ATS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Abstract Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Eduardo A. Tovar
Carlos Del Campo
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Tovar, E. A.
Right arrow Articles by Weinstein, P. B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Tovar, E. A.
Right arrow Articles by Weinstein, P. B.

Ann Thorac Surg 1995;60:1138-1142
© 1995 The Society of Thoracic Surgeons

Current Review

Postoperative Management of Cerebral Air Embolism: Gas Physiology for Surgeons

Eduardo A. Tovar, MD, Carlos Del Campo, MD, Alan Borsari, MD, Robin P. Webb, Ccp, Jeffrey R. Dell, MD, Paul B. Weinstein, MD

Divisions of Cardiovascular Surgery and Cardiology, St. Jude Medical Center, Fullerton, and The University of California, Irvine Medical Center, Orange, California


   Abstract
Top
 Footnotes
 Abstract
Introduction
 Case Reports
 Gas Physiology
 Conclusion
 Acknowledgments
 References
 
Cerebral gaseous microemboli are present in most, if not all, cardiopulmonary bypass--assisted operations. Fortunately, the great majority are subclinical. Clinically significant cases of cerebral air embolism are largely underdiagnosed, undertreated, and underreported. The management of cerebral air embolism has been challenged due to the lack of prospective, randomized studies. Preventive measures that have been implemented throughout the years, resulting from empirically acquired knowledge, have avoided frequent major mishaps. Perfusion accidents, in which massive amounts of gas are pumped into patients, are managed intraoperatively by common-sense heroic measures which, at best, remove 50% of the embolized gas. Postoperative confirmation of a neurologic insult after a cardiopulmonary bypass--assisted operation, in which a cerebral air embolism is likely the source, is one of the most distressing situations a surgical team has to confront, due in part to the lack of pathognomonic diagnostic tools and to the absence of a ``scientifically proven'' (supported by prospective, randomized studies) therapeutic regimen. In lieu of the latter, we present the physical and physiologic bases that will justify the use of several therapeutic tools when facing a suspected CAE. These tools, when applied rationally, will represent some of the most innocuous modalities in the medical armamentarium.


   Introduction
Top
 Footnotes
 Abstract
 Introduction
Case Reports
 Gas Physiology
 Conclusion
 Acknowledgments
 References
 
Cardiopulmonary bypass (CPB) has been associated with air embolism since its inception. Alexis Carrel [1], while performing experimental operations on the heart, warned of that possibility in 1914. In April 1951, during the second attempt ever to use extracorporeal circulation in humans, Dennis and colleagues [2] experienced a sudden emptying of the arterial reservoir. The patient died intraoperatively of a massive air embolism. Despite all the experience and knowledge accumulated in more than 40 years of CPB-assisted operations, gas embolism continues to be present as gaseous microemboli in virtually every operation, particularly when a bubble oxygenator is in use [3] or when arterial filters are not being used [4]. Even though most gaseous microemboli currently observed are subclinical [5], some patients may experience massive air emboli. Stoney and co-authors [6] reported that between 1972 and 1977 one in 870 patients undergoing CPB-assisted operations experienced a massive air embolism, with 1 in 2,500 cases resulting in death or permanent injury. Kurusz and co-workers [7] reported that between 1982 and 1985 1 case of massive air embolism occurred in every 1,250 cases. One resulted in death or injury in every 8,000 cases.

There are two common sources of clinically significant cerebral air embolism (CAE). One arises from the pump and the other, by far the most common, originates in the surgical field. Although Reed and co-authors [8] and Kurusz and co-workers [9] have extensively studied the causes and prevention of the former, other investigators, including Fishman and co-authors [10], Mills and Ochsner [11], and Roe [12], among others, have established protocols to avoid mishaps that arise in the surgical field.

Currently, there is no reliable test to diagnose CAE a posteriori [13, 14]. In the course of an operation, the expression of CAE is purely electrical. The use of electroencephalography during or immediately after an episode of CAE will detect this expression, which will vary in intensity from simple slowing to complete extinction of cerebral activity in the involved hemisphere. The gravity of the intraoperative electroencephalogram does not always reflect the severity of the clinical manifestations [15]. The major determinants of the presence of symptoms are the size of the bubbles, the site of final destination within the cerebral circulation, and the type of gas embolized.

