Acid-Base Physiology Notes

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Osmosis High-Yield Notes

This Osmosis High-Yield Note provides an overview of Acid-Base Physiology essentials. All Osmosis Notes are clearly laid-out and contain striking images, tables, and diagrams to help visual learners understand complex topics quickly and efficiently. Find more information about Acid-Base Physiology:

Acid-base map and compensatory mechanisms

Metabolic acidosis

Metabolic alkalosis

Respiratory acidosis

Respiratory alkalosis

NOTES NOTES ACID-BASE PHYSIOLOGY ACID-BASE MAP & COMPENSATORY MECHANISMS osms.it/acid-base_map_and_ compensatory_mechanisms ACID-BASE MAP ▪ Main physiologic pH factors ▫ HCO3−, CO2 ▪ Acid-base map ▫ HCO3− concentration (x-axis)/CO2 partial pressure (y-axis) diagram ▪ Henderson–Hasselbalch equation ▫ pH = 6.1+log ([HCO3-]/0.03PCO2) ▫ PCO2 is partial pressure of CO2 ▪ Diagonal lines ▫ Drawn where each point on graph has same pH (isohydric lines) ▪ Drawing lines for pH = 7.35, pH = 7.45 ▫ Comprises area where all HCO3−, CO2 combinations correspond to “normal” pH pH out of normal range ▪ One of two ways ▫ Acidosis: pH ↓ 7.35, enters top-left portion of map ▫ Alkalosis: pH ↑ 7.45, enters bottomright portion of map ▪ One of two reasons ▫ Respiratory: PCO2 too ↑/↓ ▫ Metabolic: [HCO3−] too ↑/↓ COMPENSATORY MECHANISMS ▪ Simple acid-base disorder ▫ Single problem changing pH ▪ Mixed acid-base disorder ▫ Multiple problems compounding/ cancelling out Multiple compensatory mechanisms ▪ Respiratory acidosis ▫ Kidneys retain more HCO3− ▪ Respiratory alkalosis ▫ Kidneys excrete more HCO3− ▪ Metabolic acidosis ▫ Lungs blow off CO2 (deeper, more frequent breaths) ▪ Metabolic alkalosis ▫ Lungs retain CO2 (shallower, less frequent breaths) OSMOSIS.ORG 1
Figure 8.1 An acid-base map shows the relationship between pH, bicarbonate concentration, and partial pressure of carbon dioxide in respiratory and metabolic acidosis or alkalosis, and how these values are adjusted when there is renal or respiratory compensation. The accompanying tables depict the changes in PCO2, [HCO3-, and pH associated with respiratory/metabolic acidosis/alkalosis. BUFFERING & HENDERSONHASSELBALCH EQUATION osms.it/buffering_&_henderson-hasselbalch_equation BUFFERING ▪ Buffers: pH change-resisting solutions ▪ Can comprise ▫ Acidic buffer: weak acid, conjugate base ▫ Basic buffer: weak base, conjugate acid ▪ Weak acids, bases do not dissociate fully → equilibrium formation (e.g. HA ⇄ H+ + A or B + H2O ⇄ BH+ + OH-) ▫ Le Chatelier’s principle: equilibriums move forward/backward, balance products/reactants’ gain/loss Resisting pH change ▪ Acidic, basic buffers resist all pH changes ▪ Strong base added to acidic buffer ▫ OH- ions react with H+ ions → ↑ pH ▫ H+ ion loss shifts acid’s equilibrium → 2 OSMOSIS.ORG more H+ ions created, resists pH change ▪ Strong acid added to acidic buffer ▫ H+ ions would ↓ pH ▫ Shifts acid equilibrium in opposite direction → conjugate base reacts with H+ ions → resists pH change ▪ Strong acid added to basic buffer ▫ H+ ions would ↓ pH, also reacts with excess OH- ions ▫ OH- loss ions shifts base’s equilibrium → ↑ OH ion creation → resists pH change ▪ Strong base added to basic buffer ▫ OH- ions would react with H+ ions to ↑ pH ▫ Shifts base’s equilibrium in opposite direction → conjugate acid reacting with OH- ions → resists pH change
