Analyzing the Arterial Blood Gases: A Comprehensive Approach

INTRODUCTION

Understanding arterial blood gas (ABG) reports is a crucial task in determining the management of patients requiring intensive and continuous monitoring. They give us a deep insight to the oxygenation deficiencies to be differentiated from primary ventilatory deficiencies and primary metabolic acid–base abnormalities. Hence, learning to interpret them in a proper way becomes an essential agenda in any anesthesiologist’s learning diary.¹

The aims of doing a blood gas analysis are to detect the existence and intensity of oxygen- and carbon dioxide-related abnormalities in the blood levels and the degree of compensation in maintaining the acid–base equilibrium, thereby diagnosing the condition and planning their management.

The maintenance of potential hydrogen (pH) equilibrium by the three physiological processes of alveolar ventilation, oxygenation, and acid–base balance is reflected through the ABG report. There is a strong interrelation of all these three processes.

RESPIRATORY AND METABOLIC CONDITIONS

Primary modifications in ventilation lead to respiratory acidosis or alkalosis due to excessive removal or accumulation of CO₂. Metabolic conditions cause acidosis or alkalosis by alterations in the bicarbonate ions concentration.

COMPENSATION

Compensation of primary acid–base disorder is done either by the lungs or kidneys. The respiratory system compensates for the metabolic changes due to deviations in HCO₃⁻ (metabolic acidosis or alkalosis) while kidneys compensate for fluctuations in CO₂ (respiratory acidosis/alkalosis), which take around 2–5 days.

SIMPLE VS MIXED ACID–BASE DISORDER

Simple acid–base disorder consists of only a primary single process of either acidosis or alkalosis whereas mixed acid-base disorder may have more than one acid–base disorder coexisting together.

In metabolic conditions, movement of pH and HCO₃⁻ is in same direction whereas in respiratory conditions the movement of pH and PaCO₂ is in opposite direction. In simple disorders, the movement of HCO₃⁻ and PaCO₂ is in same direction while in mixed disorders, fluctuations of HCO₃⁻ and PaCO₂ are in opposite directions (Table 1).^5,6

While evaluating for the acid–base status, the pH values range between 7.35 and 7.45; PaCO₂ ranges between 35 and 45 mm Hg and HCO₃⁻ values range between 22 and 26 mEq/L. For calculation purposes, the base is taken as 7.40 for pH, PaCO₂ is taken as 40 mm Hg, and 24 mEq/L for HCO₃⁻.^7,8

The stepwise approach to the ABG Analysis⁴ was given by Narins and Emmett and modified by Morganroth in 1991.⁹

• Step 1. Evaluate if the patient has alkalosis or acidosis using the arterial pH. Low pH (%3C;7.35) is acidosis, if associated with low HCO₃⁻ is metabolic acidosis; high PaCO₂ is respiratory acidosis. High pH (%3E;7.45) is alkalosis, if associated with high HCO₃⁻ is metabolic alkalosis. Low PaCO₂ is respiratory alkalosis.
• Step 2. Based on PaCO₂ and serum HCO₃⁻ levels, check if there is a primary respiratory or metabolic disruption. pH moves in the same direction as PaCO₂/HCO₃⁻ in case of metabolic conditions. pH moves in the opposite direction as PaCO₂/ HCO₃⁻ in case of respiratory conditions.
• Step 3. In case of a primary respiratory disorder, evaluate whether it is chronic or acute. This can be done by checking ΔH⁺/ΔPaCO₂ < 0.3 indicating chronic condition, >0.8 indicating acute condition, while 0.3–0.8 indicates acute or chronic condition.
• Steps 4 and 5. In metabolic disorders, evaluate if the compensation by the respiratory system is adequate or not. In respiratory disorders, evaluate if compensation by the metabolic system is adequate or not (Table 2).
• Step 6. Check for the oxygenation status (PaO₂ and SaO₂)—if there is hypoxemia or not?
• Step 7A. In case of metabolic acidosis, calculate the anion gap (AG).

  AG = Na⁺ – (Cl⁻ + HCO₃⁻) normal < 12 and osmolar gap. In case of severe hypoalbuminemia, AG should be corrected by AGc = AG + {(4-[Albumin]) × 2.5}.

• Step 7B. In high anion gap metabolic acidosis (HAGMA), compute the sum of bicarbonate ions (HCO₃⁻) and the change in anion gap (ΔAG) to check for coexisting metabolic imbalances.

