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Effect of coronary shock on tolerance to pulmonary embolus
Effect of coronary shock on tolerance to pulmonary embolus Albert B. Lowenfels, M.D., F.A.C.S.,* Bruce J. Sobol,
M.D.**
Hans H. C. Morsch, M.D., F.A.C.S.,*** and Pedro Iral, M.D.,**** Valhalla, N. Y.
V>/ver one hundred years ago, Cruveilhier found that pulmonary embolism occurred most often in association with cardiac disorders. Since that time, several observersir>'1G have documented this relationship, and, in recent series,10' " coexisting heart disease was present in most cases of pulmonary embolus. Indeed, as pointed out by Breckenridge and Ratnoff,4 pulmonary embolism does occur in supposedly healthy patients, but this is a distinctly rare event compared to the incidence in patients with heart disease. In spite of the important relationship between heart disease and pulmonary embolus, most studies of experimental lung embolus have been performed in animals which had a normal circulatory system. In this experiment, we have studied survival after pulmonary embolism in dogs subjected to previous myocardial damage. From the Departments of Surgery, Medicine, and Pathology of New York Medical College and Grasslands Hospital, Valhalla, N. Y. 10595. Supported by U.S. Public Health Service Grant No. H E 10564-01 and grants from the Westchester Heart Association. Received for publication March 23, 1972. *Associate Director of Surgery and Associate Professor of Surgery, New York Medical College. **Director of Cardiopulmonary Laboratory and Professor of Medicine, New York Medical College. ***Assistant Attending Surgeon. * " " F o r m e r Associate Director of Pathology.
296
Method Data obtained from 25 adult mongrel dogs weighing between 14 and 21 kilograms comprise the basis of this report. Fourteen of the animals formed the experimental group, and the remaining 11 were controls. The protocol was as follows. Production of myocardial lesions. Animals were anesthetized with intravenous sodium pentobarbital until satisfactory levels of surgical anesthesia were reached. They were then placed in the supine position. After administration of heparin, 3 mg. per kilogram, we passed a double-lumen metal cannula with a balloon tip to the root of the aorta via the left carotid artery. Plastic microspheres,* 297 to 350 ^ in diameter suspended in 20 c.c. of 15 per cent gum acacia solution, were injected into the aorta just above the coronary ostia. Inflating the balloon for a 30 second period immediately before and after the injection ensured that the beads entered the coronary circulation. The technique has been described in full by Agress and co-workers.1 Intra-aortic pressures obtained from another cannula introduced via the femoral artery were measured in all animals, as was Lead II of the electrocardiogram. Proper position and occlusion of the aortic balloon was ensured by a prompt drop in systemic *Dow Chemical Corporation,
Midland, Mich.
Volume 64
Number 2
297
Pulmonary embolism in coronary shock
August, 1972
pressure to levels of 30 mm. Hg upon inflation of the balloon. The 11 dogs in the control group were prepared and studied in the same fashion except that they received only the gum acacia injection without plastic microspheres. In 5 control and 5 treated animals, we measured cardiac output with a densitometer and indocyanine green dye before and after coronary embolization. Pulmonary embolus studies. All animals that survived the initial coronary embolization procedure were kept for 1 month and then subjected to pulmonary embolization in a previously outlined method. s Glass beads (75 n in diameter) were introduced into the right side of the circulation via a short cannula in the jugular vein. The glass beads were suspended in a small amount of saline solution and injected as a bolus in a dosage of 0.1 c.c. of beads per kilogram of body weight. The animal was given repetitive injections at 10 minute intervals until death. We recorded systemic arterial pressure, right ventricular pressure, and Lead II of the electrocardiogram immediately before and for 2 minutes after each injection of the beads. Pressure measurements, electrocardiogram, and cardiac output studies were also obtained 5 minutes after each embolization. Arterial oxygen saturations were determined immediately before each embolization. At the time of death (as defined by terminal apnea), the heart was removed, photographed, weighed, and examined grossly and microscopically. Results Coronary embolus studies. Following injection of microspheres into the coronary circulation, we observed a response similar to that reported by others. 2 ' 3 - ]1 This consisted of hypotension of varying degrees, lasting from 5 to 50 minutes, accompanied by a diminished cardiac output. Eight animals sustained a 30 per cent or greater reduction in mean aortic pressure that persisted for 10 or more minutes. These ani-
i
SEVERE
I ZL.
