›The rationale is nitrogen washout that shrinks the bubble and correction of hypoxaemia
›Continue 100 percent oxygen even in a chronic carbon dioxide retainer during a life-threatening event, then titrate down once stable while monitoring for carbon dioxide narcosis
›Nitrous oxide is contraindicated
›Nitrous oxide, used at 50 to 70 percent inspired concentration for anaesthesia or analgesia, diffuses into a gas bubble far faster than nitrogen leaves it and can rapidly enlarge it
›Discontinue it immediately and do not introduce it
›Airway management if intubation is required
›Indications are refractory hypoxaemia, airway protection with depressed consciousness, or the work of breathing in cardiogenic shock
›Use haemodynamically neutral induction, for example ketamine 1 to 2 mg/kg intravenously or etomidate 0.2 to 0.3 mg/kg intravenously, with rocuronium 1 mg/kg intravenously or succinylcholine 1 to 1.5 mg/kg intravenously
›Use the lowest positive end-expiratory pressure that maintains oxygenation, because higher levels raise right atrial pressure and can promote paradoxical embolism through a patent foramen ovale
›Avoid large tidal volumes and high mean airway pressures that further impede a mechanically obstructed right ventricle
Aspiration of intracardiac air
›Aspirate through a central venous catheter when one is in place
›A multi-orifice catheter with its tip near the junction of the superior vena cava and right atrium gives the best chance of retrieving air
›Aspirate with a syringe during and after positioning, accepting that recovery of a meaningful volume is inconsistent
›Placement in an unstable patient
›If no catheter is present and the patient is in extremis, a central line may be placed for aspiration, but it must not delay chest compressions, oxygen, or vasopressors
›Bedside ultrasound of the right heart can confirm the catheter tip and the presence of air to aspirate
›Aspiration is an adjunct, not the primary treatment
›Source control, oxygen, positioning, and circulatory support take precedence
›Chest compressions may fragment a right ventricular air lock and force air into the smaller pulmonary vessels
Haemodynamic support and refractory shock
›Volume resuscitation
›Isotonic crystalloid, compound sodium lactate or 0.9 percent sodium chloride, 500 to 1000 ml intravenous bolus, then reassess
›Volume raises central venous pressure, reduces further entrainment, and supports preload for an obstructed right ventricle
›Reassess after each bolus with lung and cardiac ultrasound to avoid over-filling a failing right ventricle
›Titrate in 250 to 500 ml aliquots in the elderly or in known cardiac or renal disease
›Norepinephrine as the first-line vasopressor
›Norepinephrine, a predominant alpha-1 agonist with modest beta-1 activity that raises systemic and coronary perfusion pressure without marked tachycardia
›Start 0.05 mcg/kg/min by central infusion
›Titrate by 0.02 to 0.05 mcg/kg/min every 2 to 5 minutes to a mean arterial pressure of at least 65 mmHg
›Reduce to increments of 0.01 to 0.02 mcg/kg/min as the pressure approaches target to avoid overshoot
›Usual ceiling 1 mcg/kg/min, above which add a second agent rather than escalate alone
›Run through a large peripheral vein with extravasation vigilance only until central access is secured
›Epinephrine for refractory hypotension or arrest physiology
›Epinephrine, a combined alpha and beta agonist that provides inotropy and chronotropy for a failing right ventricle
›Infusion start 0.02 to 0.05 mcg/kg/min
›Titrate every 2 to 5 minutes toward a mean arterial pressure of at least 65 mmHg
›Decelerate the increments as perfusion recovers to limit tachyarrhythmia
›Usual ceiling 0.5 mcg/kg/min for shock, watching for tachyarrhythmia and a rising lactate
›Arrest dose is 1 mg intravenously every 3 to 5 minutes
›Vasopressin as an adjunct
›Vasopressin, a non-catecholamine vasoconstrictor with relatively less effect on pulmonary vascular resistance
›Add at a fixed 0.03 units/min and do not titrate
›Use as a second agent to spare catecholamine dose, not as sole therapy
›Right ventricular inotropy and afterload reduction when perfusion pressure allows
›Dobutamine, a beta-1 agonist inodilator
›Start 2.5 mcg/kg/min
›Titrate by 2.5 mcg/kg/min every 10 minutes to a maximum of 20 mcg/kg/min
›Decelerate once cardiac output improves to limit tachycardia
›Omit it or pair it with a vasopressor if systolic pressure is below 90 mmHg, because it can vasodilate and worsen hypotension
›Inhaled nitric oxide for severe right ventricular failure with pulmonary hypertension
›Start 20 ppm
›Wean by 5 ppm as the right ventricle recovers
