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Renal > 13 Acid Base 2: Clinical Disorders > Flashcards

13 Acid Base 2: Clinical Disorders Flashcards

1
Q

Terminology

  • Acidosis
  • Alkalosis
  • Acidemia
  • Alkalemia
  • Caution
A
  • Acidosis
    • A pathophysiologic process that decreases blood pH
  • Alkalosis
    • A pathophysiologic process that increases blood pH
  • Acidemia
    • Arterial blood pH < 7.36
  • Alkalemia
    • Arterial blood pH > 7.44
  • Caution
    • Acidemia can’t be present w/o acidosis
    • Alkalemia can’t be present a/o alkalosis
    • But acidosis & alkalosis can exist at any blood pH if >1 disturbance is present
    • Acidosis & alkalosis can occur simultaneously, in which case it could be unclear what the pH would be
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2
Q

Terminology

  • Metabolic disturbance
  • Respiratory disturbance
  • Compensation
  • Simple disturbance
  • Mixed disturbance
A
  • Metabolic disturbance
    • An acidosis or alkalosis resulting from a primary change in the serum bicarb conc
  • Respiratory disturbance
    • An acidosis or alkalosis resulting from a primary change in the PCO2
  • Compensation
    • The physiologic metabolic (renal) & respiratory changes to return the pH toward normal i.r.t. a primary acidosis or alkalosis
    • Does not return pH completely to normal
    • Time course
      • Buffering: minutes to 6 hours
      • Respiratory: minutes to 12 hours
      • Metabolic: 24 to 72 hours
  • Simple disturbance
    • A single acid-base process (acidosis or alkalosis) & its expected compensation are present
  • Mixed disturbance
    • _>_2 primary acid base disturbances are present
    • Arterial blood pH will depend on the direction & magnitude of the disturbances
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3
Q

Primary acid base disturbances

  • Metabolic acidosis
    • Primary process
    • Compensation
  • Metabolic alkalosis
    • Primary process
    • Compensation
  • Respiratory acidosis
    • Primary process
    • Compensation
  • Respiratory alkalosis
    • Primary process
    • Compensation
A
  • Metabolic acidosis
    • Primary process: ↓ [HCO3-]
    • Compensation: ↓ PCO2
  • Metabolic alkalosis
    • Primary process: ↑ [HCO3-]
    • Compensation: ↑ PCO2
  • Respiratory acidosis
    • Primary process: ↑ PCO2
    • Compensation: ↑ [HCO3-]
  • Respiratory alkalosis
    • Primary process: ↓ PCO2
    • Compensation: ↓ [HCO3-]
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4
Q

Metabolic acidosis

  • Results from…
  • Categorized on the basis of…
  • Anion gap (AG)
    • AG =
    • Made up of…
    • Normal AG
A
  • Results from…
    • Depletion of body bicarb buffers
  • Categorized on the basis of…
    • The anion that accumulates replacing the bicarb into hyperchloremic metabolic acidoses & anion gap metabolic acidosis
  • Anion gap (AG)
    • AG = [PNa] - [Cl-] - [HCO3-]
    • Made up of…
      • Measured cations: K, Ca, Mg
      • Unmeasured anions: anionic proteins, phosphates, sulfates, organic anions
    • Normal AG = 10 +/- 2 meq/L
      • 2/3 of the normal AG is accounted for by dissociated carboxyl groups on albumin
      • –> normal AG needs to be adjusted in the setting of hypoalbuminemia
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5
Q

