OLADAPO OLAYEMI

FWACS,FMCOG(NIG),MPH (JOHNS HOPKINS)

PROFESSOR
DEPT OF OBSTETRICS AND GYNAECOLOGY,
UNIVERSITY COLLEGE HOSPITAL, IBADAN
 Fluid in which cells are insulated in the body
function optimally in a narrow limit of pH
 Normal plasma pH is 7.35-7.45 at 37ºC
 Slight deviation from this normal can lead to
death of the cell. At pH of 7.00 or below,
death occurs from acidotic coma while at pH
of 7.8 or above, death occurs from tetany
 Most enzymatic reactions also must take
place in certain pH ranges including drug
actions.
 Arterial blood gas values are usually given as
pH,pO2, pCO2, [HCO3¯], base excess/deficit
and % oxygen saturation
 Less frequently venous and mixed venous
blood gases are measured
 Mixed venous blood samples are obtained
from right atrium , usually through a
pulmonary catheter
Measurement Arterial blood Mixed blood
pH 7.4(7.37-7.44) 7.36
pO2 80-100mmhg 35-40mmhg
pCO2 35-40mmhg 41-51mmhg
O2 saturation >95% 60-80%
[HCO3¯] 22-26mEq/L 22-26mEq/L
Base def/excess -2 to +2 -2 to +2

Decrease in base [HCO3¯] is termed base

deficit, increase in base is termed base
excess
 Blood gas machines measure pH, pCO2 and pO2 but
[HCO3¯] and base differences are calculated using
H/H equation.
 Henderson-Hasselbalch Equation: pH = 6.1 + log 10
(HCO3-) / (0.03 x pCO2)
 Henderson Equation: (H+) = 24 x pCO2 / (HCO3-)
 The Henderson equation is easier to use, but only
applies when pH is between 7.2 and 7.6.
 For this equation, one must calculate [H+] from pH
 [H+] = 40 mEq/L when pH is 7.4.
 The [H+] increases 10 mEq/L for a 0.1 unit drop in
pH.
 A change in pCO2 up or down 10mmhg is associated
with increase or decrease in pH of 0.08 units.
 ACIDOSIS(pH<7.37)
 ALKALOSIS( pH >7.37)
 Abnormalities in the respiratory and
metabolic/renal systems are the major causes
of acid-base disturbances
 An abnormal pCO2 will alter the pH as well as
any metabolic disturbance altering [HCO3¯]
 Any primary disturbance in acid-base
homeostasis will evoke a normal
compensatory response.
 A primary metabolic disorder leads to a
respiratory compensation and a primary
respiratory disorder leads to an acute
metabolic compensation due to the buffering
capacity of body fluids
 A more chronic compensation (1-2 days), will
require alteration in renal function
 A- B dist Primary abn Second Resp
MA [HCO3¯]  pCO2
MALK [HCO3¯]  pCO2
RA  pCO2 [HCO3¯]
RALK  pCO2  [HCO3¯]
MA= metabolic acidosis, MALK= metabolic
alkalosis, RA= Respiratory acidosis, RALK=
Respiratory alkalosis
 Metabolic acidosis is a disorder with low plasma
[HCO3-] caused by a net gain of H+ or loss of
HCO3-
 If unopposed, it will result in acidemia.
 A net gain of H+ is illustrated as follows:
 CO2 + H2O  H2CO3  H+ + HCO3-
 
 [H+] = 24  PCO2 / [HCO3-]
 
