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Acid base disordersDr. Tanuj Paul Bhatia

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BASIC TERMINOLOGY

pH : pH signifies free hydrogen ion concentration.

pH is inversely related to H+ ion concentration.

Increase in pH means H+ion is decreasing. Decrease in pH means H+ ion is increasing

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Acid and Base

Acid : A substance that can “donate” H+ ion or when added to solution raises H+ ion (i.e., lowers pH).

Base : A substance that can “accept” H+ ion or when added to solution lowers H+ ion (i.e., raises pH).

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Anion and Cation

Anion : An ion with negative charge (i.e., Cl-, HCO3

-)

Cation : An ion with positive charge (i.e., Na+, K+, Mg+)

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Acidosis and Alkalosis

Acidosis : Abnormal process or disease, which reduces pH due to increase in acid or decrease in alkali.

Alkalosis : Abnormal process or disease, which increases pH due to decrease in acid or increase in alkali.

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Clinical terminology Criteria

Normal pH 7.4 (7.35 – 7.45)

Acidaemia pH < 7.35

Alkalaemia pH > 7.45

Normal PaCO2 40 (35-45) mm of Hg (4.7-6 KPa)

Respiratory acidosis PaCO2 > 45 mm of Hg & low pH

Respiratory alkalosis PaCO2 < 35 mm of Hg & high pH

Normal HCO-3 24 (22-26) mEq/L

Metabolic acidosis HCO3 <22 mEq/L & low pH

Metabolic alkalosis HCO3 >26 mEq/L & high pH

Normal PaO2 > 90 mm of Hg (over 12 KPa)

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Regulation of pH in a narrow range of 7.35 – 7.45 is essential for normal cellular enzymatic reaction and for normal ionic concentration.

Extreme ranges of pH (less than 7.2 or more than 7.55) are potentially life threatening because of disruption of many vital cellular enzymatic reactions and physiological process.

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BASIC PHYSIOLOGY OF ACID BASE REGULATION

The body maintains pH within a normal range in spite of variation in dietary intake of acid and alkali and endogenous acid production.

The regulation of pH in a narrow range, is the function of buffers, lungs and kidneys.

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Buffers

Buffers are chemical systems, which either release or accept H+ion.

Buffers act fastest but have least buffering power. Most important buffers are -1. Bicarbonate – carbonic acid systems2. Plasma proteins

3. Haemoglobulin 4. Phosphates

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Respiratory regulation

By excreting volatile acids, lung regulates PaCo2.

Respiratory regulation acts rapidly (in seconds to minutes) and has double buffering power as compared to chemical buffer.

Failure of regulation causes Respiratory acidosis Respiratory alkalosis

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Renal regulation

The role of kidney is to maintain plasma Hco3 concentration.

It has the most powerful buffering system, which starts within hours and takes 5-6 days for the peak effect.

Failure of regulation Metabolic acidosis Metabolic alkalosis

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If initial disturbance affects Hco3

1. Metabolic acidosis (fall in bicarbonate)2. Metabolic alkalosis (raise in bicarbonate)

If initial disturbance affects PaCo2

1. Respiratory acidosis (raise in PaCo2)

2. Respiratory alkalosis (fall in PaCo2)

When you see “Metabolic” – Think of Hco3 and when you see “Respiratory” – Think of PaCo2.

4 primary acid base disorders

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Characteristics of primary acid base disorders

Basic disorder pH Primary change Secondary change

(compensatory changes)

Respiratory PaCO2 HCO3

AcidosisAlkalosis

↑↓

↑↓

Metabolic HCO3 PaCO2

AcidosisAlkalosis

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Evaluation and investigations

History and examination : Careful history and examination can provide clue for underlying clinical disorders.

Diarrhea or ketoacidosis metabolic acidosis

Presence of Kussmaul’s breathing Metabolic acidosis.

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Basic investigations are essential as they may provide clue for underlying disorders.

Most useful investigations are serum sodium, potassium, chloride, Hco3 and anion gap.

