1. Abu El-Reesh Hospital
Arterial Blood Gases (ABG)
Acid Base Balance and ABG Interpretation
An Approach for ICU Clinical Pharmacists
Shaza Aly
BCPS, ALS, ICU Clinical Pharmacist
18/11/2015
2. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
ABG Concepts and Practice
Targets you should take home:
1. Understand Acid Base disorders
2. Making ABG interpretation easy
3. Treatment of Acid Base disorders
Topics to reach targets:
Part 1 :Concepts
Aim to:
Pulmonary gas exchange concepts
Disorders of gas exchange
o Acid–base balance
o Disorders of acid–base balance
ABG sampling technique
When and why is an ABG required?
– Common ABG values
– Making ABG interpretation easy
Part 2 :Practice
Aim to:
To put all of this into practice with a series of case scenarios involving
ABG analysis
Cases
Part 3: Treatment of Acid Base disorders
3. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
Part 1 :Concepts
PULMONARY GAS EXCHANGE: THE BASICS Please do not skip them!
1. Partial Pressures
2. CO2 elimination
3. Haemoglobin Oxygen Saturation (So2)
4. Oxyhaemoglobin Dissociation Curve
5. Alveolar Ventilation And Pao2
6. Ventilation/Perfusion Mismatch And Shunting
7. Fio2 And Oxygenation
4. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
Lung
BloodOxygen
ation
1. Hb Conc
2. Saturation of Hb
with O2 (SO2):
CO2 elimination
-V/Q
-FiO2
5. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
NB
O2 comprises 21% of air, so the partial pressure of O2 in air= 21% of atmospheric
pressure
CO2 makes up just a tiny fraction of air, so the partial pressure of CO2 in inspired air
is negligible.
Extremely thin alveolar–capillary membrane), CO2 and O2 are
able to move (diffuse) between them
Arterial blood gases (ABGs) help us to assess the effectiveness
of gas exchange by providing measurements of the partial
pressures of O2 and CO2 in arterial blood (i.e. the Pao2and
Paco2).
PO2 = partial pressure of O2
PaO2 = partial pressure of O2 in arterial blood
At the alveolar–capillary membrane, air in alveoli has a higher
Po2 and lower Pco2 than capillary blood. Thus, O2 molecules
move from alveoli to blood and CO2 molecules move from
blood to alveoli until the partial pressures are equal.
6. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
1. PARTIAL PRESSURES
Partial pressure: contribution of one individual gas within a gas mixture (such as
air) to the total pressure. When a gas dissolves in liquid (e.g. blood), the amount
dissolved depends on the partial pressure
2. CARBON DIOXIDE ELIMINATION
a. Ventilation
b. Hypoxic Drive
7. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
In patients (chronic hypercapnia), the specialized receptors that
detect CO2 levels can become desensitised.The body then relies on
receptors that detect the PaO2 to gauge the adequacy of
ventilation and low PaO2 becomes the principal ventilator stimulus.
This is referred to as hypoxic drive.
In patients who rely on hypoxic drive, overzealous correction of
hypoxaemia, with supplemental O2, may depress ventilation, leading
to a catastrophic rise in PaCO2.
Patients with chronic hypercapnia must there fore begiven
supplemental O2 in a controlled fashion with careful ABG
monitoring. The same does not apply to patients with acute
hypercapnia.
8. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
3. HAEMOGLOBIN OXYGEN SATURATION (SO2)
Po2 does not actually tell us how much O2 is in blood. It only measures free,
unbound O2 molecules – a tiny proportion of the total.
In fact, almost all O2 molecules in blood are bound to Hb; Because of this, the
amount of O2 in blood depends on the following two factors:
1. Hb concentration:
2. Saturation of Hb with O2 (SO2):
NB:
SO2= O2 saturation in (any) blood while SaO2= O2 saturation in arterial blood
pulse oximeter:
– A probe (pulse oximeter) applied to the finger or earlobe.
– less accurate with saturations below 75%
– Unreliable when peripheral perfusion is poor.
