Acid-Base Physiology Notes (2024) PDF

WSUSOM Medical Physiology Rossi-Acid Base Physiology Page 1 of 18 Acid Base Compensation Acid Base: Physiologic Compensation Learning Objectives: 1. Acid base imbalance A. Identify and classify acidemia vs alkalemia B. Identify a...

WSUSOM Medical Physiology Rossi-Acid Base Physiology Page 1 of 18 Acid Base Compensation Acid Base: Physiologic Compensation Learning Objectives: 1. Acid base imbalance A. Identify and classify acidemia vs alkalemia B. Identify and classify respiratory imbalances vs metabolic imbalances 2. Physiologic compensation A. Define what is meant by compensation for acid base disorders B. Learn the role of the lungs and the kidneys compensation of acid base disorders 3. Primary (“simple”) acid base disorders A. Develop a proficiency in using the acid base map to identify and categorize acid base disorders B. Know the buffering systems involved in response to the disturbance C. Estimate the expected compensatory response for acid base disorders D. Identify the paradigm diseases associated with each of the primary acid base disorders WSUSOM Medical Physiology Rossi-Acid Base Physiology Page 2 of 18 Acid Base Compensation Acid-Base Imbalance Definitions Acid base disturbances are classified first by pH: Acidemia – condition where pH < 7.40 (normal at sea level) Alkalemia – condition where pH > 7.40 (normal at sea level) Then, sub-classified based on changes in carbonic acid or non-carbonic acid content: Respiratory imbalance – changes in pCO2/carbonic acid due to changes in ventilation § D in volatile acid: pCO2 = measure of carbonic acid unbalance § pCO2 excess = respiratory acidosis § pCO2 deficit = respiratory alkalosis Metabolic imbalance - changes in non-carbonic acid with base excess/deficit § D in nonvolatile acid § Base deficit = metabolic acidosis § Base excess = metabolic alkalosis If an arterial blood sample has abnormal pH, pCO2 and/or [HCO3-] values, then there is an acid base imbalance. The fact that the values are abnormal indicates a disturbance, but what is the SIZE of the disturbance? § the value of pCO2 is a good measure of the size of a carbonic acid imbalance but § [HCO3-] is not a direct measure of the size of a non-carbonic acid imbalance… § need to evaluate the base excess/base deficit Normal Range: Acid-Base Values The BOLD hexagon delineates the ranges of pH, pCO2 and [HCO3-] values in normal humans living near sea level with a body temperature of 37oC. - pH » 7.35 to 7.45 (really more closely regulated to within 7.38 - 7.42 than can be shown on the graph easily) - p CO2 » 35 - 45 mmHg (as for pH, really more closely regulated to 37 - 42 mmHg) - [HCO3-] » 22 - 26 mEq Normal values at sea level and 37oC are pH 7.40, HCO3- 24 mM, pCO2 40 mmHg Persons living at high altitudes (Denver, Tibet) have decreased arterial pCO2 and pO2 and [HCO3-] increased Hb concentration. We will assume sea level for all problems. (You do not need to memorize these numbers this year, but you will need to know them when you become a clinician. You will be given the normal values on the test! You will need to know how to find these normal values on the Davenport diagram.) WSUSOM Medical Physiology Rossi-Acid Base Physiology Page 3 of 18 Acid Base Compensation Definitions - ACIDEMIA Definition - ALKALEMIA Highlighted area shows ACIDEMIA. Highlighted area shows ALKALEMIA. Definition – Hypercapnia Definitions – hypocapnia Respiratory acidosis Respiratory alkalosis Highlighted area shows HYPERCAPNIA. Highlighted area shows HYPOCAPNIA. WSUSOM Medical Physiology Rossi-Acid Base Physiology Page 4 of 18 Acid Base Compensation Regulation of Acid-Base State Daily acid formation Ø 13,000 mmol/day CO2 + 70 to 100 mmol/day nonvolatile acid Lung excretion: 13,000 mmol/day CO2 Kidney excretion: 70 to 100 mmol/day H+ Ø Total Secretion » 5,000 mmoles H+ Secrete H+ to reclaim filtered HCO3-: 4,500 mmol/d