1.Arterial Blood GasArterial Blood Gas Analysis & interpretationAnalysis & interpretation Mohammed A. El-haj MPH 07/12/2011

2. What is an ABG?What is an ABG? The Components pH / PaCO2 / PaO2 / HCO3 / O2sat / BE Desired Ranges pH - 7.35 - 7.45 PaCO2 - 35-45 mmHg PaO2- 80-100 mmHg HCO3 - 21-27 O2sat - 95-100% Base Excess - +/-2 mEq/L 3. Why Order an ABG?Why Order an ABG? Aids in establishing a diagnosis Helps guide treatment plan Aids in ventilator management Improvement in acid/base management allows for optimal function of medications Acid/base status may alter electrolyte levels critical to patient status/care 4. LogisticsLogistics When to order an arterial line -- Need for continuous BP monitoring Need for multiple ABGs Where to place -- the options Radial Femoral Brachial Dorsalis Pedis Axillary 5. Acid Base BalanceAcid Base Balance The body produces acids daily 15,000 mmol CO2 50-100 mEq Nonvolatile acids The lungs and kidneys attempt to maintain balance 6. Acid Base BalanceAcid Base Balance Assessment of status via bicarbonate-carbon dioxide buffer system CO2 + H2O H2CO3 HCO3 - + H+ pH = 6.10 + log ([HCO3] / [0.03 x PCO2]) 7. Normal valuesNormal values Uncompensated acidosis pH .7 35.7 45 Uncompensated alkalosis Respiratory alkalosis CO2 35-45 Respiratory acidosis Metabolic acidosis HCO3 23-27 Metabolic alkalosis 8. CompensationCompensation 7.4 7.35 7.45 Partial compensated Partial 9. Respiratory AcidosisRespiratory Acidosis pH, CO2,Ventilation Causes CNS depression Pleural disease COPD/ARDS Musculoskeletal disorders Compensation for metabolic alkalosis 10. Respiratory AcidosisRespiratory Acidosis Acute vs Chronic Acute - little kidney involvement. Buffering via titration via Hb for example pH by 0.08 for 10mmHg in CO2 Chronic - Renal compensation via synthesis and retention of HCO3 (Cl to balance charges hypochloremia) pH by 0.03 for 10mmHg in CO2 11. Respiratory AlkalosisRespiratory Alkalosis pH, CO2, Ventilation CO2 HCO3 (Cl to balance charges hyperchloremia) Causes Intracerebral hemorrhage Salicylate and Progesterone drug usage Anxiety lung compliance Cirrhosis of the liver Sepsis 12. Respiratory AlkalosisRespiratory Alkalosis Acute vs. Chronic Acute - HCO3 by 2 mEq/L for every 10mmHg in PCO2 Chronic - Ratio increases to 4 mEq/L of HCO3 for every 10mmHg in PCO2 Decreased bicarb reabsorption and decreased ammonium excretion to normalize pH 13. Metabolic AcidosisMetabolic Acidosis pH, HCO3 12-24 hours for complete activation of respiratory compensation PCO2 by 1.2mmHg for every 1 mEq/L HCO3 The degree of compensation is assessed via the Winters Formula PCO2 = 1.5(HCO3) +8 2 14. The CausesThe Causes Metabolic Gap Acidosis M - Methanol U - Uremia D - DKA P - Paraldehyde I - INH L - Lactic Acidosis E - Ehylene Glycol S - Salicylate Non Gap Metabolic Acidosis Hyperalimentation Acetazolamide RTA (Calculate urine anion gap) Diarrhea Pancreatic Fistula 15. Metabolic AlkalosisMetabolic Alkalosis pH, HCO3 PCO2by 0.7 for every 1mEq/L in HCO3 Causes Vomiting Chronic diarrhea Hypokalemia Renal Failure 16. Mixed Acid-Base DisordersMixed Acid-Base Disorders Patients may have two or more acid-base disorders at one time Delta Gap Delta HCO3 = HCO3 + Change in anion gap >24 = metabolic alkalosis 17. The six steps to ABGs analysisThe six steps to ABGs analysis Look at the pH if it is normal/acidotic/alkalotic Look at the PaCO2 if it is normal/acidotic/alkalotic Look at the HCO3 if it is