Hyperchloremic metabolic acidosis

  • General
  • Results from…
  • Impaired renal acid excretion
  • Renal bicarb loss
  • GI bicarb loss
  • Acid (H ion) gain
A
  • General
    • Normal AG
    • Increased Cl
    • Decreased serum bicarb
      • Addition of HCl –> primary bicarb loss
  • Results from…
    • Impaired acid excretion
    • increased bicarb loss
    • H ion gain
  • Impaired renal acid excretion
    • Renal failure
    • Distal renal tubular acidosis
      • Classic / hypokalemic (type I)
      • Hyperkalemic (type IV)
  • Renal bicarb loss
    • Proximal renal tubular acidosis (type II)
    • Carbonic anhydrase inhibitors
    • Partially treated diabetic ketoacidosis
      • Due to urinary excretion of β-hydroxybutyrate and acetoacetate, which are no longer available to be metabolized to regenerate bicarb once the ketogenesis is suppressed
  • GI bicarb loss
    • Diarrhea
    • Pancreatic drainage
    • Ureteral diversion
  • Acid (H ion) gain
    • Hyperalimentation sol’ns
    • Ammonium chloride ingestion
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6
Q

Anion gap metabolic (“delta”) acidosis

  • General
  • Results from…
  • Causes (increased anions, *+)
    • Diabetic ketoacidosis*
    • Alcoholic ketolactic acidosis*
    • Lactic acidosis*
    • Renal failure
    • Toxins
      • Methanol
      • Ethylene glycol
      • Salicylate
      • Paraldehyde
A
  • General
    • Normal Cl
    • Increased AG (>20 meq/L)
      • Always represents a metabolic acidosis regardless of pH or serum bicarb
    • Decreased serum bicarb
      • Addition of strong organic acid (ex. lactic acid, beta-hydroxybuteric acid) + anion accumulation –> bicarb loss
  • Results from…
    • Excessive production, ingestion, or retention of a strong acid or compound metabolized to a strong acid
  • Causes (increased anions)
    • Diabetic ketoacidosis: β-hydroxybutyrate, acetoacetate
      • Insulin deficiency –> abnormal production of ketoacids
    • Alcoholic ketolactic acidosis: β-hydroxybutyrate, acetoacetate, lactate
      • Fasting after binge drinking –> low glucose –> decreased insulin secretion & ketosis
    • Lactic acidosis: lactate
      • Increased tissue lactate production
        • Congenital enzymatic defects
        • Tissue hypoperfusion or hypoxia
        • Enhanced metabolic rate
      • Decreased lactate utilization
        • Hypoperfusion
        • Liver disease
        • Ethanol intoxication
    • Renal failure: phosphate, sulfate, organic anions
    • Toxins
      • Methanol: formate, lactate
      • Ethylene glycol: oxylate, glycolate
      • Salicylate: ketoacids, lactate, salicylate
      • Paraldehyde: organic anions
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7
Q

Renal tubular acidosis:
Proximal renal tubular acidosis (type II RTA)

  • General
  • Characterized by…
  • Hypokalemia results from…
  • Proximal RTA in children vs. adults
  • Proximal RTA is often accompanied by…
  • Iatrogenic RTA
A
  • General
    • Defect in proximal tubular bicarb reabsorption
  • Characterized by…
    • Impaired H secretion in the proximal nephron
    • Decreased threshold for bicarb reclamation
      • Bicarb > threshold –> renal bicarb wasting
      • Bicarb < threshold –> conserved bicarb + max urinary acidification (urine pH < 5.3)
  • Hypokalemia results from…
    • Increased distal K secretion
      • Stimulated by hyperaldosteronism associated w/ mild chronic volume depletion
    • Increased distal delivery of bicarb
  • Proximal RTA in children vs. adults
    • Children: associated w/ congenital metabolic defects
    • Adults: secondary to acquried proximal tubular damage
      • Ex. heavy metal exposure, multiple myeloma
  • Proximal RTA is often accompanied by other proximal tubular transport defects
    • Renal glycosuria
    • Phsophate wasting
    • Aminoaciduria
    • Hypouricemia (Fanconi syndrome)
  • Iatrogenic RTA
    • May result from therpay w/ carbonic anhydrase inhibitors
    • Ex. acetazolamide
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8
Q