Other relevant investigations are CBC, urine examination, urine electrolytes, blood sugar, renal function test etc.

Primary investigations

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As blood gases require arterial puncture and is relatively expensive, it should not be performed as a routine investigation.

Arterial blood gases (ABG) :

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Indications for ABG

1.Critical and unstable patients where significant acid base disorder is suspected.

2.If history, examination and serum electrolytes suggest severe progressive acid base disorders.

3.Sick patient with significant respiratory distress, secondary to acute respiratory diseases or exacerbation of chronic respiratory diseases

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Interpretation of basic Investigations

1) pHNormal value : 7.4 (7.35 - 7.45)Normal pH : It suggests either

absenceof disorders or

presenceof mixed disorder.

Low pH (<7.35) : Suggests acidosisHigh pH (> 7.45) : Suggests alkalosis.

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2. HCO3

Normal value 22-26 meq/L

Low (< 22 mEq/L) Metabolic acidosis (primarychange) or Respiratoryalkalosis (secondary change)

High (> 26 mEq/L) Metabolic alkalosis (primary change) or Respiratory acidosis (Secondary change)

Normal Hco3 Does not exclude acid base disorders.

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3. Paco2

Normal value 40(35-45) mm of Hg

High (>45 mm of Hg) Respiratory acidosis (primary change) or Metabolic alkalosis(Secondary change)

Low (<35 mm of Hg) Respiratory alkalosis (primary change) or Metabolic acidosis(secondary change)

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4. Anion gap (AG)

The charge difference between unmeasured anion and cation is termed as Anion gap (AG).

Anion gap (AG) = Na – (Cl + Hco3) = 122 mEq/L (Normal value).

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Importance of Anion Gap :

In case of mixed acid-base disorders (eg. Metabolic acidosis and metabolic alkalosis co exist) in same patient, the pH may be normal or near normal. When pH is normal an elevated AG denotes presence of metabolic acidosis.

Anion gap is most useful to establish etiological diagnosis of metabolic acidosis.

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METABOLIC ACIDOSIS

Metabolic acidosis is characterized by Fall in pH Fall in HCO3

Fall in PaCO2 (compensatory change –

hyperventilation).

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Pathophysiology :

Metabolic acidosis can result from – 1.   Loss of base – HCO3 via GI tract

or kidneys (diarrhea, proximal RTA).

2.  Over production of metabolic acids in the body (ketoacidosis or lactic acidosis)

3.  Ingestion or infusion of acid or potential acids (salicylates or NH4Cl).

4.  Failure of H+ excretion by kidney (renal failure).

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Etiology :

Calculation of anion gap is helpful in narrowing etiological diagnosis. On the basis of AG, causes of metabolic acidosis can be divided into 2 groups.

1. Normal anion gap (hyperchloraemic) acidosis

2. High anion gap (normochloraemic) acidosis

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Treatment :

1) Specific management of underlying disorder

2) Alkali therapy Indications :

a.      When blood pH drops below 7.15 b.      When HCO3 fall below 10 mEq/Lc. Treatment of hyperkalemia with metabolic

acidosis.

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Amount of HCO3 required (mEq/L) = (desired HCO3 – actual HCO3) x 0.5 x body weight in kg.

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50% of the calculated NaHCO3 is infused with 5% dextrose over 4-5 hours. Remaining 50% of NaHCO3 is infused gradually over 24 hours.

3) Correct volume and electrolyte deficits

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METABOLIC ALKALOSIS

Metabolic alkalosis is characterized by Elevated pH Elevated HCO3

Elevated PaCO2 (compensatory change –

hypoventilation)

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Pathophysiology

Generation of metabolic alkalosis : The loss of hydrogen ion form upper GI

tract (vomiting) or urine (diuretics). Addition of alkali : Administration of

HCO3 or its precursors as citrate (multiple transfusions of citrated blood).

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Urine chloride concentration differentiates metabolic alkalosis in to saline responsive and saline resistant metabolic alkalosis.

The differential diagnosis is based on urine Cl- <20 mEq/L (chloride/saline

responsive) Cl- > 20 mEq/L (chloride/saline

resistant).