v 25 mmol/L x 180 L/d = 4,500 mmol/d Secrete H+ in the form of NH4+ and H2PO4-: 70 to 100 mmol/d To remain in acid base balance the body must excrete acid. Two organs are involved the lungs and the kidneys. Note that mole for mole, more carbonic acid is generated than non-carbonic (non-volatile) acid each day. Any decrease in these excretory processes will lead to accumulation of acid in the body (acidosis). “Simple” (Single) Acid-Base Disorders Hypercapnia = respiratory acidosis Hypocapnia = respiratory alkalosis Metabolic acidosis Metabolic alkalosis Combined disorders (year 2) The four types of simple acid base disorders are listed above. The term simple means that only ONE primary disorder is present. Simple does not mean the problems will be easy or that the disorder is minor. (There are circumstances when individuals may have more than one primary acid base disorder going on but the net effect will be ONE pH. These are known as “mixed acid base disorders”. Next year…) - e.g, a person may have a metabolic acidosis which is very severe and may be difficult to diagnose or treat - The body’s physiological response to the acid base disorder is called compensation. Steps in Evaluating Acid Base Problems 1 – using the Davenport Diagram 1. obtain a sample of arterial blood 2. measure pH, pCO2 and [HCO3-] 3. plot these values on the Davenport diagram 4. make a diagnosis based on the position of the point WSUSOM Medical Physiology Rossi-Acid Base Physiology Page 5 of 18 Acid Base Compensation 5. If at all possible getting relevant history about the person (diarrhea, vomiting, diabetes, lung disease, etc.) is very helpful. 6. We will focus on simple (single) acid base disorders, that is, only one primary disturbance. Just be mindful that people can have more than one primary, independent problem at a time. Think of the patient who also develops vomiting and diarrhea together. We will tackle dual and triple acid base disorders next year. Steps in Evaluating Acid Base Problems 2 Obtain sample of arterial blood Deduce the primary malfunction – respiratory vs metabolic – add/loss volatile vs add/loss non-volatile acid Estimate compensatory response = the physiologic response to acid base unbalance Estimate time since onset of disorder (respiratory disorders: chronic vs acute) Use this as an exercise for yourself: Put the dots on a point of the graph and then determine the acid base status. Simple Acid-Base Disorders The table shows the directional changes in simple acid base disorders. Acidosis: CLEAR down arrows for pH Alkalosis: BLACK up arrows for pH Primary disorder: SOLID ARROWS Compensation: DOTTED ARROWS For example: If the pH is down and the pCO2 and [HCO3-] are both down (compared with the normal values pH 7.40, pCO2 40 mmHg and [HCO3-] 24 mEq/L) WSUSOM Medical Physiology Rossi-Acid Base Physiology Page 6 of 18 Acid Base Compensation Then, the primary disorder is the drop in [HCO3-] (the one that caused the pH problem) so the acid base disorder is metabolic (not respiratory in origin), a metabolic acidosis. The pCO2 is down as a physiologic compensatory response. Next, we shall see how this COMPENSATION works…. Unlike buffering which is a chemical response, compensation is the physiologic response to an acid/base perturbation. Compensation is the attempt by the body to counteract the disturbance. If the disturbance is acidosis, then the body will try to bring the pH back up toward normal. Likewise for alkalosis, the body will try to bring the pH down toward normal. Simple Acid-Base Disorders The figure above depicts the FOUR SIMPLE acid base disorders. “Simple” in the sense that there is only ONE acid base disorder going on. (Remember there is only ONE pH but you can have opposing primary processes such as vomiting and diarrhea). Some people prefer to use the graphs below. Others use formulas. Eventually the formulas are more helpful in