Renal tubular acidosis:
Classic distal renal tubular acidosis (type I RTA)

  • General
  • Results from either…
  • May be associated w/…
  • Types
  • Molecular defects that may account for this
A
  • General
    • Defect in distal tubular H gradient
      • Urine pH can’t be reduced below 5.5
      • Daily acid load can’t be excreted
    • PK is usually low
  • Results from either…
    • Defect in distal nephron H pumps
    • Back-leak of secreted H
  • May be associated w/…
    • Hyperclaciuria
    • Nephrocalcinosis
  • Types
    • Idiopathic
    • Secondary to a wide varity of disturbances
  • Molecular defects that may account for this
    • Impaired H ATPase function
    • Defective bicarb/Cl exchanger
    • Defective cytosolic carbonic anhydrase
    • Back-leak of H
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9
Q

Renal tubular acidosis:
Hyperkalemic distal renal tubular acidosis (type IV RTA)

  • Characterized by…
  • Aldo deficiency / resistance
  • Voltage-dependent defect in H secretion
A
  • Characterized by…
    • Hyperkalemia
    • Hyperchloremic metabolic acidosis
  • Aldo deficiency / resistance
    • Metabolic acidosis associated w/ aldo deficiency or tubular resistance to aldo
    • Primary disturbance: hyperkalemia
      • Suppresses proximal tubular ammoniagenesis
      • Produces metabolic acidosis
    • Urinary acidification is intact
    • Majority of pts have mild renal insufficiency
      • Diabetic nephropathy found in 50-60% of pts
  • Voltage-dependent defect in H secretion
    • Primary defect: CD Na reabsorption
      • Decreases voltage gradient
      • Favors H secretion
      • See hyperkalemia
    • Max urinary acidification is usually impaired
    • May be seen in a variety of disorders including obstructive uropathy
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10
Q

Metabolic acidosis of kidney disease

  • Early stages of CKD
  • Late stages of CKD
A
  • Early stages of CKD: hyperchloremic
    • Primarily due to decreased urinary buffers (impaired ammoniagenesis)
    • Urinary acidification is preserved (urine pH < 5.3)
    • RAAS is normal
    • May be accompanied by hyperkalemia
  • Late stages of CKD: increased anion gap
    • Results form retention of phosphates, sulfates, & organic anions
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11
Q

Urinary anion gap (UAG)

  • Use
  • Calculation
  • In non-renal causes of hyperchloremic acidosis (ex. diarrhea)
  • In the setting of acidemia…
  • UAG vs. ammonium
A
  • Use
    • Assesses the cause of hyperchloremic metabolic acidosis
  • Calculation
    • UAG = [UNa] + [UK] - [UCl]
  • In non-renal causes of hyperchloremic acidosis (ex. diarrhea)
    • Kidney should attempt to compensate by increasing net acid excretion
    • Major mech: increase urinary ammonium excretion
  • In the setting of acidemia…
    • Urinary ammonium production should be stimulated
    • UAG should be < 0
  • UAG vs. ammonium
    • UAG < 0 when ammonium is present & balanced by negatively charged urinary Cl –> non-renal acidosis
    • UAG > 0 when little ammonium is present –> nela acidosis
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12
Q

Respiratory compensation for metabolic acidosis

  • Normal respiratory response to metablic acidosis
  • Winter’s formula
  • Used in pts w/ metabolic acidosis to evaluate…
  • Limitation of respiratory compensation
A
  • Normal respiratory response to metablic acidosis
    • Hyperventilation
    • Compensation begins within minutes but takes 12-24 hr fo rmax response
  • Winter’s formula
    • Calculates expected PCO2 in a simple metabolic acidosis
    • PCO2 = 1.5 * [HCO3-] + 8 +/- 2
  • Used in pts w/ metabolic acidosis to evaluate…
    • Whether th eobserved PCO2 is an appropriate copmensatory repsonse
    • Whether there’s an additional…
      • Respiratory acidosis (PCO2 > predicted)
      • Alkalosis (PCO2 < predicted)
  • Limitation of respiratory compensation
    • PCO2 can’t be lowered below 10 torr
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13
Q