As far as management is concerned, Mills and Ochsner [11] have described the now-classic maneuvers employed during this emergency in the operating theater. We present maneuvers that can be implemented in the postoperative period (Fig 1Go), and their physical and physiologic bases.



View larger version (36K):
[in this window]
[in a new window]
  		Fig 1. . Postoperative management of cerebral air embolism.

 

   Case Reports
Top
 Footnotes
 Abstract
 Introduction
 Case Reports
Gas Physiology
 Conclusion
 Acknowledgments
 References
 
Patient 1
A 61-year-old woman underwent a mitral valve replacement. At the completion of CPB and after standard deairing maneuvers, while heparin was being reversed and the arterial line clamped, a large air bubble suddenly appeared in the aortic cannula. Arrhythmias and temporary ventricular dysfunction coincidentally occurred. Approximately 11/2 hours after the completion of the operation, the patient exhibited spasmodic movements of the left eyelid. Soon after, focalized seizures followed, involving the left side of the face and left upper and lower extremities. The patient's seizures were treated unsuccessfully with diazepam, lorazepam, phenytoin, and phenobarbital. Consequently, a thiopental coma was induced.

An electroencephalogram 24 hours from the time of the operation still demonstrated an epileptiform disturbance. We therefore transferred the patient to a facility equipped with a monoplace hyperbaric chamber. The patient underwent 2 hours of hyperbaric oxygen therapy at 3 absolute atmospheres (ATA) 32 hours after the initial incident. A repeat electroencephalogram the following day demonstrated that the seizure bursts had disappeared. We took the patient for a second time to the chamber, where she underwent a repeat of the original therapy. While in the chamber, the patient started to breathe spontaneously and her pupils became much more reactive. We discontinued all anticonvulsant therapy. Once all the medications were fully metabolized, the patient regained consciousness and was free of all seizure activity and neurologic deficit. She was discharged on the 15th postoperative day without any sequelae.

Patient 2
A 54-year-old man who, 12 years earlier, underwent an aortic valve replacement, presented with fever, chills, and signs of aortic insufficiency. An uncomplicated redo aortic valve replacement was performed for prosthetic valve endocarditis. The patient awakened soon after the operation, moving all four extremities. Approximately 13 hours after his admission to the intensive care unit, the patient had a grand mal seizure followed by left hemiplegia. Thirty minutes later, a second convulsive episode occurred. We treated the patient with lorazepam and phenytoin, which controlled the seizure activity. The left-sided paralysis improved over the next hours. Hyperoxia, increased blood pressure and enhanced cardiac output using inotropic medications, and surface hypothermia were instituted at the time of the first seizure. Thirty-six hours after the operation, the patient was extubated and exhibited no neurologic symptoms. On the second postoperative day, we discontinued administration of lorazepam and phenytoin. The patient progressed well and was discharged home on the fifth postoperative day.


   Gas Physiology
Top
 Footnotes
 Abstract
 Introduction
 Case Reports
 Gas Physiology
Conclusion
 Acknowledgments
 References
 
When the diagnosis of CAE has been suspected in the postoperative period, hyperbaric oxygen therapy has been accepted as the only specific therapeutic modality geared to enhance dissolution of bubbles in the intravascular space [16, 17]. In fact, bubbles have the natural tendency to dissolve [18], and several additional maneuvers can be used to accelerate this process. Although air bubbles can be present in the intravascular space for more than 48 hours after an air embolism [19], it has been calculated that a 4-mm air bubble will disappear in 560 minutes in flowing blood [20]. The size of the bubbles is important. The smaller they are the smaller the vessels that will be blocked and the larger the surface area of the gas in contact with blood (Table 1Go), thus facilitating reabsorption of the gas. How fast a bubble dissolves in the cerebral circulation may mean the difference between ischemic penumbra (during which the neurons remain structurally intact but functionally inactive) [21] and cerebral infarct.


