Acid–Base/ABG Interpretation — Acid–Base And ABG Interpretation With Clinical Response - NCLEX Rn

SECTION 1

Historical Context & Motivation

The human body maintains a remarkably narrow blood pH range of 7.35–7.45, and even slight deviations can trigger cellular dysfunction, enzyme inactivation, and hemodynamic collapse. Understanding how clinicians arrived at the modern framework of arterial blood gas (ABG) interpretation requires appreciating over a century of biochemical and technological advances. The ability to measure pH, partial pressures of carbon dioxide (PaCO₂), and bicarbonate (HCO₃⁻) in real time transformed critical care from a reactive discipline into a proactive, precision-driven science.

1909 • Sørensen Defines pH

Danish chemist Søren Sørensen introduced the pH scale at the Carlsberg Laboratory, providing a standardized measure of hydrogen ion concentration that enabled quantitative study of acid–base balance in biological fluids.

1917 • Henderson-Hasselbalch Equation

Karl Hasselbalch adapted Lawrence Henderson's earlier work on buffer equilibria into the logarithmic equation that remains the mathematical backbone of ABG interpretation, linking pH to the ratio of bicarbonate and dissolved CO₂.

1952 • Copenhagen Polio Epidemic

During the devastating poliomyelitis outbreak in Copenhagen, Bjørn Ibsen pioneered positive-pressure ventilation guided by blood gas analysis, catalyzing the birth of modern intensive care medicine and demonstrating the clinical necessity of ABG monitoring.

1958 • Severinghaus Blood Gas Electrode

John Severinghaus and A. Freeman Bradley developed the first practical PaCO₂ electrode, enabling rapid bedside measurement of arterial carbon dioxide tension and making real-time ABG analysis a clinical reality.

1977 • Point-of-Care ABG Analyzers

The introduction of automated, compact blood gas analyzers allowed nurses and respiratory therapists to obtain results within minutes at the bedside, integrating ABG interpretation into standard nursing assessment and establishing it as a core competency for critical care providers.

Today, ABG interpretation is an essential nursing skill tested on the NCLEX-RN because recognizing and responding to acid–base disturbances directly affects patient survival. The central clinical question is: Given a set of ABG values, can the nurse identify the specific acid–base disorder, determine whether compensation is occurring, and initiate the appropriate clinical response?

SECTION 2

Core Principles & Definitions

Before interpreting any ABG, you must internalize the normal reference ranges and the physiological roles of the three primary components. The body employs three interrelated systems to maintain acid–base homeostasis: chemical buffer systems (responding in seconds), the respiratory system (responding in minutes to hours by adjusting CO₂ elimination), and the renal system (responding over hours to days by excreting or reabsorbing H⁺ and HCO₃⁻). When one system fails or is overwhelmed, the others attempt to compensate, and the ABG provides a snapshot of where this compensatory process stands.

pH: The Master Indicator

Normal range: 7.35–7.45. A pH below 7.35 is acidosis; above 7.45 is alkalosis. The pH always tells you the primary direction of the disturbance.

PaCO₂: The Respiratory Component

Normal range: 35–45 mmHg. Carbon dioxide is a volatile acid regulated by the lungs. Hypoventilation raises PaCO₂ (respiratory acidosis), while hyperventilation lowers it (respiratory alkalosis).

HCO₃⁻: The Metabolic Component

Normal range: 22–26 mEq/L. Bicarbonate is the primary base regulated by the kidneys. Low HCO₃⁻ indicates metabolic acidosis; elevated HCO₃⁻ indicates metabolic alkalosis.

PaO₂ & SaO₂: Oxygenation Status

Normal PaO₂: 80–100 mmHg; normal SaO₂: 95–100%. While not directly part of acid–base classification, hypoxemia often coexists with respiratory acid–base disorders and drives compensatory mechanisms.

Compensation: The Body's Response

When a primary disorder exists, the opposite system attempts correction. Respiratory compensation adjusts PaCO₂; renal compensation adjusts HCO₃⁻. Full compensation returns pH near normal but rarely overcorrects.

