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Interpretation of Arterial Blood Gas Analysis

Volume 2, Oct 2013

Kapil D. Soni, MD, Jeetendra Sharma, MD, IFCC, Mukesh K. Gupta, MD, FNB; New Delhi, India; Gurgaon, India

J Clin Prev Cardiol. 2013;2(4):207-13

 Blood gas analysis (arterial and/or venous) is a routine test and commonly used monitoring modality. Blood gas has vast information; when this information is interpreted with background clinical condition it helps in diagnosis
 
Indications for Arterial Blood Gas (ABG)

  • Severe respiratory or metabolic disorders
  • Clinical features of hypoxia or hypercarbia
  • Shock
  • Sepsis
  • Decreased cardiac output
  • Renal failure
  • Multiorgan dysfunction
  • Diabetic ketoacidosis

Samples Collection and Transport
 
Ideal artery for sampling is radial. One must perform “Allen Test” to ensure collateral blood supply by ulnar artery before puncturing radial artery (Table 1).
 
Indwelling arterial line of radial or femoral artery can be used for sample collection.
 


Precautions for collection of blood sample
 
  1. Heparin is acidic and lowers pH. Use heparin of lower strength (1000 instead of 5000 units per ml) or heplock solution.
  2. Use small volume of heparinised saline just for lubricating syringe and plunger. If volume is more, dissolved oxygen in heparinised saline may increase PaO2.
  3. Avoid air bubble and let syringe fill spontaneously.
  4. It is desirable to use a glass syringe as plastic syringes are permeable to air.
  5. The sample should be processed immediately, preferably within 30 minutes. Blood is a living medium. The cells consume oxygen and produce CO2. Drop in PaO2 depends on initial PaO2. If the latter is very high, significant drop may be noticed. The changes are as depicted in Table 2. Slush of ice (not cubes) should be used for storing samples till processing. The sample should be shaken before putting in machine (Fig. 1).



For minimal error, blood sample should be stored at 4°C, if it cannot be processed immediately for minimal error.

Terminology and Normal ABGs
 
Terminology
 
Acidosis pH <7.35
Alkalosis pH >7.45
 
Acidemia and alkalemia refer to blood while acidosis, alkalosis to tissue pH.
 
 
THb
 
THb is total hemoglobin of patient. Few machines measure hemoglobin, others need this information to be fed. Hemoglobin is required to calculate oxygen content (O2CT) of blood.
 
Temp
 
Patient temperature has to be fed into machine because the machine measures all values at 37°C. Temperature affects pH, PaCO2 and PaO2. Hence, it is desirable to have values corrected for patient temperature.
 
BE, St BE(SBE), BB
 
Base excess (BE) refers to actual base excess in variance from (above or below) total buffer base (BB). Normal BB is 48–49 mmol/l. If BB is 40, it means buffer base is reduced by nearly 8 mmol/l, or BE is –8 (also called base deficit). If BB is 60, it means buffer base is increased by nearly 12 mmol/l, or BE is +12.
 
Standard base excess (SBE) is the BE adjusted for temprature of 30oC and PaCO2 of 40 mmHg.
 
BB is dependent on hemoglobin, as 25% of BB is constituted by hemoglobin buffer. Fifty percent of BB is contributed by bicarbonate and 25% by other buffers (proteins, phosphate, sulfate).
 
HCO3; St HCO3 (SBC); TCO2

TCO2 is sum of HCO3- and amount of CO2 dissolved in plasma. For each mmHg PaCO2, 0.03 ml CO2 is dissolved per 100 ml of plasma. As HCO3- values change with CO2 levels, standard bicarbonate (st HCO3-) is used to denote value of HCO3-, independent of CO2 changes (i.e., at PaCO2 of 40 and temperature of 37°C).
 
St. pH

Standard pH (st. pH) is the pH adjusted for temperature of 37°C and PaCO2 of 40 mmHg. This would represent pH value purely due to metabolic status.
 
[H+]

It is the concentration of hydrogen ions in nmol/l at 37°C patient’s temperature.

[H+]nEq/l = 24 × (PaCO2/ HCO3)
 
O2CT

It is the sum of oxygen bound to hemoglobin and oxygen dissolved in plasma. For each gram saturated Hb, 1.34 ml O2 is bound to hemoglobin and for each mmHg PaO2 0.003 ml oxygen is dissolved per 100 ml of plasma.
 
O2CT = 1.34 × Hb × SaO2 + 0.003 PaO2

SaO2 sat
 
It is the proportion/percentage of arterial hemoglobin which is saturated with oxygen.

AaDO2
 
This refers to the alveolar-to-arterial oxygen gradient. Normal value is 5–15 mmHg.
 
