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Davenport Diagram Pathology > Renal Pathologies > Renal Pathologies Davenport Diagram Pathology > Renal Pathologies > Renal Pathologies DAVENPORT DIAGRAMS: • Davenport diagrams are graphic displays of acid-base states. • They illustrate the dynamic relationships between arterial blood pH, bicarbonate and non-bicarbonate buffers, and the partial pressure of carbon dioxide. • An isopleth represents all possible combinations of bicarbonate and pH values at a given carbon dioxide partial pressure. 4 simple acid-base disorders prior to compensation Graph Features: - The x-axis tracks pH; the healthy homeostatic arterial blood value = 7.4 - Values less than this reflect acidosis; values higher reflect alkalosis. - The y-axis tracks bicarbonate concentration; the healthy homeostatic value 24 millimolar. - Recall that, as bicarbonate concentration increases, pH becomes more alkaline. - Isopleth for a partial pressure of carbon dioxide of 40 mmHg. - A straight line to represent the combination of all non-bicarbonate buffer titration curves. Disorders that cause the blood to become more acidic. • Metabolic acidosis occurs when the reduction in bicarbonate concentration lowers the pH. - Notice that, because this is a non-respiratory disorder, PaCO2 is unaffected. • Respiratory acidosis occurs when the lungs retain excess carbon dioxide, so the partial pressure of carbon dioxide is elevated above normal, which lowers the pH. - Recall that respiratory acidosis produces an elevated bicarbonate concentration, which is reflected in our graph. Disorders that cause the blood to become alkalotic (aka, basic). • Metabolic alkalosis occurs when bicarbonate concentration is elevated. - As in metabolic acidosis, the PaCO2 remains on the 40 mmHg isopleth. 1 / 4 • Respiratory alkalosis occurs when the lungs release too much carbon dioxide - Lowers the PaCO2 and increases pH. Compensatory Mechanisms • The lungs and kidneys respond to acid-base disorders via compensatory mechanisms that bring pH back to normal. When metabolic acidosis triggers release of carbon dioxide from the lungs, PaCO2 falls and pH increases. • Thus, our point of interest lies lower and to the right than on our original graph. - Shaded area represents all possible outcomes of partial compensation for metabolic acidosis; the extent of the original disturbance and the magnitude of compensation determine the specific blood outcome. When respiratory acidosis triggers increased renal excretion of hydrogen ions and conservation of bicarbonate, pH increases. • The partial pressure of carbon dioxide remains elevated until the source of the disorder is treated, because the lungs are unable to expel CO2. When metabolic alkalosis triggers respiratory and renal mechanisms to conserve hydrogen ions, pH lowers. • However, because the respiratory component of compensation requires conservation of carbon dioxide, its partial pressure remains elevated. When respiratory alkalosis triggers renal mechanisms that conserve hydrogen ions, pH lowers. • But, until the source of the disorder is treated, the partial pressure of carbon dioxide will remain below 40 mmHg. Perfect Compensation - Blood pH returned to 7.4 - The blood profile end-states reflect both the original disorders and the compensatory mechanisms. If the original disorder was metabolic acidosis or respiratory alkalosis, both the bicarbonate concentration and the partial pressure of carbon are reduced (isohydric hypocapnia). • In the case of metabolic acidosis, this new state is accounted for by: - The cause of the disorder, which was a low concentration of bicarbonate relative to hydrogen ions. - The respiratory component of compensation, which required increased release of carbon dioxide. 2 / 4 • In the case of respiratory alkalosis, this new state is accounted for by: - The cause of the disorder, which was the excessive release of carbon dioxide, and, - Renal compensatory mechanisms that excreted bicarbonate. If the original disorder was respiratory acidosis or metabolic alkalosis, both the bicarbonate concentration and the partial pressure of carbon dioxide are elevated above normal (isohydric hypercapnia). • In the case of respiratory acidosis, this is state is accounted for by: - The cause of the disorder, which was over-retention of carbon dioxide, and, - Renal compensatory mechanisms that conserved bicarbonate. • In the case of metabolic alkalosis, this state is accounted for by: - The cause of the disorder, which was an increased bicarbonate to hydrogen ion ratio - The respiratory component of compensation, which required increased carbon dioxide retention in the lungs. Compound Disturbances: • If both metabolic and respiratory acidosis are in play, pH is reduced more so than if just one disorder was influencing pH; the shaded area shows the range of