Chapter 8 Renal System HENDERSON-HASSELBALCH EQUATION ▪ Henderson–Hasselbalch equation determines buffer’s pH ▫ pH = pK + log([A-]/[HA]) ▪ This is derived ▫ Weak acid equilibrium: equilibrium constant K → K = [H+][A-]/[HA] ▫ Solving for H+ → [H+] = K([HA]/[A-]) ▫ Negative log of both sides → pH = pK + log([A-]/[HA]) ▪ Note ▫ If [A-] = [HA], then pH = pK PHYSIOLOGIC pH & BUFFERS osms.it/physiologic-pH-and-buffers PHYSIOLOGIC pH ▪ Measures balance between acids, bases in body ▪ pH: -log[H+] ▫ [H+]: hydrogen ion concentration ▪ Ideal: [H+] = 40 x 10-9 Eq/L = 40 nEq/L → pH = 7.4 (slightly alkaline) ▫ Acidemia: pH < 7.4 ▫ Alkalemia: pH > 7.4 ▪ ↑ [H+] → ↓ pH (negative sign in equation) ▪ pH, [H+] has logarithmic (not linear) relationship PHYSIOLOGIC BUFFERS ▪ Physiologic buffers occur naturally in body ▫ Maintains stable pH between 7.35–7.45 Bicarbonate buffer system ▪ Extracellular, most important ▪ Acidic buffer: carbonic acid (H2CO3) ▪ Conjugate base: bicarbonate ion (HCO3-) ▪ Carbonic acid can be formed from H2O, CO2 (carbonic anhydrase catalyzes reaction) ▪ Equilibrium reaction ▫ H2O + CO2 ⇄ H2CO3 ⇄ H+ + HCO3▪ Excess ▫ CO2 blown off by lungs ▫ HCO3- eliminated by kidneys Phosphate buffer system (extracellular) ▪ Acidic buffer: dihydrogen phosphate (H2PO4- ) ▪ Conjugate base: monohydrogen phosphate (HPO42-) ▪ Equilibrium reaction ▫ H2PO4- ⇄ H+ + HPO42Protein buffer system (extracellular) ▪ Protein amino acids may have exposed carboxyl (-COOH), amine (NH2) groups ▪ Results in separate acidic (-COOH ⇄ -COO- + H+ ), basic (-NH2 + H+ ⇄ -NH3+) buffers Intracellular buffer systems ▪ Hemoglobin: buffer in red blood cells (selectively binds H+ ions) ▪ Organic phosphates (e.g. ATP) can buffer similarly OSMOSIS.ORG 3
PLASMA ANION GAP osms.it/plasma-anion-gap PLASMA ANION GAP ▪ Cations, anions coexist within plasma ▫ To keep plasma electrically neutral sum of cation charges must equal sum of anion charges ▪ Not all cation, anion concentrations can be measured ▫ Often gap (“plasma anion gap”) between measured cation charges (mainly Na+), smaller measured anion charges sum (mainly Cl−, HCO3- ) ▪ Plasma anion gap range: 3–11 mEq/L ▫ High gap → high unmeasured anion number ▫ Low gap → low unmeasured anion number ▪ Unmeasured anions include anion component of several organic acids, negatively charged plasma proteins (e.g. albumin) DIAGNOSTIC TOOL ▪ Plasma anion gap serves as useful diagnostic tool ▫ Organic anions aren’t measured → plasma anion gap ↑ ▫ Organic acids include lactic acid, ketoacids, oxalic acid, formic acid, hippuric acid ▪ Some cases (e.g. diarrhea/renal tubular acidosis) ▫ Kidneys reabsorb more Cl− ions → plasma anion gap remains normal (hyperchloremic metabolic acidosis) High gap may suggest ▪ Unmeasured anion buildup (e.g. hyperphosphatemia, hyperalbuminemia) ▪ Metabolic alkalosis (high pH triggers albumin to release H+ ions → negative charge ↑ on unmeasured albumin molecules) Low gap may suggest ▪ Unmeasured anion ↓ (e.g. hypoalbuminemia) ▪ Unmeasured cation ↑ (rarely) ▫ E.g. hyperkalemia, hypercalcemia, hypermagnesemia Metabolic acidosis ▪ Organic acids’ H+ ions convert HCO3- into H2CO3 THE ROLE OF THE KIDNEY IN ACID-BASE BALANCE osms.it/kidney_and_acid-base_balance KIDNEYS' FUNCTION ▪ Kidneys maintain acid-base balance in two ways ▫ HCO3- reabsorption: urine into blood ▫ H+ secretion: blood into urine 4 OSMOSIS.ORG ▪ Kidneys consist of nephrons ▫ Each has glomerulus (capillaries clump) ▪ During filtration, plasma leaves glomerulus entering renal tubule (consists of proximal convoluted tubule, loop of Henle, distal convoluted tubule)
