Acid base balance

and
blood gas interpretation

Dr. Asoka Gunaratne

 What is an acid?
What is a base?
Acid A compound that dissociates and
release H+
Strong acid release more H+ (e.g. HCl)
Weak acid less tendency to dissociate and
release less H+ (e.g. H2CO3)
Base A compound that react with H+
Strong base rapidly react with H+ (e.g. OH-)
Weak base slowly react with H+ (e.g. HCO3-)
 Normal H+ concentration
40 neq/l (0.00000004 meq/l)

Sources of acid
Non volatile acid production - 80 mEq/day
Acid ingestion amount ?

As the H+ concentration is very low it is

expressed as pH

Normal pH = -log(0.00000004)
= 7.4
 Henderson Hasselbalch
Equation
K = HCO3- H+ /H2CO3
H+ = K H2CO3 /HCO3-
H2CO3 CO2
H + = K CO2 / HCO3-
-log H = -logK -logCO2 / HCO3-
pH = pK log HCO3- / CO2
Defences against changes in H+
Buffers quick
Bicarbonate buffer
Phosphate buffer
proteins
Respiratory compensation
Few minutes by altering the ventilation
Volatile acid (CO2) excretion
Renal compensation hours to few days
Filtration of bicarbonate
H+ secretion
Re-absorption and formation of bicarbonate
Formation of ammonia
 Buffering power of a buffer
depends on

pK of it
pH at which it is working
Concentration of it
 When the concentrations are equal it
becomes log of 1 which is o
Then the pH=pK

If the acid base disturbance is due to

HCO3- it is referred to as metabolic and if
due to CO2 respiratory
 HCO3- buffer
CO2 + H2O H2CO3 H+ + HCO3-
Is the most important buffer in blood and
in proximal renal tubule
pK is 6.1
In lungs shift to right by removing CO2
In peripheral tissues shift to left by adding
CO2
Carbonic anhydrase is found in red cells,
renal tubular cells and alveolar cells
Bicarbonate titration curve
 Phosphate buffer

H+ + NaHPO4- NaH2PO4
Important buffer in DCT and ICF
pK is 6.8
Filtrate is concentrated with phosphate
buffer in DCT
 Hb and other proteins
50% of buffering is done by Hb in blood
Proteins found in abundance in the cell
H+ react with negatively charged COO- &
NH2- in proteins
pK of the system is 7.4
Accounts for most of the intracellular
buffering (70% of all buffering is
intracellular)
 Respiratory regulation
CO2 is eliminated by lungs
Increase H+ concentration stimulates respiration
in via central chemo receptors indirectly by
elevated CO2
Hyperventilation causes CO2 washouts and
removal of volatile acid
Acidosis is corrected
In alkalosis respiration is inhibited to cause
retention of CO2 (accumulate volatile acid)
pH of Arterial Blood and Ventilation
 Renal control of AB balance
4320 m.eq of bicarbonate is filtered daily
Filtered bicarbonate is reabsorbed
Formation of bicarbonate
Excretion of H+
Formation of ammonia and excretion of H +
in the form of ammonium ion (non-titratable
acid excretion)
Re-absorption of bicarbonate
Generation of new bicarbonate
Excretion of H +
 In DT cells
Active secretion of H+ to lumen
Important in forming maximally
concentrated urine
H+ produced in excess of HCO3- in the
tubule is buffered by the phosphate
system
Role of NH3 in H Excretion
+
 Strong ion difference
In 1983 Stewart postulated that pH is dependent
on 3 variables
1.Pco2
2.SID difference between plasma strong
cations (Na+,K+,Ca2+,Mg2+) and anions
(Cl- ,lactate, sulfate, KA, FA)

3.Atot total plasma concentration of non

volatile buffers (albumin,globulin &
phosphate)
 Henderson- Hasselbalch equation
provides an estimate of the magnitude of
the problem but not the mechanism of its
development

