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Learning Objectives in Acid-Base Physiology

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Learning Objectives in Acid-Base Physiology Learning objectives in acid-base physiology CHAPTER 1 Water 1.1. Describe and explain properties of water which are important in physio­ logical mechanisms. 1.2. State how much water there is in the body. Explain why we differentiate between "intracellular' and "extracellular' fluid; give the magnitudes of each. 1.3. Write the reaction for the dissociation of water and indicate the general significance of the fact that water dissociates. 1.4. Define 'acid', 'base' 'alkali'. Write the reaction for the dissociation of an acid; describe what is meant by 'strong' and 'weak' acids. 1.5. State and explain the law of mass action. 1.6. Define and write an equation for the 'ionic product of water'; give its value. pH and buffers 1.7. Define pH. 1.8. Calculate the approximate pH of a given concentration (e.g. M, M/10, M/100) of strong acid or alkali. 1.9. Explain what is meant by buffering. Write down the chemical reactions occurring when a weak acid and its salt are added to an aqueous solution. Identify the buffer acid and the buffer base. 1.10. Explain why a mixture of a weak acid and its conjugate base acts as a buffer. 1.11. Derive the Henderson-Hasselbalch equation. 1.12. Define the pK of a weak acid or base. 110 1 1 LEARNING OBJECTIVES IN ACID-BASE PHYSIOLOGY ~----------------------------------------------------~ 1.13. Define and explain 'buffer value', describe how, for a particular buffer, this varies with pH. Explain why a buffer pair has its greatest buffer value at a pH which equals its pK. col-bicarbonate system 1.14. Derive the expressions pH= pK + log[HC03 -]/[C02]. State that the· pK in this instance is 6.1 when [HC03 -]and [C02] are measured in M. 1.15. State the relationship between concentration of a gas in dilute solution and its partial pressure; define 'solubility coefficient'. 1.16. State that [C02] in mM equals a x Pco2 , Pco2 in mmHg and a= 0.03 (the solubility coefficient for C02 in water). 1.17. Explain that the CO2 and H CO 3 - buffer pair is a poor chemical buffer because its pK is more than one pH unit away from the pH of the body. Explain that the buffer pair is physiologically important because the body can manipulate the concentrations of both the buffer acid (via the lungs) and the buffer base (via lungs and kidney). CHAPTER2 The range of extracellular [H +] 2.1. Give a typical value for the extracellular pH and the limits normally compatible with survival. Give corresponding values for [H+]. Compare the physiological range with that for sodium and chloride ions; explain any difference. 2.2. Explain the consequences of wide variations of extracellular [H +]. 2.3. Indicate why hyperventilation may result in hypocalcaemic tetany; include the importance of extracellular [H+] variation. 2.4. Describe which tissues provide buffering power. Graphic representation of acid-base status 2.5. Describe in outline how the concentrations of H+, C02 and HC03 - of a solution are estimated. 2.6. On a graph of Pco2 (abscissa) and [HC03 -](ordinate), draw lines join­ ing points of equal pH. 2.7. On the graph of 2.5, show and explain the effects of changes in Pco2 on [HC03 -]for: (a) distilled water; (b) sodium bicarbonate solution; (c) sodium bicarbonate solution plus a non bicarbonate buffer. LEARNING OBJECTIVES IN ACID-BASE PHYSIOLOGY I 171 I 2.8. On a graph of Pco2 - [HC03 -], draw the relationships for normal plasma and for normal blood in vitro. The graph should show typical numerical values for Pco2 and [HC03 -]in normal arterial blood. CHAPTER3 3.1. Explain that C02 can be regarded as volatile, since it can be retained or removed by the lung. HC03 - can be retained or removed by the kidney. Other acids and alkalis are non-volatile or fixed. Disturbances of acid-base balance 3.2. Define - acidaemia and acidosis, alkalaemia and alkalosis. Respiratory disturbances 3.3. On the graph ofPco2 - [HC03 -],indicate the immediate effects of hypo­ ventilation and hyperventilation and deduce the effects on [HC03 -] and [H+]. Also on the graph, indicate and explain the delayed effects, mediated by the kidney, occurring if the primary respiratory disorder persists. Hence define uncompensated and compensated respiratory acidosis and alkalosis. 3.4. Define partial, complete and over-compensation. 3.5. Explain that the renal compensation of altered [H+] involves alterations in blood biochemistry to restore the blood pH; compensation does not mean the restoration of normal blood biochemistry. Metabolic disturbances 3.6. Define and explain the meaning of 'metabolic disturbances of acid-base physiology'. Give examples. 