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Would the Hemoglobin–Oxygen Dissociation Curve Shift with Fetal Hemoglobin Compared with Adult Hemoglobin?

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Would the Hemoglobin–Oxygen Dissociation Curve Shift with Fetal Hemoglobin Compared with Adult Hemoglobin? ❖ CASE 19 A 23-year-old man with no medical problems is brought to the emergency cen- ter by family members who found him to be confused, nauseated, short of breath, and complaining of a headache. The patient was found in the basement of their home next to a furnace, where he was trying to stay warm on a cold winter day. On examination, the patient is lethargic and confused. His lips appear a bright pink. A urine drug screen is obtained and is negative. His serum carboxyhemoglobin level is elevated. The patient is diagnosed with car- bon monoxide poisoning and is admitted to the hospital for further treatment. ◆ What is the mechanism by which carbon monoxide causes hypoxia? ◆ In which direction (right or left) would the hemoglobin–oxygen dissociation curve shift with fetal hemoglobin compared with adult hemoglobin? ◆ What is the most common way in which carbon dioxide is transported in venous blood? 154 CASE FILES: PHYSIOLOGY ANSWERS TO CASE 19: OXYGEN-CARBON DIOXIDE TRANSPORT Summary: A 23-year-old man has confusion, nausea, shortness of breath, and headache after being found near a furnace in the basement. The patient has clinical and laboratory findings consistent with carbon monoxide poisoning. ◆ Hypoxia with carbon monoxide: Decreased oxygen-binding capacity of hemoglobin. ◆ Fetal hemoglobin–oxygen dissociation curve: Shift to the left. ◆ Most common way carbon dioxide is transported in the blood: - Bicarbonate (HCO3 ). CLINICAL CORRELATION Carbon monoxide is a gas that is produced commonly by internal combustion engines, fossil-fuel home appliances (heaters, stoves, furnaces), and incom- plete combustion of nearly all natural and synthetic products. Poisoning with carbon monoxide, if a person is exposed for a long period, can be fatal. Symptoms include headache, shortness of breath, confusion, impaired judg- ment, nausea, respiratory depression, coma, and even death. It is particularly a challenging problem because the gas is odorless and colorless; also, because the hemoglobin molecule is saturated, the patient is “pink” but hypoxemic. Carbon monoxide is inhaled through the lungs and binds to the oxygen- binding site of hemoglobin with a significantly higher affinity than does oxy- gen. The combination of carbon monoxide and hemoglobin makes carboxyhemoglobin, which can be measured in a patient’s blood. The eleva- tion of the carboxyhemoglobin level may give some indication of the severity of the disease. After a person’s removal from the carbon monoxide exposure, the carbon monoxide slowly dissociates and is excreted through the lungs. Treatment of the poisoning includes removal from the carbon dioxide expo- sure and the administration of 100% oxygen (non-rebreather mask). At times patients need intubation (coma, seizures, or cardiovascular instability) or treat- ment with hyperbaric oxygen (extremely elevated carboxyhemoglobin levels). APPROACH TO OXYGEN-CARBON DIOXIDE TRANSPORT Objectives 1. Know about the structure and function of hemoglobin. 2. Understand the hemoglobin–oxygen dissociation curves and the fac- tors which may change them. 3. Know about carbon dioxide transport in the blood. CLINICAL CASES 155 Definitions Oxygen carrying capacity of blood: The sum of the amount of dissolved O2 plus the amount of O2 bound to hemoglobin in the presence of 100% O2. Oxygen content of blood: The sum of the amount of dissolved O2 plus the amount of O2 bound to hemoglobin at any given PO2. Bohr effect: In the presence of CO2 hemoglobin has a lower binding affin- ity for O2. Because of the Bohr effect, increasing CO2 or lowering the pH of the blood decreases the O2 affinity of hemoglobin favoring O2 release. Haldane effect: Deoxygenation of hemoglobin increases its ability to bind CO2. DISCUSSION Oxygen Transport Metabolism consumes O2 and produces CO2. Gas exchange in the lungs occurs when blood passing through the pulmonary capillaries releases CO2 and takes up O2. The arterial concentrations of CO2 and O2 are in equilibrium with their concentrations in the alveolar compartment. The gas concentration in the blood is expressed as its partial pressure, and its content is determined by its partial pressure and its solubility in blood. The solubility of oxygen in aqueous solution is low, and the amount of O2 that can be dissolved in nor- ∞ mal plasma, or the O2 content, at 37 C is 0.3 mL/100 mL at a normal arterial partial pressure of 100 mm Hg. The O2 content of plasma is much too low to meet a person’s metabolic demands; however, hemoglobin greatly increases the amount of O2 the blood can carry. The O2-carrying capacity of blood is