RQ
 
Respiratory quotient (RQ) is the amount of CO2 liberated per minute divided by amount of O2 utilized per minute. Normal values are 200 ml/250 ml = 0.8.
 
FiO2
 
It is inspired oxygen fraction (FiO2) concentration. This value has to be fed to machine; it is required for calculation of alveolar oxygen concentration.
 
Details about pH
 
pH= pK + log10 (HCO3-/H2CO3) (Henderson–Hasselbach euqation)
 
Normal pH = 7.35 – 7.45


Types of Acid–base Disorder

  • Metabolic acidosis
  • Metabolic alkalosis
  • Acute respiratory acidosis
  • Chronic Respiratory acidosis
  • Acute respiratory alkalosis
  • Chronic Respiratory alkalosis
 
Metabolic acidosis
 
Metabolic acidosisis is a process that causes primary decrease in plasma bicarbonate concentration. This can be due to gain in acid or loss of bicarbonate (Table 3).
 
Types of metabolic acidosis are as follows:
 
   A. High anion gap (AG)
   B. Non-AG acidosis or normal AG acidosis


High-AG acidosis
 
High-AG acidosis results from production of endogenous acid. It results from addition of hydrogen ion and an unmeasured anion in the blood. The hydrogen ions are buffered by bicarbonate causing decrease in its concentration.

Anion gap = Unmeasured anions – Unmeasured cations
 
AG = Na- (Cl+ HCO3-)
 
Normal AG = 12 ± 2 mEq/l
 
Reference AG is influenced by albumin concentration in blood.
 
Adjusted AG = Observed AG + 2.5 [4.0 – measured albumin (g/dl)]
 
If an elevated AG metabolic acidosis is present, the “delta–delta ratio” should be calculated to determine if a second metabolic disorder is present.
 
The delta–delta calculation compares the deviation from normal of the AG with that of HCO3- (normal [HCO3-] ≈ 22–26 mEq/l). In a simple AG acidosis, these values would be expected to roughly equal one another (HCO3- decreasing by one unit for every unit the AG increases); however because not all H+ is buffered by HCO3-, the Δ in the AG usually exceeds the Δ in HCO3-.
 
If Δ AG/Δ HCO3- <1, an elevated gap metabolic acidosis and a normal gap acidosis are both present.
 
If Δ AG/Δ HCO3- = 1–2, a simple elevated gap metabolic acidosis is present.
 
If Δ AG/Δ HCO3- >2, an elevated gap metabolic acidosis and a metabolic alkalosis are both present.

Non-AG acidosis or normal AG acidosis
 
It is also known as hyperchloremic acidosis and drop in bicarbonate is the primary pathology. Sometime increased chloride can cause non-AG acidosis.





than 30, low HCO3, with a pH of 7.3–7.4.
 
Expected PaCO2 = (1.5 × HCO3-) + (8±2)

In uncompensated metabolic acidosis, the following conditions prevail:
 
  • Normal PaCO2, low HCO3- and a pH less than 7.30
  • Occurs as a result of increased production of acids and/or failure to eliminate these acidsIn uncompensated metabolic acidosis, the following conditions prevail:

Respiratory system is not compensating by increasing alveolar ventilation (hyperventilation).

Metabolic alkalosis
 
Metabolic alkalosis is a process that causes primarily increase in HCO3- concentration. It can be either generated by loss of hydrogen ion or gain of HCO3- and compensated by respiratory system.
 
Expected PaCO2 = (0.7 × HCO3-) + (21±2)
 
Causes of metabolic alkalosis are as follows:

  • Extracellular fluid volume depletion
  • Severe potassium depletion
  • Mineralocorticoid excess syndrome




Acute respiratory acidosis
 
  • PaCO2 is elevated and pH is acidotic
  • The decrease in pH is accounted for entirely by the increase in PaCO2
  • Bicarbonate and base excess will be in the normal range because the kidneys have not had adequate time to establish effective compensatory mechanisms
 
Causes are as follows:
 
  • Respiratory pathophysiology (airway obstruction, severe pneumonia, chest trauma/pneumothorax)
  • Acute drug intoxication (narcotics, sedatives)
  • Residual neuromuscular blockade
  • Central nervous system disease (head trauma)
 
 
Chronic respiratory acidosis
 
  • PaCO2 is elevated with a pH in the acceptable range
  • Renal mechanisms increase the excretion of H+ within 24 hours and may correct the resulting acidosis caused by chronic retention of CO2 to a certain extent 
 
Causes are as follows:
 
  • Chronic lung disease (e.g., chronic obstructive pulmonary disease)
  • Neuromuscular disease
  • Extreme obesity
  • Chest wall deformity
 
