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Air embolism and cardiac arrest in a patient with a pulmonary artery catheter: A possible association
113
Resuscitation, 14 (1986) 113-119 Elsevier Scientific Publishers Ireland Ltd.
AIR EMBOLISM AND PULMONARY ARTERY
MICHAEL S. JASTREMSKI
CARDIAC ARREST IN A PATIENT WITH CATHETER: A POSSIBLE ASSOCIATION
A
and LAKSHMIPATHI CHELLURI
Department of Critical Care and Emergency Medicine, University Hospital, Sciences Center at Syracuse, 750 East Adams Street, Syracuse, NY 13210 (U.S.A.)
Health
(Received February 27th, 1986) (Revision received May 12th, 1986) (Accepted May 21st, 1986)
SUMMARY
This patient with acute mitral insufficiency suddenly developed hemoptysis and electromechanical dissociation. A post mortem chest X-ray demonstrated a large amount of air in the right ventricular cavity. It is postulated that this air embolism resulted from a catheter-induced rupture of the pulmonary artery.
Key words: Air embolism
- Pulmonary
artery catheter
INTRODUCTION
Since its introduction in 1970, bedside hemodynamic monitoring by right heart catheterization has become a widely used and valuable technique in the management .of critically ill patients (Swan, Ganz, Forrester, Marcus, Diamond and Chonette, 1970; Connors, McCaffree and Gray, 1983; Goldenheim and Kazemi, 1984; Weidman, Matthay and Matthay, 1984). Several recent reviews summarize the myriad of complications from pulmonary artery catheterization that have been reported (Weidman et al., 1984; Sprung, 1983). Physical trauma to the lungs has included retrograde dissection of the pulmonary artery (Gomez-Arnau, Montero, Luengo, Gilsanz and Avello, 1982), at least 32 incidents of rupture of the pulmonary artery (Sprung, 1983), tension pneumothorax (Culpepper, Setter and Rinaldo, 1982; Farber, Rose, Bassell and Eugene, 1981), false aneurysm of 0 1986 Elsevier Scientific Publishers Ireland Ltd. 0300-9572/86/$03.50 Printed and Published in Ireland
114
the pulmonary artery (Kron, Piepgrass, Carabello, Crisler, Testmeyer and Nolan, 1982), and pulmonary artery bronchial fistula (Fiol, Ibanez, Marse, Garcia-Moris and Marcos, 1980). The following case illustrates yet another manifestation of pulmonary trauma from this technique. CASE REPORT
C.P. was a 75-year-old female who had been in good health until she developed severe left sided chest pain and marked dyspnea on the day of admission. When she arrived at the emergency ward she was cyanotic and unresponsive. Pulse was 130 beats/min, blood pressure 150/90 mmHg, and the respiratory rate 40 breaths/min. There were rales to the apices of both lungs. The heart was enlarged with a grade II soft systolic murmur at the
Fig. 1. AP chest X-ray demonstrating lower lobe.
the tip of the pulmonary artery catheter in the left
115
apex. The extremities were mottled and cold. An endotracheal tube was passed and 100% oxygen was given. She received 20 mg furosemide, 10 mg morphine, and 100 mg lidocaine intravenously. Blood pressure then fell to 60/O mmHg and a dopamine infusion was started which raised the blood pressure to 110/60 mmHg. A chest X-ray obtained at this time confirmed the diagnosis of pulmonary edema. The electrocardiogram showed sinus tachycardia and left bundle branch block. Initial laboratory data included hemoglobin 14.2 gm/dl, white count 11,70O/dl, normal urinalysis, sodium 144 mEq/l potassium 3.3 mEq/l, chloride 96 mEq/l, COZ 24 mEq/l, BUN 26 mg%, glucose 394 mg%, CPK 50 I.U./l, SGOT 45 p/ml (normal lo-15 p/ml), and LDH 260 p/ml (normal 90-200 p/ml). Arterial blood gases on 100% oxygen were pH 7.49, PCO, 36 mmHg, and PO, 218 mmHg. The patient was transferred to the Coronary Care Unit where an arterial line was placed in the left radial artery and a 5F Swan-Ganz catheter was inserted using pressure monitoring. A chest X-ray (Fig. 1) showed that the catheter tip was in the peripheral left lung. Oxygen saturation was 75% in both the right atrium and right ventricle. Pulmonary artery pressure was 30/10 mmHg with a wedge pressure of 11 mmHg. There was a prominent V wave present. During the next several hours the patient began to diurese, became awake and responsive, and no longer required dopamine to support her blood pressure. However, she remained in pulmonary edema and her pansystolic murmur had increased to grade IV in intensity. The blood pressure was 150/ 90 mmHg with a pulmonary artery pressure of 40/26 mmHg, a wedge pressure of 26 mmHg, and