All about Oxygen.

All about Oxygen

Introduction As you know… It is tasteless, ordorless
Supports combustion Vital for life May be mixed with other gases (He, CO2, N2, NO2) Comprises 21% of the atmopheric gas Normally mmHg in the blood, 100 in the lung, 40 in the venous blood

Introduction As you know… Critical temperature is 118.6 °C (-181 °F)
Can be stored as a liquid or gas Produced through fractional distillation Stored in cylinders or bulk supply systems Used in the home with concentrators Is a FDA drug, must be at least 99% pure, prescribed by a MD and approved by insurance before use by a pulmonary stress test

Introduction As you know…
Filtered in a concentrator by a molecular sieve, gives up to 90% O2 Semi permeable membranes give up to 40% O2 May be blended to form Heliox Given in either a high flow or low flow environment

Indications for Oxygen
Pneumothorax: Give 100% for Nitrogen washout COPD/chronic lung disease: Low concentrations (below 30%) Pulmonary Fibrosis: low flow, 25-40% O2 Trauma/emergencies: typically give 100% O2 with a non-rebreathing mask Ex: Car accident, hypovolemia

Indications for O2 Dyspnea Increased WOB/SOB MI (up to 4L)
CVA, chest pain, high altitude sickness, pulmonary edema, restrictive diseases… Orthopnea Tachypnea Pre-suctioning Platypnea Low Spo2, hypoxemia, anemia, hypoxia…. If a patient is not breathing: Must supply positive pressure with 100% O2 via bag/mask

Indications for O2 Without proper oxygenation a patient will develop hypoxemia which will produce symptoms of: Tachypnea Tachycardia Cyanosis Hypoxia/cell death Anoxia/brain death Heart failure Low CaO2, PaO2, SaO2, SpO2 Confusion, lethargy, weakness, malnutrition SOB/WOB/Dyspnea…

Indications Oxygen is used to: Decrease Ventilatory demand
Decrease Work of breathing Decrease Cardiac output Oxygen is required when: SaO2 less than 90% PaO2 less than 60 mm Hg

Determining the requirement of oxygen you must assess
Neurologic status (is there lethargy, anoxic events…) Pulmonary status (check all O2 indices and assessments) Cardiac status (HR, recent MI, poor EF, cardiac inflammation, valve problems…)

Why is Oxygen considered toxic?
High inspired oxygen concentrations cause toxicity by causing formation of oxygen free radicals (which damage tissues), and by causing absorption atelectasis and V/Q mismatch. The issue of oxygen toxicity has been topical for a generation, following the discovery that therapeutic oxygen causes blindness in premature babies (retrolental fibroplasias) with respiratory distress syndrome. In addition, it has been established that high inspired concentrations of oxygen may cause acute lung injury, probably 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. The extent of injury appears to depend on: 1. The FiO2, 2. The duration of exposure, 3. The barometric pressure under which exposure occurred. It appears that the critical FiO2 for toxicity is around 50% (1), above which lung recruitment maneuvers should be condidered (CPAP). High concentrations of inspired oxygen may cause absorption atelectasis. In addition high FiO2 may cause increased peripheral vascular resistance in congestive heart failure leading to reduced cardiac output.

How much oxygen is safe is a moot point. It is more important that you do not withhold life saving oxygen therapy than to be concerned about oxygen toxicity. It is, nonetheless, important that FiO2 is minimized to normalization of blood gas in intensive care patients: i.e. there is little to be gained in having a PaO2 of greater than 100mmHg. Often elevated oxygen requirements can be compensated for by appropriate patient positioning and increasing mean airway pressures to improve matching of ventilation and perfusion.

