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38 Cards in this Set
- Front
- Back
Hydrogen Ion
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a proton freed of its electrons; exists in aqueous solutions as H3O+
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Acid
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proton donor, by donating a proton it dissociates into its conj base and a free proton
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Base
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Proton Acceptor, and by accepting the proton it becomes its conj acid
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What are the conjugat bases for the followin acids:
HCL, H2PO4-, NH4+, H2CO3 |
Cl- + H+
HPO42- + H+ NH3 + H+ HCO3- + H+ |
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Measurement of Acidity
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pH = -log10[H+], Eq/L
[H+] = antilog(9-pH), nEq/L range of pH compatable with life is ab 7.0-7.7 9 refers to nanoequivalents (i.e., 10-9 Eq) |
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Law of Mass Action
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HA <------> A- + H+
At equilibrium: [H+] [A-] K’ = -------------- [HA] The larger the K’ (and the lower the pK’), the stronger the acid, and vice versa. any given rxn can be driven in either direction dep upon the conc of the products on either side of the reaction. Every rxn has an eq constant K. Strong acid will have hi K, weak will have low K. pKa- low if hi K pKa hi if low K |
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Buffers
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Weak acids or bases, when dissolved in water, undergo only partial dissociation--all species of the parent molecule are present.
These solutions can resist changes in acidity (provide buffering capacity). |
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The Carbonic Acid- Bicarbinate Buffer System
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CO2dis + H2O carbonic anhydrase <--> H2CO3 <---> H+ + HCO3-
most imp buffer system [H+] [HCO3-) K’ = ---------------------- [H2CO3] Henderson equation: comes from K eqation 24 PaCO2 [H+] = ----------------------- [HCO3-] carbonic acid is a weak acid. |
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non bicarb buffer systems
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are biologically crucial
are effective buffers because their pKs are near the pH of plasma (pH = 7.4) include: proteins (mainly hemoglobin)- has hi conc histidine which can serve as buffer bc it can donate and accept free H+. phosphates inorganic: major urinary buffers organic: intracellular buffers ammonium NH4+ NH3 + H+ |
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PaCO2 and CO2 balance
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15,000 mmol (300 L) CO2 produced by tissues daily
transported in a nongaseous form to minimize impact on acidity (since PaCO2 determines [H2CO3]) PaCO2 proportional to CO2 production and ind proportional to alveolar ventilation. ventilation under control of central ([H+]) and peripheral chemoreceptors (PaCO2, PaO2) carotid bodies and aortic arch |
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Transportation of CO2 from peripheral tissues to lungs
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CO2 in muscle cell diffuses out of cell into tissues down conc gradient. Some diffuses directly into plasma (sm amt). Some CO2 diffuses directly into RBCs taken up by Hb making carboxy Hb. Most of it combines with H2O catalyzed by carbonic anhydrase making carbonic acid, then dissociates into bicarb and free protons which are neutralized by Hb (histidine buffer). Bicarb that is left will diffuse out of plasma in exchange for Cl to maintain electrical neutrality. When CO2 and bicarb gets to lung reverse rxns occur. Free CO2 if liberated and ventilated off
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Sources of acid and alkali gain and losses
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Dietary intake (acid gain)
Metabolism / catabolism (acid gain) Gastrointestinal H+ or HCO3- loss Renal HCO3- filtration (potential loss) nearly 100% of bicarb is filtered Renal HCO3- reabsorption and generation Renal H+ secretion |
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H+ load must be buffered
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plasma HCO3- ab 50%
plasma and interstitial proteins ab 1% intracellular and bone proteins, phosphates, HCO3 and bone carbonate- up to 50% |
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Renal Regulation of H+ balance
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The kidneys must:
conserve all existing HCO3- generate new HCO3- to repay alkali deficit secondary to 1 mEq/kg/d of H+ input |
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Proximal nephron and H+ balance
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reclaims ~ 90% of filtered HCO3-
generates NH3 generates “new” HCO3- via H+ secretion and NH4+ production |
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How H+ ions get from blood stream to urin
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H+ can get from blood to prox tub epith cells fairly easily down an electrochemical gradient. To go from epith cells to lumen must go against pH and electrochem gradient. H+ must have an active transport process to get them into the urin.
H+ are secreted out of the cell into the urinary space. They combine with bicarb filtered thru the glom- to form carbonic acid and can dissociate into CO2 and H2O via carbonic anhydrase on the brush border membrane of the prox tub epith cell. H2O excreted in urine, CO2 diffuses back into cell (down conc grad) CO2 then combined with water to form Carbonic acid and dissoc partially into bicarb and protons, protons can be resecreted bicarb goes down conc gradient into blood. H+ secretion occurs via an active process, no pump on apical side of tubular epith cell, they are exchanged for K, Na K ATP ase drives this exchange. Secondary active transport. Bicarb diffuses out of cell with Na to maintain electrical nutrality. |
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NH3 / NH4+ production
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proximal nephron also produces ammonia.