  ΔAG = [HCO₃⁻] + (AG-12)

  Table 2: Compensation of simple acid–base imbalance

  Simple acid–base imbalance	Compensation	Formula
  Metabolic acidosis	PaCO2 decreases 1.2 mm Hg per 1.0 mEq/L drop in HCO3−	Expected PaCO2 = [(1.5 × HCO3−) + 8] ± 2 (Winter’s formula)
  Metabolic alkalosis	PaCO2 rises 0.7 mm Hg per 1.0 mEq/L rise in HCO3−	Expected PaCO2 = [(0.7 × HCO3−) + 21] ± 1.5
  Respiratory acidosis	[HCO3−] increases
  Acute	[HCO3−] increases 1.0 mEq/L per 10 mm Hg rise of PaCO2	ΔHCO3− = ΔPaCO2 × 0.1 ± 3
  Chronic (3–5 days)	[HCO3−] increases 4 mEq/L per 10 mm Hg rise of PaCO2	ΔHCO3− = 4 (ΔPaCO2 × 0.1)
  Respiratory alkalosis	[HCO3−] decreases
  Acute	[HCO3−] decreases 2.0 mEq/L per 10 mm Hg fall of PaCO2	ΔHCO3− =2 (ΔPaCO2 × 0.1)
  Chronic	[HCO3−] decreases 5.0 mEq/L per 10 mm Hg fall of PaCO2	ΔHCO3− = 5(ΔPaCO2 × 0.1)

  If > 24, consider additional hidden metabolic alkalosis. If < 24, consider a hidden nonanion gap metabolic acidosis.

  We can also calculate Delta ratio^10,11 in case of HAGMA:

  Delta ratio = Increase in AG/decrease in HCO₃⁻

  Delta ratio < 1 suggests a greater decrease in HCO₃⁻ than expected from the change in AG, i.e., additional nonanionic gap metabolic acidosis

  Delta ratio ranging between 1 and 2 suggests HAGMA.

  Delta ratio > 2 suggests a less decrease in HCO₃⁻ than expected, i.e., additional metabolic alkalosis

• Step 7C. In case of nonanion gap acidosis, calculate the urinary anion gap that is necessary to differentiate between renal and nonrenal causes.

If compensation is as per calculation, it is a single acid–base disorder. If compensation is less than or greater than calculated expected value, then it is mixed acid–base problem.

METABOLIC ACIDOSIS

The pathophysiological causes of metabolic acidosis¹¹ include: (1) HCO₃⁻ loss either due to renal or gastrointestinal tract (GIT) causes; (2) greater formation of nonvolatile acids, exogenous acids, lactates, ketoacids, and poisons; and (3) fall in renal acid secretion.

Causes of HAGMA include: (1) lactic acidosis; (2) diabetic ketoacidosis, alcoholic ketoacidosis, and starvation; (3) chronic renal failure; (4) rhabdomyolysis; (5) salicylate toxicity, methanol toxicity, and ethylene glycol toxicity.

Causes of normal AG metabolic acidosis (NAGMA): (1) HCO₃⁻ loss due to GIT causes—biliary or pancreatic drainage, diarrhea, ketoacidosis during treatment, renal-proximal (type II) renal tubular acidosis (RTA), urinary diversions (ureterosigmoidostomy); (2) reduced renal acid excretion: renal failure, hyperkalemia (type IV) RTA, distal (type I) RTA; (3) miscellaneous: ammonium chloride (NH₄Cl) therapy, HCl therapy (treatment of severe metabolic alkalosis), hyperalimentation, and cholestyramine ingestion.

Diagnosing cause of metabolic acidosis:

Plasma osmolality = 2[Na⁺] + [Gluc]/18 + [BUN]/2.8. Plasma osmolality gap is defined as the difference between the calculated and measured plasma osmolality.

In HAGMA:

If the plasma osmolality gap is more than 15–20 mOsm/kg, then it shows presence of high osmolar substances like alcohol in the blood.

Ketones and hyperglycemia indicate diabetic ketoacidosis while ketones with normal glucose point to alcoholism and starvation. Serum lactate levels more than 2 indicate lactic acidosis.

In NAGMA:

Urine AG (UAG) is calculated. If positive UAG, then it indicates RTA; urine pH > 5.5 indicates type I RTA. If pH %3C; 5.5 and high K⁺, it indicates type IV RTA; if pH < 5.5 and low potassium (K⁺), it indicates type II RTA.

