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Arterial Blood Gases

58

 

Rahul Pandit

 

A 45-year-old alcoholic male patient was admitted to the hospital for 2 weeks. He was being treated for pyogenic lung abscess. He seemed to be improving but became unwell again. A blood gas analysis showed pH 7.31, PaCO2 30 mmHg, PaO2 106 mmHg (0.3 FiO2), HCO314 mmol/L, standard base excess (SBE) 15 mmol/L, Na+ 131 mmol/L, K+ 5 mmol/L, Cl96 mmol/L, osmolar gap 8 mmol/Kg, lactate 2 mmol/L, and albumin 3 g/dL.

Arterial blood gas analysis is an essential component of diagnosing and managing critically ill patients in the ICU. The proper understanding and application of the concepts of acid–base balance will help the clinician to follow the progress of the patient and also to evaluate the effectiveness of the treatment provided to them.

Step 1: Take an arterial blood sample

If possible, take an arterial blood gas (ABG) sample at room air and start oxygen supplementation immediately.

The radial artery is preferred for collecting the sample.

Prefer to use 22-gauge needle.

Avoid air bubbles.

Cool the sample immediately. A. Potential sampling error.

Air contamination—spurious increase in PO2.

Duration of exposure is more important than volume of air bubbles.

Expel air immediately.

Discard the sample if froth is present.

R. Pandit, M.D., F.C.I.C.M. (*)

Department of Critical Care, Seven Hills Hospital, Mumbai, India e-mail: dr_rapandit@yahoo.com

R. Chawla and S. Todi (eds.), ICU Protocols: A stepwise approach,

455

DOI 10.1007/978-81-322-0535-7_58, © Springer India 2012

 

456

R. Pandit

 

 

B. Venous sample—absence of flash of blood on entry into the vessel and pulsations during syringe filling and absence of autofilling of the syringe.

Venous admixture.

Cross-check with pulse oximetry and clinical status.

Anticoagulant effects: Dilution error—drop in PCO2 and PO2. pH usually remains unchanged.

D.Metabolism: Blood cells consume O2, produce CO2, and lower pH. Magnitude of changes depends on the initial level.

Step 2: Take detailed history and do proper clinical examination

Very often, it is the presenting symptom or signs which are a clue to the interpretation of the acid–base status.

For example in a patient with vomiting, the primary acid–base problem could be metabolic alkalosis (due to loss of hydrochloric acid) as opposed to someone with diarrhea, whose primary problem could be metabolic acidosis (due to loss of bicarbonate ions).

The important aspect to remember is that it is the underlying disorder of the patient which determines the acid–base status and not just the pH of the blood.

A stepwise approach helps to interpret ABG correctly.

Interpretation of serum electrolytes is also important for an accurate estimation of mixed acid–base disorders.

Step 3: Know the normal values

 

Normal range

For calculation

pH

7.34–7.45

7.4

PCO2

35–45

40

HCO3

22–26

24

PO2

>80

>95

Step 4: Assess oxygenation (Ref Appendix 2)

Look at oxygenation (PaO2 and SaO2).

Look at the PaO2/FiO2 ratio.

Normally, the ratio is around 1:400–1:500 given the fact that at 0.21 FiO2, the PaO2 is approximately 100 mmHg.

Less than 1:400—suggestive of V–Q mismatch or diffusion defect or intracardiac shunt.

Less than 300 with bilateral lung infiltrate in chest skiagram—ARDS.

A-a gradient

A-a gradient = PAO2 − PaO2

Here, PAO2 is alveolar PO2 (calculated from the alveolar gas equation) and PaO2

is arterial PO2 (measured in arterial blood A-a gradient).

 

 

In general, the A-a gradient can be calculated by:

/ 0.8)

 

A a gradient = FiO2 × (Patm PH2 O)(PaCO2

PaO2

 

 

 

 

58 Arterial Blood Gases

457

 

 

On room air and at sea level, the FiO2 is 0.21, the Patm is 760 mmHg, and PH2O is 47 mmHg.

– On room air, PAO2 can be calculated by:

150 PaCO2 / 0.8

Normal A-a gradient in a 20-year-old person is 5 mmHg, which increases to 10 mmHg in a 35-year-old person. If A-a gradient is 20 mmHg at any age, it is abnormal. If FiO2 is above 0.21, it is unreliable.