Chapter 8 Renal System ▪ Tubules lined with brush border cells (apical surface facing tubular lumen, basolateral surface facing peritubular capillaries) HCO3- reabsorption ▪ Primarily in proximal convoluted tubule ▫ Na+ ions exchanged for H+ ions through apical surface → bind with HCO3- → form H2CO3 ▫ Carbonic anhydrase type 4 splits H2CO3 into H2O, CO2 ▫ H2O, CO2 diffuse across membrane ▫ Carbonic anhydrase type 2 recombines them into H2CO3 ▫ H2CO3 dissolve into H+,HCO3- ▫ Sodium/chloride bicarbonate cotransporters on basolateral surface snatch up HCO3- , nearby sodium/ chloride ion, moving both into blood H+ secretion ▪ Primarily in proximal convoluted tubule ▫ Sodium-hydrogen countertransport: H+ ions exchanged for Na+ ions through apical surface ▫ Another mechanism in distal convoluted tubule, collecting ducts involving alphaintercalated cells ▫ Chemical buffers (ammonia, phosphate) prevent urine pH from dropping too low in tubules (< 4.5) METABOLIC ACIDOSIS osms.it/metabolic-acidosis METABOLIC ACIDOSIS ▪ HCO3 ion reduction → blood pH ↓ to < 7.35 - TYPES ▪ Distinguished by high/normal anion gap ▫ Measured cation concentration ▫ E.g. Na+ ions, minus measured anion concentration (e.g. Cl−, HCO3− ions) High anion gap ▪ H+ ions from organic acids convert HCO3- to H2CO3 ▫ ↓ HCO3− ion concentration (measured in anion gap), ↑ organic anion concentration (not measured) ▫ Naturally-occurring organic acids: e.g. lactic acid production (lactic acidosis), ketoacid production (diabetic ketoacidosis), excessive uric, sulfurcontaining acid retention (chronic renal failure) ▫ Ingestible organic acids: e.g. oxalic acid (antifreeze), formic acid (methanol), hippuric acid (toluene) Normal anion gap ▪ HCO3- lost in various ways, Cl− ↑ prevents anion gap change (hyperchloremic metabolic acidosis) ▪ Possible causes ▫ Diarrhea, renal tubular acidosis REGULATORY MECHANISMS ▪ Body has several regulatory mechanisms to reverse ↓ pH ▫ H+ ions moved from blood into cells, exchanged for K+ ions (may cause hyperkalemia); if organic anions present, can enter cells with H+ ions → K+ ions are not released ▫ Chemoreceptors fire more in low pH → ↑ respiratory rate, breath depth → ↑ ventilation, CO2 movement out of body ▫ H+ ions excreted by kidneys → HCO3reabsorbed (with normal renal function) OSMOSIS.ORG 5
Figure 8.2 Illustration depicting the two kinds of metabolic acidosis: high anion gap (where H+ from organic acids converts HCO3- to H2CO3), and normal anion gap (where a Cl- increase maintains the normal anion gap). METABOLIC ALKALOSIS osms.it/metabolic-alkalosis METABOLIC ALKALOSIS ▪ HCO3 ion gain → blood pH ↑ > 7.45 - CAUSES ▪ Associated with direct HCO3- ion gain/ loss of H+ ion loss (thus → HCO3- ion gain), usually both ▪ Hypokalemia ▫ Metabolic alkalosis cause ▫ May also be result of other