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Acid-Base Physiology

Costanzo-Acid-Base Physiology

normal range of arterial pH 7.37 to 7.42 pH<7.37 called acidemia pH>7.42 alkalemia pH range compatible with life 6.8 to 8
CO2 (acid production) volatile acid=>expired in the lungs end product of aerobic respiration with help of carbonic anhydrase reacts with water and converted into carbonic acid within RBCs (weak acid)
carbonic anhydrase catalyzes conversion of CO2 + H2O => H2CO3
fixed acid produced from metabolism of proteins (sulfuric acid) and phospholipids (phosphoric acid) produced in excess in pathophysiological states may be ingested not volatile=>must be buffered in body fluid until kidney excretion causes metabolic aci
fixed acids from pathological states diabetes=>beta-hydroxybutyric acid and acetic acid strenuous exercise/hypoxic tissues=>lactic acid
fixed acids from ingestion salicylic acid=>aspirin overdose formic acid=>methanol ingestion glycolic and oxalic acids=>ethylene glycol ingestion
buffer mixture of weak acid and its conjugate base OR weak base and its conjugate acid resists change in pH=>important 1st defense against changes in pH
pK characteristic of value of buffer pair strong acids=>low pK weak acid=>high pK pH=pK=>equal concentrations of HA and A- small pH changes occur in linear portion of pK titration curves
bicarbonate buffer most important extracellular buffer first line of defense when H+ gained/lost from body because 1)concentration of HCO3- high (24 mEq/L) 2)pK=6.1=>close to pH of ECF 3)CO2 is volatile and can be expired by lungs
acid-base map represents Henderson-Hasselbach equation=>shows relationships between Pco2 and HCO3- isohydric lines have same pH and gives all combos of Pco2 and HCO3- that yield same value of pH *abnormal combinations can yield normal values of pH
phosphate buffer major buffer of ECF pK=6.8
plasma protein buffers H+ can either bind H+ or Ca2+=>relationship between plasma proteins, H+, and Ca2+
organic phosphates ATP, AMP, glucose-1-phosphate, 2,3-diphosphoglycerate (2,3-DPG)
hemoglobin most significant intracellular buffer=>deoxyhemoglobin more effective buffer present in high concentration inside RBCs
respiratory compensation stimulated by acidemia and carotid chemoreceptors in the carotid bodies=>produces immediate hyperventilation excess CO2 is expired
EFC volume expansion inhibits isosmotic reabsorption in the proximal tubule
ECF volume contraction stimulates isosmotic reabsorption in the proximal tubule
angiotensin II activated by ↓ in ECF volume stimulates Na+-H+ exchange in proximal tubule
contraction alkalosis metabolic alkalosis secondary to ECF volume contraction occurs during loop diuretics/thiazide diuretics treatment can be caused by vomiting treatment: infusing isotonic NaCl
respiratory acidosis Pco2 is ↑ => ↑ generation of H+ for secretion by Na+-H+ exchanger=> ↑ reabsorption of HCO3- => ↑ arterial pH (compensation)
respiratory alkalosis Pco2 ↓ => ↓ generation of H+ for secretion by Na+-H+ exchanger =>less HCO3- reabsorbed=> ↓ arterial pH (compensation)
titratable acid H+ excreted with urinary buffers=>phosphate buffer the most important bc high concentration in urine and ideal pK primarily excreted in alpha-intercalated cells of distal tubule and collecting ducts
H+-ATPase mechanism for H+ secretion=>located in alpha-intercalated cell luminal membrane stimulated by aldosterone
H+-K+ ATPase mechanism for H+ secretion=>located in alpha-intercalated cell luminal membrane also responsible for K+ reabsorption
minimum urine pH 4.4
nephron segments that participate in excreting H+ as NH4+ proximal tubule=>secreted by Na+-H+ exchanger (after glutamine metabolism) thick ascending limb of Henle's loop=>exchanged for K+ in Na+-K+-2Cl- cotransporter (participates in countercurrent multiplication) alpha-intercalated cells of collecting d
NH3 diffusion NH3 lipid soluble diffuses from high concentration in medullary interstitial fluid into the lumen of the collecting duct=>combines with H+ to form NH4+=>stuck in lumen bc of diffusion trapping
diffusion trapping of NH4+ NH4+ not lipid soluble=>trapped in collecting duct lumen and excreted
