Air embolism may appear in either the right or the left side of the circulatory system.

Involvement of the
right side of the circulation is referred to asvenous orpulmonary air embolism. Generally, venous air is
well tolerated, but death can occur when the volume of air reaches 5 to 8 mL/kg. The rate at which air
moves into the circulation and the body's position are important determinants of the volume that can
be tolerated. If the body's position allows dispersion of air into the peripheral circulation, more air can
be tolerated, although the damage to peripheral structures and end-organs can be extensive. Rapid
death usually results from obstruction of the right ventricle or the pulmonary outflow tract. Injuries to
the vena cava or the right ventricle can also create portals of entry into the right circulatory system.

Air embolism involving the left side of the circulatory system is referred to asarterial orsystemic air
embolism. The lethal volume depends on the organs to which it is distributed. As little as 0.5 mL of air in
the left anterior descending coronary artery can lead to ventricular fibrillation. Two milliliters of air
injected into the cerebral circulation can be fatal. The formation of traumatic bronchovenous fistulas
creates potential entry points for air to move into the left side of the circulatory system. The only
requirement is the formation of an air-blood gradient conducive to the inward movement of air.
Although lowered intravascular pressure from hemorrhage is a risk factor, the most important element
in all reports of air embolism has been the use of positive pressure ventilation.46

In a review of 447 cases of major thoracic trauma, Yee and coworkers47 found adequate chart data to
suggest the diagnosis of air embolism in 61 patients. Approximately 25% of patients with air embolism
have blunt trauma, with associated lung injury secondary to multiple rib fractures or hilar disruption.
The overall mortality is higher than 50%.

The diagnosis of air embolism is easily overlooked because the signs and symptoms are similar to those
of hypovolemic shock. Two valuable signs that are present in 36% of patients are hemoptysis and the
occurrence of cardiac arrestafter intubation and ventilation. The development of focal neurologic
changes, seizures, or central nervous system dysfunction in the absence of head injury is also suggestive
of the diagnosis.48 Overall, the diagnosis is subtle and must be considered when there is no evidence of
the more common causes of extremis in a trauma patient.

Air Emboli

Lisa Wise-Faberowski, Christian Seefelder, in Complications in Anesthesia (Second Edition), 2007

Implications

Significant pulmonary air emboli can result in decreased cardiac output, arterial hypotension, and
cardiovascular collapse as a result of one or more of the following:
•

Obstruction of peripheral pulmonary vessels by gas bubbles

Air lock from gas in large pulmonary vessels or the heart

Reflex pulmonary vasoconstriction

Right ventricular failure secondary to pulmonary hypertension

Electromechanical dissociation or arrhythmias

Myocardial ischemia from reduced coronary perfusion pressure, coronary paradoxical air emboli, or
hypoxemia

Impaired pulmonary function with carbon dioxide retention and arterial oxygen desaturation can result
from the following:

Ventilation-perfusion mismatch from pulmonary vascular obstruction with increased dead-space

ventilation

Reactive bronchoconstriction with increased airway resistance

•
Interstitial pulmonary edema

Gas bubbles enter the arterial circulation directly or through intracardiac communications. Most
neonates have a patent foramen ovale, usually with left-to-right shunting. Although the foramen ovale
may be probe-patent in 25% to 50% of infants and in 20% to 30% of adults, rarely is shunting
demonstrated. However, increased right-sided pressures with venous air emboli may facilitate
paradoxical air emboli across a patent foramen ovale. Paradoxical air emboli can result in myocardial or
cerebral ischemia.