In the distal nephron: NH3 neutralizes H+ in the tubular lumen NH4+ in the tubular lumen allows excretion of H+ (secreted by the α-intercalated cells, via H+/K+ ATP-ase) Generated HCO3- is transported into the blood glutamine is brken down into ammonia plus glutamate, then ammonia travels to distal nephron where it titrates H+ ions present within urinary space via secretory process and by the H+ from the intercalated cells. allows urinary tract to excrete H+ only having min impact on urinary pH. no ammonia would cause super acidic pH bicarb is also produced from the breakdown of glutamine |
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Distal Nephron and H+ balance
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reabsorbs any remaining HCO3- (approx the other 10 % prox tubule didnt get)
generates “new” HCO3- via H+ secretion and titration of urinary buffers (HPO43-, NH3) |
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Blood Gas Measurements
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Arterial measurement usually necessary, especially regarding oxygenation / respiratory status. (venous gives us an idea of waste products dumped into blood stream) Arterial blood has been filtered etc
Compared to arterial measurements, venous blood gases have the following characteristics: pH 0.02-0.04 units lower PaCO2 6-8 mmHg higher HCO3 1-2 mEq/L higher PaO2 approximately 60 mmHg lower Avoid excessive amounts of heparin (lowers PaCO2 by dilution). often hep in tubes to prevent clotting.- thnk of this if labs dont match up to clinical scenario Keep specimen on ice (continued anaerobic glycolysis by RBCs and WBCs will lower pH at room temperature). |
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Steps in the interpretation of acid-base disorders:
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Is the pH acidemic or alkalemic? This indicates the direction of the predominant acid-base disorder. normal ph is 7.4, pCO2 is 40 and bicarb is 24
Is the abnormal pH due to changes in the PaCO2 (respiratory component) or HCO3- (metabolic component)? -if pH and bicarb move in same direction = metabolic process, if opp = resp process Is appropriate compensation present? use rule of 7's What is the anion gap? |
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acidosis vs acidemia
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acidosis- process that if not compensated for will result in overall state of acidity
acidemia- refers to state of organism as a whole- or the blood stream. acidemic- lo pH blood stream poss to have metaolic acidosis and resp alkalosis, may have acidemia |
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Rule of 7's
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Place disorders in ABC order, then list- first formula is winter's doesnt follow rule
Disorder Correct compensation ( 2) Metabolic acidosis pCO2 = 1.5 x HCO3 + 8 Metabolic alkalosis 10 HCO3 = _6__ pCO2 Respiratory acidosis, acute 10 pCO2 = _1__ HCO3 Respiratory acidosis, chronic 10 pCO2 = _3.5 HCO3 Respiratory alkalosis, acute 10 pCO2 = _2__ HCO3 Respiratory alkalosis, chronic 10 pCO2 = _5__ HCO3 |
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Calculation of Anion Gap
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Cations = Na+, K+ (measured)
Ca2+, Mg2+, NH4+, proteins+ (unmeasured) Anions = Cl-, HCO3- (measured) SO42-, PO43-, alb-, organic acids- (unmeasured) SO: Na - (CL and HCO3) |
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Differential Dx of Metabolic Acidosis
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metabolic acidosis is only acid base disorder that can lead to incr anion gap
Elevated anion gap (MUDPILES): >12 Methanol-formic acid Uremia Diabetic ketoacidosis Paraldehyde, propylene glycol Iron, isoniazid, inhalants, idiopathic Lactic acidosis Ethylene glycol Salicylates Normal anion gap: Loss of bicarbonate (GI) -Diarrhea, ileal loop bladder Loss of bicarbonate or failure of acid secretion (renal) -Renal tubular acidosis, adrenal insufficiency, carbonic anhydrase inhibitors Addition of hydrochloric acid -E.g., ammonium chloride, arginine-HCl, lysine-HCl |
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Systemic effects of Metabolic Acidosis
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Cardiovascular
Hypotension, arrhythmia Pulmonary Hyperventilation, reduced O2 delivery Gastrointestinal Hypomotility, decreased absorption Renal Na+, K+ wasting; uric acid retention Metabolic Protein catabolism; altered catecholamine, aldosterone, PTH, vitamin D production and response |
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Salicylate toxicity
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only drug toxicity that causes metabolic acidosis and resp alkalosis, not compensatory- mixed disorder
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95% of all metabolic acidoses will have
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increased anion gap. 5% will be normal and most of those will be from diarrhea
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Correction of metabolic acidosis
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Goals: ph>7.2 and bicarb >12
Calculate HCO3 deficit or H+ surplus: (measured bicarb from art bg) (HCO3 desired - HCO3 measured) x .5 x body weight kg administrate alkali to titrate one hal of H+ surplus over 6-12 hrs and the remainder over the next 12 -24 hrs (usu given IV NAHCO3) Can give up to 150 mEq of NaHCO3 per liter of D5W (5% dextrose in water solution) |
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Metabolic Alkalosis (factors which lead to initiation and maintenance):