COMPLEX or MIXED acid base disorders where there is more than one process going on…that is in year 2!!! Factors Affecting HCO3 Reabsorption It will be good to review the factors affecting HCO3- reabsorption from the kidney lecture on urinary acidification at this time. WSUSOM Medical Physiology Rossi-Acid Base Physiology Page 7 of 18 Acid Base Compensation Normal Range: Acid-Base Values: pH 7.40, pCO2 40 mmHg and HCO3- 24 mM Compensation Respiratory Acidosis (Hypercapnia): Carbonic Acid Excess In respiratory acidosis (also known as hypercapnia) the primary problem is an excess of carbonic acid (an increase in CO2 content) which is reflected in the elevated pCO2. Recall that the carbonic acid is buffered by Hgb-Im resulting in the formation of HCO3- H2CO3 + Hgb-Im « HgbHIm+ + HCO3- The biochemical response to this rise in pCO2 is an increase in [HCO3-] = buffering This occurs rapidly. The physiologic response to the rise in pCO2 (which leads to a decrease in pH) is that the kidney will reabsorb more HCO3- and secrete more NH4+. This will result in an increase in serum [HCO3-] = compensation. This takes more time than buffering. Thus, both biochemical buffering and physiologic response will tend to offset the decrease in pH (increase in [H+]). The rise in [HCO3-] is known as the compensatory (secondary) response. Malfunctions Causing Respiratory Acidosis (Hypercapnia) WSUSOM Medical Physiology Rossi-Acid Base Physiology Page 8 of 18 Acid Base Compensation These Medical conditions are often seen with primary hypercapnia (respiratory acidosis). Notice that the disorders fall into 3 major groups: 1. airway and lung disease 2. restriction of expansion the chest cavity 3. suppression of central respiratory drive You will be held responsible for knowing the diseases in the boxes as there are paradigmatic ones. Acute vs Chronic Respiratory Acidosis (or Hypercapnia): compensation Abnormal steady state of acid-base unbalance - Disorder = high pCO2 and low pH (move to higher isobar) - Response o Buffered by Hgb (HCO3- ­) o Compensation: kidneys increase H+ excretion manifest as further increase in [HCO3- ] along the same isobar (renal COMPENSATION) o This “titrates” pH toward “normal” The kidney needs time to reabsorb more bicarbonate. So, after the acute response wherein the bicarb goes up by 1-2 mM, if the respiratory acidosis persists in a chronic situation, then the bicarbonate will rise further as the kidney excretes H+ and reabsorbs HCO3-. The physiologic compensatory response reaches a new steady state level (hours to days). This increase in [HCO3-] titrates the ECF towards a higher pH along the abnormal pCO2 isobar. (This isobar is dictated by the disease and its severity and is not changed by buffering or compensation (e.g, COPD, sedation, etc.) Example: Arterial blood sample from patient has pH = 7.37, pCO2 = 60 mmHg, [HCO3-] = 34 WSUSOM Medical Physiology Rossi-Acid Base Physiology Page 9 of 18 Acid Base Compensation How did she get there? acutely the pCO2 increased from 40 to 60 mmHg (follow the titration curve from point O to the 1/2 hr point at isobar 60 mmHg) and is buffered by Hgb-Im over time the compensatory physiologic response to this higher pCO2 shows the person “sliding” along the 60-isobar as the kidney reabsorbs more HCO3- (note [HCO3-] increases from 27 mEq/L at 1/2 hr to 34 mEq/L at point A) (This may NOT take 14 days). This new steady state level (Point A) is described in many different ways: - “compensated hypercapnia” - “compensated respiratory acidosis - “primary respiratory acidosis with appropriate compensation” Do NOT call this “primary respiratory acidosis with metabolic alkalosis”…that implies TWO PRIMARY diseases: one driving the respiratory acidosis and a separate disease leading to metabolic alkalosis (e.g., vomiting). There is only ONE disease and it is being compensated appropriately. IMPORTANT POINT: Renal compensation