normal/acidotic/alkalotic If the pH match with the PCO2 or with the HCO3 If the value goes opposite direction of the pH (determine the compensation). Look at the Po2 and oxygen saturation 18. Sample problemSample problem pH 7.49 PCO2 40 HCO3 28 Uncompensated metabolic alkalosis Vomiting/dearrhea In this example the Bicarb is matching the pH No compensation (Partial) 19. Sample problemSample problem pH 7.10 PCO2 25 HCO3 7 Uncompensated metabolic acidosis DKA/Dearrhea/shock/bleeding /sepsis In this example the Bicarb is matching the pH No compensation (Partial) Severe metabolic acidosis 20. Sample problemSample problem pH 7.42 PCO2 18 HCO3 11 PO2 150 O2 sat 99% compensated respiratory alkalosis This pt is hyperventilated for too long (blowing off CO2) 21. Sample problemSample problem pH 7.35 PCO2 60 HCO3 32 PO2 92 O2 sat 96% No need for correction or treatment because pH is normal Compensation is bringing the pH to the side of 7.4 but doesn't to the opposite side (stop in 7.4) 22. Sample problemSample problem pH 7.37 PCO2 33 HCO3 18 Metabolic acidosis Fully compensated 23. Sample problemSample problem pH 7.36 PCO2 62 HCO3 34 PO2 70 O2 sat. 90% Respiratory acidosis Fully compensated E.g. COPD 24. Respiratory AlkalosisRespiratory Alkalosis Most common causes of respiratory alkalosis are: 1. Hypoxemia ( PaO2< 60mmHg and O2 sat. 7.45 Acidosis:is a process that will result in acidemia if left unopposed. Alkalosis:is a process that will result in alkalemia if left unopposed Metabolic refers to a disorder that results from a primary alteration in [H+] or [HCO3-]. Respiratory refers to a disorder that results from a primary alteration in PCO2 due to altered CO2 elimination. Normal HCO3- 24 meq/L; Normal PCO2 40 mm Hg ; Normal pH 7.35-7.45 32. Definitions (Continued)Definitions (Continued) PH: - is a negative logarithm of Hydrogen ion concentration; and it is the initials of these two wards (puiessence Hydrogen) that mean the power of hydrogen 33. Definitions (Continued)Definitions (Continued) An acid: - is a hydrogen ion or proton donor, and a substance which causes a rise in H+ concentration on being added to water. A base: - is a hydrogen ion or proton acceptor, and a substance which causes a rise in OH- concentration when added to water. Strength of acids or bases refers to their ability to donate and accept H+ ions respectively. 34. Importance of acid-base balanceImportance of acid-base balance The hydrogen ion (H+)concentration must be precisely maintained within a narrow physiological range Small changes from normal can produce marked changes in enzyme activity & chemical reactions within the body 35. Acidosis - CNS depression, coma (pH ~ 6.9) Alkalosis - CNS excitability, tetany, siezures Hydrogen ion concentration is most commonly expressed as pH (= negative logarithm of the H+ concentration) 36. ACID-BASE CALCULATIONSACID-BASE CALCULATIONS The Henderson equation is easier to use, but only applies when pH is between 7.2 and 7.6. For this equation, one must calculate [H+] from pH. [H+] = 40 nEq/L when pH is 7.4. The [H+] increases 10 nEq/L for a 0.1 unit drop in pH. Henderson Eq. [H+] = 24 PCO2 / [HCO3-] 37. ph H+ (nmol/l) 7 100 7.1 80 7.2 63 7.3 50 7.36 44 7.4 40 7.44 36 7.5 32 7.6 25 7.7 20 38. Normal pH: Arterial blood: 7.35 - 7.45 Venous blood, interstitial fluid: 7.35 Intracellular: 6.0-7.4 (average 7.0) 39. Regulation of pHRegulation of pH *Buffer systems - very rapid (seconds), incomplete *Respiratory