Updated: 6/9/2018

Acid-Base Disorders

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Introduction
  • The kidneys play an important role in regulating the body's acid-base status via
    • HCO3 reabsorption
      • this is the major extracellular buffer and is thus why it is important to conserve HCO3
        • ~99.9% of filtered HCO3 is reabsorbed
          • the proximal convoluted tubule is the site where most of the filtered HCO3 is reabsorbed
      • Na+H+ exchanger secretes H+ into the tubular lumen and combines with filtered HCO3to form H2CO3
        • H2CO3 is converted into CO2 and H2O with the aid of brush border carbonic anhydrase
          • CO2 and H2O enters the proximal tubular cell to be converted into H2CO3 via intracellular carbonic anhydrase
            • H2CO3 becomed HCO3 and H+
              • H+ gets secreted by the Na+-H+ exchanger to reabsorb more HCO3
                • there is no net secretion of H+ since it is being recycled
                • angiotensin II stimulates the Na+-H+ exchanger which subsequently increases HCO3 reabsorption
                  • this explains contraction alkalosis
              • HCO3 gets transported into the blood via
                • Na+-HCO3 cotransport
                • Cl-HCO3 exchanger
        • excess of HCO3 exceeds HCO3 reabsorption capacity and results in HCO3excretion
        • arterial CO2 and renal compensation
          • not completely understood
          • respiratory acidosis
            • increased CO2 exposed to renal cells generates more H+ to be secreted by the Na+-H+ exchanger 
              • this increases HCO3reabsorption
          • respiratory alkalosis
            • decreased CO2 exposed to renal cells decrease H+ secretion by the the Na+-H+ exchanger
              • this decreases HCO3 reabsorption
    • H+ excretion
      • H+ excretion is accompanied by new HCO3 synthesis and reabsorption
      • there are two mechanisms involved
        • excretion of titratable acid (e.g., urinary buffers such as inorganic phosphate)
          • this is accomplished by H+ATPase (which can be stimulated by aldosterone) and H+-K+ ATPase on α-intercalated cells of the late distal convoluted tubule and collecting ducts
            • H+ binds to HPO4-2 to form H2PO4 (the titratable acid)
              • every titratable acid that excreted results in the synthesis of HCO3
        • excretion of NH4+
          • proximal convoluted tubule
            • NH4+ is secreted via the Na+-H+ exchanger
              • glutamine is metabolized into glutamate and NH4+ by the enzyme glutaminase in the proximal convoluted tubular cells
              • NH3 is lipid soluble and diffuses from the tubular cell into the lumen because it is lipid soluble
                • Na+-Hexchanger secretes H+ which will bind to NH3 to form NH4+
                  • this is diffusion trapping
          • collecting duct
            • H+-ATPase and H+-K+ ATPase on α-intercalated cells secrete H+ to bind with NH3 and form NH4+
              • this is diffusion trapping
 Acid-Base Disorders
  • Acidosis results in acidemia due to an increased serum H+ (decreased pH)
  • Alkalosis results in alkalemia due to a decreased serum H+ (increased pH)
  • These acid base disorders may be due to primary disturbances in HCO3 (metabolic) or arterial CO2 (PCO2) (respiratory)
    • the Hendersen-Hasselbalch equation shows that changes in HCO3 or PCO2 changes pH
      • pH = pKa + log ([HCO3-]/(0.03 * PCO2)
  • Metabolic acidosis
    • due to a decrease in HCO3
      • either because of increased H+ or loss of HCO3
  • Metabolic alkalosis
    • due to an increase in HCO3
  • Respiratory acidosis 
    • due to an increase in CO2
      • secondary to hypoventilation (which retains CO2)
  • Respiratory alkalosis 
    • due to a decrease in CO2
      • secondary to hyperventilation
  • Winter's formula
    • determines expected respiratory compensation in response to metabolic acidosis 
    • PCO2 = 1.5 (HCO3-) + 8 +/- 2
      • if actual PCO2 is greater than expected PCO2 → also has a primary respiratory acidosis
      • if actual PCO2 is less than expected PCO2 also has a primary respiratory alkalosis
 