3.7. With the help of the normal blood line, describe and explain: (a) the immediate effects on blood biochemistry of a bolus injection of a strong fixed acid or alkali; (b) the respiratory compensation in each case; (c) the renal compensation in each case. Give the approximate time courses of these compensatory processes. Potassium 3.8. State the relationship between extracellular concentrations of [H+] and [K+]. 172 I Ll___ L_E_A_RN_IN_G_O_B_JE_C_T_I_V_E_S_IN_A_C_ID_-_B_A_S_E_P_H_Y_S_I_O_L_O_G_Y __ ____i 3.9. State and explain factors which contribute to this relationship. 3.1 0. State the principal adverse effects ofhyperkalaemia and hypokalaemia. Acid-base status and persistent vomiting of gastric contents 3.11. Describe the chemicals which are lost from the body in persistent vomit­ ing of gastric contents. 3.12. Explain the acid-base disturbance produced by persistent vomiting of gastric contents. 3.13. Explain the renal mechanisms called into play to compensate for the fluid loss; indicate why the compensation for fluid loss exacerbates the acid-base disorder. 3.14. Describe the movements of potassium that occur in a patient suffering from chronic vomiting. 3.15. From the above, indicate how it is that some patients arrive at the situation of having extracellular alkalosis and intracellular acidosis. 3.16. Explain how the cautious intravenous infusion of physiological saline is likely to improve the patient's condition. CHAPTER4 Assessment of acid-base status 4.1. Define the standard bicarbonate for blood and explain how it is measured; give a typical normal value. Show this point on the 'normal blood line'. 4.2. State that a change in standard bicarbonate is indicative of a metabolic component in an acid-base disorder. Explain this on the graph of the blood buffer line and explain why the magnitude of the change in standard bicarbonate is an underestimate of the magnitude of the metabolic disorders. 4.3. Explain that the blood buffer base consists mainly of HC03 - and Protein-(Pr-). Define the buffer base as ([HC03 -]+[Pr-J). 4.4. Explain that alteration of the Pco2 does not significantly alter the magnitude of the buffer base. Explain that addition of a given amount of strong acid or alkali to a blood sample results in a quantitatively equal change in buffer base. 4.5. From the preceding, and in relation to the graph of the 'normal blood line', define the terms base excess. Define 'base deficit' and describe how it can be regarded as a 'negative base excess'. 4.6. Explain how base excess can be directly determined by a 'back- titration' of 'titratable' acid or alkali. Explain why a Pco2 of 40 mmHg is used and a pH of 7.4 is the end point of the titration. LEARNING OBJECTIVES IN ACID-BASE PHYSIOLOGY 1 1 173 L---------------------------------------------------~ 4.7. Explain that the acid-base status can be deduced from the blood bio­ chemistry in cases of uncompensated respiratory or metabolic disorder. 4.8. Demonstrate examples of compensated disorders (e.g. compensated respiratory acidosis and compensated metabolic alkalosis) in which the same abnormality of blood biochemistry may be reached by different routes. Hence explain the need, in such cases, to seek each cause and evaluate its effect. The Siggaard-Andersen nomogram 4.9. Explain the advantage of using log(Pco2) as a function of pH for constructing a nomogram to measure the parameters of acid-base status. 4.10. State and explain the plots given by: (a) a solution with; no buffering power; (b) a perfect buffer; (c) plasma; (d) blood. 4.11. Explain the construction of the scale for reading off base excess. 4.12. Explain the analyses needed on a blood sample in order to be able to plot a line on the nomogram and how to use the nomogram to read off standard bicarbonate, base excess, total buffer base. 4.13. Define normal buffer base, describe how to calculate it and explain its value. 4.14. Indicate how variations in the haemoglobin concentration influence the different parameters of acid-base status and how this is accommodated in interpretation of results. CHAPTERS Sources and buffering of acid and alkali 5.1. Describe the sources of acid and alkali in the body, giving approximate values. 5.2. Describe and explain the contributions of different buffer systems to respiratory and metabolic disorders of metabolism. Composition of plasma 5.3. Give a balance sheet for the concentrations of electrolytes in plasma. 5.4. Give the quantitative contribution of proteins to (a) electrical neutrality and (b) the colloid osmotic pressure of plasma. 174 I LI___ L_E_A_R_N_IN_a_o_B_J_Ec_T_I_v_E_s_IN_A_c_m_-B_A_s_E_P_H_Y_s_I_o_L_o_a_Y __ ___, Plasma and erythrocytes in whole blood 5.5. Explain what is meant by separated plasma and true plasma. 5.6. Does the measurement of pH qn a sample of whole blood give a value representing an average for erythrocytes and plasma, for erythrocytes or for the plasma component? Explain your answer. Explain how you would calculate the [HC03 -] from measurements of pH and Pco2 . (Why does the result apply to the plasma component when the measure­ ments are made on whole blood?).
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