View this table:
[in this window]
[in a new window]
  		Table 1. . Relationship of Diameter, Volume, and Surface Areaa
 
To facilitate the understanding of gas physiology it is important to remember how, at sea level, gases are distributed (Table 2Go). Note that nitrogen (N2) and oxygen (O2) are the main components of an air bubble [23]. Oxygen is readily absorbed, whereas the remaining gas (N2) takes much longer [24]. The task is, therefore, to dissolve the remaining N2 bubble. The therapeutic tools that can be used in the management of CAE are (1) hypothermia, (2) supranormal blood pressure, (3) enhanced cardiac output, (4) hyperoxia, (5) hyperbaric pressure, (6) hyperbaric oxygen, and (7) perfluorocarbon (PFC). The rationale for using each of these tools is as follows:


View this table:
[in this window]
[in a new window]
  		Table 2. . Partial Pressures (mm Hg) at Sea Levela
 
Effect of Hypothermia on Gas Solubility Coefficient
According to Henry's law, the amount of a gas that will dissolve in a liquid at a given temperature is a function of the partial pressure of that gas in contact with the liquid and the solubility coefficient (in mL • dL-1 • mm Hg-1) of the gas for that particular fluid [25]. To illustrate this concept we will use O2 as an example. The solubility coefficient of O2 in plasma at 37°C is 0.0031 mL • dL-1 • mm Hg-1 [26]. Its use in calculating arterial O2 content is shown in the following formula: Amount of O2 bound to hemoglobin = (hemoglobin of 15 g/dL x 1.34) O2 saturation approximately 20 mL/dL (1 g of hemoglobin carries 1.34 mL of O2). The above is added to the amount in physical solution = oxygen tension of 100 mm Hg x 0.0031 = 0.3 mL/dL. The arterial O2 content in this case is 20 + 0.3 = 20.3 mL/dL. For nitrogen, the nitrogen tension of 573 x 0.0017 (solubility coefficient of N2 in plasma at 37°C) = 0.97 mL of N2/dL or 9.7 mL of N2/L of plasma. At 20°C, the solubility coefficient of N2 increases to 0.0021 [25]. This will result in the physical solution of 12 mL of N2/L of plasma.

Effect of Hypothermia on Bubble Size
Charles' law states that for any gas, a change of volume or pressure is directly related to a change in temperature. Therefore, the lower the temperature, the lower the gas volume and gas pressure [23].

Supranormal Blood Pressure
The forces that oppose a gas leaving solution are the barometric pressure and the hydrostatic pressure exerted on the gas in solution (ie, blood pressure, cerebrospinal fluid pressure, local tissue pressure). The force that favors bubble formation is the partial pressure of the gas [25].

For instance, nitrogen tension - (barometric pressure + mean blood pressure) breathing air at sea level = 573 - (760 + 70) = -257 mm Hg (if the result is a negative value there is no possibility that N2 will come out of solution) [27]. When the value becomes positive, bubble formation or growth is likely to occur. For example, during a rapid ascent to an altitude of 1/2 ATA the likelihood of bubble formation is great, particularly on the venous side of the circulation (573 - [380 + 70] = 123 mm Hg on the arterial side and 573 - [380 + 6] = 187 mm Hg on the venous side) [27]. On the other hand, at 3 ATA with an increased blood pressure (573 - [2280 + 100] = -1717), if an N2 bubble exists the tendency will be for it to redissolve [27].

Enhanced Cardiac Output
The larger the amount of blood circulating through the lungs the larger the amount of N2 that will be eliminated. At 3 ATA 100% O2, 32 mL of N2 can be displaced per liter of blood. If the cardiac output is 3 L/min, 96 mL/min will be mobilized, and if the cardiac output is 6 L/min, 192 mL/min will be displaced. Cardiac output, therefore, plays a direct role in the process called ``denitrogenation'' [28] (see below).

Effect of Hyperoxia
If serum of a person breathing air at sea level containing a nitrogen tension of 573 mm Hg is suddenly subjected to a barometric pressure of 380 mm Hg (1/2 ATA), N2 will come out of solution and a bubble will be formed [29]. Similarly, if a person is taken to an altitude equivalent to a barometric pressure of 380 mm Hg he or she will experience ``the bends'' [30] (compressed air illness). If the same individual breathes 100% O2 for about 4 hours, all N2 will be removed from the body [27] and no symptoms will be produced despite exposure to higher altitudes [30]. This process is called denitrogenation [27].

The total amount of N2 in an individual is 573 x 0.0017 = 0.97 mL/100 mL of fluid x 10 = 9.7 mL/L in a 70-kg individual with 50 L of fluid = 50 x 9.7 mL = 485 mL of N2 dissolved in the body. The difference between the arterial and venous gas pressure is the so-called oxygen window [31] (Table 3Go). The O2 window will be used to remove N2. The larger the window the more N2 can be removed. Theoretically, a 54-mm Hg window can only remove 0.0017 x 54 = 0.0918 mL/dL or 0.9 mL of N2/L of blood. At sea level with an inspired oxygen fraction of 1.0, 0.0017 x 627 = 1.06 mL of N2/dL or 10.6 mL of N2/L of blood. Hlastala and Farhi [20] observed that a bubble of N2 measuring 4 mm in diameter disappears in 560 minutes while breathing air. A similar bubble disappears in only 56 minutes while breathing 100% O2.


