高濃度酸素の投与による酸素中毒
及びCO2ナルコーシスのリスク

テルコムの酸素濃縮器の酸素濃度は【酸素中毒防止】のため敢えて50%以下に抑えました。
(但しマスク、またはフローバイでの酸素投与では90%濃度での使用も可能です)

酸素ハウス内での酸素濃度を22%~45%範囲で調節できます(在宅でも飼い主が調整できます)

1、酸素中毒

高濃度酸素による【酸素中毒】を日本救急医学会では下記の通り「用語解説」しております。

過剰な酸素が,生体の解毒機能を超えて有害な作用をきたした状態。障害の主な標的臓器は中枢神経系と肺である。2‐3気圧以上の高い分圧の酸素を吸入する高気圧酸素療法では,生体の細胞代謝が障害され,心窩部や前胸部の不快感・嘔吐・めまい・視野狭窄など,時には短時間で痙攣発作と昏睡がみられることがある。
これが急性酸素中毒である。一方,吸入気酸素濃度50%以上の高濃度酸素を長時間吸入することにより気道粘膜や肺胞が障害され,重篤な場合は呼吸不全に陥る。障害機序は酸素由来のフリーラジカルによる細胞障害が想定されている。とくに人工呼吸器による呼吸管理をおこなっているときは,動脈血酸素分圧を70‐100mmHgに維持するように吸入酸素濃度を設定すべきとする報告もある(Castleman B, et al: N Engl J Med 1970; 282: 976)。
可及的早期に吸入酸素濃度は下げるべきであるが,一般的に肺胞気酸素濃度が60%以下なら長期の酸素吸入でも安全とされている。

2、CO2ナルコーシス

Ⅱ型呼吸不全疾患では専門医の推奨する酸素濃度は25~30%です。

参考文献:
獣医学博士 城下幸仁先生執筆文献から
「犬・猫の呼吸器を診る」S/A Medicine  Vol.21 No.6 2019
(お申し込み下さい別刷り差し上げます。)

下記:城下先生より頂戴した解説を転載いたします。
https://www.sagamigaoka-ac.com/2017/11/22/Ⅱ型呼吸不全患者に対する酸素投与方法、目標と/

Ⅱ型呼吸不全患者に対する酸素投与方法、目標とするPaO2の値は?
急性呼吸促迫時には100% 酸素をFlow-byがよいと思います。開口呼吸が消失すれば、ICU管理がよく、FIO2 25-30%, 室温 22-23℃に初期設定します。
Ⅱ型呼吸不全の代表疾患である慢性閉塞性肺疾患(COPD)では、長期経過に伴いある程度の低酸素血症には適応しており、ヘモグロビン-酸素解離曲線が急峻部から平坦部のカーブが変化するPao2 60mmHg程度に安定して維持されれば、ヘモグロビンと酸素との結合力が安定し、酸素運搬能としては十分です。
逆に、低酸素血症に適応している環境で、急にFIO2 が上昇すると、体の反応としては、末梢化学受容体が即応し、negative feedback機構により呼吸抑制または停止します。その後、高炭酸ガス血症が生じ、体内の平衡と酸素療法の介入とのバランスをとることが困難な状況になり、呼吸状態が不安定となり、制御困難な状況になります。ヒトでは以下の文献のように、COPDの急性増悪時にはPao2は20-40mmHgまでに下がっていると考えられ、Pao2 60mmHgにまで回復することができれば、酸素化にも高炭酸ガス血症発症リスク回避にも適切と考えられています。したがって、急性呼吸促迫時には目標とするPao2は60mmHgです。
安定期には、患者の呼吸状態によって調整しますが、FIO2<30%での管理が適切と思います。人の文献ですが、COPD患者の酸素療法について記載されている部分を引用します。

Malley WJ. Clinical Blood Gases: Application and Noninvasive Alternatives. Philadelphia: WB Saunders, 1990. pp184-185、本文中の文献リストは以下です。Malley90-ClinicalBloodGases-COPD患者の酸素療法, FIO2の設定と管理 -文献

Oxygen-Sensitive Patients1
The approach to oxygen therapy in the patient with COPD or chronic hypercapnia is completely different. In these individuals, caution is the byword. Excessive oxygen therapy administered to these oxygen-sensi¬tive patients may have fatal consequences. Neverthe¬less, even in these patients, when hypoxia is suspected, oxygen therapy should never be withheld simply be¬cause the patient may be sensitive to oxygen. Correc¬tion of hypoxia is always the first priority.
Specifically, the first line of supportive treatment in acute exacerbation of COPD is low FIO2 therapy. Typi¬cally, the patient with COPD in acute respiratory7 failure has blood gases approximating those shown in Ex¬ample 10-1.179

Example 10-1. TYPICAL BLOOD GASES DURING ACUTE RESPIRATORY FAILURE IN PATIENTS WITH COPD
pH …………………………………….. 7.23-7.39
PaCO2 ………………………………. 60-80 mm Hg
PaO2 ………………………………… 20-40 mm Hg

