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PULMONARY AIR EMBOLI DURING CARDIAC SURGERY
P U L M O N A R Y AIR EMBOLI D U R I N G CARDIAC SURGERY Robert M. Anderson,
M.D., James M. Fritz, M.D.,
James E. O'Hare, M.D., Tucson,
and
Ariz.
T
HE occurrence of pulmonary air emboli is a significant hazard in open-heart surgery. This study was done to obtain objective evidence in support of this clinical observation. This investigation deals with only one of the possible detrimental effects of pulmonary air embolism: its effect on pulmonary pres sure due to increased pulmonary vascular resistance. The findings suggest that air emboli account for some post-bypass problems following open-heart surgery. The devastating effect of air emboli on vital organs is well documented.-' 3 ' 5> 6 Cerebral air emboli 2 ' 3 and myocardial dysfunction from coronary air em 6 boli are recognized as complications of open-heart surgery. The blocking effect of air to right heart emptying has been considered a factor in death from venous air embolism since the time of Virchow.5 Recently Wright 7 has produced pul monary vascular damage with resulting pulmonary hypertension in experimental animals by repeated venous air injections over many weeks. There has, how ever, been little mention of the deleterious effects of pulmonary air emboli occurring during open-heart surgery. CLINICAL OBSERVATION
In our early cases of heart surgery, there was occasional occurrence of moderate increase in the pulmonary artery pressure immediately after cardiopulmonary bypass. This was noted in cases in which the right heart was open for repair of septal defects, pulmonary stenosis, or when a right-sided vent had been used during the course of repair of some left-sided lesion, such as mitral insufficiency or stenosis. This pressure elevation was usually mild and of transient nature. However, in patients with severe preoperative pulmonary hypertension from pulmonary arteriosclerosis, the increase in pulmonary artery pressure after bypass was of considerable concern. The right heart failure sec ondary to increased pulmonary resistance was the mechanism of death in some cases. Furthermore, there was an occasional patient who had had an adequate repair of a simple pulmonary stenosis, or other congenital defect, whose post operative pulmonary problems were greater than expected. Tracheotomies were Prom the Department of Zoology, University of Arizona, and the Department of Surgery of Tucson Medical Center, and St. Mary's Hospital, Tucson, Ariz. Supported by research grants from the Santa Barbara California and Orange County California Heart Associations. Received for publication June 30, 1964. 440
Vol. 49, No. 3 Mard), 1965
PULMONARY AIR EMBOLI
441
frequently necessary in these cases. These occurrences were in patients in whom no other obvious insult to the lungs had occurred, and in whom a left heart vent had been used to guard against trauma to the lungs from overdistention of its vasculature with blood and the prevention of any elevation in pulmonary pressure during perfusion. 1 ' i In some of these cases, air which had entered the right heart and traversed the lung was seen coming out of the left vent. After closing the right heart, all visible air was allowed to escape through the left vent before its closure and the termination of the perfusion. In the last 130 clinical cases, since taking precautions against any air entering the pulmonary artery, there has been marked reduction in our postoperative pul monary problems. Post-bypass increase in pulmonary pressure has not been observed. Only one patient has required a tracheotomy.
^Mw^w^
Fig. 1.—Cardiotomy suction used with pump oxygenator. The bubbles in the tubing decrease the effective suction because of the surface tensions of the many menisci.
PHYSICAL PRINCIPLE INVOLVED
Bubbles in small tubes impede the flow of liquid because of the resistance of the surface tensions of their many menisci. This physical principle accounts for the increase in resistance to flow of blood in a vessel by air bubbles. To il lustrate this principle, reference is made to the cardiotomy suction used with our oxygenator (Fig. 1). With this device, a constant suction of 30 cm. water pressure is applied to a reservoir to which suction tubing is attached. When the suction tubing is filled with a column of blood without bubbles there is rapid movement of fluid in the tubing. However, the greater the number of air bubbles in the tubing the less the effective suction and the slower the move ment of the column. If the tubing is full of froth, so that the additive effect of the surface tensions of the many menisci equals the suction pressure, ef fective suction is eliminated and the flow stops. Elevating the sucker tip allows the froth to move on into the reservoir and restores the effective suction to the tip. Our observation of this phenomenon during surgery pointed to air bubbles as a possible mechanism of impeded circulation in pulmonary blood vessels following heart surgery. An attempt was made, therefore, to see if pulmonary artery pressure could be increased acutely in experimental animals by the introduction of air bubbles into the pulmonary artery.
PA
FA
CONTROL
3 0 CC.
