Arterial blood gases and oximetry
 The measurement of hydrogen ion
concentration (pH), PaO2 and PaCO2, and
bicarbonate concentration in an arterial
blood sample is essential in assessing the
degree and type of respiratory failure and for
measuring acid–base status
 The pH of the arterial plasma is normally
7.40
 Corresponds to a H+ concentration of 40
nmol/L
 An increase in H+ concentration
corresponds to a decrease in pH
 pH is under tight homeostatic regulation, so
that the it does not vary outside the range of
7.44–7.36 under normal circumstances
 To preserve function of many pH-sensitive
enzymes
 A variety of physiological mechanisms
maintain the pH of the ECF
 The first is the action of blood and tissue
buffers, of which the most important
involves reaction of H+ ions with
bicarbonate to form carbonic acid, which,
under the influence of the enzyme
carbonic anhydrase dissociates to form
CO2 and water
 CO2+ H2O --H2CO3 --H+ HCO3−
 This buffer system is important because
bicarbonate is present in relatively high
concentration in the ECF (21–28 mmol/L)
 Two of its key components are under
physiological control: the CO2 by the lungs,
and the bicarbonate by the kidneys
 Respiratory compensation for acid–base
disturbances occurs quickly
 In response to acid accumulation, pH
changes in the brain stem stimulate
ventilatory drive, serving to reduce the
PCO2 and hence drive up the pH
 Systemic alkalosis leads to inhibition of
ventilation
 The kidney also provides of defence against
disturbances of arterial pH
 When acid accumulates due to chronic
respiratory or metabolic (non-renal) causes,
the kidney has the long-term capacity to
enhance urinary excretion of acid, &
increase the plasma bicarbonate
Respiratory acidosis
 Respiratory acidosis can be due to severe
pulmonary disease, respiratory muscle
fatigue, or abnormalities in ventilatory
control and is recognized by an increase in
Paco2 and decrease in pH
 In acute respiratory acidosis, there is an
immediate compensatory elevation (due to
cellular buffering mechanisms) in HCO3–,
which increases 1 mmol/L for every 10mmHg increase in Paco2
 In chronic respiratory acidosis (>24 h), renal
adaptation increases the [HCO3–] by 4
mmol/L for every 10-mmHg increase in Paco2
Clinical features
 Vary according to the severity and duration
of the respiratory acidosis, the underlying
disease, and whether there is accompanying
hypoxemia
 A rapid increase in Paco2 may cause anxiety,
dyspnea, confusion, psychosis, and
hallucinations and may progress to coma
 Acute hypercapnia follows sudden occlusion
of the upper airway or generalized
bronchospasm as in severe asthma,
anaphylaxis, inhalational burn, or toxin
injury
 Chronic hypercapnia and respiratory
acidosis occur in end-stage obstructive lung
disease
 Restrictive disorders involving both the
chest wall and the lungs can cause
respiratory acidosis because the high
metabolic cost of respiration causes
ventilatory muscle fatigue
Treatment
 The management of respiratory acidosis
depends on its severity and rate of onset
 Acute respiratory acidosis can be lifethreatening, and measures to reverse the
underlying cause should be undertaken
simultaneously with restoration of adequate
alveolar ventilation
 This may include tracheal intubation and
assisted mechanical ventilation
 Oxygen administration should be titrated
carefully in patients with severe obstructive
pulmonary disease and chronic CO2
retention who are breathing spontaneously
 The Paco2 should be lowered gradually in
chronic respiratory acidosis, aiming to
restore the Paco2 to baseline levels
 To provide sufficient Cl– and K+ to enhance
the renal excretion of HCO3–
 Chronic respiratory acidosis is frequently
difficult to correct
RESPIRATORY ALKALOSIS
 Characterized by a primary decrease in Pco2
an increased arterial pH and decreased
plasma bicarbonate concentration
 It is most commonly the result of alveolar
hyperventilation rather than
underproduction of CO2
Causes
 Hypoxemia, due to pulmonary disease,