Anesthesia for Neurologic Surgery and Neurointerventions

Michael A. Gropper MD, PhD, in Miller's Anesthesia, 2020

Paradoxical Air Embolism

The possibility of the passage of air across the interatrial septum via a patent foramen ovale (PFO),
which is known to be present in approximately 25% of adults, is a concern.103 The risk is major cerebral
and coronary morbidity. However, the precise definition of the morbidity that can actually be attributed
to PAE is not clear. Although the minimal pressure required to open a probe PFO is not known with
certainty, the necessary gradient may be as much as 5 mm Hg. In a clinical investigation, Mammoto and
colleagues observed that PAE occurred only in the context of major air embolic events, suggesting that
significant increases in right heart pressures are an important predisposing factor of the occurrence of
PAE.104 Several clinical investigations have examined factors that influence the right atrial pressure
(RAP) to left atrial pressure (LAP) gradient. The use of positive end-expiratory pressure (PEEP) increases
the incidence of a positive RAP to pulmonary wedge pressure gradient105 and generous fluid
administration (e.g., 2800 mL/patient vs. 1220 mL/control patient106) reduces it. As a result, the use of
PEEP, which was once advocated as a means of preventing air entrainment, was abandoned.
Subsequently, the practice of more generous fluid administration for patients undergoing posterior
fossa procedures evolved. However, even when mean LAP exceeds mean RAP, PAE can still occur
because transient reversal of the interatrial pressure gradient can occur during each cardiac cycle.107

Some centers have advocated performing bubble studies preoperatively with echocardiography92 or
transcranial Doppler (TCD),108 or intraoperatively using TEE prior to positioning109 to identify patients
with a PFO with

Air embolism may occur on the right, left, or both sides of the cardiac system. Systemic air embolism is
more frequently encountered with the introduction of a transseptal catheter or in patients who have a
patent foramen ovale or other cardiac septal defects. Systemic air embolism commonly presents as
heart block or acute inferior ischemia, given the anterior location of the right coronary ostium.
Detection of air emboli may be possible with echocardiography, and arterial air emboli may be seen on
neurovascular imaging. Management is largely supportive because restoration of flow will help with the
resolution of the embolism. Increasing the fraction of inspired oxygen will also aid with resorption.

Clinical Care in Extreme Environments : High Pressure, Immersion, Drowning, Hypo- and Hyperthermia

Michael A. Gropper MD, PhD, in Miller's Anesthesia, 2020

Gas Embolism and Decompression Sickness

Introduction of gas into the arterial circulation (AGE) has traditionally been associated with scuba divers
and attributed to pulmonary barotrauma during ascent from a divewhile breathing compressed gas.
However, it may also occur iatrogenically in several clinical circumstances, such as during
cardiopulmonary bypass or as a result of inadvertent injection of air during a diagnostic arteriogram or
hemodialysis. Additionally, large amounts of gas may enter the venous system, for example during
neurosurgical procedures with the patient in the sitting position, accidental disconnection of
hemodialysis access equipment, major back surgery, total hip replacement, cesarean section,
laparoscopy, intrauterine laser surgery, arthroscopy (from air escaping from a faulty air-powered
instrument), and hydrogen peroxide irrigation or oral ingestion (due to elaboration of gaseous oxygen
from tissue and blood catalase). Venous gas embolism (VGE) can also occur when a central venous
catheter is opened to air. Severe VGE has also occurred during orogenital sex after blowing air
intravaginally.168 VGE has been reported in patients with ARDS who are being ventilated with positive
end-expiratory pressure (PEEP).169 VGE in sufficient quantity may overwhelm the ability of the
pulmonary vasculature to filter the gas, allowing bubbles to pass into the arterial circulation. Even small
amounts of venous gas (e.g., VGE caused by decompression from diving) have recently been implicated
in neurologic syndromes in scuba divers because of transatrial passage through a patent foramen
ovale.170,171

