It is a blood vessel blockage caused by one or more bubbles of air or other gas in the circulatory system.
An air embolism is also known as an air embolism.
Air embolisms can also occur in the xylem of vascular plants, especially when they are under under water stress.
Air can enter the circulation during surgical procedures, over-expansion injury to the lungs, decompression, and other causes.
Divers can suffer from arterial gas emboli due to a lung over-expansion injury.
The breathable gas introduced into the venous system of the lungs due to pulmonary barotrauma will not be trapped in the alveolar capillaries and, therefore, will be circulated to the rest of the body through the systemic arteries, with a high risk of embolism.
Inert gas bubbles that arise from decompression generally form on the venous side of the systemic circulation, where fixed gas concentrations are highest; these bubbles get typically trapped in the lungs’ capillaries, which are generally eliminated without causing the symptom.
If they are diverted into the systemic circulation through a patent foramen ovale, they can travel and lodge in the brain where they can cause a stroke, the coronary capillaries where they can cause ischemia or other tissues where the consequences are often less critical.
First aid treatment involves:
- We are administering oxygen at the highest possible concentration.
- They are treating shock.
- It is transported to a hospital where therapeutic recompression and hyperbaric oxygen therapy are the definitive treatment.
The physiological effects of venous air embolism are similar to those of pulmonary embolism.
The accumulation of air in the left ventricle prevents diastolic filling. During systole, the air is pumped into the coronary arteries, interrupting coronary perfusion—air placement in the vasculature results in acute hypoxemia and hypercapnia.
Acute changes in correct ventricular pressure result in right ventricular stress, leading to right heart failure, decreased cardiac output, right ventricular ischemia, and arrhythmia.
This can be followed by a systemic circulatory collapse and even death.
The degree of physiologic impairment depends on the volume of air, the rate of air embolism, the type of gas (i.e., ambient air, carbon dioxide, or nitrous oxide), and the patient’s position when the embolism occurs.
Emboli not only cause a reduction in perfusion distal to the obstruction, but the damage also results from an inflammatory response that initiates the air bubble.
These inflammatory changes can lead to pulmonary edema, bronchospasm, and increased airway resistance.
The severity of symptoms resulting from air embolism varies depending on the amount of air instilled and the final location of the air bubble. Patients may be asymptomatic or have complete cardiovascular collapse.
Lethal volumes of air in an acute bolus have been described and are approximately 0.5 to 0.75 ml/kg in rabbits and 7.5 to 15.0 ml/kg in dogs.
The lethal dose for humans has been theorized to be 3-5 ml/kg, and it is estimated that 300-500 ml of gas introduced at a rate of 100 ml / s is a fatal dose for humans.
In addition, the accumulation rate and the patient’s position also contribute to the fatality. In addition, air infusion rates of more than 1.5 ml/kg/min are associated with bradycardia and cardiovascular decompensation.
The true incidence of any air vascular embolism is uncertain due to presumed occurrences during procedures with subclinical responses. Furthermore, it is difficult to document a cause of death due to air absorption before autopsy.
Numerous case reports in the literature describe air embolism from various causes. The occurrence is probably more familiar as a complication of central venous catheterization.
Multiple additional clinical settings have reported the occurrence of air embolism.
These include, but are not limited to, disconnected central venous catheters, air travel, endoscopic retrograde collapse pancreatography (ERCP), hemodialysis, trauma, laparoscopic insufflations, open heart surgery, lung biopsy, radiological procedures, childbirth, head, and neck surgery and diving.
Signs and symptoms
- Short of breath.
Symptoms of arterial gas embolism include:
- Loss of consciousness.
- Cessation of breathing.
- Loss of coordination
- Loss of control of bodily functions.
- Extreme fatigue
- Limb weakness.
- Areas of abnormal sensation.
- Visual abnormalities
- I hear abnormalities.
- Personality changes
- Cognitive impairment
- Nausea or vomiting
- Bloody sputum
Symptoms of other consequences of pulmonary overexpansion may also occur, such as pneumothorax and subcutaneous or mediastinal emphysema.
An air embolism can occur when your veins or arteries are exposed, and pressure allows air to travel to them. This can happen in several ways, such as:
Small amounts of air often accidentally enter the bloodstream during surgery and other medical procedures (for example, a bubble entering an IV fluid line), but most of these air emboli enter the veins and are they stop in the lungs and, therefore, in a vein.
Air embolism showing any symptoms is very rare.
Air embolism is a diving disorder suffered by underwater divers who breathe gases at ambient pressure, and it can occur in two different ways.
This is possible if you hold your breath for too long when underwater or come out of the water too quickly.
These actions can cause the air sacs in your lungs, called alveoli, to rupture. When the alveoli rupture, air can move into the arteries and cause an air embolism.
Pulmonary barotrauma: Air bubbles can enter the bloodstream due to severe trauma to the lining of the lung after a rapid ascent while holding your breath.
The air contained within the lung expands to the point where the tissues tear (pulmonary barotrauma).
This is easy to do as the lungs give little warning through the pain until they burst. The diver will generally surface in pain and distress and may foam or spit blood.
