Acid Base Disturbance Notes PDF

Acid Base Disturbance # Extra. ! Notes " Important things doctor said I think he might bring in the exam Lecture objectives 1. Recall the physiology involved in the acid base balance of the body. 2. Describe the normal values and factors that influence normal variables....

Acid Base Disturbance # Extra. ! Notes " Important things doctor said I think he might bring in the exam Lecture objectives 1. Recall the physiology involved in the acid base balance of the body. 2. Describe the normal values and factors that influence normal variables. Acid Base Disturbance 3. Identify abnormal values and its interpretation. 4. Describe and list the differential diagnosis of respiratory acidosis. 5. Describe and list the differential diagnosis both of metabolic acidosis and alkalosis. What is the acid ? acid is the molecule that can donate hydrogen ion which is the proton. What are the hydrogen ions ? Hydrogen Ions are the representative of the acidity in the body. Which means the more the hydrogen ions the more the avidity and Vice versa. What is the base ? It’s the opposite of acid. Any molecule that can receive or accept the hydrogen ion. Is there anything common between acid and base ? Buffers are the molecules that can accept and donate at the same time. When we say disturbance what do we mean ? Body can produce everyday in children from 2-3 mil/kg acid while adults are 1-2mil/kg. 0 Acids are produced from where ? From the metabolic process Co2. We have volatile and non- volatile volatile acid(CO2) & non-volatile acid others. volatile is excreted by respiratory system whiles the non-volatile excreted by renal system. Why is it important to maintain the acid-base balance ? The functionality will be affected (metabolic processes ) How can the body maintain the balance? Through 3 mechanisms 1) respiration 2)renal 3) buffers What is the order of the body’s mechanisms to maintain the balance ? First through 1) buffers which’s target to prevent large fluctuations. Then 2) respiratory system which complete the compensation from 12-24 hours. What do we mean by compensation? The deviation of the ph will be corrected but note that it won’t web fully compensated only 70%. The respiratory system tries to wash out the co2 to maintain the acid base balance, but how? Increase in the RR or decrease in the RR to accumulate the co2 in the case of alkalosis. Lastly 3) renal which complete it’s compensation 3-4 hour( not sure didn’t hear it well ) by either excreting HCO3or hydrogen. And also can produce ammonia. Ammonia is considered as a buffer. Brønsted and Lowry defined acids as substances which are able to donate protons, and bases as substances which accept protons. Buffers are solutions that resist changes in the pH of a when acid or alkali is added. Acid base disturbances are one of the most worrying clinical problems to physician. because of subtle nature of the physiological changes which lead to them Usually the acid base imbalance indicates a serious disturbance of physiological control mechanisms. If a patient came and you want to check his ph which test you order ? Blood gas (ABG) this is the standard and most accurate. But usually we don’t use it. so what we use instead is VBG or ABG because they are easier especially the venous blood gas. what is the difference between the Arterial blood gas and the venous blood gas ? The venous have more co2 so the acidity will be higher also co2 is higher and HCO3 is less. But the difference isn’t as huge as you imagine it’s only 1-2 HCO3 less than the arterial blood gas, and the Co2 will be up to10 higher than the arterial. The arterial range of normal co2 is from 35-45. However for the venous the CO2 from 20-26 ( ‫) اﺣﺴﮫ ﻋﻜﺲ ھﻨﺎ ﺑﯿﻦ اﻟﻔﯿﻨﻮس واﻻرﺗﯿﺮﯾﺎل‬ PH stands for “ Power of Hydrogen ”. The cells of the body function within the normal range of 7.35-7.45. Death usually occurs if PH falls below 7 or rises to 7.8. Every day, metabolic processes result in the production of volatile acid(CO2) & non-volatile acid or fixed acids(sulphuric and phosphoric). a  Mechanisms of A-B regulation There are three mechanisms counteract any deviation from the normal PH by stabilize the PH at 7.4. – Blood buffers Preventlongfluitionio If – Respiratory – Renal  BLOOD BUFFERS First line of defence Act within minutes ONLY, prevent large fluctuation of PH by combining with excess (H+) OR giving off (H+). The major buffers: – Bicarbonate-carbonic acid (ECF) – Hb (ICF) 8008 OTHERS [proteins & Phosphate] (ICF)  respiratory minits howy RateandDepthof vatlatia Main advantage>> quick response. CO2 & H+ have potent stimulatory effect – Rate – Depth Wash out CO2 Only compensate by 75%  renal Days 48 Third line It’s the only organ can excrete non-volatile acids. I ÉE phosphorisf Three main renal mechanisms are responsible for regulation of A-B: – Reabsorption of bicarbonate – Active secretion of H+ – Synthesis of ammonia bulfur  DISTURBANCE OF A-B A-B imbalance is usually a complication of diseases affecting the systems which regulate the production or excretion of H+. – METABOLIC – RESPIRATORY ACIDOSIS ALKALOSIS How many types of disturbances we have ? 1) acidosis 2) alkalosis 3) mixed.. If the patient have ether alkalosis or acidosis we call it simple if it came together we call it mixed. Why is it important to know what is the kind of disturbance that happened? To know how to treat and manage. So we must take history and do physical examination. And you must know that history is the most important part in approaching the disturbance.  METABLIC ACIDOSIS Accumulation of non-carbonic acids in (ECF) of Excessive loss of HCO3 Accumulation of which types of acids ? non-volatile acid or fixed e.g:- acids(sulphuric and phosphoric). Or loss of HCO3 this can lead to metabolic acidosis. We need to calculate the anion gap and carbalaztion – DM DKA Ketone Lacticacids – Sever diarrhoea Bicarb mastromonause highAniongap NIMAG mostlydiarri – Renal failure Assume that a patient came with respiratory distress ( increased RR and decreased oxygen supply) and we took history and it turned out to be an acute issue and there is no other complication. So we also did the examination and he don’t have any signs of respiratory problems. Here we need to do the blood gas test to have an idea about what is going on. So when we order the blood gas we found out that he have acidosis and the Co2 is 25 so 25 is it respiratory acidosis? Student answer: I think maybe it’s mixed. Doctor : to say it’s mixed we need to know the HCO3 and make the compensation equation. And we found also that his HCO3 is low so this is metabolic acidosis. And the body is trying to compensate by washing out Co2.  METABOLIC ALKALOSIS H+ Or dropping in ( ‫ ) ﻣﺎﺳﻤﻌﺖ زﯾﻦ‬25:00 bicarbonate e.g:- – Loss of Gastric juice vomiting – Ingestion of bicarbonate Gastric juices are made up of HCL which is the H ion so if there is any loss in the gastric juice it’ll result in a drop of H+ causing metabolic alkalosis  RESPIRATORY ACIDOSIS Accumulation of CO2 in blood – Asthma – Pneumonia – CHF – morphine suppresi l Resp rate  RESPIRATORY ALKALOSIS Excessive washing out of CO2. – Panic attack – High altitude  ASSESSMENT OF A-B Antivic Blood PH (7.35-7.45) Pco2 (35-45) HCO3 (22-28) Anion gap (10-16) Base excess (-2 to +2) Blood gas contents are Ph level and co2 and HCO3 and electrolytes. Why does the blood gas contain electrolytes ( sodium + potassium + chloride) ? Generally disturbance in acid base cause disturbance in electrolytes. metabolic acidosis we need to calculate the anion gap so we need the electrolytes. How to calculate anion gap ? Anion Gap = Sodium - (Chloride + Bicarbonate) some people use other ways to calculate. Anion gap usually is +/- 12. But if we calculate potassium with the anion gap it becomes 16+/- 4. When we want to evaluate the blood gas the first thing we should look to is the PH then Co2 and HCO3. Assuming that the ph is slightly acidic 7.3 and the co2 is 55 and the HCO3 is 28. This is most likely what? Respiratory acidosis. To know if it was respiratory or metabolic we will evaluate the co2 and HCO3. Co2= acid so if co2 increase this means it is acidosis. HCO3= alkaline so if it increases this means it is alkalosis. In case it was mixed there will be compensation like in the case of metabolic acidosis the HCO3 will be low and co2 will be low. So there will be washing out of co2. So how we can know if it was simple or mixed ? There is an equation which is co2= 1.5*HCO3+8+/-2. If the result was equal to the Pco2 this is simple but if the result was higher or less this is mixed. In case of metabolic alkalosis the co2 will be increased. To say that this is a pure or simple metabolic alkalosis the body will compensate by increasing the co2 7 for each increased HCO3 for e.g if HCO3 is 35 the body will compensate by increasing the co2 by 7 in this case this is simple. Metabolic Acidosis PCO2 = 1.5 x HCO3 + (8 +/- 2) Metabolic Alkalosis PCO2 = 0.7 x HCO3 + (21 +/- 2) I have a rule of 1,2,3,4 1. In case of respiratory the all equations are based on that HCO3 is 10. The body will compensate by increasing HCO3 1 for each 10 increase in co2. This is in the case of acute respiratory acidosis. 2. In case of acute respiratory Alkalosis the body will compensate by decrease the HCO3 by 2 for each 10 co2 drop. What is the BE ? This is the base excess it has a rule which gives us a hint about the acidosis and alkalosis. if it’s negative mostly it means that it is alkalosis. And if it is positive ‫ اﻧﻘﻄﻊ ﻣﺠﺮى اﻟﺤﺪﯾﺚ ھﻨﺎ‬. 43:00. Low cl- in the urine means it is from GI. Follow the numbers in the slides bc there are many sources with different values. pH < 7.35 PCO2 BE / [sHCO3 -] – Respiratory acidosis Compensated pH < 7.35 PCO2 BE / [sHCO3 -] respiratory acidosis pH < 7.35 PCO2 - BE / [sHCO3 -] Metabolic acidosis pH < 7.35 PCO2 BE / [sHCO3 -] Metabolic acidosis pH > 7.45 PCO2 BE / [sHCO3 -] – Alkalosis pH > 7.45 PCO2 BE / [sHCO3 -] pH > 7.45 PCO2 - BE / [sHCO3 -] Metabolic alkalosis Metabolic alkalosis pH > 7.45 PCO2 BE / [sHCO3 -] If we had a very low anion gap one of the most common causes is hypoalbuminemia. The delta ratio is used to Evaluate if the metabolic acidosis is pure or mixed high anion gap. Read about it if you have time. # RESPIRATORY ALKALOSIS Excessive washing out of CO2. – Panic attack – High altitude High anion gap which is usually a topic for mcqs ‫ﻗﺮأھﺎ اﻟﺪﻛﺘﻮر‬ ‫ﻛﻠﮭﺎ ورﻛﺰ ﻋﻠﯿﮭﺎ‬ * Uremia = Renal failure which usually suffer from both excretion of acid and reabsorption of HCO3 which causes high anion gap metabolic acidosis What is the cause of normal metabolic acidosis anion gap or the most common cause is diarrhea. Until proven otherwise. Diarrhea causes acidosis due to the loss of HCO3 from intestines. Or increase in acid. Or because of dehydration which will cause hypoperfusion which will increase the lactate.  CHAPTER 37 Acid-Base Disorders 139 may interfere with normal growth and development, whereas the chronic lung disease. Formulas are available for calculating acute, severe changes in pH can be fatal. Control of acid-base the appropriate metabolic or respiratory compensation for the balance depends on the kidneys, the lungs, and the intracellular six primary simple acid-base disorders (Table 37.1). Appropriate and extracellular buffers. compensation is expected in a simple disorder; it is not optional. The lungs and kidneys maintain a normal acid-base balance. If a patient does not have appropriate compensation, a mixed Carbon dioxide (CO2) generated during normal metabolism is a acid-base disorder is present. weak acid. The lungs prevent an increase in the partial pressure of CO2 (PCO2) in the blood by excreting the CO2. Production of CO2 varies depending on the body’s metabolic needs. The rapid METABOLIC ACIDOSIS pulmonary response to changes in CO2 concentration occurs via central sensing of the PCO2, and a subsequent increase or Decision-Making Algorithm decrease in ventilation to maintain a normal PCO2 (35-45 mm Available @ StudentConsult.com Hg). Acidemia The kidneys excrete endogenous acids. An adult normally produces about 1-2 mEq/kg per day of hydrogen ions, whereas a child produces 2-3 mEq/kg per day. The hydrogen ions from Metabolic acidosis occurs frequently in hospitalized children; endogenous acid production are neutralized by bicarbonate, diarrhea is the most common cause. For a patient with an potentially causing the bicarbonate concentration to fall. The unknown medical problem, the presence of metabolic acidosis kidneys regenerate this bicarbonate by secreting hydrogen ions, is often diagnostically helpful because it suggests a relatively maintaining the serum bicarbonate concentration in the normal narrow differential diagnosis (Table 37.2). range (20-28 mEq/L). CLINICAL ASSESSMENT OF TABLE 37.1 Appropriate Compensation During Simple ACID-BASE DISORDERS Acid-Base Disorders DISORDER EXPECTED COMPENSATION* Decision-Making Algorithms Available @ StudentConsult.com Metabolic acidosis PCO2 = 1.5 × [HCO3− ] + 8 ± 2 Acidemia Metabolic alkalosis PCO2 increases by 7 mm Hg for each Alkalemia 10 mEq/L increase in the serum [ HCO3− ] Respiratory acidosis Acute Acidemia is a pH below normal (7.45). Acidosis is a pathological process Hg increase in the PCO2 that causes an increase in the hydrogen ion concentration, and Chronic [ HCO3−] increases by 3.5 for each 10 mm alkalosis is a pathological process that causes a decrease in the Hg increase in the PCO2 hydrogen ion concentration. A simple acid-base disorder is a Respiratory alkalosis single primary disturbance. During a simple metabolic disorder, Acute there is respiratory compensation; the PCO2 decreases during [ HCO3− ] falls by 2 for each 10 mm Hg decrease in the PCO2 metabolic acidosis and increases during metabolic alkalosis. With metabolic acidosis, the decrease in the pH increases the Chronic [ HCO3−] falls by 4 for each 10 mm Hg ventilatory drive, causing a decrease in the PCO2. The fall in decrease in the PCO2 the CO2 concentration leads to an increase in the pH. This *[HCO3−] is expressed in mEq/L. appropriate respiratory compensation for a metabolic process happens quickly and is complete within 12–24 hours. During a primary respiratory process, there is metabolic compensation mediated by the kidneys. The kidneys respond TABLE 37.2 Causes of Metabolic Acidosis to a respiratory acidosis by increasing hydrogen ion excre- tion, increasing bicarbonate generation, and raising the serum NORMAL ANION GAP bicarbonate concentration. The kidneys increase bicarbonate Diarrhea excretion to compensate for a respiratory alkalosis; the serum Renal tubular acidosis bicarbonate concentration decreases. In contrast to a rapid Urinary tract diversions respiratory compensation, it takes 3-4 days for the kidneys Posthypocapnia to complete appropriate metabolic compensation. However, Ammonium chloride intake there is a small and rapid compensatory change in the bicarbon- ate concentration during a primary respiratory process. The INCREASED ANION GAP expected appropriate metabolic compensation for a respiratory Lactic acidosis (shock) disorder depends on whether the process is acute or chronic. Ketoacidosis (diabetic, starvation, or alcoholic) A mixed acid-base disorder is present when there is more Kidney failure than one primary acid-base disturbance. An infant with broncho- Poisoning (e.g., ethylene glycol, methanol, or salicylates) pulmonary dysplasia may have respiratory acidosis from chronic Inborn errors of metabolism lung disease and metabolic alkalosis from a diuretic used to treat 140 SECTION 7 FLUIDS AND ELECTROLYTES tubular acidification is intact, but leads to metabolic acidosis Etiology due to bicarbonate wasting. The plasma anion gap is useful for evaluating patients with Increased anion gap metabolic acidosis occurs with lactic metabolic acidosis. It divides patients into two diagnostic groups: acidosis, ketoacidosis, chronic renal failure, and toxic inges- normal anion gap and increased anion gap. The following tions. Lactic acidosis most commonly occurs when inadequate formula determines the anion gap: oxygen delivery to the tissues leads to anaerobic metabolism and excess production of lactic acid. Lactic acidosis may be Anion Gap = Na+ − (Cl− + HCO3− ) secondary to shock, severe anemia, or hypoxemia. Inborn errors of carbohydrate metabolism produce a severe lactic acidosis A normal anion gap is 12 ± 2 mEq/L. (see Chapter 52). In diabetes mellitus, inadequate insulin leads Normal anion gap metabolic acidosis occurs in the setting to hyperglycemia and diabetic ketoacidosis (see Chapter 171). of diarrhea and renal tubular acidosis (RTA). Diarrhea causes a Renal failure (see Chapter 165) causes metabolic acidosis because loss of bicarbonate from the body. The amount of bicarbonate the kidneys are unable to excrete the acid produced by normal lost in the stool depends on the volume of diarrhea and the metabolism. bicarbonate concentration of the stool, which tends to increase A variety of toxic ingestions cause metabolic acidosis. Acute with more severe diarrhea. Diarrhea often causes volume salicylate intoxication occurs after a large overdose. Chronic depletion because of losses of sodium and water, potentially salicylate intoxication is possible because of the gradual buildup exacerbating the acidosis by causing hypoperfusion (shock) of the drug. Patients may also have a respiratory alkalosis. Other and a lactic acidosis. symptoms of salicylate intoxication include fever, seizures, leth- There are three forms of RTA: argy, and coma. Hyperventilation may be particularly marked. 1. Distal (type I) Tinnitus, vertigo, and hearing impairment are more likely with 2. Proximal (type II) chronic salicylate intoxication. Ethylene glycol, a component 3. Hyperkalemic (type IV) of antifreeze, is converted in the liver to glyoxylic and oxalic In distal RTA (dRTA), children may have accompanying acids, causing a severe metabolic acidosis. Excessive oxalate hypokalemia, hypercalciuria, nephrolithiasis, and nephrocal- excretion causes calcium oxalate crystals to appear in the urine, cinosis; rickets is a less common finding. Failure to thrive, and calcium oxalate precipitation in the kidney tubules can cause resulting from chronic metabolic acidosis, is the most common renal failure. The toxicity of methanol ingestion also depends presenting complaint. Autosomal dominant (relatively mild) on liver metabolism; formic acid is the toxic end product that and autosomal recessive (more severe) forms of dRTA exist. causes the metabolic acidosis and other sequelae, which include Autosomal recessive dRTA is often associated with deafness damage to the optic nerve and central nervous system. secondary to a defect in the gene for a H+-ATPase that is present There are many inborn errors of metabolism that may cause in the kidney and the inner ear. dRTA also may be secondary metabolic acidosis (see Section 10). Metabolic acidosis may be to medications or congenital or acquired renal disease. Patients due to excessive production of ketoacids, lactic acid, or other with dRTA cannot acidify their urine and have a urine pH organic anions. Some patients may have accompanying hyperam- greater than 5.5, despite metabolic acidosis. monemia. In most patients, acidosis occurs only episodically Proximal RTA is rarely present in isolation. In most patients, during acute decompensations, which may be precipitated by proximal RTA is part of Fanconi syndrome, a generalized the ingestion of specific dietary substrates (proteins), the stress dysfunction of the proximal tubule. Along with renal wasting of a mild illness (fasting, catabolism), or poor adherence with of bicarbonate, Fanconi syndrome causes glycosuria, aminoac- dietary or medical therapy. iduria, and excessive urinary losses of phosphate and uric acid. The chronic hypophosphatemia is more clinically significant because it ultimately leads to rickets in children. Rickets or failure Clinical Manifestations to thrive may be the presenting complaint. Fanconi syndrome is The underlying disorder usually produces most of the signs rarely an isolated genetic disorder, with pediatric cases usually and symptoms in children with a mild or moderate metabolic secondary to an underlying genetic disorder, most commonly acidosis. The clinical manifestations of the acidosis are related cystinosis. Medications, such as ifosfamide or valproate, may to the degree of acidemia; patients with appropriate respiratory cause Fanconi syndrome. The ability to acidify the urine is compensation and less severe acidemia have fewer manifestations intact in proximal RTA, and untreated patients have a urine than patients with a concomitant respiratory acidosis. At a pH less than 5.5. serum pH less than 7.20, there is impaired cardiac contractility In hyperkalemic RTA, renal excretion of acid and potas- and an increased risk of arrhythmias, especially if underlying sium is impaired because of either an absence of aldosterone heart disease or other predisposing electrolyte disorders are or an inability of the kidney to respond to aldosterone. In present. With acidemia, there is a decrease in the cardiovascular severe aldosterone deficiency, as occurs with congenital response to catecholamines, potentially exacerbating hypotension adrenal hyperplasia secondary to 21α-hydroxylase deficiency, in children with volume depletion or shock. Acidemia causes the hyperkalemia and metabolic acidosis are accompanied vasoconstriction of the pulmonary vasculature, which is by hyponatremia and volume depletion from renal salt especially problematic in neonates with primary pulmonary wasting. Incomplete aldosterone deficiency causes less severe hypertension of the newborn (see Chapter 61). The normal electrolyte disturbances; children may have isolated hyper- respiratory response to metabolic acidosis—compensatory kalemic RTA, hyperkalemia without acidosis, or isolated hyperventilation—may be subtle with mild metabolic acidosis, hyponatremia. but it causes discernible increased respiratory effort with Distal and hyperkalemic RTA are similar in that distal tubular worsening acidemia. Chronic metabolic acidosis causes failure acidification is impaired. Conversely, in proximal RTA, distal to thrive.  CHAPTER 37 Acid-Base Disorders 141 Diagnosis TABLE 37.3 Causes of Metabolic Alkalosis Calculating the anion gap can help narrow the differential CHLORIDE RESPONSIVE (URINARY CHLORIDE 20 mEq/L) of a normal or increased anion gap is not always reliable in High Blood Pressure differentiating the causes of a metabolic acidosis, especially when the metabolic acidosis is mild. Some patients have more Adrenal adenoma or hyperplasia than one explanation for their metabolic acidosis, such as a Glucocorticoid-remediable aldosteronism child with diarrhea and lactic acidosis secondary to shock. Renovascular disease Renin-secreting tumor Treatment 17α-hydroxylase deficiency The most effective therapeutic approach for patients with a 11β-hydroxylase deficiency metabolic acidosis is correction of the underlying disorder, if Cushing syndrome possible. The administration of insulin in diabetic ketoacidosis or restoration of adequate perfusion in lactic acidosis from 11 β-hydroxysteroid dehydrogenase deficiency shock eventually results in normalization of acid-base balance. Licorice ingestion The use of bicarbonate therapy is indicated when the underlying Liddle syndrome disorder is irreparable; examples include RTA and chronic renal Normal Blood Pressure failure. In salicylate poisoning, alkali administration increases renal clearance of salicylate and decreases the amount of Gitelman syndrome salicylate in brain cells. Short-term base therapy is often neces- Bartter syndrome sary in other poisonings and inborn errors of metabolism. Base administration METABOLIC ALKALOSIS Etiology The causes of a metabolic alkalosis are divided into two categories Clinical Manifestations based on the urinary chloride (Table 37.3). The alkalosis in The symptoms in patients with metabolic alkalosis often are patients with a low urinary chloride is maintained by volume related to the underlying disease and associated electrolyte depletion. They are called chloride responsive because volume disturbances. Hypokalemia is often present and occasionally repletion with fluid containing sodium chloride and potassium severe (see Chapter 36). Children with chloride-responsive chloride is necessary to correct the metabolic alkalosis. Emesis, causes of metabolic alkalosis often have symptoms related to which causes loss of hydrochloride and volume depletion, is volume depletion (see Chapter 33). In contrast, children with the most common cause of a metabolic alkalosis. Diuretic use chloride-unresponsive causes may have symptoms related to increases chloride excretion in the urine. Consequently, while hypertension. Severe alkalemia may cause arrhythmias, hypoxia a patient is receiving diuretics, the urinary chloride is typically secondary to hypoventilation, or decreased cardiac output. high (>20 mEq/L). After the diuretic effect resolves, the urinary chloride is low ( 7.45 (alkalemia): Primary disorder is an alkalosis. 2. Evaluate pCO2 (partial pressure of carbon dioxide in blood, reference range: 33–45 mm Hg) to determine whether the primary acid-base disorder is respiratory or metabolic: pH and pCO2 change in the opposite direction: respiratory disorder pH and pCO2: respiratory acidosis pH and pCO2: respiratory alkalosis pCO2 and pH change in the same direction: metabolic disorder pH and pCO2: metabolic acidosis (calculate anion gap to identify the possible causes) pH and pCO2: metabolic alkalosis Suspect a mixed acid-base disorder if: pCO2 or HCO3- is abnormal and pH is normal or did not change as expected (e.g., a very high pCO2 and a mild acidosis). pCO2 and HCO3- shift towards acidosis ( pCO2 and HCO3-) or alkalosis ( pCO2 and HCO3‑). Lesser- or greater-than-expected compensatory response (see “Compensation” below) 3. Evaluate HCO3- (reference range: 22–28 mEq/L): High: metabolic alkalosis or compensated respiratory acidosis Normal: uncompensated respiratory disorders Low: metabolic acidosis or compensated respiratory alkalosis 4. Evaluate pO2: High: hyperoxemia Low: hypoxemia Example pH = 7.5, pCO2 = 20 mmHg, HCO3 = 22 mEq/L, pO2 = 70 mmHg Alkalosis ( pH), respiratory disorder ( pCO2), uncompensated (normal HCO3), hypoxemia ( pO2): uncompensated respiratory alkalosis with hypoxemia SMORE: change of pCO2 in the Same direction as pH Metabolic disorder; change of pCO2 in the Opposite direction of pH REspiratory disorder Compensation (acid-base) Definition: physiological changes that occur in acid-base disorders in an attempt to maintain normal body pH Compensatory changes In metabolic disorders: rapid compensation within minutes by changes in minute ventilation In respiratory disorders: typically slow compensation over several hours to days by changes in the urinary pH Compensation mechanisms in acid-base disorders Primary disorder Compensatory process Expected compensation* Metabolic acidosis Arterial and CSF pH (with HCO3-) Winter formula stimulation of the medullary chemoreceptors Expected PCO2 = respiratory rate and/or tidal volume ( (1.5 x HCO3-) + 8 hyperventilation) CO2 washout PCO2 (+/- 2) Interpretation Measured PCO2 > expected PCO2: respiratory acidosis in addition to metabolic acidosis Measured PCO2 < expected PCO2: respiratory alkalosis addition to metabolic acidosis Metabolic alkalosis Arterial and CSF pH (with HCO3-) Expected pCO2 = (0.7 stimulation of the medullary chemoreceptors x HCO3-) + 20 (+/- 5) respiratory rate and/or tidal volume ( hypoventilation) CO2 retention PCO2 Respiratory Acute Buffers in blood Expected HCO3- = 24 + [0.1 x (pCO2 - 40)] acidosis compensation (+/- 3) Chronic Arterial pH (with PCO2) HCO3- via: Expected HCO3- = 24 Reabsorption of HCO3- by the + [0.4 x (pCO2 - 40)] compensation proximal convoluted tubule (+/- 3) Excretion of H+ as H2PO4- and NH4+ by the distal convoluted tubule and collecting duct Respiratory Acute Buffers in blood Expected HCO3- = 24 - [0.2 x (40 - pCO2)] alkalosis compensation (+/- 3) Chronic Arterial pH (with PCO2) HCO3- via: Expected HCO3- = 24 Reabsorption of HCO3- by the - [0.5 x (40 - pCO2)] compensation proximal convoluted tubule (+/- 3) Renal excretion of H+ *If the expected compensation does not occur, a secondary acid-base disturbance will be present in addition to the primary disorder. Anion gap An anion gap represents the difference between the concentration of unmeasured anions and the concentration of unmeasured cations. Calculation Anion gap = [Unmeasured anions] - [Unmeasured cations] [Unmeasured anions] = [Total anions] - [Routinely measured anions] [Unmeasured cations] = [Total cations] - [Routinely measured cations] Since maintenance of electrical neutrality requires that the total concentration of cations approximate that of anions, the anion gap formula can also be expressed as: anion gap = [Routinely measured cations] - [Routinely measured anions] If potassium concentration is normal, anion gap ≈ [Na+] - ([Cl-] + [HCO3-]) (reference range: 6–12 mmol/L) If potassium levels are also taken into consideration: anion gap = ([Na+] + [K+]) - ([Cl-] + [HCO3-]) ( reference range: 10–16 mmol/L) An increase of unmeasured anions can increase the anion gap (see “High anion gap metabolic acidosis” below). Interpretation Normal anion gap metabolic acidosis (also known as hyperchloremic acidosis) Primary loss of HCO3- compensated with Cl- normal anion gap Etiology Endogenous: diarrhea; , biliary or pancreatic fistula; , renal tubular acidosis; , Addison disease Exogenous: drugs (e.g., carbonic anhydrase inhibitors), uptake of acids containing chloride ions (e.g., HCl) Further evaluation: urine anion gap = [urine Na+] + [urine K+] - [urine Cl-] Positive urine anion gap: renal acidification (e.g., due to renal tubular acidosis) Negative urine anion gap: GI loss of bicarbonate (e.g., due to diarrhea) High anion gap metabolic acidosis Increased concentration of organic acids such as lactate, ketoacids (beta-hydroxybutyrate, acetoacetate), oxalic acid, formic acid, or glycolic acid; no compensatory increase of Cl- anion gap Etiology Endogenous: lactic acidosis, diabetic ketoacidosis, renal insufficiency/uremia Exogenous: salicylate intoxication, ethanol intoxication, methanol intoxication, ethylene glycol intoxication (a component of antifreeze products) Further evaluation: delta ratio = (anion gap - 12) / (24 - [HCO3-]) Delta ratio < 1 : A hyperchloremic or normal anion gap metabolic acidosis is present in addition to a high anion gap metabolic acidosis. Delta ratio 1–2 : Only a high anion gap metabolic acidosis is present. Delta ratio > 2 : A chronic respiratory acidosis or a metabolic alkalosis is present in addition to a high anion gap metabolic acidosis. Abnormal anion gap without metabolic acidosis Hypoalbuminemia [Unmeasured anions] anion gap Paraproteinemia (e.g., multiple myeloma), severe hypercalcemia, severe hypermagnesemia, and/or lithium intoxication [Unmeasured cations] anion gap Severe hyperphosphatemia [Unmeasured anions] anion gap Severe hypocalcemia and/or hypomagnesemia [Unmeasured cations] anion gap Causes of high anion gap acidosis (MUDPILES): Methanol intoxication, Uremia, Diabetic ketoacidosis, Paraldehyde, Isoniazid or Iron overdose, Inborn error of metabolism, Lactic acidosis, Ethylene glycol intoxication, Salicylate intoxication Causes of normal anion gap acidosis (FUSEDCARS): Fistula (biliary, pancreatic), Ureterogastric conduit, Saline administration, Endocrine (Addison disease, hyper-PTH), Diarrhea, Carbonic anhydrase inhibitor, Ammonium chloride, Renal tubular acidosis, Spironolactone A neGUTive urine anion gap implies GI loss of bicarbonate. Treatment Treatment of acid-base disorders should always address the underlying cause. Some steps in urgent management are listed below. Respiratory acidosis: Treat underlying cause; (see “Treatment” in “COPD”, “Opioid intoxication”, and “ Benzodiazepine overdose” articles). Respiratory alkalosis: Treat underlying cause. Metabolic acidosis Acute severe metabolic acidosis: intravenous sodium bicarbonate Chronic metabolic acidosis: oral sodium bicarbonate along with treatment of the underlying cause (e.g., diarrhea, renal tubular acidosis) Electrolyte disturbances: correction (e.g., see “Disorders of potassium balance”) See “Diabetic ketoacidosis” and “Salicylate toxicity”. Metabolic alkalosis Volume depletion: isotonic saline to increase urinary bicarbonate excretion and correct extracellular volume loss Bicarbonate excess: acetazolamide Electrolyte disturbances: correction References 1. Kasper DL, Fauci AS, Hauser SL, Longo DL, Lameson JL, Loscalzo J. Harrison's Principles of Internal Medicine. McGraw-Hill Education ; 2015 2. Tuchscherer J, Rehman H. Metabolic acidosis in toluene sniffing. CJEM. 2013; 15 (04): p.249- 252. doi: 10.2310/8000.2013.130974. | Open in Read by QxMD 3. Spital A. Physiological approach to assessment of acid-base disturbances.. N Engl J Med. 2015; 372 (2): p.193. doi: 10.1056/NEJMc1413880. | Open in Read by QxMD 4. Meltem AC, Figen C, Nalan MA, et al. A hypokalemic muscular weakness after licorice ingestion: a case report. Cases Journal. 2009; 2 (1): p.8053. doi: 10.4076/1757-1626-2-8053. | Open in Read by QxMD 5. Kraut JA, Madias NE. Metabolic acidosis: pathophysiology, diagnosis and management. Nature Reviews Nephrology. 2010; 6 (5): p.274-285. doi: 10.1038/nrneph.2010.33. | Open in Read by QxMD 6. Jaber S, Paugam C, Futier E, et al. Sodium bicarbonate therapy for patients with severe metabolic acidaemia in the intensive care unit (BICAR-ICU): a multicentre, open-label, randomised controlled, phase 3 trial. Lancet. 2018; 392 (10141): p.31-40. doi: 10.1016/s0140- 6736(18)31080-8. | Open in Read by QxMD 7. Costanzo LS. Physiology Board review series. Lippincott Williams & Wilkins ; 2014 8. Marano M. Evaluation of the expected ventilatory response to metabolic acidosis in chronic hemodialysis patients. Hemodial Int. 2017; 22 (2): p.180-183. doi: 10.1111/hdi.12602. | Open in Read by QxMD 9. Rastegar A. Use of the DeltaAG/DeltaHCO3- ratio in the diagnosis of mixed acid-base disorders.. J Am Soc Nephrol. 2007; 18 (9): p.2429-31. doi: 10.1681/ASN.2006121408.| Open in Read by QxMD 10. Lee S, Kang KP, Kang SK. Clinical usefulness of the serum anion gap.. Electrolyte & blood pressure : E & BP. 2006; 4 (1): p.44-6. doi: 10.5049/EBP.2006.4.1.44. | Open in Read by QxMD 11. Sadjadi SA, Pi A. Hyperphosphatemia, a Cause of High Anion Gap Metabolic Acidosis: Report of a Case and Review of the Literature. American Journal of Case Reports. 2017; 18 : p.463-466. doi: 10.12659/ajcr.902862. | Open in Read by QxMD 12. Herold G. Internal Medicine. Herold G ; 2014 13. Acid Base Online Tutorial. http://fitsweb.uchc.edu/student/selectives/TimurGraham/compensatory_responses_respiratory _alkalosis.html. Updated: February 21, 2017. Accessed: February 21, 2017. 14. Barrett KE, Barman SM, Boitano S, Brooks HL. Ganong's Review of Medical Physiology (Enhanced EB). McGraw Hill Professional ; 2009 © 2020 AMBOSS Medical Knowledge Terms and Conditions Privacy Privacy Settings Legal Notice Get Support & Contact Us Multiple Choice Questions- Acid Base Balance Q.1- A person was admitted in a coma. Analysis of the arterial blood gave the following values: PCO2 16 mm Hg, HCO3- 5 mmol/l and pH 7.1. What is the underlying acid-base disorder? a) Metabolic Acidosis b) Metabolic Alkalosis c) Respiratory Acidosis d) Respiratory Alkalosis Q.2- In a man undergoing surgery, it was necessary to aspirate the contents of the upper gastrointestinal tract. After surgery, the following values were obtained from an arterial blood sample: pH 7.55, PCO2 52 mm Hg and HCO3- 40 mmol/l. What is the underlying disorder? a) Metabolic Acidosis b) Metabolic Alkalosis c) Respiratory Acidosis d) Respiratory Alkalosis Q.3- A young woman is found comatose, having taken an unknown number of sleeping pills an unknown time before. An arterial blood sample yields the following values: pH – 6.90, HCO3- 13 meq/liter, PaCO2 68 mmHg. This patient’s acid-base status is most accurately described as a) Uncompensated metabolic acidosis b) uncompensated respiratory acidosis c) simultaneous respiratory and metabolic acidosis d) respiratory acidosis with partial renal compensation Q.4- A student is nervous for a big exam and is breathing rapidly, what do you expect out of the followings a) Metabolic Acidosis b) Metabolic Alkalosis c) Respiratory Acidosis d) Respiratory Alkalosis Q.5- A 45- year-old female with renal failure, missed her dialysis and was feeling sick, what could be the reason ? a) Metabolic Acidosis b) Metabolic Alkalosis c) Respiratory Acidosis d) Respiratory Alkalosis Q.6- An 80-year-old man had a bad cold. After two weeks he said, “It went in to my chest, I am feeling tightness in my chest, I am coughing, suffocated and unable to breathe!” What could be the possible reason? a) Metabolic Acidosis b) Metabolic Alkalosis c) Respiratory Acidosis d) Respiratory Alkalosis Q.7- A post operative surgical patient had a naso gastric tube in for three days. The nurse caring for the patient stated that there was much drainage from the tube that is why she felt so sick. What could be the reason? a) Metabolic Acidosis b) Metabolic Alkalosis c) Respiratory Acidosis d) Respiratory Alkalosis Q.8- The p H of the body fluids is stabilized by buffer systems. Which of the following compounds is the most effective buffer system at physiological pH ? a) Bicarbonate buffer b) Phosphate buffer c) Protein buffer d) All of the above Q.9- Which of the following laboratory results below indicates compensated metabolic alkalosis? a) Low p CO2, normal bicarbonate and, high pH b) Low p CO2, low bicarbonate, low pH c) High p CO2, normal bicarbonate and, low p H d) High pCO2, high bicarbonate and High pH Q.10- The greatest buffering capacity at physiological p H would be provided by a protein rich in which of the following amino acids? a) Lysine b) Histidine c) Aspartic acid d) Leucine Q.11- Which of the following is most appropriate for a female suffering from Insulin dependent diabetes mellitus with a pH of 7.2, HCO3-17 mmol/L and pCO2-20 mm HG a) Metabolic Acidosis b) Metabolic Alkalosis c) Respiratory Acidosis d) Respiratory Alkalosis Q.12- Causes of metabolic alkalosis include all the following except. a) Mineralocorticoid deficiency. b) Hypokalemia c) Thiazide diuretic therapy. d) Recurrent vomiting. Q.13- Renal Glutaminase activity is increased in- a) Metabolic acidosis b) Respiratory Acidosis c) Both of the above d) None of the above Q.14- Causes of lactic acidosis include all except- a) Acute Myocardial infarction b) Hypoxia c) Circulatory failure d) Infections Q.15- Which out of the following conditions will not cause respiratory alkalosis? a) Fever b) Anxiety c) Laryngeal obstruction d) Salicylate toxicity Q.16- All are true about metabolic alkalosis except one- a) Associated with hyperkalemia b) Associated with decreased ionic calcium concentration c) Can be caused due to Primary hyperaldosteronism d) Can be caused due to Renin secreting tumor Q.17- Choose the incorrect statement out of the followings a) Deoxy hemoglobin is a weak base b) Oxyhemoglobin is a relatively strong acid c) The buffering capacity of hemoglobin is lesser than plasma protein d) The buffering capacity of Hemoglobin is due to histidine residues. Q.18- Carbonic anhydrase is present at all places except- a) Gastric parietal cells b) Red blood cells c) Renal tubular cells d) Plasma Q.19- All are true for renal handling of acids in metabolic acidosis except a) Hydrogen ion secretion is increased b) Bicarbonate reabsorption is decreased c) Urinary acidity is increased d) Urinary ammonia is increased. Q.20- Choose the incorrect statement about anion gap out of the followings a) In lactic acidosis anion gap is increased b) Anion gap is decreased in Hypercalcemia c) Anion gap is decreased in Lithium toxicity d) Anion gap is decreased in ketoacidosis. Q.21- Excessive citrate in transfused blood can cause which of the following abnormalities? a) Metabolic alkalosis b) Metabolic acidosis c) Respiratory alkalosis d) Respiratory acidosis Answers- 1-a, 2-b, 3-c, 4-d, 5-a, 6-c, 7-b, 8-a, 9-d, 10-b, 11-a, 12-a, 13-c, 14-d, 15-c, 16-a, 17-c, 18-d, 19-b, 20-d, 21-a