Treatment of metabolic acidosis

  • Primary treatment
  • Acute metabolic acidosis
    • Acute alkali replacement if…
    • Goal of therapy
    • Volume of distribution of bicarb
  • ​Chronic metabolic acidosis
    • Goal of therapy
A
  • Primary treatment
    • Remove underlying cause
    • Alkali replacement: only under certain circumastances of acute & metabolic acidosis
  • Acute metabolic acidosis
    • Acute alkali replacement if pH < 7.1
      • Max respiratory compensation
        • Any further drop in serum bicarb –> decrease pH
      • Myocardial depression becomes a risk
    • Goal of therapy
      • Restore serum bicarb to a safe range (12-15 mmol/L)
      • Full correction could –> overshoot metabolic alkalosis if the pt subsequently metabolizes the unmeasured anions (ex. lactate, ketones) to bicarb
    • Volume of distribution of bicarb = 50% body weight
      • If acute bicarb replacement is indicated, estimate amt administered:
      • HCO3- dose (mmol) = 0.5 * BW (kg) * ( [HOC3-]desired - [HCO3-]actual )
  • ​Chronic metabolic acidosis
    • Goal of therapy
      • Prevent long-term sequelae of metabolic acidosis
        • Bone disease
        • Growth failure
        • Nephorcalcinosis
        • Nephrolithiasis
      • Normalize serum bicarb conc
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14
Q

Metabolic alkalosis

  • Characterized by…
  • Due to…
  • Accompanied by…
  • Kidney excretion of excess bicarb
  • Presence of sustained metabolic alkalosis implies…
  • Pathogenesis takes into account…
A
  • Characterized by…
    • Increased arterial blood pH
  • Due to…
    • Primary elevation in bicarb conc
    • Gain of bicarb or loss of acid/H
  • Accompanied by…
    • Increase in PCO2
  • Kidney excretion of excess bicarb
    • Kidney has a high capacity for excreting excess bicarb
    • When bicarb > tubular max for reabsorption –> excess bicarb excreted in urine
    • Infusion of bicarb only –> transietn alkalosis that corrects itself as soon as the infusion is stopped
  • Presence of sustained metabolic alkalosis implies…
    • Defect in renal bicarb excretion
  • Pathogenesis takes into account…
    • Cause for its generation & maintenance
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15
Q

Generation of metabolic alkalosis

  • Acid loss
    • Renal acid loss
    • GI acid loss
  • Alkali gain
A
  • Acid Loss
    • Renal acid loss
      • Diuretic therapy
      • Mineralocorticoid excess
      • Cushing’s syndrome
      • Severe potassium depletion
      • Bartter’s and Gitelman’s syndromes
      • Liddle’s syndrome
    • GI acid loss
      • Gastric acid loss (vomiting, nasogastric drainage)
      • Chloride diarrhea
  • Alkali gain
    • Bicarbonate administration
    • Milk-alkali syndrome
    • Infusion of organic anions
      • Citrate
      • Acetate
      • Lactate
    • Rapid correction of chronic hypercapnia
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16
Q

Maintenance of metabolic alkalosis

  • Requires…
  • Decreased GFR
  • Increased proximal tubular bicarbonate reclamation
  • Increased hydrogen ion excretion
A
  • Requires impairment of renal bicarb excretion due to…
    • Increased H excretion
    • Increased PT bicarb reclamation
    • Decreased GFR (decreased filtered load of bicarb)
  • Decreased GFR
    • Decreased effective arterial blood volume (pre-renal state)
    • Renal insufficiency
  • Increased proximal tubular bicarbonate reclamation
    • Decreased effective arterial blood volume (pre-renal state)
    • Chloride depletion
  • Increased hydrogen ion excretion
    • Mineralocorticoid excess
    • Hypokalemia
17
Q