Pulmonary barotrauma is usually apparent and can present quite differently from decompression sickness.
Decompression sickness (ED): Inert gas bubbles form in the bloodstream if the gas dissolved in the blood under pressure during the dive does not have enough time to be removed from the solution during the ascent.
Symptoms can be subtle and are not immediately noticeable, and can develop for some time after the appearance of the surface.
Ventilator-induced by pulmonary barotrauma
Trauma to the lung can also cause an air embolism. This can happen after a patient is placed on a respirator and air is forced into an injured vein or artery, causing sudden death.
Holding your breath while ascending from diving can also force air from the lung into the pulmonary arteries or veins similarly due to the pressure difference.
Air can be accidentally injected directly into a vein or artery during clinical procedures.
The incorrect use of a syringe to meticulously remove air from the vascular tube of a hemodialysis circuit can allow air to enter the vascular system.
Venous air embolism is a rare complication of diagnostic and therapeutic procedures that require catheterization of a vein or artery.
If a significant embolism occurs, the cardiovascular, pulmonary, or central nervous system may be affected.
Interventions to eliminate or mitigate the embolism may include procedures to reduce the size of the bubbles or the removal of air from the right atrium.
There have been rare cases of air embolisms caused by air entering the bloodstream of the uterus or by tears in the female genitalia.
The risk appears to be higher during pregnancy when a tear in the placenta may have occurred.
Cases resulting from attempted abortion by syringe have been reported. They were due to damage to the placenta that allowed air to enter the bloodstream.
Patent foramen ovale in underwater divers is considered a risk factor for arterial gas embolism due to the shunting of what would otherwise be asymptomatic venous bubbles in the systemic arteries.
Air embolism can occur when a blood vessel is open, and a pressure gradient favors the entry of gas.
Because the circulatory pressure in most arteries and veins is higher than atmospheric pressure, and air embolus does not usually occur when a blood vessel is injured.
In veins above the heart, such as in the head and neck, venous pressure may be less than atmospheric, and an injury may allow air to enter.
This is one reason why surgeons must take special care when operating on the brain and why the head of the bed tilts down when a central venous catheter is inserted or removed from the jugular or subclavian veins.
When air enters the veins, it travels to the right side of the heart and then to the lungs. This can cause the vessels in the lung to constrict, increasing pressure on the right side of the heart.
If the pressure rises sufficiently in a patient who is one of the 20% to 30% of the population with a patent foramen ovale, the gas bubble can travel to the left side of the heart and the brain or coronary arteries.
Such bubbles are responsible for the most severe gas embolic symptoms.
Venous or pulmonary air embolism occurs when air enters the systemic veins and is transported to the right side of the heart and to the pulmonary arteries, where it can lodge, blocking or reducing blood flow.
Gas in the venous circulation can cause heart problems by obstructing the pulmonary circulation or forming an air blockage that raises central venous pressure and lowers pulmonary and systemic arterial pressure.
Animal experiments show that the amount of gas required to occur is quite variable. Human case reports suggest that injecting more than 100 ml of air into the venous system at rates greater than 100 ml / s can be fatal.
Massive and symptomatic amounts of venous emboli can also occur on rapid decompression in severe diving or decompression accidents. They can interfere with circulation in the lungs and result in respiratory distress and hypoxia.
Air embolism in a systemic artery, called an arterial air embolism (AGE), is more severe than in a vein because a gas bubble in a route can directly stop blood flow to an area fed by the artery.
Symptoms of “arterial gas embolism” depend on the area of blood flow and maybe stroke for a cerebral embolism (CAGE) or heart attack if the heart is affected.
The amount of arterial air embolism that causes symptoms depends on the location: 2 ml of air in the cerebral circulation can be fatal, while 0.5 ml of air in a coronary artery can cause cardiac arrest.
Prevention and detection
If a patent foramen ovale (PFO) is suspected, an echocardiographic examination may be performed to diagnose the defect.
In this test, fantastic bubbles are introduced into a patient’s vein by swirling saline in a syringe to produce the bubbles and then injecting them into a vein in the arm.
These bubbles can be seen on the ultrasound image a few seconds later as they travel through the patient’s right atrium and ventricle.
At this time, bubbles can be seen directly crossing a septal defect, or a patent foramen ovale can be temporarily opened for the patient to perform the Valsalva maneuver. In contrast, the bubbles pass through the right heart.
An action that will open the foramen. It flaps and shows bubbles that pass to the left heart.
Such bubbles are too small to cause damage to the test. Still, such a diagnosis can alert the patient to potential problems that can arise from more giant bubbles formed during activities such as diving underwater, where bubbles can grow during decompression.
A patent foramen ovale test may be recommended for divers who wish to be exposed to relatively high decompression stress in deep technical diving.
Treatment for an air embolism has three goals:
- Stop the source of the air embolism.
- Prevent air embolism from damaging your body.
- Resurrect you if necessary.
In some cases, your doctor will know how air enters your body.