Oxygen Toxicity Oxygen can be toxic, with high concentrations (>50%) over 24 hours it can lead to: · Decreased DLCO · Decreased CL · Increase PAO2 – PaO2 gradient · Decreased VC · Bilateral infiltrates on CXR · Absorption atelectasis · O2 induced hypoventilation · Formation of hyaline membrane · ROP

Titrate O2!! Wean patients off O2 or to a safe FIO2 as soon as tolerated in order to avoid complications associated with O2 toxicity Acceptable SpO2 Ranges: COPD/Pulmonary Fibrosis: 88-92% Adults w/o Lung disease: >92% Pediatrics: >94% Recent MI: >94%

Wean O2 Discontinue O2 once the SpO2 reaches 92% on adult patients to avoid toxicity, wean FIO2 if SpO2 is greater than 92% Oxygen can be administered by low flow or high flow devices. High flow devices include venturi masks which can be affected by: Blocked entrainment ports (causes the devices total output flow to decreases, increases the percent of O2 from less entrained room air and it also changes the FIO2 received by the patient)

If a patient develops SOB on a venturi mask, assure that total flow is adequate, increase flow to mask as needed Venturi masks go up to 50% FIO2 Stable FIO2 requires the mask to provide all the gas needed by the patient during inspiration. They can provide variable FIO2 values under some clinical conditions. They always deliver O2 concentrations less than 100%. yield a set FIO2 only if their flow exceeds the patient's.

High Flow Oxygen Actual O2 provided by an air-entrainment system depends on: O2 input flow to the jet air-to-O2 ratio of the device resistance downstream from the jet Most low flow oxygen devices are not stable, they are easy to apply, disposable, have a low cost but are not stable, meaning they can come off the patients face easily.

Assessing O2 Remember oxygenation is reflected by looking at PaO2 while ventilation is reflected by looking at PaCO2 Selecting a proper Oxygen delivery system for a patient requires: Knowledge of general performance of the device Individual capabilities of the equipment

What is the Oxygen Cascade?
The oxygen cascade describes the process of declining oxygen tension from atmosphere to mitochondria The purpose of the cardio-respiratory system is to extract oxygen from the atmosphere and deliver it to the mitochondria of cells. Oxygen, being a gas, exerts a partial pressure, which is determined by the prevailing environmental pressure. At sea level, the atmospheric pressure is 760mmHg, and oxygen makes up 21% of inspired air: so oxygen exerts a partial pressure of 760 x 0.21 = 159mmHg. This is the starting point of the oxygen cascade, as one moves down through the body to the cell, oxygen is diluted down, extracted or otherwise lost, so that at cellular level the PO2 may only be 3 or 4mmHg.

Oxygen Cascade The first obstacle that oxygen encounters is water vapor, which humidifies inspired air, and dilutes the amount of oxygen, by reducing the partial pressure by the saturated vapor pressure (47mmHg). This will, obviously, affect the PIO2 (the partial pressure of inspired oxygen), which is recalculated as: ( ) x = 149mmHg.

Oxygen Cascade Air consists of oxygen and nitrogen, but as gas moves into the alveoli, a third gas, carbon dioxide, is present. The alveolar carbon dioxide level, the PACO2, is usually the same as the PaCO2, which can be measured by a blood gas analyzer. The alveolar partial pressure of oxygen PAO2 can be calculated from the following equation: PAO2 = PIO2 – PaCO2/R. R is the respiratory quotient, which represents the amount of carbon dioxide excreted for the amount of oxygen utilized, and this in turn depends on the carbon content of food (carbohydrates high, fat low). For now let us assume that the respiratory quotient is 0.8, the PAO2 will then be 149 – (40/0.8) = 100mmHg (approx).

Oxygen Cascade The next step is the movement of oxygen from alveolus to artery, and as you would expect, there is a significant gradient, usually 5 –10 mmHg, explained by small ventilation perfusion abnormalities, the diffusion gradient and physiologic shunt (from the bronchial arteries). Oxygen is progressively extracted thru the capillary network, such that the partial pressure of oxygen in mixed venous blood, PVO2, is approx 47mmHg.

Oxygen Cascade What is essential to understand about the oxygen cascade is that if there is any interference to the delivery of oxygen at any point in the cascade, significant injury can occur downstream. The most graphic example of this is ascension to altitude. At 19,000 feet (just above base camp at Mount Everest, the barometric pressure is half that at sea level, and thus, even though the FiO2 is 21%, the PIO2 is only 70mmHg, half that at sea level. Conversely, if the barometric pressure is increased, such as in hyperbaric chambers, the PIO2 will actually be higher.