congestive heart failure, and high-altitude
living, or anemia
 Mechanical ventilation
Primary stimulation of the central
chemoreceptor as seen in
 Endotoxemia
 Hepatic cirrhosis
 Salicylate intoxication
 Correction of metabolic acidosis
 Hyperthermia
 Pregnancy
 Cortical hyperventilation from anxiety and
pain
Clinical Manifestations
 Symptoms of acute hypocapnia are largely
attributable to the alkalemia and include
dizziness, perioral or extremity paresthesias,
confusion, asterixis, hypotension, seizures,
and coma
 Symptoms are due to decreased cerebral
blood flow or reduced free calcium (because
alkalosis increases calcium's protein-bound
fraction)
Treatment
 Address the underlying cause of the
disturbance
 Patients who exhibit symptoms, such as
tetany and syncope, and do not have more
serious causes of hyperventilation can be
treated with a rebreathing mask
Metabolic acidosis
 Metabolic acidosis occurs when an acid
other than carbonic acid (due to CO2
retention) accumulates in the body,
resulting in a fall in the plasma bicarbonate
 The pH fall is blunted by hyperventilation,
resulting in a reduced PCO2
 If the kidneys are normal, renal excretion of
acid is gradually increased over days to
weeks, raising the plasma bicarbonate and
hence the pH towards normal
Two typesof metabolic acidosis
 In type A, a mineral acid (HCl)
accumulates, or there is a primary loss of
bicarbonate buffer from the ECF
 There is no addition to the plasma of a new
acidic anion
 In this case, the ‘anion gap’ is normal since
the plasma chloride increases to replace the
depleted bicarbonate levels
 Anion gap is the difference between the
main measured cations (Na+ + K+) and the
anions (Cl− + HCO3−)
 This ‘gap’, normally around 15 mmol/L
 is made up of anions such as phosphate,
sulphate and multiple negative charges on
plasma protein molecules
 Normal anion gap metabolic acidosis
(typeA) is usually due either to diarrhoea,
where the clinical diagnosis is generally
obvious, or to renal tubular acidosis
 In pattern B, an accumulating acid is
accompanied by its corresponding anion,
which adds to the unmeasured anion gap,
while the chloride concentration remains
normal
 The cause is usually apparent from
associated clinical features
 Uncontrolled diabetes mellitus
 Renal failure
 Shock
 Methanol poisoning where pts will present
with visual complaints
 Lactic acidosis
Lactic acidosis
 Accumulation of lactic acid
 Normal maximal level is 2 mmol/L
 Two types
 Type 1, due to tissue hypoxia and peripheral
generation of lactate, as in patients with
circulatory failure and shock
 Type 2, due to impaired metabolism of
lactate as in liver disease
 A number of drugs and toxins also impair
lactate metabolism, including metformin
Renal tubular acidosis (RTA)
 This condition should be suspected when
there is a hyperchloraemic (normal anion
gap) acidosis
 no evidence of gastrointestinal disturbance
 Urine pH is inappropriately high (i.e. > 5.5
in the presence of systemic acidosis)
 Defective reabsorption of bicarbonate in the
 proximal tubule (proximal RTA)
 Defective acid secretion in the late
distal/cortical collecting duct (distal RTA)
 Defective sodium reabsorption in the late
distal/cortical collecting duct, with reduced
secretion of both potassium and acid
(hyperkalaemic distal RTA)
 Management of metabolic acidosis
 identify and correct the cause
 This may involve control of diarrhoea,
treatment of diabetes mellitus, correction of
shock, cessation of drug administration, or
dialysis to remove toxins
 Since metabolic acidosis is frequently
associated with sodium and water depletion,
resuscitation with appropriate intravenous
fluids is often needed
 Use of intravenous bicarbonate in this
setting is controversial
 Rapid correction of acidosis can induce
 hypokalaemia or reduce plasma ionised
calcium
 use of bicarbonate infusions is best reserved
for situations where the underlying disorder
cannot be readily corrected and the acidosis
is critical (pH < 7.00) and associated with
evidence of tissue dysfunction