Advanced Pathophysiology Unit 8: Acid/Base/Lytes Page 1 of 31

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1 Advanced Pathophysiology Unit 8: Acid/Base/Lytes Page 1 of 31 Learning Objectives for this File: 1. Review acids, bases and chemical relationship. 2. Understand acid dissociation, conjugate base 3. Review clinical correlates of acidosis and alkalosis 4. Review the ph scale 5. Understand what buffer systems do 6. Understand the concept of base excess 7. Review the physiologic buffer systems respiratory, chemical, renal and how they work 8. Review each of the metabolic acid-base derangements metabolic acidosis & alkalosis and associated electrolyte & clinical findings 9. Understand how to use the anion gap in acidosis to determine if the cause is gained acid or lost base 10. Review each of the respiratory acid-base derangements respiratory acidosis & alkalosis and associated electrolyte & clinical findings 11. Recognize the expected physiologic compensatory responses to an acid-base derangement 12. Understand how to proceed through a clinical algorithm to determine the type of acid-base derangement, its cause, its expected compensatory response, and if it is acute or chronic 13. Understand how to use the acid-base nomogram to determine the clinical diagnosis based on ABG results

2 Advanced Pathophysiology Unit 8: Acid/Base/Lytes Page 2 of 31 ACID-BASE BALANCE THESE ARE ALL RELATED TOPICS: Acid-base analysis which includes the Anion Gap analysis which prepares you to actually USE a clinical Arterial Blood Gas (ABG) analysis These topics could also easily fit into the RENAL or PULMONARY sections They are all connected topics since pulmonary and renal systems work together to insure homeostasis of acid-base balance Add in oxygenation and you ve got it all tied together ONLINE RESOURCES: these are all pretty terrific!! GREAT Tutorials on acid-base interpretation: Great historical explanations why the terminology is so weird!! o Go to: o See Awkward Inverses Merck Manual Online: discussion starts at the link below, keep going to the rest of the sections in this chapter to see all the pathology discussions. o id-base_regulation_and_disorders/acid-base_regulation.html?qt=&sc=&alt= Excellent website showing all about how to obtain an actual ABG: Clinical discussion: (Berend, DeVries & Gans, 2014, New England Journal of Medicine) Great charts and clinical algorithms Williams AJ. Assessing and interpreting arterial blood gases and acid-base balance. BMJ1998;317: ( 31 October ) at: Includes discussion of tutorial on actually TAKING the ABG from a live person and analyzing the results: This is from year 1998 but still really good!!!! (register for free access)

3 Advanced Pathophysiology Unit 8: Acid/Base/Lytes Page 3 of 31 HOW TO TAKE AN ARTERIAL BLOOD GAS (ABG): Excellent website showing all about how to take ABG: (These pictures from the above website) Method: obtain from arterial site Arterial Stick: Usually done on radial artery (very accessible) perform Allen s test first to verify patency of palmar arch vessels first compress BOTH ulnar and radial arteries at the SAME time to see the hand blanch then, release ONLY the ulnar artery the whole hand should pink up within 8 seconds if not, the ulnar artery is not enough to perfuse the hand and you should NOT perform radial artery catheterization Allen s Test Arterial Puncture More below on Allen s test

4 Advanced Pathophysiology Unit 8: Acid/Base/Lytes Page 4 of 31 Allen s test: Note the normal color of the palmar surface of the hand (pink from perfusion) Now, Allen s test is blanching the hand (turns white) due to complete compression of BOTH the radial & ulnar arteries Now, ONLY release the ulnar artery the hand completely pinks up and you know that the ulnar artery ALONE is capable of perfusing the hand This person can now have an arterial stick for a blood gas even if a hematoma develops that obstructs the radial artery, the ulnar artery alone will be able to maintain adequate perfusion of the hand In some people, when the ulnar artery is released, only the ulnar side of the hand is perfused (the radial side stays white) this person needs to have their ABG taken from a larger artery (e.g. femoral) this actually has happened when I demonstrated this in a physical diagnosis class on one of the students! She had no idea and was considering tattooing on her person do not take ABG from radial artery!! From: Williams AJ. Assessing and interpreting arterial blood gases and acid-base balance. BMJ1998;317: ( 31 October ) at: Includes discussion of tutorial on actually TAKING the ABG from a live person and analyzing the results: This is from year 1998 but still really good!!!! (register for free access)