A giant air bubble in the heart (as may follow specific traumas in which air freely gains access to large veins) will present a constant murmur of “machinery.”
It is essential to quickly place the patient in the Trendelenburg position (head down) and on their left side (left lateral decubitus position).
The Trendelenburg position keeps an air bubble from the left ventricle away from the coronary artery ostia (close to the aortic valve) so that air bubbles don’t get in and clog the coronary arteries (causing a heart attack).
The left lateral decubitus position helps trap air in the non-dependent segment of the right ventricle (where it is more likely to remain rather than progress into the pulmonary artery and impede it).
The left lateral decubitus position also prevents air from passing through a patent foramen ovale (present in up to 30% of adults) and entering the left ventricle, from which it could embolize into the distal arteries (which could cause occlusive symptoms, such as running).
Administration of a high percentage of oxygen is recommended for venous and arterial air embolism. This is intended to counteract ischemia and accelerate the reduction in the size of the bubbles.
For venous air embolism, Trendelenburg or the left lateral position of a patient with a right ventricular air-blocking obstruction can move the air bubble in the ventricle and allow blood to flow below the drop.
Hyperbaric therapy with 100% oxygen is recommended for patients with clinical features of arterial air embolism. It accelerates the removal of nitrogen from the bubbles by solution and improves the oxygenation of the tissues.
This is especially recommended for cases of cardiopulmonary or neurological compromise. Early treatment has the most significant benefits but can be effective for up to 30 hours after injury.
First aid oxygen treatment is helpful for suspected victims of air embolisms or divers who have made rapid ascents or missed decompression stops.
Most closed-circuit respirators can provide sustained high concentrations of oxygen-rich breathing gas and could be used as an alternative to pure open-circuit oxygen resuscitators.
However, pure oxygen from an oxygen cylinder through a non-rebreather mask is the optimal way to deliver oxygen to decompression sickness patients.
Recompression is the most effective, albeit slow, treatment of air embolism in divers. Typically this takes place in a recompression chamber.
As pressure increases, the solubility of a gas increases, reducing the size of the bubble by accelerating the absorption of the gas into the blood and surrounding tissues.
In addition, the volumes of gas bubbles decrease inversely with ambient pressure, as described by Boyle’s law. In the hyperbaric chamber, the patient can breathe 100% oxygen at ambient pressures to a depth equivalent to 18 MSW.
Under hyperbaric conditions, oxygen diffuses into the bubbles, displacing the nitrogen from the bubble and the solution in the blood. Oxygen bubbles are more easily tolerated.
Diffusion of oxygen to blood and tissues under hyperbaric conditions supports body areas that are deprived of blood flow when arteries are blocked by gas bubbles. This helps reduce ischemic injury.
The effects of hyperbaric oxygen also counteract the damage that can occur with reperfusion of previously ischemic areas; this damage is mediated by leukocytes (a type of white blood cell).
High incidence of relapse after hyperbaric oxygen treatment due to delayed cerebral edema.
In terms of the epidemiology of air embolisms, the intraoperative period is found to have the highest incidence.
For example, vascular air embolism in neurological cases varies up to 80%, and the incidence of obstetric and gynecological surgeries can increase up to 97% for VAE (vascular air embolism).
In divers, the incidence rate is 7 / 100,000 per dive. Air embolism has been reported since the 19th century, both in pediatric and adult surgical practice.
The nonspecific nature of the signs and symptoms of vascular air embolism, as well as the difficulty in documenting the diagnosis, do not allow us to know its actual incidence.
With central line placement, it is estimated to occur in approximately 0.2% to 1% of patients. Treatment may be useless if the air bolus is greater than 50 ml.
The interventional radiology literature reports an incidence of venous air embolism of 0.13% during insertion and removal of central venous catheters despite optimal techniques and positioning.
Furthermore, massive air embolism in cardiac bypass procedures is between 0.003% and 0.007%, with 50% of adverse results.
Based on a series of reported cases, the frequency of venous air embolism with central venous catheter placement varies, ranging from 1 in 47 to 1 in 3,000.
It is most commonly associated with otorhinolaryngology and neurosurgical procedures. This is due to the location of the surgical incision, which is usually higher than the heart at a distance more significant than the central venous pressure.
The sitting position in posterior craniotomies is considered especially risky, and the complications of the venous air related to the procedure are estimated between 10% and 80%.
Air embolisms generally occur in the xylem of vascular plants because a drop in hydraulic pressure causes cavitation. The decrease in hydraulic pressure occurs due to water stress or physical damage.
Several physiological adaptations serve to prevent cavitation and recover from it. Cavitation can be prevented from spreading through the narrow pores in the walls between the vessel elements.
Sap from the plant’s xylem can be diverted around cavitation through interconnections.
Water loss can be reduced by closing the leaf stomata to reduce perspiration, or some plants produce positive xylem pressure at the roots.
When the pressure of the xylem increases, the cavitation gases can dissolve.
In summary, vascular air embolism is a rare but potentially fatal complication of several procedures, including access to the central venous catheter. The severity of the symptoms varies, but the worst case is sudden cardiac death.