The effects of gas embolism can be partly due to vessel obstruction by bubbles, but bubble-endothelial
interaction causes increased capillary permeability and extravasation of fluid,172-174 resulting in
hemoconcentration. Impaired endothelial function also occurs.175 Another effect has been
demonstrated in a model of AGE in anesthetized rabbits176,177: small doses of intracarotid air may pass
through the cerebral microcirculation yet produce vasoplegia, delayed reduction of cerebral blood flow,
and neurophysiologic impairment. This reduction in blood flow is abolished when there is neutropenia;
thus it has been concluded that leukocytes are a major component of the pathophysiology.178 This
phenomenon of delayed reduction of cerebral blood flow may be responsible for the clinical observation
of initial neurologic improvement after AGE, followed by delayed deterioration.179

A related syndrome that results from pathologic effects of tissue and blood gas bubbles is DCS, seen in
aviators and compressed gas divers. The gas bubbles in these situations occur because of a decrease in
ambient pressure at a rate sufficient to induce local inert gas supersaturation, resulting in formation of
bubblesin situ from tissue stores. Manifestations of AGE classically consist of impaired consciousness,
hemiparesis, or seizures, but may be of a less severe nature. DCS most commonly presents as any
combination of joint pain, paresthesias, motor weakness, bladder or bowel sphincter dysfunction,
vertigo, tinnitus, and hearing loss.180,181

ANESTHETIC MANAGEMENT FOR POSTERIOR FOSSA SURGERY

David S. Smith, in Cottrell and Young's Neuroanesthesia (Fifth Edition), 2010

Use of Positive End-Expiratory Pressure

VAE and positive end-expiratory pressure (PEEP) may both increase right atrial pressure, and PEEP may
raise cerebral venous pressure. PEEP has been proposed as a prophylactic measure against VAE.69
However, it may impair surgical conditions, decrease venous return, and increase the chance that right
atrial pressure will exceed left atrial pressure, thus predisposing an at-risk patient to PAE. Giebler and
colleagues70 found no reduction in the incidence of air embolism when they compared 10 cm PEEP with
no PEEP in a prospective randomized study of patients operated on in the sitting position; these
researchers suggested that the use of PEEP in sitting cases be abandoned. Jugular venous compression
has been demonstrated to be effective in reducing air entry.71,72

Air Embolism and Diving Injury

Robert A. van Hulst, ... Peter Radermacher, in Mechanical Ventilation, 2008

CONCLUSIONS

Air embolism, the entry of gas into the vascular structures, is a mainly iatrogenic clinical problem that
can result in serious morbidity and even death. In most cases, gas embolism is actually air embolism,
although the medical use of other gases such as carbon dioxide, nitrous oxide, nitrogen, and helium can
also result in embolism. Significant amounts of in vivo data demonstrate that cerebral damage is caused
by even small volumes of arterial gas. However, the exact relevance of these data for the clinical
situation has not yet been fully elucidated. Although data on the morbidity and mortality of air
embolism in humans are scarce, many case reports and retrospective studies on small numbers of
patients suffering from CAE have shown that HBO2 is the treatment of choice for this complication.

Cardiac Patients Requiring Emergent Noncardiac Surgery

Lev Deriy MD, ... Brian Starr MD, in Essentials of Cardiac Anesthesia for Noncardiac Surgery, 2019

Venous Air Embolism

Venous air embolism (VAE) can occur in any surgery in which a pressure gradient occurs favoring air
entrainment rather than bleeding, typically when the surgical site lies above the level of the heart. The
prevalence of VAE is highest in posterior fossa neurosurgical patients, but also can occur during spine
surgery, shoulder surgery involving beach chair positioning, or hip or femur surgery. The consequences
of VAE depend on the rate of air entry, with massive VAE causing an air lock in the right ventricle and
cardiovascular collapse. More commonly, VAE occurs more slowly, leading to increased pulmonary
vascular pressure, RV strain and failure, increased CVP, and systemic hypotension. Paradoxical air
embolus is the passing of air via an intracardiac defect, leading to coronary artery obstruction (ischemia)
or stroke. The diagnosis of VAE occurs best with TEE and precordial Doppler, but other modalities can
also be used (Fig. 16.8).