CORONARY SHOCK
1
i
I
™ ' ^^^ZLmm '
MILD CORONARY SHOCK
I CONTROLS
6
30*
60
MINUTES
TO*
Fig. 1. Survival time after pulmonary embolus. Horizontal bars represent individual survival times. Average values (vertical lines) were as follows: Severe coronary group, 23 minutes. Mild coronary group, 44 minutes. Controls, 40 minutes. The difference between the severe coronary shock and control groups is statistically significant (p < 0.005).
mals were considered to have sustained moderate-to-severe coronary shock. The remaining 6 animals exhibited lesser degrees of hypotension and were placed in a separate category of mild coronary shock. Some reduction in mean aortic pressure was noted in all of the control animals after injection of only gum acacia. However, in this group the hypotension was transient, and within 10 minutes after the injection the mean aortic pressure had returned to normal. Pulmonary embolus studies. The results during subsequent pulmonary embolization in both the control and treated groups are shown in Figs. 1 and 2. We found that the dogs sustaining moderate-to-severe coronary shock had a shorter survival time than either the control group or the mild coronary shock group (Fig. 1). This difference was statistically highly significant (p < 0.005). No difference was observed when the mild coronary shock group was compared to the control group.
298
The Journal of
Lowenfels et al.
Thoracic and Cardiovascular Surgery
|
| CONTROLS
ARY
HMRY
rfcr^
lOOi
si CONTROL
|-
2 3 PULMONARY
4 5 EMBOLUS -
J_LH
Fig. 2. Hemodynamic results observed during pulmonary embolus. After an initial control period, repetitive pulmonary emboli were given at 10 minute intervals. Measurements recorded here are average values taken midway between each episode, except for oxygen saturations, which were obtained just before each bead injection. Numbers within bottom columns represent the number of animals alive before each embolus. CO., Cardiac output. M.A.P., Mean arterial pressure. R.V.S.P., Right ventricular systolic pressure.
Mean aortic pressures declined gradually with successive pulmonary emboli in all groups, whereas the right ventricular systolic pressures gradually rose to levels that in some animals approached or exceeded systemic levels. Right ventricular diastolic pressures rose only as a terminal event in all groups and are not shown in Fig. 2. The initial cardiac output studies prior to pulmonary embolization were similar in all groups. In many of the dogs, there was a slight increase in cardiac output following the first one or two embolic episodes, and only at death did the cardiac output fall. Changes in cardiac output were much less severe during pulmonary embolism than during coronary embolization. Arterial oxygen saturations fell progressively during pulmonary embolism. The
lowest level reached in all three groups was 60 to 70 per cent. Pathologic findings. At autopsy, all of the dogs subjected to coronary embolization had some abnormalities within the heart, whereas none of the control dogs had any changes resulting from injection of the acacia solution. After coronary embolization, discrete, patchy, subendocardial lesions, varying in size from 2 mm. to 1 cm., were found. These lesions were located entirely in the left ventricle and septum and were never found in the free wall of the right ventricle. Many small coronary vessels had been occluded by the beads, and often there was hypertrophy of the arterial wall proximal to the block. The average heart weights expressed in grams per kilogram of body weight were
Volume 64 Number 2 August, 1972
as follows: control animals 7.3 ± 1.4, mild coronary shock group 7.3 ± 0.5, and severe coronary shock group 8.3 ± 1.0. These group differences were not significant, but there was good correlation between the individual heart weight of each dog subjected to coronary embolism and the survival time following subsequent pulmonary embolus (Fig. 3). Discussion Coronary embolization. The method used in this experiment to produce myocardial damage has several advantages over other methods. It can be performed without opening the chest, it produces diffuse lesions, and it produces graded forms of heart damage by alteration of the dose. However, even when carried out in a standard fashion, there was considerable individual difference in the hemodynamic response, as originally pointed out by Agress.2 In our studies, we found that a dose of 4 mg. per kilogram of beads produced moderately severe coronary shock in 57 per cent of the animals. Attempts to increase the extent of myocardial damage by increasing the dose of beads led to a prohibitive mortality rate. Embolization of the lungs evoked a prompt hemodynamic response in all of our animals. This was characterized by a progressive fall in arterial oxygen saturation and in systemic blood pressure accompanied by a rise in right ventricular systolic pressure. At first these findings were only transient, but with each succeeding embolus the findings became more marked and more sustained. The combination of systemic hypotension and right ventricular hypertension was tolerated poorly by the severe coronary shock group; most dogs died shortly after the onset of these hemodynamic events. In general, the changes were quite similar to those reported by other investigators who used a variety of embolic agents. The cardiac output studies during pulmonary embolus were of interest in that this measurement remained the same or in many animals increased following the first few embolic episodes. Only as a terminal event
299
Pulmonary embolism in coronary shock
fi
40 —"«C
*
20-
0
^^_ • 5
6
7
HEART
8
9
10
n
WEIGHT
(G/Kg Body Wt.)