 
Acute respiratory alkalosis
 
  • PaCO2 is low and the pH is alkalotic
  • The increase in pH is accounted for entirely by the decrease in PaCO2
  • Bicarbonate and base excess will be in the normal range because the kidneys have not had sufficient time to establish effective compensatory mechanisms
 
Causes are as follows:
 
  • Pain
  • Anxiety
  • Hypoxemia
  • Restrictive lung disease
  • Severe congestive heart failure
  • Pulmonary emboli
  • Drugs
  • Sepsis
  • Fever
  • Thyrotoxicosis
  • Pregnancy
  • Overaggressive mechanical ventilation
  • Hepatic failure

Chronic respiratory alkalosis
 
In chronic respiratory alkalosis, metabolic component compensates almost completely. Therefore there will be little change in pH.
 
Oxygenation Assessment
 
A–a gradient. The alveolar–arterial oxygenation gradient is the difference between PAO2 and PaO2 [a normal A–a gradient ≈ (age in years + 10)/4]. The source of this normal gradient is a physiological shunt due to bronchial blood flow (which bypasses the alveoli and is therefore not oxygenated) and a small portion of coronary venous blood that drains directly into the left ventricle via the thebesian veins.
 
A–a oxygen ratio = PaO2 / PAO2
 
Normal range > 0.77
 
PAO2 = FIO2 × 713 – (PaCO2/RQ)
 
It is used to approximate the change expected in PaO2 for a given increase in FIO2.
 
PaO2/ FiO2 ratio: Normal range = 300–500;
 
Gas exchange derangement = 200–300;
 
Severe hypoxia < 200.
 
 
ABG Interpretation – Steps
 
First, does the patient have an acidosis or an alkalosis?
 
Second, what is the primary problem – metabolic or respiratory?
 
Third, is there any compensation by the patient?
 
Respiratory compensation is immediate while renal compensation takes time.

Putting it together:
 
 
Respiratory
 
  • PaCO2> 45 with a pH < 7.35 represents a respiratory acidosis
  • PaCO2< 35 with a pH > 7.45 represents a respiratory alkalosis
  • For a primary respiratory problem, pH and PaCO2 move in the opposite direction
    • For each deviation in PaCO2 of 10 mmHg in either direction, 0.08 pH units change in the opposite direction

Metabolic
 
  • HCO3< 22 with a pH < 7.35 represents a metabolic acidosis
  • HCO3> 26 with a pH > 7.45 represents a metabolic alkalosis
  • For a primary metabolic problem, pH and HCO3- are in the same direction, and PaCO2 is also in the same direction
  • Fourth, look for compensation
    • The body’s attempt to return the acid/base status to normal (i.e., pH closer to 7.4)




Expected Compensation
 
Respiratory acidosis (1/4)
 
  • Acute – the pH decreases 0.008 units for every 1 mm Hg increase in PaCO2; HCO3-1 mEq/l per 10 mm Hg PaCO2
  • Chronic – the pH decreases 0.003 units for every 1 mm Hg increase in PaCO2; HCO3-4 mEq/l per 10 mm Hg PaCO2
 
 
Expected compensation
 
Respiratory alkalosis (2/5)
 
  • Acute – the pH increases 0.008 units for every 1 mmHg decrease in PaCO2; HCO3- 2mEq/l per 10 mmHg PaCO2
  • Chronic – the pH increases 0.0017 units for every 1 mmHg decrease in PaCO2; HCO3- 5 mEq/l per 10 mmHg PaCO2
 
Expected Compensation
 
Metabolic acidosis
 
  • Expected PaCO2 = 1.5(HCO3) + 8 (±2)
  • PaCO2 1-1.5 per 1 mEq/l HCO3
  •  
 
Metabolic alkalosis
 
  • Expected PaCO2 = 0.7(HCO3) + 21 (±2)
  • PaCO2 0.5–1.0 per 1 mEq/l HCO3


References
 
  1. Acid–base evaluations (Chapter 31). In: Marino’s The ICU Book (4th edn.). Marino PL (ed.). Lippincott Williams & Wilkins; 2013.
  2. Oh’s Intensive Care Manual (7th edn.). Acid–base balance and disorders (Chapter 92). Philadelphia, PA: Butterworth Heinemann; 2013.
  3. Ghosh AK. Diagnosing acid–base disorders. JAPI. 2006;54:720–4.
  4. Androgue HJ, Madias NE. Management of life-threatening acid–base disorders. N Engl J Med. 1998;338:26–34.
  5. Androgue HJ, Madias NE. Management of life-threatening acid–base disorders: second of two parts. N Engl J Med.1998;338:107–11.
  6. http//:www. newbornwhocc.org

 
 

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