responses - rapid (minutes), incomplete *Renal responses - slow (hours to days), complete 40. BackgroundBackground H+ + H+ CO3 - H2CO3 H2O + CO2 -Metabolic Disorders: Affect HCO3 -: (Normal 22-26 meq/L) -Metabolic Acidosis Acid neutralizes HCO3 - H+ CO3 - , pH -Metabolic Alkalosis H+ CO3 - Production Drives Rxn to Right H+ pH 41. Primary Abnormality in AcidPrimary Abnormality in Acid Base DisordersBase Disorders Acidosis Alkalosis Respiratory pCO2 Metabolic H+ + H+ CO3 - H2CO3 H2O + CO2 42. Primary Abnormality in AcidPrimary Abnormality in Acid Base DisordersBase Disorders Acidosis Alkalosis Respiratory pCO2 pCO2 Metabolic H+ + H+ CO3 - H2CO3 H2O + CO2 43. Primary Abnormality in AcidPrimary Abnormality in Acid Base DisordersBase Disorders Acidosis Alkalosis Respiratory pCO2 pCO2 Metabolic H+ CO3 - H+ + H+ CO3 - H2CO3 H2O + CO2 44. Primary Abnormality in AcidPrimary Abnormality in Acid Base DisordersBase Disorders Acidosis Alkalosis Respiratory pCO2 pCO2 Metabolic H+ CO3 - H+ CO3 - H+ + H+ CO3 - H2CO3 H2O + CO2 45. Simple Acid-Base Disorders: Type of Disorder pH PaCO2 [HCO3] Metabolic Acidosis Metabolic Alkalosis Acute Respiratory Acidosis Chronic Respiratory Acidosis Acute Respiratory Alkalosis Chronic Respiratory Alkalosis 46. Simple Acid-Base Disorders: Type of Disorder pH PaCO2 [HCO3] Metabolic Acidosis Metabolic Alkalosis Acute Respiratory Acidosis Chronic Respiratory Acidosis Acute Respiratory Alkalosis Chronic Respiratory Alkalosis 47. Simple Acid-Base Disorders: Type of Disorder pH PaCO2 [HCO3] Metabolic Acidosis Metabolic Alkalosis Acute Respiratory Acidosis Chronic Respiratory Acidosis Acute Respiratory Alkalosis Chronic Respiratory Alkalosis 48. Simple Acid-Base Disorders: Type of Disorder pH PaCO2 [HCO3] Metabolic Acidosis Metabolic Alkalosis Acute Respiratory Acidosis Chronic Respiratory Acidosis Acute Respiratory Alkalosis Chronic Respiratory Alkalosis 49. Simple Acid-Base Disorders: Type of Disorder pH PaCO2 [HCO3] Metabolic Acidosis Metabolic Alkalosis Acute Respiratory Acidosis Chronic Respiratory Acidosis Acute Respiratory Alkalosis Chronic Respiratory Alkalosis 50. Simple Acid-Base Disorders: Type of Disorder pH PaCO2 [HCO3] Metabolic Acidosis Metabolic Alkalosis Acute Respiratory Acidosis Chronic Respiratory Acidosis Acute Respiratory Alkalosis Chronic Respiratory Alkalosis 51. Simple Acid-Base Disorders: Type of Disorder pH PaCO2 [HCO3] Metabolic Acidosis Metabolic Alkalosis Acute Respiratory Acidosis Chronic Respiratory Acidosis Acute Respiratory Alkalosis Chronic Respiratory Alkalosis 52. Simple Acid-Base Disorders: Type of Disorder pH PaCO2 [HCO3] Metabolic Acidosis Metabolic Alkalosis Acute Respiratory Acidosis Chronic Respiratory Acidosis Acute Respiratory Alkalosis Chronic Respiratory Alkalosis 53. CompensationCompensation For each acid-base disorder , there is a compensatory response mediated by the kidneys or the lungs that tends to bring the pH back towards normal. Compensation is never complete (i.e. pH never returns to 7.4). Therefore if the pH < 7.4, the primary process is an acidosis. If the pH > 7.4 the primary process is an alkalosis 54. Compensated Abnormality in AcidCompensated Abnormality in Acid Base DisordersBase Disorders Acidosis Alkalosis 1 Respiratory Compensation pCO2 pCO2 1 Metabolic Compensation H+ CO3 - H+ CO3 - H+ CO3 - H+ CO3 - pCO2 pCO2 H+ + H+ CO3 - H2CO3 H2O + CO2 55. Compensation (Continued)Compensation (Continued) Formulas predict