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![BUFFERS
• Buffers are substances that attenuate the change in pH that occurs when acids
or bases are added to the body.
• Extracellular buffers accomplish buffering of metabolic causes and intracellular
buffers to that of respiratory causes.
• The pH at which a buffer is 50% dissociated is its pKa ( ionization constant
of acid).
• The best physiologic buffers have a pKa close to 7.40 .When a pH is lower
than pKa of a buffer ,there is more acid than base and vice versa.
• pH of body fluids is calculated using the Henderson-Hasselbach equation
which expresses the relationship among pH , pKa and the concentrations of an
acid and its conjugate base. This relationship is valid for any buffer.
• Equation: pH = 6.1 + 𝑙𝑜𝑔
[𝐻𝐶𝑂3
−]
[𝐶𝑂2]](https://image.slidesharecdn.com/abgfinal-220624095507-9bd7cba1/85/Acid-Base-Disorders-3-320.jpg)
![COMPENSATIONS
Disorder Primary Event Compensation
Metabolic Acidosis ↓ [HCO3
¯] ↓ pCO2
Metabolic Alkalosis ↑ [HCO3
¯] ↑ pCO2
Respiratory Acidosis
Acute (<24 hours) ↑ pCO2 ↑ [HCO3
¯]
Chronic (3-5 days) ↑ pCO2 ↑↑ [HCO3
¯]
Respiratory Alkalosis
Acute (<24 hours) ↓ pCO2 ↓ [HCO3
¯]
Chronic (3-5 days) ↓ pCO2 ↓↓ [HCO3
¯]](https://image.slidesharecdn.com/abgfinal-220624095507-9bd7cba1/85/Acid-Base-Disorders-19-320.jpg)
![PLASMA ANION GAP
• Plasma Anion gap is the difference between measured cations (Na+) and the
measured anions (Cl-+ HCO3
-). It is also the difference between unmeasured
cations (K , Mg , Ca) and the unmeasured anions ( albumin, phosphate, urate,
sulfate).
• Formula : Na – (Cl – HCO3)
• Normal value 8-12 meq/l or 12±2meq/l
• A 1g/dl decrease in albumin concentration decreases anion gap by 2.5 meq/l. So,
anion gap corrected for albumin is
[Na]-[Cl+HCO3]+2.5(4-albumin)
• High anion gap metabolic acidosis(HAGMA)-AG is high as HCO3 gets
overconsumed to neutralise accumulated acids and increase in unmeasured
anions.
• Normal anion gap metabolic acidosis(NAGMA)- AG is normal as HCO3 loss is
accompanied by Cl reabsorption ( hyperchloremic metabolic acidosis)](https://image.slidesharecdn.com/abgfinal-220624095507-9bd7cba1/85/Acid-Base-Disorders-23-320.jpg)
More Related Content
Similar to Acid Base Disorders
Acid Base Disorders
- 1. ACID BASE DISORDER Presenter: Dr. Sneha Das Moderator : Dr. Some Suvra Bose
- 2. ACID BASE BALANCEPHYSIOLOGY • Human body is always pro acidic as every living cell needs energy molecule i.e. ATP molecules. • During ATP production in cell , acid is generated . • But, the normal blood pH is 7.35-7.45 ( slightly basic ) and the urine pH is 6.5-7.0 (slightly acidic). • Mechanisms of Acid Base Balance Regulating pH 1. Buffering ( Tissue level) Extracellular: HCO3- (most imp), albumin Intracellular: PO42-(bones), Haemoglobin 2. Respiratory Regulation ( minor role ) 3. Renal regulation (most potent) by acidification of urine.