– Oximetry does not provide information on PaCO2 and, therefore, should not be used as a
9. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
substitute for ABG analysis in ventilator impairment
Keypoint
PO2 is not a measure of the amount of O2 in blood – ultimately, the SaO2 and the Hb
concentration determine the O2 content of arterial blood
4. OXYHAEMOGLOBIN DISSOCIATION CURVE:
– We now know that the amount of O2 in blood depends on the Hb
concentration and the So2. So what is the significance of the Po2?
Po2 can be thought of as the driving force for O2 molecules to bind to Hb:
as such, it regulates the So2.
– The oxyhaemoglobin dissociation curve shows the So2 that will result from
any given Po2
10. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
Key points:
• PO2 is not the amount of
O2 in blood but is the
driving force for
saturating Hb with O2.
• Note the sigmoid shape: it is
relatively flat when PO2 is
greater than 80 mmHg but
steep when PO2 falls below
60 mmHg
11. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
5.ALVEOLAR VENTILATION AND PaO2
We have now seen how Pao2 regulates the Sao2. But what determines Pao2?
Three major factors dictate the Pao2:
1. Alveolar ventilation
• Key point
Both oxygenation and CO2 elimination depend on alveolar ventilation: impaired
ventilation causes PaO2 to fall and PaCO2 to rise.
2. Matching of ventilation with perfusion(V˙/Q˙)
• Not all blood flowing through the lung meets well-ventilated alveoli and not all
ventilated alveoli are perfused with blood – especially in the presence of lung
disease. This problem is known as ventilation/perfusion (V˙/Q˙) mismatch.
• If alveoli in one area of the lung are poorly ventilated (e.g. due to collapse or
consolidation). Blood passing these alveoli returns to the arterial circulation
with less O2 and more CO2 than normal. This is known as shunting
Key points
• V˙/Q˙mismatch allows poorly oxygenated blood to re-enter the arterial circulation, thus lowering
PaO2 and SaO2.
• Provided overall alveolar ventilation is maintained, theV˙/Q˙mismatch does not lead to an increase
in PaCO2.
13. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
1. Concentration of O2 in inspired air (FiO2)
• The fraction of inspired oxygen (Fio2) refers to the percentage of O2 in the air we
breathe in. The Fio2 in room air is 21%, but can be increased with supplemental O2.
• A low Pao2 may result from either V˙/Q˙ mismatch or inadequate ventilation and, in both
cases, increasing the Fio2 will improve the Pao2
• When the cause is inadequate ventilation, it must be remembered that increasing Fio2 will
not reverse the rise in Paco2.
• A useful rule of thumb is that the difference between Fio2 and Pao2 (in kPa) should not
normally be greater than 10
14. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
DISORDERS OF GAS EXCHANGE
1. HYPOXIA, HYPOXAEMIA AND IMPAIRED OXYGENATION
2. HYPERVENTILATION
1. HYPOXIA, HYPOXAEMIA AND IMPAIRED OXYGENATION:
• Hypoxia refers to any state in which tissues receive an inadequate supply of O2
to support normal aerobic metabolism It may result from impaired blood
supply to tissues (ischaemia). It is often associated with lactic acidosis as cells
resort to anaerobic metabolism
• Hypoxaemia refers to any state in which the O2 content of arterial blood is
reduced. It may result from impaired oxygenation , low haemoglobin (anaemia)
or reduced affinity of haemoglobin for O2 (e.g. carbon monoxide).
• Impaired oxygenation refers to hypoxaemia resulting from reduced transfer of
O2 from lungs to the blood stream. It is identified by a low Pao2 (<10.7 kPa;
<80 mmHg).
16. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
Type 1 Respiratory Impairment
• Type 1 respiratory impairment: low Pao2 with normal or low Paco2.
• The Paco2 is often low due to compensatory hyperventilation.