a V wave of 35-40 mmHg. A nitroprusside drip was then started and titrated to maintain her wedge pressure between 14 and 18 mmHg with a systolic blood pressure of no less than 95 mmHg. With this regimen her V wave decreased to 8-10 mmHg, her pulmonary edema cleared, and the intensity of the murmur decreased. Twelve hours after admission she was extubated. On the day after admission she was clinically stable but nitroprussidedependent, since each attempt in tapering the nitroprusside resulted in worsening of her mitral regurgitation. During the day she coughed up a small amount of blood streaked sputum. Coagulation studies at this time were normal with a prothrombin time of 13.4 s with a control of 12.9 s, a partial thromboplastin time of 29.1 s with a control of 32.4 s, and a platelet count of 172 000. On the evening of the second hospital day, the patient suddenly became agitated and told the nurse she was about to die. While one author was at her bedside, she coughed up several hundred milliliters of frothy bright red blood and quickly became unresponsive with sinus tachycardia but a flat line on the intraarterial pressure tracing. The wedge pressure was 14 mmHg a few minutes before the arrest. A nasogastric tube was in place and draining clear yellow gastric contents. CPR was started, the patient was intubated, and a large amount of blood suctioned from the trachea. She was given
116
saline, sodium bicarbonate, calcium chloride and 100% oxygen; but received no intracardiac injections. Arterial blood gases during CPR showed a pH of 7.44, a Pace, of 38 mmHg, and aPa& of 114 mmHg. The sinus tachycardia soon degenerated to ventricular fibrillation, and she was finally pronounced dead approximately 20 min after the onset of the hemoptysis. Unfortunately, permission for an autopsy could not be obtained, but a post mortem lateral chest X-ray (Fig. 2) showed a large amount of air in the right ventricle. DISCUSSION
Although autopsy confirmation of the mechanism of death was not obtained, the simultaneous appearance of blood in the airway and air in the vascular system may have resulted from a physical communication between the tracheobronchial tree and the pulmonary vasculature. The usual manifestation of trauma to the lung from pulmonary artery catheterization is hemoptysis, but in three other cases there has also been evidence of barotrauma. Two patients had simultaneous development of hemoptysis and
Fig. 2. Lateral chest X-ray showing air in the right ventricle artery catheter and producing an air fluid level (arrows).
silhouetting
the pulmonary
117
tension pneumothorax after catheter manipulation (Culpepper et al., 1982; Farber et al., 1981) and in one case a pulmonary artery-bronchial fistula was documented with angiography (Fiol et al., 1980). Barash and co-workers have described several mechanisms by which a catheter might injure the pulmonary artery including tip performation, over inflation of the balloon, or normal inflation of the balloon in a small distal artery (Barash, Nardi, Hammond, Walker-Smith, Capuano, Laks, Kopriva, Baue and Geha, 1981). We suspect the latter occurred in this case since the tip of the catheter was quite distal. Because the pulmonary artery and bronchus are contiguous structures it is easy to see how both structures could be simultaneously injured. In fact, for hemoptysis to result from a pulmonary artery catheter there has to be some injury to the airway. Fistulas between a bronchus and a pulmonary vessel, both natural and experimental, have clearly been proven to allow air entry into the vasculature, although the pressure differential should favor bleeding into the bronchus during spontaneous breathing (Graham, Beall, Mattox and Vaughan, 1977). However, the institution of positive pressure ventilation might make intrabronchial pressure greater than intravascular pressure and thus favor air entry into the vessel. This is suggested by a pressure tracing obtained from the distal port of this patient’s pulmonary artery catheter shortly after she arrested (Fig. 3). We feel that venous air embolism with obstruction of right ventricular outflow was the most likely cause of our inability to resuscitate this patient.
Fig. 3. EKG tracing (top) and pressure recording from the tip port of the pulmonary artery catheter during the resuscitation. The increase in pressure to 50 mmHg coincided with positive pressure ventilation from a bag-valve device. Scale is in mmHg.