Fig. 3. Relationship between heart weight and survival time after pulmonary embolus. Both mild and severe coronary shock groups are included. (r = 0.58; p < 0.05).
did cardiac output decrease. This is in agreement with previous experimental0 as well as clinical findings in patients with angiographically proved pulmonary embolus.7- 14 The reason for this somewhat surprising finding is not clear, but acute hypoxia has been suggested as one possible cause.12 Previous experiments in our laboratory 8 have demonstrated that the average survival time with this method of pulmonary embolus is 44 minutes. Almost the same results were obtained in the current experiments for both control and mild coronary shock animals. However, in animals which had previously sustained severe coronary shock, survival time was greatly reduced, averaging only 23 minutes. In terms of volumes of embolic agent, the average lethal pulmonary embolus for the control and mild coronary shock groups was 0.4 c.c. of beads per kilogram as compared to a dose of 0.2 c.c. of beads per kilogram in the severe coronary shock dogs. Gross inspection of the interior of the heart and of cut sections through the muscular wall revealed a gradation of discrete, usually subendocardial lesions. As in studies in man, these pathologic changes were never found in the free wall of the right ventricle, suggesting that this part of the canine heart is particularly resistant to infarction. Although there was some correlation between the number of these lesions and the survival time following pulmonary
The Journal of
300
Lowenfeh
et al.
embolus, a much better correlation was found between heart weight and survival time. When confronted with a patient who has sustained a massive pulmonary embolus, the physician faces a serious therapeutic decision: Will this gravely ill patient survive with only medical treatment or will he require embolectomy? Clinical experience suggests that patients with unilateral pulmonary artery embolus who are younger than 50 years of age rarely die9 and rarely need surgerys unless there is pre-existing cardiopulmonary disease. Indeed, some observers1'1 believe that pre-existing cardiopulmonary disease is just as important a determinant for survival as is the size of the embolus. Our experiments support this point of view and suggest that, in patients with known coronary artery disease, pulmonary embolectomy might be considered necessary for a smaller embolus than in normal patients. Conclusions The response to pulmonary embolus was studied in animals which had survived previous production of coronary shock. Myocardial damage was found to be a major factor in determining subsequent tolerance to pulmonary embolus. Animals which had previously sustained severe coronary shock exhibited a significant decrease in subsequent survival time after pulmonary embolus. Those which had sustained mild coronary shock fared the same as control animals. In all animals subjected to prior coronary shock, there was good correlation between heart weight and tolerance to pulmonary embolus.
Thoracic and Cardiovascular Surgery
3 4
5
6
7
8
9 10
11
12
13
14
We thank Ruthven Ferreira and John Holly for
their help.