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KEY TAKEAWAY

Think of acid–base balance like a seesaw in a playground. On one side sits CO₂ (acid, controlled by the lungs), and on the other side sits HCO₃⁻ (base, controlled by the kidneys). The pH is the position of the fulcrum. When one side gets too heavy—say CO₂ rises due to poor ventilation—the seesaw tips toward acidosis. The kidneys then try to add weight to the bicarbonate side to re-level it. An ABG is essentially a photograph of the seesaw at one moment in time, telling you which side is heavier and whether the other side is actively trying to compensate.

SECTION 3

Visual Explanation: The ABG Interpretation Algorithm

The four-step ABG interpretation algorithm. Begin with pH to determine acidosis versus alkalosis (Step 1), then evaluate PaCO₂ and HCO₃⁻ to identify the respiratory or metabolic origin (Step 2). Assess whether compensation is absent, partial, or full (Step 3), and finally determine the appropriate clinical response (Step 4).

The algorithm depicted above provides the systematic framework that every nursing student should commit to memory. The first step—evaluating pH—is non-negotiable because it establishes the direction of the primary disturbance and prevents the common error of fixating on a single abnormal value. Step 2 requires you to determine which system (respiratory or metabolic) is responsible for the pH deviation; the component that "matches" the pH direction is the primary culprit. For example, if the pH is low (acidotic) and PaCO₂ is elevated, the elevated CO₂ is driving the acidosis—this is respiratory acidosis. Step 3 assesses the opposing system: if HCO₃⁻ is also abnormal (elevated in this case), the kidneys are attempting to compensate. The pH determines whether compensation is partial (pH still abnormal) or full (pH returned to 7.35–7.45). Step 4 translates interpretation into clinical action.

SECTION 4

The Mathematical & Physiological Framework

The quantitative relationship underpinning all acid–base physiology is captured by the Henderson-Hasselbalch equation. While the NCLEX does not require you to perform logarithmic calculations, understanding this equation reveals why pH, PaCO₂, and HCO₃⁻ are interdependent and why changing one variable necessarily affects the others. The equation also explains the clinical rationale behind interventions such as sodium bicarbonate administration or mechanical ventilation adjustments.

HENDERSON-HASSELBALCH EQUATION

pH = 6.1 + log₁₀ ( [HCO₃⁻] / (0.03 × PaCO₂) )

Where 6.1 is the pKa of the carbonic acid buffer system, [HCO₃⁻] is the bicarbonate concentration in mEq/L, 0.03 is the solubility coefficient of CO₂ in plasma, and PaCO₂ is the partial pressure of arterial CO₂ in mmHg. The ratio of HCO₃⁻ to dissolved CO₂ is normally approximately 20:1, which yields a pH of 7.40.

BICARBONATE-CO₂ RATIO

[HCO₃⁻] / (0.03 × PaCO₂) ≈ 24 / (0.03 × 40) = 24 / 1.2 = 20 : 1

The normal bicarbonate concentration of 24 mEq/L divided by dissolved CO₂ (0.03 × 40 mmHg = 1.2) gives the critical 20:1 ratio. Any condition that shifts this ratio—whether by raising PaCO₂, lowering HCO₃⁻, or both—will move the pH away from 7.40.

ANION GAP CALCULATION

Anion Gap = Na⁺ − (Cl⁻ + HCO₃⁻) [Normal: 8–12 mEq/L]

The anion gap helps differentiate causes of metabolic acidosis. An elevated anion gap (>12) suggests accumulation of unmeasured acids such as lactate, ketoacids, or uremia (mnemonic: MUDPILES). A normal anion gap acidosis results from direct bicarbonate loss, as seen in diarrhea or renal tubular acidosis.

Physiologically, the respiratory system compensates for metabolic disturbances by adjusting the rate and depth of ventilation. In metabolic acidosis, chemoreceptors detect elevated H⁺ and trigger Kussmaul respirations—deep, rapid breathing that lowers PaCO₂ and shifts the Henderson-Hasselbalch equation toward a higher pH. Conversely, metabolic alkalosis triggers hypoventilation to retain CO₂, although this compensation is limited because hypoxemia eventually overrides the drive to retain carbon dioxide. Renal compensation for respiratory disorders involves adjusting bicarbonate reabsorption in the proximal tubule and H⁺ secretion in the distal nephron, a process that takes 24–72 hours to reach full effect.

