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At least 19 recordsLinked to original sources
PubMed1994

[Sound frequency analysis for identification of venous air embolism].

Air emboli occurring during surgery are considered to be life-threatening incidents. With the aim of achieving acoustic identification of venous air emboli, a frequency analysis of the sounds induced by an air embolism (millwheel murmurs) as well as of all other unusual sounds, was undertaken during 20 operations, and in experiments with animals. The frequency spectra of the sounds induced by air emboli are characterised by an increase in the amplitudes in the frequency range 1,100 to 3,000 Hz, while the amplitudes of normal heart sounds continuously decrease with increasing frequency. The frequency spectrum was examined for characteristics using an electronic filter system. The sounds induced by air emboli can be clearly distinguished from normal heart sounds. During operations on patients, suction sounds occur, the frequency patterns of which are not easy to distinguish from those of embolus-induced sounds, although an acoustic distinction can be made via a stethoscope or a loudspeaker. With optimal adjustment of the filter system, 73 out of 81 (90%) embolism-related sounds were correctly identified in animal experiments. On no occasion were normal heart sounds wrongly identified as due to an embolus. However, an embolus sound was frequently mimicked by interfering sounds such as those produced by artificial respiration, and other ambiend sounds. By modifying the oesophageal catheter to achieve optimal suppression of interfering sounds, this filter system could be developed into an alarm.

Animals↗
PubMed1992

[Air embolism].

Air embolism is a dramatic event which threatens the patient's life during invasive therapeutic and diagnostic procedures. Immediately after establishment of the diagnosis treatment in a hyperbaric chamber should be started. The prognosis depends to a certain extent on how quickly the patient is transferred into a hyperbaric chamber. Treatment with hyperbaric oxygen is based on fundamental physical and physiological principles of the action of compressed air and the supply of a large amount of oxygen in a dissolved form into the ischaemic tissue beyond the obstruction. Installation of hyperbaric chambers in hospitals would make successful and prompt treatment of all cases of embolism possible, as well as of some other diseases indicated for hyperbaric oxygen therapy.

Embolism, Air↗
PubMed2005

[Ischemic brain infarction after an air embolism. Case report].

Ischemic stroke due to embolic air is uncommon. There are few reports of patients with air embolic stroke as a complication of endoscopic procedures. The temporal relationship between the stroke and this procedure is the most important clue for the diagnosis. CT scan and MRI of the brain are confirmatory tests. The morbidity and mortality is high. Patients should be hospitalized in a critical care service and treated as soon as possible with oxygen in a pressure camera. We report a 52 years old woman with an ovarian cancer that, during an upper gastrointestinal endoscopy, had a severe alteration of consciousness that did not respond to the use of Flumazenil. A CT scan showed multiple areas of air embolism in the watershed area between anterior and middle right cerebral arteries. A conservative treatment was decided and the patients died 48 hours later.

Anterior Cerebral Artery↗
PubMed1999

[Venous paradoxical air embolism].

Paradoxical air embolism may occur with any venous air embolism. Air may either enter the systemic circulation through a patent foramen ovale or through transpulmonary passage of air. While small venous air emboli are mostly well tolerated, even the smallest paradoxical air emboli can have fatal consequences in the systemic circulation. Therapy and prophylaxis of paradoxical air embolism equal those of venous air embolism. This is especially true, since paradoxical air embolism may not become obvious under general anesthesia. More specific therapeutic regiments, such as hyperbaric oxygenation and the infusion of perfluorocarbons, are still in an experimental stage.

Embolism, Air↗
PubMed1997

Activation of complement and neutrophils increases vascular permeability during air embolism.

Pulmonary air embolism occurs in diving and aviation during acute pressure reductions and in clinical complications. Undoubtedly physical obstructions play a role, but bubbles in blood can produce a number of indirect effects leading to tissue injury. In the present study, we investigated the involvement of the complement system and polymorphonuclear leukocytes (PMN) in altering segmental vascular resistance, lung weight gain, and filtration coefficient (Kf), by using isolated and perfused rat lungs. After establishing ventilation with air and 5% CO2, the lung was removed en bloc and suspended in a humidified chamber at 37 degrees C. Lung weight and arterial and venous pressures were monitored continuously. The buffered salt perfusate contains 4% Ficoll for osmotic balance. We used four series of perfusates containing 20% of: a) normal plasma; b) decomplemented plasma (from donor rats pretreated with a cobra venom factor); c) normal plasma and PMN at 2 x 10(6).ml-1; and d) decomplemented plasma and PMN at 2 x 10(6).ml-1. Pulmonary air embolism, air bubbles introduced through the pulmonary artery, increased pulmonary arterial resistance and pulmonary arterial blood pressure. The lung weight and lung water content were greater than those in the control groups. Air embolism increased vascular permeability, which was shown by an elevated Kf after air infusion. After air embolism, Kf was 0.63 +/- 0.05 g.min-1.cm H2O-1.100 g-1 in lungs perfused with both PMN and plasma, which was significantly greater than those in lungs perfused with either plasma (0.49 +/- 0.04), decomplemented plasma (0.44 +/- 0.03), or PMN and decomplemented plasma (0.47 +/- 0.03). These results demonstrated that air embolism increases vascular permeability of the lung by pulmonary hypertension, activation of the complement, and activation of PMN.