 A rise in [H+] results in a decrease in pH
 The ↑[H+] drives conversion of HCO3- to
H2CO3 and the conversion of H2CO3 to CO2
 Thus there is an increase in [H+] and a
decrease in pH
 In chronic metabolic acidosis, acidemia
triggers respiratory compensation
 The ↓ pCO2 drives the conversion of H2CO3 to CO2,
and the conversion of H+ and HCO3- to H2CO3
 This will result in a ↓ in [H+] and an ↑ in pH towards
normal
 Respiratory compensation begins within the first hour
and is complete by 12 to 24 hours
 However, even with maximum respiratory
compensation acidemia persists
 Metabolic acidosis can be anion gap or a nonanion gap
acidosis
 Anion gap acidosis is caused by decrease in [HCO3¯]
by an increase in an unmeasured acid ion either from
endogenous or exogenous ingestion (normochloremic)
 Nonanion gap acidosis (AG 8-12mEq/L). This
is due to decrease in [HCO3¯] balance by an
increase in chloride (hyperchloremic acidosis)
 methanol ingestion
uremia
diabetic ketoacidosis/starvation or
ethanol ketoacidosis
paraldehyde ingestion
iron toxicity (rare)
lactic acidosis
ethylene glycol
rhabdomyolysis
salicylates poisoning
Fistulae, diarrhoea, starvation
 Metabolic alkalosis is a disorder with high plasma
[HCO3-] caused by a net gain of HCO3- or loss of
H+
 If unopposed, it will result in alkalemia.
 A net loss of H+ is illustrated as follows:
 CO2 + H2O  H2CO3  H+ + HCO3-
 
 [H+] = 24  PCO2 / [HCO3-]
 
 A ↓ in [H+] results in an ↑ in pH
 The reduced [H+] drives conversion of H2CO3 to
HCO3-. Thus [HCO3-] is increased.
 A net gain of HCO3- is illustrated as follows:
 CO2 + H2O  H2CO3  H+ + HCO3-
 
 [H+] = 24  pCO2 / [HCO3-]
 
 There is an increase in [HCO3-]
 The ↑ [HCO3-] drives the consumption of H+, thus
↓ [H+] and ↑ pH
 With a gain of HCO3- or a loss of H+, [H+] is
reduced, [HCO3-] is ↑ed, and pH is ↑ed
 Alkalemia then triggers respiratory compensation
 With respiratory compensation, ↓ed alveolar
ventilation results in a ↓ in CO2 elimination and an
↑ in pCO2
 The ↑ed pCO2 drives the conversion of CO2 to
H2CO3 and the dissociation of H2CO3 into H+ and
HCO3-
 This results in an ↑ in [HCO3-], an ↑ in [H+]
and a ↓ in pH towards normal
 Alkalemia also triggers ↑ed glycolysis and
lactic acid production
 This also helps ↑ [H+] and ↓ pH towards
normal
 Respiratory compensation begins within the
first hour and is complete by 12 to 24 hours.

 Chloride–responsive (urine Cl < 10 mEq/L):
vomiting, NG drainage, diuretics, post–
hypercapneic, cystic fibrosis, villous adenoma,
congenital chloride diarrhea.
 Chloride–resistant (urine Cl > 10mEq/L):
hypokalemia, primary aldosteronism, secondary
aldosteronism (CHF, cirrhosis & ascites), Cushing’s
syndrome, Steroid administration
 Miscellaneous: poorly resorbed anion (high
dose carbenicillin, refeeding alkalosis,
administration of alkali (e.g. overshoot from
treatment of acidosis, massive transfusions with
citrate anticoagulant, milk alkali).
 Respiratory acidosis is a disorder with high
pCO2 caused by reduced CO2 elimination (or
hypoventilation). There is a compensatory
rise in plasma[HCO3]. If unopposed, it will
result in acidaemia.
 Respiratory acidosis is illustrated as follows:
 CO2 + H2O  H2CO3  H+ + HCO3- 
 
 [H+] = 24  PCO2 / [HCO3-]
 
 In acute respiratory acidosis, ↑pCO2 drives → CO2 to
H2CO3, and H2CO3 → ↑ HCO3- and ↑ H+, and ↓PH
 In chronic respiratory acidosis, ↑ PCO2 triggers renal
compensation
 There is an ↑ H+ excretion into the urine and ↑ generation
of new HCO3- in the blood by the kidney
 The resultant effects are:↑ [HCO3-], ↓H+], and ↑pH towards
normal
 Renal compensation begins within 24 hours and is complete
in 5 days
 Despite compensation, the pH remains in the lower range of
normal.
 Treat by increasing ventilation- intubate and place on
ventilator, increase ventilator rate. If sedation was given,
reverse with Nalaxone
 Respiratory center inhibition (sedatives,
opiates, O2 in CO2 retainer)
 Neuromuscular disorder (Guillain–Barré,
myasthenia gravis, hypokalemia)
 Chest wall disorder (rib fractures, pulmonary
oedema, severe pnuemonia)
 Airway obstruction (acute- asthma, chronic-
COPD)
 Acute and chronic lung disease
 Respiratory alkalosis is a disorder with ↓ pCO2
cause by ↑CO2 elimination (hyperventilation).
 If unopposed, it will result in alkalemia
 Respiratory alkalosis is illustrated as follows:
 CO2 + H2O  H2CO3  H+ + HCO3- [H+] = 24  PCO2 / [HCO3-]
    
