Louis Al-Saleem 5/4/13 OXYGEN PHYSIOLOGY AND PULSE OXIMETRY A very experienced senior resuscitation nurse approached me at work recently, and asked if there was any circulating academic evidence about removing oxygen from critically ill patients. After I had picked myself up from off the floor, I enquired further and to my horror, she reported several of the doctors from ED had been attending MET calls (Rapid Response Calls) and had been rebuking the use of high flow oxygen, and in some cases even removing it. She then recalled such paradigms she had heard from these death dealers as: They don t need oxygen, their sats are ok... and: Oxygen won t help them and the old favourite: The toxicologists don t like it (anyone who has worked at the Calvary Mater ED knows EXACTLY what I mean). Time to dispel this silliness with some basic oxygen physiology: The P02 of inspired air at sea level is: (760-47) x 0.21 = ~150 mmhg Barometric Pressure mmhg - Water Vapour Pressure mmhg X 02 fraction in air = P02 inspired air at sea level.
The normal physiological oxygen cascade is such that from inspired air in the atmosphere to the mitochondria where the oxygen is utilized, the partial pressure drops significantly so that the tissue p02 is remarkable lower than the alveolar p02. So small changes in ALVEOLAR p02 make for big differences in TISSUE p02. Oxygen is carried in the blood in 2 ways: 1. Dissolved (in accordance with Henry s Law, equivocating to 3ml O2 per litre of plasma). But our bodies require up to 3000ml/minute so this isn't really good enough. 2. Attached to Haemoglobin. The main transport mechanism. Increases the blood carrying capacity by 70 times ( round 208ml O2 / litre of blood).
Hypoxia - An abnormally low P02 in the tissues. There are 4 basic types: Hypoxic Hypoxia (decreased absorption from the lung) Decreased p02 in the blood caused by lung disease and poor gas exchange). This is the most common. Anaemic Hypoxia (decreased oxygen carrying capacity of the blood). Circulatory Hypoxia (Circulatory failure from local obstruction or systemic shock meaning reduced oxygen delivery to the tissues). Histiocytic Hypoxia (decreased utilization of oxygen by the tissues, such as in cyanide poisoning where cytochrome oxidase is inhibited in the mitochondria). Hypoxic hypoxia is the most common type in clinical practice and encompasses hypoventilation, shunt, diffusion abnormalities and V/Q mismatching. For the most part, these are correctable by applying supplemental oxygen to increase the alveolar or inspired P02 thus affecting the cascade at the top. The exception is shunt, where blood is bypassing the lungs and emptying into the systemic circulation deoxygenated although supplemental oxygen can help to a small degree but increasing the amount of dissolved oxygen carried by the plasma.
They don t need oxygen, their sats are ok... Yup. This is a really good way to get yourself smacked in the face. Pulse Oximetry is a measurement of how saturated the haemoglobin molecules in the blood are with oxygen. It works on the theory that pulsatile blood absorbance or IR or red light changes with regard to the degree of oxygenation. From the Hb-02 dissociation curve, we can see that approximations can be made between Sa02 and p02. But: Pulse Oximetry does not tell you ANYTHING about Tissue Hypoxia It does not take into account anaemia, dyshbaemias, CO poisoning. It s limited in poor perfusion states and shock. It s proven to be inaccurate at Sp02 < 80%
Pulse Ox Latency In a normal patient, Sp02 pulse ox reading is 30-60 seconds in the past. In a shocked patient it can be up to 3 minutes in the past. It as simple as the fact that the blood in the extremity having not been in the central circulation for some time. Quantitative waveform ETC02 is a more useful reading in terms of monitoring ventilation. Is too much oxygen bad for you? We can universally agree that oxygen is good for you. But there can be dangers of giving too much for too long. We know that in experiments, guinea pigs placed in 100% O2 at atmosphere pressure for 48 hours develop pulmonary oedema. In humans, after 30minutes of 100% O2 evidence of impaired gas exchange has been demonstrated. Volunteers who breathe 100% O2 at atmospheric pressure for 24 hours complain of substernal distress aggravated by deep breathing and diminished vital capacity due to a phenomenon known as Absorption Atelectasis (rapid alveolar collapse due to large diffusion gradients between alveoli and the blood). High inspired concentrations of oxygen for prolonged periods can also cause acute lung injury due to oxygen free radical production - superoxide, hydroxyl, hydrogen peroxide and singlet O2 molecules. These agents damage biomolecules such as membrane lipids, enzymes and nucleic acids. Premature babies breathing 100% oxygen develop blindness because of retrolental fibroplasia due to local vasoconstriction caused by high P02. This study even suggested that high flow oxygen may cause harm to a subset of patients, thus many coronary units advocate moderate to low supplemental oxygen delivery only. Emerg Med J. 2011 Nov;28(11):917-23. doi: 10.1136/emj.2010.103564. Epub 2011 Feb 23. Oxygen therapy for acute myocardial infarction: a systematic review and meta-analysis. Burls A, Cabello JB, Emparanza JI, Bayliss S, Quinn T. Department of Primary Health Care, University of Oxford, Oxford, UK
So In Summary: Oxygen is good for you almost all of the time. Peripheral Pulse Oximetry does not reflect tissue hypoxia. The Sats probe is a real life time machine, only not based on a Delorean. Don t gauge a patients oxygen requirements by pulse oximetry reading, it doesn't make sense. Be aware of dangers of 100% oxygen for prolonged periods, but remember in a ward or ED setting, a non-rebreather mask on 15L/min wall oxygen delivers you around 50% on a good day. Don t say They don t need oxygen, their sats are ok, The toxicologists don t like it and don t take oxygen off critically ill patients. It makes you look like a total dummy. References Appel PL, Shoemaker WC. Relationship of oxygen consumption and oxygen delivery in surgical patients with ARDS. Chest 1992; 102(3):906-911. Shoemaker WC, Appel PL, Kram HB. Role of oxygen debt in the development of organ failure sepsis, and death in high-risk surgical patients. Chest 1992; 102(1):208-215. Crossley DJ, McGuire GP, Barrow PM, Houston PL. Influence of inspired oxygen concentration on deadspace, respiratory drive, and PaCO2 in intubated patients with chronic obstructive pulmonary disease. Crit Care Med 1997; 25(9):1522-1526. Register SD, Downs JB, Stock MC, Kirby RR. Is 50% oxygen harmful? Crit Care Med 1987; 15(6): 598-601. West, J.B. Pulmonary Physiology, the essentials 5th ed, Lippincott Williams and Wilkins, 1998