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Blood Gas Interpretation Acid-Base Homeostasis • The vast majority of processes in the body are pH sensitive. • pH of extracellular fluid is tightly regulated and maintained between a pH of 7.35- 7.45. • pH outside the range of 6.8-7.8 is not compatible with life. • An acid is anything that adds H ions, whereas an alkali removes H ions.+ - Effect of PCO2 and [HCO 3 ] on pH CO +2H O 2 H 2O 3 HCO 3-+ H + - • The Henderson-Hasselbalch equation shows how changes in PCO2 and [HCO ] affect3pH.Maintaining Acid- Base Homeostasis Extracellular and Intracellular Buffering • Extracellular buffering-bicarbonate ions are the main buffer within extracellular fluid (ECF). When acid is added to body fluid (or alkali lost), bicarbonate ions are utilised to neutralise the acid load, ultimately leading to decreased concentration of bicarbonate ions. When alkali is added to body fluid (or acid lost), hydrogen ions are consumed, causing increased dissociation of H 2O a3d therefore, increased concentration of bicarbonate ions. • Intracellular buffering (relies on movement of hydrogen ions into/out of cells) When acid is added to body fluid, hydrogen ions move into cells. When alkali is added to body fluid, hydrogen ions move out of cells. Extracellular and Intracellular Buffering - + CO +2H O 2 H 2O 3 HCO 3 + H • When there is increased PCO , 2O mov2s into the cell and the reaction shifts to the right. The H is buffered within the cells, while the HCO e3its the cell, increasing the ECF [HCO ]. - 3 • When there is decreased PCO , t2e reaction shifts to the left, reducing the ECF - [HCO ]3 Respiratory Compensation • Rate of ventilation can be altered to bring about changes in PCO . Central and peripheral 2 chemoreceptors monitor changes in PCO and p2 and the ventilation rate is altered appropriately. • When metabolic acidosis occurs, ventilation rate increases, causing a decrease in PCO . 2 • When metabolic alkalosis occurs, ventilation rate decreases, increasing PCO 2. • The respiratory response to metabolic acid-base disturbances can take hours to complete. Renal Compensation • Metabolism of carbohydrates and fats leads to production of large amount of carbon dioxide which is eliminated via the lungs. • Metabolism of dietary amino acids leads to net production of acids, which are immediately neutralized by the bicarbonate in ECF. This bicarbonate needs to be replenished and this is where the kidneys play a role. • The kidneys maintain acid-base balance by: 1. reabsorption of HCO , 2) - 3 regulation of H excretion and 3) creation of new HCO . - 3Renal Compensation - 1. Reabsorption of HCO 3 Approx. 80% of HCO is r3absorbed in the proximal convoluted tubule. Asimilar mechanism is utilised in the thick ascending limb of the Loop of Henle.Renal Compensation Asmall percentage of HCO is absorbed in the 3 distal convoluted tubule and collecting ducts via alpha-intercalated cells. Beta-intercalated cells secrete HCO , 3nto tubular fluid, while H is reabsorbed. In most cases, H secretion predominates, however, when there is metabolic alkalosis, the beta-cells activity increases to excrete excess HCO . - 3 Renal Compensation 2. Regulation of H+ excretion • Acidosis stimulates excretion of H . Alkalosis causes reduced excretion of H . + + • In the case of metabolic/respiratory acidosis, the decreased intracellular pH creates a favourable gradient for excretion of H via the apical membrane. • The change in pH also causes changes in the kinetics of transport proteins and causes increased shuttling of transporters to the membrane, causing increased excretion of H . + • With long-term acidosis, there is an increase in the number of membrane transporters due to changes in transcription and translation. • In the case of metabolic/respiratory alkalosis, the responses are reversed. Renal Compensation 3. Creation of new HCO3- - + Tubular fluid reaching the DCT and collecting ducts contains minimal HCO . Therefore, w3en H is excreted into the tubular fluid there, it combines with non HCO buffers3such as PO 43-and is excreted as a titratable acid. HCO gene3ated from the - cells here is returned to ECF as new HCO . 