5 Advanced Pathophysiology Unit 8: Acid/Base/Lytes Page 5 of 31 ACID-BASE BASICS Acids & Bases: A base (alkali) is something that can accept an H+ in solution An acid is something that gives up an H+ in solution What is H+? it is a hydrogen atom with its electron removed o Thus it is mainly a proton o It is also called the hydronium ion because in water it combines with H2O (H+) + (H2O) (H3O+) This is how H+ ions exist in human systems since we are water-based critters o You will hear this referred to as a proton, a hydronium ion, a hydrogen ion Remember that substances with an electrical charge are ions o H+ is a free proton that can interact with negatively charged chemical o Positive (H+) and negative ions attract & combine o Remember that positive ions are cations and negative ions are anions Where do we get the H+ ions?? o In solution, acids are chemical substances that break apart ("dissociate") to form hydronium ion(s) o When you make a hydronium ion, you also make a conjugate base o The word conjugate means to pair (i.e., conjugal prison visit ) o So for the creation of every bit of acid, there is an equal creation of conjugate base (another substance that is a base) o The -ic acid creates the -ate base (carbonic acid creates bicarbonate) o the strength of the acid depends on how readily the acid releases its H + ions See ph scale next page for some examples of acids & bases Examples of acids & conjugate bases commonly found in the body are: o hydrochloric HCl (HCl H+ and Cl-), conjugate base: chloride ion (Cl-) o carbonic H2CO3 (H2CO3 H+ and HCO3-), conjugate base: bicarbonate ion (HCO3-) o phosphoric H2PO4 - o ammonium NH4 + (NH4+ H+ and NH3), conjugate base: ammonia (NH3) o note that some of these acids are also charged substances Concentration of H + in our body s fluids is important for homeostasis o Our internal environment requires narrow ph concentration limits o Mostly so enzymes and other proteins can work properly o Remember the function of any protein depends on how it folds up in 3D space o This folding up (configuration) is dependent on temperature and ph o So most of our homeostasis is a focus on maintaining temperature & ph!!!

6 Advanced Pathophysiology Unit 8: Acid/Base/Lytes Page 6 of 31 How do we describe and measure acids and bases? The ph system A mathematical way to handle very small numbers These acids and bases exist in very small amounts in our body fluids (which is water) ph: mathematical function helping us deal with super small numbers like H + concentrations of a logarithm function ph means the negative logarithm of the H + concentration expressed to the base 10, ph = log 1/(H + ) = - log (H + ) o example: H+ conc = 10-7, the ph = 7 there is an inverse relationship of ph to H + concentration SO a low ph number means a high number of H+ ions and MORE acidity SO a high ph number means a low number of H+ ions and LESS acidity (more alkalinity)

7 Advanced Pathophysiology Unit 8: Acid/Base/Lytes Page 7 of 31 ph of body fluids: Usually the ph is maintained in these fluids to enhance the function of enzymes and other proteins in that area o The reaction time of enzymes is dependent on ph and temperature o The function of structural proteins is also dependent on ph and temperature Blood: o arterial blood ph = 7.4, venous blood ph = 7.35 (more CO2, which acts as an acid due to its conversion with H2O to carbonic acid) o intracellular ph is low (more metabolic acid waste products) & is lower still if hypoxic and unable to perform oxidative metabolism and/or rid cell of waste due to poor circulation. Limits of life = ph range of 6.8 to 8.0. Other body fluids: o Urine: can range from 4.5 to 8.0 (in order to rid the body of acid or alkali as needed). o Stomach fluid: can go as low as 0.8 due to parietal (oxyntic) cell secretion of HCl. (Coca-Cola is ph of about burns off car paint). o Feces: alkalotic. Optimum enzyme function depends on ph