Animals↗
PubMed1997

Pharmacologic modulation of pulmonary vascular permeability during air embolism.

Pulmonary air embolism induces the generation of vasoactive and cytotoxic substances leading to lung injury. In the present study we investigated, in isolated and perfused rat lungs, the involvement of arachidonic acid metabolites in the alterations of vascular pressure, lung water content, and the filtration coefficient (Kf). We also tested the effects of a beta-agonist, a calcium channel blocker, and a cyclo-oxygenase inhibitor on the hemodynamic and the permeability changes following pulmonary air embolism. The artificially ventilated rat lungs were removed en bloc and suspended in a humidified chamber at 37 degrees C. The salt and buffered perfusate contained 4% Ficoll as albumin substitute for osmotic balance. We introduced air bubbles through the pulmonary artery. Air embolism increased pulmonary arterial resistance and caused pulmonary hypertension. Lungs receiving air infusion contained 88.6 +/- 0.6% water, which was significantly greater than the lung water content in the control groups (81.9 +/- 0.4%). Air embolism increased Kf by 145 +/- 19% from the baseline value. Pretreatment with indomethacin, isoproterenol, or nifedipine significantly reduced post-air-embolism lung water content to 85.8 +/- 0.5%, 84.1 +/- 0.4%, and 86.5 +/- 04%, respectively, and reduced the Kf increase to 17 +/- 8%, 1 +/- 9%, and 72 +/- 8%, respectively. These interventions did not alter the hemodynamic responses, except for the isoproterenol infusion, which shortened the half-time (T1/2) for pressure recovery after ending air infusion compared to the group with air embolism alone. Our results showed that indomethacin prevented vascular permeability increase and reduced pulmonary edema, suggesting that the cyclo-oxygenase products partially mediate the lung injury following air embolism. Furthermore, isoproterenol and nifedipine prevented or reduced the permeability increase, suggesting that alterations of the intracellular cAMP and cytosolic Ca2+ level play an important role in the pathophysiology of pulmonary air embolism.

Animals↗
PubMed2001

Arterial air embolism after venous air infusion in newborn piglets.

UNLABELLED: In the newborn period, decreased right atrial pressure results in functional closure of the foramen ovale (FO). The objective of this study was to investigate whether air bubbles infused in the vena cava will pass through the FO into the arterial circulation in a newborn animal. Since air tends to rise to the highest point in a fluid, the study also investigated whether the animal's position could influence arterialization of air. Twelve 1-3-d-old piglets were anaesthetized and mechanically ventilated, and had catheters placed in the vena cava for infusion of air, in the aorta for blood gas and blood pressure measurements, and in the pulmonary artery for pressure measurements. After stabilization, 0.05 ml kg(-1) per minute of air was infused for 25 min followed by a 3 h observation period. Six piglets were placed in the left, and six in the right lateral recumbent position. Air bubbles in the left atrium or ventricle was monitored by echocardiography. Ultrasound Doppler probes were placed on both carotid arteries for detection of air embolism. Gas bubbles were detected in the left ventricle within 45 s of air infusion in 11 of 12 piglets. Eight piglets had air bubbles in the carotid arteries. Mean pulmonary arterial pressure (PAP) increased significantly after 1 min of air infusion, whereas mean systemic arterial pressure remained unchanged. When arterial air embolism occurred, PAP had not increased significantly. The time to reach maximum PAP with the animals in the left recumbent position was significantly shorter than in the right. CONCLUSION: This study shows that venous gas bubbles enter the arterial circulation through the FO in newborn piglets and that body position may influence the haemodynamic effect of these bubbles.

Air↗
PubMed1997

Retrograde cardioplegia preserves myocardial function after induced coronary air embolism.

