1.Arterial Blood GasInterpretationPRESENTER- Dr. Shankerdeep SondhiResident IIInd Yr Department of Medicine

2. OBJECTIVESABGSamplingInterpretation of ABGCase Scenarios 3. ABG Procedure and Precautions Site- (Ideally) Radial Artery Brachial Artery Femoral Artery Ideally - Pre-heparinised ABG syringes- Syringe should be FLUSHED with 0.5mlof 1:1000 Heparin solution and emptied.DO NOT LEAVE EXCESSIVE HEPARIN IN THESYRINGEHEPARIN DILUTIONAL HCO3 EFFECT PCO2Only small 0.5ml Heparin for flushing and discard itSyringes must have > 50% blood. 4. Ensure No Air Bubbles. Syringe must be sealed immediatelyafter withdrawing sample. Contact with AIR BUBBLESAir bubble = PO2 150 mm Hg , PCO2 0 mm HgAir Bubble + Blood = PO2 PCO2 ABG Syringe must be transported at the earliest to thelaboratory for EARLY analysis via COLD CHAIN 5. ABG ELECTRODESA. pH (Sanz Electrode) Measures H+ ion concentration of sample against a known pH in a reference electrode, hence potential difference. Calibration with solutions of known pH (6.384 to 7.384)B. P CO2 (Severinghaus Electrode) CO2 reacts with solution to produce H+ higher C02- more H+ higher P CO2 measuredC. P 02 (Clark Electrode) 02 diffuses across membrane producing an electrical current measured as P 02. 6. Interpretation of ABG 7. Acid Base Homeostasis1. Plasma Acid Homeomostasis: Chemical buffering H+ influenced by Rate of endogenous production Rate of excretion Buffering capacity of body Buffers effective at physiologic pH are Hemoglobin Phosphate Proteins Bicarbonate 8. 2. Alveolar Ventilation:pCO2 action is immediate. Stimulation of respiratorycenter washes off the excess CO2 increasing pH, and vice versa3. Excretion:Liver: uses HCO3 to make urea which further prevents accumulation of ammonia and traps H+ in renal distal tubuleKidney: regulate plasma [HCO3] through three main processes: reabsorption of filtered HCO3 formation of titratable acid excretion of NH4+ in the urine.Proximal tubule reclaims 85% filtered HCO3Distal tubule reclaims 15%, and excretes H+4060 mmol/d of protons is excreted to maintain balance 9. Acid Base Balance H+ ion concentration in the body isprecisely regulated The body understands the importance of H+and hence devised DEFENCES against anychange in its concentration-BICARBONATERESPIRATORYRENALBUFFER REGULATION REGULATIONSYSTEM Acts in fewActs in hours toActs in fewminutesdaysseconds 10. BUFFER SYSTEM 1st line of defence in pH regulation. Determine capacity of ECF totransport acids from site of productionto site of excretion without unduechange in pH. They resist change in pH on additionof acid/alkali in media wherever theyare. 11. PLASMARBC BUFFERSBUFFERS NaHCO3/H2CO KHCO3/H2CO33 K2HPO4/KH2P4 Na2HPO4/ KHb/HHbNaH2PO4 Na-Pr/H-Pr 12. BICARBONATE BUFFER NAHCO3/H2CO3 = 20/1 = Alkali reserve. conversion of strong & non volatile acidin ECF, in weak & volatile acid at theexpense of NaHCO3 component ofbuffer. H2CO3 thus formed is eliminated by lungas CO2.Directly linked with respiration &healthy lungs essential for its function. High concentration in blood,so very goodphysiological buffer. Weak chemical buffer. 