Disorders of Acid

Base Balance
Respiratory Acidosis
 Arterial pCO2 rises to a level higher than
expected
 paCO2 α VCO2 / VA
 Causes of Respiratory Acidosis
 Inadequate Alveolar Ventilation
 Over-production of CO2
 Increased Intake of CO2
Inadequate Alveolar Ventilation
 Central Respiratory Depression
 Drugs
 CNS trauma, infarct, haemorrhage
 Hypoventilation of obesity (Pickwickian syndrome)
 Cervical cord lesions
 High central neural blockade
 Poliomyelitis

 Weaning from mechanical ventilation

 Nerve or Muscle Disorders

 Lung or Chest Wall Defects

 Airway Disorders

 Inadequate mechanical ventilation

 Over-production of Carbon Dioxide

 Malignant Hyperthermia
 Thyrotoxic crisis

Increased Intake of Carbon Dioxide

 Rebreathing
 Addition of CO2 to inspired gas
 Insufflation of CO2 into body cavity
Metabolic Effects of Respiratory Acidosis

 Depression of Intracellular Metabolism

 Stimulation of ventilation
 Cerebral vasodilation: ↑ CBF, ↑ ICP
 Stimulation of the sympathetic nervous system:
tachycardia, peripheral vasoconstriction, sweating
 Peripheral vasodilation by direct effect
 Central depression at very high levels of pCO 2
Effects on cardiovascular system
 Patient is warm, flushed, sweaty, tachycardic
and has a bounding pulse
 Hypoxaemia
 Arrhythmias
 Arterial pCO2 > 90 mmHg not compatible with
life in patients breathing room air
Compensatory Mechanisms
 Acute Respiratory Acidosis - Buffering
 99% of this buffering occurs intracellularly
 proteins (including Hb) and phosphates most
important buffers

 Chronic Respiratory Acidosis - Renal

Bicarbonate Retention
 takes 3 - 4 days to reach maximum
 Mechanism:
 ↑CO2 in proximal tubular cells H+ secretion into
tubular lumen, HCO3- crosses basolateral
membrane and enters the circulation

 Na+ reabsorption in exchange for H+ and less in

exchange for Cl-

 ↑ NH3 production to buffer the H+ in the tubular

lumen (urinary excretion of NH4Cl increases)
Correction of Respiratory Acidosis

 Restoration of adequate alveolar ventilation

 Precautions:
 chronic respiratory acidosis
 severe chronic obstructive airways disease
 asthmatic with severe bronchospasm but not
respiratory arrest
 Post hypercapnic alkalosis
Assessment of severity
 Coexisting metabolic acid-base disorders
cause compensatory changes in pCO2

 Difference between 'actual' and 'expected'

pCO2

 Eg. Coexisting metabolic acidosis:

Expected pCO2 = 1.5 x [HCO3] + 8
Metabolic Acidosis
 ↑ fixed acids in blood

 plasma bicarbonate level lower than

expected- due to titration of HCO3- by H+
Causes
 Patho-physiological Mechanism
 gain of strong acid
 loss of base

 Anion Gap
 'high anion gap metabolic acidosis'
 'normal anion gap metabolic acidosis'
Causes of Metabolic Acidosis
 High Anion-Gap Acidosis

 1. Ketoacidosis: Diabetic, Alcoholic, Starvation

 2. Lactic Acidosis
 Type A: Impaired perfusion
 Type B: Impaired carbohydrate metabolism
 3. Renal Failure: Uraemic acidosis, ARF
 4. Toxins: Ethylene glycol, Methanol, Salicylates
 Normal Anion-Gap Acidosis
(Hyperchloraemic acidosis)

 1. Renal Causes: Renal tubular acidosis,

Carbonic anhydrase inhibitors
 2. GIT Causes: Severe diarrhoea, small bowel
fistula
 3. Other Causes: Recovery from ketoacidosis,
addition of HCl, NH4Cl
 Metabolic effects
 Respiratory Effects:
 Hyperventilation ( Kussmaul respiration)

 Shift of oxyhaemoglobin dissociation curve to the

right

 ↓ 2,3 DPG levels in red cells

 Cardiovascular Effects
 ↓Myocardial contractility
 Sympathetic overactivity
 Resistance to catecholamines
 Peripheral arteriolar vasodilatation
 Venoconstriction of peripheral veins
 Pulmonary Vasoconstriction
 Effects of hyperkalaemia on heart

 Other Effects
 Increased bone resorption (chronic acidosis only)
Compensation
 Hyperventilation to decrease the arterial
pCO2

 Maximal compensation takes 12 to 24 hours

 Maintain hyperventilation in ventilated

patients
Correction
 Accurate diagnosis

 Treat the underlying disorder

 Supportive treatment (fluids, oxygen,

treatment for hyperkalaemia)