SECTION 5

The Four Primary Acid–Base Disorders & Clinical Causes

The four primary acid–base disorders organized by direction (acidosis vs. alkalosis) and origin (respiratory vs. metabolic). Each disorder lists common clinical causes and the characteristic ABG pattern. The lower panel summarizes the expected compensatory responses and the time required for each system to reach full effect.

The diagram above serves as a clinical reference for rapid pattern recognition. Notice that respiratory compensation is fast but limited—the lungs can adjust ventilation within minutes, but they cannot maintain extreme rates indefinitely. Renal compensation is slower, requiring 24–72 hours, but it is more powerful and sustained once established. This timing difference is clinically significant: if a patient presents with metabolic acidosis and a normal PaCO₂, the lungs have not yet begun compensation (or the patient has a concurrent respiratory problem preventing compensation). Similarly, if a patient with chronic respiratory acidosis suddenly shows a normal HCO₃⁻, you should suspect an acute-on-chronic process where a new insult has overwhelmed previously established renal compensation.

Disorder	pH	PaCO₂	HCO₃⁻	Key Clinical Signs
Respiratory Acidosis	↓ (< 7.35)	↑ (> 45)	Normal or ↑	Dyspnea, confusion, drowsiness, headache
Metabolic Acidosis	↓ (< 7.35)	Normal or ↓	↓ (< 22)	Kussmaul respirations, fatigue, nausea, confusion
Respiratory Alkalosis	↑ (> 7.45)	↓ (< 35)	Normal or ↓	Tachypnea, lightheadedness, paresthesias, tetany
Metabolic Alkalosis	↑ (> 7.45)	Normal or ↑	↑ (> 26)	Hypoventilation, muscle cramps, hypokalemia, dysrhythmias

Summary of the four primary acid–base disorders with ABG value patterns and clinical manifestations

SECTION 6

Worked Example: Interpreting an ABG with Clinical Response

A 68-year-old patient with a history of COPD is admitted with increasing dyspnea and confusion. The nurse obtains an ABG with the following results: pH 7.28, PaCO₂ 58 mmHg, HCO₃⁻ 26 mEq/L, PaO₂ 55 mmHg. The patient is on 2 L/min nasal cannula. Let us systematically interpret these values and determine the appropriate nursing response.

ABG Interpretation: COPD Patient in Acute Distress

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Step 1 — Evaluate the pH

The pH is 7.28, which falls below the normal range of 7.35–7.45. This tells us the patient is in acidosis. The pH is the master indicator—regardless of what the other values show, the primary process is acidotic.

pH 7.28 → Acidosis
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Step 2 — Identify the Primary Cause

PaCO₂ is 58 mmHg, which is elevated (normal: 35–45 mmHg). An elevated PaCO₂ causes acidosis because CO₂ combines with water to form carbonic acid. Since the pH is acidotic and the PaCO₂ is elevated (both point in the same direction—acidosis), the PaCO₂ "matches" the pH disturbance. HCO₃⁻ is 26 mEq/L, which is within or at the upper end of normal (22–26 mEq/L). This confirms the primary disorder is respiratory acidosis.

PaCO₂ 58 ↑ matches acidotic pH → Primary Respiratory Acidosis
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Step 3 — Assess Compensation

HCO₃⁻ at 26 mEq/L is at the high end of normal, suggesting minimal or early renal compensation. In a fully compensated chronic respiratory acidosis, we would expect HCO₃⁻ to be significantly elevated (often 30–35 mEq/L), and the pH would be closer to normal. Since the pH remains markedly abnormal (7.28) and HCO₃⁻ is only borderline elevated, this represents uncompensated or acute respiratory acidosis—consistent with an acute COPD exacerbation where the kidneys have not yet had time (24–72 hours) to retain enough bicarbonate.

HCO₃⁻ 26 (near normal) + pH still very low → Uncompensated Acute Respiratory Acidosis
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Step 4 — Assess Oxygenation

PaO₂ is 55 mmHg, well below the normal range of 80–100 mmHg. This patient is hypoxemic, which is consistent with the COPD exacerbation and ventilation-perfusion mismatch. The hypoxemia compounds the danger of the respiratory acidosis and requires immediate intervention.