- 3. BUFFERS • Buffers aresubstances that attenuate the change in pH that occurs when acids or bases are added to the body. • Extracellular buffers accomplish buffering of metabolic causes and intracellular buffers to that of respiratory causes. • The pH at which a buffer is 50% dissociated is its pKa ( ionization constant of acid). • The best physiologic buffers have a pKa close to 7.40 .When a pH is lower than pKa of a buffer ,there is more acid than base and vice versa. • pH of body fluids is calculated using the Henderson-Hasselbach equation which expresses the relationship among pH , pKa and the concentrations of an acid and its conjugate base. This relationship is valid for any buffer. • Equation: pH = 6.1 + 𝑙𝑜𝑔 [𝐻𝐶𝑂3 −] [𝐶𝑂2]
- 4. BICARBONATE BUFFER SYSTEM •It is based on the relationship between CO2 and HCO3¯ • CO2+H2O H+ + HCO3¯ • CO2 acts as an acid which after combining with water releases H+, bicarbonate acts as its conjugate base in that it accepts an H+. • The pKa of this reaction is 6.1 . • The bicarbonate buffer system is very effective because of the high concentration in the body (24 meq/l) and because it is an open system. The remaining body buffers are in closed system. • As the lungs increase CO2 excretion when the blood CO2 concentration increases.
- 5. BICARBONATE BUFFER SYSTEM •When acid is added to the body, following reaction occurs: H+ + HCO3¯ CO2 + H2O • In closed system, the CO2 would increase. The higher CO2 concentration would lead to an increase in the reverse reaction CO2 + H2O H+ + HCO3¯ This will increase H+, limiting the buffering capacity of bicarbonate. As the lungs excrete excess CO2 , the reverse reaction doesn’t occur thus enhancing the buffering capacity of bicarbonate. Same mechanism holds with addition of base.
- 6. NON BICARBONATE BUFFERS 1.Phosphate • Can bind upto 3 hydrogen molecules so it can exist as PO4 3¯, HPO4 2¯, H2PO4¯, H3PO4 . However, at a physiological pH most phosphate exists either as HPO4 2¯ or H2PO4 - • H2PO4¯ = H+ + HPO4¯ • The pKa of this reaction is 6.8, making it an effective buffer. 2. Protein • Large numbers of histidine in the Hb makes it an effective buffer. pKa of this reaction is 6.8. • Plasma proteins have lesser number of histidine residues than hemoglobin and hence they are not very effective. pKa of this reaction is 6.8.
- 7. ENDOGENOUS ACID PRODUCTION •Normally when food is metabolized, 2 types of acids are added to ECF 1. Volatile acid in the form of carbonic acid ( H2co3), which determines the level of CO2 in the blood ( PaCO2) and is excreted by lung. 2. Non volatile acids like sulphuric acid and phosphoric acids are produced by dietary and endogenous protein catabolism. They are excreted by the kidney.
- 8. RESPIRATORY REGULATION • Therespiratory compensation begins almost immediately within minutes and is fully established by 24 hr. • The lungs participate in regulating pH by increasing or decreasing the elimination of CO2. • With acidosis, pH changes around the brainstem stimulate hyperventilation and the reverse is observed with alkalosis. • However, the respiratory compensation is not completely effective in restoring pH as only volatile acids i.e CO2 is taken care by the lungs. • Failure of respiratory regulation results in respiratory acidosis or alkalosis.
- 9. RENAL REGULATION • Itis the most powerful buffering system, which starts within hours and takes 5-6 days for peak effect. • Involved in the removal of non volatile acids or bases through several active transport mechanism. • In response to acidosis- 1. Renal tubules reabsorb bicarbonate that is filtered at the glomerulus 2. Tubular secretion of H+ mostly in the collecting duct, with a small role in distal tubule. • Adequate excretion of endogenous acids requires presence of 2 urinary buffers – Phosphate and ammonia.
- 10. BICARBONATE REABSORPTION INPROXIMAL TUBULE • The reabsorption of filtered bicarbonate is first step in renal regulation of acid base balance. • The proximal tubule reclaims approximately 85% of the filtered bicarbonate. • Remaining 15% is reclaimed mostly in the ascending limb of the loop of Henle.
- 11. BICARBONATE REABSORPTION INPROXIMAL TUBULE • Increased HCO3- reabsorption occurs in 1. Volume depletion 2. Hypokalemia 3. Increased PCO2 (Respiratory Acidosis) • Decreased HCO3- reabsorption occurs in 1. Decreased PCO2 ( Respiratory Alkalosis) 2. Hyperparathyroidsm ( PTH decreases HCO3- reabsorption). 3. Carbonic anhydrase inhibitors such as as acetazolamide 4. Disorders that can cause proximal RTA.