Acid-Base Disorders
Acid-Base Disorder pH PCO2 [HCO3-] Compensatory Response
Metabolic acidosis
  • ↓ (primary disturbance)
  • Hyperventilation
Metabolic alkalosis 
  • ↑ (primary disturbance)
  • Hypoventilation
Respiratory acidosis
  • ↑ (primary disturbance)
  • ↑ renal HCO3- reabsorption
Respiratory alkalosis
  • ↓ (primary disturbance)
  • ↓ renal HCO3- reabsorption

 

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Questions (4)
Lab Values
Blood, Plasma, Serum Reference Range
ALT 8-20 U/L
Amylase, serum 25-125 U/L
AST 8-20 U/L
Bilirubin, serum (adult) Total // Direct 0.1-1.0 mg/dL // 0.0-0.3 mg/dL
Calcium, serum (Ca2+) 8.4-10.2 mg/dL
Cholesterol, serum Rec: < 200 mg/dL
Cortisol, serum 0800 h: 5-23 μg/dL //1600 h:
3-15 μg/dL
2000 h: ≤ 50% of 0800 h
Creatine kinase, serum Male: 25-90 U/L
Female: 10-70 U/L
Creatinine, serum 0.6-1.2 mg/dL
Electrolytes, serum  
Sodium (Na+) 136-145 mEq/L
Chloride (Cl-) 95-105 mEq/L
Potassium (K+) 3.5-5.0 mEq/L
Bicarbonate (HCO3-) 22-28 mEq/L
Magnesium (Mg2+) 1.5-2.0 mEq/L
Estriol, total, serum (in pregnancy)  
24-28 wks // 32-36 wks 30-170 ng/mL // 60-280 ng/mL
28-32 wk // 36-40 wks 40-220 ng/mL // 80-350 ng/mL
Ferritin, serum Male: 15-200 ng/mL
Female: 12-150 ng/mL
Follicle-stimulating hormone, serum/plasma Male: 4-25 mIU/mL
Female: premenopause: 4-30 mIU/mL
midcycle peak: 10-90 mIU/mL
postmenopause: 40-250
pH 7.35-7.45
PCO2 33-45 mmHg
PO2 75-105 mmHg
Glucose, serum Fasting: 70-110 mg/dL
2-h postprandial:<120 mg/dL
Growth hormone - arginine stimulation Fasting: <5 ng/mL
Provocative stimuli: > 7ng/mL
Immunoglobulins, serum  
IgA 76-390 mg/dL
IgE 0-380 IU/mL
IgG 650-1500 mg/dL
IgM 40-345 mg/dL
Iron 50-170 μg/dL
Lactate dehydrogenase, serum 45-90 U/L
Luteinizing hormone, serum/plasma Male: 6-23 mIU/mL
Female: follicular phase: 5-30 mIU/mL
midcycle: 75-150 mIU/mL
postmenopause 30-200 mIU/mL
Osmolality, serum 275-295 mOsmol/kd H2O
Parathyroid hormone, serume, N-terminal 230-630 pg/mL
Phosphatase (alkaline), serum (p-NPP at 30° C) 20-70 U/L
Phosphorus (inorganic), serum 3.0-4.5 mg/dL
Prolactin, serum (hPRL) < 20 ng/mL
Proteins, serum  
Total (recumbent) 6.0-7.8 g/dL
Albumin 3.5-5.5 g/dL
Globulin 2.3-3.5 g/dL
Thyroid-stimulating hormone, serum or plasma .5-5.0 μU/mL
Thyroidal iodine (123I) uptake 8%-30% of administered dose/24h
Thyroxine (T4), serum 5-12 μg/dL
Triglycerides, serum 35-160 mg/dL
Triiodothyronine (T3), serum (RIA) 115-190 ng/dL
Triiodothyronine (T3) resin uptake 25%-35%
Urea nitrogen, serum 7-18 mg/dL
Uric acid, serum 3.0-8.2 mg/dL
Hematologic Reference Range
Bleeding time 2-7 minutes
Erythrocyte count Male: 4.3-5.9 million/mm3
Female: 3.5-5.5 million mm3
Erythrocyte sedimentation rate (Westergren) Male: 0-15 mm/h
