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Acid-Base Disorders
CSN Vittal

Normal Values
pH : 7.35 – 7.45
PaCO2 : 35 – 45 mm Hg
PaO2 : > 70 mm Hg
HCO3- : 22 – 26 mEq/L
BE : -2.0 to +2.0 mEq/L
pH
Depends on the ratio between acid and base
Proportional to HCO3- / H2CO3
pH change to HCO3- is metabolic
pH change to H2CO3 (CO2) is respiratory

Base Excess
Difference between patient’s actual buffering capacity and normal buffering capacity
Normal Values : +/- 2.0 mEq/L
Follows changes in HCO3-

Sources of acid gain:
1. Carbon dioxide (since CO2 and H2O form HCO3-, bicarbonate, and H+, a proton, in the presence of carbonic anhydrase)
2. Production of nonvolatile acids from the metabolism of proteins and other organic molecules
3. Loss of bicarbonate in faeces or urine
4. Intake of acids or acid precursors

Sources of acid loss:
1. Use of hydrogen ions in the metabolism of various organic anions
2. Loss of acid in the vomitus or urine


Primary & Compensatory Changes

Resp. Acidosis - Increased PaCo - 2 Increased HCO3
Resp. Alkalosis - Decreased PaCo2 - Decreased HCO3
Met. Acidosis - Decreased HCO3 - Decreased PaCo2
Met. Alkalosis - Increased HCO3 - Increased PaCo2

Diagnosis of Acid Base Disorders

  • Consider the history
  • Look for clues on physical exam
  • Examine the electrolytes
  • PCO2
  • Potassium
  • Anion Gap
  • Review other laboratory data
  • Analyze the arterial blood gas
  • History

  • Loose Stools and decreased Intake
  • Polyphagia, Polydipsia of DM
  • History of Renal Insufficiency
  • Possibilty of Poisoning in Toddlers
  • Fever and Increasing Sickness
  • Sign of CNS Disorder
  • Medication history
  • Examination

  • Signs of Sepsis
  • Signs of dehydration
  • Signs of meningeal irritation
  • Signs of Addison's disease
  • FSigns of Neuromuscular disorder
  • 5 Step Approach

    1. pH: Normal, acid or alkaline?
    2. Respiratory component – Is it like pH?
    3. Metabolic component – Is SBE like pH?
    4. Magnitude of change – minor, moderate or major?
    5. Recognizing compensation

    Step 1
    Acidemic or Alkalotic?
    Acidemic : pH < 7.35
    Alkalotic : pH > 7.45
    * A normal pH does not rule out acid base disorder


    Step 2

    Respiratory Component : PCO2
    If the respiratory change is like the pH,
    i.e., both acid, then
    the cause is respiratory
    The exception : when the metabolic component is also acid -> both are contributing to the acid pH.

    Step 3
    Metabolic Component : SBE
    If the Standard Base Excess (SBE) is the component which is like the pH, i.e., both acid (a negative base excess), then the cause is metabolic.
    The exception, - is when the respiratory component is also acid; then both contribute to the acid pH.

    Step 4
    Magnitude of Disturbance
    Just try to judge minor, moderate, or major, for clinical comment.
    Whenever the pH is normal, i.e., pH = 7.4. then the PCO2 and the SBE are equal and opposite.
    The slope for BE / PCO2 when pH = 7.4 gives us this ratio:
    3 units of change in SBE = 5 mm Hg change in PCO2.

    Step 5
    Recognizing compensation
    If a pt. with a respiratory problem has a high PCO2, e.g., 60 mmHg (raised by 20mmHg) then for "complete compensation" the SBE would have to be about 12
    (using the 5 to 3 ratio given above).
    If the SBE were zero = "no compensation" - typical of an acute process of recent onset.
    Most likely - the patient is somewhere in the middle (SBE = 6 mEq/L) which is typical for "compensation for chronic respiratory acidosis”.

    Step 5
    Recognizing compensation
    Inverse example:
    if a patient with a metabolic problem has a low SBE, e.g., -12, then the PCO2 would have to be reduced by hyperventilation to about 20 mmHg to achieve "complete compensation".
    If the PCO2 were still normal then there would be "no compensation".
    Again, far the most likely, the patient is somewhere in the middle (30 mmHg) which is typical for "compensation for metabolic acidosis".

    Logical Approach to an Acid pH
    Are the pH and the PCO2 both acid? If so the PCO2 contributes to the condition.
    If not (i.e., PCO2 is alkaline) then the metabolic component is the cause and the PCO2 is compensatory.
    Is either PCO2 or SBE normal? Because, if so, there is no compensation and you have a pure acidosis:
    (pure respiratory acidosis occurs fairly frequently, metabolic rarely)
    To be typical the compensation must lie roughly half way between no compensation and complete compensation - use the rule 3 mEq/L = 5 mmHg to work out complete compensation.
    If both components are acid, you don't have a typical single condition, you have a combined metabolic and respiratory acidosis.