AIR
5 WIN.
1 0 WIN.
2 0 WIN.
30 WIN.
60 WIN.
Pig. 2.—Dog 6. Pulmonary pressure response to 30 c.c. of air injected into the main pulmonary artery.
15
>
w
O
JS
H ►3
W
w O
Pi
B
to
Vol. 49, No. 3
March, 1965
PULMONAEY AIR EMBOLI
443
PROCEDURE
Eight dogs weighing from 25 to 60 pounds were used for this study. A left thoracotomy in the fourth intercostal space was made under general anes thesia. Ventilation was maintained by endotracheal intubation with the use of a Stanton small animal respirator. With this device the respirator rate and the degree of inflation of the lungs gave some indication of the compliance of the lungs at any given time. An increase in the resistance to the flow of air in this respirator is the trigger in changing from inspiration to expiration. A pericardiotomy was made over the main pulmonary artery. Animals were heparinized with 3 mg. per kilogram of body weight. Through a 2-0 silk purse-string suture a No. 205 polyethylene catheter was introduced 1 cm. into the main pulmonary artery. This catheter was connected to a transducer and recordings of pressures were obtained. A femoral artery catheter was also inserted for pressure recording. Frequent observations were made as to the respiratory rate and degree of inflation of the lungs. Any apparent cyanosis of the mucous membranes was recorded. Air bubbles of small size were produced for injection into the main pul monary artery by aspirating blood from the femoral vein through polyethylene tubing which had a No. 27 needle introduced into it to create an, air leak which would allow the introduction of small air bubbles. The aspiration of approxi mately 4 c.c. of blood allowed the formation of 20 c.c. of froth of relatively small bubbles. The froth was then injected into the main pulmonary artery and the tubing was then cleared of any air bubbles by irrigation with 2 c.c. of Ringer's lactate solution. It was found that injection of plain air had the same pressure effect as the injection of froth, as the air was broken up into small bubbles as it entered the pulmonary artery from the catheter. The air given was insufficient to cause myocardial dysfunction from coronary air emboli from bubbles traversing the pulmonary circuit. In 7 animals the pulmonary air embolization was diffuse to both lungs. I n 1 it was limited to a single lung. This was accomplished by clamping one pulmonary artery before the injection of air. This study was done primarily as acute experiments; however, 4 animals were allowed to survive for long-term observation. FINDINGS
Air introduced into the main pulmonary artery of dogs caused immediate increase in the pulmonary artery pressure. The pressure responses of the sub jects to 1 c.c. of air per pound of body weight injected into the main pulmonary artery is shown in Table I. The elevation was present to a significant degree in every case. Fig. 2 (Dog 6) shows the typical pulmonary artery pressure re sponse, with an instantaneous rise and then a gradual decrease toward normal in approximately 30 minutes. Fig. 3 demonstrated the pulmonary artery pres sure elevation from air emboli to be from increased pulmonary vascular re sistance by contrasting it with the high cardiac output elevation in pulmonary artery pressure that results from Adrenalin. In both cases there is an increase
444
ANDERSON, FRITZ, O'HARE
J. Thoracic and Cardiovas. Surg.
in pulmonary artery systolic pressure. However, the Adrenalin elevation has a low pulmonary diastolie pressure and is associated with systemic artery hyper tension, whereas, the elevation after air embolism has a high diastolie pressure and occurs in the presence of decreased systemic pressure. In Dog 3 (Table I ) , the left pulmonary artery was clamped before air embolization of the main pulmonary artery. No pressure change occurred from this clamping of the left pulmonary artery. Then, with all the blood flow going to the right lung, air
Fig. 3.—The elevated pulmonary artery pressure with decreased circulation rate from in jection of air in the pulmonary artery is contrasted with the high cardiac output and elevated pulmonary artery pressure from administration of 2 c.c. of 1/10,000 Adrenalin in a 35 pound dog.
injected into the main pulmonary artery caused an accentuated increase in pul monary artery pressure to over three times the control. Then there was an in stantaneous return back to normal after release of the left pulmonary artery clamp which allowed blood to flow to the protected lung. In some of the animals, repeated injections of air was found to cause a slightly greater pressure response which was of longer duration than the response after the initial injection. Fig. 4 (Dog 7) is the tracing of a response of a 35 pound greyhound to a small in jection of air and later a lethal 100 c.c. embolism. This demonstrates the abrupt increase in pulmonary artery pressure with reduced systemic arterial blood pressure and obviously reduced cardiac output. Terminally it shows the oc currence of high pulmonary artery pressure and its persistence in the presence of very marked reduction in circulatory rate with severe systemic hypotension.
