ABG for ICU Clinical PhARMACIST

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

Shaza Aly BPharm, BCPS, ALS, ICU Clinical Pharmacist [email protected]

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


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


Lung

Blood Oxygen

ation

1. Hb Conc 2. Saturation of Hb with O2 (SO2):

CO2 elimination

-V/Q

-FiO2


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.


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


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.


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


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


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


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(V̇/Q̇)

• 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 • V̇ / Q̇ mismatch allows poorly oxygenated blood to re-enter the arterial circulation, thus lowering

PaO2 and SaO2.

• Provided overall alveolar ventilation is maintained, theV̇ /Q̇ mismatch does not lead to an increase

in PaCO2.


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


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).


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

•


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)


SUMMARY OF GAS EXCHANGE ABNORMALITIES


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).


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+.


DISTURBANCES OF ACID–BASE BALANCE


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


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.


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


a. METABOLIC ACIDOSIS AND

ANION GAP

b. LACTIC ACIDOSIS

c. DIABETIC KETOACIDOSIS DKA


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


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


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)


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.


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


MAKING ABG INTERPRETATION EASY

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.


INTERPRETING ACID–BASE STATUS


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)


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.


https://courses.kcumb.edu/physio/adaptations/alveolar%20oxygen.htm

https://courses.kcumb.edu/physio/adaptations/alveolar%20oxygen.htm


Answer:


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-mm Hg

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).


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


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

ABG for ICU Clinical PhARMACIST

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