- 12. DISTAL TUBULE ACIDIFIACTION •Distal tubule acidification requires 2 urinary buffers- Phosphate and ammonia. • Almost 15% of the filtered HCO3- is absorbed in TAL via apical Na/H exchanger. • Type A IC cells in the distal tubule secretes H+ via H-ATPase and H+/K+ ATPase present in the apical membrane. • The secreted H+ combines with HPO42- to form H2PO4- , a titrable acid which is excreted. • H+ ATPase is stimulated by aldosterone
- 13. AMMONIUM EXCRETION • Inthe proximal tubule, NH3 is produced from glutamine in the renal cells. • H+ is secreted by Na+-H+ exchanger and NH3 diffuses into the lumen. • NH4 + is reabsorbed by Na+-K+- 2Cl− cotransporter in the TALH and deposited in the medullary interstitial fluid. • In the collecting ducts, NH3 diffuses from the medullary interstitium into the lumen, combines with secreted H+ in the lumen, and is excreted as NH4 +.
- 14. AMMONIUM EXCRETION • Acidexcretion by the collecting duct increases in 1. Primary hyperaldosteronism and secondary hyperaldosteronism due to volume depletion 2. Hypokalemia ( stimulates NH3 production in proximal tubule and increases H+ secretion in the collecting duct).
- 15. INDICATION OF ABG •Severe respiratory or metabolic disorders • Clinical features of hypoxia or hypercarbia • Shock • Sepsis • Decreased urine output • Renal failure • Monitoring of babies in ventilator
- 16. ALGORITHM FOR SIMPLEACID BASE DISORDER Blood pH Acidemi a (↓pH) Alkalemi a (↑pH) Respiratory Acidosis Metaboli c Acidosis Respiratory Acidosis with compensatory metabolic alkalosis Metabolic Acidosis with compensatory respiratory alkalosis Respiratory Alkalosis Metaboli c Alkalosis Respiratory Alkalosis with compensatory metabolic acidosis Metabolic Alkalosis with compensatory respiratory acidosis ↑pCO2 ↑pCO2 ↓pCO2 ↓HCO3 ¯ ↑HCO3 ¯ ↑HCO3 ¯ ↓pCO2 ↓HCO3 ¯
- 17. STEPS OF ABGINTERPRETATION 1. Is there an acid base disorder?- Look at the PaCO2 and HCO3 to determine whether they are in the normal range. Normal values- pH-7.35-7.45(7.40) , HCO3 – 22-26 meq/l (24), PaCO2- 35-45mm of Hg(40) 2. Is there acidosis or alkalosis? pH<7.35 -Acidosis pH>7.45 -Alkalosis
- 18. 3. What isthe primary acid base disorder? Determine the primary defect from the pH, HCO3 and PaCO2 If pH <7.35 – acidosis , may be either • Metabolic acidosis- Low HCO3 • Respiratory acidosis- High PaCO2 If pH >7.45- alkalosis , may be either • Metabolic alkalosis – High HCO3 • Respiratory alkalosis- Low PaCO2 STEPS OF ABG INTERPRETATION
- 19. COMPENSATIONS Disorder Primary EventCompensation Metabolic Acidosis ↓ [HCO3 ¯] ↓ pCO2 Metabolic Alkalosis ↑ [HCO3 ¯] ↑ pCO2 Respiratory Acidosis Acute (<24 hours) ↑ pCO2 ↑ [HCO3 ¯] Chronic (3-5 days) ↑ pCO2 ↑↑ [HCO3 ¯] Respiratory Alkalosis Acute (<24 hours) ↓ pCO2 ↓ [HCO3 ¯] Chronic (3-5 days) ↓ pCO2 ↓↓ [HCO3 ¯]
- 20. 4. Calculate theexpected compensation Metabolic Acidosis WINTER’S formula-Expected CO2= (1.5xHCO3)+ 8 ±2 Metabolic Alkalosis Expected CO2= (HCO3 + 15 ) Respiratory Acidosis • Acute- For every 10 mm increase in pCO2 , HCO3 increases by 1. • Chronic- For every 10 mm increase in pC02, HCO3 increases by 3.5. Respiratory Alkalosis • Acute- For every 10 mm decrease in pCO2, HCO3 decreases by 2. • Chronic- For every 10 mm decrease in pC02, HCO3 decreases by 4. STEPS OF ABG INTERPRETATION