possible values that could result. • When alkalosis results from both metabolic and respiratory origins, pH is elevated more so than if only one disorder was present. - Be aware that while this information can tell us if there are one or two sources of the pH disturbance, it cannot tell us which preceded the other. FULL-LENGTH TEXT ¬ Here we will learn how to draw and interpret Davenport diagrams. To begin, start a table, and denote some key principles of Davenport diagrams: Davenport diagrams are graphic displays of acid-base states; They illustrate the dynamic relationships between arterial blood pH, bicarbonate and non-bicarbonate buffers, and the partial pressure of carbon dioxide. An isopleth represents all possible combinations of bicarbonate and pH values at a given carbon dioxide partial pressure. Let's begin with a Davenport diagram of the four simple acid-base disorders prior to compensation. First, set up the basic graph parameters: The x-axis tracks pH; indicate the healthy homeostatic arterial blood value 7.4; Indicate that values less than this reflect acidosis; values higher reflect alkalosis. The y-axis tracks bicarbonate concentration; indicate the healthy homeostatic value 24 millimolar. Recall that, as bicarbonate concentration increases, pH becomes more alkaline. Next, draw the isopleth for a partial pressure of carbon dioxide of 40 mmHg. Then, indicate the healthy homeostatic starting point, where pH is 7.4, bicarbonate concentration is 24 millimolar, and the partial pressure of carbon dioxide is 40 mmHg. Lastly, draw a straight line to represent the combination of all non-bicarbonate buffer titration curves. Now, we're ready to show the uncompensated acid-base disorders on our graph. First, we'll show the disorders that cause the blood to become more acidic. Indicate metabolic acidosis occurs when the reduction in bicarbonate concentration lowers the pH. Notice that, because this is a non-respiratory disorder, PaCO2 is unaffected. Then, show that, because respiratory acidosis occurs when the lungs retain excess carbon dioxide, the partial pressure of carbon dioxide is elevated above normal, which lowers the pH. Recall that respiratory acidosis produces an elevated bicarbonate concentration, which is reflected in our graph. Now, let's show the disorders that produce alkalotic (aka, basic) states. Indicate that metabolic alkalosis occurs when bicarbonate concentration is elevated; as in metabolic acidosis, the PaCO2 remains on the 40 mmHg isopleth. Show that when respiratory alkalosis occurs, the lungs release too much carbon dioxide, which, in turn, lowers the PaCO2 and increases pH. The lungs and kidneys respond to acid- base disorders via compensatory mechanisms that bring pH back to normal. Let's see what the arterial blood profile 3 / 4 looks like when compensation is only partially complete: First, re-draw the original graph, and include the curves to show the 40 mmHg isopleth and the non-bicarbonate buffer line. Then, show that when metabolic acidosis triggers release of carbon dioxide from the lungs, PaCO2 falls and pH increases; thus our point of interest lies lower and to the right than on our original graph. Shade in the area that represents all possible outcomes of partial compensation for metabolic acidosis; the extent of the original disturbance and the magnitude of compensation determine the specific blood outcome. Likewise, show that when respiratory acidosis triggers increased renal excretion of hydrogen ions and conservation of bicarbonate, pH increases. The partial pressure of carbon dioxide remains elevated until the source of the disorder is treated, because the lungs are unable to expel CO2. Then, show that when metabolic alkalosis triggers respiratory and renal mechanisms to conserve hydrogen ions, pH lowers; however, because the respiratory component of compensation requires conservation of carbon dioxide, its partial pressure remains elevated. Similarly, when respiratory alkalosis triggers renal mechanisms that conserve hydrogen ions, pH lowers; but, until the source of the disorder is treated, the partial pressure of carbon dioxide will remain below 40 mmHg. Next, re-draw the graph to show the outcomes when pH is returned to 7.4 via perfect compensation. As we'll see, the blood profile end-states reflect both the original disorders and the compensatory mechanisms. If the original disorder was metabolic acidosis or respiratory alkalosis, both the bicarbonate concentration and the partial pressure of carbon are reduced (isohydric hypocapnia). In the case of metabolic acidosis, this new state is accounted for by: The cause of the disorder, which was a low concentration of bicarbonate relative to hydron ions, and, The respiratory component of compensation, which required increased release of carbon dioxide.
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