8 Advanced Pathophysiology Unit 8: Acid/Base/Lytes Page 8 of 31 Buffers: any system that resists a ph change that might occur due to the addition of acid or alkali to the solution o chemicals in the solution absorb either the acid or alkali, neutralizing the effect of their being added to the solution in humans, it is the acid buffer system that is of most importance o there is continuing accumulation of acids in the body (result of metabolic processes) o the more hypermetabolic (e.g. infection, inflammation) the more acidic that area of the body becomes o we always a need to buffer their addition to body systems many buffers in our bodies are anions that combine with H+ buffer systems absorb the H + ion to protect the ph o thus, the H+ is not able to react with other chemicals o eventually, the body excretes the excess acid via urine (fixed acid excretion in water) renal pathway ventilation (volatile acid excretion in expired CO2 breath) lung pathway a buffer reaction looks like this: o BUFFER + H + H-Buffer o Buffer grabs the acid, reaction can go both ways to also release the H+ again Review the Human buffer systems: THREE buffer systems in our body 1) chemical buffers in water solution within a fraction of a second will combine with acid include proteins (such as hemoglobin) most buffering takes place inside our RBC o Protein + (H+) (Protein-H+) loose association o very rapid but can t handle TOO MUCH acid addition includes carbonic anhydrase buffer system: (H+) + (HCO3-) (H2CO3) (CO2) + (H2O) Acid + bicarbonate carbonic acid carbon dioxide + water Thus, whenever we say CO2 WE ARE SAYING ACID because of the interrelation above 2) respiratory center "buffer" (sometimes called a physical buffer ) pulmonary ventilation removes CO2 this is a volatile (gas CO2) acid called blowing off acid when we breathe out CO2 very rapid but not powerful enough to manage our acid-base balance on its own 3) renal buffers the kidneys can excrete either acid or alkaline urine as needed thus the acid excretion would be a fixed acid excretion (in water) very powerful, but can take days to complete this action

9 Advanced Pathophysiology Unit 8: Acid/Base/Lytes Page 9 of 31 ACIDOSIS: Most acids in our bodies are weak o strong acid: HCl o weak acid: H2CO3 o note that the HCl is mostly found in the gastric (stomachic) juices, where there are multiple mechanisms in place to protect the gastric mucosa o when we have GERD (acid reflux disease) the esophagus is terribly damaged (esophagitis, which can lead to cancer) because those protective mechanisms are not found outside the stomach lining Acidemia means increased acid in the bloodstream (the -emia ending means blood) o DEFINITION: ph of arterial blood is < 7.35 Acidosis means increased acid in the body in general (any derangement with excess acid) o The excess acid can come from either respiratory problems, or metabolic problems, or both (mixed) o CAUSE IS: acid gain or alkali loss ALKALOSIS: a molecule or ion that can accept an H+ is called a base o this type of substance is also called alkaline (alkali) Amino acids make up protein o Most have negative charges, therefore function as bases o Thus, most proteins in the body can function as bases important when we consider acid-base balance and buffers (protect body against changes in acid-base status) The strength of the base is how strongly the base accepts the H + and removes it from solution o strong base: NaOH -- lye, weak base: HCO3 - o True alkalis are really the alkaline metals such as Na+, K+, Li+ in combination with an hydroxyl ( OH - ) ion. Most acids/bases in body solutions/systems are weak Alkalemia means excess base in the blood o DEFINITION: ph of arterial blood is > 7.45 Alkalosis means excess base in the body in general (any derangement of alkalinity being too high) o CAUSE is: acid loss or alkali gain