• If the arterial blood gas (ABG) is drawn from a patient on supplemental O2, the Pao2
may not be below the normal range, but will be inappropriately low for the Fio2
•
17. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
Type 2 Respiratory Impairment
• Type 2 respiratory impairment is defined by a high Paco2 (hypercapnia) and
is due to inadequate alveolar ventilation
• It is important to note that any cause of type 1 impairment may lead to type
2 impairment if exhaustion supervenes
• Supplemental O2 improves hypoxaemia but not hypercapnia and, therefore,
treatment of type 2 respiratory impairment should also include measures to
improve ventilation (e.g. reversal of sedation, relief of airways obstruction,
assisted ventilation).
• The overzealous supplemental O2 to some patients with chronic type 2
impairment may further depress ventilation by abolishing hypoxic drive
• Because pulse oximetry provides no information on Paco2, it is not a suitable
substitute for ABG monitoring in type 2 respiratory impairment
2. HYPERVENTILATION
• Hyperventilation leads to a low Paco2 (hypocapnia) and a corresponding rise
in blood pH .
• Hyperventilation also occurs as a compensatory response to metabolic
acidosis (secondary hyperventilation)
18. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
SUMMARY OF GAS EXCHANGE ABNORMALITIES
19. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
ACID–BASE BALANCE: THEBASICS
MAINTAINING ACID–BASEBALANCE:
What generates H+ ions in our bodies?
The breakdown of fats and sugars for energy generates CO2,
which, when dissolved in blood, forms carbonic acid
H+ ions must, therefore, be removed to maintain normal blood
pH.
What removes H+ ions from our bodies?
Respiratory mechanisms
Our lungs are responsible for
removing CO2.
Paco2, the partial pressure of
carbon dioxide in our blood, is
determined by alveolar
ventilation.
If CO2 production is altered,
we adjust our breathing to
exhale more or less CO2, as
necessary, to maintain Paco2
within normal limits.
The bulk of the acid produced
by our bodies is in the form of
CO2, so it is our lungs that
excrete the vast majority of
the acid load.
Renal (metabolic) mechanisms
Kidneys secrete H+ ions into urine
and reabsorb HCO3− from urine.
HCO3− is a base (and therefore
accepts H+ ions), so it reduces the
concentration of H+ ions in blood.
also maintain stable
concentrations of the major
electrolytes (e.g. sodium and
potassium) and try to preserve
electro neutrality (i.e. the overall
balance between positively and
negatively charged particles in the
body).
20. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
MAINTAINING ACID–BASE BALANCE
H2O + CO2 ↔ H2CO3 ↔ H+ + HCO3 -
it predicts that blood pH depends not on the absolute amounts of CO2
or HCO3 present but on the ratio of CO2 to HCO3.
Thus, a change in CO2 will not lead to a change in pH if it is balanced by
a change in HCO3 that preserves the ratio (and vice versa).
Because CO2 is controlled by respiration and HCO3 by renal excretion,
this explains how compensation can prevent changes in blood pH.
Balancing acts in kidney
There are two major ‘balancing acts’ that influence acid–base regulation:
Cl− and HCO3:
• are the main negatively charged ions
(anions) that have to balance
(cations; predominantly Na+ and
K+).
• During times of high Cl− loss, more
HCO3 − is retained;
• when HCO3 − losses are high (via the
kidney or gastrointestinal tract),
more Cl− is retained.
1. Sodium ions (Na+) are
retained by swapping them for
either a potassium ion (K+) or
H+. When K+ is in short
supply, H+ has to take up the
slack (and vice versa), and
therefore, more H+ are
excreted in exchange for Na+.
21. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
DISTURBANCES OF ACID–BASE BALANCE
22. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
compensation :
• The renal and respiratory systems operate jointly to maintain blood pH within normal
limits.
• If one system is overwhelmed, leading to a change in blood pH, the other usually
adjusts, automatically, to limit the disturbance (e.g. if kidneys fail to excrete metabolic
acids, ventilation is increased to exhale more CO2). This is known as compensation.
COMPENSATED ACID–BASE DISTURBANCE:
When faced with such an ABG, how can we tell which is the primary disturbance and which is
the compensatory process?
• the patient is more important than the ABG. When considering an ABG, one
must always take account of the clinical context.
