ABG Analysis: Comprehensive Notes

ABG Basics and Context

• ABGs quantify hydrogen ion activity in the blood to assess acid–base balance.

• Because the hydrogen ion concentration in blood is very small, the body uses an inverse logarithm to express pH: the normal pH range is 7.35 to 7.45. In words: a pH below 7.35 is acidemia; above 7.45 is alkalemia.

• Normal acid–base balance is supported by a base-to-acid ratio of about 20:1. Buffers in the blood (proteins, etc.) can absorb excess hydrogen ions when needed, acting like sponges; when hydrogen ions are in excess, buffers release ions back into solution.

• Buffers act quickly; respiratory compensation can adjust CO₂ within minutes to hours; renal compensation (kidneys) takes hours to days and provides longer-term adjustment.

• Four classic abnormal states to memorize:

  • Respiratory acidosis

  • Respiratory alkalosis

  • Metabolic acidosis

  • Metabolic alkalosis

• Real-world relevance: compensation mechanisms aim to restore pH toward normal to preserve enzyme function, hormonal signaling, neuromuscular activity, and overall homeostasis.

Normal reference ranges (typical for many labs)

• pH: 7.35 \le pH \le 7.45

• PaCO₂ (part of respiratory component): 35 \le PaCO_2 \le 45 mmHg

• HCO₃⁻ (metabolic component): 23 \le [\mathrm{HCO_3^-}] \le 30 mEq/L

• Note on lab variation:

  • Some courses use [\mathrm{HCO_3^-}] \in [22,26] as normal.

  • Others use [\mathrm{HCO_3^-}] \in [21,28] or as high as 30.

  • In this material, keep in mind the common teaching ranges:

  • Lab-typical: 22 \le [\mathrm{HCO_3^-}] \le 26

  • Course-specific: 23 \le [\mathrm{HCO_3^-}] \le 30

• Practical note: when a textbook uses a different normal range for HCO₃⁻, use the same approach but rely on the same analysis steps; the pattern (pH, PaCO₂, HCO₃⁻) remains consistent.

• Goldilocks pH reference: pH around 7.40 is the target normal point; still, compensation may move values around while trying to restore pH toward 7.40.

How to analyze ABGs: the matching game (step-by-step)

• Step 1: Determine the primary problem by pH

  • If pH < 7.35 → acidemia

  • If pH > 7.45 → alkalemia

  • If pH is within 7.35–7.45 → pH is normal (possible compensation)

• Step 2: Evaluate the respiratory component (PaCO₂)

  • If PaCO₂ > 45 → respiratory acidosis tendency

  • If PaCO₂ 35–45 → respiratory component normal

  • If PaCO₂ < 35 → respiratory alkalosis tendency

• Step 3: Evaluate the metabolic component (HCO₃⁻)

  • If HCO₃⁻ < 22 → metabolic acidosis tendency

  • If HCO₃⁻ 22–26 → metabolic component normal

  • If HCO₃⁻ > 26 → metabolic alkalosis tendency

• Step 4: Identify the primary disorder

  • Match the abnormal pH with the abnormal secondary parameter(s) to identify the primary disorder (respiratory vs metabolic).

• Step 5: Determine compensation

  • Compensation exists when the non-primary system is out of range and in the opposite direction to the primary disorder.

  • Rule 1: Both the respiratory (PaCO₂) and metabolic (HCO₃⁻) indicators must be out of range and in opposite directions for compensation to be occurring.

  • Rule 2: If the pH has returned to the normal range (7.35–7.45), the patient is fully compensated; if the pH remains abnormal but both non-pH indicators are out of range in opposite directions, compensation is partial.

• Step 6: Interpret clinical significance

  • Abnormal pH with appropriate compensation implies a managed/compensated disorder.

  • Abnormal pH with little or no compensation suggests an acute primary disorder or an insufficient compensatory response.

Common ABG disorder patterns with examples

• Respiratory Acidosis

  • Primary: PaCO₂ > 45 mmHg; pH < 7.35

  • Compensatory response: increased HCO₃⁻ (kidney retention of bicarbonate) over time

• Respiratory Alkalosis

  • Primary: PaCO₂ < 35 mmHg; pH > 7.45

  • Compensatory response: decreased HCO₃⁻ (renal excretion of bicarbonate) over time

• Metabolic Acidosis

  • Primary: HCO₃⁻ < 22 mEq/L; pH < 7.35

  • Compensatory response: decreased PaCO₂ (hyperventilation) via respiratory compensation

