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Oxygen Delivery and Consumption in the Critically Ill R M Leach, D F Treacher

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Oxygen Delivery and Consumption in the Critically Ill R M Leach, D F Treacher Downloaded from thorax.bmj.com on January 11, 2012 - Published by group.bmj.com 170 REVIEW SERIES The pulmonary physician in critical care c 2: Oxygen delivery and consumption in the critically ill R M Leach, D F Treacher ............................................................................................................................. Thorax 2002;57:170–177 Early detection and correction of tissue hypoxia is OXYGEN TRANSPORT essential if progressive organ dysfunction and death are Oxygen transport describes the process by which to be avoided. However, hypoxia in individual tissues oxygen from the atmosphere is supplied to the tissues as shown in fig 1 in which typical values or organs caused by disordered regional distribution of are quoted for a healthy 75 kg individual. The oxygen delivery or disruption of the processes of cellular phases in this process are either convective or dif- oxygen uptake and utilisation cannot be identified from fusive: (1) the convective or “bulk flow” phases global measurements. Regional oxygen transport and are alveolar ventilation and transport in the blood from the pulmonary to the systemic microcircula- cellular utilisation have an important role in maintaining tion: these are energy requiring stages that rely on tissue function. When tissue hypoxia is recognised, work performed by the respiratory and cardiac treatment must be aimed at the primary cause. “pumps”; and (2) the diffusive phases are the movement of oxygen from alveolus to pulmonary Supplemental oxygen may be life saving in some capillary and from systemic capillary to cell: these situations but cannot correct inadequate oxygen delivery stages are passive and depend on the gradient of caused by a low cardiac output or impaired ventilation. oxygen partial pressures, the tissue capillary den- sity (which determines diffusion distance), and Recent innovations include artificial oxygen carrying the ability of the cell to take up and use oxygen. proteins and “haemoglobin” molecules designed to This review will not consider oxygen transport improve tissue blood flow by reducing viscosity. within the lungs but will focus on transport from Regulating cell metabolism using different substrates or the heart to non-pulmonary tissues, dealing spe- cifically with global and regional oxygen delivery, drugs has so far been poorly explored but is an exciting the relationship between oxygen delivery and area for further research. A minimum level of global consumption, and some of the recent evidence oxygen delivery and perfusion pressure must be relating to the uptake and utilisation of oxygen at the tissue and cellular level. maintained in the critically ill patient with established “shock”, but advances in the understanding and control of regional distribution and other “downstream” factors OXYGEN DELIVERY Global oxygen delivery (DO2) is the total amount in the oxygen cascade are needed to improve outcome of oxygen delivered to the tissues per minute irre- in these patients. spective of the distribution of blood flow. Under .......................................................................... resting conditions with normal distribution of cardiac output it is more than adequate to meet the total oxygen requirements of the tissues (VO2) and ensure that aerobic metabolism is main- lthough traditionally interested in conditions tained. affecting gas exchange within the lungs, the Recognition of inadequate global DO2 can be Arespiratory physician is increasingly, and difficult in the early stages because the clinical appropriately, involved in the care of critically ill features are often non-specific. Progressive meta- patients and therefore should be concerned with bolic acidosis, hyperlactataemia, and falling O systemic as well as pulmonary oxygen transport. mixed venous oxygen saturation (Sv 2), as well as Oxygen is the substrate that cells use in the great- organ specific features such as oliguria and est quantity and upon which aerobic metabolism impaired level of consciousness, suggest inad- equate DO . Serial lactate measurements can indi- and cell integrity depend. Since the tissues have no 2 cate both progression of the underlying problem storage system for oxygen, a continuous supply at a rate that matches changing metabolic require- ments is necessary to maintain aerobic metabolism ................................................. and normal cellular function. Failure of oxygen Abbreviations: SO , oxygen saturation (%); PO , oxygen See end of article for supply to meet metabolic needs is the feature com- 2 2 partial pressure (kPa); PIO , inspired PO ;PEO , mixed authors’ affiliations 2 2 2 mon to all forms of circulatory failure or “shock”. expired PO ;PECO , mixed expired PCO ;PAO , alveolar ....................... 