Systematic review. Tibbles, Patrick M. Thom, Stephen R. Suppl 1 : S. Gehring, Hartmut, et al. Error assessment based on differences among identical blood gas analyzer devices of five manufacturers. Toffaletti, John, and Willem G.
Braunitzer, G. Gregory, I. Legrand, Matthieu, et al. Oxygen carrying capacity of whole blood. Previous chapter: Perfusion-limited and diffusion-limited transfer of gases Next chapter: Fraction of oxygenated haemoglobin.
All SAQs related to this topic. All vivas related to this topic. It has come up several times in the past papers: Question 1 from the first paper of where it formed half of the answer to the question, "outline the determinants of oxygen delivery to the tissues". References Chapler, C.
This is painful when it occurs. Thalassemia is a rare genetic disease caused by a defect in either the alpha or the beta subunit of Hb. Patients with thalassemia produce a high number of red blood cells, but these cells have lower-than-normal levels of hemoglobin.
Therefore, the oxygen-carrying capacity is diminished. Sickle cell anemia : Individuals with sickle cell anemia have crescent-shaped red blood cells. Diseases such as this one cause a decreased ability in oxygen delivery throughout the body. Dissolution, hemoglobin binding, and the bicarbonate buffer system are ways in which carbon dioxide is transported throughout the body. Carbon dioxide molecules are transported in the blood from body tissues to the lungs by one of three methods:.
Several properties of carbon dioxide in the blood affect its transport. First, carbon dioxide is more soluble in blood than is oxygen. About 5 to 7 percent of all carbon dioxide is dissolved in the plasma. Second, carbon dioxide can bind to plasma proteins or can enter red blood cells and bind to hemoglobin. This form transports about 10 percent of the carbon dioxide.
When carbon dioxide binds to hemoglobin, a molecule called carbaminohemoglobin is formed. Binding of carbon dioxide to hemoglobin is reversible. Therefore, when it reaches the lungs, the carbon dioxide can freely dissociate from the hemoglobin and be expelled from the body.
Third, the majority of carbon dioxide molecules 85 percent are carried as part of the bicarbonate buffer system. In this system, carbon dioxide diffuses into the red blood cells. Carbonic anhydrase CA within the red blood cells quickly converts the carbon dioxide into carbonic acid H 2 CO 3.
Since carbon dioxide is quickly converted into bicarbonate ions, this reaction allows for the continued uptake of carbon dioxide into the blood, down its concentration gradient. The newly-synthesized bicarbonate ion is transported out of the red blood cell into the liquid component of the blood in exchange for a chloride ion Cl- ; this is called the chloride shift. Each subunit surrounds a central heme group that contains iron and binds one oxygen molecule, allowing each hemoglobin molecule to bind four oxygen molecules.
Molecules with more oxygen bound to the heme groups are brighter red. As a result, oxygenated arterial blood where the Hb is carrying four oxygen molecules is bright red, while venous blood that is deoxygenated is darker red.
Figure 1. The protein inside a red blood cells that carries oxygen to cells and carbon dioxide to the lungs is b hemoglobin. Hemoglobin is made up of four symmetrical subunits and four heme groups. Iron associated with the heme binds oxygen. It is the iron in hemoglobin that gives blood its red color. It is easier to bind a second and third oxygen molecule to Hb than the first molecule.
This is because the hemoglobin molecule changes its shape, or conformation, as oxygen binds. The fourth oxygen is then more difficult to bind. The binding of oxygen to hemoglobin can be plotted as a function of the partial pressure of oxygen in the blood x-axis versus the relative Hb-oxygen saturation y-axis.
The resulting graph—an oxygen dissociation curve —is sigmoidal, or S-shaped Figure 2. The taut form predominates in the tissues a high carbon dioxide, low pH environment promoting oxygen release, whereas the relaxed form binds oxygen more avidly in areas of high pH, low carbon dioxide tension, and high partial pressures of oxygen such as in the alveoli.
This relationship between haemoglobin, oxygen binding, carbon dioxide tension, and pH is known as the Bohr effect. Carbon dioxide is returned to the lungs from the tissues dissolved in the plasma, either directly or as bicarbonate, and through the formation of carbaminohaemoglobin species within the erythrocyte. Deoxygenated blood has a greater ability to transport carbon dioxide when compared with oxygenated blood, and this is known as the Haldane effect. In combination therefore, the Bohr and Haldane effects promote oxygen binding and carbon dioxide release in the pulmonary capillaries, with the reverse occurring in the tissues.
Haemoglobin has a maximum theoretical oxygen-carrying capacity of 1. However, due in part to the existence of abnormal forms of haemoglobin such as methaemoglobin and carboxyhaemoglobin, which reduce the oxygen-carrying capacity of haemoglobin, empirically this value seems to be closer to 1.
It is a marker of haemoglobin's affinity for oxygen and is used to compare changes in the position of the curve. The ODC position changes in the face of various chemical and physiological factors, and also with different haemoglobin species. The various factors and their effects on the curve are described in Table 1 , and also the effects of a change in position of the curve on oxygen loading and unloading.