• For example, if the patient has a diabetic, with high levels of ketones in the
urine, it would be obvious that the metabolic acidosis was a primary process
(diabetic ketoacidosis).
MIXED ACID–BASE DISTURBANCE:
When a primary respiratory disturbance and primary metabolic
disturbance occur simultaneously, there is said to be a mixed acid–base
disturbance
If these two processes oppose each other, the pattern will be similar to a
compensated acid–base disturbance and the resulting pH derangement will
be minimized.
A good example is salicylate poisoning, where primary hyperventilation
(respiratory alkalosis) and metabolic acidosis (salicylate is acidic) occur
independently.
By contrast, if the two processes cause pH to move in the same direction
(metabolic acidosis and respiratory acidosis or metabolic alkalosis and
respiratory alkalosis), a profound acidaemia or alkalaemia may result
23. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
EVALUATION OF ACID–BASE
DISORDERS
Acid–base disorders should be evaluated using a stepwise approach:
1. Obtain a detailed patient history and clinical assessment.
2. Check the arterial blood gas, sodium, chloride, and HCO−3 .
3. Identify all abnormalities in pH, Paco2, and HCO−3 .
4. Determine which abnormalities are primary and which are Compensatory
based on pH.
a. If the pH is less than 7.40, then a respiratory or metabolic acidosis is primary.
b. If the pH is greater than 7.40, then a respiratory or metabolic alkalosis is
primary.
c. If the pH is normal (7.40) and there are abnormalities in Paco2 and HCO−3 , a
mixed disorder is probably present because metabolic and respiratory
compensations rarely return the pH to normal.
4. Always calculate the anion gap. If it is equal to or greater than
20, a clinically important metabolic acidosis is usually present even if the pH
is within a normal range.
5. If the anion gap is increased,
• calculate the excess anion gap (anion gap – 10).
• Add this value to the HCO−3 to obtain corrected value.
24. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
a. If the corrected value is greater than 26, a metabolic alkalosis is also
present.
b. If the corrected value is less than 22, a non anion gap metabolic acidosis is
also present.
6. Consider other laboratory tests to further differentiate the cause of the
disorder.
If the anion gap is high, measure serum ketones and lactate.
7. Compare the identified disorders to the patient history and begin patient-
specific therapy
1. METABOLIC ACIDOSIS
Metabolic acidosis is characterized by:
Loss of bicarbonate from the body,
Decreased acid excretion by the kidney,
Or increased endogenous acid production
Two categories of simple metabolic
acidosis (i.e., normal anion gap and increased anion gap)
The anion gap (AG) represents the concentration of unmeasured negatively
charged (anions) in excess of the concentration of unmeasured positively charged
substances (cations) in the extracellular fluid
Of the unmeasured anions, albumin is perhaps the most important:
In critically ill patients with hypoalbuminemia, the
calculated AG should be adjusted using the following formula:
adjusted:
AG= AG+ 2.5 × (normal albumin – measured albumin in g/dL),
where a normal albumin concentration is assumed to be
4.4 g/dL.
The severity of a metabolic acidosis should be judged according to
both the underlying process and the resulting acidaemia.
An HCO3 less than 15 mmol/L (or BE < −10) indicates a severe acidotic
process, whereas a pH below 7.25 constitutes serious acidaemia.
The dominant symptom in metabolic acidosis is often hyperventilation
(Kussmaul respiration) owing to the respiratory compensation
https://www.youtube.com/watch?v=TG0vpKae3Js
25. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
a. METABOLIC ACIDOSIS AND
ANION GAP
b. LACTIC ACIDOSIS
c. DIABETIC KETOACIDOSIS DKA
26. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
a. METABOLIC ACIDOSIS AND ANION GAP
Calculating the anion gap may help to establish the cause of a metabolic
acidosis.
Metabolic acidosis with a normal
anion gap
Metabolic acidosis with a high
anion gap
Caused by excessive loss of
HCO3− (e.g. renal tubular
acidosis) or GIT (e.g. diarrhea).