• Metabolic Alkalosis

  • Primary: HCO₃⁻ > 26 mEq/L; pH > 7.45

  • Compensatory response: increased PaCO₂ (hypoventilation) via respiratory compensation

Worked ABG practice problems (per transcript)

• Case 1: pH = 7.47; PaCO₂ = 42; HCO₃⁻ = 32

  • pH: alkalemia → alkalosis

  • PaCO₂: 42 in normal range → no respiratory abnormality

  • HCO₃⁻: 32 high → metabolic alkalosis

  • Conclusion: Metabolic alkalosis (no respiratory compensation observed in this snapshot)

• Case 2: pH = 7.51; PaCO₂ = 28; HCO₃⁻ = 22

  • pH: alkalemia

  • PaCO₂: 28 (low) → respiratory alkalosis tendency

  • HCO₃⁻: 22 (low end of normal) → metabolic component not clearly elevated

  • Conclusion: Respiratory alkalosis (primary respiratory cause)

• Case 3: pH = 7.51; PaCO₂ = 28; HCO₃⁻ = 22

  • Same as Case 2; Respiratory alkalosis with respiratory primary cause

• Case 4: pH = 7.28; PaCO₂ = 62; HCO₃⁻ = 23

  • pH: acidemia

  • PaCO₂: 62 (high) → respiratory acidosis

  • HCO₃⁻: 23 normal

  • Conclusion: Respiratory acidosis (no metabolic compensation yet)

• Case 5: pH = 7.30; PaCO₂ = 44; HCO₃⁻ = 17

  • pH: acidemia

  • PaCO₂: 44 normal → not a respiratory abnormality here

  • HCO₃⁻: 17 low → metabolic acidosis

  • Conclusion: Metabolic acidosis (no apparent respiratory compensation yet)

• Case 6: pH = 7.36; PaCO₂ = 49; HCO₃⁻ = 30

  • pH near normal (slightly low-normal)

  • PaCO₂: 49 high → respiratory acidosis tendency

  • HCO₃⁻: 30 high → metabolic alkalosis tendency

  • Both non-pH indicators out of range in opposite directions with pH normal → Fully compensated respiratory acidosis (respiratory system cannot correct acidity alone; metabolic compensation has occurred until pH normal)

• Case 7: pH = 7.43; PaCO₂ = 49; HCO₃⁻ = 29

  • pH near normal (slightly alkalemic side of normal)

  • PaCO₂: 49 high → respiratory acidosis tendency

  • HCO₃⁻: 29 high → metabolic alkalosis tendency

  • Outcome: Fully compensated metabolic alkalosis (primary metabolic alkalosis with respiratory compensation keeping pH near normal)

• Case 8: pH = 7.29; PaCO₂ = 31; HCO₃⁻ = 16

  • pH: acidemia

  • PaCO₂: 31 low → respiratory alkalosis tendency

  • HCO₃⁻: 16 very low → metabolic acidosis tendency

  • Both non-pH indicators out of range in opposite directions with abnormal pH → Partially compensated metabolic acidosis

• Case 9: Diabetic ketoacidosis (DKA) scenario

  • DKA is a metabolic acidosis with compensatory respiratory response (Kussmaul respirations)

  • Expected ABG pattern: low pH, low HCO₃⁻, low PaCO₂ due to hyperventilation

  • In practice: pH < 7.35, HCO₃⁻ low, PaCO₂ decreased due to compensation; if severe, PaCO₂ may approach normal or be higher depending on respiratory fatigue

  • Important teaching point: Deep, rapid respirations signal compensation; do not assume a primary respiratory issue without considering metabolic cause

• Case: Vomiting for three days

  • Primary disorder: Metabolic alkalosis (loss of gastric acid)

  • Expected compensation: hypoventilation with increased PaCO₂ to retain CO₂

  • ABG pattern: high pH, high HCO₃⁻, elevated PaCO₂ with partial/complete compensation possible depending on time course

• Case: High altitude exposure (hypoxemia)

  • Key pattern: Respiratory alkalosis due to hyperventilation in response to hypoxia

  • ABG signature: high pH, low PaCO₂, variable HCO₃⁻ depending on duration of exposure and compensation

• Case: Opioid overdosing (sedative overdose)

  • Primary disorder: Respiratory acidosis due to hypoventilation

  • ABG: high PaCO₂, low pH; compensation may begin with metabolic changes if prolonged

• Case: Emphysema/chronic COPD

  • Primary disorder: Chronic respiratory acidosis (due to impaired CO₂ exchange)

  • ABG: high PaCO₂ with pH near normal or slightly low; long-standing compensation with elevated HCO₃⁻ over time