13. Bicarbonate Buffer SystemCO2 + H2O carbonic anhydrase H2CO3H+ + HCO3- In Acidosis - Acid = H+H+ + HCO3 H2CO3CO2 + H2O In Alkalosis - Alkali + Weak Acid = H2CO3CO2 + H20H2CO3 HCO3- + H++ALKALI 14. PHOSPHATE BUFFER Na2HPO4/NaH2PO4 =AlkPO4/AcidPO4 = 4/1. NaH2PO4 excreted by kidneys.Directly linked with kidneys & healthykidneys necessary for its functioning. Concentration in blood is low so notgood physiological buffer. Very good chemical buffer as pKaaprroches pH. 15. PROTEIN BUFFER Na+Pr- / H+Pr- = salt/acid. Proteins can act as a base In acidicmedium nd as an acid in basicmedium..with COOH& NH2 group. Buffering capacity of plasma proteinsis much less than Hb. 16. Respiratory Regulation of Acid Base Balance- ALVEOLARH+ VENTILATION PaCO2ALVEOLARH+VENTILATIONPaCO2 17. Renal Regulation of Acid Base BalanceKidneys control the acid-base balance by excreting either an acidic or a basic urine,This is achieved in the following ways-ReabsorptionSecretion of H+ of HCO3 ions in tubules in bloodand excretion PCO2 K+ in ECF AldosteroneH+ ionProximal ConvulatedTubules (85%)Thick Ascending Limb ofECF VolumeLoop of Henle (10%)Angiotensin IIDistal Convulated TubuleCollecting Tubules(5%) 18. Definitions and Terminology ACIDOSIS presence of a process which tends topH by virtue of gain of H + or loss of HCO3- ALKALOSIS presence of a process which tendsto pH by virtue of loss of H+ or gain of HCO3-If these changes, change pH, suffix emia is added ACIDEMIA reduction in arterial pH (pH7.45) 19. Simple AcidBase Disorder/ Primary Acid Base disorder a single primary process of acidosis or alkalosis due to an initial change in PCO2 and HCO3. Compensation - The normal response of the respiratory system or kidneys to change in pH induced by a primary acid-base disorder The Compensatory responses to a primary Acid Base disturbance are never enough to correct the change in pH , they only act to reduce the severity. Mixed AcidBase Disorder Presence of more than one acid base disorder simultaneously . 20. Normogram (for simple acid-base ds) 21. Characteristics of Primary ACID BASE DisordersPRIMARY PRIMARY RESPONSES COMPENSATORYDISORDERH+ ion pHPrimary RESPONSESConc.DefectMetabolic PCO2Acidosis H+ pH HCO3AlveolarHyperventilationMetabolic PCO2AlkalosisH+ pH HCO3 AlveolarHypoventilationRespiratoryAcidosis H+ pHPCO2HCO3RespiratoryAlkalosisH+ pHPCO2HCO3 22. CompensationMetabolic Disorders Compensation in these disorders leads toa change in PCO2 METABOLICACIDOSIS For every 1mmol/l in HCO3 the PCO2 falls by 1.25 mm Hg METABOLIC ALKALOSIS For every 1mol/l in HCO3 thePCO2 by 0.75 mm Hg 23. In Respiratory DisordersPCO2KidneyHCO3 ReabsorptionCompensation begins to appear in 6 12 hrs and is fullydeveloped only after a few days.1.ACUTEBefore the onset of compensationResp. acidosis 1mmHg in PCO2 HCO3 by 0.1meq/lResp. alkalosis 1mmHg in PCO2 HCO3 by 0.2 meq/l2.CHRONIC (>24 hrs)After compensation is fully developedResp. acidosis 1mmHg in PCO2HCO3 by 0.4meq/lResp. alkalosis 1mmHg in PCO2HCO3 by 0.4meq/l 24. Bodys physiologic response to Primary disorderin order to bring pH towards NORMAL limitFull compensationPartial compensationNo compensation. (uncompensated)BUT never overshoots,If a overshoot pH is there,Take it granted it is a MIXED disorder 25. STEP WISE APPROACHto Interpretation Of ABG reports 26. Normal ValuesANALYTENormal Value Units pH 7.35 - 7.45PCO2 35 45mm HgPO280 100 mm Hg` [HCO3]22 26meq/LSaO295-100%Anion Gap 10 + 2meq/L HCO3 +2 to -2 meq/L 27. STEP 0 Is this ABG Authentic?STEP 1 ACIDEMIA or ALKALEMIA? RESPIRATORY or METABOLIC?STEP 2STEP 3 Is COMPENSATION adequate?STEP 4 If METABOLIC ANION GAP? If High gap Metabolic AcidosisSTEP 5 GAP GAP? 28. Step 0 Authentic or Not?Verify that the ABG values are internallyaccurate. The accuracy of the values can be establishedby confirming that they satisfy a simplified formof the Henderson-Hasselbalch equation:[H+](nmol/L) = 24 pCO2(mm Hg) [HCO3-] (mEq/L) [H+] = 10 exp(-pH). Within the pH range of 7.26to 7.45 [H+] in nmol/L = 80 the decimal of thepH (e.g., for pH = 7.25, [H+] = 80 25 = 55 29. Example: using Kassirer-Bleich equation [H+](nmol/L) = 24 pCO2(mm Hg) [HCO3-](mEq/L) ABG: pH = 7.25, pCO2 = 30, HCO3- = 223055 = 24 x2255 32 LAB ERROR 30. STEP 1ACIDEMIA OR ALKALEMIA? Look at pH 7.45 alkalemia RULE An acid base abnormality is present even ifeither the pH or PCO2 are Normal. 