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Treatment :

A) Treatment of underlying causeB) Saline (chloride / volume) responsive

alkalosis. Aim of therapy is adequate correction of volume, chloride

and K+ deficit. IV isotonic saline with KCl or isolyte G are preferred

infusion. Treatment with H2 inhibitors or proton pump inhibitors will

reduce gastric acid secretion and will minimize further H+ loss due to vomiting or nasogastric suction.

Avoid or discontinue exogenous source of alkali such as NaHCO3 infusions, ringer’s lactate, acetate or citrate.

In severe metabolic alkalosis, diluted Hcl can be given IV to lower the plasma HCO3 concentration.

Dialysis therapy may be useful in occasional patients with severe metabolic alkalosis, volume overload and renal failure.

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C) Saline (chloride/volume) resistant metabolic acidosis :

Metabolic alkalosis due to certain causes like oedemaotus states, mineralocorticoid excess, may be saline resistant.

It needs specific treatment of underlying causes (surgical treatment of pituitary tumor or adrenal adenoma in Cushings syndrome) or supportive treatment such as potassium sparing diuretics (amiloride, spiranolactone), correction of hypokalemia and sodium restriction.

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RESPIRATORY ACIDOSIS

Respiratory acidosis is characterized by Fall in pH Elevated PaCO2

Elevated HCO3 (Compensatory change)

It occurs when the effective alveolar ventilation (CO2 excretion by lung) fails to keep pace with the rate of CO2 production.

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Clinical features

Mild to moderate hypercapnia – Sleep disturbances, day time

somnolence, loss of memory, personality changes, tremor, and myoclonic jerks.

Severe hypercapnia – Headache, dyspnoea, hallucination,

psychosis, papilloedema and coma.

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Treatment

A) General measures : The major goal of therapy is to identify

and treat the underlying cause promptly.

Establish patent airway and restore adequate oxygenation.

If a patient with chronic hypercapnia develops sudden increase in PaCO2, search for the aggravating factor. Vigorous treatment of pulmonary infection, bronchodilator therapy and removal of secretions can offer considerable benefits in such patients.

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B) Oxygen therapy :

Role of oxygen therapy in respiratory acidosis is like a “double edged sword”.

In acute respiratory acidosis, major threat to life is hypoxia. So oxygen supplementation is needed.

In chronic hypercapnia, hypoxemia may be the primary and only stimulus to respiratory, injudicious therapy can be lead to further reduction in alveolar ventilation and aggravate hypercapnia drastically.

If PaO2 is 50mm of Hg or higher, O2 therapy is generally not needed. If PaO2 is less than 50 mm of Hg, O2 should be given.

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C) Mechanical ventilatory (MV) support :

Indications : Unstable, symptomatic or

progressively hypercapnic (PaCO2 > 80mm of Hg) patients.

If the patient exhibits signs of muscle fatigue, start MV before respiratory failure occurs.

Refractory severe hypoxia or apnoea. Depression of respiratory center (eg.

Drug over dose)D) Alkali therapy : Avoid alkali therapy, except in

patients with associated metabolic acidosis.

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RESPIRATORY ALKALOSIS

Respiratory alkalosis is characterized by

Elevated pH Fall in PaCO2

Fall in HCO3 (compensatory change)

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Clinical features

Light headache, Tingling of extremities, Circumoral anaesthesia, Cardiac arrhythmias and Infrequent tetany or seizures.

PaCO2 below 20-25 mm of Hg is a grave prognostic sign.

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Treatment

1. Vigorous treatment of underlying cause.2. Mild alkalosis with few symptoms need no

direct treatment. 3. As hypoxemia is the common cause of

hyperventilation, O2 supplementation is essential along with etiological diagnosis and treatment.

4. In the absence of hypoxemia, hyperventilation needs reassurance and rebreathing in a paper bag.

5. Pretreatment with acetazolamide minimizes symptoms due to hyperventilation at high altitude.

6. Associated treatment of hypocalcemia.

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