Acid Base Lecture Notes PDF

Acid Base for Beginners/ Intermediates THE POWER OF HYDROGEN Dr Andrew Miller ACKNOWLEDGEMENT OF COUNTRY I’d like to begin today by acknowledging and paying respect to the Komumberri people and the Yugembah speaking people, the Minjungbal and Nandawul people, all Elders past, present and emerging on...

Acid Base for Beginners/ Intermediates THE POWER OF HYDROGEN Dr Andrew Miller ACKNOWLEDGEMENT OF COUNTRY I’d like to begin today by acknowledging and paying respect to the Komumberri people and the Yugembah speaking people, the Minjungbal and Nandawul people, all Elders past, present and emerging on whose land this lecture was prepared and presented. I’d like to specifically acknowledge the ongoing work that Australian First Nations health workers contribute to our workplace and improvement in health outcomes for all First Nations People. LECTURE OUTLINE Importance of acid-base and system effects Some theory Some definitions Some simple practical examples DEFINITION pH is -ve logarithm of [H+] Increase [H+] = decreased pH Normal serum pH ~ 7.35 -> 7.45 Intracellular pH ~ 7.2 Acidaemia/ Alkalaemia is state of blood as a result of an underlying process multiple processes Acidosis/ Alkalosis is underlying process differentiate for phrasing IMPORTANCE Cellular effects Denatures proteins De-functions enzymes and transmembrane transport System effects? range of effects arrythmias, reduced cardiac performance controlled acid/base metabolism vital stop working vasodilation increased pulmonary vascular resistance Morbidity and mortality? need to intervene and diagnose to avoid increased morbidity or potential mortality resp - electrolyte shifts K+ shift - CV collapse Risk of acute kidney injury mesenteric ischaemia coagulopathic - not clot easily (platelet activity reduced) affect all cells in body acidotic PRACTICALITY Bedside test Lots of information in ~ 5 minutes significant information e.g. blood gas blood gas to aid treatment PHYSIOLOGY No agreement on best model to use Henderson-Hasselbach (physiological) H20 + CO2 H2CO3 H+ + HCO3increase CO2 - increase hydrogen, decrease pH Under control of carbonic anhydrase Standard base excess Amount of base required to return sample to pH of 7.4 Under normal temperature, pressure and CO2 remove CO2 Stewart (quantitative) electrochemical balance Probably the most accurate/ realistic Definitely the most confusing add or subtract hydrogen affect pH PHYSIOLOGY No agreement on best model to use We will keep it simple (this time) and use the classic. The O.G. Henderson-Hasselbach (physiological model) H20 + CO2 H2CO3 H+ + HCO3- acidaemic - increase CO2, increase tachypnoea the focus Under control of carbonic anhydrase RESPIRATORY SYSTEM Oxygenation versus ventilation Control of O2 and CO2 Different receptors/ pathways more you breathe, more CO2 Oxygenation is less affected by minute ventilation OXYGENATION Primarily under control of carotid and aortic bodies Alveolar gas equation PAO2 = (FiO2 x (Patm-PH2O)) - (PaCO2/RQ) = FiO2 x 713 - PaCO2/0.8 VENTILATION Primarily under control of medullary chemoreceptors responsible for recognising changes in CO2 CO2 diffuses easily across BBB Then reacts to change H+ [] more easily than oxygen and bicarb H+ & HCO3 diffuse slowly across BBB BUFFERS Location Buffer/s Renal H+ excretion H2CO3 NH3 PO4Na/ Cl control lots of renal control Hb good buffer H2CO3/ Cl Protein Blood Intracellular fluid Interstitial fluid slightly different pH intracellular and extracellular buffer to maintain - via proteins phosphates Protein PO4H2CO3 via ammonia and phosphoric acid electrochemical and acid/base balance Haldene effects quicker buffer than renal system Albumin buffer acid/base RENAL HANDLING Bicarbonate Resorption kidneys upregulate or downregulate resorb sodium in same fashion Proximal tubule ++ relies on glomerular filtration Source: P. Kumar & M. Clark: Kumar and Clark’s Clinical Medicine, Eighth Edition Copyright Elsevier. RENAL HANDLING H+ excretion acidaema - excrete more of acid/H alkylaemia - excrete less of acid Distal tubule > proximal (proximal will just be resorbed) distal more than proximal excrete phosphoric acid or ammonia Excreted as phosphoric acid and ammonium Source: P. Kumar & M. Clark: Kumar and Clark’s Clinical Medicine, Eighth Edition Copyright Elsevier. metabolism FATE OF METABOLIC ACIDS kidney injury quickly develop acidosis as fail to excrete transport and excrete DERANGEMENTS Failure of respiratory system with regards to CO2 clearance too much or too little CO2 Failure of metabolic system with regards to H+/ HCO3- balance Acidosis or alkalosis RESPIRATORY ACIDOSIS Decreased CO2 clearance Decreased respiratory drive (TBI, drugs) Obstructive lung disease (COPD, OSA) brain telling to hyperventilate to clear CO2, but cannot clear Increased CO2 production RESPIRATORY ALKALOSIS Increased CO2 clearance hyperventilating to increase CO2 due to hypoxaemia? Pain Anxiety Hypoxia decondary to compensate for primary METABOLIC ACIDOSIS cannot clear electrolytes Added exogenous