Presentation on theme: "Approach to Acid-Base Disorders"— Presentation transcript:
1Approach to Acid-Base Disorders Antonio Renato B. Herradura, M.D.F.P.C.P, F.P.C.C.PUERMMMC
2Importance of Acid-Base Disorders Among the most common clinical problems encountered in hospitalized patients, especially ICU patientsLead to significant physiologic effectsProper management may be life-savingPneumonia >>>>respiratory alkalosis; Diarrhea >>>>metabolic acidosis; persistent vomiting >>>>metabolic alkalosisMet acidosis >>>> predisposes to cardiac arrhythmias, pulmonary congestion; bone calcium loss (chronic)Respiratory acidosis >>>> transient increase ICP, headache, hypertensionResp alkalosis >>>> decreased ionized calcium >>>>sx of hypocalcemia
3Acid – Base Disorders Principles of A-B homeostasis and disturbances Recognition of A-B disordersSpecific disorders: common etiologies, pathogenesis, clinical features, general principles of managementInterpretation of ABG and electrolyte results
4Normal Arterial Blood Values pH:pCO2: mmHgHCO3: 22 – 26 mmol/LpO2, O2 saturation, base excess/deficitHCO3 is not measured but just calculated from H-H equation.A chemistry panel shows the [total CO2], [Cl-], [K+] and [Na+], [glucose], [BUN] and [creatinine].Normal [H+] = nmol/L or neq/L
5Normal Arterial Blood Values pH:pCO2: mmHgHCO3: 22 – 26 mmol/LpO2, O2 saturation, base excess/deficitChemistry panel:Sodium: mmol/L Potassium: mmol/LChloride: 96 – 109 mmol/L Total CO2: mmol/LGlucose, BUN, CreatinineHCO3 is not measured but just calculated from H-H equation.A chemistry panel shows the [total CO2], [Cl-], [K+] and [Na+], [glucose], [BUN] and [creatinine].Normal [H+] = nmol/L or neq/L
6Maintenance of blood pH pH = log [HCO3](pCO2)(0.0301)Equation describes the relationship between blood pH, pCO2 and HCO3.
7Maintenance of blood pH pH = log [HCO3](pCO2)(0.0301)pH α [HCO3]pCO2pH 1/α pCO2(pCO2)(0.301) = [CO2] in mmoles/liter;May use the H-H equation to determine if the results are accurate
8CO2 production ≈ pCO2 elimination Regulation of pCO2CO2 production ≈ pCO2 eliminationglucose metabolism ventilatory forcesneural drivebellows apparatusairwaysThe respiratory-neural drive system is the chief determinant of pCO2.
9Regulation of plasma HCO3- Via kidneys:Reabsorption of filtered HCO3Formation of titratable acidExcretion of NH4+ in urine
10Maintenance of blood pH Maintenance of the ratio of HCO3 to pCO2 via compensatory responses by the kidneys and lungs
11Maintenance of blood pH Maintenance of the ratio of HCO3 to pCO2 via compensatory responses by the kidneys and lungsChemical buffering:includes HCO3, phosphates, proteins, hemoglobin, bone carbamates
12Compensation for Acid – Base Disorders Primary metabolic Compensatory disturbance respiratory responseHCO pH (met. acidosis) pCO2HCO pH (met. alkalosis) pCO2
13Compensation for Acid – Base Disorders Primary respiratory Compensatorydisturbance metabolic responsepCO pH (resp. alkalosis) HCO3pCO pH (resp. acidosis) HCO3
14Prediction of Compensatory Responses on Simple Acid - Base Disorders Primary Acid-Base DisorderExpected Range of CompensationLimits of CompensationMetabolic AcidosisPCO2 =1.5[HCO3-] + 812-14 mm HgMetabolic Alkalosis PCO2 =0.6 mm Hg for each 1 mEq/L [HCO3-]55 mm HgRespiratory Acidosis [HCO3-] =1(acute) – 4 (chronic) mEq/L for each 10 mm Hg PCO2[HCO3-] =45 mEq/LRespiratory Alkalosis [HCO3-] =2 (acute) -5 (chronic) mEq/L for each 10 mm Hg PCO212-15 mEq/LImportant rule: compensation is not complete.Compensation does not result in over correction of pH.Harrison: Resp Alk HCO3 increases by 4/10 pCO2
16Anion Gap AG = Na+ - (Cl- + HCO3) Normal: 10 - 14 e.g. AG = ( ) = 140 – 129 = 11Represents those unmeasured anions in the plasmaIncrease in AG is due to increased in the amount of unmeasured anions, and less commonly due to a decrease in unmeasured cationsNormal values: [Na+]: mEq/L; [K+]: mEq/L; [Cl-]: mEq/L; [total CO2] :24-30 mEq/LIf AG > 20 high AG metabolic acidosis is present regardless of the pH or HCO3.
17Determinants of AG Unmeasured Anions Unmeasured Cations Albumin (15mEq/L) Calcium (5 mEq/L)Organic Acids (5 mEq/L) Potassium (4.5 mEq/L)Phosphate (2 mEq/L) Magnesium (1.5 mEq/L)Sulfate (1 mEq/L)Total UA (23 mEq/L) Total UC (11 mEq/L)AG = UA – UC = 12 mEq/LAG represents those unmeasured anions in the plasmaIf albumin is decreased by 50%, AG = 4-5 mEq/LIncrease in AG is due to increased in the amount of unmeasured anions, and less commonly due to a decrease in unmeasured cationsIf AG > 20 high AG metabolic acidosis is present regardless of the pH or HCO3.