10 Advanced Pathophysiology Unit 8: Acid/Base/Lytes Page 10 of 31 Measure of metabolic acid-base disturbance what is the Base Excess : The buffer base = total of all anion buffers in blood o these are usually the conjugate bases like bicarbonate (HCO3-), sulfate, phosphates Measuring the base excess is looking at how far the patient s ph is deviating form normal (how much extra conjugate base is needed to balance the acid in the blood) thus a measure of metabolic disturbance Clinically, this is determined from values on the ABG o Just using the deviation from the normal bicarbonate value (normal bicarbonate is 24) may not be accurate, since the bicarbonate value is calculated from pco2 and ph o The base excess is more accurate, taking into account other buffers and remaining accurate even with anemia (and reduction of hemoglobin s buffering capacity) This can be a negative value o example: if acidotic your base excess is negative you would have to take away acid to come to normal, in other words, you d have to add base so therefore, you have less base than you need for balance There is a BASE EXCESS and a STANDARD BASE EXCESS o Base Excess: Base excess is the quantity of acid or alkali to return blood under standard conditions (ph 7.40, 37C, PCO2 40 mm Hg) Normal Base excess is between -3 and +3mEq/L General rule: a base excess > +3 = metabolic alkalosis a base excess < -3 = metabolic acidosis o Standard Base Excess Standard base excess is the quantity of acid or base required to return the plasma (ECF) to a normal ph under standard conditions (ph 7.40, 37C, PCO2 40 mm Hg) If available on your lab report, this is a more reliable value to use and is not affected by anemia The idea is that this represents the acid-base status of the entire body, not just blood

11 Advanced Pathophysiology Unit 8: Acid/Base/Lytes Page 11 of 31 MORE ON ACID BASE IMBALANCE: COMPENSATIONS WHAT CAN THE BODY DO TO RESTORE HOMEOSTASIS? Remember, the primary problem could be o metabolic causes o respiratory causes o or mixed metabolic/respiratory Then, the compensatory response of the body would then be either/both o metabolic (kidney actions & buffering actions) o respiratory (lung actions) RESPIRATORY compensation (response) to a primary METABOLIC acid-base imbalance: Excretion of the volatile acids (CO2) o in equilibrium with the bicarbonate buffer system o INCREASED CO2 excretion means LOSS of ACID o DECREASED CO2 excretion means GAIN of ACID Biofeedback between ventilatory rate and ph/pco2 maintains homeostasis This is called the "physical" buffer For an Acute ACIDOSIS from primary metabolic cause: o GAIN of acid exists in equilibrium with CO2 due to carbonic anhydrase system o increased PCO2 level indirectly drives this buffer system by feedback to the brain's respiratory centers o CO2 CSF converts to H2CO3 H+ ion crosses into respiratory center chemosensitive cells of medulla decreased ph in CNS causes increased RR o This effect tapers off after a few days in chronic acidosis, the renal compensatory system takes over for long-term compensation For an Acute ALKALOSIS from primary metabolic cause: o the ventilation rate is lowered to try and retain CO2 (to retain acid, and lower ph) o BUT since this ALSO leads to hypoxemia the drive for respiration picks up again. LESSON TO BE LEARNED: o the respiratory system alone cannot completely return the ph to normal if there is extra-respiratory cause of acid-base imbalance o it can only help restore ph in the right direction o we need the KIDNEY for final compensation to return to homeostasis

12 Advanced Pathophysiology Unit 8: Acid/Base/Lytes Page 12 of 31 METABOLIC (RENAL & BUFFERING) compensation (response) to RESPIRATORY acidbase imbalance: Respiratory system pathology can lead to acid-base imbalance, examples: o retained CO2 in emphysema respiratory acidosis o hyperventilation respiratory alkalosis & hypocalcemic symptoms such as carpopedal spasm For an Acute ACIDOSIS from primary respiratory cause: o ICF Potassium exchanges with ECF hydrogen ion for immediate reduction in acidosis potassium LEAVES the cells and HYDROGEN ION enters the cells this is why serum hyperkalemia is usually associated with acute acidosis o Intracellular buffering occurs (mostly using Hemoglobin in the RBC) o Same carbonic anhydrase buffering as described above increased CO2 means GAIN of ACID o Renal compensation responses include: Increased reabsorption of bicarbonate (to gain base) Actual synthesis of new bicarbonate (to gain base) Secretion of titratable (fixed) acids (to excrete more acid) For an Acute ALKALOSIS from primary respiratory cause: o Usually, if from hyperventilation the person passes out and starts breathing normally! o If from other causes of hyperventilation may require sedation and mechanical ventilation e.g. CNS hemorrhage, pregnancy (progesterone effect), drug effects o Pregnant women NORMALLY have a different ABG profile ph normally more alkalotic approximately ph = 7.46 in the third trimester More on the renal compensatory responses below