- 21. 5 . Determinethe presence of mixed acid base disorder • If either of the pH or PaCO2 is normal and the other abnormal, then there is a mixed metabolic and respiratory disorder. • If the pH is normal in a setting of acid base disorder , there is always a mixed acid base disorder in the opposite direction. • In metabolic acidosis, there may be mixed HAGMA and NAGMA or a mixed HAGMA + metabolic alkalosis ( or pre existing compensated respiratory acidosis ) • Delta Ratio is measured in high anion gap metabolic acidosis. 6. Clinical correlation and to establish the etiological diagnosis STEPS OF ABG INTERPRETATION
- 22. SAME MIXED DISORDERS SameMixed Disorders – Which came first? • If the trend of change in PaCO2 and HCO3 is the same, check the percent difference. The one , with greater % difference between the two is the one that is the dominant disorder. • Eg : pH=7.25, HCO3=16, PaCO2=60 • Here, the pH is acidotic and both PaCO2 and HCO3 explain its acidosis, so look at the % difference • HCO3 % difference= (24-16)/24 = 0.33 • PaCO2 % difference= (60-40)/40= 0.5 • So, respiratory acidosis is the dominant disorder
- 23. PLASMA ANION GAP •Plasma Anion gap is the difference between measured cations (Na+) and the measured anions (Cl-+ HCO3 -). It is also the difference between unmeasured cations (K , Mg , Ca) and the unmeasured anions ( albumin, phosphate, urate, sulfate). • Formula : Na – (Cl – HCO3) • Normal value 8-12 meq/l or 12±2meq/l • A 1g/dl decrease in albumin concentration decreases anion gap by 2.5 meq/l. So, anion gap corrected for albumin is [Na]-[Cl+HCO3]+2.5(4-albumin) • High anion gap metabolic acidosis(HAGMA)-AG is high as HCO3 gets overconsumed to neutralise accumulated acids and increase in unmeasured anions. • Normal anion gap metabolic acidosis(NAGMA)- AG is normal as HCO3 loss is accompanied by Cl reabsorption ( hyperchloremic metabolic acidosis)
- 25. IMPORTANCE OF ANIONGAP • Useful to establish the etiological diagnosis of metabolic acidosis. • Useful in diagnosis of mixed disorder.
- 26. DELTA RATIO • Ifthere is high anion gap metabolic acidosis then calculate the delta ratio or delta gap to determine additional hidden metabolic acidosis or metabolic alkalosis. • Formula : (AG-12)/(24-HCO3) • <0.4 –Pure NAGMA • 0.4-0.8- Mixed NAGMA+HAGMA • 0.8-2- Pure HAGMA • >2- Mixed HAGMA + metabolic alkalosis
- 27. METABOLIC ACIDOSIS • Itis characterized by fall in plasma HCO3- and fall in pH (<7.35). The PaCO2 is reduced secondarily by hyperventilation , which minimizes fall in pH. • 3 basic mechanisms- 1. Loss of bicarbonate from the body 2. Impaired ability to excrete acid by the kidney 3. Addition of acid to the body ( endogenous or exogenous)
- 28. CLASSIFICATION AND CAUSESOF METABOLIC ACIDOSIS I. Overproduction of H+ 1. Toxins and drugs –methanol , ethylene glycol, salicylate etc 2. Ketoacidosis- DKA, starvation 3. Lactic acidosis- • Type A – shock, anaemia, CO poisoning • Type B- Liver failure, renal failure , metformin , zidovudine, INH II. Underexcretion of H+ Renal failure- uraemic acidosis( GFR<15ml/1.73m2/min) III. Excess loss of HCO3 1. GIT causes- diarrhea, pancreatic fistula, ureterosigmoidostomy 2. Renal causes- RTA , drugs such as ACEi, aldosterone antagonist, CA inhibitors I, II- HAGMA III- NAGMA
- 29. URINARY ANION GAP •It helps in differentiating the causes of normal anion gap metabolic acidosis. • Urinary anion gap reflects the ability of the kidney to excrete NH4Cl • Formula – Urinary (Na+K-Cl) =80 –NH4 • Normally UAG is zero or has a positive value around 30-35meq/l, due to the presence of dissolved anions. • UAG is negative in GIT causes of metabolic acidosis due to intact mechanism of renal acidification resulting in enhanced NH4Cl excretion. • UAG is positive in all forms of RTA due to low renal NH4+ excretion.