REFERENCES 1 Agress, C. M., Rosenburg, M. J., Jacobs, H. I., Binder, M. J., Schneiderman, A., and Clark, W. G.: Protracted Shock in Closed Chest Dog Following Coronary Embolization With Graded Microspheres, Am. J. Physiol. 170: 536, 1952. 2 Agress, C. M., Glassner, H. F., Binder, M. J.,
15
16
and Fields, J.: Hemodynamic Measurements in Experimental Coronary Shock. J. Appl. Physiol. 10: 469, 1957. Bloch, J. H., Pierce, C. H., Manax, W. G., and Lillehei, R. C : Treatment of Experimental Cardiogenic Shock, Surgery 58: 197, 1965. Breckenridge, R. T., and Ratnoff, O. D.: Pulmonary Embolism and Unexpected Death in Supposedly Normal Persons, N. Engl. J. Med. 270: 298, 1964. Cross, F . S., and Mowlem, A.: A Survey of the Current Status of Pulmonary Embolectomy for Massive Pulmonary Embolism, Circulation 35: 86, 1966 (Suppl. I). Daicoff, G. R., Chavez, F. R., and Swenson, E. W.: Pulmonary Venous Hypertension in Massive Pulmonary Embolism, Am. J. Cardiol. 21: 95, 1968. Dalen, J. E., Banas, J. S., Brooks, H. L., Evans, G. L., Paraskos, J. A., and Dexter, L.: Resolution Rate of Acute Pulmonary Embolism in Man, N. Engl. J. Med. 280: 1194, 1969. Emirgil, C , Lowenfels, A. B., and Sobol, B. J.: Veno-arterial Shunting Without Oxygenation in Experimental Pulmonary Embolism, J. Surg. Res. 8: 167, 1968. Gorham, L. W.: A Study of Pulmonary Embolism, Arch. Intern. Med. 108: 189, 1961. Herman, R. E., Davis, J. H., and Holden, W. D.: Pulmonary Embolism. A Clinical and Pathologic Study With Emphasis on the Effect of Prophylactic Therapy With Anticoagulants, Am. J. Surg. 102: 19, 1961. Jacobey, J. A., Taylor, W. J., Smith, G. T., Gorlin, R., and Harken, D. E.: A New Therapeutic Approach to Acute Coronary Occlusion: Experimental Study, Am. J. Cardiol. 9: 60, 1962. Kontos, H. A., Levasseur, J. E., Richardson, D. W., Mauck, H. P., Jr., and Patterson, J. L., Jr.: Comparative Circulatory Responses to Systemic Hypoxia in Man and in Unanesthetized Dog, J. Appl. Physiol. 23: 381, 1967. Mclntyre, K. M., and Sasahara, A. A.: Determinants of the Hemodynamic Response to Pulmonary Embolism (abstr.) Clin. Res. 17: 254, 1969. Mclntyre, K. M., and Sasahara, A. A.: Hemodynamic Response to Pulmonary Embolism in Patients Without Prior Cardiopulmonary Disease, A m . J. Cardiol. 28: 288, 1971. Miller, R. D., Jordan, R. A., Parker, R. L., and Edwards, J. E.: Thrcmboembolism in Acute and in Healed Myocardial Infarction: Systemic and Pulmonary Arterial Occlusion, Circulation 6: 7, 1952. Moran, T. J.: Autopsy Incidence of Pulmonary Embolism in Coronary Heart Disease, Ann. Intern. Med. 32: 949, 1950.
M.D.**
Hans H. C. Morsch, M.D., F.A.C.S.,*** and Pedro Iral, M.D.,**** Valhalla, N. Y.
V>/ver one hundred years ago, Cruveilhier found that pulmonary embolism occurred most often in association with cardiac disorders. Since that time, several observersir>'1G have documented this relationship, and, in recent series,10' " coexisting heart disease was present in most cases of pulmonary embolus. Indeed, as pointed out by Breckenridge and Ratnoff,4 pulmonary embolism does occur in supposedly healthy patients, but this is a distinctly rare event compared to the incidence in patients with heart disease. In spite of the important relationship between heart disease and pulmonary embolus, most studies of experimental lung embolus have been performed in animals which had a normal circulatory system. In this experiment, we have studied survival after pulmonary embolism in dogs subjected to previous myocardial damage. From the Departments of Surgery, Medicine, and Pathology of New York Medical College and Grasslands Hospital, Valhalla, N. Y. 10595. Supported by U.S. Public Health Service Grant No. H E 10564-01 and grants from the Westchester Heart Association. Received for publication March 23, 1972. *Associate Director of Surgery and Associate Professor of Surgery, New York Medical College. **Director of Cardiopulmonary Laboratory and Professor of Medicine, New York Medical College. ***Assistant Attending Surgeon. * " " F o r m e r Associate Director of Pathology.
296
Method Data obtained from 25 adult mongrel dogs weighing between 14 and 21 kilograms comprise the basis of this report. Fourteen of the animals formed the experimental group, and the remaining 11 were controls. The protocol was as follows. Production of myocardial lesions. Animals were anesthetized with intravenous sodium pentobarbital until satisfactory levels of surgical anesthesia were reached. They were then placed in the supine position. After administration of heparin, 3 mg. per kilogram, we passed a double-lumen metal cannula with a balloon tip to the root of the aorta via the left carotid artery. Plastic microspheres,* 297 to 350 ^ in diameter suspended in 20 c.c. of 15 per cent gum acacia solution, were injected into the aorta just above the coronary ostia. Inflating the balloon for a 30 second period immediately before and after the injection ensured that the beads entered the coronary circulation. The technique has been described in full by Agress and co-workers.1 Intra-aortic pressures obtained from another cannula introduced via the femoral artery were measured in all animals, as was Lead II of the electrocardiogram. Proper position and occlusion of the aortic balloon was ensured by a prompt drop in systemic *Dow Chemical Corporation,
Midland, Mich.
