9.3 Arterial Blood Gas (ABG) Interpretation & Acid-Base Disturbances

Arterial Blood Gas (ABG) Interpretation & Acid-Base Disturbances

Clinical Core Insight: Arterial Blood Gas (ABG) interpretation is a foundational diagnostic skill in acute nursing and critical care. In the Irish health service, ABG machines report partial pressures of gases in kilopascals (kPa), the International System of Units (SI), though familiarity with conventional millimetres of mercury (mmHg) remains essential (conversion: $1\text{ kPa} \approx 7.5\text{ mmHg}$; $1\text{ mmHg} \approx 0.133\text{ kPa}$). A structured, algorithmic approach prevents diagnostic errors when identifying primary acid-base disorders, compensatory physiological responses, and mixed pathologies.

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Normal ABG Reference Ranges

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Systematic 4-Step ABG Interpretation Framework

+-----------------------------------------------------------------------------+
|                   4-STEP SYSTEMATIC ABG INTERPRETATION                      |
+-----------------------------------------------------------------------------+
| STEP 1: EXAMINE pH                                                          |
|   * pH < 7.35  --> Acidaemia                                                |
|   * pH > 7.45  --> Alkalaemia                                               |
|   * pH 7.35 - 7.45 --> Normal (or fully compensated disorder)               |
+-----------------------------------------------------------------------------+
| STEP 2: EXAMINE PaCO2 (Respiratory Component)                               |
|   * PaCO2 > 6.0 kPa (45 mmHg) --> Respiratory Acidosis (CO2 retention)      |
|   * PaCO2 < 4.7 kPa (35 mmHg) --> Respiratory Alkalosis (CO2 washout)       |
|   * PaCO2 4.7 - 6.0 kPa       --> Normal respiratory status                 |
+-----------------------------------------------------------------------------+
| STEP 3: EXAMINE HCO3- & BASE EXCESS (Metabolic Component)                   |
|   * HCO3- < 22 mmol/L / BE < -2 --> Metabolic Acidosis                      |
|   * HCO3- > 26 mmol/L / BE > +2 --> Metabolic Alkalosis                     |
|   * HCO3- 22 - 26 mmol/L / BE -2 to +2 --> Normal metabolic status          |
+-----------------------------------------------------------------------------+
| STEP 4: DETERMINE PRIMARY DISTURBANCE & DEGREE OF COMPENSATION              |
|   * Uncompensated: pH abnormal; one parameter abnormal; other normal       |
|   * Partially Compensated: pH abnormal; both parameters abnormal in same dir|
|   * Fully Compensated: pH normal (7.35-7.45); both parameters abnormal      |
+-----------------------------------------------------------------------------+

Step 1: Examine the pH

• If $\text{pH} < 7.35$, the patient has acidaemia.
• If $\text{pH} > 7.45$, the patient has alkalaemia.
• If $\text{pH}$ is within the normal range (7.35–7.45), the gas is either completely normal or reflects a fully compensated underlying acid-base disorder. In fully compensated states, look at whether the pH sits on the acidotic side ($< 7.40$) or alkalotic side ($> 7.40$) of absolute neutral (7.40) to deduce the original primary disturbance.

Step 2: Examine the PaCO2 (Respiratory Component)

$\text{PaCO}_2$ reflects alveolar ventilation and the respiratory regulation of volatile carbonic acid ($\text{H}_2\text{CO}_3 \rightleftharpoons \text{H}_2\text{O} + \text{CO}_2$):

• $\text{PaCO}_2 > 6.0\text{ kPa}$ ($> 45\text{ mmHg}$): Hypercapnia, indicating alveolar hypoventilation and respiratory acidosis.
• $\text{PaCO}_2 < 4.7\text{ kPa}$ ($< 35\text{ mmHg}$): Hypocapnia, indicating alveolar hyperventilation and respiratory alkalosis.
• Compare the directional shift of $\text{PaCO}_2$ with the pH: if pH is low ($< 7.35$) and $\text{PaCO}_2$ is high ($> 6.0\text{ kPa}$), the primary driver is respiratory.

Step 3: Examine the HCO3- and Base Excess (Metabolic Component)

Serum bicarbonate ($\text{HCO}_3^-$) and Base Excess (BE) reflect renal metabolic acid-base buffering:

• $\text{HCO}_3^- < 22\text{ mmol/L}$ (and $\text{BE} < -2.0\text{ mmol/L}$): Indicates a deficit of bicarbonate or accumulation of non-volatile acids, signifying metabolic acidosis.
• $\text{HCO}_3^- > 26\text{ mmol/L}$ (and $\text{BE} > +2.0\text{ mmol/L}$): Indicates an excess of bicarbonate or loss of hydrogen ions, signifying metabolic alkalosis.
• If pH is low ($< 7.35$) and $\text{HCO}_3^-$ is low ($< 22\text{ mmol/L}$), the primary driver is metabolic.

