25. Acid–Base Balance Flashcards
Intro
Why important
What tryingto maintain as normal
How
A stable pH in body fluids is essential to maintain 1 normal enzyme function, 2 ion distribution and 3 protein structure.
Homeostatic acid–base regulatory mechanisms aim to maintain a pH between 7.35 and 7.45 ([H+] of 45–35 nmol/L) via:
> Buffers in tissue and blood
> Excretion of acids by kidneys
and
lungs
Normal acid–base balance relies on the following variables:
> pH ~ 7.40
> PCO2 ~ 5.3 kPa (40 mmHg)
> HCO3 – ~ 24 mmol/L
An acid–base disturbance occurs when at
least two of these three variables are abnormal.
The primary change determines whether a disturbance is respiratory (alteration of PCO2) or metabolic (alteration of the bicarbonate buffer system by means other than PCO2).
Base
Proton acceptor,
or hydroxide (OH-) producer,
pH > 7.0
Acid:
> Strong acid (e.g. HCl):
> Weak acid
Acid
proton donor, pH < 7.0
The strength of an acid is defined by its ability to give up protons:
Strong Acid
fully dissociates in solution
Weak Acid (e.g. carbonic acid): does not fully dissociate, and together with its conjugate base, it acts as an acid–base buffer system to resist a change in pH.
pH:
measure of the acidity of a solution and is calculated as the negative logarithm to the base 10 of the hydrogen ion concentration.
> Normal serum pH
> Normal serum pH
is 7.40 (range 7.36–7.44).
Acidosis
Acidosis: a process
where there is acid accumulation
or alkali loss.
Acidaemia
Acidaemia:
occurs when the arterial
pH < 7.35 or [H+] > 45 nmol/L.
Alkalosis
Alkalosis:
a process where there
is acid loss or
alkali accumulation.
Alkalaemia:
Alkalaemia:
occurs when the
arterial pH > 7.45 or [H+] < 35 nmol/L.
Standard bicarbonate
define
what does it represent
Standard bicarbonate:
plasma concentration of bicarbonate when arterial PCO2 has been corrected to 5.3 kPa, haemoglobin is fully saturated and the body temperature is 37 °C.
It represents what the actual bicarbonate
would be after eliminating
any respiratory component of
acid–base disturbance.
Base excess (deficit):
What is it
when is positive and negative
What can be used to derive it
The amount of acid or base required to restore 1 litre of blood to normal pH at a PaCO2 of 5.3 kPa and at body temperature.
It is negative in acidosis and positive in alkalosis, and is a useful marker of severity of the metabolic component of acid–base disturbances.
The Siggaard–Anderson nomogram can be used to derive the base deficit and standard bicarbonate if the pH, PCO2 and haemoglobin are know
pKa
pKa:
the pH of an acid at
which it is 50% dissociated,
or in equilibrium with its conjugate base.
It is a measure of the strength
of an acid
(the lower the pKa, the stronger the acid)
and is calculated as the
negative logarithm to the
base 10 of the
dissociation constant of an acid.
What compensatory mechanisms exist?
Why do the exist
What way doe they respond to primary change
Compensation
How long does each mechanism take
These aim to restore the pH
towards normal,
and are based on maintaining
the ratio PaCO2 /[HCO3–];
therefore, the variable in the compensatory
response always changes
in the same direction as the variable responsible
for the primary imbalance.
Correction occurs when
all three variables
(pH, HCO3– and PaCO2) are
restored to normal levels.
> Initial compensation is by
intracellular buffering
(carbonic acid– bicarbonate buffer system
and haemoglobin)
and occurs within 2 hours.
> Respiratory compensation reaches
its maximum by 24 hours and is by:
• Hyperventilation in the presence
of a metabolic acidosis.
• Hypoventilation in the presence
of a metabolic alkalosis.
> Renal compensation is by:
• Increased acid (H+) secretion
and HCO3 – retention
(reabsorption and
regeneration) in the
presence of a respiratory (and metabolic) acidosis.
• Decreased acid (H+) secretion
and HCO3 – retention
(reabsorption and regeneration)
in the presence of a respiratory
(and metabolic)
alkalosis.
The generation of bicarbonate, through urinary excretion of ammonium and phosphate, restores the depleted HCO3 – and buffer base reserves over 2–3 days.
Table 25.1 Primary changes and compensatory mechanisms in acid–base
disorders
Table 25.1 Primary changes and compensatory mechanisms in acid–base
disorders
Identify the abnormalities of
these arterial blood gases: pH 7.0;
PaCO2 7 kPa; PaO2 7 kPa.
Abnormality: Acidaemia (pH < 7.4)
Process: Acidosis (excess production of acid, in the form
of CO2)
Primary change:
Respiratory (↑PaCO2 and ↓PaO2, i.e. type 2
respiratory failure)
Acute v. chronic:
Likely acute as uncompensated
Base excess/deficit: Negative
Standard bicarbonate:
Low in acute setting, as slow renal
compensation is incomplete
What would you expect the pH to
be in patients with a chronically
elevated PaCO2 at 7 kPa?
In chronic respiratory acidosis,
the renal compensatory mechanisms result in
a chronic elevation of plasma bicarbonate,
which in turn restores the pH to
within the normal range.
Typically, renal compensation is not complete, and
the normal level of pH 7.40 is never reached
How does metabolic compensation take place?
The increased PaCO2 in the
renal tubular cells results
in an increased secretion of H+ ions.
Their secretion results in the following:
• Reabsorption of bicarbonate
by the dissociation of carbonic acid
• Regeneration of bicarbonate
by the excretion of H+ with
ammonia and phosphate in urine.
Metabolic compensation takes place over 2–3 days.
Describe the physiological process accounting for the low pH.
Respiratory acidosis is a consequence
of hypoventilation or ventilation perfusion inequalities.
The resulting elevated PCO2
disrupts the ratio of HCO3− to PCO2
and causes a drop in pH.
Comment on PaO2 of 7 with the above gas of pco2 7 ph 7
This is lower than normal, suggesting either a problem with ventilation, diffusion, shunt or a ventilation–perfusion mismatch.
Assuming the inspired concentration of
oxygen is known,
the alveolar partial pressure of oxygen
can be calculated using the
alveolar gas equation.
The A-a gradient can then be
worked out and type of
hypoxia can be assessed,
to help establish the cause.
`Define anion gap and list causes
of an increased gap.
T he anion gap (AG) is the difference
between measured cations
(positively charged ions)
and measured anions
(negatively charged ions) in serum.
> This difference (gap) can be accounted
for by the presence of unmeasured anions,
such as albumin, lactic acid, ketones
(β-hydroxybutyrate and acetoacetate),
phosphates and sulphates.
AG Eqn
> C lassically it has been calculated using the equation:
• AG = ([Na+] + [K+]) − ([Cl−] + [HCO3−])
- Normal range of 10–20 mmol/L
- [K+] may be excluded from the equation
(as its value is negligible compared
to the other measured ions)
giving a normal AG range of
8–16 mmol/L.
• Modern analysers now predict a
normal range of 3–11 mmol/L.
> In the presence of acidic unmeasured anions, there is a secondary loss of bicarbonate ions due to their buffering capacity,
but chloride concentration remains
unchanged in order to maintain electroneutrality.
The AG, therefore, becomes elevated.