Oxygen Cascade Four factors influence transmission of oxygen from the alveoli to the capillaries 1. Ventilation perfusion mismatch 2. Right to left shunt 3. Diffusion defects 4. Cardiac output. The amount of oxygen in the bloodstream is determined by the oxygen carrying capacity, the serum hemoglobin level, the percentage of this hemoglobin saturated with oxygen, the cardiac output and the amount of oxygen dissolved The PVO2 is determined by whole body oxygen demand, and the capacity of the tissues to extract oxygen. In sepsis there appears to be a fundamental abnormality of tissue oxygen extraction.

How much oxygen is in the blood?
The amount of oxygen in the blood is calculated using the formula: [1.34 x Hb x (SaO2/100)] x PO2 = 20.8ml Oxygen is carried in the blood in two forms: dissolved and bound to hemoglobin. Dissolved oxygen obeys Henry’s law – the amount of oxygen dissolved is proportional to the partial pressure. For each mmHg of PO2 there is ml O2/dl (100ml of blood). If this was the only source of oxygen, then with a normal cardiac output of 5L/min, oxygen delivery would only be 15 ml/min. Tissue O2 requirements at rest are somewhere in the region of 250ml/min, so this source, at normal atmospheric pressure, is inadequate.

Hemoglobin is the main carrier of oxygen. Each gram of hemoglobin can carry 1.34ml of oxygen. This means that with a hemoglobin concentration of 15g/dl, the O2 content is approximately 20ml/100ml. With a normal cardiac output of 5l/min, the delivery of oxygen to the tissues at rest is approximately 1000 ml/min: a huge physiologic reserve. Hemoglobin has 4 binding sites for oxygen, and if all of these in each hemoglobin molecule were to be occupied, then the oxygen capacity would be filled or saturated. This is rarely the case: under normal conditions, the hemoglobin is 97% to 98% saturated. The amount of oxygen in the blood is thus related to the oxygen saturation of hemoglobin.

Taking all of these factors into account, we can calculate the oxygen content of blood where the PO2 is 100mmHg, and the hemoglobin concentration is 15g/L: [1.34 x Hb x (saturation/100)] x PO2 = 20.8ml As one would expect, this figure changes mostly with the hemoglobin concentration: when the patient is anemic the oxygen content falls, when polycytemic, it rises. In either case the O2 saturation of hemoglobin may be 97 – 100%, but there may be a large discrepancy in content.

How much oxygen is delivered to the tissues per minute?
The delivery of oxygen to the tissues per minute is calculated from: DO2 = [1.34 x Hb x SaO2 + (0.003 x PaO2)] x Q The following is the single most commonly quoted equation in critical care, and it’s worth remembering

The Delivery of oxygen (DO2) to the tissues is determined by: The amount of oxygen in the blood: the oxygen binding capacity of hemoglobin x the concentration of hemoglobin x the saturation of hemoglobin + the amount of dissolved oxygen all Multiplied by the Cardiac Output (Q). The cardiac output is determined by preload, afterload and contractility. The hemoglobin concentration is determined by production, destruction and loss.

The SaO2 (the saturation of hemoglobin at arterial level with oxygen - as opposed to the SpO2 which is measured by pulse oximetery) is determined by: The oxygen saturation curve: which equates PaO2 (arterial oxygen tension) against SaO2. So if a patient has a hemoglobin of 15g/l, a cardiac output of 5L, a PaO2 of 100 and a SaO2 of 100%, what is his oxygen delivery? DO2 = [1.39 x 15 x (0.003 x PaO2)] x Q = 1000 ml

How much oxygen is extracted per minute?
Tissue oxygen extraction is calculated by subtracting mixed venous oxygen content from arterial oxygen content. The Fick equation is used to calculate the VO2, the oxygen consumption. This is computed by figuring out how much oxygen has been lost between the arterial side and the venous side of the circulation and multiplying the result by the cardiac output. In the following equation, VO2 is the oxygen consumption per minute, CaO2 is the content of oxygen in arterial blood, and CvO2 is the content of oxygen in venous blood: VO2 = Q x (CaO2-CvO2) mlO2/min