Kidneys respond to the drop in
HCO3− by retaining Cl−,
preserving electro-neutrality.
Because it entails an increase in
Cl−, normal anion gap acidosis is
also referred to as
‘hyperchloraemic metabolic
acidosis’.
usually caused by :
– Ingestion of an exogenous acid
– Or increased production of an
endogenous acid.
Because the anion that is
paired with H+ to form these
acids is typically not measured
(e.g. lactate, salicylate), its
presence leads to an increase
in the gap.
In high anion gap acidosis, the
size of the gap is usually
proportionate to the severity
of the acidosis.
easy pneumonic to remember
:ACCRUED.
A = Ammonium chloride/acetazolamide
(urine bicarbonate loss)
C = Chloride intake (PN, intravenous
solutions)
C = Cholestyramine (GI bicarbonate
loss)
R = Renal tubular acidosis
U = Urine diverted into the intestine
fistula)
Lactic acidosis and diabetic ketoacidosis
(DKA) – two common and clinically
important causes of high anion gap
metabolic acidosis
27. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
E = Endocrine disorders (e.g.,
aldosterone deficiency)
D = Diarrhea or small/large bowel
fluid losses (e.g., enterocutaneous
fistulas)
The anion gap explained
In blood, positively charged ions (cations) must be balanced by negatively charged
ions (anions). However, when the two main cations (Na+ + K+) are compared with
the two main anions (Cl− + HCO3−), there appears to be a shortage of anions or an
anion gap.
Anion gap = (Na+ + K + ) - (Cl- + HCO3 - )
–18 mmol/L]
The gap is made up of unmeasured anions such as phosphate and sulphate
and negatively charged proteins (these are difficult to measure).
A raised anion gap (>18 mmol/L) therefore indicates the presence of
increased unmeasured anions.
Every acid consists of an H+ ion paired with an anion. For example, lactic acid
is the combination of H+ with the negatively charged lactate ion. Thus,
during conditions of increased lactic acid production there is accumulation of
both H+ (causing acidosis) and the lactate anion (causing a high anion gap).
b.LACTIC ACIDOSIS:
This is the most common cause of metabolic acidosis in ICU
patients.
It is defined by a low HCO3 in association with a plasma lactate
concentration greater than 4 mmol/L
28. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
When the supply of O2 to tissues is inadequate to support normal
aerobic metabolism, cells become dependent on anaerobic
metabolism – a form of energy generation that does not require O2
but generates lactic acid as a by-product
In particular, the initial serum lactate concentration is a powerful predictor
of death in patients with sepsis.
Types of lactic acidosis (lactate greater than 18/dL and pH less than 7.35)
Type A: Hypoperfusion (cardiogenic or septic shock, regional ischemia,
severe anemia)
Type B: Metabolic – No tissue hypoxia
o B1 = sepsis without shock, liver disease, leukemia, lymphoma, AIDS
o B2 = drugs/toxins (metformin, didanosine/stavudine/zidovudine,
ethanol, linezolid, propofol, propylene glycol toxicity caused by
intravenous lorazepam or pentobarbital), nitroprusside (cyanide)
toxicity
o B3 = inborn errors of metabolism (pyruvate dehydrogenase deficiency)
c.DIABETIC KETOACIDOSIS DKA
In the absence of insulin, the body cannot metabolise glucose and,
therefore, increases metabolism of fats.
The breakdown of fats produces ketones – small organic acids that provide
an alternative source of energy but can accumulate, leading to acidosis.
DKA is therefore characterised by the triad of:
1. A high anion gap metabolic acidosis
2. An elevated plasma glucose (hyperglycaemia)
3. The presence of ketones (detectable in blood or urine)
29. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
2.METABOLIC ALKALOSIS
A metabolic alkalosis is any process, other than a fall in Paco2, that acts to
increase blood pH.
It is characterised on ABG by an elevated plasma HCO3 and an increase in
BE.
Loss of H+ ions may initiate the process but the kidneys have huge scope to
correct threatened alkalosis by increasing HCO3 excretion. But it is not that
easy:
3. RESPIRATORY ACIDOSIS
A respiratory acidosis is, simply, an increase in Paco2.