13 Advanced Pathophysiology Unit 8: Acid/Base/Lytes Page 13 of 31 RENAL regulation of acid-base (Things the Kidney can do): 1) Tubular reabsorption of bicarbonate: Hydrogen ion is secreted into the urine using a Na-H+ counter-transport carrier molecule (early nephron) this requires an ATP expenditure at the opposite side of the cell where the Na-K pump is setting up the Na+ gradient. Hydrogen ion combines with the filtered bicarbonate to form carbonic acid o this dissociates into CO2 & H2O o the CO2 diffuses back into the renal cell o converts to carbonic acid o dissociates into bicarbonate & H+ o bicarbonate now can diffuse back into the ECF (reabsorbed).

14 Advanced Pathophysiology Unit 8: Acid/Base/Lytes Page 14 of 31 2) Excretion of FIXED (non-volatile acids): Phosphate buffer system: 1) excretion of fixed, non-volatile acid; 2) phosphate in filtrate combines with H+ to form phosphoric acid Ammonia buffer system: 1) dominant way acid is excreted in chronic acidosis. 2) Ammonia is secreted by proximal tubular cells (coupled to acid secretion) & accepts H+ ion in the collecting tubules yielding ammonium (NH4 + ) 3) Coupled bicarbonate reabsorption & hydrogen ion (acid) secretion: both base is retained & acid is excreted in the distal nephron (intercalated cells) stimulated by aldosterone Acid secretion only works down to urine ph of 4.5 o excess Aldosterone (Conn's syndrome) can therefore lead to alkalosis

15 Advanced Pathophysiology Unit 8: Acid/Base/Lytes Page 15 of 31 4) In TERRIBLE acidosis the kidney makes brand-new bicarbonate (base): renal cell can also make new bicarbonate and add this into the ECF Uses amino acid glutamine o bicarbonate is synthesized and reabsorbed o ammonium is excreted OVERVIEW SUMMARY: What the kidney does in acidosis: LOSS of ACID o an acid urine would be produced in acidotic conditions, especially chronic acidosis o increased excretion of non-volatile (fixed) acids such as phosphoric acid & ammonium o increased excretion of H+ coupled to increased bicarbonate reabsorpton o LOSS of ACID in response to acidosis GAIN of BASE o increased reabsorption of bicarbonate to add base to the system o possibly synthesis of new bicarbonate as well (coupled to ammonium excretion) What the kidney does in alkalosis: a basic urine would be produced in alkalotic conditions. reduced reabsorption of bicarbonate (loss of base)

16 Advanced Pathophysiology Unit 8: Acid/Base/Lytes Page 16 of 31 METABOLIC DERANGEMENTS: 1. METABOLIC ACIDOSIS: LOSS of bicarbonate (diarrhea) GAIN of acid either endogenous acid production (Diabetic ketoacidosis, DKA) or retention (uremic kidney failure) or exogenous addition (salicylate poisoning). Correlates: THINK HYPERKALEMIA!!! except in a renal condition, called Renal Tubular Acidosis Compensatory response: since the problem is metabolic, the compensation is respiratory blow off CO2 (volatile acid) Increased depth & rate of respiration Kussmaul respirations. Presentation: Kussmaul respirations, abdominal pain, increased uric acid, increased K+, increased Calcium levels (released from albumin as ph goes down). The Calcium change causes skeletal muscle flaccidity & increased cardiac tone & conduction (arrhythmias). Treatment: oxygen (for CO poisoning) dialyze (uremia, toxins) insulin (in diabetic ketoacidosis (DKA) to move glucose and potassium acutely into cells)