normal compensation in both acute and chronic conditions. Inadequate compensation tells you that something else is wrong! Metabolic compensation takes time and is more complete in chronic conditions than acutely 56. Buffer Systems A substance that can prevent major changes in the pH of body fluids by removed or releasing hydrogen ions ,they can act quickly to prevent excessive changes in hydrogen ion concentration Bicarbonate, phosphate and protein buffering systems are the three major buffering systems 57. Bicarbonate buffer system *Primary extracellular buffer system (>50% of extracellular buffering) *Accurate assessment - readily calculated from PCO2 and pH using available blood gas machines *Consists of carbonic acid (weak acid) and bicarbonate 58. *CO2 regulated by the lungs - rapidly *HCO3- is regulated by the kidneys slowly *Not powerful *pKa = 6.1)the pK of a buffer system identifies the pH at which the concentration of acid and base in that system is equal) 33222 HCOHCOHCOOH ++ + 59. Protein buffer system *Most powerful *75 % of all intracellular buffering *Hemoglobin -important extracellular buffer due to large concentration of hemoglobin in blood -buffering capacity varies with oxygenation -reduced hemoglobin is a weaker acid than oxyhemoglobin -dissociation of oxyhemoglobin results in more base available to combine w/ H+ 60. Plasma protein *acid buffer *important intracellular buffer system 61. Phosphate buffer system *H2PO4- and HPO42- *important renal buffering system *extracellular concentration, 1/12 that of bicarbonate *pKa = 6.8 *phosphate is concentrated in the renal tubules 62. Respiratory Responses occurs within minutes of alteration in pH due to stimulation/depression of respiratory centers in the CNS H+ acts directly on respiratory center in Medulla Oblongata alveolar ventilation increases/decreases in response to changes in CO2 alveolar ventilation is inversely proportional to PaCO2 *2 x ventilation pH 7.4 to 7.63 * ventilation pH 7.4 to 7.0 incomplete response because as the change in alveolar ventilation brings pH back towards normal, the stimulus responsible for the change in ventilation decreases . 63. Renal Responses the kidneys regulate pH by either acidification or alkalinization of the urine complex response that occurs primarily in the proximal renal tubules with acidosis, rate of H+ secretion exceeds HCO3- filtration with alkalosis, rate of HCO3- filtration exceeds H+ secretion occurs over hours/days, and is capable of nearly complete restoration of acid/base balance 64. Renal & Respiratory CompensationRenal & Respiratory Compensation Primary Disorder Primary change Predicted Compensatory Response Metabolic acidosis HCO3 1.2 PaCO2 per 1 meg HCO3 Metabolic Alkalosis HCO3 .7 PaCO2 per 1meq HCO3 Respiratory acidosis: Acute PaCO2 1 meq HCO3 per 10 mm PaCO2 Respiratory acidosis: Chronic PaCO2 3.5 meq HCO3 per 10 mm PaCO2 Respiratory alkalosis: Acute PaCO2 2 meq HCO3 per 10mm PaCO2 Respiratory alkalosis: Chronic PaCO2 4 meq HCO3 per 10mm PaCO2 65. SUMMARY OF SIMPLE ACID-BASE DISORDERS ANDSUMMARY OF SIMPLE ACID-BASE DISORDERS AND COMPENSATIONCOMPENSATION Primary Acid- Base Disorder Primary Defect Effect on pH Compensatory Response Expected Range of Compensation Limits of Compensatio n Respiratory Acidosis Hypoventilati on (PCO2) HCO3- Generation [HCO3-] = 1-4 mEq/L for each 10 mm Hg PCO2 [HCO3-] = 45 mEq/L Respiratory Alkalosis Hyperventilati on (PCO2) HCO3- Consumption [HCO3-] = 2-5 mEq/L for each 10 mm Hg PCO2 [HCO3-] = 12-15 mEq/L Metabolic Acidosis Loss of HCO3- or gain of H+( HCO3-) Increase in Ventilation (PCO2) PCO2 = 1.5[HCO3-] + 8 PCO2 = 12-14 mm Hg Metabolic Alkalosis Gain of HCO3- or loss of H+ ( HCO3-) Decrease in Ventilation (PCO2 ( PCO2 = 0.6 mm Hg for each 1 mEq/L [HCO3-] PCO2 = 55 mm Hg 66. GENERAL ASPECTS OFGENERAL ASPECTS OF ACID-BASE DISORDERSACID-BASE DISORDERS A primary alteration in [H+], [HCO3-] or PCO2 results in abnormal pH. The body has several mechanisms to correct pH towards the normal range. -In the acute phase (minutes to hours), the extra- and intra- cellular buffer systems (most importantly the bicarbonate system) minimize the pH changes. - In the chronic phase (hours to days), renal or respiratory compensation partially or completely restore pH towards normal. There are limits to both types of compensation. Compensation does not result in over correction of pH. 67. DATA REQUIRED TO DIAGNOSEDATA REQUIRED TO DIAGNOSE ACID-BASE DISORDERSACID-BASE DISORDERS An arterial blood gas shows the blood pH, PCO2 and [HCO3-]. A chemistry panel shows the [total CO2], [Cl-], [K+] and [Na+], [glucose], [BUN] and [creatinine]. The [total CO2] is the sum of the measured [CO2] + [HCO3-]. Thus the [HCO3-] from the blood gas and the [total CO2] from the electrolyte panel usually are within 2 mEq/L. Otherwise the measurements are in error or were taken at different times. 68. NORMAL LABORATORYNORMAL LABORATORY VALUESVALUES Arterial Blood Gas: pH 7.35-7.45 [H+] 35-45 nmol/L or neq/L PCO2 35-45 mm Hg [HCO3-] 22-26 mmol/L or mEq/L Plasma Electrolytes [Na+] 135-145 mEq/L [K+ ] 3.5-5.0 mEq/L [Cl-] 96-109 mEq/L [total CO2] 24-30 mEq/L 69. SIMPLE ACID-BASE DISORDERSSIMPLE ACID-BASE DISORDERS Simple acid-base disorders have one primary abnormality. The four primary disorders are respiratory acidosis, respiratory alkalosis, metabolic acidosis and metabolic alkalosis. Mixed acid-base disorders have more than one abnormality. Two to three primary disorders can be combined together to result in a mixed disorder. 70. Metabolic AcidosisMetabolic Acidosis Secondary to Acid production or H+ CO3 - loss Characterized by low serum H+ CO3 - ( by hyperventilation PCO2 HCO3- ) Divided into two categories: Anion gap metabolic acidosis (High anion gap) NonAnion gap metabolic acidosis (Normal anion gap) 71. Anion GapAnion Gap The anion gap (AG) represents the difference between the major plasma cations and anions ,and reflects usually unmeasured anions such as sulfate. Anion Gap = [Na+ ] - ( [H+ CO3 - ]+ [Cl- ] ) Normal 14 +/- 2 72. Why does this help us in patients with metabolic acidosis? Secondary to Acid production or H+ CO3 - loss In disorders associated with acid production there anions accumulate anion gap whereas In disorders associated with H+ CO3 - loss, there is no accumulation of unmeasured anions and the anion gap is normal 73. Unmeasured anions whichUnmeasured anions which accumulateaccumulate Anion Gap AcidosisAnion Gap Acidosis Lactate Ketones Sulfates and phosphates Other organic acids 74. Lactic AcidosisLactic Acidosis Fundamentally what causes a lactic acidosis? Answer: Anaerobic metabolism 75. The differential diagnosis ofThe differential diagnosis of Lactic AcidosisLactic Acidosis Lactic acidosis occurs whenever the cells are unable to utilize aerobic respiration: i.e. whenever the cells are unable to obtain or utilize oxygen Consider Murphys law: Whatever can go wrong will go wrong! (i.e. take each step in oxygen absorption and distributionany one of them can go away and cause lactic acidosis.) 