Pulmonary Air Embolism Research Articles

Hydrodynamic features of pulmonary air embolism: a model study.

To elucidate the hydrodynamic events during pulmonary air embolism, experiments were conducted in a branching-tube apparatus and in small vessels. It was found that, as long as there existed an elevation differential between the two branches of a bifurcation, the vast majority of air bubbles always entered the higher branch. This finding is explained in terms of buoyancy, shear forces, and liquid flow velocity and is consistent with the in vivo finding of increased blood perfusion in the dependent lung regions during air embolization (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 51: 211-217, 1981). The pressures required to drive air bubbles through various small vessels were determined using three aqueous solutions of different surface tensions. Based on these measurements and a theoretical analysis, the diameter of air bubbles that could not pass through the pulmonary vessels was calculated to be 20-30 micrometers, agreeing well with a recent in vivo measurement (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 47: 537-543, 1979).

Redistribution of pulmonary blood flow during experimental air embolism

The effect of experimental pulmonary air embolism on pulmonary perfusion was studied in 14 closed-chest, anesthetized, paralyzed dogs. During constant-rate air infusion through a femoral vein, regional distribution of lung perfusion was measured with radioactive xenon boluses injected via a catheter positioned distally to the pulmonary valve. The results obtained from nine prone dogs indicate a large shift of blood perfusion toward the dependent areas of the lung during air embolism; the results obtained in five supine dogs were similar but statistically less significant. Concomitant with the perfusion shift, pulmonary arterial pressure increased, more acutely during the first 30 min. Switching from air to N2O-O2 ventilation accentuated the perfusion shift, which may be reverted towards control values by intravenous administration of 0.4 mg of isoproterenol. Other alterations observed included moderate increase of pulmonary resistance and decrease of cardiac output. It is concluded, based on these results and an adjunct model study, that the observed changes were predominantly due to aggregation of air bubbles in the upper part of the pulmonary vasculature.

Response of pulmonary veins to increased intracranial pressure and pulmonary air embolization.

Brain compression with subdural air causes pulmonary hypertension and noncardiogenic pulmonary edema (A. B. Malik, J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 42: 335-343, 1977). To see whether air emboli to the lungs rather than brain compression caused these findings, anesthetized dogs received intravenous air infusions, subdural air infusions, or brain compression from balloons inflated in the subdural space. Subdural air and intravenous air resulted in similar vascular responses. Pulmonary artery pressure (Ppa) increased 160% (P less than 0.01) and pulmonary venous pressure transiently rose 13 +/- 5 Torr (P less than 0.05) without an increase in left atrial pressure or cardiac output (Q). The end-tidal PCO2 fell 55% (P less than 0.01) and the postmortem weight of the lungs increased 55% (P less than 0.05). Brain compression with a subdural balloon instead of air only caused a 20% rise in Ppa and Q without pulmonary edema. Thus, pulmonary air emboli rather than brain compression accounts for the edema and pulmonary hypertension caused by subdural air. Catheters in pulmonary veins and the left atrium showed that air emboli cause transient pulmonary venous hypertension as well as a reproducible form of noncardiogenic pulmonary endema.

AN AUDIBLE ALARM FOR MONITORING AIR EMBOLISM DURING NEUROSURGERY

✓ The sensitivity of various monitors during experimental pulmonary air embolization was measured in five dogs. Changes in vital signs, electrocardiogram, Doppler sound, and end tidal CO2 were observed. An audible alarm was incorporated in the end tidal CO2 monitor. The results showed that a 0.01 cc to 0.02 cc/kg dose of air triggered the Doppler consistently, but the changes in heart sounds were heard only transiently. The fall in end tidal CO2 occurred at 0.5 to 1.0 cc/kg of intravenously injected air and was confirmed by pen write-out. The audible alarm device was constructed to sound after four consecutive breaths with preset percentage fall in end tidal CO2. The changes in vital signs occurred at doses of 4 to 8 cc/kg of air and death occurred at 8 to 10 cc/kg. The sound alarm was used in 30 patients during sitting craniotomies. Eight patients developed air emboli initially detected by transient change in Doppler sound. The alarm called attention to the fall in end tidal CO2 and confirmed the occurre...

Effects of pulmonary gas embolism on circulation and respiration in the dog. V. Effect of changing breathing gas composition on pulmonary gas embolization.