17 Advanced Pathophysiology Unit 8: Acid/Base/Lytes Page 17 of 31 THE ANION GAP and METABOLIC ACIDOSIS: WHAT IS IT? This is a concept introduced in 1977, to help narrow DDX in acid-base disturbances by deciding if it is due to: o a loss of bicarbonate (in GI fluid or urine) o OR addition of acid Additional endogenous acid (production & retention: uremia, DKA) Addition of exogenous acid (toxins) Doing some math on measured cations & anions (from chemistry labwork) determines if results are normal or abnormal (there is a "gap"). Based on the clinical setting, this leads to etiology. HOW TO DO IT: Electrolytes are charged particles occurring in living systems, cations = positively charged electrolytes and anions = negatively charged electrolytes. First, you must determine if the patient is acidotic (using an ABG). Then, determine if the anion gap is normal, decreased, or increased. The formula to do this is main cation minus main anions Na - (Cl + HCO3) = 12 (normal gap) (Na anions = 12) OR (Na + K) (Cl + HCO3) = 14 (cations anions = 14) CLINICAL CORRELATES mostly used in ACIDOTIC patients: Acidosis: arterial ph < 7.40 (need an ABG to know this) An increased anion gap in acidosis is assumed to be caused by the net gained acids A normal anion gap in acidosis would be due to net loss of anion (bicarb) o So metabolic acidosis is often referred to as: Anion gap acidosis (GAINED acid from endogenous or exogenous source) Non-anion gap acidosis (LOSS of bicarbonate base) Anion-gap acidosis gained acid: increased endogenous anions (lactate, sulfate, phosphate, ketones) o e.g. uremia (kidney failure), diabetic ketoacidosis increased exogenous acids o e.g. ingestions of salicylate, methanol, ethanol, paraldehyde, ethylene glycol Non-anion gap acidosis lost base: Loss of alkali (base) Usually, bicarbonate losses o e.g. due to diarrhea, RTA, drugs (carbonic anhydrase inhibitors like acetazolamide), pancreatic fistula Note that although the anion gap is normal, the base excess will be abnormal NOTE: it is also used in non-acidotic patients, but not very much, so I am not going to discuss that here.

18 Advanced Pathophysiology Unit 8: Acid/Base/Lytes Page 18 of 31 From: Berend, K., de Vries, A.P.J. & Gans, R.O.B. (2014) Physiological approach to assessment of acid-base disturbances, New England Journal of Medicine, 371(15), Retrieve from This is a great review article with lots of charts and clinical algorithms

19 Advanced Pathophysiology Unit 8: Acid/Base/Lytes Page 19 of METABOLIC ALKALOSIS: GAIN of base (bicarb therapy) LOSS of acid (vomiting, NG tube losses, sometimes diuretic therapy).

20 Advanced Pathophysiology Unit 8: Acid/Base/Lytes Page 20 of 31 Clinical Correlates: THINK HYPOKALEMIA in alkalosis!!! Compensatory mechanism: retain acid can't hold your breath long enough to build up CO2 (acid), so renal mechanisms must compensate increased renal bicarbonate excretion -- requires good renal blood flow. If volume contracted (reduces renal blood flow), hyperaldosterone state occurs and paradoxical bicarbonate reabsorption occurs. Symptoms: confused (brain ph) Calcium levels decrease (bound more tightly to albumin with increasing ph) cardiac flaccidity (poor cardiac output, bradycardia) & skeletal muscle tetany. Treatment: normal saline to volume expand and is self-correcting especially since fluids have chloride which enhance renal bicarb excretion.