dependent on the hemoglobin concentration. At saturating oxygen levels, hemoglobin binds about 1.34 mL of O2 per gram of hemoglobin. Normal blood has about 15 g of hemoglobin per 100 mL; thus, at saturation, the amount of O2 bound to hemoglobin is ¥ ¥ 15 g Hb 1.34 mL O2/g Hb 100% saturation = 20.1 mL O2/100 mL blood The amount of O2 bound at saturation is the O2-binding capacity of hemo- globin. The normal arterial PO2 is about 100 mm Hg. At this partial pressure, hemoglobin is 97.5% saturated and the amount of O2 that is bound is ¥ ¥ 15 g Hb 1.34 mL O2/g Hb 97.5% saturation = 19.6 mL O2/100 mL blood The total amount of O2 in the blood is the sum of the dissolved O2 and the bound O2: O2dis = 0.3 mL/100 mL blood O2bound = 19.6 mL/100 mL blood O2content = 19.9 mL/100 mL blood 156 CASE FILES: PHYSIOLOGY The majority of O2 is transported in the blood bound to hemoglobin. Any factors that influence the amount of functional hemoglobin will influence O2 transport in the blood. Hemoglobin is the major blood protein constituent; it is contained within the red cells of the blood and is central to gas transport and maintenance of hydrogen ion homeostasis and acid–base balance. It is a tetrameric complex a b of two subunits and two subunits, each of which binds an O2 molecule. The binding of the first oxygen to hemoglobin causes a structural shift that favors the binding of additional oxygen molecules. This cooperativity yields a characteristic sigmoidal affinity curve for O2 binding. Several important physiologic parameters contribute to the binding affinity of hemoglobin for O2 and affect the shape of the curve. Variables such as temperature, pH, and CO2 alter the binding affinity for O2. The structural shift induced by O2 bind- ing alters the ionization state of important amino acid residues, causing a shift + in their H dissociation constant (pKa). O2 binding results in a decreased affin- ity of hemoglobin for H+ and a release of H+ from the molecule. The reaction is readily reversible and is in equilibrium. Thus, not only does O2 binding or + + release cause a change in [H ], the H concentration influences O2 binding by hemoglobin. Although seemingly minor, the O2 binding affinity of hemoglo- bin is pH-dependent and is important to the overall physiologic function of hemoglobin. Also, hemoglobin contributes to H+ ion homeostasis by becom- + ing a weaker acid (higher affinity for H ) upon O2 dissociation. This shift in the pKa is the basis of both the Haldane effect and the Bohr effect. Finally, hemoglobin also binds CO2 with the formation of carbamino groups. The binding is weak and readily reversible but has two important consequences: The binding of CO2 alters O2 affinity, and hemoglobin contributes to CO2 transport in the blood. + An increase in H or PCO2 will shift the O2 dissociation curve to the right with a resultant decrease in the affinity for O2. This phenomenon is known as the Bohr effect. Another important regulator of the O2 binding affin- ity of hemoglobin is 2,3-diphosphoglycerate (DPG). DPG is produced by red cells and is increased during hypoxia. An increase in DPG shifts the affinity curve to the right, decreasing the affinity for O2 and favoring oxygen release in the tissues (See Figure 19-1). The effect of pH, PCO2, temperature, and 2,3-DPG on O2 binding to hemo- globin is central to gas transport by the blood. Figure 19-1 is the oxygen- binding curve of hemoglobin. Because of the steeply sigmoidal nature of the curve through much of the physiologic range, even slight changes in the bind- ing affinity for O2 can cause large changes in the percent of O2 saturation at a + given PO2. Thus increases in H ,CO2, temperature, or 2,3-DPG will cause O2 dissociation from hemoglobin. Conversely, a decrease in any of these factors will increase the affinity for O2 favoring its binding to hemoglobin. CLINICAL CASES 157 100 98100 97 N 91 90 90 Shift to the left: Hypothermia N 80 Hypocapnia 80 Alkalosis 70 ↓2,3 DPG Shift to the right: 70 N Hyperthermia Hypercapnia 60 60 Acidosis ↓ 2,3-DPG A 50 50 40 40 % Hemoglobin saturation 30 30 20 20 10 10 0 27 0 0 10 20 30 40 50 60 70 80 90 100 PO2 (mm Hg) Figure 19-1. Oxygen dissociation curve with shifts based on various factors. Carbon Dioxide Transport The transport of CO2 by the blood occurs through several different mecha- nisms. CO2 has a higher solubility than does O2; therefore, a larger fraction is carried as dissolved CO2. More important, CO2 spontaneously reacts with water to form carbonic acid: Æ Æ + - CO2 + H2O H2O CO3 H + HCO3 + - Carbonic acid dissociates to H and HCO3 . The enzyme carbonic anhy- drase catalyzes this reaction and is contained in red cells. CO2 freely diffuses + − − into the red cell and reacts with water to form H and HCO3 . The HCO3 is − − transported rapidly out of the red cell by the Cl / HCO3 exchanger in the red cell membrane.
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