It was found in previous investigations that during venous gas infusion at low rates (1--5 ml/min-1) circulatory and respiratory variables reached a constant level after about 10--15 min. The present study demonstrates that this steady state can be disturbed by changing the composition of the breathing gas mixture. Alteration from air to 21% O2 in helium rapidly increased the embolic effects up to a maximum within 1.5--2 min; in the next 5--8 min the circulatory and respiratory variables returned to their previous levels during air breathing. Reverse effects occurred when changing from 21% O2 in helium to air. Similar phenomena were seen after switching from air to pure oxygen and from 21% O2 helium to pure oxygen. However, the extent of the circulatory and respiratory changes differed depending on the composition of the respective alternating breathing gas mixtures and on the initial embolic level as determined by infusion rate and kind of infusion gas. Gas movements between intravascular bubbles and alveolar space might be responsible for these changes.

Effects of pulmonary gas emoblism on circulation and respiration in the dog. VI. Influence of body position on the effects of pulmonary gas embolism.

In the present study the influence of body position on the effects of venous gas infusion was examined. The body position of anesthetized dogs ventilated artifically varied between supine, right-side-down and left-side-down position. Without venous gas infusion the change of body position hardly affected pulmonary arterial pressure (Pap) and alveolar CO2 fractional concentration (FACO2). However, during venous gas infusion a change of body position immediately elicited a rapid increase Pap and a decrease in FACO2 completed within a few seconds. Thereafter both variables gradually returned to their initial levels as before the change of body position. The extent of change in Pap and FACO2 due to alteration of body position depended on the initial embolic level (determined by the rate of infusion and the nature of the gas used) and on the change of body position.

An audible alarm for monitoring air embolism during neurosurgery.

The sensitivity of various monitors during experimental pulmonary air embolization was measured in five dogs. Changes in vital signs, electrocardiogram, Doppler sound, and end tidal CO2 were observed. An audible alarm was incorporated in the end tidal CO2 monitor. The results showed that a 0.01 cc to 0.02cc/kg dose of air triggered the Doppler consistently, but the changes in heart sounds were heard only transiently. The fall in end tical CO2 occurred at 0.5 to 1.0 cc/kg of intravenously injected air and was confirmed by pen write-out. The audible alarm device was constructed to sound after four consecutive breaths with preset percentage fall in end tidal CO2. The changes in vital signs occurred at doses of 4 to 8 cc/kg of air and death occurred at 8 to 10 cc/kg. The sound alarms was used in 30 patients during sitting craniotomies. Eight patients developed air emboli initially detected by transient change in Doppler sound. The alarm called attention to the fall in end tidal CO2 and confirmed the occurence of air emboli.

Effects of pulmonary gas embolism on circulation and respiration in the dog. II. Effects on respiration.

In mongrel dogs weighing 15--25 kg and anesthetized with thiopental-gamma-hydroxybutyric acid the effects of venous gas infusion and injection on several respiratory variables were investigated. During spontaneous respiration pulmonary gas embolism caused an increase of the ventilatory minute volume depending on the degree of embolization. The contribution of breathing frequency and tidal volume to the increase of ventilatory minute volume varied from one animal to the other. During constant artificial ventilation pulmonary gas embolism impaired the pulmonary gas exchange depending on the degree of embolization. How far a steady-state phase in gas exchange can be reached during continuous venous gas infusion depended on the adaptation of the circulation. At severe degrees of embolization circulation as well as gas exchange became deficient. Increasing artificial ventilation during pulmonary gas embolism improved the wash-out of carbon dioxide, but hardly affected the uptake of oxygen. The most important origin of the disturbed gas exchange in pulmonary gas embolism seemed to be an increased inequality of the ventilation-perfusion ratio distribution.

Effects of pulmonary gas embolism on circulation and respiration in the dog. I. Effects on circulation.

