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Welcome back to the tasty morsels of critical care podcast.
Today we’re going to talk about a fairly rare and niche issue in critical care – gas embolism. The venerated stone tablets of Oh’s Manual do not mention it in any great detail but my alternative and go to textbook has been Irwin & Rippe’s weighty tome/deadweight, and chapter 177 here is dedicated to gas embolism syndromes.
This can quickly be split into venous and arterial emboli and we’ll start with the venous side
There are a few causes for this and a reproducible short list might include
- Surgical causes
- sitting awake craniotomy the classic case where air gets into a venous sinus
- any procedure with an open vein
- it is worth noting that when this is searched for in surgeries that are considered high risk it is very common to find signs of air in the venous circulation on doppler. It is a testament to the lungs as a protective filter that it doesn’t cause more issues
- Traumatic causes
- a stab wound to a big vein
- major thoracic injury
- Procedural
- CVC being the most obvious one we think of
- it has been reported with peripheral IVs and even epidurals (though I can’t quite get my head around the mechanism there)
Ultimately there needs to be some kind of pressure gradient between the atmosphere and the vein in question hence why position and vigorous respiratory effort are risk factors as both induce a pressure gradient and rapid flow toward the right atrium. The air can get trapped anywhere between the entry point and the pulmonary circulation and it is then obstruction of flow through and out of the right heart that causes all the drama.
100mls is considered to be a fatal “dose” in case you were wondering.
Paradoxical emboism is a very real concern here. 1 in 5 of us is walking around with a PFO and generally it’s not a problem as the slightly higher pressure in the LA vs the RA ensures that the little flap of tissue sits closed. However in the scenario of raised right heart pressures (say when there is 50 mls of air trapped in the RV) then the PFO can blow open and air can enter the left sided circulation converting the scenario from a venous gas embolism to the as yet unmentioned arterial gas embolism situation.
In terms of making the diagnosis the context is everything – what was the situation when the haemodynamic collapse occurred? Did they rip out their vascath while sitting upright attacking staff with an IV pole prior to their cardiac arrest?
There is apparently a mill-wheel murmur that has been described that i suspect is useful only as an answer in an exam. In reality this will probably be a tricky echo diagnosis or a slightly late and embarrassing CT diagnosis. Hopefully you’ll have nailed it at the context stage and proceded to treatment.
Treatment involves stopping any further gas entering the circulation which will likely involve clamps on vascular devices or sticking a finger on the hole in the vessel. The ninja move that is needed next is to lie the patient on their left side in the hope that the air lodges in the RV apex and allows an unobstructed conduit from RA through RV and on to PA. Next try and get a catheter into the RV and aspirate some air. This always make me think of some form of reverse John Travolta/Uma Thurman in Pulp Fiction precordial syringe stab but in reality it’ll be a CVC placed in a rush.
100% O2 is considered a good idea as physiologically you might replace the insoluble nitrogen in the apex of the RV with pure metabolisable O2 but this didn’t really pan out in PTX and I suspect is useful only in theory. This is another time to suggest hyperbaric oxygen but again, in reality, taking a critically ill dying patient to a single person compression chamber seems like a recipe for disaster but perhaps it is something that is done.
Let’s turn to the arterial side.
Overall the venous side will tolerate gas somewhat better than the arterial side, with the lungs acting as a giant filter however once it gets big enough you can obstruct your RV and the usual RV spiral of death beings. Air in the left side is much less problematic haemodynamically but neurologically is devastating.
The list of causes is similar to those for venous gas embolism as many of them can shunt through a PFO In addition some important ones to note include
- cardiac surgery
- angiography
- traumatic injuries like a bronchovenous fistula will rapidly entrain blood into the LA and LV
- decompression sickness
- carotid endarterectomy
The pathophys is one of simple obstruction to flow in the brain but there is a corresponding endothelial injury that has its own consequences
The treatment here is much less exciting as all we can really do is give 100% O2 as a strategy and consider HBO. And by HBO i mean hyperbaric oxygen not the TV channel.
References:
Irwin & Rippe’s Intensive Care Chapter 177