    Example A
    pH = 7.2, PCO2 = 60 mmHg, SBE = 0 mEq/L
    Overall change is acid.
    Respiratory change is also acid - therefore contributing to the acidosis.
    SBE is normal - no metabolic compensation.
    Therefore, pure respiratory acidosis.
    Typical of acute respiratory depression.
    Magnitude: marked respiratory acidosis

    Example B
    pH = 7.35, PCO2 = 60 mmHg, SBE = 7 mEq/L
    Overall change is slightly acid.
    Respiratory change is also acid - therefore contributing to the acidosis.
    Metabolic change is alkaline - therefore compensatory.
    The respiratory acidosis is 20 mmHg on the acid side of normal (40). To completely balance plus 20 would require 20 * 3 / 5 = 12 mEq/L SBE
    The actual SBE is 7 mEq/L, which is roughly half way between 0 and 12, i.e., a typical metabolic compensation.
    Magnitude: marked respiratory acidosis with moderate metabolic compensation

    Example C
    pH = 7.15, PCO2 = 60 mmHg, SBE = - 6 mEq/L
    Overall change is acid.
    Respiratory change is acid - therefore contributing to the acidosis.
    Metabolic change is also acid - therefore combined acidosis.
    The components are pulling in same direction - neither can be compensating for the other
    Magnitude: marked respiratory acidosis and mild metabolic acidosis

    Example D
    pH= 7.30, PCO2 = 30 mmHg, SBE = -10 mEq/L
    Overall change is acid.
    Respiratory change is alkaline - therefore NOT contributing to the acidosis.
    Metabolic change is acid - therefore responsible for the acidosis.
    The components are pulling in opposite directions. SBE is the acid component so it is primarily a metabolic problem with some respiratory compensation
    The metabolic acidosis is 10 mEq/L on the acid side of normal (0). To completely balance 10 would require 10 * 5 / 3 = 17 mmHg respiratory alkalosis (= 23 mmHg)
    The actual PCO2 is 30 mEq/L which is roughly half way between 23 and 40, i.e., a typical respiratory compensation..
    Magnitude: marked metabolic acidosis with mild respiratory compensation.

    Respiratory Acidosis
    Acute
    The PaCO2 is elevated above the upper limit of the reference range (i.e., > 45 mm Hg) with an accompanying acidemia (i.e., pH < 7.35).
    Chronic
    The PaCO2 is elevated above the upper limit of the reference range, with a normal or near-normal pH secondary to renal compensation and an elevated serum bicarbonate (i.e., HCO3- > 30 mm Hg).

    Respiratory Disturbances
    Is it Acute or Chronic ? Respiratory Acidosis
    Acute:
    pH decrease = 0.008 X (PaCO2 – 40)
    Chronic:
    pH decrease = 0.003 X (PaCO2 – 40)
    Respiratory Alkalosis
    Acute:
    pH Increase = 0.008 X (PaCO2 – 40)
    Chronic:
    pH Increase = 0.003 X (PaCO2 – 40)

    Respiratory Acidosis - Acute
    Abrupt failure of ventilation, h PaCO2
    Neuromuscular disorders
    CNS Depression
    Brain stem Injury
    Musculoskeletal Disorders
    GBS
    Myasthenia
    Airway Obstructive Disease
    Asthma
    Foreign Body
    Laryngeal Edema
    Pulmonary Embolism
    Drugs
    Sedatives
    Barbiturates

    Respiratory Acidosis - Chronic
    COPD
    Obesity hypoventilation syndrome (i.e., Pickwickian syndrome)
    Neuromuscular disorders
    Amyotrophic lateral sclerosis
    Severe restrictive ventilatory defects
    Interstitial fibrosis and
    Thoracic deformities


    Respiratory Acidosis
    Symptoms:
    Symptoms of the disease that causes respiratory acidosis are usually noticeable
    shortness of breath
    easy fatigue
    chronic cough, or
    wheezing.
    When respiratory acidosis becomes severe,
    Confusion
    irritability, or
    lethargy may be apparent.

    Respiratory Acidosis
    Treatment:
    Treat the underlying cause
    Improve alveolar gas exchange
    Assisted ventilation

    Respiratory Alkalosis
    Hyperventilation, i PaCO2
    Catastrophic CNS Events
    Hemorrhage
    Hysterical
    Assisted ventilation
    Drugs
    Salicylates (early stages)
    Interstitial Lung Disease
    Cirrhosis, Liver Failure
    Anxiety
    Gram negative Septicemia
    Hypoxia and severe anemia or high altitude

    Respiratory Alkalosis
    Symptoms
    Tingling and numbness
    Parasthesias
    Lethargy
    Tetany
    Unconsciousness
    Vasospasm of cerebral vassals - Hypercapnia
    Respiratory Alkalosis
    Treatment
    Treat underlying cause
    Metabolic Acidosis
    Increased H+ Load
    Increased HCO3- Loss

    Metabolic Acidosis
    Anion Gap Metabolic Acidosis
    Accumulation of unmeasured anions
    Low HCO3 and h AG