View this table:
[in this window]
[in a new window]
  		Table 3. . Rate of N2 Desaturation (Denitrogenation) Is Proportional to the Size of the ``O2 Window''
 
Hyperbaric Pressure
Boyle's law states that at a constant temperature the volume of a gas will vary inversely to the pressure to which the gas is subjected and vice versa. The volume of a gas will decrease to one half at 2 ATA, to one third at 3 ATA, and to one sixth at 6 ATA. However, the diameter of the gas bubble will have much more modest decreases. At 2 ATA it will be 79.3% of the initial diameter, at 3 ATA 69.3%, and at 6 ATA 55% [26].

Hyperbaric Oxygen
The combination of hyperbaric pressure and hyperoxia has a synergistic effect. This is limited by the effects of oxygen toxicity. No more than 3 ATA of 100% O2 can be used before severe O2 toxicity will ensue [32].

Notice in Table 4Go how the magnitude of the O2 window varies in three different conditions. At 3 ATA and an inspired oxygen fraction of 1.0 it is 1,894 mm Hg, which is the same as at 6 ATA and an inspired oxygen fraction of 0.5 (1,894 x 0.0017 = 3.2 mL of N2/dL or 32 mL of N2/L of blood). At 6 ATA breathing compressed air the O2 window is only 911 mm Hg (15.5 mL of N2/L of blood). Notice that at 6 ATA breathing compressed air, the nitrogen tension in plasma will increase sixfold, with the likelihood of adding this gas to a bubble with a nitrogen tension of 573 mm Hg [33, 34]. This problem is circumvented by using 50% O2 and 50% helium [30, 35]. It is difficult, however, to decide whether the 19% reduction of the bubble's diameter between 3 ATA and 6 ATA, with no difference in the O2 window, justifies its use in these critically ill patients.


View this table:
[in this window]
[in a new window]
  		Table 4. . Magnitude of O2 Window at Different ATA and Inspired Oxygen Fractionsa
 
A second effect of hyperbaric oxygen is that at 3 ATA of 100% O2 the usual amount of O2 removed by the tissues (arteriovenous oxygen difference) of 6 mL/100 mL of blood will be present in physical solution (2,193 x 0.0031 = 6.7 mL of O2/100 mL of plasma) and there will be no need to use hemoglobin-bound O2 [25, 26, 36]. Therefore, areas not available to erythrocytes will still be oxygenated. In addition, O2 diffusion distance increases from 64 µm to 247 µm at the arterial end of the capillary and from 36 µm to 64 µm at the venous end [37].

Perfluorocarbon Emulsions
Although PFC emulsions have never been used in the clinical management of CAE, their use has been advocated for this purpose [38, 39]. The rationale for using PFC emulsions is briefly presented below.

The solubility coefficient of N2 in a 20% PFC emulsion is 0.0076 mL • dL-1 • mm Hg-1 [40], resulting in an N2 carrying capacity of 43.5 mL/L, whereas, as shown above, only 9.7 mL/L will dissolve in plasma.

What limits the use of PFC emulsions is the amount that can be infused to patients. For the purpose of this article let us assume that 1 L of 20% PFC emulsion is added to 4 L of blood. The N2 carrying capacity of the resulting mixture is 16.5 mL/L, which represents only a modest increase over plasma alone.


   Conclusion
Top
 Footnotes
 Abstract
 Introduction
 Case Reports
 Gas Physiology
 Conclusion
Acknowledgments
 References
 
If during arousal from anesthesia after a CPB-assisted operation the patient presents with a neurologic injury, there is a good possibility that air or other gas has made its way into the cerebral circulation. Mistaken treatment of a neurologic deficit that results from any source other than CAE during CPB will rarely be criticized. Failure to treat a patient who has sustained a CAE may result in a disabling neurologic injury and perhaps death. Based on physical and physiologic principles, the use of surface hypothermia, supranormal blood pressure, enhanced cardiac output, hyperoxia, and hyperbaric oxygen is validated in promoting prompt resolution of gas bubbles in the intravascular space.