31. STEP 2RESPIRATORY or METABOLIC?IS PRIMARY DISTURBANCE RESPIRATORY ORMETABOLIC?pH HCO3 orpH HCO3METABOLICpH PCO2 or pHPCO2 RESPIRATORYRULE- If either the pH or PCO2 is Normal, there is amixed metabolic and respiratory acid base disorder. 32. Step 3 Is CompensationAdequate? 33. DisorderPrediction of CompensationpH HCO3 PaCO2Metabolic PaCO2 will 1.25 mmHg per mmol/L inacidosis[HCO3-] LowLow LowMetabolicPaCO2 will 0.75 mmHg per mmol/L in High HighHighalkalosis [HCO3-] 34. DisorderPrediction of CompensationpH HCO3 PaCO2Respiratory High Low LowalkalosisAcute [HCO3-] will 0.2 mmol/L per mmHg inPaCO2 Chronic[HCO3-] will 0.4 mmol/L per mmHg inPaCO2Respiratory LowHighHighacidosisAcute [HCO3-] will 0.1 mmol/L per mmHg inPaCO2 Chronic[HCO3-] will 0.4 mmol/L per mmHg inPaCO2 35. STEP 0 Is this ABG Authentic?STEP 1 ACIDEMIA or ALKALEMIA? RESPIRATORY or METABOLIC?STEP 2STEP 3 If Respiratory ACUTE or CHRONIC?STEP 4 Is COMPENSATION adequate?STEP 4 If METABOLIC ANION GAP? If High gap Metabolic AcidosisSTEP 6 GAP GAP? 36. Electrochemical Balance in Blood100%UC UA 90% 80% HCO3 Na Sulfate 70%Phosphate 60%Mg- OACl 50%K - Proteins 40%Ca-HCO3 30%Na- Cl 20% 10%0% CATIONS ANIONS 37. Anion GapAG based on principle of electroneutrality: Total Serum Cations = Total Serum Anions M cations + U cations = M anions + U anions Na + (K + Ca + Mg) = HCO3 + Cl + (PO4 + SO4 + Protein + Organic Acids) Na + UC = HCO3 + Cl + UA But in Blood there is a relative abundance of Anions, hence Anions > Cations Na (HCO3 + Cl)= UA UC Na (HCO3 + Cl)= Anion Gap 38. METABOLIC ACIDOSIS-STEP 4ANION GAP?IN METABOLIC ACIDOSIS WHAT IS THE ANION GAP? ANIONGAP(AG) = Na (HCO3 + Cl) Normal Value = 10 + 2Adjusted Anion Gap = Observed AG +2.5(4.5- S.Albumin)50%in S. Albumin 75% in Anion Gap !!!High Anion Gap Metabolic AcidosisMetabolic AcidosisNormal Anion Gap Acidosis 39. STEP 5CO EXISTANT METABOLIC DISORDER Gap Gap?C/O HGAG METABOLIC ACIDOSIS,ANOTHER DISORDER? Anion Gap = Measured AG Normal AG Measured AG 12 HCO3 = Normal HCO3 Measured HCO324 Measured HCO3Ideally,Anion Gap = HCO3For each 1 meq/L increase in AG, HCO3 will fall by 1 meq/LAG/ HCO3- = 1 Pure High AG Met Acidosis AG/ HCO3- > 1 Assoc Metabolic Alkalosis AG/ HCO3- < 1 Assoc N AG Met Acidosis 40. CLINICAL CASESCENARIO 41. Case ScenarioA patient with a severe postoperativeileus requires the insertion of anasogastric (NG) tube fordecompression. After several days onthe floor, he develops a line infection andis moved to the ICU once he becomespressor dependent. The patients ABGreveals a pH = 7.44, pCO2 = 12, and[HCO3-] = 8. The [Na+] = 145 with [Cl-] =102. 42. ABG: pH = 7.44, pCO2 = 12, [HCO3-] = 8, [Na+] = 145 with [Cl-] = 102 With knowledge of the common clinicalscenarios leading to acid-basedisturbances, this patient is at risk fordeveloping a metabolic alkalosis from NGsuction and a metabolic acidosis andrespiratory alkalosis from sepsis. Step 1. [H+] = 80 44 = 36. Does 36 = 24 12 / 8? It does. Step 2. The patient is mildly alkalemic, whichcan be explained by the low pCO2 but not bythe low [HCO3-], suggesting that a respiratoryalkalosis may be the primary derangement. 