see also: [[Oxygen dissociation curve]], [[Diving injuries and Dysbarism#Diving Physics]] source: Advanced Ventilator Book William Owens >[!key points] >- *Cardiac output* has greatest influence on O2 delivery to tissues >- anaemia has a more pronounced effect on oxygen delivery than hypoxaemia >- oxygen consumption ↑ by 30-50% during critical illness >- the heart consumes a high percentage of delivered oxygen because it receives a smaller fraction of total cardiac output >- the difference between arterial and venous oxygen content is normally 3-5mL O2/dL blood >>**DO2** - oxygen delivery >>**VO2** - Oxygen consumption >>**SVO2** - venous oxygen saturation (measured with pulm artery catheter) ## Oxygen delivery equation >*Equation:* $\text{DO}_{2} = \text{CO} * \text{CaO}_{2} * 10$ where $\text{DO}_{2}$ = delivery of oxygen, CO = cardiac output, and $\text{CaO}_{2}$ = Oxygen content - once arterial blood loaded with O2, it is delivered to tissues - the amount of blood circulated per minute is the *cardiac output* (L blood/min ; CO = HR x SV) - if normal CO is 5L/min, then DO2 is 1020 mL O2/min - ==the cardiac output has the greatest influence on oxygen delivery== - even during periods of arterial hypoxemia, a ↑ in CO can be sufficient to deliver necessary O2 ot tissues - **anaemia has a more pronounced effect on oxygen delivery than hypoxemia** - *an increase in cardiac output can offset hypoxemia* DO2 can be indexed for body surface area. a "typical" BSA is 1.7 m^2, so typical DO2 indexed would be 1020/1.7 = 600 mL O2/min/m^2. > table below shows the effect that ↑ CO can have on oxygen delivery, even with significant anaemia or hypoxia. > it also shows that anemia has a more pronounced effect on oxygen delivery than hypoxia. ### table: relationship btwn CO, Hb, SaO2, DO2 | CO <br>(L/min) | Hb<br>g/dL | SaO2 | DO2<br>mL O2/min | | -------------- | ---------- | ---- | ---------------- | | 3 | 15 | 100% | 604 | | 8 | 7 | 100 | 750 | | 5 | 15 | 100 | 1005 | | 8 | 15 | 75 | 1206 | impaired oxygen delivery is always due to either low cardiac output, anaemia, or hypoxaemia. ## Oxygen content equation > *Oxygen content:* $\text{CaO}_{2} = 1.34 * \text{Hgb} * \text{SaO}_{2} + [\text{PaO}_{2} * 0.003]$ - each gram of Hb can bind 1.34 mL of O2 when fully saturated - tiny amount of O2 also carried in plasma (PaO2) - with normal Hb of 15g/dL, SaO2 of 100%, O2 content of arterial blood is 20.4mL O2/dL blood - the fracction contributed by dissolved O2 is negligible - if FiO2 on ventilator increased to bring PaO2 up to 500mmHg (keeping SaO2 at 100%), only 1.2 mL O2/dL would be added to O2 content because Hb binds 98.5% of O2 content - keeping PaO2 elevated beyond what is necessary for adequate saturation of the hemoglobin is unlikely to be consequential *except in cases of profound anaemia* (Hb <5 g/dL) or hyperbaric conditions - *therefore*: **the SaO2 is what matters, not the PaO2** ## Oxygen consumption > *Oxygen consumption:* VO2 - during rest, oxygen consumption, VO2, is ~200-250mL O2/min. - indexed for BSA, resting VO2 is ~ 120-150 mL O2/min/m2. - recall indexed DO2 delivery is ~ 600 mL O2/min/m2. - increase VO2 during exercise x10 - ==during critical illness like septic shock, multisystem trauma, or burn== *VO2 increases by 30-50%*. - oxygen consumption varies by organ system - brain and heart consume most O2 - however, ==organs vary in their cardiac output receipt==; brain consumes most O2, but also recieves 15% of cardiac output. coronary circulation accounts for only 5% of total cardiac output, *so the percentage of delivered O2 that is consumed is much higher*. total body VO2 can be measured with a *pulmonary artery catheter* or using cardiac output monitor (eg PICCO) with central venous oxygen saturation: > *Central venous oxygen content:* > $\text{CVO}_{2} = 1.34 * \text{Hb} * \text{SvO}_{2} + [\text{PVO}_{2} * 