If negative UAG, the urine osmolality gap is calculated. If increased it’s due to iatrogenic acid gain and if normal it’s due to GIT causes.

Example 1: Patient comes with diabetic ketoacidosis at 0 hours at presentation. pH 7.06, CO₂ = 10.3, HCO₃⁻ = 6.1, Na⁺/Cl⁻ 142/106

• pH acidemia, primary condition metabolic with pH and HCO₃⁻ both decreased
• AG = 142 – (106 + 6.1) = 30↑↑ = HAGMA
• Compensation for metabolic acidosis: Winter’s formula: Expected CO₂ = (1.5 × 6) + 8 = 17, but actual value 10 < 17, indicating respiratory alkalosis (hyperventilation)
• Delta ratio = AG-12/HCO₃⁻ -24 = 18/18 = 1, no non-AG acidosis (Cl⁻ normal)

Thus, patient has HAGMA with respiratory alkalosis.

Same patient after 6 hours of treatment with insulin and saline, pH 7.22, CO₂ = 24, HCO₃⁻ = 10.2, Na⁺/Cl⁻ 140/120

• pH = acidemia, primary condition metabolic with pH and HCO₃⁻ both decreased
• AG = 140–130 = 10, now normal indicating NAGMA
• Metabolic acidosis compensation: Expected CO₂ = (1.5 × 10) + 8 = 23 matches the measured CO₂ (Winter’s formula). Thus, compensation is adequate.
• Delta AG = (AG – 12) + measured HCO₃⁻ = 2 + 10 = 12 < 24, indicating hidden NAGMA (Cl⁻ 120). Delta ratio which is the ratio of difference in AG and bicarbonates = (AG - 12)/(HCO₃⁻–24) = 2/14 < 1.

With saline, hyperchloremic acidosis sets in. Thus, the patient now has NAGMA owing to the treatment. Ketoacids are being cleared (AG ↓), thus indicating a good response. Only HCO₃⁻ will not indicate adequacy of response.

Treatment of metabolic acidosis includes treating underlying cause, HCO₃⁻ therapy as per the formula 0.5 × weight (kg) × HCO₃⁻ deficit (mEq/L). The objective is to raise the pH to %3E;7.2 and HCO₃⁻ > 10 mEq/L.

METABOLIC ALKALOSIS

Metabolic alkalosis is commonly (up to 50% of all disorders) associated with significant mortality.

Pathophysiological causes of metabolic alkalosis are the following:¹¹

(1) HCO₃⁻ accumulation: massive blood transfusion, giving large amounts of HCO₃⁻, ingestion (milk-alkali syndrome); (2) H⁺ loss: GIT—loss of gastric secretions, chloride losing diarrheal diseases; renal: mineralocorticoid excess, diuretics (loop/thiazide), Bartter’s syndrome, high-dose intravenous penicillin, post-chronic hypercapnia, hypercalcemia; (3) H⁺ movement into cells—hypokalemia, refeeding. Most in ICU are Cl⁻ responsive (urinary Cl⁻ %3C; 15 mEq/L) due to vomiting, nasogastric suction, diuretics, laxative, and volume depletion. Cl⁻ resistant (urinary Cl⁻ %3E; 25 mEq/L) due to severe hypokalemia and high aldosterone.

Example 2: A 70-year-old male with history of poor oral intake associated with areflexia and weakness. pH 7.54↑, CO₂ 54↑, HCO₃⁻ 44, Na⁺/K⁺/Cl⁻ 145/2.1/86

• pH = alkalemia, condition being metabolic since both pH and HCO₃⁻ high
• AG = 145 − (86 + 44) = 15 normal
• Expected CO₂ = 0.7 × HCO₃⁻ + 21 ± 2 = 0.7 × 44 + 21 ± 2 = 51.8 ± 2, which is seen as per reading.
• Diagnosis is severe metabolic alkalosis due to severe hypokalemia (K⁺ = 1.9).

Treatment: Immediate goal of therapy is partial correction of the alkalosis. The objective is reducing pH less than 7.55 and decreasing HCO₃⁻ less than 40 mEq/L.

Cl⁻ responsive type metabolic alkalosis is the most severe form. Treating the causes responsible for chloride and volume depletion. Administration of 3–5 L of 150 mEq/L sodium chloride should be done in patients with established signs of volume contraction. In case of chloride-resistant metabolic alkalosis, chloride should be repleted as potassium chloride. For metabolic alkalosis due to mineralocorticoid excess, spironolactone, which is a K⁺-sparing diuretic, proves beneficial.