2 2 2 2 Prevention, early identification, and correction of PO2;PaO2, arterial PO2;SaO2, arterial SO2;SvO2, mixed O O Correspondence to: tissue hypoxia are therefore necessary skills in venous S 2; Qt, cardiac output; Hb, haemoglobin; Ca 2, arterial O content; CvO , mixed venous O content; VO , Dr D Treacher; managing the critically ill patient and this requires 2 2 2 2 David.Treacher@ oxygen consumption; VCO2,CO2 production; O2R, oxygen an understanding of oxygen transport, delivery, gstt.sthames.nhs.uk return; DO2, oxygen delivery; Vi/e, minute volume, ....................... and consumption. inspiratory/expiratory. www.thoraxjnl.com Downloaded from thorax.bmj.com on January 11, 2012 - Published by group.bmj.com Oxygen delivery and consumption in the critically ill 171 PaO2 (13) (P50) SaO2 (97) CaO2 (200) DO2 Qt Hb (150) Qt (5) (1000) Diffusion of O2 in tissues LV Inspired (dry) LA Capillary PIO2 (21) venous arterial VO2 (5.3) (13) (250) Interstitial Vi/e (5.32.7) Lungs shunt (5) Intracellular (2.71.3) Expired (dry) PEO2 (15.9) RV PECO2 (4.2) Mitochondrial RA (1.30.7) PAO2 VCO2 (14) (200) Q O R t Hb (150) Q (5) 2 t (750) PvO2 (5.3) (P50) SvO2 (75) CvO2 (150) Figure 1 Oxygen transport from atmosphere to mitochondria. Values in parentheses for a normal 75 kg individual (BSA 1.7 m2) breathing air (FIO2 0.21) at standard atmospheric pressure (PB 101 kPa). Partial pressures of O2 and CO2 (PO2,PCO2) in kPa; saturation in %; contents (CaO2, CvO2) in ml/l; Hb in g/l; blood/gas flows (Qt, Vi/e) in l/min. P50 = position of oxygen haemoglobin dissociation curve; it is PO2 at which 50% of haemoglobin is saturated (normally 3.5 kPa). DO2 = oxygen delivery; VO2 = oxygen consumption, VCO2 = carbon dioxide production; PIO2, PEO2 = inspired and mixed expired PO2;PEC O2 = mixed expired PCO2;PAO2 = alveolar PO2. and the response to treatment. Raised lactate levels increases markedly above 100 g/l. This impairs flow and (>2 mmol/l) may be caused by either increased production or oxygen delivery, particularly in smaller vessels and when the reduced hepatic metabolism. Both mechanisms frequently perfusion pressure is reduced, and will therefore exacerbate apply in the critically ill patient since a marked reduction in tissue hypoxia.1 Recent evidence suggests that even the DO2 produces global tissue ischaemia and impairs liver traditionally accepted Hb concentration for critically ill function. patients of approximately 100 g/l may be too high since an Table 1 illustrates the calculation of DO2 from the oxygen improved outcome was observed if Hb was maintained content of arterial blood (CaO2) and cardiac output (Qt) with between 70 and 90 g/l with the exception of patients with cor- examples for a normal subject and a patient presenting with onary artery disease in whom a level of 100 g/l remains hypoxaemia, anaemia, and a reduced Qt. The effects of provid- appropriate.2 With the appropriate Hb achieved by transfu- ing an increased inspired oxygen concentration, red blood cell sion, and since the oxygen saturation (SaO2) can usually be transfusion, and increasing cardiac output are shown. This maintained above 90% with supplemental oxygen (or if emphasises that: (1) DO2 may be compromised by anaemia, necessary by intubation and mechanical ventilation), cardiac oxygen desaturation, and a low cardiac output, either singly or output is the variable that is most often manipulated to in combination; (2) global DO2 depends on oxygen saturation achieve the desired global DO2 levels. rather than partial pressure and there is therefore little extra benefit in increasing PaO2 above 9 kPa since, due to the OXYGEN CONSUMPTION sigmoid shape of the oxyhaemoglobin dissociation curve, over Global oxygen consumption (VO2) measures the total amount 90% of haemoglobin (Hb) is already saturated with oxygen at of oxygen consumed by the tissues per minute. It can be that level. This does not apply to the diffusive component of measured directly from inspired and mixed expired oxygen oxygen transport that does depend on the gradient of oxygen concentrations and expired minute volume, or derived from partial pressure. the cardiac output (Qt) and arterial and venous oxygen Although blood transfusion to polycythaemic levels might contents: × seem an appropriate way to increase DO2, blood viscosity VO2 =Qt (CaO2 –CvO2) Table 1 Relative effects of changes in PaO2, haemoglobin (Hb), and cardiac output (Qt) on oxygen delivery (DO2) Dissolved O2 FIO2 PaO2 (kPa) SaO2 (%) Hb (g/l) (ml/l) CaO2 (ml/l) Qt (l/min) DO2 (ml/min) DO2 (% change)‡ Normal* 0.21 13.0 96 130 3.0 170 5.3 900 0 Patient† 0.21 6.0 75 70 1.4 72 4.0 288 – 68 ↑ FIO2 0.35 9.0 92 70 2.1 88 4.0 352 + 22 ↑↑ FIO2 0.60 16.5 98 70 3.8 96 4.0 384 + 9 ↑Hb 0.60 16.5 98 105 3.8 142 4.0 568 +48 ↑Qt 0.60 16.5 98 105 3.8 142 6.0 852 +50 × × × × DO2 =CaO2 Qt ml/min, CaO2 =(Hb SaO2 1.34) + (PaO2 0.23) ml/l where FIO2 = fractional inspired oxygen concentration; PaO2,SaO2,CaO2 = partial pressure, saturation and content of oxygen in arterial blood; Qt = cardiac output. 1.34 ml is the volume of oxygen carried by 1 g of 100% × saturated Hb. PaO2 (kPa) 0.23 is the amount of oxygen in physical solution in 1 l of blood, which is less than <3% of total CaO2 for normal PaO2 (ie <14 kPa).
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