0.003]$ as with arterial oxygen content equation, minor contribution made by disolved oxygen (PvO2) can be omitted from calculation - therefore, for Hb of 15 and normal SvO2 of 75%, venous oxygen content is 15.1 mL O2/dL blood. the *oxygen consumption*, VO2, can be calculated by multiplying the arterial-venous oxygen difference by cardiac output and converting the units: >*oxygen consumption:* $\text{VO}_{2} = \text{CO} * [\text{CaO}_{2} - \text{CvO}_{2}] * 10$ >$\text{VO}_{2} = \text{CO} * 1.34 * \text{Hb} * (\text{SaO}_{2} - \text{SvO}_{2}] * 10$ ## Using DO2 and VO2 - known DO2 or VO2 in isolation is not particularly useful - the clinical question is *whether the delivery of O2 is adequate to meet teh body's consumption requirements* - DO2:VO2 ratio can be helpful for this . ration should be 4:1 or 5:1 (cardiac output increases DO2 to meet VO2 demands) - the DO2 can vary widely as the VO2 remains constant due to this existing physiologic reserve - as DO2 declines, it can reach a point where a further drop in O2 delivery causes a drop in consumption. this is the **hypoxic, or anaerobic, threshold** - at this point, reserve is exhausting and consumption becomes supply-dependent - a patient at or below this point for a prolonged period will become severely acidotic and will not survive - occurs at roughly the 2:1 mark due to variable oxygen consumption of different organ systems | DO2:VO2 | SvO2 | | ------- | ---- | | 5:1 | 80% | | 4:1 | 75% | | 3:1 | 67% | | 2:1 | 50% | > measuring the SVO2 can be a surrogate for DO2:VO2 relationship, and used to identify when a patient has insufficient oxygen delivery to meet consumption requirements (hence popularity of pulmonary artery catheter in goal-directed sepsis resuscitation) ## Oxygen extraction ratio (SaO2 - SvO2)/ SaO2 normal is 20-25% O2 ER >30% warrants investigation, and O2 ER >40% suggests approaching anaerobic threshold DO2:VO2 ratio reflect balance btwn delivery and consumption; they do NOT represent a specific target for intervention ## How much Oxygen is really needed? - not perfectly well known, many variables - degree of tolerable hyoxemia varies - mitochondrial PO2 in cardiac and skeletal muscle normally btwn 1-5 mmHg; oxidative phosphorylation doesn't begin to fall until PO2 btwn 0.1 and 1 mmHg - climbers on Everest have had PaO2 in 24-28 mmHg range - in septic shock, primary problem is not delivery; it s inability of tissues to properly metabolise delivered oxygen. not fully understood, but can die even though SvO2 80% - in [[ARDSnet ventilator settings|ARDSNet trials]] PaO2 as low as 55 mmHg with SaO2 of 88% considered acceptable. - pts in trial with higher tidal volumes had higher oxygenation, but also higher mortality rate. ==suggests that preventing lung injury was more important than improving oxygenation==. - many interventions have been shown to improve oxygenation in mechanically ventilated pts, but not improve survival ## what about lactate? - most [[Lactic acidosis|lactate]] production in critical illness is NOT due to anaerobic metabolism - instead, it is due to ↑ pyruvate production in setting of impaired or altered glycolysis and gluconeogenesis - lactate is the preferred fuel for cardiac myocytes in the setting of adrenergic stimulation and is produced by *aerobic* cellular respiration - therefore, *lactate should be viewed as a non-specific marker of physiologic stress* - lactate is not a goal in itself ## Oxygen toxicity > give the patient just as much oxygen as they need; may be less than you think. > cardiac output has a much more significant effect on oxygen delivery than the saturation, and focus on signs of adequate or inadequate oxygen delivery rather than strictly the SaO2 and PaO2 - neonates with ↑ FiO2 a/w retinopathy and bronchopulmonary dysplasia - adults ↑ O2 a/w worse outcomes