 Role of sodium bicarbonate

Ancillary Indices- anion gap &
delta ratio
 Anion gap

 Unmeasured anions in the plasma

 AG = [Na+] + [K+] - [Cl-] - [HCO3-]

 Reference range is 8 to 16 mmol/l

 Hypoalbuminaemia causes a low anion gap

 Delta Ratio
Increase in Anion Gap ÷ Decrease in bicarbonate

Delta Ratio Assessment Guideline

< 0.4 Hyperchloraemic normal anion gap acidosis

0.4 - 0.8 Consider combined high AG & normal AG acidosis

often <1 in acidosis associated with renal failure

1 to 2 Usual for uncomplicated high-AG acidosis

Lactic acidosis: average value 1.6
DKA more likely to have a ratio closer to 1 due to urine ketone
loss (esp if patient not dehydrated)

>2 Suggests a pre-existing elevated HCO3 level so consider:

 a concurrent metabolic alkalosis, or
 a pre-existing compensated respiratory acidosis
Lactic Acidosis
 Excessive tissue production or impaired
hepatic metabolism of lactate- mostly a
combination of the two mechanisms
 Hyperlactaemia: 2- 5 mmol/l
 Severe Lactic Acidosis: > 5 mmols/l
 Lactate level alone not a good predictor of
outcome unless the cause is also considered
Treatment of lactic acidosis
 Diagnose and correct underlying condition

 Restore adequate tissue oxygen delivery

 Avoid sodium bicarbonate (except for

treatment of associated severe
hyperkalaemia)
 Structured Approach to Assessment
of Acid-Base Disorders

1. pH: deviation from normal

2. Pattern of bicarbonate & pCO2
3. Additional clues from other investigations
4. Appropriateness of compensatory
response
5. Bring the information together and make
the acid base diagnosis
6. Confimation: Consider additional tests,
revise the diagnosis if necessary
Assessment of compensation
 Acute Respiratory Acidosis
 Expected [HCO3] = 24 + { (Actual pCO2 - 40) / 10}

 Chronic Respiratory Acidosis

 Expected [HCO3] = 24 + 4 { (Actual pCO2 - 40) /
10}
 Acute Respiratory Alkalosis
 Expected [HCO3] = 24 - 2 { ( 40 - Actual pCO2) /
10 }

 Chronic Respiratory Alkalosis

 Expected [HCO3] = 24 - 5 { ( 40 - Actual pCO2 ) /
10
 Metabolic Acidosis
 Expected pCO2 = 1.5 x [HCO3] + 8

 Metabolic Alkalosis
 Expected pCO2 = 0.7 [HCO3] + 20
Approaches to ABGs
 Boston approach

 Copenhagen approach

 Stewart approach
Boston approach
 Based on actual experimental work in humans

 Magnitude of compensation to graded degrees of acid-

base disturbance determined

 Results presented as graphs or as a set of formulae

 Comparison of the ‘actual’ and ‘expected’ values

 ‘Expected’ value incorporates adjustments for

interaction between pCO2 and HCO3
Copenhagen approach
pCO2-independent indices
 Standard bicarbonate: bicarbonate concentration
when the pCO2 has been adjusted to 40 mmHg

 Buffer Base: concentration of all the buffers present

in plasma or blood

 Base Excess: a measure of how far Buffer Base has

changed from its normal value
Stewart approach
 Quantitative physicochemical approach to acid-
base physiology
 H+ ion concentration depends on dissociation
equilibria of all fully dissociated and partially
dissociated ionic compounds in solution
 Three simple rules to be applied
 Electrical neutrality must be maintained
 Conservation of mass must occur
 All dissociation equilibria must be satisfied
 [H+] is a function of three independent
variables: SID, ATOT, pCO2

 SID = { [Na+] + [K+] + [Ca++] + [Mg++] } - { [Cl-] + [A-] }

= 40- 44 mEq/L

 [ATot] - total concentration of weak acid in the solution

 Major non-volatile weak acids present are
proteins and phosphate
 [Albumin] an estimate of ATot in plasma
[H+] can be derived by solving the following equations:
1. Water Dissociation Equilibrium:
[H+] x [OH-] = K’w
2. Electrical Neutrality Equation:
[SID] + [H+] = [HCO3-] + [A-] + [CO3-2] + [OH-]
3. Weak Acid Dissociation Equilibrium:
[H+] x [A-] = KA x [HA]
4. Conservation of Mass for “A”:
[ATot] = [HA] + [A-]

5. Bicarbonate Ion Formation Equilibrium:

[H+] x [HCO3] = KC x pCO2

6. Carbonate Ion Formation Equilibrium:

[H+] x [CO3-2] = K3 x [HCO3-]