3 HCO3- is also generated by the production of NH , which i4 produced by the metabolism of glutamine in the PCT. Glutamine metabolism produces 2 NH , plus an anion. The anion formed is then metabolised to form HCO , which is - 4 3 reabsorbed. The NH , 4ecreted in the PCT is reabsorbed in the thick ascending loop of the loop of Henle and accumulates in the interstitial tissue before being excreted in the collecting duct. Blood Gas Interpretation OABC Approach O- Oxygenation • Accepted range for PO2 is 11-14 kPa. • PO2 <11 kPa indicates hypoxaemia. * If patient on high flow oxygen, PO 2hould be no more than 10 kPa less than the inspired PO2. • If pO2 < 8 kPa, this is termed respiratory failure. • Type 1 respiratory failure- hypoxia, with normal or low PCO . 2 • Type 2 respiratory failure- hypoxia with high PCO . 2 A-Acidosis vs Alkalosis •Accepted range for pH is 7.35-7.45. •pH <7.35 represents acidosis. •pH >7.45 represents alkalosis. B- Buffers (Bicarb/CO2 system) • Acidosis (pH <7.35) • If PCO 26 kPa- respiratory acidosis - • If [HCO ]3<22 mEq/L- metabolic acidosis • Alkalosis (pH >7.45) • If PCO 24 kPa- respiratory alkalosis - • If [HCO ]3>28 mEq/L- metabolic alkalosis C- Chronic/Compensated • Acidosis (pH <7.35) • If PCO >62kPa- respiratory acidosis→ if [HCO ] > 28 mEq/L, ch3onic • If [HCO ] <32 mEq/L- metabolic acidosis→ if PCO <4 kPa, chronic 2 • Alkalosis (pH >7.45) • If PCO <42kPa- respiratory alkalosis → if [HCO ] < 22 mEq/L, ch3onic • If [HCO ] >38 mEq/L- metabolic alkalosis → if PCO > 6 kPa, chronic 2 Base Excess • Refers to the amount of strong acid that must be added to the blood to maintain a pH of 7.40. • If the value of BE is negative, this indicates that there is a base deficit. • Normal range is -2 to +2 mEq/L. • Value > +2 indicates metabolic alkalosis. • Value < -2 indicates metabolic acidosis. Questions 1. 70M presents to ED with 3/7 hx of worsening SOB and productive cough. Patient is pyrexial on triage and saturating 88% on 40% FiO2. CXR showed R basal consolidation with hyperinflated lung-fields bilaterally. What is the likely diagnosis and interpret the followingABG (on 40% FiO ).2 pH 7.28 pCO 7289 kPa Bicarb 30 mEq/L PO 27 kPa Questions 2. 19M BIBAafter being found unrousable by partner. Collateral hx reveals diagnosis of T1DM with poor compliance- patient not taken insulin in over a week. ABG showed the following: pH 7.18 pCO 2.0 kPa Bicarb 14 mEq/L PO 23 kPa Questions 3. 75M 2/7 post-op following repaired fractured NOF, develops central pleuritic chest pain and is noted to be tachycardic and tachypnoeic. ABG (room air) showed the following: pH 7.47 pCO 2.8 kPa Bicarb 23 mEq/L PO 2.5 kPa Questions 4. 45F presented to ED with persistent vomiting. Patient’s daughter recently contracted norovirus. ABG (room air) showed the following: pH 7.50 pCO 2.8 kPa Bicarb 32 mEq/L PO 23 kPa References • Berne and Levy- Physiology (Sixth Edition)- Chapter 36 • Davidson’s Principles and Practice of Medicine (Twenty-third Edition)- Chapter 17 • https://i0.wp.com/www.aliem.com/wp-content/uploads/HHEq.png?fit=937%2C300&ssl=1 • https://encrypted- tbn0.gstatic.com/images?q=tbn:ANd9GcSt3Hwt9WYCYlS19ClQnL3SYMZRhtsUDJH8Jg&s • https://doctorlib.info/physiology/physiology/physiology.files/image761.jpg