- 30. CLINICAL FEATURES OFMETABOLIC ACIDOSIS I. Manifestations of underlying disorder II. Manifestations of metabolic acidosis • Pulmonary changes- Kussmauls breathing • Cardiovascular changes- In severe acidemia (pH <7.2), there is increased susceptibility for arrythmias, decreased response to inotropes, secondary hypotension due to depressed myocardial contractility and arterial vasodilation. • Neurological changes- Ranges from headache, confusion, lethargy, drowsiness to coma. • Chronic acidemia as with renal failure can cause rickets.
- 31. APPROACH TO METABOLICACIDOSIS I. History II. Investigations III. Management History- Kussmaul’s breathing is the most important diagnostic presentation. H/o diabetes, toxin ingestion, diarrhoea, FTT, rickets, bone pains, recurrent episode of dehydration, vomiting etc Investigations- • ABG- Low HCO3, low pH, compensatory fall in PaCO2. • Plasma AG • Delta Gap • Urinary AG Management • Specific management of underlying disorder • Correct volume and electrolyte deficits • Alkali therapy with NaHCO3 and Tromethamine • Amount of IV NaHCO3 required is calculated as – B.W x base deficit x0.3
- 32. ALKALI THERAPY INMETABOLIC ACIDOSIS Indication of bicarbonate therapy • Serum pH <7.10 and/or plasma HCO3 <10 meq/l in conditions of normal anion gap metabolic acidosis. Disadvantages of bicarbonate therapy • Hypernatremia and volume overload especially in CHF or renal failure. • Increased PaCO2. Therefore, patients ventilatory status should be assessed before administration. • Hypokalemia and hypocalcemia • Overshoot or rebound alkalosis in organic acidosis (i.e ketoacidosis , lactic acidosis ) due to conversion of accumulated organic anions into bicarbonate .
- 33. APPROACH TO METABOLICACIDOSIS Metabolic Acidosis (pH<7.35, HCO3<22meq/l, PaCO2<35mmHg) Calculate plasma pH HAGMA • Toxins • Ketoacidosis • Lactic acidosis NAGMA GIT CAUSES • Diarrhoea • Pancreatic fistula • Ureterosigmoidost omy RENAL CAUSES • RTA UAG NEGATIVE POSITIVE GIT CAUSES RTA
- 34. APPROACH TO METABOLICACIDOSIS NAGMA UAG POSITIVE N / ↓K+ ↑K+ Urine pH Urine pH pH < 5.3 pH > 5.3 pH < 5.3 pH > 5.3 PRTA Distal RTA RTA Type IV Hyper K+ Distal RTA
- 35. CAUSES AND CLASSIFICATIONOF METABOLIC ALKALOSIS Metabolic Alkalosis Urine Chloride Diuretics Persistant vomiting, NG suction Villous adenoma Cystic fibrosis Post hypercapnia Chloride diarrhea Blood pressure Plasma renin, aldosterone Bartter syndrome Gitelman syndrome High renin High aldosterone Low renin High aldosterone Low renin Low aldosterone Renovascular stenosis Renin secreting tumor Adrenal hyperplasia, adenoma, carcinoma GRA Liddle syndrome AME, Cushing syndrome Exogenous steroids CAH (11β- or 17α- Chloride Responsive Low (<20mEq/L) Chloride Unresponsive High (>20mEq/L) High Normal
- 38. APPROACH TO METABOLICALKALOSIS I. History II. Investigations III. Management History-H/o vomiting, swelling of the body, recurrent respiratory infections , polyuria, dehydration urine output, diarrhoea in newborn, FTT, shock, HTN etc. Investigations • ABG- High HCO3, high pH, compensatory increase in PaCO2 • Urine Cl levels • Serum renin and aldosterone levels • BP