43. ABG: pH = 7.44, pCO2 = 12, [HCO3-] = 8, [Na+] = 145 with [Cl-] = 102 Step 3 a. The drop in [HCO3-] might be an appropriatecompensation for a chronic respiratory alkalosis([HCO3-] is 0.4 mmol/L per mmHg in PaCO2)However, 24 [(40 12) 0.4] = 12.8, which is notclose to the observed [HCO3-] of 8. A mixed disorder isimplied. b. AG = 145 102 8 = 35. There is an elevatedAG, suggests a concomitant metabolic acidosis. c. Delta anion gap=35 10 = 25. d. Delta bicarbonate= 24 8 =16. Ratio of above two is more than 1 suggestive ofassociated metabolic alkalosis. This has proven to bea triple acid-base disorder with an elevated aniongap acidosis, a metabolic alkalosis, and arespiratory alkalosis, as was alluded to in Step 1 44. Metabolic Acidosis Metabolic acidosis can occur because of increase in endogenous acid production (lactate and ketoacids) loss of bicarbonate (as in diarrhea) accumulation of endogenous acids (as in renal failure). Effects on the respiratory, cardiac, and nervoussystems. Kussmaul respiration Intrinsic cardiac contractility may be depressed, but inotropicfunction can be normal because of catecholamine release. Both peripheral arterial vasodilation and centralvenoconstriction can be present The decrease in central and pulmonary vascular compliancepredisposes to pulmonary edema with even minimal volumeoverload. Central nervous system function is depressed, withheadache, lethargy, stupor, and, in some cases, even coma. 45. Metabolic Acidosis: Essentials ofDiagnosis Decreased HCO3 with acidemia. Classified into high anion gap acidosisand normal anion gap (hyperchloremic)acidosis. The high anion gap acidoses are seen inlactic acidosis, ketoacidosis, renal failureor toxins. Normal anion gap acidosis is mainlycaused by gastrointestinal HCO3 loss orRTA. Urinary anion gap may help distinguish between these causes. 46. Causes of High-Anion-Gap Metabolic Acidosis1. Lactic acidosis Poor tissue perfusion (type A) Aerobic disorders (type B)2. Ketoacidosis Diabetic Alcoholic Starvation3. Toxins Ethylene glycol Methanol Salicylates Propylene glycol: as vehicle of medications Pyroglutamic acid: acetaminophen toxicity4. Renal failure (acute and chronic) 47. Ketacidosis Diabetic Ketoacidosis (DKA): DKA is caused by increased fatty acidmetabolism and the accumulation of ketoacids(acetoacetate and -hydroxybutyrate). DKA usually occurs in insulin-dependentdiabetes mellitus in association with cessation of insulin or an intercurrent illness, such as an infection, gastroenteritis, pancreatitis, or myocardial infarction, which increases insulin requirements temporarily and acutely. The accumulation of ketoacids accounts for theincrement in the Anion Gap and isaccompanied most often by hyperglycemia[glucose > 17 mmol/L (300 mg/dL)]. 48. Glucose,a mmol/L (mg/dL)13.933.3 (250600)Sodium, meq/L 125135PotassiumaNormal to MagnesiumaNormal ( plasma levels may be normal or high atpresentation, total-body stores are usuallydepleted)Chloridea NormalPhosphateaCreatinineSlightly Osmolality (mOsm/mL)300320Plasma ketonesa ++++Serum bicarbonate,a meq/L 3.3 mmol/L 50. Management Assess patient: What precipitated the episode(noncompliance, infection, trauma, infarction, cocaine)?Initiate appropriate workup for precipitating event(cultures, CXR, ECG). Measure capillary glucose every 12 h; electrolytes (especially K+, bicarbonate, phosphate) and aniongap every 4 h for first 24 h. Monitor blood pressure, pulse, respirations, mentalstatus, fluid intake and output every 14 h. Replace K+: 10 meq/h when plasma K+ < 5.5 meq/L, ECG normal, urine flowand normal creatinine documented; administer 4080 meq/h when plasma K+ < 3.5 meq/L or ifbicarbonate is given. Continue above until patient is stable, glucose goal is 150250 mg/dL, and acidosis is resolved. Insulin infusion may bedecreased to 0.050.1 