118
Although blood loss may have been a contributing factor, the volume of hemorrhage was not great enough to have caused refractory electricalmechanical dissociation. The absence of hypoxia and acidosis in the blood gases during the resuscitation argue against ineffective gas exchange from drowning the lungs in blood as a cause of the unsuccessful resuscitation. If the possibility of an air embolism had been considered, several additional procedures might have facilitated her resuscitation. First, the endotracheal tube could have been advanced into the right mainstem bronchus, thus protecting the right lung from further blood aspiration and shutting off the further flow of air into the vasculature. Second, the right ventricular outflow obstruction might have been relieved by placing her in the left lateral decubitus Trendelenburg position and pulling the catheter back into the right ventricle for aspiration of the air (Nicholson, 1956; Bartlett, 1985). This case serves to reemphasize several important safeguards that should be followed in using the pulmonary artery catheter. First, catheter tips should not be allowed to remain in the peripheral position but rather should be maintained in a proximal pulmonary artery and allowed to float distally with the balloon inflated to obtain wedge recordings. The balloon should not be inflated when the pressure tracing shows a wedge pressure wave form. Second, hemoptysis should be regarded as a serious sign in a patient with a pulmonary artery catheter, especially if the patient is anticoagulated; and its appearance requires immediate reassessment of the catheter’s position and withdrawal if it has migrated to a distal position. Finally, air embolism with right ventricular outflow obstruction should be considered in the differential diagnosis of any patient with a pulmonary artery catheter who suddenly develops electromechanical dissociation. REFERENCES Barash, P.G., Nardi, D., Hammond, G., Walker-Smith, G., Capuano, D., Laks, H., Kopriva, C.J., Baue, A.E. and Geha, A.S. (1981) Catheter-induced pulmonary artery perforation. Mechanisms, management, and modifications. J Thorac Cardiovasc Surg 82(l), 5-12. Bartlett, R.L. (1985) Resuscitative thoracotomy. In: Clinical procedures in emergency medicine, pp 247-248. Editors: J.R. Roberts and J.R. Hedges. W.B. Saunders, Philadelphia. Connors, A.F., McCaffree, D.R. and Gray, B.A. (1983) Evaluation of right-heart catheterization in the critically ill patient without acute myocardial infarction. NEJM 308,263-267. Culpepper, J.A., Setter, M. and Rinaldo, J.E. (1982) Massive hemoptysis and tension pneumothorax following pulmonary artery catheterization. Chest 82(3), 380-382. Farber, D.C., Rose, D.M., Bassell, G.M. and Eugene, J. (1981) Hemoptysis and pneumothorax after removal of a persistently wedged pulmonary artery catheter. Crit Care Med 9,494-495. Fiol, M., Ibanez, J., Marse, P., Garcia-Moris, S. and Marcos, J. (1980) Pulmonary artery bronchial fistula. A new complication of bedside pulmonary arteriography [letter]. Chest 78(2), 355. Goldenheim, P.D. and Kazemi, H. (1984) Cardiopulmonary monitoring of critically ill patients. NEJM 311, 776-780.
119 8 Gomez-Arnau, J., Montero, C.G., Luengo, C., Gilsanz, F.J. and Avello, F. (1962) Retrograde dissection and rupture of pulmonary artery after catheter use in pulmonary hypertension. Crit Care Med lO(lO), 694-695. 9 Graham, J.M., Beall, A.C., Mattox, K.L. and Vaughan, G.D. (1977) Systemic air embolism following penetrating trauma to the lung. Chest 72, 449-454. 10 Kron, I.L., Piepgrass, W., Carabello, B., Crisler, N., Testmeyer, C.J. and Nolan, S.P. (1982) False aneurysm of the pulmonary artery: a complication of pulmonary artery catheterization. Ann Thorac Surg 33(6), 629-630. 11 Nicholson, M.J. (1956) Emergency treatment of air embolism. Lahey Clin Bull 9, 239-246. 12 Sprung, C.L. (1983) Complications of pulmonary artery catheterization. In: The pulmonary artery catheter: methodology and clinical applications, pp 73-101. Editor: C.L. Sprung. University Park Press, Baltimore. 13 Swan, H.J.C., Ganz, W., Forrester, T., Marcus, M., Diamond, G. and Chonette, D. (1970) Catheterization of the heart in man with use of a flow-directed balloon-tipped catheter. NEJM 233,447-451. 14 Weidemann, H.P., Matthay, M.A. and Matthay, R.A. (1984) Cardiovascular monitoring in the intensive care unit. Chest 85, 537-549, 656-668.