Step 5: Assess acid–base disorder (Ref Appendix 2)

I. Look at the pH—is there acidemia or alkalemia?

A normal pH would suggest a mixed disorder or a normal acid–base status.

II.Check CO2 and HCO3to determine whether the primary problem is metabolic or respiratory in origin.

III.If the primary disorder is respiratory, determine whether it is an acute disorder or a chronic disorder.

IV. Apply the rules of compensation to know if it is a simple or a mixed disorder. V. Mind the gaps—anion gap, delta gap, and osmolar gap.

I.Look at the pH

The pH is actually the −log [H+]. By altering either the PCO2 or the HCO3, [H+] will change, and so will pH.

An acidemia (low pH) can result from either a low HCO3 or a high CO2.

An alkalemia (high pH) can result from either a high HCO3 or a low CO2.

II. Look at the CO2 and HCO3to determine if the primary problem is metabolic or respiratory in origin

The primary acid–base disturbances include the following:

Low HCO3—metabolic acidosis

High HCO3—metabolic alkalosis

High PCO2—respiratory acidosis

Low PCO2—respiratory alkalosis A. Metabolic acidosis

Metabolic acidosis results from a primary decrease in plasma [HCO3−].

It is due to either an excretion of bicarbonate-containing fluids or by utilization of bicarbonate.

It is very important to calculate the anion gap (AG) if the primary disorder is metabolic acidosis.

AG = Na+ − (Cl− + HCO3−); the normal AG is 12 ±2 mEq/L.

A higher gap usually denotes the presence of unmeasured anions in the body (Table 58.1).

In non-AG metabolic acidosis, the bicarbonate losses are accompanied by cation loss, hence no change in AG (Table 58.2).

458

R. Pandit

 

 

Table 58.1 Causes of a raised AG metabolic acidosis (MUDPILERS)

M Methanol

U Uremia (chronic)

DDiabetic ketoacidosis

PParaldehyde

IIsoniazid, iron

LLactate

EEthanol, ethylene glycol

RRhabdomyolysis/renal failure

SSalicylate

Table 58.2 Causes of a non-AG metabolic acidosis (HARDUP)

H Hyperalimentation

A Acetazolamide

R Renal tubular acidosis

D Diarrhea

U Uremia (acute)

P Post ventilation hypocapnia

Remember to correct AG for hypoalbuminemia, which is very common in ICU patients. For this, for every 1 g% drop in albumin below 4 g%, add 2–3 to the calculated gap.

Check urinary AG in non-AG metabolic acidosis (U Na+ +U K−U Cl)

Normal—negative

Nonrenal loss of bicarbonate (diarrhea)—negative

Renal loss of bicarbonate or decrease H+ excretion (renal tubular acidosis)—positive

B.Metabolic alkalosis (high HCO3)

Metabolic alkalosis reflects an increase in plasma [HCO3−].

It is due to either gain of HCO3− or extracellular volume contraction.

It can be classified into saline responsive or nonresponsive. For this, spot urinary chloride can be checked.

More than 20 mEq/L urinary chloride is saline unresponsive (Table 58.3), and less than 20 mEq/L urinary chloride is saline responsive (Table 58.4).

C.Respiratory acidosis (high PCO2)

Respiratory acidosis is due to a primary rise in CO2.

Hypercapnia almost always results from alveolar hypoventilation due to one of the following causes:

1. Respiratory center depression

2. Neuromuscular disorders

3. Upper airway obstruction

4. Pulmonary disease

58 Arterial Blood Gases

459

 

 

Table 58.3 Urine Clmore than 20 mEq/L (usually saline unresponsive)

Primary hyperaldosteronism

Cushing’s syndrome, ectopic ACTH

Exogenous steroids, licorice ingestion, tobacco chewing

Adrenal 11 or 17 OH defects

Liddle’s syndrome

Bartter’s syndrome

K+ and Mg2+ deficiency

Milk-alkali syndrome

Hypercalcemia with secondary hypoparathyroidism

Table 58.4 Urine Clless than 20 mEq/L (usually saline responsive)

Vomiting, nasogastric suctioning

Chloride-wasting diarrhea

Villous adenoma of colon

Posthypercapnia

Poorly reabsorbed anions like carbenicillin

Diuretic therapy

D.Respiratory alkalosis (low PCO2)

A respiratory alkalosis is due to decrease in PCO2.