Diagnosis of metabolic alkalosis & respiratory compensation

  • Etiology
  • Urine Cl
  • Urine Na
  • Respiratory compensation for metabolic alkalosis
A
  • Etiology
    • Deduced from H&P
  • Urine Cl
    • < 20 mmol/L –> volume depletion
    • > 20 mmol/L –> excess mineralocorticoid effect or Bartter’s syndrome
    • May not be reliable if pt is receiving a diuretic
  • Urine Na
    • Less reliable indicator of volume depletion
    • During the generation or treatment of metabolic alkalosis, the threshold for bicarb may be exceeded
    • Any bicarb spilling into the urine oligates excretion of a cation (ex. Na)
      • May increase urine Na
  • Respiratory compensation for metabolic alkalosis
    • Hypoventilation
    • Not as predictable as hyperventilation for metabolic acidosis
    • limited by hypoxemia (storng respiratory stimulant)
18
Q

Treatment for metabolic alkalosis

  • Stratified based on…
  • Saline-responsive metabolic alkalosis
  • Saline-resistant metabolic alkalosis
A
  • Stratified based on…
    • Responsiveness to intravascular volume expansion
    • If maintenance of metabolic alkalosis is…
      • Volume contraction –> saline responsive
      • Mineralocorticoid excess, hypokalemia, or renal insufficiency –> saline resistant
  • Saline-responsive metabolic alkalosis
    • Volume expansion w/ isotonic saline
      • Re-expansion + Cl repletion –> decrease PT bicarb reabsoprtion –> bicarbonaturia –> decrease serum bicarb
    • If severe K depletion –> correct w/ KCl
    • Responders to saline administration
      • Gastric acid losses
      • Diuretics
      • Cl depletion
      • Post-hypercapnic state
  • Saline-resistant metabolic alkalosis
    • Pts aren’t volume or Cl depleted (high urine Cl conc)
    • If due to minearlocorticoid excess (ex. Conn’s syndrome)
      • Inhibit mineralocorticoid action by aldo antagonist (spironolactone, eplerenone)
      • Ultimate therapy: surgical or chemical ablation of adrenal glands
    • If due to severe hypokalemia (K < 2 mmol/L)
      • K repletion corrects enhanced tubular H excretion, increased ammoniagenesis, & Cl wasting
    • Persistent k wasting
      • Ex. mineralocorticoid excess, Bartter’s or Gitelman’s syndromes, & Liddle’s syndrome
      • Treat w/ K sparing diuretics (ex. amiloride, triamterene)
    • Acetazolamide
      • Inhibits bicarb reabsorption in the PT
19
Q

Respiratory acidosis

  • Primary process
  • Etiologies
  • Renal compensation
    • Acute respiratory acidosis
    • Chronic respiratory acidosis
  • In the presence of chronic hypercapnia
  • Symptoms of acute hypercapnia (CO2 narcosis)
  • Treatment
A
  • Primary process
    • Increase arterial PCO2 (hypercapnia) due to abnormal respiratory function
  • Etiologies
    • Impaired alveolar gas exchange
    • Obstructive airway disease
    • Disorders of the respiratory muscles and chest wall
    • Inhibition of CNS control of ventilation
  • Renal compensation: slow
    • Acute respiratory acidosis
      • Renal compensation doesn’t have a chance to occur
      • Minimal increase in serum bicarb
    • Chronic respiratory acidosis
      • Hypercapnia –> renal acid excretion –> increase serum bicarb by 3.5-5 mmol/L for each 10 torr increase in PCO2
      • Rarely rises to >35-40 mmol/L
      • Max compensation requires 48 hrs
  • In the presence of chronic hypercapnia
    • Major stimulus for ventilation: hypoxemia
    • Oxygen therapy inhibits ventilation & worsens hypercapnia
      • Must be used w/ extreme caution
  • Symptoms of acute hypercapnia (CO2 narcosis)
    • Headache
    • Asterixis
    • Confusion
    • Lethagy
    • Obtundation
  • Treatment
    • Treat underlying problem
    • Severe: mechanical ventilation
20
Q

