Acid-Base Balance & ABG Analysis PDF

Acid-Base Balance ABG Analysis Clay Freeman, DNP, CRNA Science in Anesthesia 1 Objectives Readings: Nagelhout: p.630-632 Barash: Chap 16 • Define Acid/Base • Detail Acid-Base Concept Models • Describe Acid-Base Maintenance • Kidneys, Lungs, Buffers • Detail Acid-Base Derangements • Interpret AB...

Acid-Base Balance ABG Analysis Clay Freeman, DNP, CRNA Science in Anesthesia 1 Objectives Readings: Nagelhout: p.630-632 Barash: Chap 16 • Define Acid/Base • Detail Acid-Base Concept Models • Describe Acid-Base Maintenance • Kidneys, Lungs, Buffers • Detail Acid-Base Derangements • Interpret ABG Values • Discuss Acid-Base Interventions 2 Acid/Base Defined Arrhenius (1880s): In an aqueous solution… - Acids dissociate to produce hydrogen ions - Bases dissociate to produce hydroxyl ions Brønsted-Lowry (1923): ▪ Acids are Proton (H+) Donors ▪ Bases are Proton (H+) Acceptors ➢ First clinically useful approach ➢ Introduced Acid-Base conjugates Lewis Approach (1923): ▪ Acids are acceptors of electrons ▪ Bases are donors of electrons ➢ Includes CO2 & H+ 3 Acid-Base Reactions Proton-transfer within a reaction Base & Conjugate Acid • When an acid transfers a H+ it converts to a conjugate base • When a base accepts a H+ it converts to a conjugate acid Goal of reaction is to reach Neutralization H2CO3 + OH- ↔ HCO3- + H2O Acid & Conjugate Base It’s all about balance: Weak acids/bases: form a dynamic equilibrium in water between molecular & ionized form HCl + H2O ↔ Cl- + HCO3+ Strong acids/bases: completely ionize/dissociate in water 4 pK Equilibrium Constant (K): Predicts the point of equal molar concentrations between product and reactants • Ka/Kb subscript added when discussing acid/base ionization • A higher Ka/Kb value indicates a strong acid/base +][A-] [H Ka = HA +][OH-] [BH Kb = B pKa/pKb: -log of Ka/Kb • Logarithmic relationship provides a manageable value • pH of solvent at which 50% of solute is Ionized and 50% of solute is Non-Ionized • Lower pKa/pKb indicates a strong acid/base • pKa + pKb = 14 5 pH The hydrogen ion [H+] is a hydrogen atom missing its electron It is highly reactive since it cannot exist in this state in perpetuity In normal physiology, H+ occurs in miniscule concentrations pH is the negative logarithm of [H+]: pH = -log [H+] • Therefore, a small change in pH reflects a large change in H+ • Gross inaccuracies pH scale ranges from 1 to 14 • 7 is neutral • 6.8-7.8 is compatible with life 6 Henderson-Hasselbalch (1909) Conjugate base Acid • Describes the mathematical relationship of pH due to pKa and solute concentrations • pH is a function of the ratio of dissociated to non-dissociated acid • “Acid-base balance” described by solving for pH within buffer solution 7 Acid-Base Balance Concepts Boston Approach (Schwartz/Relman-1950s): • Related the Henderson-Hasselbalch equation to clinical practice of predicting acid-base disorders • Difficult to discern metabolic derangements pKH2CO3 is the equilibrium constant of buffer system = 6.1 S is the solubility coefficient of CO 2 = 0.03 Eq This equation states that the pH in blood is equal to a constant (pK) plus the log ratio of bicarbonate to pCO2 • Ultimately, pH = HCO3:CO2 ratio 8 Acid-Base Balance Concepts Copenhagen Approach Siggaard/Andersen-1950s): • Introduced additional buffers into acid-base analysis • Introduced concept of base excess/deficit • Difficult to discern chronic and multifactorial derangements Anion Gap Approach (Emmett/Narins-1977): Anion Gap = (Na+ + K+) - (Cl- + HCO3-) • Details difference between physiologic cations & anions • Sum of the difference in charge of common extracellular ions reveals “gap” Stewart Model (1983): • Based on law of electroneutrality, law of dilution, and law of conservation of mass • Uses Arrhenius definition of acid/base to predict physiologic shifts of ions • Applied several formulas together to keep variables independent of one another (HCO3, CO2, ions) 9 Stewart’s PhysicoChemical Approach pH is dependent on variables of PaCO2, Atot , SID Strong Ion Difference (SID): Balance of strong ions: measurable cations - anions (Na+ + K+ + iMg++ + iCa++) – (Cl- + lactate) = 40mEq/L (Normal) Total Amount of Weak Acid (Atot): • Non-bicarbonate “buffers” include albumin, phosphate, & plasma proteins • Albumin makes the greatest contribution to ionic charge o Minimal contribution from phosphate • Overall minimal effect on acid-base balance except in chronic disease processes (liveralbumin, kidney-phosphate) Strong Ion Gap: Provides a more detailed evaluation of acid-base balance with both inorganic & organic acids SID – (Atot + CO2) 10 Dissociation of Water The water molecule has an unequal charge distribution giving it unique physicochemical properties ▪ Water is considered an Amphiprotic Species: It acts as either an acid (H3O+) or base (OH-) within reactions ▪ Water itself acts as an acid or base when it dissociates to become the source of H+ and OH- ions ➢ Temperature is a crucial factor in determining balance 11 Acid-Base Balance An acid-base load is imposed via diet, metabolic processes, cellular shifts, and iatrogenic interventions Control of H+ is necessary to prevent electrochemical imbalances from interfering with transcellular transport mechanisms Three primary systems to maintain acid-base balance: 1) Buffer System 2) Lungs 3) Kidneys 12 Chemical Buffering Buffer: A solution that resists shifts in pH due to addition of either an acid or base. • “Shock Absorber” - Rapidly guards against sudden shifts in H + concentrations • Protects enzymes which function within a narrow pH range Extracellular - principle buffer is the bicarbonate system (Most Important) Intracellular - principle buffers include phosphates and proteins 13 Bicarbonate Buffer System Instantaneous chemical equilibrium between carbonic acid and bicarbonate ions work to resist sudden changes in pH Bicarbonate buffer system converts • Strong bases to a weak base (bicarbonate ion) • Strong acids to a weak acid (carbonic acid) Process is sped up by presence of Carbonic Anhydrase in erythrocytes When an Increase in pH (alkalosis) occurs… H2CO3 → HCO3– + H+ Carbonic acid dissociates to H+ = lowering the pH When a Decrease in pH (acidosis) occurs… H2CO3  HCO3– + H+ Bicarbonate binds with H+ = raising the pH 14 Lungs CO2 (the major by-product of oxidative metabolism) is transported to the lungs and eliminated through alveolar ventilation in order to control pH More fun facts: • CO2 is a volatile acid that diffuses intracellular easily • CO2 is the major source of acid in the body • produces 12,500 mEq of H+ per day • CO2 is lipid-soluble and rapidly crosses the Blood-Brain Barrier into the CSF • H+ & HCO3 are slow to cross into CSF Central Chemoreceptors regulate pH of CSF by controlling speed and depth of ventilation • Compensatory responses within minutes 15 Kidneys Kidneys excrete H+ & regenerate HCO3 • Effectively at a 1:1 exchange ratio H+ excreted as NH4 and H2PO4 in urine - Gradual stepwise excretion (reach max at ~4 days) Na+ and Cl- ions are used as cotransporters • Cl- excreted in metabolic acidosis • Na+ & K+ excreted in metabolic alkalosis • Only way to excrete fixed acids is through kidneys (70mEq/day) • Intrinsic control in the kidney (not CNS mediated) • Compensatory responses take hours to days 16 Intracellular fluid shifts Shifting of ions across cell