Resuscitation, 14 (1986) 113-119 Elsevier Scientific Publishers Ireland Ltd.
AIR EMBOLISM AND PULMONARY ARTERY
MICHAEL S. JASTREMSKI
CARDIAC ARREST IN A PATIENT WITH CATHETER: A POSSIBLE ASSOCIATION
A
and LAKSHMIPATHI CHELLURI
Department of Critical Care and Emergency Medicine, University Hospital, Sciences Center at Syracuse, 750 East Adams Street, Syracuse, NY 13210 (U.S.A.)
Health
(Received February 27th, 1986) (Revision received May 12th, 1986) (Accepted May 21st, 1986)
SUMMARY
This patient with acute mitral insufficiency suddenly developed hemoptysis and electromechanical dissociation. A post mortem chest X-ray demonstrated a large amount of air in the right ventricular cavity. It is postulated that this air embolism resulted from a catheter-induced rupture of the pulmonary artery.
Key words: Air embolism
- Pulmonary
artery catheter
INTRODUCTION
Since its introduction in 1970, bedside hemodynamic monitoring by right heart catheterization has become a widely used and valuable technique in the management .of critically ill patients (Swan, Ganz, Forrester, Marcus, Diamond and Chonette, 1970; Connors, McCaffree and Gray, 1983; Goldenheim and Kazemi, 1984; Weidman, Matthay and Matthay, 1984). Several recent reviews summarize the myriad of complications from pulmonary artery catheterization that have been reported (Weidman et al., 1984; Sprung, 1983). Physical trauma to the lungs has included retrograde dissection of the pulmonary artery (Gomez-Arnau, Montero, Luengo, Gilsanz and Avello, 1982), at least 32 incidents of rupture of the pulmonary artery (Sprung, 1983), tension pneumothorax (Culpepper, Setter and Rinaldo, 1982; Farber, Rose, Bassell and Eugene, 1981), false aneurysm of 0 1986 Elsevier Scientific Publishers Ireland Ltd. 0300-9572/86/$03.50 Printed and Published in Ireland
114
the pulmonary artery (Kron, Piepgrass, Carabello, Crisler, Testmeyer and Nolan, 1982), and pulmonary artery bronchial fistula (Fiol, Ibanez, Marse, Garcia-Moris and Marcos, 1980). The following case illustrates yet another manifestation of pulmonary trauma from this technique. CASE REPORT
C.P. was a 75-year-old female who had been in good health until she developed severe left sided chest pain and marked dyspnea on the day of admission. When she arrived at the emergency ward she was cyanotic and unresponsive. Pulse was 130 beats/min, blood pressure 150/90 mmHg, and the respiratory rate 40 breaths/min. There were rales to the apices of both lungs. The heart was enlarged with a grade II soft systolic murmur at the
Fig. 1. AP chest X-ray demonstrating lower lobe.
the tip of the pulmonary artery catheter in the left
115
apex. The extremities were mottled and cold. An endotracheal tube was passed and 100% oxygen was given. She received 20 mg furosemide, 10 mg morphine, and 100 mg lidocaine intravenously. Blood pressure then fell to 60/O mmHg and a dopamine infusion was started which raised the blood pressure to 110/60 mmHg. A chest X-ray obtained at this time confirmed the diagnosis of pulmonary edema. The electrocardiogram showed sinus tachycardia and left bundle branch block. Initial laboratory data included hemoglobin 14.2 gm/dl, white count 11,70O/dl, normal urinalysis, sodium 144 mEq/l potassium 3.3 mEq/l, chloride 96 mEq/l, COZ 24 mEq/l, BUN 26 mg%, glucose 394 mg%, CPK 50 I.U./l, SGOT 45 p/ml (normal lo-15 p/ml), and LDH 260 p/ml (normal 90-200 p/ml). Arterial blood gases on 100% oxygen were pH 7.49, PCO, 36 mmHg, and PO, 218 mmHg. The patient was transferred to the Coronary Care Unit where an arterial line was placed in the left radial artery and a 5F Swan-Ganz catheter was inserted using pressure monitoring. A chest X-ray (Fig. 1) showed that the catheter tip was in the peripheral left lung. Oxygen saturation was 75% in both the right atrium and right ventricle. Pulmonary artery pressure was 30/10 mmHg with a wedge pressure of 11 mmHg. There was a prominent V wave present. During the next several hours the patient began to diurese, became awake and responsive, and no longer required dopamine to support her blood pressure. However, she remained in pulmonary edema and her pansystolic murmur had increased to grade IV in intensity. The blood pressure was 150/ 90 mmHg with a pulmonary artery pressure of 40/26 mmHg, a wedge pressure of 26 mmHg, and a V wave of 35-40 mmHg. A nitroprusside drip was then started and titrated to