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Acid-Base Balance. By: Hannah Coakley 2/27/2014. Quick Review: Acids. Acids are compounds which function as hydrogen (H+) donors in biochemical equations/solutes The more free H+ ions available for donation, the more acidic the compound
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Acid-Base Balance By: Hannah Coakley 2/27/2014
Quick Review: Acids Acids are compounds which function as hydrogen (H+) donors in biochemical equations/solutes The more free H+ ions available for donation, the more acidic the compound Many foods that are “acidic” in taste are actually metabolized into basic compounds in the body
Quick Review: Bases Bases are compounds which can accept H+ ions. This is accomplished by having an excess of OH- (hydroxide) ions The terms “basic” and “alkaline” are used interchangeably
Quick Review: pH pH is the –log of H+ concentration in any given solute Its range spans from 0 – 14 A lower pH implies a high H+ concentration (acidic). A higher pH implies a low H+ concentration (basic)
Role of pH in the Body Intra and extracellular pH levels are tightly regulated:
Acids & Bases in the Body The body naturally produces more H+ than OH- ions This occurs in several ways: -- The metabolism of fats (fatty acids) and proteins (amino acids) -- The byproduct of cellular respiration: where carbonic acid breaks down into CO2 and H20 to be breathed out by the lungs
The Chemical Buffer System Works to regulate pH by taking up or releasing H+ ions accordingly Protects neutrality, usually by pairing a weak acid with a base Also functions by substituting a strong acid or base for a weak one
Methods of Excretion The other primary way to maintain pH homeostasis is through the excretion of excess acids or bases. Respiratory excretion of CO2 using rate and depth of breath Renal excretion, whicheliminates acids and can also regulate the amount of circulating bicarbonate (HCO3-)
Defining Acidosis and Alkalosis Acidosis: • pH< 7.35 • Primary effect is in suppression of the CNS decreased Ca binding to protein, high I-Cal • Weakness, coma, death Alkalosis: • pH > 7.45 • Primary effect is in overstimulation of CNS & PNS increased Ca binding to protein, low I-Cal • Lightheadedness, spasms/tetany, death
Metabolic vs Respiratory Metabolic Acidosis loss of relative concentration of bicarbonate ion (< 22 mEq/L) (Symptoms: Headache, lethargy, N/V/D, coma) Metabolic Alkalosis excess of relative concentration of bicarbonate ion (> 26 mEq/L) (Symptoms: electrolyte depletion, tetany, slow and/or shallow breathing, tachycardia)
Metabolic vs Respiratory Respiratory Acidosis carbonic acid excess leading to hypercapnia(pCO2 > 45 mm Hg) (Symptoms: warm, flushed skin vasodilation, breathlessness, hypoventilation, disorientation, tremors) Respiratory Alkalosis carbonic acid deficit leading to hypocapnia(pCO2 < 35 mm Hg) (Symptoms: dizziness, lightheaded, numbness of extremities)
Compensatory Mechanisms Depending upon the primary acid-base imbalance, the body will compensate using a secondary mechanism in order to return pH homeostasis to the body
Compensation: Metabolic Metabolic Acidosis • Increased Ventilation to eliminate excess CO2 (Hyperventilation) • K+ & PO4 shifting from ICF to ECF to function as a buffer (H+ shifts into the cells) Metabolic Alkalosis • Decreased ventilation (Hypoventilation) limited by constraints of hypoxia
Compensation: Respiratory Respiratory Acidosis • Kidneys eliminate excess H+ ions, retain Bicarbonate ions Respiratory Alkalosis • Kidneys conserve H+ ions and excrete excess Bicarb ions • K+ shift from ECF to ICF to increase circulating H+ (sudden low serum K+)
Interpreting the Anion Gap If the Anion gap is > than 26 mEq/L this is considered normochloremic acidosis If the anion gap is WNL (6 – 12 mEq/L), this is considered hyperchloremic acidosis
Mixed Acid-Base Disorders More than one acid/base disturbance can occur concomitantly in the body If unexpected lab values are noted, there is good reason to suspect a mixed acid-base disorder
Treatment Strategies: Metabolic Acidosis If Hyperchloremic: IV-Lactate solution is given, this is converted to bicarb in the liver, thus raising the relative concentration of bicarbonate in the blood (shift of K+ back into ICF and may cause a need for it to be repleted) If Normochloremic: Identify and correct sources of excess acids
Treatment Strategies: Metabolic Alkalosis Saline Responsive (urine Cl- < 10 mEq/L) IV-NaCl solution is given to physiologically replace the excess bicarbonate ions in the blood with Cl ** Administration of KCl is also essential, as adequate K+ buffer in the ECF is essential to fully correcting the alkalosis
Treatment Strategies: Respiratory Acidosis -- Treat the underlying dysfunction or disease -- Restore appropriate ventilation -- Add IV-lactate to aid in compensatory bicarb production -- Ensure that the patient is not being overfed, as this will prolong acidosis (via excess CO2 production)
Treatment Strategies: Respiratory Alkalosis -- Treat underlying dysfunction or disease -- Attempt to slow respiration -- Add IV-Cl to aid in compensatory replacement of excess bicarb -- Replete K+ as needed, since K+ shifts intracellularly in exchange for H+ in the ECF
Correcting Acid/Base Imbalance:Step By Step • Analyze the pH 2) Analyze the pCO2 3) Analyze the HCO3 4) Match the pCO2 or the HCO3 with the pH 5) Assess AG and BE 6) Assess directionality/compensation 7) Analyze the pCO2 and O2 saturation
Check Your Knowledge Scenario #1a: pH: acidic // CO2: high // HCO3: high What is the primary imbalance? Is there evidence of compensation? #1b: What if HCO3 was normal? Low?
Take Home:What is the RD’s Role? • Monitoring • Treatment (Repletion of electrolytes and fluids) • Maintenance (appropriate TF or TPN)
References Brantley, Susan. The ABCs of ABGs. Support Line. UT Medical Center, Knoxville, TN. Langley, Ginger. Fluid, Electrolytes, and Acid-Case Disorders. A.S.P.E.N Nutrition Support Core Curriculum, 2007. Gilmore, Diane M. Acid Base Balance and Imbalance. Arkansas State University, Dept of Pathophysiology, 2012. Ebihara, L. & West, John. Acid-Base Balance, A Respiratory Approach. Repiratory Physiology, The Essentials. 2011 Jaber, Bertrand. Metabolic Acidosis. Tufts University Open Courseware, Renal Pathophysiology. 2007. Kibble, Jonathan D.& Colby R. Halsey, Medical Physiology: The Big Picture. 2009. Skujor, Mario & Mira Milas. Endocrinology. Cleveland Clinic: Center for Continuing Education. 2013