Volume 64
Number 2
297
Pulmonary embolism in coronary shock
August, 1972
pressure to levels of 30 mm. Hg upon inflation of the balloon. The 11 dogs in the control group were prepared and studied in the same fashion except that they received only the gum acacia injection without plastic microspheres. In 5 control and 5 treated animals, we measured cardiac output with a densitometer and indocyanine green dye before and after coronary embolization. Pulmonary embolus studies. All animals that survived the initial coronary embolization procedure were kept for 1 month and then subjected to pulmonary embolization in a previously outlined method. s Glass beads (75 n in diameter) were introduced into the right side of the circulation via a short cannula in the jugular vein. The glass beads were suspended in a small amount of saline solution and injected as a bolus in a dosage of 0.1 c.c. of beads per kilogram of body weight. The animal was given repetitive injections at 10 minute intervals until death. We recorded systemic arterial pressure, right ventricular pressure, and Lead II of the electrocardiogram immediately before and for 2 minutes after each injection of the beads. Pressure measurements, electrocardiogram, and cardiac output studies were also obtained 5 minutes after each embolization. Arterial oxygen saturations were determined immediately before each embolization. At the time of death (as defined by terminal apnea), the heart was removed, photographed, weighed, and examined grossly and microscopically. Results Coronary embolus studies. Following injection of microspheres into the coronary circulation, we observed a response similar to that reported by others. 2 ' 3 - ]1 This consisted of hypotension of varying degrees, lasting from 5 to 50 minutes, accompanied by a diminished cardiac output. Eight animals sustained a 30 per cent or greater reduction in mean aortic pressure that persisted for 10 or more minutes. These ani-
i
SEVERE
I ZL.
CORONARY SHOCK
1
i
I
™ ' ^^^ZLmm '
MILD CORONARY SHOCK
I CONTROLS
6
30*
60
MINUTES
TO*
Fig. 1. Survival time after pulmonary embolus. Horizontal bars represent individual survival times. Average values (vertical lines) were as follows: Severe coronary group, 23 minutes. Mild coronary group, 44 minutes. Controls, 40 minutes. The difference between the severe coronary shock and control groups is statistically significant (p < 0.005).
mals were considered to have sustained moderate-to-severe coronary shock. The remaining 6 animals exhibited lesser degrees of hypotension and were placed in a separate category of mild coronary shock. Some reduction in mean aortic pressure was noted in all of the control animals after injection of only gum acacia. However, in this group the hypotension was transient, and within 10 minutes after the injection the mean aortic pressure had returned to normal. Pulmonary embolus studies. The results during subsequent pulmonary embolization in both the control and treated groups are shown in Figs. 1 and 2. We found that the dogs sustaining moderate-to-severe coronary shock had a shorter survival time than either the control group or the mild coronary shock group (Fig. 1). This difference was statistically highly significant (p < 0.005). No difference was observed when the mild coronary shock group was compared to the control group.
298
The Journal of
Lowenfels et al.
Thoracic and Cardiovascular Surgery
|
| CONTROLS
ARY
HMRY
rfcr^
lOOi
si CONTROL
|-
2 3 PULMONARY
4 5 EMBOLUS -
J_LH
Fig. 2. Hemodynamic results observed during pulmonary embolus. After an initial control period, repetitive pulmonary emboli were given at 10 minute intervals. Measurements recorded here are average values taken midway between each episode, except for oxygen saturations, which were obtained just before each bead injection. Numbers within bottom columns represent the number of animals alive before each embolus. CO., Cardiac output. M.A.P., Mean arterial pressure. R.V.S.P., Right ventricular systolic pressure.