   Acknowledgments
Top
 Footnotes
 Abstract
 Introduction
 Case Reports
 Gas Physiology
 Conclusion
 Acknowledgments
References
 
We are indebted to Kiumars Saketkhoo, MD, John C. Tufts, Parker T. Bailey, Dennis E. Rogers, Ronald J. Eickhoff, Joseph V. Malave, and David L. Smith, members of the hyperbaric unit at Presbyterian Intercommunity Hospital, for their professionalism and dedication. We also sincerely appreciate and acknowledge Jean L. Burnette for her assistance in the preparation of the manuscript.


   Footnotes
Top
 Footnotes
Abstract
 Introduction
 Case Reports
 Gas Physiology
 Conclusion
 Acknowledgments
 References
 
Address reprint requests to Dr Tovar, 100 E Valencia Mesa Dr, Suite 301, Fullerton, CA 92635.


   References
Top
 Footnotes
 Abstract
 Introduction
 Case Reports
 Gas Physiology
 Conclusion
 Acknowledgments
 References
 

  1. Carrel A. Experimental operations on the orifices of heart. Ann Surg 1914;60:1–6.[Medline]
  2. Dennis C. Perspective in review: one group's struggle with development of a pump-oxygenator. Trans Am Soc Artif Organs 1985;31:1–11.
  3. Van der Linden J, Casimir-Ahn H. When do cerebral emboli appear during open heart operations? A transcranial Doppler study. Ann Thorac Surg 1991;51:237–41.[Abstract]
  4. Padyachee TS, Parsons S, Theobold R, Gosling RG, Deverall PB. The effect of arterial filtration on reduction of gaseous microemboli in the middle cerebral artery during cardiopulmonary bypass. Ann Thorac Surg 1988;45:647–9.[Abstract]
  5. Topol EJ, Humphrey LS, Borkon AM, et al. Value of intraoperative left ventricular microbubbles detected by transesophageal two-dimensional echocardiography in predicting neurologic outcome after cardiac operations. Am J Cardiol 1985;56:773–5.[Medline]
  6. Stoney WS, Alford WC, Burrus GR, Glassford DM Jr, Thomas CS Jr. Air embolism and other accidents using pump oxygenators. Ann Thorac Surg 1980;29:336–40.[Abstract]
  7. Kurusz M, Conti VR, Arens JR, et al. Perfusion accident survey. Proc Am Acad Cardiovasc Perfusion 1986;7:57–65.
  8. Reed CC, Kurusz M, Lawrence AE Jr. Safety and techniques in perfusion. Stafford, TX: Quali-Med, Inc, 1988:239--57.
  9. Kurusz M, Wheeldon DR. Risk containment during cardiopulmonary bypass. Semin Thorac Cardiovasc Surg 1990;2:400–9.[Medline]
  10. Fishman NH, Carlsson E, Roe BB. The importance of the pulmonary veins in systemic air embolism following open-heart surgery. Surgery 1969;66:655–62.[Medline]
  11. Mills NL, Ochsner JL. Massive air embolism during cardiopulmonary bypass: causes, prevention, and management. J Thorac Cardiovasc Surg 1980;80:708–17.[Abstract]
  12. Roe BB. Air embolism prevention. Ann Thorac Surg 1987;44:212–3.[Abstract]
  13. Adkisson GH, Macleod MA, Hodgson M, et al. Cerebral perfusion deficits in dysbaric illness. Lancet 1989;2:119–22.[Medline]
  14. Warren LP Jr, Djang WT, Moon RE, et al. Neuroimaging of scuba diving injuries to the CNS. AJR 1988;151:1003–8.[Abstract/Free Full Text]
  15. Dutka AJ, Mink R, McDermott J, Clark JB, Hallenbeck JM. Effect of lidocaine on somatosensory evoked response and cerebral blood flow after canine cerebral air embolism. Stroke 1992;23:1515–20.[Abstract/Free Full Text]
  16. Peirce EC II. Specific therapy for arterial air embolism. Ann Thorac Surg 1980;29:300–3.[Medline]
  17. Kol S, Ammar R, Weisz G, Melamed Y. Hyperbaric oxygenation for arterial air embolism during cardiopulmonary bypass. Ann Thorac Surg 1993;55:401–3.[Abstract]
  18. Butler BD, Luehr S, Katz J. Venous gas embolism: time course of residual pulmonary intravascular bubbles. Undersea Biomed Res 1989;16:21–9.[Medline]
