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Lecture 12

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University of Toronto Scarborough
Biological Sciences
Stephen Reid

1    Lecture 12: Blood Gas Transport 1. Partial Pressures of Gases throughout the Circulatory System In blood flowing through the pulmonary artery intothe lungs, oxygen levels are relatively low (40 mmHg) and CO leve2s quite high (46 mmHg). Note: mmHg is often referred to as 'Torr'; they are the same unit. The blood reaches the lungs, where it interacts with alveolar air. Alveolar air is not the same as atmospheric air; atmospheric air has a PO of 160 mmHg and a PCO2 of 0.3 mmHg, 2 whilst alveolar air has a PO 2 of 100 mmHg and a P CO 2 of 40mmHg. There are several reasons for this: firstly, gas exchange occurs through the capillaries in the alveoli with the atmospheric air before it has a chance to reach theblood of the systemic circuit; secondly, there is mixing of the air in the anatomical dead space; and thirdly, the alveoli are filled with water vapour as well, with a relative humidity of approximately - and we have to subtract the partial pressure of water vapour from the partial pressure of oxygen and carbon dioxide. The blood flowing through the lungs equalizes with the partial pressures of the alveolar air (100 Torr O 2nd 40 Torr CO ) an2 remains at these values throughout the systemic arteries. When the blood enters the systemic capillaries (tissues) and begins oxygenating the tissues and carrying away carbon dioxide, the partial pressure of oxygen drops to 40 Torr and the partial pressure of carbon dioxide rises to 46 Torr. Within the mitochondria oxygen levels can be as low as 1 Torr. The deoxygenated blood flows through the venous system back to the right side of the heart, maintaining these partial pressure values until it returns to the lungs. 2. Perfusion versus Diffusion Limitation In human lungs), the uptake of O2 and the excretion of CO2 are perfusion limited. This refers to the fact that the limitingfactor in the oxygenation ofour tissues (and the removal of CO2 from our tissues) is the rate of blood flowto our lungs and tissues. However,some animals such as fish, and humans in certain circumstances, are insteaddiffusion limited, meaning that the limiting factor in oxygenation of the tissues is the diffusion rate ofoxygen from the lung gas into the blood flowing through the lungs. The rate of O 2 uptake, and CO e2cretion, is a function of the distance the blood has to travel through the pulmonary capillaries. Within the first third of the length of a pulmonary capillary, the blood has changed from being deoxygenated and high in CO (40mmHg 2 ; 46mmHg CO )2to 2 being oxygenated and low in CO 2(100mmHg O ; 402mHg CO ). What 2his means is that we have a large reserve distance in the lungs for gas exchange; two thirds of the capillary length is not even used in normal gas exchange. In very highly-trained athletes, at the peak of their performance, however, diffusion limitations do begin to apply. 2    3. Determination of Alveolar Ventilation The rate of gas exchange at the lungs depends upon our metabolic demands. The amount of oxygen that is being consumed, or carbon dioxide excreted, will affect the amount of alveolar ventilation. The ratio of CO 2roduction to O co2sumption in our tissues is called therespiratory quotient and it is a measure of our metabolic rate (in the lungs this ratio is referred to as the respiratory exchange ratio). Regular breathing which is sufficient to meet our metabolic demands is called eupnea or eupneic breathing. When metabolic demands increase, for example during exercise, alveolar ventilation must increase to meet this heightened demand; this is called hyperpnea. Apnea is the term for the absence of breathing, and dyspnea is the term for difficult or laboured breathing. 4. Hyperventilation and Hypoventilation Everyone has heard the terms hyperventilation and hypoventilation before; colloquially we use these terms to refer to an increase or decrease inbreathing, but clinically they are defined in terms of blood gas levels. If breathing isreduced enough that the partial pressure of oxygen inthe arterial blood falls below 100mmHg and/or the P CO 2rises above 46Hg, we referto this ashypoventilation. If breathing increases such that PO 2rises above 100mmHg, and CO fall2 below 40mmHg, then we refer to this as hyperventilation. 