How much oxygen is extracted per minute?
The major difference between the two is obviously the hemoglobin saturation, which is roughly 100% on the arterial side and 75% on the venous side. Substituting inwards, where hemoglobin is 15g/dl: CaO2 is approx 20ml/100ml, CvO2 is 15ml/100ml: the difference is 5ml/100ml = 50 ml/l multiplied by a cardiac output of 5L = O2 consumption per minute is 250ml. So the mixed venous O2 saturation can be used to calculate the oxygen consumption: if SvO2 is decreasing, the O2 consumption is increasing.

What is the oxyhemoglobin dissociation curve and why is it important?
The Oxyhemoglobin dissociation curve describes the non-linear tendency for oxygen to bind to hemoglobin: below a SaO2 of 90%, small differences in hemoglobin saturation reflect large changes in PaO2 The oxyhemoglobin dissociation curve mathematically equates the percentage saturation of hemoglobin to the partial pressure of oxygen in the blood. The strange sigmoid shape of the curve relates to peculiar properties of the hemoglobin molecule itself

Hemoglobin and oxygen act a little like parents and children. When all are living at home (i.e. hemoglobin is fully saturated) then the parents don’t want any to leave: but once one has flown the nest (i.e. dissociated from hemoglobin) – parents find it progressively easier to let go. What this means that the conformation of the hemoglobin molecule depends on the number of molecules bound: as one molecule of oxygen becomes unbound, the affinity for the others falls [and vice-versa]. This is represented by the oxyhemoglobin dissociation curve.

The lack of linearity of the curve makes interpretation of the oxygen content of blood difficult. At higher saturation levels, above 90%, the curve is flat, but below this level the PaO2 declines sharply, such that at 75% saturation the PaO2 is about 47mmHg (mixed venous blood), at 50% saturation the PaO2 is 26.6mmHg, and at 25% saturation the PaO2 is a miserable 15mmHg.

The position of this curve may shift rightwards (lower saturation for given PaO2) or leftwards (higher saturation for a given PaO2). Certain circumstances make the blood more likely to dump oxygen into the tissues, and others make it more likely to cling on to oxygen. Active muscle needs more oxygen, so heat, exercise, acidosis, hypercarbia and increased 2,3-DPG all cause a shift in the curve rightwards – releasing oxygen. Conversely, when activity is minimal – such as in cold weather or during rest, when the tissues are cold, alkalotic, hypocarbic and low 2,3-DPG, then hemoglobin holds onto oxygen. The curve also shifts leftwards in carbon monoxide poisoning.

What problems are associated with right to left shunting?
Right to left shunting causes hypoxemia resistant to oxygen therapy. When blood passes through the lungs without coming in contact with air, a right to left shunt exists. This deoxygenated blood mixes with well oxygenated blood on the far side of the lung, and reduces the percentage saturation of hemoglobin. In all individuals a small physiologic shunt is present, principally arising from blood in the bronchial circulation. This has little effect on blood oxygen content. Larger shunts may cause significant problems, however.

The addition of mixed venous blood, slides the patient down the curve to the steep slope, where severe hypoxemia may result. Shunt classically does not respond to oxygen, although the administration of 100% oxygen may increase the dissolved oxygen content and increase the mixed venous oxygen saturation. The higher the SVO2, the less damaging a shunt is. The PaCO2 is usually normal, as the patient increases minute ventilation to blow off CO2 derived from the shunt, due to activation of chemoreceptors. The shunt equation is used to calculate the magnitude of a shunt: Qs/Qt = CcO2 – CaO2/CcO2 – CvO2

Qs/Qt = CcO2 – CaO2/CcO2 – CvO2 where CcO2 is the capillary oxygen content in the ideal capillary, CaO2 is the arterial oxygen content, and CvO2 is the mixed venous oxygen content. As one would expect, the greater the magnitude of the shunt, the larger the PAO2 – PaO2 difference.