PaO₂ 55 → Hypoxemia requiring intervention
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Step 5 — Determine Clinical Response

The nursing priorities for uncompensated acute respiratory acidosis with hypoxemia include: (1) Position the patient in high Fowler's to optimize diaphragm excursion; (2) Administer prescribed bronchodilators (e.g., albuterol) and corticosteroids; (3) Titrate supplemental oxygen cautiously—COPD patients may rely on hypoxic drive, so aim for SpO₂ of 88–92%; (4) Anticipate the possible need for BiPAP or intubation if the patient does not improve; (5) Notify the provider of the ABG results and the patient's clinical status; (6) Reassess ABGs after interventions (typically 20–30 minutes). Monitor closely for signs of worsening—increasing lethargy, decreasing respiratory rate, or further pH decline.

FINAL: Uncompensated Acute Respiratory Acidosis with Hypoxemia → Elevate HOB, bronchodilators, controlled O₂, prepare for BiPAP, notify provider

SECTION 7

Nursing Interventions by Disorder Type

Interpreting ABG values is only half the equation—the NCLEX expects you to connect each disorder to the appropriate nursing response. The table below summarizes evidence-based interventions organized by the four primary acid–base disturbances. Note that the underlying cause always dictates the specific treatment, but the general patterns of nursing care are consistent across scenarios.

Disorder	Priority Nursing Interventions	Key Monitoring Parameters
Respiratory Acidosis	Improve ventilation: elevate HOB, administer bronchodilators, suction airway, assist with BiPAP/intubation if needed. Cautious O₂ in COPD patients (target SpO₂ 88–92%)	Respiratory rate/depth, LOC, serial ABGs, SpO₂, cough effectiveness
Metabolic Acidosis	Treat underlying cause (insulin for DKA, fluids for lactic acidosis, dialysis for renal failure). Administer NaHCO₃ only if pH < 7.10 per provider order. Maintain IV access for fluid resuscitation	Blood glucose, electrolytes (K⁺), anion gap, I&O, LOC, respiratory pattern (Kussmaul), cardiac rhythm
Respiratory Alkalosis	Address underlying cause (anxiolytics for anxiety, antipyretics for fever, adjust ventilator settings). Coach slow breathing. Rebreathing mask ONLY if appropriate and ordered	Respiratory rate, anxiety level, LOC, paresthesias, tetany, electrolytes (Ca²⁺), ECG for dysrhythmias
Metabolic Alkalosis	Replace chloride and potassium (0.9% NaCl, KCl). Discontinue causative agents (antacids, diuretics). Administer antiemetics for vomiting. Monitor NG tube output	Electrolytes (K⁺, Cl⁻, Ca²⁺), cardiac rhythm, respiratory rate/depth, I&O, mental status

Priority nursing interventions and monitoring parameters for each primary acid–base disorder

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CLINICAL PEARL

On the NCLEX, when faced with an ABG question, always think in terms of the nursing process: Assess (interpret the ABG), Analyze (identify the disorder and cause), Plan (determine priority interventions), Implement (carry out the intervention), and Evaluate (reassess via repeat ABGs). The exam rarely asks you to simply label the disorder—it wants to know what you would DO about it. Remember the cardinal rule: treat the patient, not the numbers. An ABG must always be interpreted in the context of the patient's clinical presentation, history, and physical assessment.

SECTION 8

Mixed Disorders & Advanced Acid–Base Concepts

While the NCLEX primarily tests your ability to interpret straightforward acid–base disturbances, understanding mixed acid–base disorders strengthens your clinical reasoning and prepares you for real-world ICU practice. A mixed disorder occurs when two or more primary disturbances coexist simultaneously—for example, a patient in diabetic ketoacidosis (metabolic acidosis) who also develops aspiration pneumonia (respiratory acidosis). In such cases, both the PaCO₂ and HCO₃⁻ move in the same acidotic direction, and the pH becomes severely depressed because neither system can compensate for the other.