21 Advanced Pathophysiology Unit 8: Acid/Base/Lytes Page 21 of 31 RESPIRATORY DERANGEMENTS: 1. RESPIRATORY ACIDOSIS: common decreased ph from retained CO2 compensation is metabolic (renal) increased renal exretion of acid and increased renal reabsorption of bicarbonate (base). symptoms the same as for metabolic acidosis. Acute: respiratory arrest Chronic: o lung pathology impairing ventilation o so that acid (CO2) is chronically retained (e.g. COPD) = hypercarbia (too much CO2) Clinical Correlates: respiratory drive from CO2 is lost in COPD -- chronic hypercarbia Do not use O2 at high levels by nasal cannula if they lose their O2 respiratory drive, they won t breathe at all! Since the CO2 drive is gone. Treatment: fix the underlying ventilatory pathology Compensatory mechanism: since the etiology is respiratory, renal mechanisms must compensate increased renal acid excretion & increased renal bicarbonate reabsorption.

22 Advanced Pathophysiology Unit 8: Acid/Base/Lytes Page 22 of RESPIRATORY ALKALOSIS: not common. Decreased CO2 from hyperventilation renal compensation of decreased bicarb reabsorption. Correlate: free ionized serum Calcium levels decrease (bound more to albumin as in any alkalosis) skeletal muscle tetany (carpopedal spasm of hyperventilation), cardiac flaccidity.

23 Advanced Pathophysiology Unit 8: Acid/Base/Lytes Page 23 of 31 ACID-BASE IMBALANCE INTRODUCTION OVERVIEW: is there acidosis or alkalosis? what is the PRIMARY derangement? is it pure metabolic or pure respiratory? is it a mixed disorder what is the compensation to restore the ph to normal? The idea of COMPENSATION: (SEE MORE BELOW) If something goes wrong, your body tries to fix it by COMPENSATING SO: o In a METABOLIC problem, the RESPIRATORY system tries to compensate o In a RESPIRATORY problem, the METABOLIC system tries to compensate Respiratory compensation: o If acidotic: Blow off volatile acid CO2 by hyperventilating and excreting acid as CO2 Rapid but not very powerful Example: Kussmaul breathing in diabetic ketoacidosis o If alkalotic: Hold onto more acid in the body by NOT breathing (hold onto your CO2) obviously you can t do this too long you would suffocate from lack of oxygen!! Not a good method Metabolic compensation: o If acidotic: Kidneys excrete more fixed acids in urine & reabsorb more bicarbonate Kidney can even synthesize bicarbonate (making more base for the body) Very powerful, but slow (can take days) o If alkalotic: Excrete less acid in urine Reduce reabsorption of bicarbonate from filtrate How do we approach the problem using laboratory diagnostics? ask a series of questions remember o If it is METABOLIC cause, there is RESPIRATORY compensation. o If it is RESPIRATORY cause, there is METABOLIC compensation.

24 Advanced Pathophysiology Unit 8: Acid/Base/Lytes Page 24 of 31 ASK yourself: 1) is it acidosis or alkalosis? Obtain a arterial blood gas (ABG) and look at the ph value Normal arterial blood ph = 7.40 (+/-) 0.02 Acidemic: ph < 7.38 Alkalemic: ph > ) Is the problem due to METABOLIC or RESPIRATORY causes or BOTH (mixed)? check the ph direction change and the direction change of bicarb & PCO2 o the compensation itself may be acute or chronic (long-term problem?) o and, the problem may be pure or mixed Pure Metabolic: o ph changes in the SAME direction as bicarb & pco2 (see arrows on chart) o Metabolic Acidosis: ph decreased AND bicarb decreased (<22) (primary problem) AND PaCO2 decreased (compensatory) PCO2 = bicarb + 15 PCO2 = last two digits of ph x 100 o Metabolic Alkalosis: ph increased AND bicarb increased (>26)(primary problem) AND PaCO2 increased (compensatory) increase PCO2 for every 1 increase in bicarb Pure Respiratory: o ph changes in OPPOSITE direction of bicarb & PCO2 (see arrows on chart) o RespiratoryAcidosis: ph decreased AND PaCO2 increased (>42)(primary problem) AND bicarb increased (compensatory) Acute: bicarb goes up 1-2 for every 10 increase in PCO2 Chronic: bicarb goes up 2-4 for every 10 increase in PCO2 o Respiratory Alkalosis: ph increased AND bicarb & PaCO2 decreased (<38) Acute: bicarb goes down 1-2 for every 10 decrease in PCO2 Chronic: bicarb goes down 4-5 for every 10 decrease in PCO2 (Bicarb units are mmol/l) Changes in ph will result in compensations to try and return the ph to normal. These stabilize over time in chronic conditions.