PULMONABY A I R EMBOLI
Vol. 49, No. 3 March, 1965
445
Fig. 5 (Dog 8) shows the typical response to air with reduction in systemic arterial blood pressure and elevation in pulmonary artery pressure with gradual return to normal. The pulmonary pressure elevation occurred in the presence of a fall in systemic pressure, indicating a decreased cardiac output. TABLE I*
DOG NO.
p. A. PRESSURE BEFORE EMBOLI
1 2
3t
28/16 25/15 30/16
4 5
33/10 40/18
P. A. PRESSURE AFTER EMBOLI
56/26 55/26 95/35 and 34/18 72/50 60/30
RECOVERY TIME
30min. 30 min. Immediate
lhr. Died from coronary bubbles 78/57 lhr. 34/12 6 42/18 22/8 30 min. t 7 15-30 min. 50/30 28/8 8 •Pulmonary artery pressures before and after 1 c.c. of air per pound of body weight was introduced into the main pulmonary artery of dogs. The time required for the pressure to re turn to normal after this insult is indicated. tDog 3 shows main pulmonary artery pressure to be normal after clamping of the left pulmonary artery. Then there is an accentuated pressure rise after embolization of the right lung with prompt return to normal pressure after release of the clamp to the protected left lung.
After injection of air into the pulmonary artery the respiratory rate in creased and there was decreased inflation of the lungs with a given air pressure. This decrease in lung compliance was noted in every animal. Transient cyanosis was present which may have been due to poor ventilation from the decreased compliance or to slow circulator}^ rate from the increased pulmonary resistance. The cyanosis disappeared concomitantly with the return to normal of the pul monary artery pressure. In every case, after the initial pulmonary artery pressure rise there was gradual return toward normal (Table I and Figs. 4 and 5). This fell rapidly in the first 15 minutes then more slowly so that usually it was normal in one half hour. Simultaneously as the pulmonary artery pressure decreased, the systemic pressure rose toward normal (Figs. 4 and 5). METHOD OF PREVENTION OF PULMONARY AIR EMBOLI DURING SURGERY
Two precautions have been used to prevent air entering the pulmonary vasculature during operation: clamping of the main pulmonary artery and pre vention of deep respiratory motion of the patient during bypass. In right-sided lesions the pulmonary artery is clamped prior to making any right-sided heart opening after the start of cardiopulmonary bypass. This is done after the right atrium and ventricle have emptied themselves of blood. As soon as the main pulmonary artery is clamped, the atrium, ventricle, or pul monary artery between the clamp and the right ventricle, whichever is ap plicable, is opened. Circumferential pulmonary artery tape with keeper is some times preferred to a clamp. After repair of the defect, the right heart is filled with blood and the incision is closed before removal of the clamp. Care is taken
30 c c .
AIR
:Liij'- I.-:i..:ani:t!i:!u-..:i.?:!ii:a'a3i3a3aB;iis;:iiiiai-.8tai.-ij I\, 10. c = . «IR Fig. 4.—Dog 7 shows typical pressure responses to pulmonary air embolism. After administration of 100 c.c. of air resulting in shock levels, femoral artery pressure, and marked slowing of cardiac output, the pulmonary artery pressure remains high.
