedema. nitroprusside and dopamine. If nitroprusside or A "'state of the art" review has been pub- nitroglycerine are used in treatment of pulmonary lished 5" regarding the controversy surrounding oedema there must be close monitoring of Pap2. the intravenous use of crystalloid or colloid for NitroprUssides2,s~ has been shown to impede resuscitation and prevention or treatment of pul- hypoxic pulmonary vasoconstriction and in this monary oedema. I will not restate the arguments, way to increase pulmonary shunting and reduce but express the view that the controversy stems Pao2. from our inability to measure tissue "reserves" All of these therapies have potentially serious in Starling's equation and interstitial oedema. complications and an optimum level of applica- Until we know COPT and P'r we cannot know tion, so that either more or less would result in which patient has low or absent tissue" reserves" patient deterioration. For these reasons close and therefore may need colloids. Again, because monitoring of these patients during therapy must we can not measure COP-r and PT. we do not even be undertaken. If the patient is so ill that in- know if colloids will restore these tissue "re- travenous isuprel, dobutamine, adrenaline, ni- serves" to normal. The initial point at which tis- troprusside, nitroglycerine and/or phentolamine sue "reserves" and lymphatic drainage from the therapy is necessary, a Swan Ganz catheter lung are overwhelmed, leading to interstitial should be placed and Q determined so that the oedema, is difficult to diagnose because intersti- optimum preload contractility afterload relation- tial oedema may not result in hypoxaemia, physi- ship can be established and the best drug combi- cal findings or changes in chest radiographs. nation and dosage for the particular patient used. These clinical problems need to be solved. In the The optimum PAP pressure for most patients is meantime estimates of who will benefit from the between 1.6-2 kPa (12-15 mm Hg). In 15 patients infusion of colloids and who will not, have to be NOBLE; PULMONARY OEDEMA 299 made on the best information we have, which therapeutic manoeuvres are available and the includes Pmv, COPmv and an estimate of how P'r anaesthetist should be conversant with their use and COPy might be expected to change in given during the surgical procedure in order to provide circumstances. The potential benefits of colloid optimal care. Postoperatively, intensive infusions must be balanced against the risks of monitoring and care must be applied. Oxygena- increasing Pmv and of proteins moving extravas- tion is best maintained by applying CPPV, as- cu[arly, as the patient who may benefit from col- suming the cardiovascular system will tolerate it, loids probably has limited cardiorespiratory and rather than by increasing the Fto~ which may, by nutritional reserves. itself, damage the lungs. The patient with a normal cardiorcspiratory system should not develop pulmonary oedema V[ IMPLICATIONS OF PULMONARY OEDEMA TO because of the large reserves implicit in Starling's THE ANAESTHETIST equation. Even so, these reserves should not be Since pulmonary oedema is associated with encroached upon and fluid and other therapy hypoxaemia and often with myocardial disease, it should be applied with Starling's forces in mind. goes without saying that surgical and anaesthetic stress should not be added to this already life ACKNOWLEDGEMENTS threatening situation. There are seldom excep- I would like to thank the fellows and techni- tions to this, but these exceptions might include a cians who collaborated with me, and whose pa- patient in chronic pulmonary oedema whose pers are referenced in this article. Drs. R.J. condition and drug doses are considered op- Byrick, L. Casella, R. Chisolm and M. Kolton, timum; a patient for emergency surgery where and Mr. J.C. Kay were most helpful in reviewing delay would be disastrous (but even here one or and Mrs. P. Slusarenko in preparing the manu- two hours of intensive therapy before operation script. might be useful); and a patient to undergo a procedure that would reduce the pulmonary oedema such as mitral valve replacement. If patients in REFERENCES these conditions are anaesthetized, intravenous 1. STARLING, E.H. On the absorption of fluids from fluids, drugs (both anaesthetic and other) and the connective tissue spaces. J. 