- 39. CAUSES AND CLASSIFICATIONOF METABOLIC ALKALOSIS Management of metabolic alkalosis Cl responsive • Administration of sufficient NaCl,KCl. Replacement of NG suction. • Diuretics usage- potassium supplementation or potassium sparing diuretics is used • Rarely acetazolamide can be helpful in severe metabolic alkalosis Cl resistant With HTN • Volume repletion is C/I • Adrenal adenomas- resected • Renovascular dis- can be repaired • Glucocorticoid remediable aldosteronism, CAH- glucocorticoid administration • Cushing syndrome- spironolactone • Liddle syndrome- Triamterene, amiloride Without HTN • Barter and Gitelman syndrome- includes oral potassium and sodium supplements
- 40. RESPIRATORY ACIDOSIS Causes ofRespiratory Acidosis Central Nervous System Depression • Pacephalities • Head Trauma • Brain Tumor • Central sleep apnea • Primary pulmonary hypoventilation(Ondine curse) • Stroke • Hypoxic Brain Damage • Obesity- hypoventilation(pickwickian) syndrome • Increased Intracranial pressure • Medications Narcotics Barbiturates Anaesthesia Benzodiazepines Propofol Alcohols Respiratory Muscle Weakness • Muscular dystrophy • Hypothyroidism • Malnutrition • Hypokalemia • Hypophosphatemia • Medications Succinylcholine Corticosteroids Disorders of Spinal Cord, Peripheral Nerves, or Neuromuscular Junction • Diaphragmatic paralysis • Guillain-Barre syndrome • Poliomyelitis • Acute flaccid myelitis • Spinal muscular atrophies • Tick paralysis • Botulism • Myasthenia • Multiple sclerosis • Spinal cord injury • Medications Vecuronium Aminoglycosides Organophosphates(pesticides)
- 41. RESPIRATORY ACIDOSIS Causes ofRespiratory Acidosis Pulmonary Disease • Pneumonia • Pneumothorax • Asthma • Bronchiolitis • Pulmonary edema • Pulmonary hemorrhage • Acute respiratory distress syndrome • Neonatal respiratory distress syndrome • Cystic fibrosis • Bronchopulmonary dysplasia • Hypoplastic lungs • Meconium aspiration • Pulmonary thromboembolus • Intestinal fibrosis Miscellaneous • Flail Chest • Cardiac Arrest • Kyphoscoliosis • Decreased diaphragmatic movement due to ascites dialysis Upper Airway Disease • Aspiration • Laryngospasm • Angioedema • Obstructive sleep apnea • Tonsillar hypertrophy • Vocal cord paralysis • Extrinsic tumor • Extrinsic or intrinsic hemangioma
- 42. TREATMENT OF RESPIRATORYACIDOSIS Respiratory acidosis is best managed by treatment of underlying etiology. All patients with acute respiratory acidosis are hypoxic and need supplemental oxygen or mechanical ventilation ( PaCO2 >60). • Respiratory acidosis caused by CNS disease require mechanical ventilation as hypercarbia causes cerebral vasodilation and raised ICT. This is dangerous for the child. Patients with chronic respiratory acidosis, oxygen should be used cautiously as it blunts the respiratory drive and further increases PaCO2. • It is best to avoid mechanical ventilation in chronic respiratory acidosis as extubation is difficult. • When intubation is necessary , the PaCO2 should be lowered only to the patients normal baseline.