CONTROL
15
O W S>
JSI
cc O
b W
fc
Vol. 49, No. 3 March, 1965
PULMONARY AIR EMBOLI
447
to o •a
£ «*
448
ANDERSON, FRITZ, O'HARE
J. Thoracic and Cardiovas. Surg.
not to allow overdistention of the right heart during this closure. If, during a procedure, ventricular fibrillation occurs and if the right heart is opened to prevent its overdistention, the pulmonary artery is clamped or care is taken not to suck air into the right heart by preventing any forceful respiration. Just prior to defibrillation, the heart is filled with blood, the right vent is closed, and the clamp is removed. A defibrillating shock is then given. In patients with a left heart incision, such as repair of a mitral valve, retrograde suction of air into the pulmonary veins by respiratory motion is prevented by the anesthesi ologist. Concurrently with the prevention of pulmonary air emboli, systemic air emboli and overdistention of the pulmonary vasculature are avoided in openheart surgery by use of a left ventricular "mushroom" vent. 1 DISCUSSION
This study indicates that pulmonary air emboli of a small volume of air increases the pulmonary artery pressure for a considerable time by the me chanical presence of the small bubbles. The instantaneous pressure rise makes it unlikely that this reaction is a hormonal response. The absence of pulmonary pressure elevation, if one lung is protected against embolism, gives further sup port that the pressure elevation is mechanical in nature rather than reflex or hormonal. It is necessary to obstruct over half of the vascular bed of the lungs to cause a rise in pulmonary pressure. This is demonstrated in Dog 3 (Table I ) . In this animal the left pulmonary artery was cross-clamped with no pressure change occurring in the main pulmonary artery. Therefore, vascular occlusion by air emboli must exceed this amount of lung to elevate the pressure. It can, therefore, be concluded that, as the pulmonary pressure reaches normal after elevation from air emboli, a major portion of the lung may still have stagnant blood with no flow for some time. Return to normal pulmonary artery pressure indicates only that the necessary number of vessels have been flushed free of bubbles to allow low resistance flow. Because of the slow absorption of nitrogen from stagnant vessels and the small pressure gradient across a capillary bed, air emboli may stay in the lung vessels a long time. Fries and co-workers3 found air bubbles still present in pial vessels 48 hours after carotid artery air injec tion. From the work of Wright 7 it is evident that the air bubbles stay long enough to cause permanent damage to the vascular bed of the lungs. This is consistent with the pulmonary problems seen post-bypass in patients having pulmonary air embolism. Engorged atelectatic "liver' lungs" have not been present in clinical cases protected against pulmonary air emboli and pulmonary hypertension during cardiopulmonary bypass. Pulmonary air emboli are not as devastating to normal lungs with their large vascular and ventilation reserve as systemic air emboli are to other organs. Pulmonary air emboli, however, may be the "final straw" in poor risk patients whose preoperative vascular resistance is already great because of sclerotic changes. Also, patients with mitral disease with pulmonary hypertension and those with congenital heart disease with pul monary hypertension have a greater pressure response to a small amount of intravascular air as their vessels are already partially obstructed.
Vol. 49, No. 3
PULMONARY A I R EMROLI
449
March, 1965
Experience with unilateral embolization of the lungs in Dog 3 and its failure to cause pressure elevation gives support to the procedure of turning patients who receive accidental venous air emboli on their left sides. This would allow the air to rise and be directed to the uppermost lung, saving the other for low resistance circulation. This may be more significant than the effect of trapping the air in the right atrium in this case. This study also would indicate that there is merit in preventing any intravascular introduction of air into the donor organ during organ transplant pro cedures. CONCLUSIONS
1. Transient pulmonary hypertension lasting up to an hour can be pro duced in dogs by the introduction of air into the pulmonary artery. 2. This pressure elevation is due to mechanical increase in pulmonary vas cular resistance by the surface tensions of the many bubbles in small vessels. 3. Pulmonary air emboli, besides increasing pulmonary artery pressure, causes at least temporary decrease in compliance and decrease in pulmonary function. 4. A major portion of a normal lung's vascular bed needs to be obstructed by air emboli before any pressure change is apparent. 5. Pulmonary air embolism during open-heart surgery, although tolerated in a person with normal lungs, may result in significant increase in pulmonary hypertension at the critical time of bypass termination in patients with preoperative pulmonary vascular changes. 6. Prevention of pulmonary air embolism at operation by clamping of the pulmonary artery before opening the right heart, and prevention of forceful respiratory motions when the heart is open, has resulted in concomitant re duction in postoperative pulmonary complications after open-heart surgery. REFERENCES
1. Anderson, R. M., and Bloomer, W. E . : A Reliable Left Heart Vent, Surgery 51: 220-221, 1962. 2. Fazio, C , and Sacchi, XJ.: Experimentally Produced Red Softening of the Brain, J . Neuro path. & Exper. Neurol. 13: 476, 1954. 3. Fries, C , Levowitz, B., Adler, S., Cook, A.,. Karlson, K., and Dennis, C.: Experimental Cerebral Gas Embolism, Ann. Surg. 145: 461-470, 1957. 4. Groves, L., and Effler, D . : A Needle-Vent Safeguard Against Systemic Air Embolism in Open-Heart Surgery, J . THORACIC & CAEDIOVAS. SURG. 4 7 : 349-355, 1964.
5. Higgins, G. A., and Batchelder, T. L . : Air Embolism Following Transdiaphragmatie Pneumoperitoneum, J . THORACIC & CAEDIOVAS. SURG. 41: 159-161, 1961.
6. Eguchi, S., and Bosher, L. H., J r . : Myocardial Dysfunction Resulting From Coronary Air Embolism, Surgery 51: 103-111, 1962. 7. Wright, R. R.: Experimental Pulmonary Hypertension Produced by Recurrent Air Em boli, Med. Thorae. 19: 231-235, 1962.