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RI~SUME. L'~ed~me pulmonaire est le r~sultat du d~rangement d'un m~canisme physiologique qui permet la production et le retrait eonlinuels de l'eau extravasculaire pulmonaire selon les principes basds sur I'dquation de Starling qHi contrdlent les mouvements des fluides ~, travers une membrane semi-permdable. Tous les parametres de l'equation de Starling ne peuvent pas &re mesur~s. Cependant, I'expdrimentation permet de penser que l'augmentation de la pression capillaire hydrostatique pousse Ic liquide clans I'espace extravasculaireet dilue ainsi la pression osmotique colloide tout en augmentant la pression hydrostatique des fluides du tissus pulmonaire. Lorsque ces reserves et la capacitfi du syst~me lymphatique pulmonaire sont d~bordees. I'oedeme pulmonaire survient. L'0edi:me peut aussi rdsulter d'une diminution de la pression osmotique colloide 5. I'intdrieur des capillaires pulmonaires et d'une augmentation de la perm~abilit~ de ces m~mes capillaires en I'absence d'une pression osmotique capillaire pul monaire 61ev~e. Si l'cedbme pulmonaire se forme lentement au d~part, et se ddveloppe beaucoup plus rapidcment dans les stages avane~s, il est probable que c'est i cause de I'ensemble des r~serves formdes par la pression colloide osmotique des fluides tissulaires, de la pressin hydrostatique des fluides du tissus pulmonaire et du drainage lymphatique. La vitesse de formation de l'ced~me peut aussi &re en rapport avec le dommage caus6 au poumon par l'ced~me interstitiel, qui ouvre la voie au stage plus avance de ~ed~me alvdolaire. Bien que la compliance pulmonaire soit diminude avec I'augmentation progressive de l'o~d~me, I'augmentation du shunt et de l'hypoxdmie du poumon normal ne surviennent qu'avec I'0eddme alvdolaire. Le diagnostic de l'ced~me puhnonaire se fair par la recherche de se causes et par la radiographic du poumon. Son traitement doit commencer par le maintien de I'oxyg~nation, et la meilleur moyen d'atteindre cet objectif esl la ventilation h pression positive continue (CPPV). Celte ma- nteuvre n'enl~ve pas l'eau du poumon ten r~allt6 elle peut I'augmenter I~g~rement) mais elle amdliore I'oxygdnation en ventilant des alvdoles d~jS~ remplies de liquide. Cette amelioration de I'oxygbnation nous permel de temporiser en attendant une thdrapeutique approprifie h la cause scion la Ioi de Starling. L'dtat actuel de nos connaissances ne nous permet pas de trailer l'hyperpormdabilit~ capillaireautrement qu'en abolisant sa cause: il ne nous est pas possible non plus de rfiduire la pression osmotique des colloides tissulaires, ni d'augmenter la pression hydrostatique des fluides contenus dans le tissus pulmonaire ou la pression colloide intracapillaire ou encore le flux lymphatique. 11 ne nous reste done pour trailer I'ced~me pulmonaire que deux manoeuvres: soit I'augmentation de la pression osmotique des colloides intracapillaires soit la diminution de la pression hydrostatique pulmonaire. Mals l~ de colloides pout constituer un danger Iorsque la compliance ventriculaire gauche est diminude par l'augmeotation du volume intravasculaire qui s'ensuit, ce qui aura pour effet d'61ever la pression hydrostatique capillaire pulmonaire et d'aggraver I'oed~me. Si c'est I'augmentation de perm~abilit~ capillaire qui est en cause, il s'en suivra une fuite vers I'espace extra-vasculaire de colloides avec entrainement d'eau. Si on fait abstraction du traitement causal, la thdrapeutique la plus imporlante de I'ced~me pulmonaire devient donc la rdduction de la pression capillaire by- 302 CANADIAN ANAESTHETISTS' SOCIETY JOURNAL

drostatique. D'apr~s la cause de I'~dbme et la valeur du d6bit cardiaque, la pression capillaire pulmonaire peut &re r~duite en diminuant la pr~-charge ventriculaire gauche, r augmentant la contractibilit6 ou par une association dc cos dcux mano.'uvres. Les implications pour I'anesth~siste sont que les r~serves de Starling sont vastes el que I'~cd~me pulmonaire ne devrait pas survenir chez le sujet normal. A la p~:riode pr~-op6ratoire. chez le malade atteinl d'cedeme pulmonaire ou d'une r6serve cardiopulmonaire basse, lous les efforts doivent ~:tre tent~s pour optimiser les forces de Starling avant d'induire I'anesth~sie darts des conditions qui risquent de devenir catastrophiques.