5. Daily Oxygen Consumption Minute ventilation is about 6 L per minute. Of this 6 litres of air that we breathe every minute, some ventilates the dead space of the conducting zone so only approximately 4.2 L per minute actually reaches the alveoli. We know that air contains about 21% oxygen so therefore approximately 882 ml (4 200 ml x 21%) of oxygen reaches the alveoli every minute. Only about 250 ml of this 882 ml of oxygen actually diffuses intothe blood. If we multiply this by the number of minutes in a day, we find that per day, a human consumes about 360 litres of oxygen. We can't get this amount of oxygen to our tissues by relying on oxygen dissolved in the blood - if we did, cardiac output would have to be 83.3 L of blood a minute, far more than the 5 L of blood actually pumped per minute. So how do we get so much oxygen to the tissues? 6. Haemoglobin The answer is haemoglobin. Haemoglobin contains 98.5% of the O 2in the blood. Each molecule of haemoglobin consists of 4 globin subunits (2 alpha and 2 beta) with each subunit containing a heme group which consists of a porphyrin ring with an iron molecule in the centre. The iron molecule is the site of O2binding so each haemoglobin molecule can bind up to four O mole2ules. Fetal haemoglobin is slightly different; it contains different globin molecules and fetal haemoglobin has a greater affinity for oxygen than the haemoglobin of the mother allowing for efficient oxygen transfer from the maternal blood to the fetal blood. Sickle-cell anaemia is a genetic disorder that causes red blood cells to be abnormally ('sickle') shaped. It is caused by the production of an abnormal form of haemoglobin and results in the red 3    blood cells being less efficient at O t2ansport, as well as being viable for shorter periods of time and tending to clog blood vessels.A single-point mutation in the haemoglobin beta chains, causing haemoglobin molecules to adhere together in a distorted fashion, is the primary cause. Fatigue is the most common symptom of the disorder, but canseverely limit exercise and ability to undertake strenuous activity. 7. Linking Oxygen and Carbon Dioxide Transport in the Blood Carbonic anhydrase (CA) is an enzyme that is found throughout the body. CA’s function is to catalyse the reversible hydration/dehydration reaction whereby CO reacts with water to form an + - 2 H ion and a HCO ion.3Carbonic anhydrases are found in thered blood cells, inthe kidney tissues (where it is important for bicarbonate reabsorption and acid-base balance), in the parietal cells lining the stomach and in other tissues. However it is not present in the plasma. The CO hydration/dehydration reaction (H O + CO ↔ HCO + H ) is critical for O and CO 2 2 2 3 2 2 transport in the blood. The other reaction involved in this process describes the binding of oxygen to haemoglobin. These two equations summarize the relationship between CO 2and O t2ansport in the blood and we can model gas exchange in a red blood cell inthe lung (and tissues) using these two equations. In the lungs O 2diffuses into the blood and then into the red cell. It binds to haemoglobin, and as + + - shown in the equation, causing haemoglobin to lose H ions. These free H ions react with HCO 3 ions in the cell (these enter the cell via chloride bicarbonate exchanger gates) to produce CO and 2 H 2O, and then this CO di2fuses out into the alveolar gas and is lost as we expire. In the tissues, CO2 diffuses into the red cell and reacts with water to form a proton and a bicarbonate ion. The proton thenbinds to oxygenated Hb causing the oxygen molecule to come off the Hb molecule. It is then free to diffuse into the tissues. Both the CO 2 hydration/dehydration reaction and the oxygenation/deoxygenation of Hb are influenced by H + ions. Given this, pH can have a significant effect on oxygen-haemoglobin binding. CO in the systemic arterial blood can be found inmany forms, but primarily (89.6%) it is found as 2 bicarbonate ions in the blood. 5.5%is dissolved in the blood
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