M.D., James M. Fritz, M.D.,
James E. O'Hare, M.D., Tucson,
and
Ariz.
T
HE occurrence of pulmonary air emboli is a significant hazard in open-heart surgery. This study was done to obtain objective evidence in support of this clinical observation. This investigation deals with only one of the possible detrimental effects of pulmonary air embolism: its effect on pulmonary pres sure due to increased pulmonary vascular resistance. The findings suggest that air emboli account for some post-bypass problems following open-heart surgery. The devastating effect of air emboli on vital organs is well documented.-' 3 ' 5> 6 Cerebral air emboli 2 ' 3 and myocardial dysfunction from coronary air em 6 boli are recognized as complications of open-heart surgery. The blocking effect of air to right heart emptying has been considered a factor in death from venous air embolism since the time of Virchow.5 Recently Wright 7 has produced pul monary vascular damage with resulting pulmonary hypertension in experimental animals by repeated venous air injections over many weeks. There has, how ever, been little mention of the deleterious effects of pulmonary air emboli occurring during open-heart surgery. CLINICAL OBSERVATION
In our early cases of heart surgery, there was occasional occurrence of moderate increase in the pulmonary artery pressure immediately after cardiopulmonary bypass. This was noted in cases in which the right heart was open for repair of septal defects, pulmonary stenosis, or when a right-sided vent had been used during the course of repair of some left-sided lesion, such as mitral insufficiency or stenosis. This pressure elevation was usually mild and of transient nature. However, in patients with severe preoperative pulmonary hypertension from pulmonary arteriosclerosis, the increase in pulmonary artery pressure after bypass was of considerable concern. The right heart failure sec ondary to increased pulmonary resistance was the mechanism of death in some cases. Furthermore, there was an occasional patient who had had an adequate repair of a simple pulmonary stenosis, or other congenital defect, whose post operative pulmonary problems were greater than expected. Tracheotomies were Prom the Department of Zoology, University of Arizona, and the Department of Surgery of Tucson Medical Center, and St. Mary's Hospital, Tucson, Ariz. Supported by research grants from the Santa Barbara California and Orange County California Heart Associations. Received for publication June 30, 1964. 440
Vol. 49, No. 3 Mard), 1965
PULMONARY AIR EMBOLI
441
frequently necessary in these cases. These occurrences were in patients in whom no other obvious insult to the lungs had occurred, and in whom a left heart vent had been used to guard against trauma to the lungs from overdistention of its vasculature with blood and the prevention of any elevation in pulmonary pressure during perfusion. 1 ' i In some of these cases, air which had entered the right heart and traversed the lung was seen coming out of the left vent. After closing the right heart, all visible air was allowed to escape through the left vent before its closure and the termination of the perfusion. In the last 130 clinical cases, since taking precautions against any air entering the pulmonary artery, there has been marked reduction in our postoperative pul monary problems. Post-bypass increase in pulmonary pressure has not been observed. Only one patient has required a tracheotomy.
^Mw^w^
Fig. 1.—Cardiotomy suction used with pump oxygenator. The bubbles in the tubing decrease the effective suction because of the surface tensions of the many menisci.
PHYSICAL PRINCIPLE INVOLVED
Bubbles in small tubes impede the flow of liquid because of the resistance of the surface tensions of their many menisci. This physical principle accounts for the increase in resistance to flow of blood in a vessel by air bubbles. To il lustrate this principle, reference is made to the cardiotomy suction used with our oxygenator (Fig. 1). With this device, a constant suction of 30 cm. water pressure is applied to a reservoir to which suction tubing is attached. When the suction tubing is filled with a column of blood without bubbles there is rapid movement of fluid in the tubing. However, the greater the number of air bubbles in the tubing the less the effective suction and the slower the move ment of the column. If the tubing is full of froth, so that the additive effect of the surface tensions of the many menisci equals the suction pressure, ef fective suction is eliminated and the flow stops. Elevating the sucker tip allows the froth to move on into the reservoir and restores the effective suction to the tip. Our observation of this phenomenon during surgery pointed to air bubbles as a possible mechanism of impeded circulation in pulmonary blood vessels following heart surgery. An attempt was made, therefore, to see if pulmonary artery pressure could be increased acutely in experimental animals by the introduction of air bubbles into the pulmonary artery.
PA
FA
CONTROL
3 0 CC.
AIR
5 WIN.
1 0 WIN.
2 0 WIN.