18Metabolic Acidosis PATHOGENESIS May be due to: Increased endogenous acid production (e.g. lactate and ketones)Loss of bicarbonate (e.g. diarrhea)Decreased excretion of endogenous acids (e.g. renal failure)
19Common Causes of Metabolic Acidosis HIGH ANION GAP NORMAL ANION GAPLactic Acidosis DiarrheaKetoacidosis Isotonic saline infusionESRD Early renal insufficiencyMethanol ingestion RTAEthylene glycol ingestion AcetazoleamideSalicylate toxicity UreteroenterostomyNAG acidosis = hyperchloremic acidosis
20Metabolic Acidosis CLINICAL EFFECTS Kussmaul breathing, dyspnea Headache, nausea, vomiting, confusion, stupor, comaDecreased myocardial contractility and response to catecholamine; peripheral vasodilatation with central venoconstriction predisposing to pulmonary edema; arrhythmias
21Metabolic Acidosis MANAGEMENT Identify and treat underlying cause. Give alkali therapy (oral or i.v.) to patients with normal AG acidosis, mixed hyperchloremic and AG acidosis, and AG acidosis due to nonmetabolizable anion in the face of renal failure.Give modest quantities of i.v. alkali in patients with pure AG acidosis due to metabolizable organic acid anionGoal: increase pH to 7.15 or [HCO3] to 10 mEq/L
22Metabolic Alkalosis PATHOGENESIS Due to net gain of HCO3 or loss of volatile acid (usually HCl by vomiting)2 stages:GENERATIVE STAGE: loss of acidMAINTENANCE STAGE: failure of kidneys to compensation by excreting HCO3, because of volume contraction, low GFR, or depleted K+ or Cl-Addition of alkali is unusual
23Metabolic Alkalosis CLINICAL EFFECTS increases the affinity of hemoglobin for oxygen decrease tissue unloadingDecreases ventilationDecreases ionized calcium neuromuscular hyperirritabilitySupraventricular and ventricular arrhythmias
24Metabolic Alkalosis MANAGEMENT Identify and correct the underlying stimulus for HCO3 generationRemove the factors that sustain HCO3 reabsorption (e.g. ECF contraction or hypoK+)AcetazoleamideDilute 0.1N HCl or NH4ClHemodialysis
25ETIOLOGY and PATHOGENESIS Respiratory AcidosisETIOLOGY and PATHOGENESISmay be due to severe pulmonary disease (e.g. advanced COPD), respiratory muscle fatigue, or abnormalities in ventilatory control (e.g. stroke)
26Respiratory Acidosis CLINICAL EFFECTS depends on severity and acutenessmay be dyspneic or tachypneicSystemic vasodilation especially cerebral vasodilation increased ICP pseudotumor cerebriMyoclonic jerks, asterixis, tremors, restlessness, coma
27Respiratory Acidosis MANAGEMENT Depends on severity and rate of onset May be life-threateningMeasures to reverse underlying causeRestoration of adequate alveolar ventilationAvoid rapid correction of hypercapneaMay need tracheal intubation and mechanical ventilation.Rapid correction of pCO2 may cause the same complications noted with acute respiratory alkalosis (e.g. cardiac arrhythmias, reduced cerebral perfusion, seizures)
28Respiratory Alkalosis ETIOLOGY and PATHOGENESISDevelops when a sufficiently strong ventilatory stimulus causes CO2 output in the lungs to exceed its metabolic production in the tissuesMay be due to stimulation of CNS (e.g. pain, anxiety), peripheral chemoreceptors (e.g. hypoxemia 2o to pneumonia), chest receptors (e.g. PTE).
29Respiratory Alkalosis CLINICAL EFFECTSPanic, weakness, and sense of impending doomParesthesias about the hands and feetTrousseau’s and Chvostek’s signsPossible tetany, seizures
30Respiratory Alkalosis MANAGEMENTDirected toward alleviation of underlying disorderChange in dead space, tidal volume and respiratory frequency, if on MVRe-breathing from paper bag during symptomatic attacks of hyperventilation syndrome
31Interpretation of Acid - Base Disorders Determine if sample is arterial or venous.Compare HCO3 on ABG and electrolyte panel to verify accuracyDetermine if pH or pCO2 are normal or abnormal.If any of above are abnormal determine primary A-B disturbanceCompute for expected compensation to determine presence of mixed disorders.The HCO3 value on the ABG result should fall within 2 mmol/L of the measured [HCO3] or total CO2 on the electrolyte panel.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.If pH and pO2 are normal, check AG: if normal then normal A-B
32Interpretation of Acid - Base Disorders Calculate the Anion GapRULE: If AG > 20 high AG metabolic acidosis is present regardless of the pH or HCO3.Compare the change in AG (ΔAG) with change in HCO3 (ΔHCO3).RULE: If change (i.e. increase) in AG is < change( i.e. drop) in HCO3, there is combined high AG met acidosis and normal AG (hyperchloremic) acidosis.RULE: If ΔAG is > ΔHCO3, there is combined high AG metabolic acidosis and metabolic alkalosis.If AG > 20 high AG metabolic acidosis is present regardless of the pH or HCO3.ΔAG = patient’s AG – 10 (normal AG)ΔHCO3 = 24 (Normal HCO3) minus patient’s HCO3If change (i.e. increase) in AG is < change( i.e. drop) in HCO3, there is combined high AG met acidosis and normal AG (hyperchloremic) acidosis.If ΔAG is > ΔHCO3, there is combined high AG metabolic acidosis and metabolic alkalosis.