effect of urinary pH on excretion of NH4+ as urinary pH ↓ =>excretion of H+ as NH4+ ↑ underlying mechanism based on diffusion trapping of NH3/NH4+
chronic acidosis adaptive ↑ in NH3 synthesis in proximal tubule ↓ in intracellular pH induces synthesis of enzymes involved in glutamine metabolism what happens in DKA
hyperkalemia effect on NH3 synthesis inhibits NH3 synthesis reduces ability to excrete H+ as NH4+=>causes type 4 renal tubular acidosis
hypokalemia effect on NH3 synthesis stimulates NH3 synthesis ↑ ability to excrete H+ as NH4+
diabetic ketoacidosis cause of metabolic acidosis=> ↑ fixed acid production induces NH4+ synthesis
chronic renal failure cause of metabolic acidosis progressive loss of nephrons=>renal mechanisms for excreting fixed acid severely impaired
acidemia caused by acidosis=> ↑ in H+ concentration in blood=> ↓ in pH
alkalemia caused by alkalosis=> ↓ in H+ concentration in blood=> ↑ pH
metabolic acidosis caused by ↓ in HCO3- concentration=> ↓ pH=>respiratory compensation leads to ↓ Pco2 caused by gain of fixed H+ in the body or loss of HCO3- ex)diarrhea, type 2 renal tubular acidosis
metabolic alkalosis caused by ↑ in HCO3- concentration=> ↑ in pH caused by loss of fixed H+ from body or gain of HCO3-
respiratory acidosis caused by hypoventiliation=>CO2 retention=> ↑ Pco2=> ↓ pH
respiratory alkalosis caused by hyperventilation=>CO2 loss=> ↓ Pco2=> ↑ pH
respiratory/renal compensation rule of thumb if acid-base disturbance metabolic=>compensatory response respiratory=>adjust Pco2 if disturbance respiratory=>compensatory response renal=>adjust HCO3- concentration compensatory response always in same direction as original disturbance
anion gap of plasma based on principle of electroneutrality in all body fluid compartments useful measurement in diagnosis of acid-base disorders=>primarily metabolic acidosis PAG=[Na+]-([HCO3-]+[Cl]) =>normal range 8-16 mEq/L
increased ion gap often seen in several forms of metabolic acidosis=>accumulation of organic anion ex. of metabolic acidosis with ↑ anion gap: DKA, lactic acidosis, salicylate poisoning, methanol poisoning, ethylene glycol poisoning, chronic renal failure
osmolar gap normally little difference between measured and estimated plasma osmolarity
hyperchloremic metabolic acidosis with a normal anion gap seen in few forms of metabolic acidosis=>diarrhea, renal tubular acidosis no organic anion accumulation=> ↓ in HCO3- offset by ↑ in Cl- concentration
metabolic acidosis sequence of events 1)gain of fixed H+ 2)buffering=> ↓ HCO3- concentration=> ↓ pH=>hyperkalemia can occur 3)respiratory compensation=>hyperventilation=> ↓ Pco2 4)renal correction=>excess H+ excreted and new HCO3- synthesized and reabsorbed
metabolic alkalosis sequence of events 1)loss of fixed acid (ex. vomiting)=> ↑ in HCO3- concentration=> ↑ in pH 2)buffering=>hypokalemia can occur 3)respiratory compensation=>hypoventilation=> ↑ Pco2 4)renal correction=>complicated by ECF volume contraction
ECF volume contraction/contraction alkalosis effects maintain metabolic alkalosis 1) ↑ HCO3-reabsorption in proximal tubule 2)stimulates RAA system=>ATII stimulates Na+-H+=>promotes reabsorption of HCO3- 3) ↑ levels of aldosterone stimulate secretion of H+ and reabsorption of HCO3-
respiratory acidosis sequence of events 1) retention of CO2=> ↑ in Pco2=> ↓ pH 2)buffering=>occurs exclusively in ICF (esp. RBC) 3)no respiratory compensation 4)renal compensation=> ↑ H+ secretion and reabsorption of new HCO3-
acute respiratory acidosis renal compensation hasn't started=>pH low
chronic respiratory acidosis renal compensation started=>pH somewhat normalized from ↑ HCO3- concentration
respiratory alkalosis sequence of events 1)loss of CO2=> ↓ in Pco2=> ↑ in pH 2)buffering=>exclusively in ICF (esp. RBCs) 3)no respiratory compensation 4)renal compensation=> ↓ H+ excretion with ↓ synthesis and reabsorption of new HCO3-
acute respiratory alkalosis renal compensation hasn't started=>pH high
chronic respiratory alkalosis renal compensation started=>pH somewhat normalized from ↓ HCO3- concentration
Created by: kphom001



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