  19. Fries CC, Levowitz B, Adler S, Cook AW, Karlson KE, Dennis C. Experimental gas embolism. Ann Surg 1957;145:461–70.[Medline]
  20. Hlastala MP, Farhi LE. Absorption of gas bubbles in flowing blood. J Appl Physiol 1973;35:311–6.[Free Full Text]
  21. Astrup J, Symon L, Branston NM, Lassen NA. Cortical evoked potential and extracellular K+ and H+ at critical levels of brain ischemia. Stroke 1977;8:51–7.[Abstract/Free Full Text]
  22. Previte JJ. Human physiology. New York: McGraw-Hill, 1983:488.
  23. Shilling CW, Carlston CC, eds. The physicians' guide to diving medicine. New York: Plenum, 1983:39.
  24. Durant T, Oppenheimer MJ, Webster MR, Long J. Arterial air embolism. Am Heart J 1949;38:481–500.[Medline]
  25. D'Aoust BG. The physiological basis of hyperbaric therapy. In: Davis JC, ed. Hyperbaric and undersea medicine. San Antonio: Medical Seminars, 1981:2--7.
  26. Bassett BE, Bennett PB. Introduction to the physical and physiological bases of hyperbaric therapy. In: Davis JC, Hunt TK, eds. Hyperbaric oxygen therapy. Bethesda, MD: Undersea Medical Society, 1977:15.
  27. Heimbach RD, Sheffield PJ. Decompression sickness and pulmonary overpressure accidents. In: DeHart RL, ed. Fundamentals of aerospace medicine. Philadelphia: Lea & Febiger, 1985:135--8.
  28. Groom AC, Song SH, Ohta Y, Farhi LE. Effect of anesthesia on rate of N2 washout from body stores. In: Farhi LE, Rahn H, eds. Studies in pulmonary physiology. San Antonio: USAF School of Aerospace Medicine, 1974:254--62.
  29. Downey VM, Worley TW, Hackworth R, Whitley JL. Studies on bubbles in human serum under increased and decreased atmospheric pressure. Aerospace Med 1963;34:116–8.
  30. Behnke AR. A brief history of hyperbaric medicine. In: Davis JC, Hunt TK, eds. Hyperbaric oxygen therapy. Bethesda, MD: Undersea Medical Society, 1977:7.
  31. Brown SD, Piantadosi CA. Diving medicine and near drowning. In: Hall JB, Schmidt GA, Wood LDH, eds. Principles of critical care. New York: McGraw-Hill, 1992:875.
  32. Clark JM, Fisher AB. Oxygen toxicity and extension of tolerance in oxygen therapy. In: Davis JC, Hunt TK, eds. Hyperbaric oxygen therapy. Bethesda, MD: Undersea Medical Society, 1977:68.
  33. Goodman MW. Decompression sickness treated with compression to 2--6 atmospheres absolute. Aerospace Med 1964;35:1204–12.[Medline]
  34. Goodman MW, Workman RD. Minimal-recompression, oxygen-breathing approach to treatment of decompression sickness in divers and aviators. Washington, DC: US Navy Experimental Diving Unit. BuShips Project SF 011 06 05, Tack 11513-2, 1965, #5-65.
  35. Kindwall EP. Massive surgical air embolism treated with brief recompression to six atmospheres followed by hyperbaric oxygen. Aerospace Med 1973;44:663–6.[Medline]
  36. Boerema I, Meyne NG, Brummelkamp WK, et al. Life without blood: a study of the influence of high atmospheric pressure and hypothermia on dilution of blood. J Cardiovasc Surg 1960;1:133–46.
  37. Krogh A. The number and distribution of capillaries in muscle with calculations of the oxygen pressure head necessary for supplying the tissue. J Physiol 1919;52:409–15.[Free Full Text]
  38. Cassuto Y, Nunneley SA, Farhi LE. Inert gas washout in rats: enhancement by fluorocarbon infusion. In: Farhi LE, Rahn H, eds. Studies in pulmonary physiology. San Antonio: USAF School of Aerospace Medicine, 1974:274--7.
  39. Menasché P, Pinard E, Desroches A-M, et al. Fluorocarbons: a potential treatment of cerebral air embolism in open heart surgery. Ann Thorac Surg 1985;40:494–7.[Abstract]
  40. Tuman K, Spiess BD, McCarthy RJ, Ivankovich AD. Cardiorespiratory effects of venous air embolism in dogs receiving a perfluorocarbon emulsion. J Neurosurg 1986;65:238–44.[Medline]