Mongrel dogs weighing 15-25 kg and anesthetized with thiopental-gamma-hydroxybutyric acid were used to investigate the effects of pulmonary gas embolism on pulmonary arterial pressure (Pap), systemic arterial pressure (Pa) and cardiac output (Q). Pulmonary gas embolism was produced either by venous injecton or by venous infusion. The most marked effect of pulmonary gas embolism on circulation was an increase in Pap which returned to the original level after stopping the gas administration. 1. After gas injection Pap rose to a maximum within 30--60 s. The extent of this rise in Pap showed a positive correlation with the volume of the injected gas. The kind of gas (oxygen, helium, neon, nitrogen, air), however, did not influence the extent of the rise in Pap, but did influence the time of return of Pap to the original level. Carbon dioxide showed an exceptional behavior in that it had almost no effect on Pap at all. P a hardly changed with the volume of the gas injections (20--60 ml injected within 1 s); Q was not measured after gas injection (the direct Fick method is not usable in this situation). 2. Gas infusion caused a slow rise of Pap, its steepness and extent depending on the rate of infusion and on the physical properties of the infused gas. When the right ventricle was able to maintain its output, a constant level of Pap was reached after 10--15 min. In this circulatory steady state Pap appeared to be a measure of the degree of embolization. However, this relationship no longer held when the right ventricle failed as evidenced by a fall in Pap, Pa and Q. It may be concluded that pulmonary gas embolism produces a transient partial obstruction in the pulmonary circulation and that the performance of the right ventricle determines the maximum degree of embolization compatible with a sufficient circulation.

Effects of pulmonary gas embolism on circulation and respiration in the dog. III. Excretion of venous gas bubbles by the lung.

Intravenous injection of gas (10-60 ml) causes acute pulmonary embolism, which disappears completely within 10-20 min. Intravenous infusion of gas (1-5 ml min-1) can be continued for a long time. During these infusions a steady state is reached in which pulmonary arterial pressure is increased and cardiac output remains unaltered. This indicates that the degree of embolization has reached a constant level despite the continuous gas infusion. These findings can be explained by a gradual disappearance of the bubbles from the pulmonary circulation. The purpose of this study was to measure the possible excretion of gas from the intravascular gas bubbles into the alveolar air after venous administration. Neon was used as a test gas since its fractional concentration in ambient air is low (0.00018) and it can be detected by gas chromatography with sufficient accuracy. It could be demonstrated that after injection neon was present in the expiration gas. During the steady state of infusion the rate of excretion in the expiration gas appeared to be equal to the rate of infusion. Changes in the pulmonary arterial pressure curve were reflected in the neon wash-out curve. It may be concluded that during pulmonary gas embolism the administered gas is excreted into the alveolar air and that the excretion rate largely depends on the increased pulmonary arterial pressure due to the obstructing bubbles themselves.

Effects of pulmonary gas embolism on circulation and respiration in the dog. IV. Origin of arterial hypoxemia during pulmonary gas embolism.

Effects of pulmonary gas embolism on circulation and respiration in the dog. IV. Origin of arterial hypoxemia during pulmonary gas embolism.

Intraoperative pulmonary air embolism. Follow-up of eight documented cases

Intraoperative pulmonary air embolism. Follow-up of eight documented cases

Lung mechanics and respiratory gas exchange during pulmonary air embolization in the dog.

Lung mechanics and blood gases were studied in 7 open-chest dogs and one whose chest was intact. Balloon occlusion of one pulmonary artery induced inconsistent changes except for a 3–13% decrease in compliance. After air embolization, on the other hand, pulmonary compliance fell on an average 30%, pulmonary airflow resistance increased 19%, arterial oxygen pressure decreased markedly, and mean pulmonary arterial pressure doubled. The fall in compliance and the rise in PA pressure were not significantly correlated. Compliance and arterial oxygen values were restored, at least temporarily, by hyperinflation of the lungs. It is concluded that the changes in pulmonary ventilatory mechanics and arterial blood gases acutely after embolization are probably caused by constriction in peripheral bronchioles.

Pulmonary venous air embolism in hyaline membrane disease.

Two cases of pulmonary venous air embolism (PVAE) as a complication of mechanical ventilation during the course of hyaline membrane disease are presented. PVAE in these cases, as well as in those previously reported was associated with pulmonary interstitial emphysema (PIE). The pathophysiology of PIE and of pVAE is discussed. Radiographic recognition of PVAE depends upon visualizing gas within the vascular system and especially within hepatic veins. The value of postmortem radiographs in the detection of this entity is emphasized.

Acute changes in lung mechanics following pulmonary emboli of various gases in dogs.