A 17 year old male presents to the emergency room after being stabbed in the chest, on chest x-ray his right lung was fully collapsed, and yet his SpO2 was 94% on room air - why?

What is hypoxic pulmonary vasoconstriction?
Hypoxic Pulmonary Vasoconstriction is a physiologic protective mechanism which prevents right to left shunting of blood. Right to left shunt causes hypoxemia unresponsive to oxygen therapy One would expect that this patient would have a 50% shunt due to perfusion but no ventilation of the right lung; this does not happen. Hypoxic pulmonary vasoconstriction (HPV) takes place. Many of the tissues in the body are capable of regulating their own blood flow – the heart, the kidney, the brain and the gut all autoregulate blood flow

It appears that HVP is a similar mechanism within the lung, to prevent right to left intrapulmonary shunting, and thus the presence of deoxygenated blood in the peripheral circulation. This process is most florid in utero, when blood is diverted away from the lungs through the ductus arteriosis, due to high pulmonary arterial pressures. We know that pulmonary smooth muscle cells are extremely sensitive to alveolar oxygen tensions, but the mechanism of vasoconstriction is unknown. HPV is probably multifactorial in origin and modulated by a variety of endothelium dependent factors (nitric oxide, endothelin, prostacyclin etc).

Certain pharmacological interventions and disease processes interfere with HPV: general anesthesia with volatile agents such as isoflurane, and the use of systemic vasodilators such as sodium nitroprusside and prostacyclin, reverse HPV and may cause ventilation-perfusion mismatch. Acute lung injuries and, in particular, lung contusions, may have a similar effect. The result is ventilation-perfusion mismatch and possible right to left shunting of deoxygenated blood. The treatment is recruitment of collapsed alveoli using continuous positive airway pressure (CPAP), and positioning the patient away from the injury side (good side down, always).

V/Q mismatch Ventilation perfusion mismatch occurs along a spectrum: on one end alveoli are ventilated but not perfused (pure dead space ventilation), and on the other end alveoli are perfused but not ventilated (pure shunt). The best ventilation perfusion (V/Q) ratios occur in dependent regions of the lung, due to the preferential effect of gravity on both ventilation and perfusion. The non dependent regions are relatively better ventilated than perfused (alveolar dead space). Extensive ventilation perfusion mismatch occurs due to lung injuries, whether due to consolidation (filling alveoli with exudates), perioperative atelectasis, or “acute lung injury” where there is alveolar edema and capillary microthrombosis.

V/Q mismatch Hypoxemia due to ventilation-perfusion mismatch can usually be reversed with application of supplemental oxygen. Where there is extensive atelectasis due to gas absorption or mucus plugging, the treatment is oxygen, bronchial toilet and perhaps CPAP, to recruit collapsed airways. Stiff lungs (low compliance) may induce an overwhelming workload to breathing, and additional inspiratory support may be required to reduce workload and improve V/Q matching

What is “absorption atelectasis”?
Absorption atelectasis refers to the tendency for airways to collapse if proximally obstructed. Alveolar gases are reabsorbed; this process is accelerated by nitrogen washout techniques. Oxygen shares alveolar space with other gases, principally Nitrogen. Nitrogen is poorly soluble in plasma, and thus remains in high concentration in alveolar gas. If the proximal airways are obstructed, for example by mucus plugs, the gases in the alveoli gradually empty into the blood along the concentration gradient, and are not replenished: the alveoli collapse, a process known as atelectasis

What is “absorption atelectasis”?
This is limited by the sluggish diffusion of Nitrogen. If nitrogen is replaced by another gas, that is if it is actively “washed out” of the lung by either breathing high concentrations of oxygen, or combining oxygen with more soluble nitrous oxide in anesthesia, the process of absorption atelectasis is accelerated. It is important to realize that alveoli in dependent regions, with low V/Q ratios, are particularly vulnerable to collapse.