acids IE alcohols, normal saline Increased production endogenous acids IE keto acids, lactic acid Decreased clearance of endogenous acids IE urea, renal tubular acidosis, aldosterone antagonists Loss of bicarbonate IE renal tubular acidosis, pancreatic fluid loss, diarrhoea lose bicarbonate in stool - metaboic acidosis big picture... ANION GAP Merely the difference between measured cations and anions Na - Cl - HCO3 up to 16 Usually a gap of approximately 12 (some excluded anions IE albumin, lactate, etc) normal gap normal anion gap acidosis or high? Ketones or urea Based on principal of electroneutrality If the gap is widened then there are unmeasured anions Either added acids or endogenous unmeasured acids SIMPLE CONCEPT Na+ Clshould be matched HCO3if larger - extra anions e.g ketoacids, lactate... unmeasured can cause acidosis Albumin unmeasured ?K+ ??Anions Anion Gap 12 or less HAGMA if unmeasured -more likely Typically lactate, ketones or urea most common Can be other toxins Toxic alcohols Salicylates Paracetamol (Pyroglutamic acidosis) accumulation of unknown MUDPILES or KULT NAGMA Typically saline administration Can also commonly be aldosterone antagonists or diarrhoea Multiple other causes however aldosterone antagonists PANDARUSH METABOLIC ALKALOSIS Increased loss of endogenous acids IE vomiting, diuretic use, steroids more mortality associated than acidosis Gain of bicarbonate IE iatrogenic administration COMPENSATION Respiratory derangement will result in metabolic adjustment to maintain homeostasis Vice versa hypercarbic Respiratory compensations quick (IE minutes -> hours) retain to offset due to pain or anxiety bicarbonate changes as result pH down = try and decrease CO2 Metabolic compensations slower (IE hours -> days) renal depends on person and compensation OTHER STUFF (FOR NEXT TIME) uncover different acid-base issue Base Excess Compensation rules Delta gap Osmolar gap Strong Ion Difference IT JUST KEEPS GETTING BETTER!!!!! WORKED EXAMPLES Treat blood gases like ECG’s and CXR Understand the physiology Then practice Rinse & Repeat 1 65 yr old pH 7.17 Increasing SOB for 2-3 days PaCO2 75 Hx of COPD, on home oxygen HCO3 28 acidosis metabolic alkylosis GCS 14, slightly drowsy 40 normal 24 normal increased 1 (ANSWER) History suggests respiratory cause pH 7.17 -> acidaemia (so primary acidosis cause likely) PaCO2 75 -> increased so respiratory acidosis HCO3 28 -> increased so metabolic alkalosis (compensation) std body pH - 7.35-7.45 2 55yr old pH 7.28 acidosis closer to normal now Increasingly drowsy PaCO2 90 resp acidosis History of OSA, non compliant with CPAP HCO3 44 renal compensation No recent infections or illnesses acidaemia 2 (ANSWER) History non specific pH 7.28 -> acidaemia PaCO2 90 -> significantly increased so respiratory acidosis likely primary cause HCO3 44 -> significantly increased so metabolic alkalosis (compensation) 3 22yr old pH 7.55 Presents to ED with anxiety attack and tachypnoea PaCO2 20 Has some personal tingling HCO3 24 No oxygen requirement alkylosis respiratiory alkylosis not able to compensate yet 3 (ANSWER) History suggests respiratory cause (although tachypnoea can be a compensation for metabolic acidosis) pH 7.55 -> alkalaemia PaCO2 20 -> decreased so respiratory alkalosis likely primary cause HCO3 24 -> normal so no metabolic component 4 33yr old Hx of type 1 diabetes pH 6.95 DKA PaCO2 17 acidaemic low pCO2 respiratory alkylosis Recent binge over weekend and non compliant with medications BSL 30 on arrival, ketones 4.5 HCO3 6 very low 4 (ANSWER) History suggests metabolic component pH 6.95 -> significant acidaemia PaCO2 17 -> decreased so respiratory alkalosis (likely compensation) HCO3 6 -> significantly decreased so metabolic acidosis (likely primary cause) 5 72 year old pH 7.55 Recently started on frusemide by GP PaCO2 50 Feeling unwell and presented to ED HCO3 40 ALKYLAMIA high - mild resp acidosis high moderate alkylaemia 5 (ANSWER) History non specific pH 7.55 -> alkalaemia PaCO2 50 -> elevated so respiratory acidosis HCO3 40 -> significantly elevated so metabolic alkalosis as likely primary cause SUMMARY Walk before you run Understand the concepts and basics then apply in real life situations Plentiful resources for both basic sciences and worked examples THAT’S IT! [email protected] Happy to answer any questions but will have the questions/ answers put through to everyone Feedback is appreciated through the formal feedback channels REFERENCES K.E. Barrett, S.M. Baman, H.L. Brooks, X.J. Yuan: Ganong’s Review of Medical Physiology. Twenty-Sixth Edition. McGraw-Hill Education H. Gomez & J. Kellum, Understanding acid base disorders. Critical Care Clinics. 2015; 31:849860. J. Kellum & P. Elbers: Stewart’s Textbook of Acid Base. Second Edition. lulu.com P. Kumar & M. Clark: Kumar and Clark’s Clinical Medicine. Tenth Edition. Elsevier WEBSITES http://www.anaesthesiamcq.com/AcidBaseBook/ABindex.php https://derangedphysiology.com/main/cicm-primary-exam/requiredreading/acid-base-physiology https://litfl.com/acid-base-disorders/