Mean aortic pressures declined gradually with successive pulmonary emboli in all groups, whereas the right ventricular systolic pressures gradually rose to levels that in some animals approached or exceeded systemic levels. Right ventricular diastolic pressures rose only as a terminal event in all groups and are not shown in Fig. 2. The initial cardiac output studies prior to pulmonary embolization were similar in all groups. In many of the dogs, there was a slight increase in cardiac output following the first one or two embolic episodes, and only at death did the cardiac output fall. Changes in cardiac output were much less severe during pulmonary embolism than during coronary embolization. Arterial oxygen saturations fell progressively during pulmonary embolism. The
lowest level reached in all three groups was 60 to 70 per cent. Pathologic findings. At autopsy, all of the dogs subjected to coronary embolization had some abnormalities within the heart, whereas none of the control dogs had any changes resulting from injection of the acacia solution. After coronary embolization, discrete, patchy, subendocardial lesions, varying in size from 2 mm. to 1 cm., were found. These lesions were located entirely in the left ventricle and septum and were never found in the free wall of the right ventricle. Many small coronary vessels had been occluded by the beads, and often there was hypertrophy of the arterial wall proximal to the block. The average heart weights expressed in grams per kilogram of body weight were
Volume 64 Number 2 August, 1972
as follows: control animals 7.3 ± 1.4, mild coronary shock group 7.3 ± 0.5, and severe coronary shock group 8.3 ± 1.0. These group differences were not significant, but there was good correlation between the individual heart weight of each dog subjected to coronary embolism and the survival time following subsequent pulmonary embolus (Fig. 3). Discussion Coronary embolization. The method used in this experiment to produce myocardial damage has several advantages over other methods. It can be performed without opening the chest, it produces diffuse lesions, and it produces graded forms of heart damage by alteration of the dose. However, even when carried out in a standard fashion, there was considerable individual difference in the hemodynamic response, as originally pointed out by Agress.2 In our studies, we found that a dose of 4 mg. per kilogram of beads produced moderately severe coronary shock in 57 per cent of the animals. Attempts to increase the extent of myocardial damage by increasing the dose of beads led to a prohibitive mortality rate. Embolization of the lungs evoked a prompt hemodynamic response in all of our animals. This was characterized by a progressive fall in arterial oxygen saturation and in systemic blood pressure accompanied by a rise in right ventricular systolic pressure. At first these findings were only transient, but with each succeeding embolus the findings became more marked and more sustained. The combination of systemic hypotension and right ventricular hypertension was tolerated poorly by the severe coronary shock group; most dogs died shortly after the onset of these hemodynamic events. In general, the changes were quite similar to those reported by other investigators who used a variety of embolic agents. The cardiac output studies during pulmonary embolus were of interest in that this measurement remained the same or in many animals increased following the first few embolic episodes. Only as a terminal event
299
Pulmonary embolism in coronary shock
fi
40 —"«C
*
20-
0
^^_ • 5
6
7
HEART
8
9
10
n
WEIGHT
(G/Kg Body Wt.)
Fig. 3. Relationship between heart weight and survival time after pulmonary embolus. Both mild and severe coronary shock groups are included. (r = 0.58; p < 0.05).
did cardiac output decrease. This is in agreement with previous experimental0 as well as clinical findings in patients with angiographically proved pulmonary embolus.7- 14 The reason for this somewhat surprising finding is not clear, but acute hypoxia has been suggested as one possible cause.12 Previous experiments in our laboratory 8 have demonstrated that the average survival time with this method of pulmonary embolus is 44 minutes. Almost the same results were obtained in the current experiments for both control and mild coronary shock animals. However, in animals which had previously sustained severe coronary shock, survival time was greatly reduced, averaging only 23 minutes. In terms of volumes of embolic agent, the average lethal pulmonary embolus for the control and mild coronary shock groups was 0.4 c.c. of beads per kilogram as compared to a dose of 0.2 c.c. of beads per kilogram in the severe coronary shock dogs. Gross inspection of the interior of the heart and of cut sections through the muscular wall revealed a gradation of discrete, usually subendocardial lesions. As in studies in man, these pathologic changes were never found in the free wall of the right ventricle, suggesting that this part of the canine heart is particularly resistant to infarction. Although there was some correlation between the number of these lesions and the survival time following pulmonary
The Journal of
300
Lowenfeh
et al.