    Differential Dx of high-anion gap acidosis:
    "SLUMPED":
    Salicylates
    Lactic acidosis
    Uremia
    Methanol intoxication
    Paint sniffing (toluene) / Paraldehyde
    Ethylene glycol intoxication
    DKA or alcoholic ketoacidosis

    Non Anion Gap Metabolic Acidosis
    Loss of HCO3 or External acid infusion
    Low HCO3 AG < 12
    GI Losses of Bicarbonate (Diarrhoea)
    Renal Losses
    Renal Tubular Acidosis
    Renal Toxins
    Carbonic Anhydrase Inhibitors
    Ureteral Diversion
    Compensation for Resp. Acidosis
    HCl or NH4Cl Infusion, TPN

    Decrease in Anion Gap Metabolic Acidosis
    Paraproteinemias, multiple myeloma
    Lithium intoxicaion
    Excessive K+, Ca++ and Mg++
    Albumin - Low
    Bromism
      Mnemonic : PLEAB

    Metabolic Acidosis
    Increased work of breathing :
    Deep rapid breathing (Kussmaul’s)
    Peripheral Vasodilatation,
    collapse, shock, impaired cardiac function
    Lethargy, drowsiness, confusion, stupor
    Hyperkalemia
    Nonspecific : Nausea, Vomiting
    Chronic Acidosis:
    Osteopenia – CaCo3 loss
    Muscle weakness – Glutamine loss

    Metabolic Acidosis
    Management Principles:
    Identify cause
    Initial goal : Bring the pH ~ 7.25
    (For cardiac contractility & responsiveness to catecholamines)
    Sodabicarb :
    1-2 mEq/Kg [1 ml of 7.5% NaHCO3 = 0.9 mEq]
    [Bicarb deficit (mEq/L) = Body wt.(Kg) X 0.3 X Base excess]
    Half as bolus
    Half as infusion over 12 – 24 hrs.

    Metabolic Acidosis
    Potassium replacement :
    Serum K+ should be > 3.5 mEq/L before administering HCO3 -
    THAM (tromethamine; tris-hydroxymethyl aminomethane) - An amino alcohol
    Indication :
    In partients with CHF who may not be able to tolerate additional Na+ burden if treated with Sodabicarb.
    Dose : Body wt. (Kg) X Base excess
    Administration: As infusion over 3 - 6 hours


    Metabolic Acidosis – Specific Situations
    DKA
    Lactic Acidosis
    RTA
    Uremia
    Salicylate toxicity

    Metabolic Alkalosis
    Very Dangerous:
    Shifts O2 dissociation curve to Lt.
    Causes vasoconstriction of all vessels except pulmonary circulation
    Suppresses ventilation
    Decreases ionized Ca++ and shifts K+ into cells – hypocalcemia and hypokalemia
    Metabolic Alkalosis
    What generated the alkalosis?
    What is maintaining the alkalosis – what is preventing kidney from excreting the alkali ?

    Metabolic Alkalosis
    Loss of acid:
    GI Losses
    Vomiting
    NG suction
    Acid diarrhoea (Congenital chloridorrhoeas, villous adenomas)
    Renal H+ Loss
    Diuretics (thiazides, furosemide)
    Bartter’s Syndrome
    Mg deficiency
    Hyperaldosteronism, Cushing’s
    Metabolic Alkalosis
    Volume contraction (Chloride responsive)
    Potassium deficiency
    Chloride depletion
    Increased mineralocorticoids
    (Chloride resistant)

    Metabolic Alkalosis
    Identify and treat the underlying cause
    Correction of volume depletion with Normal saline (isotonic or 1⁄2 isotonic)
    Use of carbonic anhydrase inhibitors in patients who need use of diuretics
    Ammonium chloride / Arginine chloride : in resistant alkaloses ( massive gastric losses)
    Hemo or peritoneal dialysis : in severe alkaloses with hyperosmolar states

    Mixed Acid – Base Disorders
    • Respiratory Acidosis + Metabolic Acidosis Eg.Resp. Distress Syndrome
    • Respiratory Acidosis + Metabolic Alkalosis Eg. Excessive diuretic therapy, Chronic respiratory acidosis with C.C.F.
    • Metabolic Acidosis + Respiratory Acidosis Eg. Hepatic Failure
    • Respiratory Alkalosis + Metabolic Acidosis Eg. Salicylate intoxication, Gm – ve sepsis


    When to suspect a mixed acid base disorder:
    1. The expected compensatory response does not occur
    2. Compensatory response occurs, but level of compensation is inadequate or too extreme
    3. Whenever the PCO2 and [HCO3-] becomes abnormal in the opposite direction.
    4. pH is normal but PCO2 or HCO3- is abnormal
    5. In anion gap metabolic acidosis, if the change in bicarbonate level is not proportional to the change of the anion gap.
    6. In simple acid base disorders, the compensatory response should never return the pH to normal. If that happens, suspect a mixed disorder.


    Thank You
    - VittalA