This article has been cited by other articles:


Home page
 Eur Respir JHome page
P. G. Jorens, E. Van Marck, A. Snoeckx, and P. M. Parizel
Nonthrombotic pulmonary embolism
Eur. Respir. J., August 1, 2009; 34(2): 452 - 474.
[Abstract] [Full Text] [PDF]

Home page
 Br J AnaesthHome page
B. M. P. Rademaker, F. A. Groenman, P. A. van der Wouw, and E. A. Bakkum
Paradoxical gas embolism by transpulmonary passage of venous emboli during hysteroscopic surgery: a case report and discussion
Br. J. Anaesth., August 1, 2008; 101(2): 230 - 233.
[Abstract] [Full Text] [PDF]

Home page
 J. Thorac. Cardiovasc. Surg.Home page
T. Kunihara, T. Grun, D. Aicher, F. Langer, O. Adam, O. Wendler, Y. Saijo, and H.-J. Schafers
Hypothermic circulatory arrest is not a risk factor for neurologic morbidity in aortic surgery: A propensity score analysis
J. Thorac. Cardiovasc. Surg., September 1, 2005; 130(3): 712 - 718.
[Abstract] [Full Text] [PDF]

Home page
 SEMIN CARDIOTHORAC VASC ANESTHHome page
K. Prasongsukarn and M. A. Borger
Reducing Cerebral Emboli During Cardiopulmonary Bypass
Seminars in Cardiothoracic and Vascular Anesthesia, June 1, 2005; 9(2): 153 - 158.
[Abstract] [PDF]

Home page
 J. Thorac. Cardiovasc. Surg.Home page
M. A. Borger, C. M. Peniston, R. D. Weisel, M. Vasiliou, R. E. A. Green, and C. M. Feindel
Neuropsychologic impairment after coronary bypass surgery: Effect of gaseous microemboli during perfusionist interventions
J. Thorac. Cardiovasc. Surg., April 1, 2001; 121(4): 743 - 749.
[Abstract] [Full Text] [PDF]

Home page
 NeurologyHome page
D. A. Hinkle, D. M. Raizen, M. L. McGarvey, and G. T. Liu
Cerebral air embolism complicating cardiac ablation procedures
Neurology, March 27, 2001; 56(6): 792 - 794.
[Abstract] [Full Text] [PDF]

Home page
 NEJMHome page
C. M. Muth and E. S. Shank
Gas Embolism
N. Engl. J. Med., February 17, 2000; 342(7): 476 - 482.
[Full Text] [PDF]

Home page
 StrokeHome page
H. Bot, E.F. Bruggemans, B.J. Delemarre, G.L. van Rijk-Zwikker, A. van der Kleij, M. Kaps, J. Hansen, M. Weiher, K. Tiffert, and D. Droste
Microembolic Signals Under Increased Ambient Pressure • Response
Stroke, May 1, 1998; 29(5): 1069 - 1070.
[Full Text]

Home page
 PerfusionHome page
X. M Mueller, H. T Tevaearai, K. van Ness, J. Horisberger, M. Augstburger, M. Burki, and L. K von Segesser
Air trapping ability of the Spiral GoldTM membrane oxygenator: an ex vivo study
Perfusion, January 1, 1998; 13(1): 53 - 57.
[Abstract] [PDF]

Home page
 PerfusionHome page
P. D Beckley, P. D Shinko, and J. P Sites
A comparison of gaseous emboli release in five membrane oxygenators
Perfusion, March 1, 1997; 12(2): 133 - 141.
[Abstract] [PDF]

Home page
 PerfusionHome page
F. Dexter, B. J Hindman, and J. S Marshall
Estimate of the maximum absorption rate of microscopic arterial air emboli after entry into the arterial circulation during cardiac surgery
Perfusion, November 1, 1996; 11(6): 445 - 450.
[Abstract] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
Eduardo A. Tovar
Carlos Del Campo
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Tovar, E. A.
Right arrow Articles by Weinstein, P. B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Tovar, E. A.
Right arrow Articles by Weinstein, P. B.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS