Downloaded 501 times
![8
pH Review
• pH = - log [H+]
• H+ is really a proton
• Range is from 0 - 14
• If [H+] is high, the solution is acidic; pH < 7
• If [H+] is low, the solution is basic or
alkaline ; pH > 7](https://image.slidesharecdn.com/acidbasedisorders1-151018011214-lva1-app6891/75/Acidosis-and-alkalosis-8-2048.jpg)
![Delta ratio
Delta ratio Assessment
<0.4 Hyperchloraemic normal anion gap acidosis
0.4 – 0.8
Combined high AG and normal AG acidosis
Note that the ratio is often <1 in acidosis associated
with renal failure
1 - 2
Uncomplicated high-AG acidosis
Lactic acidosis: average value 1.6
DKA more likely to have a ratio closer to 1 due to urine
ketone loss (if patient not dehydrated)
>2
Pre-existing increased [HCO3
-]:
concurrent metabolic alkalosis
pre-existing compensated respiratory acidosis
𝛥 ratio = 𝛥Anion gap/𝛥[HCO3
-] = (AG – 12)/(24 - [HCO3
-])](https://image.slidesharecdn.com/acidbasedisorders1-151018011214-lva1-app6891/75/Acidosis-and-alkalosis-76-2048.jpg)
![Calculate the anion gap
AG = Na – Cl – HCO3 (normal 12 ± 2)
AG corrected = AG + 2.5[4 – albumin]
If there is an anion Gap then calculate the Delta/delta
gap (step 6). Only need to calculate delta gap (excess
anion gap) when there is an anion gap to determine
additional hidden metabolic disorders (nongap metabolic
acidosis or metabolic alkalosis)
If there is no anion gap then start analyzing for non-anion
acidosis](https://image.slidesharecdn.com/acidbasedisorders1-151018011214-lva1-app6891/75/Acidosis-and-alkalosis-95-2048.jpg)
Uploaded bynahakul poudel
Acidosis and alkalosis
The document discusses acid-base balance and how it is maintained in the human body. It provides details on: 1. The body aims to keep pH between 7.35-7.45, but produces more acid than base during metabolism. 2. Acids are removed through respiration (exhaling volatile acids like CO2) and the kidneys (excreting non-volatile acids). 3. When acid-base levels are disturbed and pH moves outside the normal range, the body uses buffer systems, respiration, and the kidneys to compensate and return pH to normal.
More Related Content
Similar to Acidosis and alkalosis
Acidosis and alkalosis
- 1. Biochemical basis ofAcid Base Balance
- 2. Q.How acid basebalance is maintained in normal human being? • Normal body pH=7.4 equivalent to 40 nmole H con. Per liter. This level is very important for normal biological activity. this level of pH should be maintained for proper functioning of the body. on an average, the pH range may fluctuate from 7.35-7.45. • During normal metabolic activity, body produces both acid and bases but the acid production is greater than the base production.
- 3. • So bodyis a net acid producer.in a normal adult two types of metabolic acid are produced. • 1.Volatile acid- 15 mole/day in the form of co2 • 2. Non volatile acid-70 mEq/day in the form of H2so4, HCl, H3Po4. • These metabolic acid has a major consequences in alter the normal body pH.
- 4. • Volatile acidsare excreted through lung via pulmonary route.non volatile acids are excreted through kidney via urine. • Before their excreation respiratory system takes some time and kidney system also takes certain time.
- 5. Excreation of volatileacid: • Co2 produced in cellular level due to metabolic activity diffused into blood.in blood co2 is transported in three form. • A.in dissolved state=7% • B. in the form of HCO3 -&H+ (H2Co3)=70% • In combination of Hb=23% • From blood CO2 is diffused into alveoli of lungs and their into the atmosphere.
- 6. Transport of carbondioxide in the blood
- 7. Approach • History -subjective information concerning events, environment, trauma, medications, poisons, toxins • Physical examination - objective information assessing organ system status and function • Differentials - potential reasons for presentation • Clinical and laboratory studies - degree of changes from normal • Compensation - assessment of response to initial problem
- 8. 8 pH Review • pH= - log [H+] • H+ is really a proton • Range is from 0 - 14 • If [H+] is high, the solution is acidic; pH < 7 • If [H+] is low, the solution is basic or alkaline ; pH > 7
- 9.
- 10.
- 11. 11 • Acids areH+ donors. • Bases are H+ acceptors, or give up OH- in solution. • Acids and bases can be: –Strong – dissociate completely in solution • HCl, NaOH –Weak – dissociate only partially in solution • Lactic acid, carbonic acid
- 12. 12 The Body andpH • Homeostasis of pH is tightly controlled • Extracellular fluid = 7.4 • Blood = 7.35 – 7.45 • < 6.8 or > 8.0 death occurs • Acidosis (acidemia) below 7.35 • Alkalosis (alkalemia) above 7.45
- 13.
- 14. 14 Small changes inpH can produce major disturbances • Most enzymes function only with narrow pH ranges • Acid-base balance can also affect electrolytes (Na+, K+, Cl-) • Can also affect hormones
- 15. 15 The body producesmore acids than bases • Acids take in with foods • Acids produced by metabolism of lipids and proteins • Cellular metabolism produces CO2. • CO2 + H20 ↔ H2CO3 ↔ H+ + HCO3 -
- 16. 16 Control of Acids 1.Buffer systems Take up H+ or release H+ as conditions change Buffer pairs – weak acid and a base Exchange a strong acid or base for a weak one Results in a much smaller pH change
- 17. 17 Bicarbonate buffer • SodiumBicarbonate (NaHCO3) and carbonic acid (H2CO3) • Maintain a 20:1 ratio : HCO3 - : H2CO3 HCl + NaHCO3 ↔ H2CO3 + NaCl NaOH + H2CO3 ↔ NaHCO3 + H2O
- 18. 18 Phosphate buffer • Majorintracellular buffer • H+ + HPO4 2- ↔ H2PO4- • OH- + H2PO4 - ↔ H2O + H2PO4 2-
- 19. 19 Protein Buffers • Includeshemoglobin. • Carboxyl group gives up H+ • Amino Group accepts H+
- 20. 20 2. Respiratory mechanisms •Exhalation of carbon dioxide • Powerful, but only works with volatile acids • Doesn’t affect fixed acids like lactic acid • CO2 + H20 ↔ H2CO3 ↔ H+ + HCO3 - • Body pH can be adjusted by changing rate and depth of breathing
- 21. 21 3. Kidney excretion •Can eliminate large amounts of acid • Can also excrete base • Can conserve and produce bicarb ions • Most effective regulator of pH • If kidneys fail, pH balance fails
- 22. 22 Rates of correction •Buffers function almost instantaneously • Respiratory mechanisms take several minutes to hours • Renal mechanisms may take several hours to days
- 23.
- 24.
- 25. 25 Acid-Base Imbalances • pH<7.35 acidosis • pH > 7.45 alkalosis • The body response to acid-base imbalance is called compensation • May be complete if brought back within normal limits • Partial compensation if range is still outside norms.
- 26. 26 Compensation • If underlyingproblem is metabolic, hyperventilation or hypoventilation can help : respiratory compensation. • If problem is respiratory, renal mechanisms can bring about metabolic compensation.
- 27. 27 Acidosis • Principal effectof acidosis is depression of the CNS through ↓ in synaptic transmission. • Generalized weakness • Deranged CNS function the greatest threat • Severe acidosis causes –Disorientation –coma –death
- 28. 28 Alkalosis • Alkalosis causesover excitability of the central and peripheral nervous systems. • Numbness • It can cause : – Nervousness – muscle spasms or tetany – Convulsions – Loss of consciousness – Death
- 29.
- 30. 30 Respiratory Acidosis • Carbonicacid excess caused by blood levels of CO2 above 45 mm Hg. • Hypercapnia – high levels of pCO2 in blood • Chronic conditions: – Depression of respiratory center in brain that controls breathing rate – drugs or head trauma – Paralysis of respiratory or chest muscles – Asthma,Pneumonia,Emphysema
- 31. 31 Respiratory Acidosis • Acuteconditons: – Adult Respiratory Distress Syndrome – Pulmonary edema – Pneumothorax
- 32. 32 Compensation for Respiratory Acidosis •Kidneys eliminate hydrogen ion and retain bicarbonate ion. • Mechanism:↓pH→↑H+→H ion+ HCO3 - → H2CO3 → CO2 + H20 →pH backs towards normal.
- 33. 33 Signs and Symptomsof Respiratory Acidosis • Breathlessness • Restlessness • Lethargy and disorientation • Tremors, convulsions, coma • Respiratory rate rapid, then gradually depressed • Skin warm and flushed due to vasodilation caused by excess CO2
- 34. 34 Treatment of RespiratoryAcidosis • Restore ventilation • IV lactate solution • Treat underlying dysfunction or disease
- 35.
- 36. 36 Respiratory Alkalosis • Carbonicacid deficit • pCO2 less than 35 mm Hg (hypocapnea) • Most common acid-base imbalance • Primary cause is hyperventilation • Hysteria • Hyperapnoea at high altitude. • Meningitis,enchephalitis. • Hepatic failure
- 37. 37 Respiratory Alkalosis • Conditionsthat stimulate respiratory center: – Oxygen deficiency at high altitudes – Pulmonary disease and Congestive heart failure – caused by hypoxia – Acute anxiety – Fever, anemia – Early salicylate intoxication – Cirrhosis – Gram-negative sepsis
- 38. 38 Compensation of Respiratory Alkalosis •By renal system • Kidneys conserve hydrogen ion • Excrete bicarbonate ion.
- 39. 39 Treatment of RespiratoryAlkalosis • Treat underlying cause • Breathe into a paper bag • IV Chloride containing solution – Cl- ions replace lost bicarbonate ions
- 40.
- 41. 41 Metabolic Acidosis • DecreasedpH due to HCO3 - deficit is called metabolic acidosis. • Bicarbonate deficit - blood concentrations of bicarb drop below 22mEq/L • Causes: – Loss of bicarbonate through diarrhea or renal dysfunction – DM, Accumulation of acids (lactic acid or ketones) – Failure of kidneys to excrete H+
- 42. • Ingestion ofacid • Formation of excessive quantities of metabolic acid in the body. • Loss of excessive alkali from the body. • Intravenous administration of metabolic acid. • Poisoning by acidic eg. Acetyl salicylates (aspirin) and methyl alcohol.
- 43. 43 Symptoms of MetabolicAcidosis • Headache, lethargy • Nausea, vomiting, diarrhea • Coma • Death
- 44. 44 Compensation for Metabolic Acidosis •By respiratory system • Increased ventilation • Renal excretion of hydrogen ions if possible • K+ exchanges with excess H+ in ECF • ( H+ into cells, K+ out of cells) • Mechanism: ↓pH→↑respiration→ ↓ pCO2 to match the lowered HCO3 - →pH backs towards normal.
- 45. 45 Treatment of MetabolicAcidosis • IV lactate solution
- 46.
- 47. 47 Metabolic Alkalosis • Bicarbonateexcess - concentration in blood is greater than 26 mEq/L • Causes: – Excess vomiting = loss of stomach acid – Excessive use of alkaline drugs – Certain diuretics – Endocrine disorders – Heavy ingestion of antacids – Severe dehydration
- 48. 48 Compensation for Metabolic Alkalosis •Alkalosis most commonly occurs with renal dysfunction, so can’t count on kidneys • Respiratory compensation difficult – hypoventilation limited by hypoxia
- 49. 49 Symptoms of MetabolicAlkalosis • Respiration slow and shallow • Hyperactive reflexes ; tetany • Often related to depletion of electrolytes • Atrial tachycardia • Dysrhythmias
- 50. 50 Treatment of MetabolicAlkalosis • Electrolytes to replace those lost • IV chloride containing solution • Treat underlying disorder
- 51.
- 52. 52 Diagnosis of Acid-BaseImbalances 1. Note whether the pH is low (acidosis) or high (alkalosis) 2. Decide which value, pCO2 or HCO3 - , is outside the normal range and could be the cause of the problem. If the cause is a change in pCO2, the problem is respiratory. If the cause is HCO3 - the problem is metabolic.
- 53. Acid-Base Biochemistry Physiology • 2different processes • Bicarbonate regeneration (incorrectly reabsorption) • Hydrogen ion excretion
- 54. Acid-Base Biochemistry Importance ofRenal Bicarbonate Regeneration • Bicarbonate is freely filtered through the glomerulus so plasma and glomerular filtrate have the same bicarbonate concentration • At normal GFR approx 4300 mmol of bicarbonate would be filtered in 24 hr • Without re-generation of bicarbonate the buffering capacity of the body would be depleted causing acidotic state • In health virtually all the filtered bicarbonate is recovered
- 56. Acid-Base Biochemistry • RenalBicarbonate Regeneration involves the enzyme carbonate dehydratase (carbonic anhydrase) • Luminal side of the renal tubular cells impermeable to bicarbonate ions • Carbonate dehydratase catalyses the formation of CO2 and H2O from carbonic acid (H2CO3) in the renal tubular lumen • CO2 diffuses across the luminal membrane into the tubular cells
- 57. Acid-Base Biochemistry • withinthe renal tubular cells carbonate dehydratase catalyses the formation of carbonic acid (H2CO3) from CO2 and H2O • Carbonic acid then dissociates into H+ and HCO3- • The bicarbonate ions pass into the extracellular fluid and the hydrogen ions are secreted back into the lumen in exchange for sodium ions which pass into the extracellular fluid • Exchange of sodium and hydrogen ions an active process involving Na+/K+/H+ ATP pump • K+ important in electrolyte disturbances of acid-base
- 58. Acid-Base Biochemistry • Regenerationof bicarbonate does not involve net excretion of hydrogen ions • Hydrogen ion excretion requires the same reactions occurring in the renal tubular cells but also requires a suitable buffer in urine • Principal buffer system in urine is phosphate • 80% of phosphate in glomerular filtrate is in the form of the divalent anion HPO4 2- • This combines with hydrogen ions • HPO4 2- + H+ ↔ H2PO4 -
- 60. Acid-Base Biochemistry • Hydrogenion excretion capacity • The minimum urine pH that Can be generated is 4.6 ( 25µmol/L) • Normal urine output is 1.5L • Without the phosphate buffer system the free excretion of Hydrogen ions is less than 1/1000 of the acid produced by normal metabolism
- 61. Acid-Base Biochemistry • Thephosphate buffer system increases hydrogen ion excretion capacity to 30-40 mmol/24 hours • In times of chronic overproduction of acid another urine buffer system • Ammonia
- 62. Acid-Base Biochemistry • Ammoniaproduced by deamination of glutamine in renal tubular cells • Catalysed by glutaminase which is induced by chronic acidosis • Allows increased ammonia production and hence increased hydrogen ion excretion via ammonium ions • NH3 + H+ ↔ NH4 +
- 63. Acid-Base Biochemistry • Atnormal intracellular pH most ammonia is present as ammonium ions which can’t diffuse out of the cell • Diffusion of ammonia out of the cell disturbs the equilibrium between ammonia and ammonium ions causing more ammonia to be formed • Hydrogen ions formed at the same time! • These are used up by the deamination of glutamine to glutamate during gluconeogenesis
- 65. Acid-Base Biochemistry • Carbondioxide transport • Carbon dioxide produced by aerobic respiration diffuses out of cells and into the ECF • A small amount combines with water to form carbonic acid decreasing the pH of ECF • In red blood cells metabolism is anaerobic and very little CO2 is produced hence it diffuses into red cells down a concentration gradient to form carbonic acid (carbonate dehydratase) buffered by haemoglobin .
- 66. Acid-Base Biochemistry • Haemoglobinhas greatest buffering capacity when it is dexoygenated hence the buffering capacity increases as oxygen is lost to the tissues • Net effect is that carbon dioxide is converted to bicarbonate in red cells • Bicarbonate diffuses out of red cells down concentration gradient and chloride ions diffuse in to maintain electrochemical neutrality (chloride shift)
- 68. •Acid-Base Biochemistry • Inthe lungs this process is reversed • Haemoglobin is oxygenated reducing its buffering capacity and generating hydrogen ions • These combine with bicarbonate to form CO2 which diffuses into the alveoli • Bicarbonate diffuses into the cells from the plasma
- 72.
- 73. Reference ranges andpoints Parameter Reference range Reference point pH 7.35-7.45 7.40 PCO2 33-44 mm Hg 40 mm Hg PO2 75-105 mm Hg HCO3 - 22-28 mEq/L 24mEq/L Anion gap 8-16 mEq/L 12 mEq/L Osmolar gap <10 mOsm/L
- 74. Treatment of Metabolic Alkalosis •Electrolytes to replace those lost • IV chloride containing solution • Treat underlying disorder 74
- 75. 75 Diagnosis of Acid-BaseImbalances 1. Note whether the pH is low (acidosis) or high (alkalosis) 2. Decide which value, pCO2 or HCO3 - , is outside the normal range and could be the cause of the problem. If the cause is a change in pCO2, the problem is respiratory. If the cause is HCO3 - the problem is metabolic.
- 76. Delta ratio Delta ratioAssessment <0.4 Hyperchloraemic normal anion gap acidosis 0.4 – 0.8 Combined high AG and normal AG acidosis Note that the ratio is often <1 in acidosis associated with renal failure 1 - 2 Uncomplicated high-AG acidosis Lactic acidosis: average value 1.6 DKA more likely to have a ratio closer to 1 due to urine ketone loss (if patient not dehydrated) >2 Pre-existing increased [HCO3 -]: concurrent metabolic alkalosis pre-existing compensated respiratory acidosis 𝛥 ratio = 𝛥Anion gap/𝛥[HCO3 -] = (AG – 12)/(24 - [HCO3 -])
- 77. Compensation Primary Disturbance pH HCO3 - PCO2Compensation Respiratory acidosis <7.35 Compensatory increase Primary increase Acute: 1-2 mEq/L increase in HCO3 - for every 10 mm Hg increase in PCO2 Chronic: 3-4 mEq/L increase in HCO3 - for every 10 mm Hg increase in PCO2 Respiratory alkalosis >7.45 Compensatory decrease Primary decrease Acute: 1-2 mEq/L decrease in HCO3 - for every 10 mm Hg decrease in PCO2 Chronic: 4-5 mEq/L decrease in HCO3 - for every 10 mm Hg decrease in PCO2 Metabolic acidosis <7.35 Primary decrease Compensatory decrease 1.2 mm Hg decrease in PCO2 for every 1 mEq/L decrease in HCO3 - Metabolic alkalosis >7.45 Primary increase Compensatory increase 0.6-0.75 mm Hg increase in PCO2 for every 1 mEq/L increase in HCO3 - , PCO2 should not rise above 55 mm Hg in compensation
- 78. Respiratory acidosis PCO2 greaterthan expected Acute or chronic Causes excess CO2 in inspired air (rebreathing of CO2-containing expired air, addition of CO2 to inspired air, insufflation of CO2 into body cavity) decreased alveolar ventilation (central respiratory depression & other CNS problems, nerve or muscle disorders, lung or chest wall defects, airway disorders, external factors) increased production of CO2 (hypercatabolic disorders)
- 79. Racid acute A 65-year-oldman with a history of emphysema comes to the physician with a 3-hour history of shortness of breath. pH 7.18 PO2 61 mm Hg PCO2 58 mm Hg HCO3 - 26 mEq/L History suggests hypoventilation, supported by increased PCO2 and lower than anticipated PO2. Respiratory acidosis (acute) due to no renal compensation.
- 80. Description pH 7.18 PO2 61mm Hg PCO2 58 mm Hg HCO3 - 26 mEq/L 1-2 mEq/L increase in HCO3 - for every 10 mm Hg increase in PCO2. PCO2 increase = 58-40 = 18 mm Hg. HCO3 - increase predicted = (1-2) x (18/10) = 2-4 mEq/L add to 24 mEq/L (reference point) = 26-28 mEq/L
- 81. Racid chronic A 56-year-oldwoman with COPD is brought to the physician with a 3-hour history of severe epigastric pain. pH 7.39 PO2 62 mm Hg PCO2 52 mm Hg HCO3 - 29 mEq/L History suggests hypoventilation, supported by increased PCO2. Respiratory acidosis (chronic) with renal compensation.
- 82. Description pH 7.39 PO2 62mm Hg PCO2 52 mm Hg HCO3 - 29 mEq/L 3-4 mEq/L increase in HCO3 - for every 10 mm Hg increase in PCO2. PCO2 increase = 52-40 = 12 mm Hg. HCO3 - increase predicted = (3-4) x (12/10) = 4-5 mEq/L add to 24 mEq/L (reference point) = 28-29 mEq/L
- 83. Respiratory alkalosis PCO2 lessthan expected Acute or chronic Causes increased alveolar ventilation (central causes, direct action via respiratory center; hypoxaemia, act via peripheral chemoreceptors; pulmonary causes, act via intrapulmonary receptors; iatrogenic, act directly on ventilation)
- 84. Ralk acute A 17-year-oldwoman is brought to the physician with a 3- hour history of epigastric pain and nausea. She admits taking a large dose of aspirin. Her respirations are full and rapid. pH 7.57 PO2 104 mm Hg PCO2 25 mm Hg HCO3 - 23 mEq/L History suggests hyperventilation, supported by decreased PCO2. Respiratory alkalosis (acute) due to no renal compensation.
- 85. Description pH 7.57 PO2 104mm Hg PCO2 25 mm Hg HCO3 - 23 mEq/L 1-2 mEq/L decrease in HCO3 - for every 10 mm Hg decrease in PCO2. PCO2 decrease = 40-25 = 15 mm Hg. HCO3 - decrease predicted = (1-2) x (15/10) = 2-3 mEq/L subtract from 24 mEq/L (reference point) = 21-22 mEq/L
- 86. Ralk chronic A 81-year-oldwoman with a history of anxiety is brought to the physician with a 2-hour history of shortness of breath. She has been living at 9,000 ft elevation for the past 1 month. Her respirations are full at 20/min. pH 7.44 PO2 69 mm Hg PCO2 24 mm Hg HCO3 - 16 mEq/L History suggests hyperventilation, supported by decreased PCO2. Respiratory alkalosis (chronic) with renal compensation.
- 87. Description pH 7.44 PO2 69mm Hg PCO2 24 mm Hg HCO3 - 16 mEq/L 4-5 mEq/L decrease in HCO3 - for every 10 mm Hg decrease in PCO2. PCO2 decrease = 40-24 = 16 mm Hg. HCO3 - decrease predicted = (4-5) x (16/10) = 6-8 mEq/L subtract from 24 mEq/L (reference point) = 16-18 mEq/L
- 88. Metabolic acidosis Plasma HCO3 -less than expected Gain of strong acid or loss of base Alternatively, high anion gap or normal anion gap metabolic acidosis Causes high anion-gap acidosis (normochloremic) (ketoacidosis, lactic acidosis, renal failure, toxins) normal anion-gap acidosis (hyperchloremic) (renal, gastrointestinal tract, other)
- 89. Macid high AG 20-year-oldman with a history of diabetes is brought to e emergency department with a 3-day history of feeling ill. e is non-adherent with his insulin. Urine ketones are 2+ d glucose is 4+. pH 7.26 Na+ 136 mEq/L PO2 110 mm Hg K+ 4.8 mEq/L PCO2 19 mm Hg Cl- 101 mEq/L HCO3 - 8 mEq/L CO2, total 10 mEq/L Glucose 343 mg/dL Urea 49 mg/dL Creatinine 1 mg/dL story suggests d NC iabetic ketoacidosis. etabolic acidosis with appropriate respiratory mpensation.
- 90. Description pH 7.26 Na+136 mEq/L PO2 110 mm Hg K+ 4.8 mEq/L PCO2 19 mm Hg Cl- 101 mEq/L HCO3 - 8 mEq/L Glucose 343 mg/dL Urea 49 mg/dL AG = 136-101-8=27 mEq/L Creatinine 1 mg/dL 1.2 mm Hg decrease in PCO2 for every 1 mEq/L decrease in HCO3 -. HCO3 - decrease = 24-8 = 16 mEq/L PCO2 decrease predicted = 1.2 x 16 = 19 mm Hg. subtract from 40 mm Hg (reference point) = 21 mm Hg
- 91. Macid normal AG A43-year-old man comes to the physician with a 3-day history of diarrhea. He has decreased skin turgor. pH 7.31 Na+ 134 mEq/L PO2 -- mm Hg K+ 2.9 mEq/L PCO2 31 mm Hg Cl- 113 mEq/L HCO3 - 16 mEq/L Urea 74 mgl/dL Creatinine 3.4 mmol/L History is limited. Metabolic acidosis with respiratory compensation.
- 92. Description pH 7.31 Na+134 mEq/L PO2 -- mm Hg K+ 2.9 mEq/L PCO2 31 mm Hg Cl- 113 mEq/L HCO3 - 16 mEq/L Urea 74 mg/dL Creatinine 3.4 mg/dL AG = 134-113-16=5 mEq/L 1.2 mm Hg decrease in PCO2 for every 1 mEq/L decrease in HCO3 -. HCO3 - decrease = 24-16 = 8 mEq/L PCO2 decrease predicted = 1.2 x 8 = 10 mm Hg. subtract from 40 mm Hg (reference point) = 30 mm Hg
- 93. Metabolic alkalosis Plasma HCO3 -greater than expected Loss of strong acid or gain of base Causes (2 ways to organize) loss of H+ from ECF via kidneys (diuretics) or gut (vomiting) gain of alkali in ECF from exogenous source (IV NaHCO3 infusion) or endogenous source (metabolism of ketoanions) or addition of base to ECF (milk-alkali syndrome) Cl- depletion (loss of acid gastric juice) K+ depletion (primary/secondary hyperaldosteronism) Other disorders (laxative abuse, severe hypoalbuminaemia)
- 94. Urinary Chloride Spot urineCl- less than 10 mEq/L often associated with volume depletion respond to saline infusion common causes - previous thiazide diuretic therapy, vomiting (90% of cases) Spot urine Cl- greater than 20 mEq/L often associated with volume expansion and hypokalemia resistant to therapy with saline infusion causes: excess aldosterone, severe K+ deficiency, current diuretic therapy, Bartter syndrome
- 95. Calculate the aniongap AG = Na – Cl – HCO3 (normal 12 ± 2) AG corrected = AG + 2.5[4 – albumin] If there is an anion Gap then calculate the Delta/delta gap (step 6). Only need to calculate delta gap (excess anion gap) when there is an anion gap to determine additional hidden metabolic disorders (nongap metabolic acidosis or metabolic alkalosis) If there is no anion gap then start analyzing for non-anion acidosis
- 96. Malk high UrineCl- An 83-year-old woman is brought to the physician with a 1- week history of weakness and poor appetite. pH 7.58 Na+ 145 mEq/L PO2 60 mm Hg K+ 1.9 mEq/L PCO2 56 mm Hg Cl- 86 mEq/L HCO3 - 52 mEq/L Urine Cl- 74 mEq/L History is limited. Metabolic alkalosis with respiratory compensation. The cause is unknown, most likely excess adrenocortical activity, current diuretic therapy, or idiopathic.
- 97. EXAMPLE • Calculate Aniongap ABG 7.23/17/235 on 50% VM BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5/ Albumin 4. AG = Na – Cl – HCO3 (normal 12 ± 2) 123 – 97 – 7 = 19 • No need to correct for albumin as it is 4
- 98. EXAMPLE : DeltaGap ABG 7.23/17/235 on 50% VM BMP Na 123/ Cl 97/ HCO3 7/BUN 119/ Cr 5/ Albumin 4. • Delta gap = (actual AG – 12) + HCO3 • (19-12) +7 = 14 • Delta gap < 18 -> additional non-gap metabolic acidosis • So Metabolic acidosis anion and non anion gap
- 99. Description pH 7.58 Na+145 mEq/L PO2 60 mm Hg K+ 1.9 mEq/L PCO2 56 mm Hg Cl- 86 mEq/L HCO3 - 52 mEq/L Urine Cl- 74 mEq/L 0.6-0.75 mm Hg increase in PCO2 for every 1 mEq/L increase in HCO3 -. HCO3 - increase = 52-24 = 28 mEq/L PCO2 increase predicted = 0.6-0.75 x 28 = 17-21 mm Hg. add to 40 mm Hg (reference point) = 57-61 mm Hg
- 100. Malk low UrineCl- An 24-year-old woman is brought to the physician with a 3- month history of weakness and fatigue. Blood pressure is 90/60 mm Hg. pH 7.52 Na+ 137 mEq/L PO2 78 mm Hg K+ 2.6 mEq/L PCO2 49 mm Hg Cl- 90 mEq/L HCO3 - 39 mEq/L Urine Cl- 5 mEq/L History and physical examination suggests bulimia. Metabolic alkalosis with respiratory compensation. The cause is most likely bulimia.
- 101. Description pH 7.52 Na+137 mEq/L PO2 78 mm Hg K+ 2.6 mEq/L PCO2 49 mm Hg Cl- 90 mEq/L HCO3 - 39 mEq/L Urine Cl- 5 mEq/L 0.6-0.75 mm Hg increase in PCO2 for every 1 mEq/L increase in HCO3 -. HCO3 - increase = 39-24 = 15 mEq/L PCO2 increase predicted = 0.6-0.75 x 15 = 9-12 mm Hg. add to 40 mm Hg (reference point) = 49-52 mm Hg
- 102. What is theprimary disorder? What disorder is present? pH pCO2 or HCO3 Respiratory Acidosis pH low pCO2 high Metabolic Acidosis pH low HCO3 low Respiratory Alkalosis pH high pCO2 low Metabolic Alkalosis pH high HCO3 high
- 103. Special Cases • Pregnancy– hyperventilation (respiratory alkalosis), hyperemesis (metabolic alkalosis or acidosis), maternal ketosis (metabolic acidosis) • Children – low bicarbonate reserve (N=12-16 mEq/L), low acid excretion reserve, inborn errors in metabolism, diabetes, and poisoning (all metabolic acidosis)