for SEVERE chronic hypercapnia (pCO2>70- 80 mmHg) is not complete since maximal H+ ion secretion rate of the renal tubules is reached, hence, the bend in the compensatory range on the graph. Luckily, pCO2>80 mmHg is rarely encountered as any lung or neuromuscular disease. Summary: Chronic Hypercapnia Body reacts to bring pH toward normal Renal maximum for HCO3- reabsorption limits the degree of compensation Overcompensation does NOT occur o pH NEVER goes into alkalemic range with compensation for hypercapnia The compensatory rise in [HCO3- ] should NOT be called “metabolic alkalosis” Be careful with the composite figure. The areas denoting the range suggest that compensation may go over to the alkalemic pH values. This does NOT occur. WSUSOM Medical Physiology Rossi-Acid Base Physiology Page 10 of 18 Acid Base Compensation Respiratory Alkalosis (or Hypocapnia): Carbonic Acid Deficit In respiratory alkalosis (also known as hypocapnia) the primary problem is a deficit of carbonic acid (a decrease in CO2 content) which is reflected in the low pCO2. Recall that the carbonic acid is buffered by Hgb-Im resulting in the formation of HCO3- 1. CO2 + H2O « H2CO3 2. H2CO3 + Hgb-Im « HgbHIm+ + HCO3- The biochemical response to a decrease in pCO2 is a decrease in H2CO3 (mass action - reaction #1 goes to the left). The lower H2CO3 leads to less [HCO3-] = buffering. This occurs within minutes. As a result of the decrease in pCO2 and decrease in [H+] (increase in pH) 1. Cells will increase lactic acid production, which will increase generation of CO2 and titrate the pH toward normal: lactic acid + HCO3- « lactate- + CO2 + H2O 2. The kidney will reabsorb LESS HCO3- and secrete less NH4+ (acid), this is the physiologic compensation and may take a few hours. Thus, the pH will tend to return down toward normal. Malfunctions Causing Respiratory Alkalosis (Hypocapnia) Note the medical conditions associated with respiratory alkalosis. These are all associated with increased ventilatory rate and removal of CO2 by the lungs. Aspirin is unusual in that it initially causes increased ventilation (central mechanism) and respiratory alkalosis. This is later followed by decreased mental status (coma) and a decrease in ventilation with respiratory acidosis. WSUSOM Medical Physiology Rossi-Acid Base Physiology Page 11 of 18 Acid Base Compensation Chronic Hypocapnia Initial low pCO2 and high pH Buffering: Hgb-Him+ releases H+ Compensation: o Kidney: reduces nonvolatile H+ excretion (= reduces HCO3- reabsorption) o That is, less NaH2PO4 and NH4Cl are excreted by the kidneys Compensation NOT complete, that is, pH comes TOWARD normal but does not overshoot. Example: Arterial blood sample from patient has pCO2 = 25 mmHg, [HCO3-] = 16 and pH 7.43. How did s/he get there? o acutely the pCO2 decreased from 40 to 25 mmHg (follow the titration curve from point O to the 1 hr point at isobar 25 mmHg) and is buffered. pH is » 7.55 and the [HCO3-] has decreased only slightly to 21 mEq/L. o over time (chronic hypocapnia) the compensatory physiologic response to this lower pCO2 shows the person “sliding” along the 25-isobar as the kidney reabsorbs less HCO3- (note [HCO3-] decreases from 20 mEq/L at 1 hr to 16 mEq/L at point F) and the pH comes closer to normal, pH 7.43. Metabolic Acidosis In metabolic acidosis the primary problem is excess non-carbonic acid. There are two major sources of non-carbonic acids in the body: 1. addition of acid: end products of metabolism that are acidic (lactic acid, b- hydroxybutyrate, acetoacetate, etc.) and organic molecules that contain phosphorus or sulfur are oxidized to phosphoric and sulfuric acids. 