membranes can function as a temporary “buffer” by decreasing extracellular acid/base load H+ ions are switched with complementary ions Ex) H+ moves intracellular → Na, K, Ca move extracellular Electroneutrality involves the coupled exchange of ions (H+/HCO3−) and (Na+/Cl−) Bone is the most vast storage of ions Response is Immediate to within 2-4hrs 17 ABG tests Measured Outputs: pH via Sanz electrode PaO2 via Clark electrode PaCO2 via Severinghaus electrode Related Measurements: electrolytes & metabolites Calculated outputs: HCO3 from the Henderson-Hasselbalch equation Base Excess from the Van Slyke equation SaO2, unless a co-oximetry is available 18 ABG tests Confidence Limits: pH pO2 pCO2 ±0.001 units ±4mmHg ±3mmHg Common errors: ▪ Air bubbles within sample • Room air bubble = 160mmHg O2 and CO2 ~0 ▪ Inadequate/excessive anticoagulant • pH of heparin is 7.0 ▪ Delayed cooling/sampling • Continuous consumption of O2 ▪ Excessive sample manipulation 19 ABG tests Perform Modified Allen’s Test: 1) 2) 3) 4) Occlude Radial & Ulnar artery, Bend patient’s elbow to lift hand for exsanguination, Release Ulnar artery to observe recirculation, Repeat to compare to Radial artery recirculation Normal/positive Allen’s test = < 10 seconds Negative Allen’s test = puncture contraindicated ➢ Refill timing should be similar between the 2 tests Negative Allen’s test occurs in less than 1% of patients 20 Acid-Base Map Shown is the relationship between pH, CO2 and HCO3-. pH 7.4 PCO2 40 HCO3- 24 Bands for the various acid-base disorders can be quickly interpreted or compared pH 21 Determine oxygenation A-a gradient Acidemia pH<7.35 Determine pH Respiratory or metabolic Respiratory or metabolic? Respiratory acidosis pCO2>40 Metabolic acidosis HCO3<24 Calculate anion gap Na+ - (Cl- + HCO3) Correct for hypoalbuminemia Gap + 2x (normal – measured albumin) Gap AG > 12 Non-gap AG < 12 Calculate ΔRatio ΔRatio = (Gap - 12) / (24 - HCO3) ΔRatio < 1 = concurrent metabolic acidosis ΔRatio 1-2 = expected ΔRatio > 2 = concurrent metabolic alkalosis Alkalemia pH>7.45 Respiratory alkalosis pCO2<40 Metabolic alkalosis HCO3> 24 Acute or chronic Acute: pH Δ 0.08 for 10mmHg change in pCO2 Chronic: pH Δ 0.03 for 10 mmHg change in pCO 2 Is respiratory compensation appropriate? Calculated pCO2 = (1.5 x HCO3) + 8 Measured > calculated = concurrent resp acidosis Measured = calculated = compensated Measured < calculated = concurrent resp alkalosis Is respiratory compensation appropriate? Calculated pCO2 = (0.7 x HCO3) + 21 Measured > calculated = concurrent resp acidosis Measured = calculated = compensated Measured < calculated = concurrent resp alkalosis 22 ABG Analysis If Respiratory: ABG Interpretation 1) Determine Acidosis (pH<7.4) vs Alkalosis (pH>7.4) 2) Differentiate primarily Respiratory vs Metabolic 3) Acute or chronic Acute = pH Δ 0.08 for 10 mmHg change in Pco2 Chronic = pH Δ 0.03 for 10 mmHg change in Pco2 If Metabolic Acidosis: 3) Check anion gap Anion gap = Na+ - (Cl- + HCO3-) 4) If anion gap exists (>12), calculate Δ Ratio Δ ratio = (anion gap – 12) + (24 - HCO3-) ΔRatio < 1 = concurrent metabolic acidosis ΔRatio 1-2 = expected ΔRatio > 2 = concurrent metabolic alkalosis If Metabolic Alkalosis: 3) Is there respiratory compensation Calculated Pco2 = (0.7 x HCO3-) + 21 Measured > calculated = concurrent resp acidosis Measured < calculated = concurrent resp alkalosis …OR… 4/5) Is there appropriate respiratory compensation? Calculated Pco2 = (1.5 x HCO3-) + 8 Measured > calculated = concurrent resp acidosis Measured < calculated = concurrent resp alkalosis 23 24 Respiratory vs Metabolic (Primary) R O Differentiate primarily Respiratory vs Metabolic Derangement: M E