Concept	Basic ABG Interpretation	Advanced ABG Analysis
Number of disorders	Single primary disorder with or without compensation	Two or three simultaneous primary disorders (mixed)
Anion gap role	Used to differentiate metabolic acidosis subtypes	Delta-delta ratio used to detect hidden second metabolic disorder
Compensation rules	Apply Winter's formula or expected PaCO₂ change	If actual compensation deviates from expected, suspect a mixed disorder
Clinical setting	Med-surg floors, general practice	ICU, emergency department, post-cardiac arrest
Key formula	Henderson-Hasselbalch equation	Winter's formula: Expected PaCO₂ = 1.5 × [HCO₃⁻] + 8 (±2)

Comparison of basic ABG interpretation and advanced acid–base analysis

As you progress in your nursing career—particularly if you pursue critical care certification (CCRN) or nurse practitioner credentials—you will encounter these complex mixed disorders regularly. For now, the essential foundation you build here in systematic single-disorder interpretation will serve as the scaffolding for all advanced acid–base reasoning. The key principle to carry forward is that whenever the degree of compensation does not match what you would expect physiologically, consider that a second primary disorder may be present. This principle transforms a mechanical ABG interpretation exercise into true clinical reasoning.

SECTION 9

Practice Problems

Question 1: CONCEPTUAL

A nurse is reviewing ABG results and notes that the pH is 7.32, PaCO₂ is 50 mmHg, and HCO₃⁻ is 24 mEq/L. Which acid–base disturbance does this represent, and what is the compensation status?

Show answer

This ABG represents uncompensated respiratory acidosis. The pH of 7.32 is below 7.35, indicating acidosis. The PaCO₂ of 50 mmHg is elevated above the normal 35–45 range, which "matches" the acidotic pH—identifying the respiratory system as the primary cause. The HCO₃⁻ of 24 mEq/L is within the normal range (22–26 mEq/L), meaning the kidneys have not yet begun to retain additional bicarbonate. Because only the respiratory component is abnormal and the metabolic component remains normal, this is an uncompensated respiratory acidosis, suggesting an acute process.

Question 2: BASIC CALCULATION

A patient with diabetic ketoacidosis has the following lab values: Na⁺ 140 mEq/L, Cl⁻ 100 mEq/L, HCO₃⁻ 10 mEq/L. Calculate the anion gap and explain what this value indicates about the type of metabolic acidosis.

Show answer

Anion gap = Na⁺ − (Cl⁻ + HCO₃⁻) = 140 − (100 + 10) = 140 − 110 = 30 mEq/L. The normal anion gap is 8–12 mEq/L, so this value of 30 is significantly elevated. An elevated anion gap indicates the presence of unmeasured acids in the blood, which in the context of diabetic ketoacidosis (DKA) are ketoacids (beta-hydroxybutyrate and acetoacetate). This is classified as a high anion gap metabolic acidosis, as opposed to a normal anion gap (hyperchloremic) metabolic acidosis that would result from direct bicarbonate loss such as in diarrhea.

Question 3: INTERMEDIATE

ABG results show: pH 7.48, PaCO₂ 48 mmHg, HCO₃⁻ 34 mEq/L. The patient has been vomiting for three days due to a bowel obstruction. Interpret the ABG, determine the compensation status, and identify the likely cause.

Show answer

This ABG represents partially compensated metabolic alkalosis. The pH of 7.48 is above 7.45, indicating alkalosis. The HCO₃⁻ of 34 mEq/L is elevated above the normal 22–26 range, which "matches" the alkalotic pH—identifying the metabolic system as the primary cause. The PaCO₂ of 48 mmHg is slightly elevated (above normal 35–45), indicating that the lungs are beginning to compensate by retaining CO₂ through hypoventilation. However, since the pH remains abnormal at 7.48, compensation is only partial. The three-day history of vomiting is the cause: loss of gastric HCl through vomiting depletes hydrogen ions and chloride, leading to a contraction alkalosis with chloride-responsive metabolic alkalosis. The nursing priority would be to administer IV normal saline to replace volume and chloride, replace potassium as ordered, and manage the bowel obstruction.

Question 4: APPLIED

A nurse is caring for a postoperative patient on a ventilator. The ABG shows: pH 7.52, PaCO₂ 28 mmHg, HCO₃⁻ 23 mEq/L, PaO₂ 110 mmHg. The patient's respiratory rate on the ventilator is set at 20 breaths/min with a tidal volume of 500 mL. What is the acid–base disturbance, and what specific nursing actions should be taken?