maintain her wedge pressure between 14 and 18 mmHg with a systolic blood pressure of no less than 95 mmHg. With this regimen her V wave decreased to 8-10 mmHg, her pulmonary edema cleared, and the intensity of the murmur decreased. Twelve hours after admission she was extubated. On the day after admission she was clinically stable but nitroprussidedependent, since each attempt in tapering the nitroprusside resulted in worsening of her mitral regurgitation. During the day she coughed up a small amount of blood streaked sputum. Coagulation studies at this time were normal with a prothrombin time of 13.4 s with a control of 12.9 s, a partial thromboplastin time of 29.1 s with a control of 32.4 s, and a platelet count of 172 000. On the evening of the second hospital day, the patient suddenly became agitated and told the nurse she was about to die. While one author was at her bedside, she coughed up several hundred milliliters of frothy bright red blood and quickly became unresponsive with sinus tachycardia but a flat line on the intraarterial pressure tracing. The wedge pressure was 14 mmHg a few minutes before the arrest. A nasogastric tube was in place and draining clear yellow gastric contents. CPR was started, the patient was intubated, and a large amount of blood suctioned from the trachea. She was given
116
saline, sodium bicarbonate, calcium chloride and 100% oxygen; but received no intracardiac injections. Arterial blood gases during CPR showed a pH of 7.44, a Pace, of 38 mmHg, and aPa& of 114 mmHg. The sinus tachycardia soon degenerated to ventricular fibrillation, and she was finally pronounced dead approximately 20 min after the onset of the hemoptysis. Unfortunately, permission for an autopsy could not be obtained, but a post mortem lateral chest X-ray (Fig. 2) showed a large amount of air in the right ventricle. DISCUSSION
Although autopsy confirmation of the mechanism of death was not obtained, the simultaneous appearance of blood in the airway and air in the vascular system may have resulted from a physical communication between the tracheobronchial tree and the pulmonary vasculature. The usual manifestation of trauma to the lung from pulmonary artery catheterization is hemoptysis, but in three other cases there has also been evidence of barotrauma. Two patients had simultaneous development of hemoptysis and
Fig. 2. Lateral chest X-ray showing air in the right ventricle artery catheter and producing an air fluid level (arrows).
silhouetting
the pulmonary
117
tension pneumothorax after catheter manipulation (Culpepper et al., 1982; Farber et al., 1981) and in one case a pulmonary artery-bronchial fistula was documented with angiography (Fiol et al., 1980). Barash and co-workers have described several mechanisms by which a catheter might injure the pulmonary artery including tip performation, over inflation of the balloon, or normal inflation of the balloon in a small distal artery (Barash, Nardi, Hammond, Walker-Smith, Capuano, Laks, Kopriva, Baue and Geha, 1981). We suspect the latter occurred in this case since the tip of the catheter was quite distal. Because the pulmonary artery and bronchus are contiguous structures it is easy to see how both structures could be simultaneously injured. In fact, for hemoptysis to result from a pulmonary artery catheter there has to be some injury to the airway. Fistulas between a bronchus and a pulmonary vessel, both natural and experimental, have clearly been proven to allow air entry into the vasculature, although the pressure differential should favor bleeding into the bronchus during spontaneous breathing (Graham, Beall, Mattox and Vaughan, 1977). However, the institution of positive pressure ventilation might make intrabronchial pressure greater than intravascular pressure and thus favor air entry into the vessel. This is suggested by a pressure tracing obtained from the distal port of this patient’s pulmonary artery catheter shortly after she arrested (Fig. 3). We feel that venous air embolism with obstruction of right ventricular outflow was the most likely cause of our inability to resuscitate this patient.
Fig. 3. EKG tracing (top) and pressure recording from the tip port of the pulmonary artery catheter during the resuscitation. The increase in pressure to 50 mmHg coincided with positive pressure ventilation from a bag-valve device. Scale is in mmHg.