Respiratory Opposite: pH and PaCO2 move in opposite directions Correlate pH to PaCO2 & HCO3 Metabolic Equal: pH & HCO3 trend in same direction 25 Respiratory Alkalosis Lab Values: Hypocarbia (PaCO2 < 40), pH high (> 7.40) Causes: Excessive ventilation (pain/anxiety, hypoxia, CNS/lung disease, sepsis, iatrogenic) Consequences: Hypokalemia, hypocalcemia, dysrhythmias, hypotension, cerebral vasoconstriction, neuronal irritability Treatment: Treat underlying cause Acetazolamide 26 Respiratory Acidosis Lab Values: Hypercarbia (PaCO2 > 40), pH low (< 7.4) Causes: • Decreased minute ventilation: Central depression(drugs), CNS injury, airway obstruction, inadequate NMB reversal • Increased dead space ventilation: COPD, PE • Increased CO2 production: Sepsis, fever, excessive parenteral feeding Consequences: Myocardial Depression, Coronary Vasodilation, Increased sympathetic tone, Tachycardia, Increased ICP, Narcosis w/ excessive PaCO2 Treatment: Acute: Intubation/Mechanical ventilation, treat underlying cause Chronic: Improvement in pulmonary function 27 Respiratory Derangements Acute vs Chronic Respiratory Derangement Acute: pH changes 0.08 for every 10mmHg change in PaCO2 away from 40mmHg Chronic: pH changes 0.03 for every 10mmHg change in PaCO2 away from 40mmHg Examples for Respiratory Acidosis: PaCO2 = 60 mmHg, pH = 7.24 PaCO2 = 60 mmHg, pH = 7.30 PaCO2 = 60 mmHg, pH = 7.34 28 Interpret pH pCO2 HCO3Na+ Cl- 7.5 28 24 128 88 29 Metabolic Alkalosis Lab Values: Hyperbicarbonatemia (>24), pH high (>7.40) Causes: Increased HCO3 reabsorption: Hypovolemia, hypokalemia, hyperaldosteronism, compensation for permissive hypercapnia, pharmaceuticals (antacids, loop diuretics) Loss of H+: Vomiting, prolonged nasogastric suction Consequences: Hypokalemia, hypocalcemia, ventricular dysrhythmias, compensatory hypoventilation, left-shift of oxyhemoglobin dissociation curve Treatment: • Volume expansion with normal saline (Increases Cl- and decreases HCO3-) • Acetazolamide (produces renal wasting of bicarbonate) • Dialysis against a high chloride/low bicarbonate dialysate 30 Metabolic Acidosis Lab Values: Hypobicarbonatemia (< 24), low pH (<7.40) Causes: Bicarbonate Buffering of endogenous or exogenous acid load High anion gap (>12) Abnormal external Loss of Bicarbonate Normal anion gap (<12) Consequences: Directly causes arteriodilation but catecholamine release increased, Myocardial depression, pulmonary congestion, insulin resistance Treatment: • Increase base load* • Decrease acidic load: low protein diet, thiazide diuretics 31 Respiratory Compensation Respiratory Compensation for Metabolic Alkalosis PaCO2 ~ (0.7 x HCO3-) + 21 Respiratory Compensation for Metabolic Acidosis PaCO2 ~ (1.5 x HCO3- ) + 8 measured PaCO2 > calculated PaCO2 = concurrent Respiratory Acidosis measured PaCO2 = calculated PaCO2 : Compensated measured PaCO2 < calculated PaCO2 = concurrent Respiratory Alkalosis 32 Anion Gap The Law of Electroneutrality suggests that an equilibrium should exist between all positive and negative charges. The anion gap is the difference between the measured anions and cations. Anion Gap = [Major Cations] – [Major Anions] [Na+] – [Cl- + HCO3-] = 12 mEq/L Simplified calculation does not account for less significant cations (Mg & Ca) and anions (albumin, PO4, lactate) Non-Gap Acidosis • HCO3- replaced in proportion to Cl- retention • ECF dilution of buffers (excessive NaCl administration) • Retention of H+ d/t kidney dysfunction High Anion Gap Acidosis • Increased organic acids • Ingestion of toxins 33 Anion Gap Anion Gap = [Major Cations] – [Major Anions] [Na+] – [Cl- + HCO3-] = 12 mEq/L 34 Resource 35 ∆Gap / Ratio ∆Gap = ∆Anion Gap ÷ ∆HCO3 = (Anion Gap – 12) ÷ (Normal HCO3 – measured) The delta gap is the difference between the change in the anion gap (ΔAG) and bicarbonate (ΔHCO 3-) ▪ HCO3 levels normally change in proportion to the anion gap in order to maintain electroneutrality ▪ A disproportionate alteration in HCO3 in relation to the anion gap, suggests an additional acid-base disorder is present. Cations AG HCO3 = Cl- 36 Again pH pCO2 HCO3Na+ Cl- 7.33 35 18 138 100 37 Another One pH pCO2 HCO3Na+ Cl- 7.43 47 32 133 92 38 Uno Mas pH pCO2 HCO3Na+ ClK+ BE 7.30 40 17 142 97 3.6 -3 39 Modified Alveolar Gas Equation A-a O2 Gradient: Comparison of alveolar oxygen tension (A) to oxygen dissolved within plasma (a) to determine if pathology causing hypoxemia exists. A-a oxygen gradient = PAO2 - PaO2 40 Work It Out 1) First, calculate alveolar oxygen tension PAO2 = (FiO2 x [Patm - PH2O]) - (PaCO2 x R) Patm = atmospheric pressure (estimated 760mmHg) PH2O = atmospheric vapor pressure (47mmHg in alveoli at 37°C) R = 1.2 (respiratory quotient if FiO2 < 0.6) 2) Next, compare PAO2 vs PaO2 to see if the Calculated A-a gradient matches the Expected A-a oxygen gradient To determine expected A-a oxygen gradient A-a oxygen gradient = 2.5 + FiO2 x age (years) 41 Oxy-Hgb Dissociation Curve Hemoglobin has a unique quaternary structure which shifts due to electrostatic reactions Electrostatic bonding is affected by both concentration gradients (CO2 & O2) & pH Trends in O2 binding with Hemoglobin is observed on the Oxy-Hgb Dissociation curve Rightward Oxy-Hgb Shift: Acidosis, Hyperthermia, • Reduced affinity of O2 to Hgb = Increased O2 released peripherally • SpO2 underestimates oxygenation (PaO2) Leftward Oxy-Hgb Shift: Alkalosis, Hypothermia • Increased affinity of O2 to Hgb = decreased O2 released peripherally • SpO2 overestimates oxygenation (PaO2) 42 Systemic Effects H+ ionizes intracellular protein molecules which affects the function of: Enzymes, Peptide Hormones, Hormone Receptors, Ion Channels, Transporters, & Mediator Proteins Acidemia • • • • • • Sympathetic Nervous System activation Myocardial Depression Increased Pulmonary Vascular resistance Increased ICP Vasopressor Resistance Insulin Resistance Alkalemia • Decreased coronary blood flow • Risk of seizures 43 Systemic Effects Alterations in pH is usually a symptom so treatment is based on the causative agent 44 Base Excess/Deficit Base Excess represents the amount of acid or alkali that must be added to 1L of blood to return the sample to a pH 7.40 while maintaining the PaCO2 at 40mmHg. BE is traditionally calculated via the Van Slyke equation Limitations: • Underlying chronic illness (Renal Failure, COPD) • Massive fluid resuscitation • Decreases in non-buffer ions (albumin, phosphate) 0 mEq/L is Normal > +2 suggests metabolic alkalosis < -2 suggests metabolic acidosis In a study by Chawla et al, of trauma patients, resuscitation decisions would have been wrong 33-58% of the time if BD or anion gap had been used as the sole criterion rather than serum lactate concentration[16] 45 Bicarb administration Prescribed during: ❑ Emergency Scenarios ❑ Hemodynamic Instability (due to pH effect on enzymes) Should not to exceed 1 mEq/kg/hr (unless emergency scenarios) NaHCO3 mEq/L = Wt(kg) x 0.3(24mEq/L – actual HCO3-) 2 Paradoxical effects of IV NaHCO3 administration: ▪ Increased levels of CO2 d/t shift in carbonic anhydrase reaction • Intracellular acidosis • acidosis in the CNS ▪ Counter anion (Na+ or K+) action and osmotic properties contribute to fluid retention and electrolyte imbalances 46 Additional Resources • https://www.youtube.com/watch?v=Ge-co-Zl1Ro • Barash. Chap 16 • https://ccforum.biomedcentral.com/articles/10.1186/cc2861#Fig3 47