76. The differential diagnosis ofThe differential diagnosis of Lactic Acidosis (2)Lactic Acidosis (2) Low environmental O2 Inability to absorb O2 O2 unable to bind Hg Unable to pump O2 Tissues unable to utilize O2 High altitude Lung Disease CO poisoning Shock (cardiogenic) Septic shock Focal vascular obstruction Cyanide poisoning 77. KetoAcidosisKetoAcidosis Occurs whenever the cells are unable to utilize glucose 78. KetoAcidosisKetoAcidosis Three etiologies Diabetic Ketoacidosis Primarily in type 1 diabetes mellitus Severe, life threatening Often associated with precipitating illness Starvation ketoacidosis Mild acidosis Alcoholic ketoacidosis Mild acidosis 79. Metabolic Acidosis Anion Gap Acidosis NonAnion Gap Acidosis Ketoacidosis Uremic Acidosis Lactic Acidosis Organic Acidosis Lung Disease CO poisening Shock (cardiogenic) Septic shock Focal vascular obstruction Cyanide poisening DKA (Type 1) Starvation Alcoholic 80. Other anion gap acidosisOther anion gap acidosis Uremia Failure to excrete daily metabolic acid load Accumulation of phosphates and sulfates Organic acidosis Methanol Ethylene Glycol Salicylates 81. Metabolic Acidosis Anion Gap Acidosis NonAnion Gap Acidosis Ketoacidosis Uremic Acidosis Lactic Acidosis Organic Acidosis Lung Disease CO poisening Shock (cardiogenic) Septic shock Focal vascular obstruction Cyanide poisening DKA (Type 1) Starvation Alcoholic Methanol Ethylene Glycol Salicylate intoxication 82. Non-anion gap metabolicNon-anion gap metabolic acidosisacidosis Bicarbonate loss Diarrhea Severe Burns Urinary loss (renal tubular acidosis) 83. Metabolic Acidosis Anion Gap Acidosis NonAnion Gap Acidosis Ketoacidosis Uremic Acidosis Lactic Acidosis Organic Acidosis Lung Disease CO poisening Shock (cardiogenic) Septic shock Focal vascular obstruction Cyanide poisening DKA (Type 1) Starvation Alcoholic Methanol Ethylene Glycol Salicylate intoxication Diarrhea Burns (severe) RTA 84. Clinical ManifestationClinical Manifestation Headache Confusion Drowsiness RR and depth Nausea and vomiting Peripheral vasodilation and decreased Cardiac output (pH 7 ) BP Hyperkalemias 85. Metabolic Acidosis: TreatmentMetabolic Acidosis: Treatment Treat underlying cause Alkali replacement Acute metabolic acidosis indicated when is pH less than ~7.15 goal is to raise serum [HCO3] to ~15mmol/L bicarbonate dose = 0.5 x BW (kg) x{[HCO3]desired - [HCO3]actual} Chronic metabolic acidosis goal of treatment is to prevent long term sequelae serum [HCO3] should be normalized 86. Metabolic AlkalosisMetabolic Alkalosis Generation Maintenance 87. Metabolic Alkalosis:Metabolic Alkalosis: GenerationGeneration Acid loss renal acid losses diuretic therapy mineralocorticoid excess Cushings syndrome severe potassium depletion Bartters syndrome Liddles syndrome gastrointestinal losses gastric acid loss chloride diarrhea 88. Metabolic Alkalosis:Metabolic Alkalosis: GenerationGeneration Alkali gain bicarbonate administration milk alkali syndrome infusion of organic anions citrate acetate lactate rapid correction of chronic hypercapnia 89. Metabolic Alkalosis: MaintenanceMetabolic Alkalosis: Maintenance Decreased GFR renal failure Increased proximal HCO3 - reabsorption chloride depletion Increased distal tubular H+ secretion hypokalemia 90. Metabolic