Without evidence of benefit, an intervention should not be presumed to be beneficial or safe.

- Rogue Medic

Will IV Oxygen Save Lives?

ResearchBlogging.org
Image credit.
 

Intravenous oxygen delivery that works?

Maybe temporary oxygenation, but not yet.

Will this change the approach to CICV (Can’t Intubate, Can’t Ventilate) patients?

No, but it may change the approach to CICO (Can’t Intubate, Can’t Oxygenate) patients.

The distinction is important. If we can deliver oxygen without ventilation, we can avoid some of the problems of hypoxia, but we will still have to deal with the acidosis that results from the inability to eliminate CO2 (Carbon DiOxide).
 

In the early 1900s, intravenous administration of oxygen gas was used in attempts to relieve refractory cyanosis (4–7). Most reported that spontaneously breathing, cyanotic animals exhibited signs of pulmonary embolism at infusion rates in excess of 0.2 to 1 ml/kg per minute and required frequent pauses in the infusion (4, 5); . . . None of these studies documented an increase in oxygen content in the blood as a result of the intervention.[1]

 

Try walking up several flights of stairs while only breathing through your nose. You will become short of breath very quickly.

Unless you are in truly horrible shape, it is not a lack of oxygen that is causing you to become short of breath. It is the inability to remove CO2 (Carbon DiOxide) that is the problem.

Most of us breathe because of a buildup of CO2, not because of a lack of oxygen.
 

The reflexive response of some people might be to give the anti-acidosis drug NaHCO3 (sodium bicarbonate). We will ignore the sodium, which at 5.8% in NaHCO3 is over 6 times the concentration of the NSS (Normal Saline Solution – 0.9% sodium) we routinely give. The sodium in NaHCO3 may be effective for treating sodium channel blocking drugs, such as antidepressnts, antiseizure medications, antiarrhythmics, and antivirals.[2]

The sodium is not the real danger. The bicarbonate (HCO3) is the problem. When binding with the excess hydrogen ions to neutralize metabolic acidosis, CO2 is produced.
 

HCO3 + H+

Produces:

CO2 + H2O
 

a patient with complex airway anatomy and difficulty maintaining oxygenation using basic airway maneuvers could avert a hypoxemic crisis during a prolonged intubation attempt. To date, safe and effective intravascular delivery of oxygen gas has not been realized.[1]

 

In the cute little bunnies used in the study (7 LOM [Lipidic Oxygen–containing Microparticles] and 6 Control), these were the results.
 


Click on images to make them larger.
 

Oxygen saturation remained between 40% and 60% with the LOM, but that was much better than the less than 20% for the controls. since the study animals received LOMs titrated to an arterial oxygen tension of greater than 30 mmHg, this is not a surprise. The controls just received fluid at a similar rate.
 


 

CO2 more than doubled for both groups.

Providing oxygen does nothing to remove CO2.
 


 

When CO2 increases, the pH will decrease (acidosis will increase).

Sodium bicarbonate will not decrease the acidosis for these patients.

Sodium bicarbonate will increase the acidosis for these patients.

Sodium bicarbonate produces CO2, which must be removed by ventilation. If we are giving LOM to patients we can adequately ventilate, maybe we do not understand what we are doing.

We should only give sodium bicarbonate to a patient who is well ventilated – unless we are trying to kill the patient.
 


 

In (F) and (G), data are means ±SEM. The blue lines end at 10.2 min because no animals treated as controls had spontaneous circulation after that time and received chest compression–only cardiopulmonary resuscitation (CPR) during the remainder of asphyxia. (H) Kaplan-Meier plot of animals experiencing cardiac arrest during asphyxia (left; P =0.0002, log-rank test), restoration of mechanical ventilation (shaded box), and subsequent recovery and observation (right).[1]

 


 

None of the bunnies reported any near-death experiences.

Consider the time involved. Many in the media have been reporting this as a way to provide half an hour of apneic oxygenation. That is ridiculously optimistic. This will be something that might provide an extra 5-10 minutes to manage a hypoxic patient, if the patient has not already died due to the hypoxia.

5-10 minutes can be the difference between life and death.

Don’t believe me?

Hold your breath for 10 minutes. Just stop breathing and hold your breath.[3]

Without LOMs, all of the bunnies were pulseless after a little more than 10 minutes, but at 15 minutes, when ventilation was resumed, almost all of the LOM bunnies still had pulses (6 out of 7).

LOMs are not just to make it possible to deliver a patient with a pulse to the hospital, so that we can say that They didn’t die in the ambulance.

That is not changing anything.

LOMs are to provide time for us to provide an airway – if this ever demonstrates safety and efficacy in humans.

Footnotes:

[1] Oxygen gas-filled microparticles provide intravenous oxygen delivery.
Kheir JN, Scharp LA, Borden MA, Swanson EJ, Loxley A, Reese JH, Black KJ, Velazquez LA, Thomson LM, Walsh BK, Mullen KE, Graham DA, Lawlor MW, Brugnara C, Bell DC, McGowan FX Jr.
Sci Transl Med. 2012 Jun 27;4(140):140ra88. doi: 10.1126/scitranslmed.3003679.
PMID: 22745438 [PubMed – indexed for MEDLINE]

Free Full Text Download in PDF format from medlive.cn
 

At the end of the asphyxial period, mechanical ventilation was restored with 100% oxygen until return of pulsations (in animals receiving chest compressions) and then titrated downward to achieve arterial saturations of >92%. Animals achieving return of spontaneous circulation after relief of asphyxia were treated with standard intensive care management, including inotropic support (dopamine, 2 to 10 mg/kg per minute, intravenous infusion) to maintain MABP of at least 40 mmHg during the follow-up period. Hyperthermia was avoided by passive ambient cooling (goal, 34 to 35° C). Animals were sacrificed 90 min after the end of asphyxia for lab and histology sampling.

Everyone seems to be using therapeutic hypothermia and trying to avoid giving too much oxygen.

[2] Management of sodium-channel blocker poisoning: the role of hypertonic sodium salts.
Di Grande A, Giuffrida C, Narbone G, Le Moli C, Nigro F, Di Mauro A, Pirrone G, Tabita V, Alongi B.
Eur Rev Med Pharmacol Sci. 2010 Jan;14(1):25-30. Review.
PMID: 20184086 [PubMed – indexed for MEDLINE]

Free Full Text in PDF format from EuropeanReview.org
 

As more substances having sodium-channel blocking properties become available, the incidence of this poisoning may be expected to increase, and clinician, particularly the emergency physician, should be familiar with this potential fatal condition.

A little evidence supports the treatment with hypertonic sodium salts, and current recommendations have not been based on randomized clinical trials.

[3] Longest time breath held voluntarily (male)
Guinness World Records
Web page.
 

The longest time holding the breath underwater was 22 min 00 sec by Stig Severinsen (Denmark) at the London School of Diving in London, UK, on 3 May 2012.

Stig was allowed to hyperventilate with oxygen prior to the attempt, and did this for 19 minutes and 30 seconds.

Kheir, J., Scharp, L., Borden, M., Swanson, E., Loxley, A., Reese, J., Black, K., Velazquez, L., Thomson, L., Walsh, B., Mullen, K., Graham, D., Lawlor, M., Brugnara, C., Bell, D., & McGowan, F. (2012). Oxygen Gas-Filled Microparticles Provide Intravenous Oxygen Delivery Science Translational Medicine, 4 (140), 140-140 DOI: 10.1126/scitranslmed.3003679

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