Theories Explaining Metabolic Acidosis - Assignment Example

Task Metabolic acidosis Metabolic acidosis is a disorder state characterised by plasma acidity increase. Acid base balance can be understood by three theories. Henderson-Hasselbalch approach This approach describes the relationship of blood pH with the components of the H2 CO3 buffering system allowing the metabolic component to be differentiated from the respiratory component of acid base balance. pH = 6.1 + log (HCO3/ H2 CO3) Bicarbonate (HCO3) is seen to be in equilibrium with the metabolic components. Here Bicarbonate production happens in the kidney and acid production from exogenous and endogenous sources. H2 CO3 = PCO2 (mm Hg) X 0.03 Carbonic acid (H2 CO3) is seen to be in equilibrium with the respiratory component Metabolic acidosis can be caused by the increase in H+ generation from endogenous sources like ketones and lactate and exogenous sources like salicylate, methanol and ethylene glycol, kidneys inability to excrete hydrogen from dietary protein intake resulting in type I, IV renal tubular acidosis, bicarbonate loss due to wasting through kidney causing type II renal tubular acidosis or wasting through gastrointestinal tract causing diarrhea and also due to a kidney response to respiratory alkalosis. Base excess theory The non-linearity of the Henderson-Hasselbalch equation which makes exact quantification of the bicarbonate deficit amount in metabolic acidosis not possible lead to the development of the base excess approach to the acid-base physiology. BE = (HCO3 – 24.4 + [2.3 X Hgb + 7.7] X [pH – 7.4]) X (1 – 0.023 X Hgb) Base excess works to provide a quantitative bicarbonate amount in mmol that is required for the addition or reduction to restore 1 L of whole blood to pH 7.4 at a pCO2 of 40 mm Hg. The following formula was developed with improved accuracy, to calculate Base Excess for Haemoglobin SBE = 0.9287 X (HCO3 – 24.4 + 14.83 X [pH – 7.4]) Strong Ion approach theory Henderson Hasselbalch or Base Excess theory does not account for acid base quantifications in critically ill patients. Both these approach assume cations and anions in plasma do not change in a patient with metabolic acidosis. However these ions are in dynamic flux in critically ill patients. The Strong Ion theory was developed by Dr. Peter Stewart which took into consideration the fluctuations of all ions dissolved in plasma. As one of this ion concentrations change, based on the electric neutrality requirement in any solution, water must dissociate into H+ or OH- to balance charge. The pH is determined by three independent variables and not the consequence of acid to base ratio. SID = [Na+ + K+ + Ca2+ + Mg2+] – [Cl- + Lactate-] Strong Ion Difference or SID where ions almost completely dissociated at physiological pH Atot = 0.325275 X [albumin] + 2 X [phosphate] Total weak acid concentration (Atot) where Ions that can exist dissociated (A-) or associated (AH) at physiologic pH (buffers) The modified Henderson Hasselbalch equation with variables from the Strong Ion Theory in order to give a more generalizeable solution to pH can be as follows. pH = pK1 ’ + log [SID] – Ka – [ATOT]/[Ka + 10–pH] SPCO2 (K1’ = equilibrium constant for the Henderson-Hasselbalch equation, Ka = the weak acid dissociation constant, and S = the solubility of CO2 in plasma.) An arterial blood gas analysis should be obtained in case of metabolic acidosis suspected due to low bicarbonate concentration. Low carbonate levels can be due to primary metabolic acidosis as well as a metabolic compensation in case of respiratory alkalosis. pH 7.45 in case of respiratory alkalosis. Normal respiratory response to metabolic acidosis is pCO2 . Failure in appropriate respiratory response represent breathing failure and should be acknowledged immediately. After appropriate respiratory response is established, the required work up can be followed for the presence of unmeasured anions using anion gap, delta delta approach or strong ion gap. This allows for the correct therapy to be applied. Metabolic acidosis results in a number of non-specific changes in several organ systems gastrointestinal, pulmonary, neurologic, cardiovascular and musculoskeletal dysfunction. Metabolic alkalosis Metabolic alkalosis is a condition in which there is an increase in serum bicarbonate concentration which happens as a consequence of H+ loss from the body orHCO3 gain. It manifests as alkalosis with a pH> 7.4. Metabolic alkalosis results in alveolar hypoventilation with an increase in arterial carbon dioxide tension as a compensatory mechanism to prevent the change in pH. A quick compensatory response is an arterial PaCO2 increase by .5 to .7 for every m Eq/L increase in bicarbonate concentration. An acid base disturbance occurs when the PaCO2 change is not within this range. When PaCO2 increase is more than .7 times bicarbonate increase metabolic alkalosis coexist with respiratory acidosis. An elevated bicarbonate level of about 35 mEq/L is caused by metabolic alkalosis. Serum anion gap calculation most often helps in differentiating between metabolic alkalosis and metabolic compensation due to respiratory acidosis. Organ systems involved in metabolic alkalosis are kidneys and the gastrointestinal tract. Metabolic alkalosis generation occur with acid loss and alkali gain or extracellular fluid compartment contraction with a consequent bicarbonate concentration change. Kidney excrete the excess bicarbonate and has the capacity to restore the normal acid-base balance by less reabsorption due to volume expansion in proximal tubule due to infused sodium bicarbonate and secretion of bicarbonate by B-type intercalated cells in collecting duct that exchange bicarbonate for chloride through the apical chloride/bicarbonate countertransporter. Alkalosis causes diffuse arteriolar constriction and tissue perfusion reduction. Alkalosis may lead to tetany, seizures, and decreased mental status by decreasing cerebral blood flow. It also decreases coronary blood flow predisposing persons to refractory arrhythmias. Metabolic alkalosis also causes hypoventilation, which might result in hypoxemia, especially in patients with poor respiratory reserve. Alkalosis decreases the ionized calcium concentration in serum by increasing calcium ion binding to albumin. It is also associated with hypokalaemia, which can result in neuromuscular weakness and arrhythmias and can precipitate hepatic encephalopathy by increased ammonia production in susceptible individuals. Respiratory acidosis Respiratory acidosis is a clinical disturbance caused due to alveolar hypoventilation due to increased partial arterial pressure of CO2 (PaCO2) in case of rapid CO2 production and failed ventilation. Normal reference range of PaCO2 which is 36-44 mm Hg increases in case of alveolar hypoventilation resulting in a decrease in bicarbonate leading to a decrease in pH. Respiratory acidosis ensue when ventilation impairments occur and when CO2 removal by lungs is less than its production in the tissues. Respiratory acidosis is of two types- acute and chronic. In acute respiratory acidosis, PaCO2 levels are elevated to greater than 45 mm Hg which is above the upper limit of the reference range with an accompanying acidaemia where pH Read More