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Troubleshoot — Cannot Desaturate

Some cus­tomers have issues desat­u­rat­ing.  This is near­ly always because of spe­cif­ic issues with user phys­i­ol­o­gy. As a rule, only well-trained ath­letes and con­di­tioned users will have pre­dictable desat­u­ra­tion responses.

See Also: Train­ing Desat­u­ra­tion Patterns

This arti­cle is split into two sec­tions. The first sec­tion explains com­mon issues with the user. The sec­ond sec­tion is a check­list for issues that may occur over time. 

There are a hand­ful of issues that may make a new user think LiveO2 isn’t work­ing prop­er­ly because a pulse oxime­ter does not read­i­ly show a decrease in oxy­gen con­cen­tra­tion in the blood while using ‑O2. This often leaves the user won­der­ing what is happening…

If the issue is with LiveO2, it’s easy to detect and cor­rect the prob­lems. When the issue is part of the user phys­i­ol­o­gy — It’s more dif­fi­cult to under­stand but still easy to test:

  • If the user ‘feels extra chal­lenge’ on ‑O2 — the sys­tem is work­ing properly. 

User-specific desaturation problems

Most of the time users can­not desat­u­rate because of one of these reasons.

#1: User metabolism challenge that interferes with blood oxygen exchange or poor hand circulation

Many new LiveO2 users have meta­bol­ic issues that inter­fere with blood gas exchange. There are three com­mon dysfunctions:

  • Cap­il­lary shunt­ing. These users exhib­it unusu­al­ly high O2 sat­u­ra­tion lev­els because issues flow restric­tions in cap­il­lary beds shunt blood around the tis­sue. Oxy­gen lev­els remain high because oxy­gen nev­er reach­es tis­sue and is underused.
  • Nutri­ent defi­cien­cies. The body requires suf­fi­cient amounts of B‑vitamins to affect gas trans­fer to the tis­sue. Defi­cien­cies inhib­it trans­fer and may inhib­it the abil­i­ty to sat­u­rate or desaturate.

These issues often hap­pen togeth­er. Each ele­ment reduces the user’s appar­ent abil­i­ty to desat­u­rate as read by a pulse oximeter.

  • Shunt­ing pre­vents oxy­gen from leav­ing the blood
  • Nutri­ent defi­cien­cies pre­vent oxy­gen from leav­ing the blood
  • Car­bon monox­ide and oxy­gen are indis­tin­guish­able by a pulse oximeter.

But… No mat­ter how these fac­tors inter­fere with the pulse oxime­ter there is a very effec­tive test.

The users will feel the ‑O2 chal­lenge. Inef­fi­cient res­pi­ra­tion makes users very sen­si­tive to reduced oxy­gen lev­els. That leads us to…

The simplest test for a new user

If your users feel extra dif­fi­cul­ty on the ‑O2 set­ting then this is a strong and reli­able indi­ca­tor that the sys­tem is work­ing properly. 

Most users will slow down on ‑O2 and speed up on +O2. Users with com­pro­mised res­pi­ra­tion will quick­ly notice the decrease in oxy­gen from 75% to 14% for LiveO2 AC

#2 User was exposed to Carbon Monoxide

Car­bon monox­ide has a high­er affin­i­ty for hemo­glo­bin than oxy­gen and may be due to envi­ron­men­tal expo­sure or inter­nal­ly gen­er­at­ed as a result of dys­func­tion­al cel­lu­lar res­pi­ra­tion. Pulse oxime­ters can­not dis­tin­guish blood-car­ry­ing car­bon monox­ide from blood sat­u­rat­ed with oxy­gen. Users with car­bon monox­ide will not desaturate. 

Car­bon monox­ide binds to hemo­glo­bin sites just like oxy­gen. Pulse oxime­ters can­not dis­tin­guish hemo­glo­bin with Car­bon Monox­ide from Oxy­gen. Car­bon monox­ide can be envi­ron­men­tal or endo­genic (from inside the body). Car­bon monox­ide binds to hemo­glo­bin about 240x more read­i­ly than oxygen.