ArticleAcute changes in lung mechanics following pulmonary emboli of various gases in dogs.M A Khan, I Alkalay, S Suetsugu, and M SteinM A Khan, I Alkalay, S Suetsugu, and M SteinPublished Online:01 Dec 1972https://doi.org/10.1152/jappl.1972.33.6.774MoreSectionsPDF (958 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByFatal systemic (paradoxical) air embolism diagnosed by postmortem funduscopy15 June 2021 | Journal of Forensic Sciences, Vol. 66, No. 5Carbon Dioxide Embolism during Laparoscopic SurgeryYonsei Medical Journal, Vol. 53, No. 3Physiologic Changes Occurring During Laparoscopy, Including Port Site ImplantationMonitoring and Management of Physiological Changes Caused by PneumoperitoneumAlternative Gases in Laparoscopic SurgeryLaparoscopic surgery and its potential for medical complicationsHeart & Lung, Vol. 26, No. 1Cardiopulmonary Physiology and Pathophysiology as a Consequence Of Laparoscopic SurgeryChest, Vol. 110, No. 3Gas Embolism: Part I. Venous Gas Emboli1 July 1996 | Journal of Intensive Care Medicine, Vol. 11, No. 4Complications of therapeutic laparoscopyCurrent Problems in Surgery, Vol. 31, No. 11Fatal Carbon Dioxide Embolism Complicating Attempted Laparoscopic Cholecystectomy—Case Report and Literature ReviewJournal of Forensic Sciences, Vol. 39, No. 6Gas Embolism: Helium Is More Lethal Than Carbon DioxideJournal of Laparoendoscopic Surgery, Vol. 4, No. 3AIR EMBOLISMAnesthesiology Clinics of North America, Vol. 11, No. 1Air EmbolismAnesthesia for Posterior Fossa SurgeryLethal air embolism during placement of a kimray-greenfield filterJournal of Cardiothoracic Anesthesia, Vol. 4, No. 5Capnography in the Intensive Care Unit30 June 2016 | Journal of Intensive Care Medicine, Vol. 5, No. 5Circulatory collapse during laparoscopyJournal of Clinical Anesthesia, Vol. 2, No. 2Air embolism during craniotomy in the seated position: a comparison of methods for detectionCanadian Anaesthetists’ Society Journal, Vol. 32, No. 2Venous air embolism. Life-threatening complication of orogenital sex during pregnancyThe American Journal of Medicine, Vol. 78, No. 2Capnography in the early diagnosis of carbon dioxide embolism during laparoscopyCanadian Anaesthetists’ Society Journal, Vol. 31, No. 4Effects of Venous Air Embolism on the Cardiovascular System and Acid Base Balance in the Presence and Absence of Nitrous OxideActa Anaesthesiologica Scandinavica, Vol. 28, No. 2Erkennung und Verhütung von Luftembolien während neurochirurgischer Eingriffe in sitzender PositionLuftembolie bei neurochirurgischen Eingriffen in sitzender PositionEffect of ventilation with different gas mixtures on experimental lung air embolismRespiration Physiology, Vol. 34, No. 3Pulmonary Vascular Changes Following Air Embolism in the Dog26 September 2008 | Archives Internationales de Physiologie et de Biochimie, Vol. 86, No. 2Effects of pulmonary gas embolism on circulation and respiration in the dogPfl�gers Archiv European Journal of Physiology, Vol. 368, No. 1-2Venous air embolism during neurosurgery A comparison of various methods of detection in manAnaesthesia, Vol. 31, No. 5Pulmonary Responses to Intravascular Platelet Aggregation in the CatActa Physiologica Scandinavica, Vol. 92, No. 4ACUTE DECOMPRESSION SICKNESSThe Lancet, Vol. 304, No. 7890Changes in Pulmonary Vascular Volumes after Induced Intravascular Aggregation of Blood PlateletsActa Physiologica Scandinavica, Vol. 92, No. 1Gas Embolism More from this issue > Volume 33Issue 6December 1972Pages 774-7 https://doi.org/10.1152/jappl.1972.33.6.774PubMed4643856History Published online 1 December 1972 Published in print 1 December 1972 Metrics

Hemodynamic effects of pulmonary air embolism

A large bolus of air was injected into the right atrium of sheep. The cardiac output, right ventricular pressure, and arterial PO 2 were studied. It was found that the cardiac output was quickly regained, in less than 10 minutes, despite relatively anoxic levels of arterial oxygen saturation. The cardiac output temporarily exceeded the preinjection level before settling back to this level. The right ventricular pressure rose, corresponding to the regained cardiac output, and then settled to its original levels. The arterial PO 2 fell precipitously and slowly started to rise over the period of study. Bubbles were seen in the coronary arteries during these experiments. A bubble trap was placed across the arch of the aorta which demonstrated that there was no major transpulmonary passage of air.