What is pathological supply dependence on oxygen?
The mixed venous oxygen saturation is a measurement of oxygen consumption, made using a pulmonary artery catheter (the measurements are made from the pulmonary artery, and are thus accurate). The SvO2 (mixed venous oxygen saturation) is proportional to SaO2 – VO2/Q x Hb (VO2 is the venous oxygen content).

We know that we can go from being completely sedentary to taking high impact exercise without developing tissue hypoxia. This is because we have a physiologic reserve. Under normal conditions, during exercise, if oxygen demand is increased, supply is increased also – by increasing minute ventilation and cardiac output. But what happens if, for example, oxygen delivery starts to fall off (e.g. in a patient who has progressively worsening respiratory or cardiovascular function)? What actually happens, in normal people, is that we compensate for this lower O2 delivery by making use of our physiologic reserve, we redistribute blood preferentially to the tissues that need them and the amount of oxygen extracted (extraction ratio) increases. Eventually reserve runs out and a critical point (point A on the diagram above) is reached: there just isn’t enough O2 to match supply, and anaerobic glycolysis takes place.

This is known as “physiological dependence of VO2 on DO2”, and can be measured by an increase in arterial lactate concentration. This plateau in VO2 is maintained by increasing the extraction ratio for oxygen (O2ER). Blood flow is redistributed to match local demand for oxygen. The meditors for this process are multiple, the most important of which are the autonomic nervous system and nitric oxide. The critical O2ER is the point where anaerobic glycolysis takes place. The critical DO2 in health is about 7 to 10ml/kg/min.

In pathological circumstances, such as systemic sepsis, this whole protective system falls apart: in diseases that affect the microcirculation, there is a loss of O2 extraction capacity. There is a school of thought that believes that DO2 needs to be maintained at a higher level that in health, as the tissues are less able to efficiently extract O2 (1;2) . There is a higher critical DO2 (to 12ml/kg/min) and pathological dependence of VO2 on DO2. A hypothesis was formed that by increasing the DO2 (supernormalization) by increasing cardiac output and oxygen carriage in sepsis, then oxygen extraction would improve. Randomized controlled trials have been disappointing. We now believe that the inability to extract oxygen occurs on the demand side, due to microcirculatory abnormalities, rather that overall oxygen delivery.

How much oxygen do I give?
The objective of oxygen therapy is to give the patient as much oxygen as is required to return the PaO2 to what is normal for the particular patient. There is no secret to this – you give as much oxygen as is required to return the PaO2 to what is normal for the particular patient. You perform a therapeutic maneuver – giving Oxygen, and you measure the result, by performing serial blood gases. There is nothing to be gained by giving too much oxygen, and a huge amount to be lost by not giving enough.

The initial inspired concentration of oxygen depends on the clinical circumstances – if the patient is only mildly hypoxemic, saturating in the late 80s, then small amounts of supplemental oxygen given by nasal cannula are all that is necessary. However, if the patient is in-extremis, then always start with 100% (or thereabouts) and work downwards. Shouldn’t I be careful about the amount of oxygen that I give COPD patients?

There is a universal misnomer that if you give too much oxygen to patients with COPD that they stop breathing, and hence medical and nursing students are often taught that COPD patients should not be given more than 28% oxygen because their respiratory drive is oxygen dependent (due to chronic CO2 retention) and they will lose their stimulus to breath. Physicians will cite rising CO2 levels in patients treated with oxygen as evidence of this

There is a fundamental flaw in this theory: It is the blood oxygen content that is important, not the inspired fraction. Patients, depending on the extent of disease, will have differing extents of ventilation-perfusion mismatch and diffusion defects: the patient needs enough inspired oxygen to return the PaO2 to what is normal for them, and the way to establish this is by starting high and working downwards with serial blood gases.

We know that high CO2 levels are well tolerated by the body, but hypoxia is not: withholding oxygen therapy for fear of hypercarbia is negligent. It is not clear that such hypercarbia results, in any case, from hypoventilation: a number of studies have demonstrated that the increase in PaCO2 after administration of oxygen is due mainly to an increase in the ratio of dead space to tidal volume (Vd/Vt). This is probably due to reversal of hypoxic pulmonary vasoconstriction. Moreover, the increase in oxygenated hemoglobin leads to an increase in CO2 release by way of the Haldane effect.