118
Although blood loss may have been a contributing factor, the volume of hemorrhage was not great enough to have caused refractory electricalmechanical dissociation. The absence of hypoxia and acidosis in the blood gases during the resuscitation argue against ineffective gas exchange from drowning the lungs in blood as a cause of the unsuccessful resuscitation. If the possibility of an air embolism had been considered, several additional procedures might have facilitated her resuscitation. First, the endotracheal tube could have been advanced into the right mainstem bronchus, thus protecting the right lung from further blood aspiration and shutting off the further flow of air into the vasculature. Second, the right ventricular outflow obstruction might have been relieved by placing her in the left lateral decubitus Trendelenburg position and pulling the catheter back into the right ventricle for aspiration of the air (Nicholson, 1956; Bartlett, 1985). This case serves to reemphasize several important safeguards that should be followed in using the pulmonary artery catheter. First, catheter tips should not be allowed to remain in the peripheral position but rather should be maintained in a proximal pulmonary artery and allowed to float distally with the balloon inflated to obtain wedge recordings. The balloon should not be inflated when the pressure tracing shows a wedge pressure wave form. Second, hemoptysis should be regarded as a serious sign in a patient with a pulmonary artery catheter, especially if the patient is anticoagulated; and its appearance requires immediate reassessment of the catheter’s position and withdrawal if it has migrated to a distal position. Finally, air embolism with right ventricular outflow obstruction should be considered in the differential diagnosis of any patient with a pulmonary artery catheter who suddenly develops electromechanical dissociation. REFERENCES Barash, P.G., Nardi, D., Hammond, G., Walker-Smith, G., Capuano, D., Laks, H., Kopriva, C.J., Baue, A.E. and Geha, A.S. (1981) Catheter-induced pulmonary artery perforation. Mechanisms, management, and modifications. J Thorac Cardiovasc Surg 82(l), 5-12. Bartlett, R.L. (1985) Resuscitative thoracotomy. In: Clinical procedures in emergency medicine, pp 247-248. Editors: J.R. Roberts and J.R. Hedges. W.B. Saunders, Philadelphia. Connors, A.F., McCaffree, D.R. and Gray, B.A. (1983) Evaluation of right-heart catheterization in the critically ill patient without acute myocardial infarction. NEJM 308,263-267. Culpepper, J.A., Setter, M. and Rinaldo, J.E. (1982) Massive hemoptysis and tension pneumothorax following pulmonary artery catheterization. Chest 82(3), 380-382. Farber, D.C., Rose, D.M., Bassell, G.M. and Eugene, J. (1981) Hemoptysis and pneumothorax after removal of a persistently wedged pulmonary artery catheter. Crit Care Med 9,494-495. Fiol, M., Ibanez, J., Marse, P., Garcia-Moris, S. and Marcos, J. (1980) Pulmonary artery bronchial fistula. A new complication of bedside pulmonary arteriography [letter]. Chest 78(2), 355. Goldenheim, P.D. and Kazemi, H. (1984) Cardiopulmonary monitoring of critically ill patients. NEJM 311, 776-780.
119 8 Gomez-Arnau, J., Montero, C.G., Luengo, C., Gilsanz, F.J. and Avello, F. (1962) Retrograde dissection and rupture of pulmonary artery after catheter use in pulmonary hypertension. Crit Care Med lO(lO), 694-695. 9 Graham, J.M., Beall, A.C., Mattox, K.L. and Vaughan, G.D. (1977) Systemic air embolism following penetrating trauma to the lung. Chest 72, 449-454. 10 Kron, I.L., Piepgrass, W., Carabello, B., Crisler, N., Testmeyer, C.J. and Nolan, S.P. (1982) False aneurysm of the pulmonary artery: a complication of pulmonary artery catheterization. Ann Thorac Surg 33(6), 629-630. 11 Nicholson, M.J. (1956) Emergency treatment of air embolism. Lahey Clin Bull 9, 239-246. 12 Sprung, C.L. (1983) Complications of pulmonary artery catheterization. In: The pulmonary artery catheter: methodology and clinical applications, pp 73-101. Editor: C.L. Sprung. University Park Press, Baltimore. 13 Swan, H.J.C., Ganz, W., Forrester, T., Marcus, M., Diamond, G. and Chonette, D. (1970) Catheterization of the heart in man with use of a flow-directed balloon-tipped catheter. NEJM 233,447-451. 14 Weidemann, H.P., Matthay, M.A. and Matthay, R.A. (1984) Cardiovascular monitoring in the intensive care unit. Chest 85, 537-549, 656-668.