Strong ion approach distinguishes 6

primary acid base disturbances
- respiratory acidosis / alkalosis
- strong ion acidosis / alkalosis
- nonvolatile buffer acidosis / alkalosis
 Acidemia results from an increase in Pco 2
or nonvolatile buffer or a decrease in SID

Alkalemia results from a decrease in Pco 2

or nonvolatile buffer or a increase in SID

pH = pK1 + log SID Atot / (1+10pKa-pH)

S Pco2

(normal SID is 42 meq/l)

Interpretation of Blood Gases
 Methodical system
Look at the pH first: acidotic or alkalotic?

Go straight to bicarb!

Correlate bicarb with PaCO2

Increase in std bicarb or a increase in BE

always indicate metabolic alkalosis and a
decrease metabolic acidosis
 Systemcontinued
After you come up with a disturbance your next
question should be is this primary or is this
compensatory

If the pH change is in the direction of the std

bicarb the primary derangement is metabolic

If the pH change is in the opposite direction the

metabolic component is compensatory
 Respiratory acidosis

IN ACUTE: Bicarb rises 1 meq/L for every

10 mmHg elevation in PCO2

IN CHRONIC: Bicarb rises 3.5 for every

10
 Respiratory alkalosis
ACUTE: Plasma bicarb falls by 2 for every
10 fall in PCO2

CHRONIC: Bicarb falls by 4 for every 10

fall in PCO2
 Compensation
The Two Given Rules of Compensation:

1. METABOLIC = BICARB (HCO3)

So if you dealing with figuring out your
disturbance and it is metabolic (up or down
HCO3), then the compensation will be
RESPIRATORY (is the PCO2 appropriately
up or down)
 Compensationcontinued

2. RESPIRATORY = PCO2
So if you are dealing with respiratory
alkalosis or acidosis, you want to know if
the METABOLIC (HCO3) compensation
is appropriate or not
 Compensation continued

If the compensation is INAPPROPRIATE,

then you automatically have a SECOND
superimposed acid/base disorder
Mixed abnormalities
Siggaard Andersen nomogram
 If metabolic acidosis
Calculate the anion gap
(Na + K) - (Cl + HCO3) = around 12
If > 12 = Anion Gap metabolic
acidosis
If < non-anion gap acidosis
 Non anion gap acidosis
HCO3 loss diarrhoea

Ureterosigmoidostomy

Renal tubular acidosis

 Anion gap acidosis
Lactic probably the commonest in ICU
causes hypoxia
hypo perfusion as in low BP
inability to utilize O2 as in sepias
Keto
Renal
Salicylate
 Investigations
PaO2
Actual HCO3-
BP, CVP
Urine ward test
keto sugar
renal protein
 Oxygenation
Check FiO2
Check PaO2
Is there a A-a gradient?
Normal A-a gradient is 0-10 mm Hg
With higher inspired O2 concentrations,
the A-a gradient will also increase
 PaO2-FiO2 ratio
Normal PaO2/FiO2 is 300-500

<300 : ALI (Acute Lung Injury)

<200 indicates a clinically significant gas

exchange derangement: ARDS (Acute
Respiratory Distress Syndrome)

Ratio often used clinically in ICU setting

 Metabolic alkalosis
Vomiting
Ingestion of alkali
Hyper aldostarinisam
Villous adenoma
Diuretics
Barters syndrome
 Management
Acidosis Rx the cause
8.4% NaHCO3 if PH< 7.1
deficiency. BW/3
give half the calculated dose

Alkalosis PPI
omit diuretics
correct low K & Cl
 Respiratory causes
Acidosis hypoventilation
causes central
airway
musculo skeletal
Alkalosis hyperventilation
causes psychogenic, pregnancy
encephalitis
thyrotoxicosis
salicylates
 Management
Acidosis ventilate

Alkalosis reassurance, re breath

change ventilatory settings
increase dead space
Gas transport in biood
Thank you