root causes Excessive H+ ion loss causes ▪ Vomiting (gastric secretions acidic) ▫ Also causes HCO3- ion buildup in pancreas (would normally neutralize gastric secretions) ▪ Abnormal renal function ▫ E.g. adrenal tumors secrete aldosterone → distal convoluted tubule dumps H+ ions, reabsorbs HCO3- ions Excessive HCO3- ion gain causes ▪ ↑ kidney reabsorption ▫ Volume contraction with loop/thiazide 6 OSMOSIS.ORG diuretics/severe dehydration cases (contraction alkalosis) ▪ Hypokalemia ▫ Diarrhea/diuretic use, triggering reninangiotensin-aldosterone mechanism → distal convoluted tubule dumps H+ ions, reabsorbs HCO3- ions ▪ HCO3- ion ingestion ▫ E.g. excessive antacid use (NaHCO3) REGULATORY MECHANISMS ▪ Body has regulatory mechanisms to reverse ↑ pH ▫ K+ ions move from blood into cells → exchanged for H+ ions (may contribute to hypokalemia) ▫ Chemoreceptors fire less in high pH → ↓ respiratory rate, breathing depth → ↓ ventilation, CO2 retention ▫ HCO3- ions excreted by kidneys → H+ reabsorbed (normal renal function)
Chapter 8 Renal System Figure 8.3 Illustration summarizing the definition and causes of metabolic alkalosis. RESPIRATORY ACIDOSIS osms.it/respiratory-acidosis RESPIRATORY ACIDOSIS ▪ CO2 gain → blood pH ↓ < 7.35 CAUSES ▪ Ventilation ↓ (frequency, breath depth) for variety of reasons → lungs blow off too little CO2 ▫ Stroke/medication overdose/etc. → respiratory-center abnormality in brainstem ▫ Obesity, trauma, neuromuscular disorders (myasthenia gravis), etc. → respiratory muscle-contraction failure ▫ Airway obstruction ▫ Alveoli damage (chronic obstructive pulmonary disease); alveoli fluid buildup (pneumonia); fluid buildup between alveoli, capillary walls (pulmonary edema) → impaired gas exchange between alveoli, capillary REGULATORY MECHANISMS ▪ Body has several regulatory mechanisms to reverse pH ↓ ▫ Low pH → chemoreceptors fire more → attempted ↑ in respiratory rate, breathing depth → ↑ ventilation ▫ H+ ions bind to basic protein molecules (mainly exposed hemoglobin -NH2 groups), although in small amounts ▫ H+ ions excreted by kidneys, HCO3reabsorbed OSMOSIS.ORG 7
RESPIRATORY ALKALOSIS osms.it/respiratory-alkalosis RESPIRATORY ALKALOSIS ▪ CO2 loss → blood pH ↑ > 7.45 CAUSES ▪ Ventilation ↑ (frequency, breath depth) for variety of reasons → lungs blowing off too much CO2 ▫ Respiratory-center abnormality in brainstem ▫ Pneumonia, pulmonary embolism, etc. → low oxygen levels (hypoxia) ▫ Anxiety, panic attacks, sepsis, salicylates overdose 8 OSMOSIS.ORG ▫ Incorrectly-set ventilator → medical intervention REGULATORY MECHANISMS ▪ Body has several regulatory mechanisms to reverse pH ↑ ▫ High pH → chemoreceptors fire less → attempted ↓ in respiratory rate, breathing depth → ↓ ventilation ▫ H+ ions released from acidic protein molecules (mainly exposed hemoglobin -COOH groups), although in small amounts ▫ HCO3- ions excreted by kidneys, H+ are reabsorbed

Osmosis High-Yield Notes

This Osmosis High-Yield Note provides an overview of Acid-Base Physiology essentials. All Osmosis Notes are clearly laid-out and contain striking images, tables, and diagrams to help visual learners understand complex topics quickly and efficiently. Find more information about Acid-Base Physiology by visiting the associated Learn Page.