Despite PaCO2 levels in excess of 60 to 65 mm Hg, many patients with COPD can be managed without mechanical ventilation.188 In general, mechanical ven¬tilation should not be initiated unless pH falls below 7.20187,188 and after all else fails.187,190 The decision to institute mechanical ventilation in COPD is always dif¬ficult and requires consideration of a host of variables.
A reasonable target PaO2 in acute exacerbation of COPD is 60 mm Hg.177,191 This level guards against hypoxia and is unlikely to cause substantial hypercap¬nia.
FIO2 Selection. A useful guideline for FIO2 selec¬tion in acute exacerbation of COPD is the fact that PaO2 increases about 3 mm Hg for each 0.01 increase in FIO2.179,192 Thus, if a patient with COPD is seen in the emergency room during an acute exacerbation with a PaO2 of 39 mm Hg on FIO2 of 0.21, the FIO2 level indicated to achieve a PaO2 of 60 mm Hg is 0.28. In other words, an FIO2 increase of 0.07 should increase PaO2 about 21 mm Hg (7 x 3 mm Hg).
The formula shown in Equation 1 may be used to determine the appropriate percentage of oxygen to be applied in acute exacerbation of COPD, assuming a target PaO2 of 60 mm Hg. Of course, this is just a guideline, and individual cases may vary considerably. It must also be remembered that this guideline applies only to the patient with COPD in acute exacerbation.
(60 mm Hg – room air PaO2)/3
= required % FIO2 increase (1)
It is noteworthy that SaO2 increases on average 3 to 4% per 0.01 increase in FIO2 in acute COPD.179This substantial increase shows the tremendous value of oxygen therapy in acute COPD. Because these patients are often on the steep portion of the oxyhemoglobin curve, the amount of oxygen actually present in the blood rises sharply with only a small increase in PaO2.
CO2 Narcosis. One must always keep in mind that increases in PaO2 in patients with COPD may also be accompanied by increases in PaCO2. Although a slight increase in PaCO2 is inconsequential, a large increase must be avoided. The patient is more likely to have an increase in PaCO2 when initial PaCO2 is greater than 70 mm Hg,192 or when the initial PaO2 is very low.191 Also, the clinician should be aware that worsening hypercarbia is usually observed several hours after the onset of oxygen therapy.188
The increase in PaCO2 also tends to be proportional to the level of FIO2 delivered. In one study, PaCO2 increased on average 5 mm Fig with administration of FIO2 0.24 and 8 mm Hg on FIO20.28.190 In another study, modest FIO2 levels of 0.35 to 0.4 substantially aggravated hypercapnia.193When excessive oxygen therapy appears to be responsible for progressive hy¬percapnia, FIO2 should be reduced gradually, because abrupt cessation of oxygen may result in further de¬terioration.
The buildup of CO2 to high levels in the blood gives rise to the syndrome known as CO2 narcosis. This syn¬drome is characterized by increasing PaCO2 levels, aci¬demia, stupor, and coma.191Additional clinical signs suggestive of mild-to-moderate hypercardia include decreased cerebral function, headache, drowsiness, lethargy, and asterixis.194 A more complete list of the signs and symptoms associated with hypercapnia is provided in Table 9-4, Chapter 9(Malley90-ClinicalBloodGases-Table9-4, Chapter9).
Sometimes, the hypercarbic patient may be rela¬tively asymptomatic. Nevertheless, the clinician must be continuously on guard for any signs or symptoms of hypercardia while administering oxygen to the pa¬tient with COPD.
Some authors suggest that high doses of oxygen therapy may be safely administered to patients with COPD if hypercapnia is not present initially.177,189 In my personal, anecdotal experience, I have observed increasing PaCO2 levels after oxygen therapy despite the absence of pre-existing hypercarbia.
The phenomenon of normal PaCO2 levels in a pa¬tient who actually has chronic hypercapnia could be explained by the observation that PaCO2 levels in some patients with COPD seem to decrease during acute exacerbation of the disease (see Chapter 14).4 Thus, when blood gases are first sampled in the hospital, PaCO2 levels could appear lower than their normal baseline. In other words, chronic CO2 retention may- go unrecognized during acute exacerbation because PaCO2 is within the normal range. In any event, it ap¬pears prudent to approach oxygen therapy cautiously in all patients with COPD, regardless of PaCO2 levels.
The device selected for the administration of oxygen is somewhat a matter of personal preference. High- flow systems such as air-entrainment masks with low FIO2 levels have the advantage of accurate FIO2 rates regardless of breathing pattern. However, the patient’s comfort and compliance with these devices are not good. In addition, these masks are often unsightly, awkward, and noisy.
Low-flow systems (e.g., nasal cannula) are more often used. They are less obtrusive, quieter, and better tolerated. For more precise FIO2 control however, flowmeters marked in flow increments less than 1 L/min may be required.195 Furthermore, one must always remember that a nasal cannula is a low-flow- system and, as such, may allow considerable FIO2 varia¬tion with changes in ventilatory pattern.