Because CO2 dissolves in blood to form carbonic acid, this has the effect of
lowering pH (↑H+ ions).
Normally, lungs are able to increase ventilation to maintain a normal Paco2 –
even in conditions of increased CO2 production (e.g. sepsis).
Thus, respiratory acidosis always implies a degree of reduced alveolar
ventilation.
30. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
This may occur from any cause of type 2 respiratory impairment or to
counteract a metabolic alkalosis.
4.RESPIRATORY ALKALOSIS
A respiratory alkalosis is a decrease in Paco2 and is caused by alveolar
hyperventilation.
Primary causes are pain, anxiety (hyperventilation syndrome), fever,
breathlessness and hypoxaemia.
It may also occur to counteract a metabolic acidosis.
MIXED RESPIRATORY AND METABOLIC ACIDOSIS
This is the most dangerous pattern of acid–base abnormality.
It leads to profound acidaemia as there are two simultaneous acidotic
processes with no compensation.
In clinical practice it is often due to severe ventilatory failure, in which the
rising Paco2 (respiratory acidosis) is accompanied by a low Pao2, resulting in
tissue hypoxia and consequent lactic acidosis.
ABG SAMPLING TECHNIQUE: Video
31. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
MAKINGABGINTERPRETATIONEASY
The golden rules:
for making ABG interpretation easy is to assess pulmonary gas exchange and acid–
base status independently
Acid–base analysis should proceed in a stepwise approach to avoid
missing complicated disorders that may not be readily apparent
ASSESSING PULMONARY GAS EXCHANGE
•Using the algorithm, classify gas exchange into one of the four possible
categories.
•If there is type 1 respiratory impairment, assess severity of hypoxaemia
•If there is type 2 respiratory impairment, establish whether it is chronic or
acute, then:
assess severity of hypercapnia and hypoxaemia
•If the category is hyperventilation, determine whether it is primary or
secondary.
34. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
INTERPRETING ACID–BASE STATUS
35. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
Interpreting delta ratio
Use of the delta ratio
For determining mixed acid-base disorders
Delta ratio =
ΔAG/ΔHCO3 = (measured AG−normal AG)/(normal HCO3−measured HCO3) =
(AG−14)/(24−measured HCO3)
36. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
Delta
Ratio
Assessment
< 0.4 Hyperchloremic normal AG acidosis
< 1 High AG acidosis and normal AG acidosis
1–2 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 High AG acidosis and concurrent metabolic alkalosis
OR a preexisting compensated respiratory alkalosis
• An alternative method (and perhaps a simpler approach) to the delta ratio is to
calculate the “excess gap” compared with the AG
• Excess gap = AG − 12 (12 being the upper limit of normal for AG).
• The excess gap is then added to the measured serum bicarbonate
concentration.
• If the sum is less than a normal serum bicarbonate concentration (e.g., 28–30
mEq/L), a mixed AG and non-AG acidosis is present.
• If the sum is greater than a normal bicarbonate concentration, the patient
likely has an
AG acidosis and concurrent metabolic alkalosis.
54. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
3. Treatment of Acid Base disorders
Treat primary etiology! This should be the focus of treating the
acid-base disorder
1. Respiratory Acidosis
1. Make sure it is not caused by excessive sedation/analgesia or overfeeding with
EN/PN.
2. Metabolic compensation,
• Compensation is different for acute versus chronic respiratory disorders because it takes about 2 days for the kidneys to
adapt to a persistent change in respiratory status
HCO3 should increase by ~4 mEq/L per 10-mmHg
increase in Pco2 > 40
2. Respiratory Alkalosis
1. Make sure the patient is getting adequate sedation/analgesia,
fever/pneumonia is being treated; nicotine and drug withdrawal regimen is/are
appropriate
2. Metabolic compensation
3. Metabolic Acidosis
a. Use of the serum anion gap (AG)
b. Use of the delta ratio for determining mixed acid-base disorders
Treatment
a. Aggressive interventional therapy unnecessary until pH less than 7.20–7.25
AGAIN: Treat primary etiology! This should be the focus of treating the acid-
base disorder.
c. IV alkali –The intent is not to normalize the pH but to improve the pH
(definitely avoid overcorrection).