Respiratory alkalosis

  • Primary process
  • Etiologies
  • Renal compensation
    • Acute respiratory alkalosis
    • Chronic respiratory alkalosis
  • Symptoms & signs
  • Treatment
A
  • Primary process
    • Decreased arteiral PCO2 via hyperventilation
  • Etiologies
    • Hypoxemia
    • Intrapulmonary disease
    • Stimulation of the medullary respiratory center
    • Mechanical ventilation
  • Renal compensation: slow
    • Acute respiratory alkalosis
      • Intracellular bufering –> small decrease in serum bicarb
    • Chronic respiratory alkalosis
      • Increased renal bicarb excretion
      • Decreased serum bicarb by 5 mmol/L for each 10 torr decrease in PCO2
  • Symptoms & signs
    • Lightheadedness
    • Parethesias
    • Carmps
    • Carpopedal spasm
    • Seizures (extreme)
  • Treatment
    • Treat underlying disorder
    • If acute hyeprventilation related to anxiety: rebreathe into a paper bag
21
Q

Mixed disturbances

  • Simple disturbance
  • Mixed disturbance
  • Additivenes of mixed disturbances
A
  • Simple disturbance
    • Primary change in HCO3 or PCO2 accompanied by a corresponding compensatory change in the other species
  • Mixed disturbance
    • >1 primary acid-base disturbance is present
      • Ex. pt w/ metabolic acidoses from diabetic ketoacidosis may also have respiratory acidosis from pneumonia
    • Each disturbance interferes w/ the compensation for the other
      • pH is lower than expected if eithe rdisturbance had been present alone
  • Additiveness of mixed disturbances
    • Mixed disordres don’t need to be additive
    • A metabolic acidoses may coexist w/ a respiratory alkalosis –> lesser pH change than either would produce alone
      • If disturbances are of equal magnitude, pH may be normal
22
Q

Diagnosis of acid-base disorders

  • History
  • Physical exam
  • Electrolytes
    • tCO2
    • Anion gap
  • Other lab data
  • Arterial blood gas
  • Compensation
A
  • History
    • Consider causes of disordres
    • Diuretics + vomiting –> metabolic alkalosis
    • Diarrhea alcoholism or diabetes mellitus –> metabolic acidosis
    • Chronic lung disease, CHF, or pneumonia –> repsiratory acidosis or alkalosis
  • Physical exam
    • Stigmata of liver disease or CHF –> respiratory alkalosis
    • Volume contraction –> metabolic alkalosis
    • Kussmaul respirations (slow deep breaths) –> respiratoyr compensation for metabolic acidosis
    • Fruity odor –> ketosis
  • Electrolytes
    • Total CO2 (tCO2)
      • Quantity measured on a set of serum electrolytes: HCO3 + H2CO3 + dissolved CO2
      • tCO2 ≈ HCO3
      • Low in metabolic acidosis or compensation for chronic respiratory alkalosis
      • High in metabolic alkalosis or compensation for chronic respiratory acidosis
    • Increased anion gap (> 20) –> metabolic acidosis
  • Other lab data
    • Increased serum Cr or hyperglycemia –> metabolic acidosis
  • Arterial blood gas
    • See if pH, PCO2, & HCO3 fit a simple disturbance
    • If metabolic acidosis, apply Winter’s formula to see if expected degree of respiratory compensation is present
    • Normal pH, PCO2, & HCO3 don’t exclude an acid-base disturbance
      • Elevated anion gap –> _>_2 disturbances must be present
  • Compensation
    • Almost never complete
23
Q