 In acute respiratory alkalosis, ↓ pCO2 drives the
conversion of H2CO3 to CO2, and the association
of HCO3- and H+ to form H2CO3
 The result is a ↓ in [HCO3-], a ↓ in [H+] and an ↑ in
pH
 In chronic respiratory alkalosis, the low pCO2
triggers renal compensation
 There is a ↓ in secretion of H+ into the urine and ↓
in generation HCO3- by the kidney
 The resultant is a ↓ in [HCO3-], an ↑ in [H+] and a ↓
in pH towards normal
 Renal compensation begins within hours and is
complete in 3 days.
 pH often can be restored to normal
 CNS disorders, anxiety, hyperventilation
syndrome, head injury, CVA, Tumors
 Hypoxia
 Pulmonary receptor stimulation (asthma,
pneumonia, pulmonary edema, PE), anxiety,
drugs (early salicylate toxicity, theophylline)
 liver failure
 Sepsis
 Fever
 Pulmonary embolus, CCF
 Pregnancy
 This occurs in seriously ill patients where two
or more different primary acid-base
disorders occur simultaneously
 The net effect may be additive eg
metabolic/respiratory acidosis resulting in
extreme alteration; or opposite eg metabolic
acidosis/ respiratory alkalosis, they will
nullify each other’s effect
 Identify primary disturbance as acidosis or
alkalosis (pH <7.37 or > 7.44)
 Identify the primary disturbance as metabolic
or respiratory eg if the blood gas is acidotic,
and if pCO2 is >40mmhg and
[HCO3¯]>24mEq/L, then the problem is
respiratory acidosis
 Identify which component is altered in the
same direction as the pH
 Checking the degree of compensation and
calculating the anion gap
 ) ANION GAP (AG) = [Na+] – ([Cl-] + [HCO3-]) =
10  2 mEq/L (8-12 mEq/L
 There are anions and cations that are easily
measured, i.e. Na+, Cl- and HCO3-
 Normally [Na+] is in excess of the sum of [Cl-] and
[HCO3-].
 This is due to the presence of unmeasured anions
 Unmeasured anions include inorganic anions
(SO42- and PO42-), and organic anions (lactate, -
hydroxybutyrate and salicylate), and anionic
proteins
 In certain types of metabolic acidosis, the unmeasured
anions are ↑ed in concentration, thus resulting in an
↑ed in the anion gap
 Suppose that metabolic acidosis is due to the net gain
in H+A-, were A- is some unmeasured anion Then
HCO3- combines with H+ to form H2CO3; H2CO3 is
converted to CO2, and CO2 is lost by alveolar
ventilation
 The net result is that HCO3- is replaced by A-
 Plasma [HCO3-] falls as [A-] increases
 Since, [Na+] and [Cl-] remain constant, the anion gap
increases
 Normal range of AG 8-12mEq/L
 Obtained from highly vascularized places eg
heel
 Commonly used for paediatric patients(
arterial blood are difficult and more traumatic
to obtain in them).
pH Same as arterial or lower (7.35-7.40)
pCO2 Same as arterial or higher 40-45
pO2 Lower than arterial 45-60
O2 Saturation >70% is acceptable
 Blood gases can give an idea of level of
oxgenation
 Usually given as pO2, % O2 saturation
 Oxygen saturation depends on pH, 2,3-DPG,
temperature.
 A shift to the right means acidosis, fever
(reduced O2) while to the left means alkalosis
eg in hypothermia, banked blood