• Case: Salicylate intoxication

  • Pattern: Metabolic acidosis (and sometimes mixed with respiratory alkalosis early)

  • ABG interpretation depends on timing and severity

• Case: Antacid use or excessive bicarbonate intake

  • Pattern: Metabolic alkalosis (elevated HCO₃⁻) with compensatory respiratory changes

• Case: Diarrhea

  • Pattern: Metabolic acidosis (loss of bicarbonate via stool) with respiratory compensation

• Case: Severe vomiting or nasogastric suction

  • Pattern: Metabolic alkalosis with CO₂ retention by hypoventilation as compensation

• Practical clinical takeaway on interpretation

  • Always determine the primary disorder first via pH, then check PaCO₂ and HCO₃⁻ to see which system is driving the problem.

  • Then assess compensation: if pH is back in the normal range, compensation is complete; if pH remains abnormal but the non-primary parameter is appropriately opposite, compensation is partial; if only one non-pH parameter is abnormal, suspect a primary disorder with little to no compensation.

  • Be mindful that electrolyte shifts (e.g., calcium in alkalosis causing paresthesias) can accompany acid–base disorders and influence symptoms (e.g., tingling, tetany).

Pathophysiology cues and clinical correlations

• Hypoxemia at high altitude drives increased ventilation leading to respiratory alkalosis.

• Lactic acidosis from hypoxia or intense activity/Seizure activity can drive metabolic acidosis (increased hydrogen ion production).

• Diabetic ketoacidosis produces metabolic acidosis via excess ketone production; compensatory hyperventilation (Kussmaul) lowers PaCO₂ but does not fully normalize pH.

• Vomiting and NG tube suction remove gastric acid, increasing bicarbonate and causing metabolic alkalosis; respiratory compensation increases CO₂ retention.

• Chronic lung diseases (e.g., COPD, emphysema) favor chronic respiratory acidosis due to impaired CO₂ elimination; kidneys gradually raise HCO₃⁻ to compensate.

• Electrolyte disturbances often accompany acid–base disorders and can affect symptoms (e.g., hypocalcemia with alkalosis may cause tingling around mouth/fingers).

Practical test-taking and clinical reasoning tips

• Use a systematic, repeatable approach (the 4-step ABG analysis) to prevent missing compensation or mislabeling the primary disorder.

• When faced with a clinical scenario, distinguish primary from compensatory processes by matching the direction of abnormal PaCO₂ and HCO₃⁻ with the pH abnormality.

• If a case mentions compensatory physiology (e.g., Kussmaul breathing in DKA), expect a corresponding ABG pattern (metabolic acidosis with respiratory compensation).

• Remember common cause-and-effect pairings to aid interpretation:

  • Vomiting/diarrhea → metabolic alkalosis or acidosis, respectively, with respiratory compensation patterns.

  • COPD/emphysema → chronic respiratory acidosis with renal compensation (elevated HCO₃⁻).

  • Hypoxia at altitude → respiratory alkalosis.

• When the source uses slightly different normal ranges for HCO₃⁻, focus on the qualitative pattern (acidosis vs alkalosis) and relative changes rather than the exact cutoff.

• For exams with “select all that apply” questions on ABGs (e.g., DKA scenario), check: pH, PaCO₂, and HCO₃⁻, then determine primary disorder and compensation; consider typical compensatory patterns (respiratory vs metabolic) and the direction of changes.

Quick reference cheat sheet (memory prompts)

• Normal pH: 7.35–7.45; primary acidemia/alkalemia determined by pH relative to this window.

• PaCO₂:

  • > 45 mmHg → respiratory acidosis tendency

  • 35–45 mmHg → respiratory normal

  • < 35 mmHg → respiratory alkalosis tendency

• HCO₃⁻:

  • < 22 → metabolic acidosis tendency

  • 22–26 → metabolic normal

  • > 26 → metabolic alkalosis tendency

• Compensation rules:

  • Opposite-direction changes in PaCO₂ and HCO₃⁻ indicate compensation.

  • pH in normal range with abnormal PaCO₂ and HCO₃⁻ indicates full compensation.

  • pH abnormal with both PaCO₂ and HCO₃⁻ abnormal in opposite directions indicates partial compensation.

Real-world practice: how this informs patient care

• Recognize which organ system is failing (lungs vs kidneys) and whether compensation is adequate, to guide treatment plans (e.g., improving ventilation, correcting volume status, addressing electrolyte disturbances).

• Identify urgent cases that require rapid intervention (e.g., severe metabolic acidosis with poor compensation or respiratory depression) and escalate care accordingly.

// End of notes