Treatment of patients with VAE involves halting the entry of venous air (flooding the field with saline,
bringing the surgical field below the level of the heart if possible, aspiration of air from the right atrium if
a CVC has been placed), and circulatory support (fluids, vasoactive medications). The cardiac patient
may tolerate a VAE poorly because of decreased cardiac reserve, potential lower ejection fraction, or
from valvulopathy (especially stenotic lesions). If the index of suspicion for VAE occurring is high in a
cardiac patient, then invasive arterial monitoring, central venous access (ideally with the tip in the right
atrium for potential VAE aspiration), and potentially TEE or precordial Doppler should be used. Surgeon
awareness of the concerns should be made with the formulation of treatment plans to occur at any
point in the operation.

Anesthesia for Plastic Surgery

Franklyn P. Cladis, ... Joseph Losee, in Smith's Anesthesia for Infants and Children (Eighth Edition), 2011

Venous Air Embolism

Venous air embolism (VAE) is a potential complication of craniofacial and neurosurgical procedures (see
Chapter 22, Anesthesia for Neurosurgery). VAE can present with hemodynamic instability and can result
in death. VAE occurs commonly in pediatric patients having cranial procedures. A prospective study
using precordial Doppler in infants and children having craniosynostosis repair detected VAE in 82% of
the patients; 31% percent developed hypotension secondary to VAE, but none developed cardiovascular
collapse (Faberowski et al., 2000). This is higher than the previously reported incidence of 66% (Harris et
al., 1987). Infants may be at increased risk for VAE, because significant hemorrhage during cranial vault
remodeling can result in low central venous pressures. In addition, the relatively large size of the infant
head may raise the surgical site above the level of the heart, thereby increasing the pressure gradient
for air entrainment. Some advocate the placement of central venous catheters to monitor the trend of
central venous pressures and minimize the risk for air embolism. However, no data suggest that central
venous pressure monitoring decreases the risk for VAE.
Management of VAE begins with preventing hypovolemic states by providing adequate volume
resuscitation and using a precordial Doppler for early detection of VAE. The precordial Doppler should
be placed over the left or right parasternal border between the third and sixth intercostal spaces
(Schubert et al., 2006). Lowering the head of the bed, left lateral positioning, flooding the surgical field
with saline, applying bone wax, discontinuing nitrous oxide, and providing inotropic support are all
measures that have been used to acutely manage VAE. Pediatric advanced life support with chest
compressions and epinephrine is required for patients who develop symptomatic low blood pressure,
bradycardia (heart rate < 60 bpm), or pulseless electrical activity.

Preoperative and Surgical Planning for Avoiding Complications

Mehmet Zileli, ... Edward C. Benzel, in Spine Surgery (Third Edition), 2005

Air Embolism

Air embolism is one of the most serious complications encountered. It is predominantly related to
operations performed above the level of the heart.28 Two precautions to avoid air embolism are
suggested: (1) if possible, avoid the sitting position, and (2) monitor the patient at risk meticulously with
Doppler ultrasound and end-tidal Pco2. In such patients a central venous catheter should be used so
that air can be emergently evacuated from the right atrium, if an air embolism is detected. The central
venous pressure should be maintained at greater than 10 cm, so that the pressure in epidural veins does
not decline. Do not use nitrous oxide when using the sitting position.

The incidence and clinical importance of air embolism is greater in the sitting position than in other
positions.1 Its incidence has been reported to be as high as 50%.28 If air embolism occurs, a central
venous catheter may be used to withdraw air from the left atrium. At the same time the surgeon should
flood the wound with Ringer's solution and inspect and control any open veins with bipolar coagulation.
Bleeding bone surfaces should be treated with wax, and the wound should be precisely packed with wet
gauze. If signs of air embolism persist, the position of the patient should quickly be changed to the right-
side-up position to aid the removal of air via the central venous catheter from the right atrium.

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