units/kg per hour. Administer intermediate or long-acting insulin as soon aspatient is eating. Allow for overlap in insulin infusion and 51. since insulin prevents production ofketones, bicarbonate therapy is rarelyneeded except with extreme acidemia (pH 1520 mmol/kg H2O, either prevails. Either the serum sodium is spuriously low, as with hyperlipidemia or hyperproteinemia (pseudohyponatremia) Osmolytes other than sodium salts, glucose, or urea have accumulated in plasma. Examples include mannitol, radiocontrast media, isopropyl alcohol, ethylene glycol, propylene 53. In this situation, the difference between thecalculated osmolality and the measured osmolality(osmolar gap) is proportional to the concentration ofthe unmeasured solute. Alcohols: With an appropriate clinical history and indexof suspicion, identification of an osmolar gap is helpfulin identifying the presence of poison-associated AGacidosis. Three alcohols may cause fatal intoxications:ethylene glycol, methanol, and isopropyl alcohol Salicylates: Salicylate intoxication in adults usuallycauses respiratory alkalosis or a mixture of high-AGmetabolic acidosis and respiratory alkalosis. Only aportion of the AG is due to salicylates. Lactic acidproduction is also often increased 54. Renal failure Acidosis The hyperchloremic acidosis of moderate renalinsufficiency is eventually converted to thehigh-AG acidosis of advanced renal failure. At GFRs below 20 mL/min, the inability toexcrete H+ with retention of acid anions suchas PO43 and SO42 results in an increasedanion gap acidosis [HCO3] rarely falls to 20 mmol/L, indicating that the acidretained in chronic renal disease is buffered byalkaline salts from bone. Results in significant loss of bone mass due toreduction in bone calcium carbonate andincreases urinary calcium excretion. 55. Treatment of high anion gapacidosis Treatment is aimed at the underlying disorder, such asinsulin and fluid therapy for diabetes and appropriatevolume resuscitation to restore tissue perfusion. Themetabolism of lactate will produce HCO3 and increasepH. Controversy regarding administration of largeamounts of HCO3 may have deleterious effects, including hypernatremia andhyperosmolality. Intracellular pH may decrease because administered HCO3is converted to CO2, which easily diffuses into cells, combineswith water to create additional hydrogen ions and worseningof intracellular acidosis and this could impair cellular function Alkaliadministration is knowntostimulatephosphofructokinase activity, thus exacerbating lactic acidosisvia enhanced lactate production. Ketogenesis is alsoaugmented by alkali therapy. 56. Treatment of high anion gap acidosis.. In salicylate intoxication, alkali therapy must be started unless blood pH is already alkalinized by respiratory alkalosis, since the increment in pH converts salicylate to more impermeable salicylic acid and thus prevents central nervous system damage. In DKA, alkali must be administered in extreme alkalemia (pH 5.5 Positive NaHCO3 (13 secretionmEq/kg/d) II. Proximal Proximal < 5.5 NormalNegative NaHCO3 orsecretion HCO3 KHCO3 (1015abspn mEq/kg/d),thiazide IV.Distal Na+ < 5.5 Positive FludrocortisoneHyporeninemic reabsorption(0.10.5 mg/d), +dietary K+ rstrn,hypoaldosteroni K secretion,and H+furosemide (40smsecretion 160 mg/d),NaHCO3 (13mEq/kg/d) 62. Treatment of normal Anion gap Acidosis Gastrointestinal: Correction of the contracted ECFV with NaCland repair of K+ deficits corrects the acid-base disorder, andchloride deficiency. RTA : administration of alkali (either as bicarbonate or citrate) tocorrect metabolic