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Acid-Base Balance KNH 413
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Acid-Base Balance Acids Donate or give up H+ ions Rise in pH as a result! Nonvolatile acids or fixed acids CO2 indirect measure of production of acid b/c of rise of pH Inorganic acids that occur through metabolism of CHO, protein, lipid Average amount 50-100 mmol/day Proteins contribute the most Lungs cannot eliminate
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Acid-Base Balance Bases Can accept or receive H+ ions Ex: bicarbonate Bicarbonate HCO 3 Kidneys provide primary regulation of acid base balance Dialysis patients deal with this on a weekly basis
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Acid-Base Balance pH Acidosis Accumulation of acid or loss of base Acidemia (*main concern) pH < 7.35 (stomach acid) Alkalosis Accumulation of base or loss of acid Alkalemia pH > 7.45 (pancreatic juice & bile)
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Regulation of Acid-Base Balance Chemical buffers-aid in maintaining balance # 1. bicarbonate increases rate and depth of breathing b/c increases the amount of CO2 production Respiratory regulation—to excrete more CO2 Kidney regulation—work to reabsorb more bicarbonate if in an acidodic condition
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Regulation of Acid-Base Balance Respiratory regulatory control: Change in respiration rate Depth of breathing Release or retention of CO 2
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Regulation of Acid-Base Balance Renal regulatory control Control of HCO 3 (bicarbonate) by the kidneys that is excreted Increased or decreased bicarbonate absorption based on need Formation of dibasic phosphate and sulfur in the urine Accepts H+
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Regulation of Acid-Base Balance Electrolyte Balance 1. Blood 2. Urine 3. ? Hydrogen and bicarbonate both electrolytes Other electrolytes affected to maintain electroneutrality Potassium, chloride, sodium—constantly looking at these blood values and altering them if necessary
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Acid-Base Disorders 4 major types Respiratory acidosis: lower pH, higher plasma bicarbonate, increased CO2 production Trying to excrete more hydrogen to regulate this Respiratory alkalosis: higher pH, lower plasma bicarbonate, decreased CO2 production Metabolic acidosis: most common; lower pH, decreased plasma bicarbonate, decreased CO2 Hyperventilation situation; hydrogen being excreted at a higher level Metabolic alkalosis: increased pH, increased plasma bicarbonate, increased CO2 production Hypoventilation
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Acid-Base Disorders Respiratory acidosis Excess acid in blood secondary to carbon dioxide retention Hypercapnia—too much CO2 in the blood Common causes d/t respiratory dysfunction – renal regulatory systems compensate
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Acid-Base Disorders Respiratory acidosis Labs Decreased pH, elevated pCO 3 Slightly elevated bicarbonate Increase in serum Ca, K, Cl Hypoxemia—inability of oxygen to flow throughout the blood Restlessness, apprehension, lethargy, muscle twitching, tremors, convulsions, coma
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Acid-Base Disorders Respiratory acidosis Treatment Correct underlying condition Increase oxygenation—increasing or decreasing ventilation Mechanical ventilation
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Acid-Base Disorders Respiratory alkalosis—hyperventilation Relative excess amount of base d/t reduction of CO 2 Hyperventilation Common causes - see Table 9.6 Shift of acid from ICF to ECF Bicarbonate moved into cells in exchange for chloride – renal compensation
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Acid-Base Disorders Respiratory alkalosis pH > 7.45 Plasma HCO 3 low in chronic, PaCO 3 low in acute Cardiac, CNS, respiratory symptoms Treat underlying cause Correction of hypoxia
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Acid-Base Disorders Metabolic Acidosis All types not caused by excessive CO 2 Common causes **Diarrhea most common cause d/t excessive loss of bicarbonate – bicarbonate- carbonic acid buffer system is stimulated Fistula drainage may occur
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© 2007 Thomson - Wadsworth
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Acid-Base Disorders Metabolic Acidosis Kussmaul breathing—deep labored breathing Common in DKA Cardiac and neurological—insult to heart/neurological as a result of being acidotic (not the norm) Treat underlying cause Raise pH to safe level – not too quickly
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Acid-Base Disorders Metabolic Alkalosis—RARE Excess amount of base (too much acetate in solution) Fluid imbalance – with volume decrease Without fluid imbalance – without volume decrease Common causes Underlying event determines pathophysiology
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Assessment of Acid- Base Disorders © 2007 Thomson - Wadsworth
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