25 Advanced Pathophysiology Unit 8: Acid/Base/Lytes Page 25 of 31 A simple acid-base disorder is a single acid-base disturbance with its accompanying compensatory response also called a pure acid-base disturbance. From Merck Manual Online

26 Advanced Pathophysiology Unit 8: Acid/Base/Lytes Page 26 of 31 More on expected changes in acid-base compensations: (from the Merck Manual online) 3) Is it PURE or MIXED? is it PURE (metabolic ONLY, or respiratory ONLY)(also called simple)? o The ph varies by units for every 1 mm Hg change in PCO2 for pure o If this is NOT seen, it may mean a mixed derangement Is it MIXED (contribution of derangement from BOTH systems?) (more below) What if it isn t PURE? In mixed disorders, the numbers don t match up like they should We use a nomogram to figure it out

27 Advanced Pathophysiology Unit 8: Acid/Base/Lytes Page 27 of 31 From: Berend, K., de Vries, A.P.J. & Gans, R.O.B. (2014) Physiological approach to assessment of acidbase disturbances, New England Journal of Medicine, 371(15), Retrieve from oi/full/ /nejmr a This is a great review article with lots of charts and clinical algorithms

28 Advanced Pathophysiology Unit 8: Acid/Base/Lytes Page 28 of 31 What is a nomogram? A graphical representation of data that connects different types of measurements o Example: West Conversion chart for pediatric height & surface are this is necessary for drug dosing in kids, estimation of dehydration, etc. connect the known height & weight and the BSA is where the line crosses the middle column

29 Advanced Pathophysiology Unit 8: Acid/Base/Lytes Page 29 of 31 HERE IS THE ACID-BASE NOMOGRAM: Match up your ph, Bicarb (HCO3), PCO2 values on the chart on the next page Where your values intersect, you can see what PURE derangement exists, and if it is ACUTE or CHRONIC If your values intersect OUTSIDE the SHADED MARKED areas, you have a MIXED derangement both metabolic AND respiratory causes of your problem Examples: o 1) ph 7.2, PCO2 of 25, bicarb of 10 where do they intersect? The section marked metabolic acidosis this is a seriously ill person with metabolic acidosis note the low bicarb (metabolic cause) and the low PCO2 (respiratory compensation) o 2) ph 7.3, PCO2 65, bicarb 36 where do they intersect? The section marked chronic respiratory acidosis this is a COPD patient with chronic acidosis from CO2 retention from pulmonary cause his kidneys (metabolic) compensate with a high bicarb o 3) ph 7.2, PCO2 45, bicarb 18 doesn t intersect anywhere in the marked shaded areas this is a derangement of both respiratory and metabolic problems together you are on your own with this one!! Who KNOWS what evil lurks here??? Small version of the chart to get the idea use the BIG chart on the next page for examples above:

30 Advanced Pathophysiology Unit 8: Acid/Base/Lytes Page 30 of 31 STEP BY STEP APPROACH IN FP NOTEBOOK: (anion gap) and (anion gap results) and (base excess) This is a fantastic resource just follow the steps to evaluation of the ABG result.

31 Advanced Pathophysiology Unit 8: Acid/Base/Lytes Page 31 of 31 Overview of Clinical Consequences of Acid-Base Disorders: From, Merck Manual Online,