30 WIN.
60 WIN.
Pig. 2.—Dog 6. Pulmonary pressure response to 30 c.c. of air injected into the main pulmonary artery.
15
>
w
O
JS
H ►3
W
w O
Pi
B
to
Vol. 49, No. 3
March, 1965
PULMONAEY AIR EMBOLI
443
PROCEDURE
Eight dogs weighing from 25 to 60 pounds were used for this study. A left thoracotomy in the fourth intercostal space was made under general anes thesia. Ventilation was maintained by endotracheal intubation with the use of a Stanton small animal respirator. With this device the respirator rate and the degree of inflation of the lungs gave some indication of the compliance of the lungs at any given time. An increase in the resistance to the flow of air in this respirator is the trigger in changing from inspiration to expiration. A pericardiotomy was made over the main pulmonary artery. Animals were heparinized with 3 mg. per kilogram of body weight. Through a 2-0 silk purse-string suture a No. 205 polyethylene catheter was introduced 1 cm. into the main pulmonary artery. This catheter was connected to a transducer and recordings of pressures were obtained. A femoral artery catheter was also inserted for pressure recording. Frequent observations were made as to the respiratory rate and degree of inflation of the lungs. Any apparent cyanosis of the mucous membranes was recorded. Air bubbles of small size were produced for injection into the main pul monary artery by aspirating blood from the femoral vein through polyethylene tubing which had a No. 27 needle introduced into it to create an, air leak which would allow the introduction of small air bubbles. The aspiration of approxi mately 4 c.c. of blood allowed the formation of 20 c.c. of froth of relatively small bubbles. The froth was then injected into the main pulmonary artery and the tubing was then cleared of any air bubbles by irrigation with 2 c.c. of Ringer's lactate solution. It was found that injection of plain air had the same pressure effect as the injection of froth, as the air was broken up into small bubbles as it entered the pulmonary artery from the catheter. The air given was insufficient to cause myocardial dysfunction from coronary air emboli from bubbles traversing the pulmonary circuit. In 7 animals the pulmonary air embolization was diffuse to both lungs. I n 1 it was limited to a single lung. This was accomplished by clamping one pulmonary artery before the injection of air. This study was done primarily as acute experiments; however, 4 animals were allowed to survive for long-term observation. FINDINGS
Air introduced into the main pulmonary artery of dogs caused immediate increase in the pulmonary artery pressure. The pressure responses of the sub jects to 1 c.c. of air per pound of body weight injected into the main pulmonary artery is shown in Table I. The elevation was present to a significant degree in every case. Fig. 2 (Dog 6) shows the typical pulmonary artery pressure re sponse, with an instantaneous rise and then a gradual decrease toward normal in approximately 30 minutes. Fig. 3 demonstrated the pulmonary artery pres sure elevation from air emboli to be from increased pulmonary vascular re sistance by contrasting it with the high cardiac output elevation in pulmonary artery pressure that results from Adrenalin. In both cases there is an increase
444
ANDERSON, FRITZ, O'HARE
J. Thoracic and Cardiovas. Surg.
in pulmonary artery systolic pressure. However, the Adrenalin elevation has a low pulmonary diastolie pressure and is associated with systemic artery hyper tension, whereas, the elevation after air embolism has a high diastolie pressure and occurs in the presence of decreased systemic pressure. In Dog 3 (Table I ) , the left pulmonary artery was clamped before air embolization of the main pulmonary artery. No pressure change occurred from this clamping of the left pulmonary artery. Then, with all the blood flow going to the right lung, air
Fig. 3.—The elevated pulmonary artery pressure with decreased circulation rate from in jection of air in the pulmonary artery is contrasted with the high cardiac output and elevated pulmonary artery pressure from administration of 2 c.c. of 1/10,000 Adrenalin in a 35 pound dog.
injected into the main pulmonary artery caused an accentuated increase in pul monary artery pressure to over three times the control. Then there was an in stantaneous return back to normal after release of the left pulmonary artery clamp which allowed blood to flow to the protected lung. In some of the animals, repeated injections of air was found to cause a slightly greater pressure response which was of longer duration than the response after the initial injection. Fig. 4 (Dog 7) is the tracing of a response of a 35 pound greyhound to a small in jection of air and later a lethal 100 c.c. embolism. This demonstrates the abrupt increase in pulmonary artery pressure with reduced systemic arterial blood pressure and obviously reduced cardiac output. Terminally it shows the oc currence of high pulmonary artery pressure and its persistence in the presence of very marked reduction in circulatory rate with severe systemic hypotension.