embolus, a much better correlation was found between heart weight and survival time. When confronted with a patient who has sustained a massive pulmonary embolus, the physician faces a serious therapeutic decision: Will this gravely ill patient survive with only medical treatment or will he require embolectomy? Clinical experience suggests that patients with unilateral pulmonary artery embolus who are younger than 50 years of age rarely die9 and rarely need surgerys unless there is pre-existing cardiopulmonary disease. Indeed, some observers1'1 believe that pre-existing cardiopulmonary disease is just as important a determinant for survival as is the size of the embolus. Our experiments support this point of view and suggest that, in patients with known coronary artery disease, pulmonary embolectomy might be considered necessary for a smaller embolus than in normal patients. Conclusions The response to pulmonary embolus was studied in animals which had survived previous production of coronary shock. Myocardial damage was found to be a major factor in determining subsequent tolerance to pulmonary embolus. Animals which had previously sustained severe coronary shock exhibited a significant decrease in subsequent survival time after pulmonary embolus. Those which had sustained mild coronary shock fared the same as control animals. In all animals subjected to prior coronary shock, there was good correlation between heart weight and tolerance to pulmonary embolus.
Thoracic and Cardiovascular Surgery
3 4
5
6
7
8
9 10
11
12
13
14
We thank Ruthven Ferreira and John Holly for
their help.
REFERENCES 1 Agress, C. M., Rosenburg, M. J., Jacobs, H. I., Binder, M. J., Schneiderman, A., and Clark, W. G.: Protracted Shock in Closed Chest Dog Following Coronary Embolization With Graded Microspheres, Am. J. Physiol. 170: 536, 1952. 2 Agress, C. M., Glassner, H. F., Binder, M. J.,
15
16
and Fields, J.: Hemodynamic Measurements in Experimental Coronary Shock. J. Appl. Physiol. 10: 469, 1957. Bloch, J. H., Pierce, C. H., Manax, W. G., and Lillehei, R. C : Treatment of Experimental Cardiogenic Shock, Surgery 58: 197, 1965. Breckenridge, R. T., and Ratnoff, O. D.: Pulmonary Embolism and Unexpected Death in Supposedly Normal Persons, N. Engl. J. Med. 270: 298, 1964. Cross, F . S., and Mowlem, A.: A Survey of the Current Status of Pulmonary Embolectomy for Massive Pulmonary Embolism, Circulation 35: 86, 1966 (Suppl. I). Daicoff, G. R., Chavez, F. R., and Swenson, E. W.: Pulmonary Venous Hypertension in Massive Pulmonary Embolism, Am. J. Cardiol. 21: 95, 1968. Dalen, J. E., Banas, J. S., Brooks, H. L., Evans, G. L., Paraskos, J. A., and Dexter, L.: Resolution Rate of Acute Pulmonary Embolism in Man, N. Engl. J. Med. 280: 1194, 1969. Emirgil, C , Lowenfels, A. B., and Sobol, B. J.: Veno-arterial Shunting Without Oxygenation in Experimental Pulmonary Embolism, J. Surg. Res. 8: 167, 1968. Gorham, L. W.: A Study of Pulmonary Embolism, Arch. Intern. Med. 108: 189, 1961. Herman, R. E., Davis, J. H., and Holden, W. D.: Pulmonary Embolism. A Clinical and Pathologic Study With Emphasis on the Effect of Prophylactic Therapy With Anticoagulants, Am. J. Surg. 102: 19, 1961. Jacobey, J. A., Taylor, W. J., Smith, G. T., Gorlin, R., and Harken, D. E.: A New Therapeutic Approach to Acute Coronary Occlusion: Experimental Study, Am. J. Cardiol. 9: 60, 1962. Kontos, H. A., Levasseur, J. E., Richardson, D. W., Mauck, H. P., Jr., and Patterson, J. L., Jr.: Comparative Circulatory Responses to Systemic Hypoxia in Man and in Unanesthetized Dog, J. Appl. Physiol. 23: 381, 1967. Mclntyre, K. M., and Sasahara, A. A.: Determinants of the Hemodynamic Response to Pulmonary Embolism (abstr.) Clin. Res. 17: 254, 1969. Mclntyre, K. M., and Sasahara, A. A.: Hemodynamic Response to Pulmonary Embolism in Patients Without Prior Cardiopulmonary Disease, A m . J. Cardiol. 28: 288, 1971. Miller, R. D., Jordan, R. A., Parker, R. L., and Edwards, J. E.: Thrcmboembolism in Acute and in Healed Myocardial Infarction: Systemic and Pulmonary Arterial Occlusion, Circulation 6: 7, 1952. Moran, T. J.: Autopsy Incidence of Pulmonary Embolism in Coronary Heart Disease, Ann. Intern. Med. 32: 949, 1950.