Car­bon monox­ide in the blood will pre­vent the pulse oxime­ter from read­ing cor­rect­ly. It will read as though the blood is sat­u­rat­ed with oxy­gen when it is not. We have also seen indi­vid­u­als who appear to have car­bon monox­ide tox­i­c­i­ty when there was no known expo­sure to car­bon monox­ide as though it was endoge­nous (made inside the body) from inef­fi­cient metabolism.

When train­ing with LiveO2 — the high bind­ing affin­i­ty of car­bon monox­ide makes it look like the per­son can­not desaturate. 

See Also:

Carboxyhemoglobin

Car­boxy­he­mo­glo­bin is pro­duced by the bind­ing of car­bon monox­ide (CO) to hemo­glo­bin. CO is gen­er­at­ed dur­ing incom­plete com­bus­tion of organ­ic prod­ucts and has tox­ic effect because it com­petes with oxy­gen for the same bind­ing site in the Fe2+ of Hb. Hemo­glo­bin bound to CO is unable to trans­port O2. Hb has a 210-fold greater affin­i­ty for car­bon monox­ide than for oxy­gen, which explains the extra­or­di­nary tox­i­c­i­ty of CO even when its con­cen­tra­tion in the inspired air is rel­a­tive­ly low. For exam­ple, breath­ing air con­tain­ing 0.02% CO for 2 h caus­es symp­toms, such as headache and nau­sea. A con­cen­tra­tion of 0.1% pro­duces loss of con­scious­ness with­in 1 h and death by asphyx­ia in only 4 h. Car exhaust gas­es con­tain between 4% and 7% CO and tox­ic con­cen­tra­tions are read­i­ly achieved in poor­ly ven­ti­lat­ed envi­ron­ments (garages). Car­boxy­he­mo­glo­bin has a cher­ry red col­or. For that rea­son, sub­jects intox­i­cat­ed with CO show appar­ent­ly “healthy” red­dish lips and cheeks.

Con­tact your train­er for sup­port. We have spe­cial­ized pro­to­cols to expe­dite car­bon monox­ide release from hemoglobin.

#3 User’s body blocks desaturation

The most com­mon rea­son user’s can­not desat­u­rate is because their body is in a stress pat­tern. This pat­tern, result­ing from chron­ic poor oxy­gena­tion, trig­gers the blood to hang-on to oxy­gen in prepa­ra­tion for a stress event. 

This pat­ten often resolves by pro­gres­sive train­ing but goes through two stages:

  • Pro­gres­sive exer­tion with train­ing with oxy­gen with esca­lat­ing challenges
  • Esca­lat­ing exer­tion chal­lenge on low oxy­gen over time 

This process uses the degrees of free­dom to grad­u­al­ly increase the body’s will­ing­ness to use reserve oxy­gen attached to hemo­glo­bin. Please con­tact your train­er to work with this.

#4 Hypotensive Shunting

Indi­vid­u­als with hypoten­sion, low blood pres­sure, often lack enough pulse pres­sure at the cap­il­lary blood entrance to push blood through the cap­il­lar­ies. Instead blood routes through bypass shunts, and fails to deliv­er oxy­gen to tissue.

When hypox­ic chal­lenge does not cause the body to send blood through cap­il­lar­ies, oxy­gen remains bound to hemo­glo­bin. Even though the air mix­ture has lit­tle oxy­gen, and the user is exert­ing, the body does not desaturate.

Hypox­ia which fur­ther dilates arter­ies, may not trig­ger the heart to pump hard enough to over­come the cap­il­lary obsta­cles. These indi­vid­u­als will have dif­fi­cul­ty desaturating.

When hypox­ic chal­lenge trig­gers the heart and vas­cu­lar sys­tem to over­come this obsta­cle, a pro­longed desat­u­ra­tion dip occurs as the break­through enables large seg­ments of the body to repay oxy­gen debt.

When this occurs, the body will remain on a low oxy­gen sat­u­ra­tion read­ing while the oxy­gen debt is paid. This can take 10 min­utes or often more.

Escalation

If you are well con­di­tioned, and use Adap­tive Con­trast, the you may want to con­sid­er upgrad­ing to LiveO2 Extreme to access more aggres­sive hypox­ia, with sim­u­lat­ed alti­tude up to 22K feet.

See Also

Updated on September 18, 2024
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