How do I administer Oxygen?
Oxygen is given thru fixed and variable performance devices. Fixed performance devices deliver a flow of oxygen equal to or in excess of peak inspiratory flow Variable performance devices use the deadspace of the nasopharynx or face masks as a reservoir of oxygen. They cannot deliver high inspired concentrations of oxygen.

Oxygen can be delivered to the upper airway by a variety of devices There are two types of devices – variable performance devices and fixed perfomance devices. The differentiation is based on the difference between the delivered concentration of oxygen FDO2 and the actual inspired concentration FiO2. Performance is based on matching the flow rate of gas leaving the device with the inspiratory flow rate entering the patient

Take a deep breath in: you have probably just inspired 1 liter of air in about 1 second. Your inspiratory flow rate is thus approximately 60 liters per minute during this deep breath. Every breath you take varies in depth and volume, but if you were in respiratory failure you may well require flow rates of this magnitude (or more). To be guaranteed a FiO2 appropriate to your flow demand, a fixed performance flow-generating device must be placed at your airway with a flow rate of 60 or so liters of oxygen-air (mixed as required) to satisfy demand. To be a fixed performance device, the gas flow must exceed the patient’s peak inspiratory flow.

Variable performance devices fit into two categories, nasal cannula and facemasks. The premise behind nasal cannula is to use the dead space of the nasopharynx as a reservoir for oxygen. When the patient inspires, entrained air mixes with the reservoir air and the inspired gas is enriched. Obviously, the FIO2 depends on the magnitude of flow of oxygen, the patient’s minute ventilation and peak flow. For most patients, each addition 1liter per minute of O2 flow with nasal cannula represents an increase in the FIO2 by 4%. So 1 liter is 24%, 2 liters is 28% and so on. At 6 liters (44%), it is not possible to raise the FIO2 further, due to turbulence, in the tubing and in the airway.

There are a couple of problems with nasal cannula: if they are not positioned at the nares, they are useless. Disorientated patients appear to be remarkably successful at dislodging cannula. Secondly, the effectiveness may be disrupted by the pattern of breathing: there appears to be little difference whether the patient is a mouth or a nose breather, but it is preferable if the patient exhales through his/her mouth rather than nose, so the reservoir is maintained. The big advantage of nasal cannula is comfort for the patient – they can eat and speak easily while receiving oxygen.

Standard oxygen masks provide a reservoir for oxygen, but the FIO2 is difficult to calculate unless calibrated Venturi devices are attached. With Venturis, there are slits in the oxygen delivery system which become smaller or larger depending whether a high or low FIO2 is required. The rate of delivery of oxygen is calibrated for the size of the Venturi and amount of mixing therein. For example, a 50% oxygen Venturi requires 15L/min fresh gas flow. Standard masks struggle to provide an FIO2 of greater than 50%. A non rebreather reservoir bag can be attached to the facemask, to provide a larger reservoir (the bag fills when the patient is not actively inspiring), the two liter capacity should, in theory at least, allow the patient to inspire 100% oxygen.

Clinical Scenario 1 An 18 year old male is brought to the recovery room following an appendectomy. He has just been extubated. He is awake and breathing normally, but his SpO2 is 88%. You administer 60% oxygen, and after a few moments his SpO2 increases to 99%. What has just happened?

Clinical Scenario 1 An 18 year old male is brought to the recovery room following an appendectomy. He has just been extubated. He is awake and breathing normally, but his SpO2 is 88%. You administer 60% oxygen, and after a few moments his SpO2 increases to 99%. What has just happened? This is a process known as diffusion hypoxia, which is not uncommon after anesthesia with nitrous oxide. This agent is floods back into the alveoli from the blood at termination of anesthesia, along the concentration gradient, and displaces oxygen. As the partial pressure of oxygen in the alveoli has fallen, so too has the tension of oxygen in the blood. The treatment is to increase the FiO2, which, according to the alveolar gas equation, will increase the PAO2. Patients who hypoventilate, such as those given opioids, have increased alveolar levels of CO2 and may require supplemental oxygen

Scenario 2 A 59 year old female undergoes abdominal surgery. She is extubated and returned from the recovery room to the floor. She becomes moderately short of breath three hours later. The nurse applies a pulse-oximeter. Her SpO2 is 89%. She treats the patient with 40% oxygen and calls you. When you arrive, the patient’s SpO2 is 94%. What is the cause of this patient’s hypoxemia and what is your plan of management?