PULMONABY A I R EMBOLI
Vol. 49, No. 3 March, 1965
445
Fig. 5 (Dog 8) shows the typical response to air with reduction in systemic arterial blood pressure and elevation in pulmonary artery pressure with gradual return to normal. The pulmonary pressure elevation occurred in the presence of a fall in systemic pressure, indicating a decreased cardiac output. TABLE I*
DOG NO.
p. A. PRESSURE BEFORE EMBOLI
1 2
3t
28/16 25/15 30/16
4 5
33/10 40/18
P. A. PRESSURE AFTER EMBOLI
56/26 55/26 95/35 and 34/18 72/50 60/30
RECOVERY TIME
30min. 30 min. Immediate
lhr. Died from coronary bubbles 78/57 lhr. 34/12 6 42/18 22/8 30 min. t 7 15-30 min. 50/30 28/8 8 •Pulmonary artery pressures before and after 1 c.c. of air per pound of body weight was introduced into the main pulmonary artery of dogs. The time required for the pressure to re turn to normal after this insult is indicated. tDog 3 shows main pulmonary artery pressure to be normal after clamping of the left pulmonary artery. Then there is an accentuated pressure rise after embolization of the right lung with prompt return to normal pressure after release of the clamp to the protected left lung.
After injection of air into the pulmonary artery the respiratory rate in creased and there was decreased inflation of the lungs with a given air pressure. This decrease in lung compliance was noted in every animal. Transient cyanosis was present which may have been due to poor ventilation from the decreased compliance or to slow circulator}^ rate from the increased pulmonary resistance. The cyanosis disappeared concomitantly with the return to normal of the pul monary artery pressure. In every case, after the initial pulmonary artery pressure rise there was gradual return toward normal (Table I and Figs. 4 and 5). This fell rapidly in the first 15 minutes then more slowly so that usually it was normal in one half hour. Simultaneously as the pulmonary artery pressure decreased, the systemic pressure rose toward normal (Figs. 4 and 5). METHOD OF PREVENTION OF PULMONARY AIR EMBOLI DURING SURGERY
Two precautions have been used to prevent air entering the pulmonary vasculature during operation: clamping of the main pulmonary artery and pre vention of deep respiratory motion of the patient during bypass. In right-sided lesions the pulmonary artery is clamped prior to making any right-sided heart opening after the start of cardiopulmonary bypass. This is done after the right atrium and ventricle have emptied themselves of blood. As soon as the main pulmonary artery is clamped, the atrium, ventricle, or pul monary artery between the clamp and the right ventricle, whichever is ap plicable, is opened. Circumferential pulmonary artery tape with keeper is some times preferred to a clamp. After repair of the defect, the right heart is filled with blood and the incision is closed before removal of the clamp. Care is taken
30 c c .
AIR
:Liij'- I.-:i..:ani:t!i:!u-..:i.?:!ii:a'a3i3a3aB;iis;:iiiiai-.8tai.-ij I\, 10. c = . «IR Fig. 4.—Dog 7 shows typical pressure responses to pulmonary air embolism. After administration of 100 c.c. of air resulting in shock levels, femoral artery pressure, and marked slowing of cardiac output, the pulmonary artery pressure remains high.