abnormalities and prevent nephrocalcinosis andrenal failure. Proximal RTA : Large amounts of alkali (1015 mEq/kg/d) maybe required to treat proximal RTA because most of the alkali isexcreted into the urine, which exacerbates hypokalemia. Thus, amixture of sodium and potassium salts, such as K-Shohlsolution, is preferred. The addition of thiazides may reduce theamount of alkali required, but hypokalemia may develop. Distal RTA : Correction of type 1 distal RTA requires a smalleramount of alkali (13 mEq/kg/d) and potassium supplementationas needed. Type IV RTA: dietary potassium restriction may be needed andpotassium-retaining drugs should be withdrawn. Fludrocortisonemay be effective in cases with hypoaldosteronism, but should beused with care, preferably in combination with loop diuretics.alkali supplementation (13 mEq/kg/d) may be required. 63. Metabolic Alkalosis Essentials of Diagnosis High HCO3 with alkalemia. Evaluate effective circulating volume byphysical examination and check urinarychloride concentration. This will helpdifferentiate saline-responsive metabolicalkalosis from saline-unresponsivealkalosis 64. Metabolic Alkalosis Occurs as a result of net gain of [HCO3] or lossof nonvolatile acid (usually HCl by vomiting) fromthe extracellular fluid. The disorder involves a generative stage, in which the loss of acid usuallycauses alkalosis maintenance stage, in which the kidneys fail tocompensate by excreting HCO3. Classified based on "saline responsiveness" orurinary Cl, which are markers for volume status Saline-responsive metabolic alkalosis is a signof extracellular volume contraction Saline-unresponsive alkalosis implies a volume-expanded state 65. Symptoms With metabolic alkalosis, changes in central andperipheral nervous system function are similar tothose of hypocalcemia : symptoms include Mental confusion Obtundation Predisposition to seizures Paresthesia Muscular cramping Tetany Aggravation of arrhythmias Hypoxemia in chronic obstructive pulmonarydisease. Related electrolyte abnormalities include Hypokalemia- Weakness and hyporeflexia hypophosphatemia. 66. Classification and etiology I. Saline-Responsive (UCl < 10 mEq/d) Excessive body bicarbonate content Renal alkalosis Diuretic therapy Poorly reabsorbable anion therapy: carbenicillin, penicillin, sulfate, phosphate Posthypercapnia Gastrointestinal alkalosis Loss of HCl from vomiting or nasogastric suction Intestinal alkalosis: chloride diarrhea Exogenous alkali NaHCO3 (baking soda) Sodium citrate, lactate, gluconate, acetate Transfusions Antacids Normal body bicarbonate content "Contraction alkalosis" 67. II. Saline-Unresponsive (UCl > 10 mEq/d) Excessive body bicarbonate content Renal alkalosis Normotensive Bartters syndrome (renal salt wasting andsecondary hyperaldosteronism) Severe potassium depletion Refeeding alkalosis Hypercalcemia and hypoparathyroidism Hypertensive Endogenous mineralocorticoids Primary aldosteronism Hyperreninism Adrenal enzyme deficiency: 11- and 17-hydroxylase Liddles syndrome Exogenous mineralocorticoids Licorice 68. Treatment Mild alkalosis is generally well tolerated. Severe orsymptomatic alkalosis (pH > 7.60) requires urgenttreatment. Saline-Responsive Metabolic Alkalosis Aimed at correction of extracellular volumedeficit. Depending on the degree ofhypovolemia, adequate amounts of 0.9%NaCl and KCl should be administered. Discontinuation of diuretics andadministration of H2-blockers in patientswhose alkalosis is due to nasogastric suctioncan be useful. If impaired pulmonary or cardiovascularstatus prohibits adequate volumerepletion, acetazolamide, 