Factors that affect the standard human oxygen dissociation curve. Adapted from Thomas and Lumb 6 and Leach and Treacher Of clinical relevance:. Increased 2,3-DPG production is seen in anaemia, which may minimize tissue hypoxia by right-shifting the ODC and increasing tissue oxygen release.
Inorganic phosphate is a substrate for the production of 2,3-DPG and thus capillary haemoglobin oxygen release may be impaired if hypophosphataemia is not corrected.
Causes of hypophosphataemia can be divided into: decreased intestinal absorption e. In critical care, hypophosphataemia is often seen in sepsis, after operation, in refeeding syndrome, in diabetic ketoacidosis due to increased urinary phosphate excretion , and during renal replacement therapy.
Hypophosphataemia is also noted after an acute liver injury caused by, for example, paracetamol overdose and after hepatic resection. First of all, the word delivery implies that all the oxygen so described is delivered to, and utilized by, metabolizing cells.
Secondly, the word delivery implies an active external process responsible for ensuring arrival of oxygen at the cell. Notwithstanding these comments, we will continue with oxygen delivery within the context of this article in order to remain consistent with common custom and usage.
Global oxygen delivery describes the amount of oxygen delivered to the tissues in each minute and is a product of the cardiac output and arterial oxygen content. It is important to note that this is clearly an overall measure of oxygen delivery and does not describe regional differences—oxygen flux to each tissue bed is not constant throughout the body, rather the microcirculation responds to altering tissue metabolic demands by varying the regional and local blood flow.
As can be seen from the above equation, alterations in cardiac output, arterial oxygen saturation, and haemoglobin concentration will affect oxygen delivery. Under these circumstances, cells have a relative or absolute failure of the capacity to utilize oxygen and increasing D O 2 will have little effect in correcting the hypoxia.
Any cause of microcirculatory dysfunction will affect oxygen delivery, 16 for example, sepsis where nitric oxide production is increased leading to disorders of autoregulation matching of supply with demand within the tissues along with the decreased vascular tone that manifests clinically as hypotension.
Manipulation of global oxygen delivery to improve patient outcome has been the focus of goal-directed haemodynamic therapy GDT since its inception in the s. Given that continuing evidence supports equivalent outcome with low blood transfusion triggers in many clinical contexts haemoglobin concentrations 7. The rate of oxygen consumption depends on cellular metabolic demand and can be manipulated. For example, the use of therapeutic hypothermia to reduce cerebral metabolic demand post-cardiac arrest in order to improve neurological outcome is well documented.
Factors that affect oxygen consumption. Adapted from McLellan and Walsh If D O 2 continues to decrease further below the D O 2 crit, or if V O 2 increases for a given D O 2 crit, tissue hypoxia ensues with resultant anaerobic respiration and lactate production secondary to an imbalance between ATP supply and demand producing a type A hyperlactataemia. It is also important to highlight that even if global oxygen consumption appears to be supply independent, it does not rule out pathological oxygen supply dependency at a regional or local level, which may only manifest clinically at a later stage.
Figure 2 illustrates the theoretical biphasic relationship between oxygen consumption and oxygen delivery. Points B and E depict D O 2 crit in health and critical illness, respectively. O 2 ER is known to increase during exercise, peaking at maximal exercise at 0. This is because although D O 2 increases, it does not match the increase in V O 2 required by exercise. In critical illness, however, especially sepsis, V O 2 may continue to increase, even with increasing D O 2 demonstrated by the line EF , and D O 2 crit may be greater than in health.
The gradient of slope DE is reduced in critical illness as the tissues are less able to extract oxygen. A graph depicting the relationship between V O 2 and D O 2. Within the lung, oxygen diffuses from the alveoli into the pulmonary capillaries, driven by the gradient between the partial pressure of oxygen in the alveolar space and that in the deoxygenated pulmonary capillary blood. In the tissues, oxygen diffuses down a gradient between oxygenated blood in the systemic capillaries and the oxygen-consuming cells.
Diffusion can be described by either a phenomenological approach using Fick's laws or an atomistic approach applying the principle known as the random walk of the diffusing particles another example of which is Brownian motion.
Thus, although the global oxygen delivery oxygen flux may be manipulated through changes in cardiac output and oxygen content, at a tissue level diffusion distance and partial pressure gradients will have the greatest effect in altering the diffusive oxygen flux.
This is shown in Figure 3. A diagram illustrating the importance of diffusion distance from capillary to cell and local oxygen tension in determining diffusive oxygen flow rate. Whole-body oxygen transport and utilization can be estimated using two principle approaches: It is worth noting that expired gas analysis, although less invasive, is more direct in its measurement of cellular oxygen consumption.
Estimation of oxygen mass transport, through separate measurement of cardiac output and the elements of oxygen content. In combination with the latter approach, additional measurement of mixed venous oxygen content allows calculation of oxygen extraction and therefore oxygen consumption.
Evaluation of oxygen consumption through measurement of steady state, or dynamically changing, oxygen uptake using expired gas analysis to measure gas flows and concentrations [cardiopulmonary exercise testing CPET , metabolic cart].
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