2. loss of base: loss of alkaline fluid secreted by the small intestine and lost in feces is accompanied by intestinal absorption of HCl Buffering occurs by H2SO4 + 2 NaHCO3 « Na2SO4 + 2CO2 + 2 H2O HCl + NaHCO3 « NaCl + CO2 + H2O 1 HCO3- is consumed in the process of buffering HCl. The CO2 formed in the reaction is expired by the lungs. The sodium salts are excreted by the kidney. The body now has 1 HCO3- fewer than it had before and that needs to be replaced. (This is the HCO3- the a intercalated cells have to “add back” since this HCO3- was “consumed” in the buffering process and the resulting CO2 and water were eliminated. See Kidney Lecture 8.) WSUSOM Medical Physiology Rossi-Acid Base Physiology Page 12 of 18 Acid Base Compensation The physiologic compensatory response is twofold: 1. increase in ventilatory rate (low pH stimulates ventilation) and “excretion” of the CO2 by the lungs. The loss of CO2 will bring the pH up toward normal. 2. excretion of acid (titratable and NH4+) by the kidney…with generation of new HCO3-. REMEMBER: this is an OPEN system. Malfunctions Causing Metabolic Acidosis Medical conditions associated with metabolic acidosis are listed above. 1. The LEFT column are processes that result in loss of HCO3-, thereby appearing to increase HCl in the body. 2. The RIGHT column are disorders that add an organic, non-carbonic acids due to overproduction, inability to metabolize or excrete fully, or ingestion a. ketoacids b. lactic acid c. sulfuric, phosphoric acids (renal failure) d. ingested substances that are acids (aspirin = acetylsalicylic acid) or are metabolized to organic acids (formic, glyoxylate) Metabolic Acidosis: Diarrhea § Normal: pH = 7.40, [HCO3-] = 24 § Gets diarrhea § Moves to point A on isobar 40 mmHg § Base deficit = 10 mM (L1) § Increased ventilation (respiratory compensation) moves to point B (new isobar, lungs are healthy) pH 7.30, [HCO3-] = 15, pCO2 = 32 § Steady state ½ way from A to C § With time, further increased ventilation will move from B to C. § With time, the kidney will excrete NH4+ and there may be a slight increase in HCO3- (not shown) WSUSOM Medical Physiology Rossi-Acid Base Physiology Page 13 of 18 Acid Base Compensation Example: - A normal person (Point O) gets diarrhea (loss of base in stool, gaining H+) such that the base deficit is 10 mEq/L. If a blood sample is taken “immediately” before ventilatory compensation kicks in (seconds), the HCO3- will be consumed in buffering and would decrease along the 40 mmHg isobar to Point A. As the low pH stimulates the respiratory center, CO2 is blown off and pCO2 drops to 30 mmHg (Point B) …titrating along the 12 mEq/pH titration curve (parallel to the body titration curve but shifted down). The low pH (high [H+]) increases kidney secretion of H+ as NH4+ Point C may not achieved as the low pCO2 inhibits the brain respiratory center from further increases in minute ventilation. Thus, the steady state compensated metabolic acidosis ends up at Point B with a pH 7.30, pCO2 32 mmHg and [HCO3-] 15 mEq/L Metabolic Acidosis: acute response ECF buffering: carbonic acid Non-ECF buffering (90 min) – Cellular uptake of H+ Hgb Other proteins – Carbonate release from bone Transients – Respiratory compensation – FAST (30 min) – Renal compensation – SLOW (hrs – days) – Recovery – renal H+ excretion § Not all non-carbonic acid added during primary metabolic acidosis is buffered in ECF. § Approx. 1/2 of infused strong acid disappears from the extracellular space and is taken up by muscle and other cells; part is neutralized by carbonate release from bone (especially in longstanding metabolic acidosis such as chronic kidney disease) § Respiratory compensation is FAST and for practical purposes is always in a steady state (certainly by the time the person comes to see you in the office or ER). § The renal excretion of acid is very low and may take days. During recovery the excess acid is excreted by the kidneys and the patient returns to normal (Point O). WSUSOM Medical Physiology Rossi-Acid Base Physiology Page 14 of 18 Acid Base Compensation Metabolic Alkalosis In metabolic alkalosis the primary problem is 1. loss of non-carbonic acid from the body (e.g., loss of HCl in vomiting) 2. addition of HCO3- to the body (e.g., ingestion of baking soda, NaHCO3) Buffering occurs not only in the ECF but also by H+ pumps in the membrane of many cells moving H+ out of cells. Over long periods of time, HCO3- is stored in bone where it forms calcium carbonate (CaCO3). The physiologic compensatory response is twofold: 1. decrease respiratory rate (high pH inhibits minute ventilation) and “excretion” of the CO2 by the lungs. The increase in CO2 will bring the pH down toward normal. 