Assessment of Acid-Base Status Charles L. Webber, Jr., Ph.D.

Learning Objectives: You should be able to:

• Answer the paradox as to why the quantitative assessment of a single buffer system is adequate despite the presence of multiple buffer systems.
• Explain the utility of Tullerþs analysis in cursory, first-pass diagnosis of acid-base disturbances of respiratory and renal origin.
• Give specific and detailed examples of how acid-base disturbances of primary respiratory origin can be compensated by renal responses.
• Give specific and detailed examples of how acid-base disturbances of primary metabolic origin can be compensated by respiratory responses.

Isohydric Principle    Tuller's Analysis     Primary Disturbances      Tuller Revisited     MainMenu

The Isohydric Principle

1. Multiple Buffer Systems of the Body (Fig. 19)
   • body fluids contain many buffer pairs, each of which competes for the
     same H+ ions
     • phosphate and protein buffer systems: closed systems within the body
     • bicarbonate buffer system: open system in communication with the external environment
   • only one buffer pair needs to be closely examined to understand the [H+] in the plasma space
     • this is possible because all buffer systems are linked together through H+ (isohydric principle)
     • for biomedical purposes, the bicarbonate buffer system is of primary importance
     • the hemoglobin buffer is of secondary importance

    

2. Accessing the Origin of Acid-Base Disturbances
   • malfunctioning respiratory system
     • insufficient CO2 removal (respiratory acidosis)
     • excessive CO2 removal (respiratory alkalosis)
   • malfunctioning metabolic systems
     • renal (improper processing of H+ or HCO3-)
     • extrarenal (excessive CO2 and H+ production)
   • compensations
     • the kidneys can compensate for dysfunctional lungs (renal system responds after a couple of days: slow)
     • the lung can compensate for dysfunctional kidneys (respiratory system responds within minutes: fast)
     • lungs and kidneys can both compensate for acid-base disturbances of extra-renal origin
   • the origin of acid-base disturbances and presence of compensations can be determined
     • measurement of bicarbonate buffer pair components and pH (quite simple)
     • interpretation of plasma electrolytes concentrations (more complicated)

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Tuller's Analysis

1. The Physician and His System (Fig. 20)
   • Martin A. Tuller, M.D.
     • Associate Attending Physician, Long Island Jewish-Queens Hospital, Jamaica, NY
     • analyzes the acid-base status of his patients using the bicarbonate system and electrolytes
   • relationships among variables in the bicarbonate buffer system
     • pH can be calculated from [HCO3-] and PaCO2
     • [HCO3-] can be calculated from PaCO2 and pH
     • PaCO2 can be calculated from [HCO3-] and pH

    

2. Empirical Definitions (Fig. 21)
   • normal acid-base status
     • pH, PaCO2 and [HCO3-] are all with their normal limits
   • pH out of normal range (pH < 7.35 or pH > 7.45)
     • an acid-base problem exists
   • PaCO2 out of normal range
     • (PaCO2 > 45 mm Hg or PaCO2 < 35 mm Hg)
     • the lungs are either the cause of or compensation for any acid-base disturbance
   • [HCO3-] out of normal range
     • ([HCO3-] < 22 mM or [HCO3-] > 28 mM)
     • the kidneys are either the cause of or compensation for any acid-base disturbance

    

3. Working Assumptions
   • five basic assumptions to Tuller's acid-base analysis (Fig. 22)

     Fig. 22

      

   • Tuller's fifth assumption is of key importance (Fig. 23)
     • compensations can never be complete (control systems argument)
     • how can the physician know the normal pH for each patient (normal distribution of pHs)?

    

4. Specific Examples
   • case A
     • data
       • pH = 7.35 units
       • PaCO2 = 30 mm Hg
       • [HCO3-] = 16 mmol/L
     • diagnosis
       • 1ø metabolic acidosis
       • 2ø respiratory alkalosis
       • full compensation
   • case B
     • data
       • pH = 7.45 units
       • PaCO2 = 30 mm Hg
       • [HCO3-] = 20 mmol/L
     • diagnosis
       • 1ø respiratory alkalosis
       • 2ø metabolic acidosis
       • full compensation
   • summary
     • both cases have very similar bicarbonate system values, but different diagnoses and treatments
     • the interpretation hinges on the side of normal each pH value resides
     • the physician should also closely examine each patient's history for compatibility with diagnosis

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The Four Primary Disturbances of Acid-Base Balance

1. Primary Respiratory Acidosis
   • initiating event:  VþA (hypoventilation)
     • chronic obstructive pulmonary disease (COPD)
     • weak respiratory muscles (neuromuscular diseases)
     • barbiturate poisoning (central nervous system depression)
   • resultant effects:  CO2 retention
     •  PaCO2,  [H+] and  pH
   • compensations: 2ø metabolic alkalosis
     •  HCO3- retention via PaCO2 effect on renal proximal tubules

    

2. Primary Respiratory Alkalosis
   • initiating event:  VþA (hyperventilation)
     • salicylate intoxication (over-aggressive aspirin therapy)
     • CNS disorders
     • hyperexcitability
     • psychogenic paroxysmal hyperventilation ("brown paper bag" therapy)
     • artificial ventilation
   • resultant effects:  CO2 elimination
     •  PaCO2,  [H+] and  pH
   • compensations: 2ø metabolic acidosis
     •  HCO3- retention via reverse PaCO2 effect on renal proximal tubules

    

3. Primary Metabolic Acidosis
   • initiating events: renal and extrarenal
     • diabetes mellitus and ketoacidosis (larger than normal anion gap)
     • severe shock or heart failure and lactic acidosis (larger than normal anion gap)
     • diarrhea and loss of bicarbonate ions (normal anion gap)
     • renal tubular acidosis and retention of hydrogen ions (normal anion gap)
   • resultant effects:  [H+] and/or  [HCO3-],  pH
   • compensations: 2ø respiratory alkalosis
     (with renal participation if possible)
     •  CO2 elimination via  acid drive on ventilation
     • Kussmaul respiration (characteristic deep labored breathing)

    

4. Primary Metabolic Alkalosis
   • initiating events: renal and extrarenal
     • chronic potassium ion depletion (aggressive diuretic therapy, hyperaldosteronism)
     • protracted vomiting (pyloric obstruction, gastric ulcers) and loss of gastric acids
     • dehydration and depletion of extracellular fluid volume (contraction alkalosis)
   • resultant effects:  [H+] and/or  [HCO3-],  pH
     • urine pH will be paradoxically low (acidic) if there is chronic depletion of potassium ions
   • compensations: 2ø respiratory acidosis
     (with renal participation if possible)
     •  CO2 retention via  acid drive on ventilation
     • hypoventilation also  PaO2 which may limit compensation (hypoxic drive on breathing)

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Tuller Revisited

1. Specific Examples
   • case C
     • data
       • pH = 7.55 units
       • PaCO2 = 27 mm Hg
       • [HCO3-] = 23 mmol/L
       • PaO2 = 104 mm Hg
       • SaO2 = 98%
     • diagnosis
       • 1ø respiratory alkalosis
       • no compensation whatsoever ("get the bag out!")

      

   • case D
     • data
       • pH = 7.30 units
       • PaCO2 = 34 mm Hg
       • [HCO3-] = 24 mmol/L
     • diagnosis
       • data incompatibility ("get the technician out?)

    

2. Lessons Learned
   • when in doubt, do not guess, but obtain another arterial blood sample for analysis
   • never discredit the importance of acquiring an accurate patient history

Isohydric Principle    Tuller's Analysis     Primary Disturbances      Tuller Revisited     MainMenu