Female: 0-20 mm/h
Hematocrit Male: 41%-53%
Female: 36%-46%
Hemoglobin A1c ≤ 6 %
Hemoglobin, blood Male: 13.5-17.5 g/dL
Female: 12.0-16.0 g/dL
Hemoglobin, plasma 1-4 mg/dL
Leukocyte count and differential  
Leukocyte count 4,500-11,000/mm3
Segmented neutrophils 54%-62%
Bands 3%-5%
Eosinophils 1%-3%
Basophils 0%-0.75%
Lymphocytes 25%-33%
Monocytes 3%-7%
Mean corpuscular hemoglobin 25.4-34.6 pg/cell
Mean corpuscular hemoglobin concentration 31%-36% Hb/cell
Mean corpuscular volume 80-100 μm3
Partial thromboplastin time (activated) 25-40 seconds
Platelet count 150,000-400,000/mm3
Prothrombin time 11-15 seconds
Reticulocyte count 0.5%-1.5% of red cells
Thrombin time < 2 seconds deviation from control
Volume  
Plasma Male: 25-43 mL/kg
Female: 28-45 mL/kg
Red cell Male: 20-36 mL/kg
Female: 19-31 mL/kg
Cerebrospinal Fluid Reference Range
Cell count 0-5/mm3
Chloride 118-132 mEq/L
Gamma globulin 3%-12% total proteins
Glucose 40-70 mg/dL
Pressure 70-180 mm H2O
Proteins, total < 40 mg/dL
Sweat Reference Range
Chloride 0-35 mmol/L
Urine  
Calcium 100-300 mg/24 h
Chloride Varies with intake
Creatinine clearance Male: 97-137 mL/min
Female: 88-128 mL/min
Estriol, total (in pregnancy)  
30 wks 6-18 mg/24 h
35 wks 9-28 mg/24 h
40 wks 13-42 mg/24 h
17-Hydroxycorticosteroids Male: 3.0-10.0 mg/24 h
Female: 2.0-8.0 mg/24 h
17-Ketosteroids, total Male: 8-20 mg/24 h
Female: 6-15 mg/24 h
Osmolality 50-1400 mOsmol/kg H2O
Oxalate 8-40 μg/mL
Potassium Varies with diet
Proteins, total < 150 mg/24 h
Sodium Varies with diet
Uric acid Varies with diet
Body Mass Index (BMI) Adult: 19-25 kg/m2
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(M1.RL.11) A 52-year-old man with a history of type I diabetes mellitus presents to the emergency room with increasing fatigue. Two days ago, he ran out of insulin and has not had time to obtain a new prescription. He denies fevers or chills. His temperature is 37.2 degrees Celsius, blood pressure 84/56 mmHg, heart rate 100/min, respiratory rate 20/min, and SpO2 97% on room air. His physical exam is otherwise within normal limits. An arterial blood gas analysis shows the following:

pH 7.25, PCO2 29, PO2 95, HCO3- 15.

Which of the following acid-base disorders is present? Review Topic

QID: 104285
1

Metabolic acidosis with appropriate respiratory compensation

78%

(61/78)

2

Respiratory acidosis with appropriate metabolic compensation

1%

(1/78)

3

Mixed metabolic and respiratory acidosis

18%

(14/78)

4

Metabolic alkalosis with appropriate respiratory compensation

0%

(0/78)

5

Respiratory alkalosis with appropriate metabolic compensation

1%

(1/78)

M1

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