2. excretion of less acid (NH4+) by the kidney…with generation of less new HCO3- NOTE: respiratory compensation for metabolic alkalosis is not as efficient as for metabolic acidosis. The compensation is limited by hypoxia. One can decrease ventilation only so much, but NOT breathing at all to improve acid base status is NOT an option. Malfunctions Causing Metabolic Alkalosis Causes: Loss of highly acid secretion or addition of alkali. The medical conditions associated with metabolic alkalosis are listed above. They fall into two main categories: 1. Volume contracted states (low ECF volume, LEFT column) 2. Normal or elevated ECF volume states (RIGHT column) Vomiting: When the body loses Cl-, a HCO3- is generated as the two ions are very often coupled in transporting epithelia (in kidney tubules, but also in gut). WSUSOM Medical Physiology Rossi-Acid Base Physiology Page 15 of 18 Acid Base Compensation ECV contraction: the HCO3- becomes “concentrated”; also the volume contraction sets all sorts of renal mechanisms in motion to reabsorb Na+ can you remember them. In the process, more HCO3- is reabsorbed proximally (reclaimed) and distally (new). Excess mineralocorticoid (aldosterone) increases H+ secretion by the kidney, thus increasing HCO3- reabsorption by the kidney. (Aldosterone also directly increases secretion of H+ by the H+-ATPase in the a intercalated cell. There is also an indirect effect of aldosterone due to decreasing the lumen potential…more negative…favoring H+ secretion.) Total body K+ depletion causes a shift of H+ into cells producing extracellular alkalosis and intracellular acidosis (The intracellular acidosis in the distal renal tubules will result in increased H+ secretion and HCO3- reabsorption). Eating NaHCO3 will directly increase [HCO3-]. Metabolic Alkalosis: Compensation High HCO3- and high pH – Add base or lose H+ Compensation – pCO2 rises but is limited by hypoxia (one can only hypoventilate so much before pO2 becomes an issue) – Renal compensation for metabolic alkalosis is limited as well by various factors, primarily, low ECF Some buffering due to H+ moving OUT of cells Why is renal compensation (excretion of more HCO3-) limited in metabolic alkalosis? Many reasons. 1. If the ECF is low, the primary motivating force for the kidney is to reabsorb Na+. a. Think back to the proximal tubule…if low ECF (and low blood pressure) leads to high Ang II and catecholamines which enhance H+ secretion by N/H exchanger, thereby Increasing HCO3- reabsorption! b. In the distal tubule and collecting duct, aldosterone will increase H+ secretion, also increasing HCO3- reabsorption! c. Aldosterone also increases K+ secretion and excretion, and the resulting low K+ results in more NH4+ formation and thus, more H+ excretion and more HCO3- reabsorption! Curve DOBE shows the average amount of steady state respiratory compensation for metabolic disorders. § curve OD for primary metabolic alkalosis (OD) and § curve OBE for metabolic acidosis. The region between the dashed lines is the approximate range of compensatory values found in humans. WSUSOM Medical Physiology Rossi-Acid Base Physiology Page 16 of 18 Acid Base Compensation OVERVIEW The pH-[HCO3-] diagram below can be divided into six regions by three lines - The vertical line through pH 7.40 separates acidemia from alkalemia - The pCO2 isobar = 40 mmHg separates hypercapnia from hypocapnia - the 12 mEq/pH body titration curve separates metabolic acidosis (lower left) from metabolic alkalosis (upper right) More accurately the boundaries are not lines but the areas of the bands formed by the dashed lines (removed here for clarity). You may wish to compare with the acid base chart (1st slide of this lecture) Summary Acid Base Disorders Region 1: primary metabolic acidosis with compensatory hypocapnia o pH low, pCO2 low, [HCO3-] low The low pH and low [HCO3-] are c/w metabolic acidosis. One might consider primary hypocapnia, but then the pH should be greater than normal; hence the low pCO2 is the compensatory response. (See acid/base chart, gives same answer.) Region 3: primary respiratory acidosis with renal compensation o pH low, pCO2 high, [HCO3-] high The low pH and high pCO2 are c/w primary respiratory acidosis. The high [HCO3-] is a compensatory response by the kidney. If the high [HCO3-] were primary, then the pH would be high. Region 2: primary metabolic acidosis with primary hypercapnia o pH low, pCO2 high, [HCO3-] low The low pH and low [HCO3-] are c/w primary metabolic acidosis, but then compensation would predict increased ventilation and low pCO2. BUT the pCO2 is high, so there is a primary hypercapnia (primary respiratory acidosis). What if you say the pH is low and the pCO2 is high so there is a primary respiratory acidosis? Compensation would predict the [HCO3-] to rise, but it is low, so there is a primary metabolic acidosis, too. This is a case of TWO separate acid/base disorders…known as mixed acid/base problems. Starting with either gives you the same answer! The metabolic acidosis is NOT properly compensated; the primary hypercapnia is not properly compensated. There are two separate diseases with two PRIMARY acid base disorders…but ONE pH. These “mixed disorders will NOT be on the exam this year. They ARE on the boards. Something to look forward to in year 2!) WSUSOM Medical Physiology Rossi-Acid Base Physiology Page 17 of 18 Acid Base Compensation Summary Acid Base Disorders Region 4: primary metabolic alkalosis with compensatory hypercapnia o pH high, pCO2 high, [HCO3-] high The high pH and high [HCO3-] are c/w metabolic alkalosis. One might consider primary hypercapnia, but then the pH should be lower than normal; hence the high pCO2 is the compensatory response. (see acid/base chart, gives same answer) Region 6: primary respiratory alkalosis with renal compensation o pH high, pCO2 low, [HCO3-] low The high pH and low pCO2 are c/w primary respiratory alkalosis. The low [HCO3-] is a compensatory response. If the low [HCO3-] were primary, then the pH would be low. Region 5: primary metabolic alkalosis with primary respiratory alkalosis o pH high, pCO2 low, [HCO3-] high The high pH and high [HCO3-] are c/w primary metabolic acidosis, but then compensation would predict decreased ventilation and high pCO2 (region 4). BUT the pCO2 is low, so there is a primary hypocapnia (primary respiratory alkalosis). What if you say the pH is high and the pCO2 is low so there is a primary respiratory alkalosis? Compensation would predict the [HCO3-] to decrease, but it is high; so there is a primary metabolic alkalosis, too. Whichever way you start you get the same right answer! Again, TWO separate acid/base disorders…known as mixed acid/base problems. Starting with either gives you the same answer! WSUSOM Medical Physiology Rossi-Acid Base Physiology Page 18 of 18 Acid Base Compensation In the past, students used to cut this out and use it when they go on the clinical wards. NOW we use our phone APPS! Much better…except not allowed on board exams. The Davenport Diagrams are on Step 1. (Frankly, I never used them but preferred the formulae that I give in Year 2.) However, the diagram does illustrate a bit HOW acid base disorders and their compensation progresses.