250500 mgintravenously every 46 hours, can be used. 69. Treatment.. One must be alert to the possible development ofhypokalemia, since potassium depletion can beinduced by forced kaliuresis via bicarbonaturia. Administration of acid can be used as emergencytherapy. HCl, 0.1 mol/L, is infused via a central vein(the solution is sclerosing). Dosage is calculated todecrease the HCO3 level by 50% over 24hours, assuming an HCO3 volume of distribution (L)of 0.5% body weight (kg). Patients with marked renal failure may require dialysis. Saline-Unresponsive Metabolic Alkalosis surgical removal of a mineralocorticoid-producingtumor blockage of aldosterone effect with an ACE inhibitor orwith spironolactone. primary aldosteronism can be treated only withpotassium repletion. 70. Respiratory AcidosisResults from decreased alveolar ventilation and hypercapniaboth due to pulmonary and non pulmonary disorders Central Neuromuscular Drugs Poliomyelitis (anesthetics, morphine, sedatives) Kyphoscoliosis Stroke Myasthenia Infection Muscular dystrophies Airway Miscellaneous Obstruction Obesity Asthma Hypoventilation Parenchyma Permissive hypercapnia Emphysema Pneumoconiosis Bronchitis Adult respiratory distress syndrome Barotrauma 71. Respiratory Acidosis Acute respiratory failure associated with severe acidosis and only a small increase in the plasma bicarbonate. After 612 hours, the primary increase in PCO2 evokes a renal compensatory response to generate more HCO3 , which tends to ameliorate the respiratory acidosis. This takes several days to complete. Chronic respiratory acidosis seen in patients with underlying lung disease, such as chronic obstructive pulmonary disease. Urinary excretion of acid in the form of NH4+ and Cl ions results in the characteristic hypochloremia of chronic respiratory acidosis. When chronic respiratory acidosis is corrected suddenly, especially in patients who receive mechanical ventilation, there is a 2- to 3-day lag in renal bicarbonate excretion, resulting in posthypercapnic metabolic alkalosis. 72. Symptoms and Signs With acute onset, there is somnolence and confusion, andmyoclonus with asterixis Coma from CO2 narcosis may ensue Severe hypercapnia increases cerebral blood flow andcerebrospinal fluid pressure. Signs of increased intracranialpressure (papilledema, pseudotumor cerebri) may be seen. Laboratory Findings Arterial pH is low PCO2 is increased Serum HCO3 is elevated, but not enough to completelycompensate for the hypercapnia. If the disorder is chronic, hypochloremia is seen. Treatment In all forms of respiratory acidosis, treatment is directed at theunderlying disorder to improve ventilation. Because opioid drug overdose is an important reversible cause ofacute respiratory acidosis, naloxone, 0.042 mg intravenously isadministered to all such patients if no obvious cause forrespiratory depression is present. Mechanical ventilation for oxygenation till it restores back tonormal maybe needed 73. Respiratory Alkalosis(Hypocapnia) Respiratory alkalosis, or hypocapnia, occurs when hyperventilationreduces the PCO2, which increases the pH Symptoms and Signs In acute cases (hyperventilation), there is light-headedness,anxiety, paresthesias, numbness about the mouth, and a tinglingsensation in the hands and feet. Tetany occurs in more severealkalosis from a fall in ionized calcium. In chronic cases, findings are those of the responsible condition. Laboratory Findings Arterial blood pH is elevated, and PCO2 is low. Serumbicarbonate is decreased in chronic respiratory alkalosis. Determination of appropriate compensatory changes in theHCO3 is useful to sort out the presence of an associatedmetabolic disorder the changes in HCO3 values are greater if the respiratoryalkalosis is chronic Although serum HCO3 is frequently below 15 mEq/L inmetabolic acidosis, it is unusual to see such a low level inrespiratory alkalosis, and its presence would imply asuperimposed (noncompensatory) metabolic acidosis. 