- 43. RESPIRATORY ALKALOSIS Causes ofRespiratory Alkalosis Hypoxia and Hypoxemia • High altitude or low fraction of inspired oxygen • Anemia • Hypotension or lung disease Pulmonary disorders • Pulmonary edema • Embolism • Airway obstruction • Pneumonia • Interstitial lung disease • Mechanical ventilation (ventilatory rate or tidal volume too high) Extrapulmonary disorders (severe respiratory alkalosis) • Stress • Neurologic disease (stroke, infection, trauma, tumor) • Medications Catecholamines Progesterone Methylxanthines Salicylates Doxapram Nicotine • Hyperthermia • Hepatic encephalopathy • Sepsis • Recovery from metabolic acidosis
- 44. EXAMPLES 1. A childwith DKA has the following ABG pH-7.1, HCO3- 8 mEq/l , PaCO2- 20 mm of Hg , Na 140 mEq/l , Cl- 106 mEq/l and urinary ketones 3+ • pH is low- so acidosis • Low HCO3 – suggestive of metabolic acidosis and low PaCO2 – suggestive of compensation ( same direction rule). • Expected PaCO2 is (1.5x8)+8±2 = 20±2 which matches with the expected PaCO2. • AG is 140-106-8 =26 • Delta gap: 26-12/24-8 =0.8 s/o pure HAGMA • So, this patient has HAGMA with respiratory compensation.
- 45. 2. A 12yr old girl K/c/o Type 1 DM presented with fever , nausea, vomiting and abdominal pain for 1 day. Lab inv suggests pH- 7.28, PaCO2-27, HCO3- 12, Na- 140 , Cl – 98 , BSL – 400. • Low pH – so acidosis • Low HCO3- s/o metabolic acidosis • Expected PaCO2 – (1.5x12)+8±2=26±2 • AG- 140-98-12 =30 s/o HAGMA • Delta ratio- 30-12/24-12= 1.5 s/o mixed HAGMA+ metabolic alkalosis • This girl has HAGMA( DKA) + met alkalosis (vomiting) with respiratory alkalosis. EXAMPLES
- 46. 3. ABG ofpatient with CHF on furosemide is pH-7.48, HCO3- 34 , PaCO2-49. • pH is high – so alkalosis • High HCO3 s/o metabolic alkalosis and high PaCO2 s/o respiratory compensation (same direction rule) • Expected PaCO2 = 34+15=49 which matches with the given PaCO2 s/o simple acid base disorder. • So, this patient has metabolic alkalosis with respiratory compensation. EXAMPLES
- 47. 4. A 11yr old boy was admitted with high grade fever and hypotension after a prolonged course of diarrhoea. Lab values showed pH-7.32 , HCO3-6, PCO2- 20, Na- 139, Cl- 106. • pH is low- so acidosis • HCO3 is low – primary defect metabolic acidosis • Expected PaCO2- (1.5x6)+8 ±2= 17±2 s/o respiratory compensation. • AG : 139-106-6=27 . So , HAGMA. • Delta gap 27-12/24-6= 0.8 s/o mixed HAGMA + NAGMA • So this boy has HAGMA( lactic acidosis) + NAGMA ( diarrhoea) with respiratory alkalosis EXAMPLES
- 48. 5. A 3yr old comatose child with h/o accidental ingestion of several tablets of phenobarbitone is intubated and ventilation started with 30% oxygen. ABG after 6 hr showed pH-7.28 , PaCO2- 56 mm of Hg, HCO3 -26 • Low pH- so acidosis • High PaCO2 – primary defect is respiratory acidosis and high HCO3 s/o metabolic compensation(Opposite direction rule) • It is acute. Increase in CO2 = (56-40)=16 Increase in HCO3 =(24+1.6)=25.6 • So, the patient has respiratory acidosis with metabolic compensation. EXAMPLES
- 49. EXAMPLES 6. K/c/o chroniclung disease develops severe vomiting . pH -7.4 , HCO3- 36 , PaCO2 – 60. • pH is normal so patient has either no disorder or has mixed acid base disorder. • However, abnormal value of HCO3 and PaCO2 is s/o mixed disorders. • High HCO3 suggests metabolic alkalosis ( due to vomiting). High PaCO2 is s/o respiratory acidosis (due to CLD). • Metabolic alkalosis is expected to increase the pH, while respiratory acidosis is expected to decrease the pH. • Normal pH can be explained as an end result of opposite changes caused by both primary disorders.
- 50.