›Do not stop abruptly, because rebound pulmonary hypertension can follow
›Refractory shock despite the above
›Persistent hypotension despite source control, fluids, two vasoactive agents, positioning, and attempted air aspiration is an indication to escalate
›Venoarterial extracorporeal membrane oxygenation or cardiopulmonary bypass to support the circulation while the air resorbs
›Reconsider tension pneumothorax, cardiac tamponade, thrombotic pulmonary embolism, haemorrhage, and anaphylaxis
›Confirm the source is truly sealed if end-tidal carbon dioxide stays low and pulmonary pressures stay high
Cardiac arrest management
›Follow standard advanced life support with modifications
›Pulseless electrical activity is the most common arrest rhythm, so high-quality compressions and adrenaline take priority
›Compressions may also help break up a right ventricular air lock
›Give epinephrine 1 mg intravenously every 3 to 5 minutes per the arrest algorithm
›Address reversible contributors during the arrest
›Confirm the air source is sealed
›Give 100 percent oxygen and an isotonic fluid bolus
›Exclude tension pneumothorax and tamponade with ultrasound
›Do not stop resuscitation prematurely
›Air embolism arrests can recover as the bubble load redistributes, so continue resuscitation and consider extracorporeal cardiopulmonary resuscitation where available
›Consider emergent transfer for hyperbaric therapy after return of spontaneous circulation if arterial gas embolism is suspected
Hyperbaric oxygen therapy
›Indications
›Cerebral arterial gas embolism with a neurologic deficit or seizure
›Coronary arterial gas embolism with ongoing ischaemia
›Severe or refractory cardiorespiratory compromise from venous air despite initial measures
›Mechanism and expected effect
›Raised ambient pressure compresses bubbles by Boyle's law, and a high oxygen partial pressure accelerates inert gas washout
›Improves tissue oxygenation and reduces the inflammatory and ischaemic injury from endothelial gas contact
›Practicalities
›Most effective within 6 hours, but recompression remains reasonable after a longer delay when deficits persist
›Continue resuscitation, vasoactive infusions, and mechanical ventilation inside the chamber with a hyperbaric team
›Treat any pneumothorax before compression and re-image for expansion during therapy
›Adjuncts around hyperbaric care
›Intravenous isotonic fluid to maintain perfusion, avoiding glucose-containing solutions that may worsen ischaemic brain injury
›Treat seizures with a benzodiazepine, for example lorazepam 0.1 mg/kg intravenously up to 4 mg per dose
›Manage cerebral oedema with head-of-bed neutral positioning once haemodynamically stable, and consider mannitol 0.25 to 1 g/kg intravenously over 20 to 30 minutes or hypertonic 3 percent sodium chloride 250 ml intravenously
›Corticosteroids are not recommended for cerebral arterial gas embolism, and if dexamethasone is given for another indication the dose is 10 mg intravenously then 4 mg every 6 hours
›Lidocaine has been proposed for cerebral protection at 1 to 1.5 mg/kg intravenously then 1 to 4 mg/min, but the evidence is insufficient and it is not routinely recommended
Interventions to avoid or modify
›Contraindicated or actively harmful
›Nitrous oxide at 50 to 70 percent inspired concentration, which diffuses into the bubble and enlarges it, and must be stopped
›Steep head-up positioning while air remains in the circulation
›A large abrupt Valsalva or a sudden release of high positive end-expiratory pressure, which can shunt air across a patent foramen ovale
›Not indicated against the air itself
›Systemic anticoagulation, for example a heparin infusion of about 18 units/kg/hour after an 80 units/kg bolus, has no effect on gas and is reserved for a proven concurrent thrombus
›Fibrinolysis, for example alteplase 50 mg intravenous bolus or 100 mg over 2 hours, does not act on air and should not be given for presumed air embolism
›Intra-aortic balloon counterpulsation augments the left ventricle and does not relieve a right ventricular outflow air lock, so it is not indicated
›Appropriate with modification
›Positive-pressure ventilation using the lowest effective airway pressure and positive end-expiratory pressure to limit right-to-left shunting and right ventricular afterload
›Analgesia with fentanyl 25 to 50 mcg intravenously every 5 to 10 minutes titrated to comfort, which is haemodynamically neutral
›Avoid morphine 2 to 4 mg intravenously in the hypotensive patient, because histamine-mediated venodilatation cuts preload for a preload-dependent right ventricle
›Vasopressors are appropriate and should not be withheld for fear of raising afterload