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net loss of hydrogen ions (H+) via GI tract (e.g., vomiting, nasogastric drainage) or kidney (e.g., hyperaldosteronism)
alkali loading (usually requires concomitant renal insufficiency; otherwise would need 1000 mEq HCO3-/day in normal individuals) volume contraction with disproportionate loss of chloride (e.g., diuretics) losing Cl so resorbing bicarb increased HCO3- absorption by the kidney: sodium avidity coupled with diminished availability of chloride mineralocorticoid excess will not see-idiopathic chloride-resistant alkalosis (usually seen with severe potassium depletion) |
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Metabolic Alkalosis: Chloride responsive
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(Urine Cl- < 25 mEq/L)
Gastric fluid losses (vomiting, NG suction) Diuretic therapy (post-chronic use)- cl deficient from diuretics and body is trying to compensate after being taken off Post-hypercapneic state- resp acidosis, kidneys retaining bicarb to compensate, then you ventilate them and they no longer have resp acidosis, you are left with metabolic alkalosis. Low chloride intake (rare) Stool losses (rare) Congenital chloridorrhea, villous adenoma non renal problem bc low cholride, kidneys trying to dump bicarb |
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Metabolic Alkalosis: Chloride Resistant
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Urine Cl- > 40 mEq/L)
Primary hyperaldosteronism- Na is resorbed and Cl is too Bartter’s syndrome-defect in Na K CL channel in thick ascending limb (same as loop diur) Gitelman’s syndrome- defect in same ion channel in distal tubule (same as thiazide diuretics) Cushing’s syndrome Renal failure (with bicarbonate loading) Idiopathic |
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Systemic Effects of Metabolic Alkalosis
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Cardiovascular
Hypotension, arrhythmia Pulmonary Hypoventilation Central Nervous System Obtundation, delirium, decreased seizure threshold Neuromuscular Tetany Metabolic Hypokalemia, hypophosphatemia, decreased ionized calcium, increased anaerobic glycolysis and lactic acid production, leftward shift of oxyhemoglobin curve |
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Management of Metabolic Alkalosis
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Goals: pH <7.6, bicarb < 45
Chloride-responsive alkalosis: prevention: Cl- and K+ supplements H2-antagonists, proton pump inhibitors antiemetics correction: NaCl, KCl administration acetazolamide acidifying-agents (e.g., HCl--rarely used) Chloride-resistant alkalosis: treat underlying defect (primary hyperaldosteronism, Cushing’s syndrome, etc.) ancillary measures: Na+ restriction, large amounts of K+ supplementation |
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Diff Dx of Resp Acidosis
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anything causing hypoventilation
Acute Airway obstruction (aspiration, bronchospasm, laryngospasm, obstructive sleep apnea) Circulatory collapse (cardiac arrest, pulmonary embolism) CNS depression (medications, anesthesia, stroke, central sleep apnea) Ventilatory restriction (pneumothorax, pneumonia) Iatrogenic (mechanical ventilation, bronchoscopy) Chronic Airway obstruction (chronic obstructive pulmonary disease) CNS depression (medications, stroke, central sleep apnea, brain tumor, obesity-hypoventilation syndrome) Neuromuscular impairment (muscular dystrophy, multiple sclerosis, amyotrophic lateral sclerosis, poliomyelitis) Ventilatory restriction (kyphoscoliosis, hydrothorax, interstitial fibrosis, morbid obesity) |
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Systemic Effects of Resp Acidosis
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Cardiovascular
Hypertension, arrhythmia Central Nervous System Increased cerebral blood flow and intracranial pressure Obtundation, confusion Seizures Metabolic Altered catecholamine production and response, increased renin and aldosterone production, increased renal sodium excretion |
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Management of Respiratory Acidosis
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Acute respiratory acidosis:
Treat underlying cause. Treat hypoxemia. HCO3- usually not needed, though may improve bronchodilatory and cardiovascular response to epinephrine (can actually worsen pCO2, however). Usually takes PaCO2 100 mmHg to produce pH <7.10. Chronic respiratory acidosis: treatment of chronic obstructive pulmonary disease (COPD) Look for complicating metabolic alkalosis. Rapid reduction of PaCO2 may produce life-threatening alkalemia (seizures, arrhythmias). Remember: Whenever PaCO2 HCO3-, pH will be > 7.60. |
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Clinical manifestations of Respiratory Alkalosis
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Acute hypocapnia:
paresthesias of extremities chest tightness circumoral numbness lightheadedness, seizures cardiovascular: pulse, SVR, CO, BP, cerebral blood flow Chronic hypocapnia: usually asymptomatic cardiovascular: BP, cerebral blood flow returns to normal, renal blood flow ECF volume (by 10-25%) hematocrit |
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Management of Resp Alkalosis
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Rarely life-threatening; usually a diagnostic, not a treatment problem
Exclude metabolic acidosis and/or hypoxemia before using paper bag in anxiety-hyperventilation syndrome. Consider respiratory alkalosis when arrhythmias occur in mechanically-ventilated patients. |