(BQ) Part 1 book Marinos the little ICU book has contents: Acid-Base analysis, organic acidoses, metabolic alkalosis, acute kidney injury, abdominal infections, abdominal infections, abdominal infections, nutritional requirements, parenteral nutrition, antimicrobial therapy,... and other contents.
Chapter 23 Acid-Base Analysis This chapter describes how to identify acid-base disorders using the pH, PCO2 and bicarbonate (HCO3) concentration in blood Included are: (a) simple rules for the identification of primary, secondary, and mixed acid-base disorders, (b) formulas for determining the expected acid-base changes for each of the primary acid-base disorders, and (c) a description of the “anion gap” and how it is used I ACID-BASE BALANCE According to traditional concepts of acid-base physiology, the hydrogen ion (H+) concentration in extracellular fluid is determined by the balance between the partial pressure of carbon dioxide (PCO2) and the bicarbonate (HCO3) concentration (1): [H+] = k × (PCO2/HCO3) (23.1) (k is a proportionality constant) This means that all acid-base disorders are defined by two variables: PCO2 and HCO3 This is shown in Table 23.1 A Types of Acid-Base Disorders A respiratory acid-base disorder is a change in [H+] that is a direct result of a change in PCO2 According to Equation 23.1, an increase in PCO2 will increase the [H+] and produce a respiratory acidosis, while a decrease in PCO2 will decrease the [H+] and produce a respiratory alkalosis A metabolic acid-base disorder is a change in [H+] that is a direct result of a change in HCO3 Equation 23.1 predicts that an increase in HCO3 will decrease the [H+] and produce a metabolic alkalosis, while a decrease in HCO3 will increase the [H+] and produce a metabolic acidosis Acid base disorders can be primary (the principal disturbance) or secondary (an additional disturbance) B Compensatory Responses Compensatory responses are designed to limit the change in H+ concentration produced by the primary acid-base disorder This is accomplished by changing the secondary variable in the same direction as the primary variable (e.g., a primary increase in PCO2 is accompanied by a compensatory increase in HCO3), as shown in Table 23.1 Compensatory responses not completely correct the change in [H+] produced by the primary acid-base disorder (2) The specific features of compensatory responses are described next The equations that describe these responses are shown in Table 23.2 C Responses to Primary Metabolic Disorders The response to a metabolic acid-base disorder involves a change in minute ventilation that is mediated by peripheral chemoreceptors in the carotid body, located at the carotid bifurcation in the neck Response to Metabolic Acidosis The compensatory response to metabolic acidosis is an increase in minute ventilation (tidal volume and respiratory rate) and a subsequent decrease in arterial PCO2 (PaCO2) This response appears in 30–120 minutes, and can take 12 to 24 hours to complete (2) The magnitude of the response is defined by the equation below (2) Δ PaCO2 = 1.2 × Δ HCO3 (23.2) Using a normal PaCO2 of 40 mm Hg and a normal HCO3 of 24 mEq/L, the above equation can be rewritten as follows: Expected PaCO2 = 40 – [1.2 × (24 – HCO3)] a (23.3) EXAMPLE: For a primary metabolic acidosis with a plasma HCO3 of 14 mEq/L, the ΔHCO3 is 24 – 14 = 10 mEq/L, the ΔPaCO2 is 1.2 × 10 = 12 mm Hg, and the expected PaCO2 is 40 – 12 = 28 mm Hg If the measured PaCO2 is >28 mm Hg, there is a secondary respiratory acidosis, and if the measured PaCO2 is 28 mm Hg, there is a secondary... Equation 23 .3 is then used to calculate the expected PaCO2 from the compensatory response The expected PaCO2 is 40 – [1 .2 × (24 – 16)] = 30.4 mm Hg c The expected and measured PaCO2 are then compared The measured PaCO2 (23 mm Hg) is