Coronary air embolism is a potential complication of cardiopulmonary bypass. We compared left ventricular function before and after the administration of antegrade or retrograde cardioplegic solution in a porcine model of coronary air embolism. Nineteen pigs were placed on cardiopulmonary bypass support and cooled to 32 degrees C. The heart was initially arrested with antegrade cold blood cardioplegic solution. The aortic crossclamp was released at 30 minutes and 0.02 cc/kg body weight of air was injected into the left anterior descending artery distal to the first diagonal branch. After 5 minutes the aorta was reclamped and the animals treated with 15 ml/kg body weight of 1:4 blood cardioplegic solution delivered by the antegrade (n = 6) or retrograde (n = 7) method. Control animals (n = 6) were not treated. Changes in regional preload recruitable stroke work were used to assess left ventricular performance before and after cardiopulmonary bypass. Two control animals could not be weaned from cardiopulmonary bypass. Left ventricular function was best preserved after treatment of induced coronary air embolism with retrograde cardioplegia (90% of baseline). Coronary air embolism treatment with antegrade cardioplegia resulted in diminished left ventricular performance (68% of baseline). In control animals left ventricular contractility was significantly impaired (39% of baseline). We conclude that administration of retrograde cardioplegic solution may be an effective method of treating coronary air embolism. The favorable outcome seen with cardioplegia may be in part because of its ability to protect the ischemic myocardium while the solution mechanically dislodges air from the vascular bed.

Animals↗
PubMed2007

Diagnosis and treatment of vascular air embolism.

Vascular air embolism is a potentially life-threatening event that is now encountered routinely in the operating room and other patient care areas. The circumstances under which physicians and nurses may encounter air embolism are no longer limited to neurosurgical procedures conducted in the "sitting position" and occur in such diverse areas as the interventional radiology suite or laparoscopic surgical center. Advances in monitoring devices coupled with an understanding of the pathophysiology of vascular air embolism will enable the physician to successfully manage these potentially challenging clinical scenarios. A comprehensive review of the etiology and diagnosis of vascular air embolism, including approaches to prevention and management based on experimental and clinical data, is presented. This compendium of information will permit the healthcare professional to rapidly assess the relative risk of vascular air embolism and implement monitoring and treatment strategies appropriate for the planned invasive procedure.

Catheterization, Central Venous↗
PubMed2000

Pulmonary air embolism.

Pulmonary air embolism is a well-known consequence of surgery, trauma, diving, and aviation. This article reviews the physiological effects, means of detection and methods of prevention and treatment of pulmonary air embolism. The primary physiological effects are elevated pulmonary artery pressures, increased ventilation-perfusion inhomogeneity, and right ventricular failure. The degree of physiological impairment depends on the volume of gas entrained, the rate of entrainment, the type of gas entrained, and the position of the patient when the embolism occurs. Transesophageal echocardiography is the most sensitive method of detection, but it is invasive. Precordial Doppler ultrasound is almost as sensitive and poses no risk to the patient. End-tidal carbon dioxide monitoring is used on all patients and is a moderately sensitive method of detection, which is useful during surgeries that have a low incidence of air embolism. For high-risk procedures, precordial Doppler ultrasound and a multi-orifice right heart catheter should be used to detect and treat pulmonary air embolism. Prevention measures include volume expansion, careful positioning, positive end-expiratory pressure, military anti-shock trousers, and jugular venous compression. Treatment of pulmonary air embolism includes flooding the surgical site with saline, controlling sites of air entry, repositioning the patient with the surgical site below the right atrium, aspiration of air from a central venous catheter, cessation of inhaled nitrous oxide, and resuscitation with oxygen, intravenous fluids, and inotropic agents. Some hypotheses on the effects of air in the pulmonary vasculature and investigational treatment options are discussed.

Aerospace Medicine↗
PubMed2003

[Venous air embolism].

Venous air embolism is the entry of air into the venous system as a consequence of trauma or iatrogenic complications (especially central venous cannulation or pressurized intravenous infusion systems). It also can occur following the surgical procedures. Venous air embolism results in right ventricular dysfunction and pulmonary injury. In this review article various causes, frequency, pathophysiology, clinical features, diagnosis, treatment, outcome and prevention of venous air embolism are discussed.

Adult↗
PubMed1998

Proof of fatal air embolism.

Venous air embolism is a rare cause of death. Entry of gas into the circulation is caused by trauma, mostly surgical or therapeutic, and sometimes resulting from criminal intervention. The detection of air embolisms requires special precautions during autopsy. An aspirometer has to be used for the detection, measurement and storage of gas originating from the heart ventricles. The aspirometer has to be filled completely with distilled water containing two drops of Tween 80 to reduce the surface tension of the water and to prevent adherence of small air bubbles to the wall of the aspirometer. Subsequently the gas has to be analysed by gas chromatography. When the results correspond with the main criteria defined by Pierucci and Gherson [2] the diagnosis "air embolism" is justified. The technique for the detection of air embolism is simple but requires a careful procedure which is described in detail.

Autopsy↗