74. Causes of respiratory alkalosis. Hypoxia : Decreased inspired oxygen tension High altitude Ventilation/perfusion inequality Hypotension Severe anemia CNS-mediated disorders Voluntary hyperventilation Anxiety-hyperventilation syndrome Neurologic disease: Cerebrovascular accident(infarction, hemorrhage) Infection Trauma Tumor 75. Causes Pharmacologic and hormonal stimulation :Salicylates, Nicotine, Xanthines ,Pregnancy(progesterone) Hepatic failure Gram-negative septicemia Recovery from metabolic acidosis Heat exposure Pulmonary disease Interstitial lung disease Pneumonia Pulmonary embolism Pulmonary edema Mechanical overventilation 76. Treatment Treatment is directed toward the underlying cause. In acute hyperventilation syndrome fromanxiety, reassurance , attention to underlying psychologicalstress and rebreathing into a paper bag will increase thePCO2. The processes are usually self-limited since muscleweakness caused by hyperventilation-induced alkalemia willsuppress ventilation. Sedation may be necessary if the process persists howeverAntidepressants and sedatives should be avoided Adrenergic blockers may ameliorate peripheralmanifestations of the hyperadrenergic state. Rapid correction of chronic respiratory alkalosis may resultin metabolic acidosis as PCO2 is increased in the setting ofprevious compensatory decrease in HCO3. If respiratory alkalosis complicates ventilatormanagement, changes in dead space, tidal volume, andfrequency can minimize the hypocapnia 77. Conclusion Clinical suspicion according to scenario Primary disorder from pH and bicarbonate or CO2values Degree of compensation? Inappropriate? mixeddisorder Anion gap (corrected for serum albuminchange)? Primary metabolic acidosis Corrected bicarbonate levels?More than normal- associated metabolic alkalosisLess - associated metabolic non-anion gap acidosis Review compensation for metabolic dsconfirm ifinitially suspected respiratory disorder exists 78. Metabolic acidosis: ..see AG High AG: plasma osmolal gap more.. Toxins Less.. KA, RF, LA, Normal AG acidosis: urine AG.negative..GI urinary pH .high..RTA 1 serum potassium.high..RTA4 Metabolic alkalosis: Urinary Chloride Less..saline responsiveECF contraction more ..saline non responsive Plasma Potassiumlow..K depletion HighBlood pressure Plasma renin 79. 1.PaCO2 equation:VCO2 x 0.863 VCO2 = CO2 production PaCO2 = ----------------- VA = VE VDVAVE = minute (total) ventilationVD = dead space ventilation0.863 converts units to mm HgCondition State ofPaCO2 in bloodalveolar ventilation>45 mm Hg HypercapniaHypoventilation35 - 45 mm Hg Eucapnia Normal ventilation 80 & Children Newborn40-70 70 yrs > 70 80 yrs > 60 90 yrs > 5060 yrs 80 mm Hg 1mm Hg/yr 99. Inspired O2 PaO2 Relationship FIO2 (%)Predicted Min PaO2 (mm Hg) 30150 40200 50250 80400 100 500 If PaO2 < FIO2 x 5, pt probably hypoxemic at RA 100. Hypoxemia on O2 therapy Uncorrected: PaO2 < 80 mm Hg (< expected on RA & FIO2) Corrected: PaO2 = 80-100 mm Hg (= expected on RA but < expected for FIO2) Excessively Corrected: PaO2 > 100 mm Hg (> expected on RA but < expected for FIO2) PaO2 > expected for FIO2: 1. Error in sample/analyzer 2. Pts O2 consumption reduced 3. Pt does not req O2 therapy (if 1 & 2 NA) 101. Thanks