Alkalosis: TreatmentMetabolic Alkalosis: Treatment Saline responsive intravascular volume expansion with normal saline potassium repletion Saline resistant potassium repletion mineralocorticoid antagonists acetazolamide 91. Respiratory AcidosisRespiratory Acidosis Think Murphys Law again From Brain to alveolus, many problems can cause hypoventilation PaCO2 pH (Respiratory acidosis) 92. Respiratory AcidosisRespiratory Acidosis Brain Spinal Cord Peripheral Nerve NeuroMuscular Junction Lung and Pleural disease Stroke Drug Intoxication C spine injury, Guillan Barre Myasthenia Gravis Asthma, COPD, ARDS, etc 93. Clinical ManifestationClinical Manifestation Hypercapnia Pulse RR BP Mental cloudiness Feeling of fullness in the head ICP Headache Hyperkalemia 94. Respiratory AlkalosisRespiratory Alkalosis Hyperventilation PaCO2 pH Etiologies Fever Pain Anxiety Pulmonary disease Sepsis Salicylate intoxication Neurologic disorders 95. MIXED ACID-BASE DISORDERSMIXED ACID-BASE DISORDERS Mixed acid-base disorders include all combinations of 2-3 simple acid base disorders. One must be able to recognize mixed acid- base disorders. This can be accomplished by examining the degree of compensation and calculating an anion gap. If the pH, PCO2 and [HCO3-] do not fit the rules of compensation for a simple disorder, one must hypothesize that there is a mixed acid-base disorder (or hypothesize that there is an error in the data). 96. If there is extreme acidemia or alkalemia, one could hypothesize multiple acid-base disorders that that are additive. If there is a mild acidemia or alkalemia, or pH is normal, particularly with an anion gap one could hypothesize multiple acid-base disorders that cancel each other out. 97. Summary of the Approach toSummary of the Approach to ABGsABGs 1. Check the pH 2. Check the pCO2 3. Select the appropriate compensation formula 4. Determine if compensation is appropriate 5. Check the anion gap 6. If the anion gap is elevated, check the delta-delta 7. If a metabolic acidosis is present, check urine pH 8. Generate a differential diagnosis 98. Putting it TogetherPutting it Together 99. What is the clinical picture? Generate hypothesis! What is the pH? Acidemia Alkalemia Check HCO3- & PaCO2 Is it respiratory or metabolic? Check: Is compensation appropriate? Check Anion Gap Reach Final Diagnosis Step 1 Step 2 Step 3 Step 4 Step 5 Step 6 100. Case 1Case 1 A 26 year old man with unknown past medical history is brought in to the ER by ambulance, after friends found him unresponsive in his apartment. He had last been seen at a party four hours prior. ABG: pH 7.25 Chem 7: Na+ 137 PCO2 60 K+ 4.5 HCO3 - 26 Cl- 100 PO2 55 HCO3 - 25 101. Case 2Case 2 A 67 year old man with diabetes and early diabetic nephropathy (without overt renal failure) presents for a routine clinic visit. He is currently asymptomatic. Because of some abnormalities on his routine blood chemistries, you elect to send him for an ABG. ABG: pH 7.35 Chem 7: Na+ 135 PCO2 34 K+ 5.1 HCO3 - 18 Cl- 110 PO2 92 HCO3 - 16 Cr 1.4 Urine pH: 5.0 102. Case 3Case 3 A 68 year old woman with metastatic colon cancer presents to the ER with 1 hour of chest pain and shortness of breath. She has no known previous cardiac or pulmonary problems. ABG: pH 7.49 Chem 7: Na+ 133 PCO2 28 K+ 3.9 HCO3 - 21 Cl- 102 PO2 52 HCO3 - 22 103. pH7.34pH7.34, PaCO2 60 , HCO3- 31, PaCO2 60 , HCO3- 31 Primary Disorder Primary change Predicted Compensatory Response Metabolic