It results from hyperventilation leading to decrease in CO2.

Causes of respiratory alkalosis

– Hypoxemia from any cause

– Respiratory center stimulation

– Mechanical hyperventilation

– Sepsis, pain

III.If the primary disorder is respiratory, determine whether it is an acute disorder or a chronic disorder

You must also take into consideration the patient’s history while interpreting ABG. However, the following formulae help in this:

Normal pH is 7.4

Calculate the change in pH (from 7.4)

A. In acute respiratory disorder (acidosis or alkalosis)

Change in pH = 0.008 × (PaCO2 − 40) Expected pH = 7.4 ± change in pH

B. In chronic respiratory disorder (acidosis or alkalosis)

Change in pH = 0.003 × (PaCO2 − 40) Expected pH = 7.4 ± change in pH

Compare the pH on ABG

• If pH on ABG is close to A, it is an acute disorder

• If pH on ABG is close to B, it is a chronic disorder

460 R. Pandit

IV. CO

2

and HCO

 

compensatory mechanism

 

 

 

 

Initial

3

Compen-

 

 

 

 

 

 

 

 

 

 

 

Primary

 

 

chemical

satory

Compensatory

 

 

disorder

 

 

change

 

 

response

mechanism

Expected level of compensation

Metabolic

 

↓ HCO3

 

↓ PCO2

Hyperventilation

PCO2 = (1.5 × [HCO3]) + 8 ± 2

acidosis

 

 

↑ HCO3

 

↑ PCO2

 

PCO2 = last two digits of pH

Metabolic

 

 

Hypoventilation

PCO2 = (0.7 × [HCO3]) + 21 ± 2

alkalosis

 

 

↑ PCO2

 

 

↑ HCO3

 

PCO2 = last two digits of PH

Respiratory

 

 

 

 

 

acidosis

 

 

 

 

 

 

 

 

 

Acute

 

 

 

 

 

 

Buffering—rule of 1

↑ [HCO3])] = 1 mEq/L for every

 

 

 

 

 

 

 

 

10 mmHg delta PCO2

Chronic

 

 

 

 

 

 

Generation of new

↑ [HCO3]) = 3 mEq/L for every

 

 

 

 

 

 

 

HCO —rule of 3

10 mmHg delta PCO

2

 

 

 

PCO2

 

 

HCO3

3

 

Respiratory

 

 

 

 

 

alkalosis

 

 

 

 

 

 

 

 

 

Acute

 

 

 

 

 

 

Buffering—rule of 2

↓ [HCO3]) = 2 mEq/L for every

 

 

 

 

 

 

 

 

10 mmHg delta PCO2

Chronic

 

 

 

 

 

 

Decreased

↓ [HCO3]) = 4 mEq/L for every

 

 

 

 

 

 

 

reabsorption of

10 mmHg delta PCO2

 

 

 

 

 

 

 

HCO —rule of 4

 

 

 

 

 

 

 

 

 

3

 

 

V.Mind the gaps

A1. Calculate AG in case of metabolic acidosis.

High denotes raised AG metabolic acidosis, and normal or narrow denotes nonAG acidosis.

A2. Calculate adjusted AG.

Adjusted AG = calculated AG + 2.5 × (4 − serum albumin in gm%)

B. In less obvious cases, the coexistence of two metabolic acid–base disorders may be apparent by calculating the difference between the change in AG

(delta AG) and the change in serum HCO3(delta HCO3). This calculation is called the bicarbonate gap or the delta gap:

Delta gap = delta AG − delta HCO3

Where delta AG = patient’s AG − 12 mEq/L{normal AG}

Delta HCO3= 24 mEq/L{normal HCO3} − patient’s HCO3

Normally, the delta gap is zero if there is only AG acidosis. A positive raised delta gap or a decreased delta gap denotes presence of mixed lesion.

A positive delta gap of more than 6 mEq/L is suggestive of presence of metabolic alkalosis and/or HCO3retention.

The delta gap of less than 6 mEq/L is suggestive of presence of hyperchloremic acidosis and/or HCO3excretion.

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