Scenario 2 59 year old female undergoes abdominal surgery. She is extubated and returned from the recovery room to the floor. She becomes moderately short of breath three hours later. The nurse applies a pulse-oximeter. Her SpO2 is 89%. She treats the patient with 40% oxygen and calls you. When you arrive, the patient’s SpO2 is 94%. What is the cause of this patient’s hypoxemia and what is your plan of management? This patient has atelectasis, presumably in the dependent regions of her lungs, as a result of anesthesia and surgery. This is manifesting itself as ventilation-perfusion abnormalities. The treatment is supplemental oxygen, chest physical therapy, and mobilization, hyperinflation therapy

Scenario 3 You are called to the emergency room (ER). A 62 year old male with a history of chronic bronchitis has been admitted with a lower respiratory tract infection. The ER resident is requesting admission to intensive care for mechanical ventilation. On examination, the patient is tachypneic and cyanosed. His blood gas is pH 7.34, PCO2 54, PO2 45, HCO3 30, BE-2. You request a piece of information, perform a therapeutic maneuver and 30 minutes later the patient’s blood gas is: pH 7.32 pCO2 60 PO2 55 HCO3 31 BE 0. The nurse wishes to reduce the FiO2. What information did you look for? What therapeutic maneuver did you perform, and what do you plan to do about the last blood gas?

Scenario 3 What information did you look for? What therapeutic maneuver did you perform, and what do you plan to do about the last blood gas? What you were interested in was the patient’s baseline blood gas (from a previous admission): it was pH 7.38 PCO2 55 PO2 55 HCO3 32. The patient is hypoxemic at baseline, and retains CO2. You increased the FiO2 to 40%, and have returned the PaO2 to baseline for this patient. The nurses concern about the blood gas is inappropriate: this relates to the widely held misconception that inspired oxygen tension should be minimized in COPD patients to prevent loss of respiratory drive. This is incorrect, even if there is some truth in the basic science (questionable), chemoreceptors respond to arterial oxygen tension, not what is given at the mouth. In this case, the patients PaO2 is normal for him, and he is receiving the appropriate amount of oxygen. The raised CO2 relates to ventilation-perfusion mismatch, resulting from the underlying acute injury, and release of hypoxic pulmonary vasoconstriction. The administration of oxygen may have increased the amount of dead space ventilation. In addition, raised PACO2 displaces O2 at alveolar level, requiring a higher FiO2.

Scenario 4 A 78 year old male is admitted with a six month history of shortness of breath, ankle edema, orthopnea, a productive cough, hoarseness and 30-40lb weight loss. He has a palpable mass in his abdomen, which turns out to be colonic cancer. As part of his preoperative work up, a blood gas is performed: pH 7.42 PaCO2 36 PaO2 41 SaO2 78%. He is put on 100% oxygen, has a chest x-ray performed, which is normal, and a spiral CT of his thorax, which also appears normal. His blood gas on 100% oxygen is: pH 7.46, PaCO2 36, PaO2 42, SaO2 78%. What do you think is wrong with this patient?

Scenario 4 What do you think is wrong with this patient?
Hypoxemia refractory to oxygen therapy is a right to left shunt until otherwise proven. This patient underwent echocardiography which showed a markedly enlarged right ventricle with reduced right ventricular function; there was reduced global left ventricular function. On cardiac catheterization this patient had a patent foramen ovale, a right to left shunt (with Eisenmenger physiology), and equalization of pulmonary and systemic blood pressures. Of his 8 liter cardiac output, 6 litres were shunting right to left. He was unsuitable for surgery.

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