Total bicarbonate dose (mEq) = 0.5 x Wt (kg) x (24 − HCO3)
1. Give one-third to one-half of the calculated total dose (or 1–2 mEq/kg) over
several hours to achieve a pH of around 7.25 (avoid boluses if possible).
55. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
2. Once the pH is around 7.25 or greater, slower correction without increasing
bicarbonate more than 4–6 mEq/L to avoid exceeding the target pH
3. Serial ABGs (e.g., every 6 hours), watch rate of decrease in serum potassium
o Use of sodium bicarbonate injection is controversial in patients with lactic
acidosis
Adverse effects of sodium bicarbonate excess:
i. Hypernatremia, hyperosmolality, volume overload
ii. Hypokalemia, hypocalcemia, hypophosphatemia
iii. Paradoxical worsening of the acidosis (if the fractional increase in Pco2
production exceeds the fractional bicarbonate change)
iv. Over-alkalinization
4. Metabolic Alkalosis:
PH greater than 7.45; symptoms are not usually severe until pH is greater
than 7.55–7.60
Assessment (to help guide treatment) based on urinary chloride
a. Saline responsive (urinary chloride less than 10 mEq/L)
i. Excessive gastric fluid losses
ii. Diuretic therapy (especially loop diuretics)
iii. Dehydration (contraction alkalosis)
iv. Hypokalemia
v. (Over-) Correction of chronic hypercapnia
b. Saline resistant (urinary chloride greater than 20 mEq/L)
i. Excessive mineralocorticoid activity (e.g., hydrocortisone)
ii. Excessive alkali intake
iii. Profound potassium depletion (serum potassium less than 3 mEq/L)
iv. Excess licorice (mineralocorticoid) intake
v. Massive blood transfusion
c. Respiratory compensation (highly variable and may not be possible for
ventilator-dependent patients)
d. Intravascular volume status (important for saline-responsive alkalemia)
Treatment – Saline-responsive alkalemia
56. Shaza Aly
BPharm, BCPS, ALS, ICU Clinical Pharmacist
Shaza.aly@gmail.com
a. Treat underlying cause (if possible).
b. Decreased intracellular volume? Give intravenous 0.9% sodium chloride
infusion (with potassium chloride, if necessary).
c. Increased intracellular volume? Acetazolamide 250–500 mg orally or
intravenously once to four times daily plus potassium chloride if necessary.
Hydrochloric acid therapy if alkalosis persistent or initial pH greater than
7.6
(N or 0.2 N of hydrochloric acid (use 0.2 N for patients requiring fluid
restriction). Hydrochloric acid should be given by central venous administration,
and it requires delivery in a glass bottle.
Dosage of hydrochloric acid:
(a) Chloride deficit
Dose (mEq) = 0.2 L/kg x Wt (kg) x (103 − serum chloride)
(b) Bicarbonate excess
Dose (mEq) = 0.5 L/kg x Wt (kg) x (serum HCO3- 24)
(c) Dickerson’s empiric approach:
Give one-half of calculated dose over 12 hours,
Repeat ABG at 6 and 12 hours after initiating hydrochloric acid infusion, and
readjust infusion rate if necessary; continue therapy and monitoring until pH
less than 7.5; then stop and reassess
Treatment – Saline-unresponsive alkalosis: Treat underlying cause (if possible).
a. Exogenous corticosteroids – Decrease dose or use drug with less
mineralocorticoid effect.
b. Excessive alkali intake – Alter regimen.
c. Profound hypokalemia (serum potassium less than 3 mEq/L) – Aggressive
potassium supplementation
d. Rare causes: Endogenous mineralocorticoid excess (Bartter or Gitelman
syndrome) –
Spironolactone, amiloride, or triamterene; consider surgery
e. Liddle syndrome: Amiloride or triamterene