acidosis HCO3 1.2 PaCO2 per 1 meg HCO3 Metabolic Alkalosis HCO3 .7 PaCO2 per 1meq HCO3 Respiratory acidosis: Acute PaCO2 1 meq HCO3 per 10 mm PaCO2 Respiratory acidosis: Chronic PaCO2 3.5 meq HCO3 per 10 mm PaCO2 Respiratory alkalosis: Acute PaCO2 2 meq HCO3 per 10mm PaCO2 Respiratory alkalosis: Chronic PaCO2 4 meq HCO3 per 10mm PaCO2 104. Case 1Case 1 A 52 y.o. man with COPD is admitted to the hospital with a lower extremity cellulitis. Hypothesis Labs: Na+ 139, K+ 4.9, Cl- 98, HCO3- 31 ABG: pH 7.34, PaCO2 60, PaO2 69 Is he acidemic or alkalemic? Is this metabolic (from sepsis) or respiratory (from COPD)? Is this acute or chronic? Why does that matter? 105. Case 1: AnswerCase 1: Answer A 52 y.o. man with COPD is admitted to the hospital with a lower extremity cellulitis. Labs: Na+ 139, K+ 4.9, Cl- 98, HCO3- 31 ABG: pH 7.34, PaCO2 60, PaO2 69 Why is he acidemic? Is this metabolic (from sepsis) or respiratory (from COPD)? Is this acute or chronic? Why does that matter? Dx: Chronic Respiratory Acidosis Not from sepsis No need for intubation or ICU care Note AG 10 106. Case 2Case 2 A 45 y.o. man reports 6 days of persistent nausea and vomiting. PE supine BP 100/60 pulse 105; Standing BP 85/55 pulse 125. Neck veins are flat Hypotheses? Labs: Na+ 140, K+ 2.2, Cl- 86, HCO3 42 BUN 80, Cr 1.9 ABG: pH 7.53, PaCO2 53, PaO2 82 Urine Na+ 2 meg/L Acidemic or Alkalemic? Metabolic or Respiratory? What is his acid base disorder? Why is he alkalemic? How would you fix it? Whats with the urine sodium? Answer: Metabolic alkalosis. Correct with NaCL 107. Case 3Case 3 79 y.o. woman with CC of abdominal pain Patient c/o abdominal pain for 2 days. Pain is moderately severe & diffuse, associated with vomiting. She reports passing no bowel movements or flatus for 2 days. PE: Elderly appearing woman in moderate distress; Vital signs T 38.5, RR 20, BP 115/60, HR 95. Abdominal exam: absent bowel sounds, diffusely distended, mild tenderness, without rebound or guarding. Rectal FOBT negative 108. Case 3 (continuedCase 3 (continued)) Labs: WBC 18K, 82% neutrophils, 10% bands HCT 37 Na 138, K 4.2 HCO3 - 6 CL 106 BUN 45 Cr. 1.0 Glucose 110 ABG: pH 7.10, PaCO2 20mm Hg, PaO2 90 What is her acid base disorder? What does it tell you? 109. Metabolic Acidosis Anion Gap Acidosis NonAnion Gap Acidosis Ketoacidosis Uremic Acidosis Lactic Acidosis Organic Acidosis Lung Disease CO poisening Shock (cardiogenic) Septic shock Focal vascular obstruction Cyanide poisening DKA (Type 1) Starvation Alcoholic Methanol Ethylene Glycol Salicylate intoxication Diarrhea Burns (severe) RTA 110. Who gets your last ICU bed?Who gets your last ICU bed? 75 y.o. WF with COPD with CC cough & SOB R.A. ABG 7.35, PaC02 60, Pa02 48. 70 y.o. WM with COPD with CC purulent sputum, SOB. ABG on 4L 7.2, PaC02 60, Pa02 of 70 111. What is the clinical picture? Generate hypothesis! What is the pH? Acidemia Alkalemia Check HCO3- & PaCO2 Is it respiratory or metabolic? Check: Is compensation appropriate? Check Anion Gap Reach Final Diagnosis Step 1 Step 2 Step 3 Step 4 Step 5 Step 6 112. Arterial punctureArterial puncture 113. Problems of taking arterialProblems of taking arterial blood samplesblood samples Bleeding Vessel obstruction Infection 114. Allen's test. The radial and ulnar arteries are occluded by firm pressure while the fist is clenched. The hand is opened and the arteries released one at a time to check their ability to return blood flow to the hand 115.