RESPIRATORY ACIDOSIS

Acute respiratory acidosis is caused by obstruction in elimination of CO₂: (1) ventilation-related causes, airway obstruction like aspiration, bronchospasm (severe), laryngospasm; pulmonary edema; (2) perfusion-related causes: cardiac arrest, pulmonary thromboembolism; (3) restricted chest wall: tension pneumothorax, hemothorax, flail chest; (4) musculoskeletal system: myasthenia gravis crisis, hypokalemia; (5) failure of mechanical ventilator and other problems like (a) central nervous system (CNS): trauma, stroke, drugs (anesthetics, sedatives); (b) peripheral nerves: neurotoxins (OPC, tetanus, botulism), cervical cord injury, skeletal muscle relaxants (succinyl choline, curare, pancuronium and allied drugs, aminoglycosides)

Causes of chronic respiratory acidosis are obstruction in elimination of CO₂ like (1) ventilation: interstitial lung disease, chronic obstructive pulmonary disease; (2) restricted chest wall movement: muscular dystrophy, polymyositis, etc., and (1) CNS: chronic trauma, obesity hypoventilation syndrome, brain malignancies, myxoedema, (2) peripheral nerves: diaphragmatic paralysis, poliomyelitis, multiple Sclerosis.

Example 3: A 21-year-old female presented with history of dyspnea and wheezing for 5 days. She was tachypneic with central cyanosis and bilateral wheezing present. Chest X-ray showed tubular heart with hyperinflated lung fields. pH = 7.31, CO₂ = 64, HCO₃⁻ = 30, PaO₂ = 68 mm Hg, Na⁺/Cl⁻ = 136/98

• pH = 7.31 with increased CO₂, hence dominant disorder is respiratory acidosis. Condition is chronic due to 5 days.
• AG = 136 − (98 + 30) = 8, which is normal.
• Compensation = ΔHCO₃⁻ = 0.4 × ΔPaCO₂ = 0.4 × 24 = 9.6, HCO₃⁻ = 24 + 9.6 = 33. 2 compensation is adequate.

The diagnosis is chronic respiratory acidosis.

Treatment of respiratory acidosis is correction of underlying cause, appropriate oxygenation preventing subduing of respiratory drive, and avoid rapid correction of increased PaCO₂ to avoid post-hypercapnic metabolic alkalosis (seizures, arrhythmias).

RESPIRATORY ALKALOSIS

Causes of respiratory alkalosis comprises of head trauma, brain tumor, cerebrovascular accidents and other causes like pain, anxiety, fever, and peripheral respiratory stimulation like pulmonary V/Q imbalance, pulmonary shunts, hypovolemia, heights, diffusion problems, and miscellaneous causes like drugs—NSAIDs, progesterone, thyroid hormone, catecholamines, gram–ve sepsis, pregnancy, heat exposure, mechanical ventilation.

Example 4: 15-year-old boy presented with complaints of difficulty in breathing and upper abdominal discomfort for 3 hours. On examination per abdomen and respiratory system are normal except for hyperventilation. pH = 7.5, PaCO₂ = 26 mm Hg, HCO₃⁻ = 20 mEq, PaO₂ = 100 mm Hg, Na⁺/Cl⁻ = 137/99.

• pH = 7.5 with decreased CO₂, hence dominant disorder is respiratory alkalosis.
• AG = 137 − (99 + 20) = 18, which is raised. AG is slightly raised in respiratory alkalosis. Since it occurred only 3 hours back, it is an acute respiratory alkalosis.
• Compensation ΔHCO₃ = 0.2 × ΔPaCO₂ = 0.2 × 14 = 2.8, HCO₃⁻ = 24 − 2.8 = 21.2; compensation is adequate. Diagnosis is acute respiratory alkalosis.

Treatment of respiratory alkalosis consists of treatment of underlying cause, administration of O₂. If pH > 7.55, the patient is sedated and paralyzed and put on ventilator.

CONCLUSION

Thus, we conclude that knowledge about the triad of oxygenation, ventilation, and acid–base status helps us in thorough analysis of ABG. However, ABG results are only meaningful when inferred taking into account patients’ symptomatology, pathophysiology, and treatment in details. Hence, emphasis is to treat the patient and not the ABG.

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