Show answer

This ABG represents uncompensated respiratory alkalosis caused by mechanical overventilation. The pH of 7.52 is above 7.45 (alkalosis), the PaCO₂ of 28 mmHg is below 35 (matching the alkalotic pH), and the HCO₃⁻ of 23 mEq/L is normal, confirming no metabolic compensation has occurred. The PaO₂ of 110 is above normal, further supporting that the patient is being over-oxygenated and over-ventilated. The nurse should immediately notify the respiratory therapist and provider to request a ventilator settings change—either reducing the respiratory rate or reducing the tidal volume to decrease minute ventilation and allow PaCO₂ to rise. The nurse should also assess for patient discomfort, pain, or anxiety that may be triggering additional spontaneous breaths above the set rate. Continuous SpO₂ and end-tidal CO₂ monitoring should be maintained, with repeat ABGs drawn 20–30 minutes after any ventilator adjustment.

Question 5: CRITICAL THINKING

A patient with chronic COPD (baseline PaCO₂ of 55 mmHg, HCO₃⁻ of 32 mEq/L) presents to the emergency department with worsening dyspnea. Current ABG: pH 7.22, PaCO₂ 72 mmHg, HCO₃⁻ 30 mEq/L, PaO₂ 48 mmHg. Analyze these results in the context of the patient's baseline, differentiate between the chronic and acute components, and outline your priority nursing interventions with rationale.

Show answer

This represents an acute-on-chronic respiratory acidosis with severe hypoxemia. At baseline, this COPD patient has a chronically compensated respiratory acidosis—the elevated PaCO₂ of 55 is offset by renal retention of HCO₃⁻ at 32, maintaining a near-normal pH. The current ABG shows PaCO₂ has risen acutely from 55 to 72 mmHg (a 17 mmHg increase), while HCO₃⁻ has actually decreased slightly from 32 to 30 mEq/L, indicating the kidneys have not had time to adjust to this new insult. The severely depressed pH of 7.22 confirms that the acute CO₂ rise has overwhelmed the existing renal compensation. The PaO₂ of 48 represents dangerous hypoxemia. Priority interventions: (1) Administer low-flow oxygen titrated to SpO₂ 88–92%—not higher, because chronic COPD patients may depend on hypoxic drive, and excessive oxygen could further suppress ventilation; (2) Prepare for non-invasive positive pressure ventilation (BiPAP) as a first-line measure to offload respiratory muscles and improve ventilation; (3) Administer nebulized bronchodilators and systemic corticosteroids per protocol; (4) Position in high Fowler's; (5) Continuously monitor LOC as a pH below 7.20 risks cardiac dysrhythmias and cerebral depression; (6) Have intubation equipment at bedside; (7) Notify the provider urgently because the gap between baseline and current values indicates this patient is decompensating rapidly.

SUMMARY

Acid–Base & ABG Interpretation: Complete Review

Summary

Systematic ABG interpretation follows a reliable four-step algorithm: first, evaluate the pH to determine acidosis (< 7.35) versus alkalosis (> 7.45); second, examine PaCO₂ (35–45 mmHg) and HCO₃⁻ (22–26 mEq/L) to identify whether the primary disorder is respiratory or metabolic; third, assess the compensation status (uncompensated, partially compensated, or fully compensated) by evaluating the opposing system; and fourth, translate the interpretation into an appropriate clinical response. The component that "matches" the pH direction identifies the primary disorder.

The four primary disorders are respiratory acidosis (↑PaCO₂, treated by improving ventilation), metabolic acidosis (↓HCO₃⁻, treated by addressing the underlying cause such as DKA or lactic acidosis), respiratory alkalosis (↓PaCO₂, treated by reducing hyperventilation), and metabolic alkalosis (↑HCO₃⁻, treated with chloride and potassium replacement). The Henderson-Hasselbalch equation provides the mathematical foundation, and the anion gap further differentiates metabolic acidosis subtypes. Always interpret ABGs in clinical context, act on findings using evidence-based nursing interventions, and reassess with serial ABGs to evaluate the effectiveness of treatment.