Acid base cheat sheet:
Normal values & (1) determine pH status

  • pH
  • Na
  • K
  • pCO2
  • HCO3
  • Cl
  • Determine pH status
A
  • pH
    • 7.4 - 7.44
  • Na
    • 140 - 144 mEq/L
  • K
    • 3.8 - 4.4 mEq/L
  • pCO2
    • 40 - 44 mmHg
  • HCO3
    • 24 - 28 mEq/L
  • Cl
    • 99 - 104 mEq/L
  • Determine pH status
    • pH < 7.4 –> acidemia
    • pH > 7.4 –> alkalemia
24
Q

Acid base cheat sheet:
(2) Determine primary process

  • Metabolic acidemia
    • pH
    • pCO2
    • HCO3
  • Metabolic alkalemia
    • pH
    • pCO2
    • HCO3
  • Respiratory acidemia
    • pH
    • pCO2
    • HCO3
  • Respiratory alkalemia
    • pH
    • pCO2
    • HCO3
A
  • Metabolic acidemia
    • pH: low
    • pCO2: low
    • HCO3: low
  • Metabolic alkalemia
    • pH: high
    • pCO2: high
    • HCO3: high
  • Respiratory acidemia
    • pH: low
    • pCO2: high
    • HCO3: high
  • Respiratory alkalemia
    • pH: high
    • pCO2: low
    • HCO3: low
25
Q

Acid base cheat sheet:
(3) Calculate the anion gap

A
  • Anion gap = Na - HCO3 - Cl
  • Anion gap > 20 mEq/L –> metabolic acidosis
  • For ever 1 g/dl albumin <4 –> add 2.5 to the anion gap
  • Conditions: MUD PILES
    • Methanol
    • Uremiea
    • Diabetic ketoacidosis
    • Paraldehyde
    • Iron or INH
    • Lactic acidosis
    • Ethylene glycol
    • Salicylates
26
Q

Acid base cheat sheet:
(4) Calculate compensation

  • Metabolic acidosis
  • Metabolic alkalosis
  • Respiratory acidosis
  • Respiratory alkalosis
A
  • Metabolic acidosis
    • Decrease in pCO2 = 1.3 decrease in bicarb
    • Winters Formula: pCO2 = 1.5 x [HCO3-] + 8 ± 2
    • Calculated pCO2 < actual pCO2 → additional respiratory acidosis
    • Calculated pCO2 > actual pCO2 → additional respiratory alkalosis
  • Metabolic alkalosis
    • Increase in pCO2 = 1.6 increase in Bicarb
  • Respiratory acidosis
    • Acute: for every increase in pCO2 by 10, Bicarb increases by 1
    • Chronic: for every increase in pCO2 by 10, Bicarb increase by 4
    • Increase in Bicarb > expected → additional metabolic alkalosis
    • Increase in Bicarb < expected → additional metabolic acidosis
  • Respiratory alkalosis
    • Acute: for every decrease in pCO2 by 10, Bicarb decreases by 2
    • Chronic: for every decrease in pCO2 by 10, Bicarb decrease by 5
    • Increase in Bicarb > expected → additional metabolic alkalosis
    • Increase in Bicarb < expected → additional metabolic acidosis
27
Q

Acid base cheat sheet:
(5) Delta gap for AG acidosis / urine gap for non-AG acidosis

  • Delta anion gap for AG acidosis
  • Urine anion gap for non-AG acidosis
A
  • Delta anion gap for AG acidosis
    • Every increase in AG should be accompanied by a decrease in HCO3
    • Higher (increase in AG > decrease in bicarb) –> occult metabolic alkalosis
    • Lower (increase in AG < decrease in bicarb) –> occult metabolic acidosis
  • Urine anion gap for non-AG acidosis
    • UAG = UNa + UK - UCl
    • Positive –> impaired renal acidification / RTA
    • Negative –> GI loss, normal renal acidification

Renal (24 decks)

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