Recent Advances in Monitoring Pulmonary Air Embolism

Recent Advances in Monitoring Pulmonary Air Embolism

Cardiopulmonary effects of intravenous gas embolism; with special reference to fate of intravascular gas bubbles.

To determine the graded cardiopulmonary effects and fate of pulmonary gas embolism, 11 sheep (with chronically implanted Doppler ultrasonic flow probes on pulmonary and brachiocephalic arteries) were subjected to experimental intravenous injection of nitrogen, oxygen and carbon dioxide. Three different rates of injection of each gas (0.03, 0.09 and 0.15ml/kg/min) were used for 30 minutes. Doppler ultrasonic flow probes were found to be very sensitive to the injected intravascular gas and produced characteristic chirps. The electromagnetic blood flowmeter was insensitive to the passage of these gases. Cardiopulmonary responses include elevation of pulmonary arterial pressure, diminished cardiac output and arterial hypoxemia. Nitrogen produced the greatest response and carbon dioxide the least, correlating with differences in solubility and diffusion rates. These responses developed with a one-half time of 15-20 minutes, with recovery, following cessation of injection, at the same rate. No statistically significant changes occurred in heart rate, systemic arterial pressure, pH or Pco2. Passage of intravenous gas through the pulmonary vasculature to the systemic circulation occurred only at the 0.15ml/kg/min dosage hate. The opening of the intrapulmonary arteriovenous shunts was primarily responsible for the decrease in arterial oxygen tension and passage of gas through the lung.

Unusual heart sounds associated with venous air embolism. Case report.

T HE millwheel murmur heard in pulmonary air embolism is due to the turbulent flow of blood mixed with air in the beating right ventricle. 1,4,'~ It has been induced experimentally with the intravenous injection of small amounts of air, 3 and it has been found that the nature of heart sounds changes as the quantity of air injected increases. 7 Shivpuri and coworkers 6 have shown experimentally that characteristic heart sounds precede the onset of the millwheel murmur. When air was introduced continuously by way of the femoral vein at the rate of 0.5 cc per sec in dogs in the supine position, after 10 to 15 sec the heart sounds became metallic and resonant in character and the heart rate increased. After 20 to 25 sec, with continued injection at 0.5 cc per sec, the sounds became drum-like. This characteristic metallic sound has been called the drum sign and has been considered pathognomonic of venous air embolism. The sound soon became rhythmic and louder, resembling the galloping of a horse on a wooden bridge. At 30 to 40 sec a systolic churning murmur, the millwheel murmur, first appeared. It completely replaced the precordial heart sounds at 50 to 60 sec. Thus, the drum sign may occur prior to the millwheel murmur. On the other hand, Durant, et al., in their experiments 1,2 found that the millwheel murmur was heard immediately after injection of air, coincident with air reaching the right side of the heart as demostrated by angiocardiographic studies. This sound followed the injection of air into the femoral vein of dogs in both the supine and the left lateral position as a bolus of 5.0 to 7.5 cc of air per kilogram of body weight, considerably more than the initial amounts injected in the experiments eliciting the drum sign. The following case presented characteristic features of the drum sign observed in animals, and may help to correlate the work of Shivpuri and Durant.

PULMONARY AIR EMBOLIZATION IN THE DOG: POSTMORTEM FINDINGS

The effect of acute pulmonary air embolization on lung morphology was investigated in twenty‐eight dogs. In sixteen animals, no lesions were observed. In twelve dogs, a slight oedema formation was found on histological examination only. No relation to the pulmonary arterial pressure increase was detected. Arterial hypoxaemia had appeared in oedematous as well as non‐oedematous dogs. Thus, pulmonary oedema did not seem to depend on pulmonary arterial pressure rise or to contribute to the arterial hypoxaemia after lung embolization with air.