CONTROL
15
O W S>
JSI
cc O
b W
fc
Vol. 49, No. 3 March, 1965
PULMONARY AIR EMBOLI
447
to o •a
£ «*
448
ANDERSON, FRITZ, O'HARE
J. Thoracic and Cardiovas. Surg.
not to allow overdistention of the right heart during this closure. If, during a procedure, ventricular fibrillation occurs and if the right heart is opened to prevent its overdistention, the pulmonary artery is clamped or care is taken not to suck air into the right heart by preventing any forceful respiration. Just prior to defibrillation, the heart is filled with blood, the right vent is closed, and the clamp is removed. A defibrillating shock is then given. In patients with a left heart incision, such as repair of a mitral valve, retrograde suction of air into the pulmonary veins by respiratory motion is prevented by the anesthesi ologist. Concurrently with the prevention of pulmonary air emboli, systemic air emboli and overdistention of the pulmonary vasculature are avoided in openheart surgery by use of a left ventricular "mushroom" vent. 1 DISCUSSION
This study indicates that pulmonary air emboli of a small volume of air increases the pulmonary artery pressure for a considerable time by the me chanical presence of the small bubbles. The instantaneous pressure rise makes it unlikely that this reaction is a hormonal response. The absence of pulmonary pressure elevation, if one lung is protected against embolism, gives further sup port that the pressure elevation is mechanical in nature rather than reflex or hormonal. It is necessary to obstruct over half of the vascular bed of the lungs to cause a rise in pulmonary pressure. This is demonstrated in Dog 3 (Table I ) . In this animal the left pulmonary artery was cross-clamped with no pressure change occurring in the main pulmonary artery. Therefore, vascular occlusion by air emboli must exceed this amount of lung to elevate the pressure. It can, therefore, be concluded that, as the pulmonary pressure reaches normal after elevation from air emboli, a major portion of the lung may still have stagnant blood with no flow for some time. Return to normal pulmonary artery pressure indicates only that the necessary number of vessels have been flushed free of bubbles to allow low resistance flow. Because of the slow absorption of nitrogen from stagnant vessels and the small pressure gradient across a capillary bed, air emboli may stay in the lung vessels a long time. Fries and co-workers3 found air bubbles still present in pial vessels 48 hours after carotid artery air injec tion. From the work of Wright 7 it is evident that the air bubbles stay long enough to cause permanent damage to the vascular bed of the lungs. This is consistent with the pulmonary problems seen post-bypass in patients having pulmonary air embolism. Engorged atelectatic "liver' lungs" have not been present in clinical cases protected against pulmonary air emboli and pulmonary hypertension during cardiopulmonary bypass. Pulmonary air emboli are not as devastating to normal lungs with their large vascular and ventilation reserve as systemic air emboli are to other organs. Pulmonary air emboli, however, may be the "final straw" in poor risk patients whose preoperative vascular resistance is already great because of sclerotic changes. Also, patients with mitral disease with pulmonary hypertension and those with congenital heart disease with pul monary hypertension have a greater pressure response to a small amount of intravascular air as their vessels are already partially obstructed.
Vol. 49, No. 3
PULMONARY A I R EMROLI
449
March, 1965
Experience with unilateral embolization of the lungs in Dog 3 and its failure to cause pressure elevation gives support to the procedure of turning patients who receive accidental venous air emboli on their left sides. This would allow the air to rise and be directed to the uppermost lung, saving the other for low resistance circulation. This may be more significant than the effect of trapping the air in the right atrium in this case. This study also would indicate that there is merit in preventing any intravascular introduction of air into the donor organ during organ transplant pro cedures. CONCLUSIONS
1. Transient pulmonary hypertension lasting up to an hour can be pro duced in dogs by the introduction of air into the pulmonary artery. 2. This pressure elevation is due to mechanical increase in pulmonary vas cular resistance by the surface tensions of the many bubbles in small vessels. 3. Pulmonary air emboli, besides increasing pulmonary artery pressure, causes at least temporary decrease in compliance and decrease in pulmonary function. 4. A major portion of a normal lung's vascular bed needs to be obstructed by air emboli before any pressure change is apparent. 5. Pulmonary air embolism during open-heart surgery, although tolerated in a person with normal lungs, may result in significant increase in pulmonary hypertension at the critical time of bypass termination in patients with preoperative pulmonary vascular changes. 6. Prevention of pulmonary air embolism at operation by clamping of the pulmonary artery before opening the right heart, and prevention of forceful respiratory motions when the heart is open, has resulted in concomitant re duction in postoperative pulmonary complications after open-heart surgery. REFERENCES
1. Anderson, R. M., and Bloomer, W. E . : A Reliable Left Heart Vent, Surgery 51: 220-221, 1962. 2. Fazio, C , and Sacchi, XJ.: Experimentally Produced Red Softening of the Brain, J . Neuro path. & Exper. Neurol. 13: 476, 1954. 3. Fries, C , Levowitz, B., Adler, S., Cook, A.,. Karlson, K., and Dennis, C.: Experimental Cerebral Gas Embolism, Ann. Surg. 145: 461-470, 1957. 4. Groves, L., and Effler, D . : A Needle-Vent Safeguard Against Systemic Air Embolism in Open-Heart Surgery, J . THORACIC & CAEDIOVAS. SURG. 4 7 : 349-355, 1964.
5. Higgins, G. A., and Batchelder, T. L . : Air Embolism Following Transdiaphragmatie Pneumoperitoneum, J . THORACIC & CAEDIOVAS. SURG. 41: 159-161, 1961.
6. Eguchi, S., and Bosher, L. H., J r . : Myocardial Dysfunction Resulting From Coronary Air Embolism, Surgery 51: 103-111, 1962. 7. Wright, R. R.: Experimental Pulmonary Hypertension Produced by Recurrent Air Em boli, Med. Thorae. 19: 231-235, 1962.