Step 4: Determine Compensation Status

Physiological compensation represents the body's homeostatic attempt to restore pH toward normal (7.40). The lungs compensate for metabolic disorders within minutes to hours by altering ventilation, whereas the kidneys compensate for respiratory disorders slowly over 24 to 72 hours by altering bicarbonate reabsorption and hydrogen ion secretion.

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Core Acid-Base Disturbances

1. Respiratory Acidosis

• Pathophysiology: Alveolar hypoventilation leading to systemic carbon dioxide retention and hypercapnia, forming carbonic acid which dissociates into hydrogen ions.
• Common Etiologies:
  • Chronic lung diseases (AECOPD, severe emphysema)
  • Central nervous system depression (opioid overdose, benzodiazepine toxicity, brainstem stroke)
  • Neuromuscular impairment (Guillain-Barré syndrome, myasthenia gravis, motor neurone disease)
  • Chest wall mechanical restriction (flail chest, severe kyphoscoliosis, morbid obesity hypoventilation)
• Renal Compensation: Kidneys synthesize and retain $\text{HCO}_3^-$ and excrete $\text{H}^+$ in urine; takes 2–3 days for full metabolic compensation.

2. Respiratory Alkalosis

• Pathophysiology: Alveolar hyperventilation exceeding metabolic $\text{CO}_2$ production, causing excessive elimination ("washout") of carbon dioxide.
• Common Etiologies:
  • Psychogenic hyperventilation (severe anxiety, acute panic attack)
  • Acute pain, physical trauma, or psychological distress
  • Pulmonary embolism (hypoxaemia-induced reflex hyperventilation)
  • Early Gram-negative sepsis (endotoxins directly stimulate the medullary respiratory center)
  • Early salicylate toxicity (aspirin directly stimulates central respiratory centers)
  • Mechanical ventilation with excessive tidal volume or respiratory rate
• Renal Compensation: Kidneys excrete $\text{HCO}_3^-$ into urine to restore normal pH (slow response).

3. Metabolic Acidosis & The Anion Gap

Metabolic acidosis is caused by either the accumulation of non-volatile organic/inorganic acids or the primary loss of bicarbonate. It is fundamentally categorized using the Serum Anion Gap: $\text{Anion Gap} = [\text{Na}^+] - ([\text{Cl}^-] + [\text{HCO}_3^-])$ Normal reference range: 8 to 16 mmol/L.

High Anion Gap Metabolic Acidosis (HAGMA)

Characterized by the addition of unmeasured organic anions that consume bicarbonate while serum chloride remains normal. Causes are remembered by the mnemonic GOLDMARK or MUDPILES:

• D — Diabetic Ketoacidosis (DKA): Beta-hydroxybutyrate and acetoacetate accumulation
• L — Lactic Acidosis: Tissue hypoperfusion, septic shock, cardiogenic shock, mesenteric ischemia (lactate $> 2.0\text{ mmol/L}$)
• U — Uraemia / Renal Failure: Impaired excretion of sulfate, phosphate, and organic acids
• T — Toxic Ingestions: Methanol, ethylene glycol (antifreeze), salicylates (aspirin)

Normal Anion Gap Metabolic Acidosis (NAGMA / Hyperchloraemic Acidosis)

Occurs when bicarbonate is lost directly from the body and replaced by chloride to preserve electroneutrality (serum chloride rises, keeping the anion gap within 8–16 mmol/L):

• Gastrointestinal Bicarbonate Loss: Severe prolonged diarrhoea, enterocutaneous fistulae, pancreatic drainage, ureterosigmoidostomy
• Renal Bicarbonate Loss: Renal Tubular Acidosis (Type 1 or Type 2 RTA)
• Iatrogenic: Rapid, large-volume infusion of 0.9% Normal Saline (saline contains 154 mmol/L chloride, inducing dilutional hyperchloraemic metabolic acidosis).

4. Metabolic Alkalosis

• Pathophysiology: Primary elevation of serum bicarbonate or loss of hydrogen ions from extracellular fluid.
• Common Etiologies:
  • Upper gastrointestinal fluid losses (severe prolonged vomiting, continuous nasogastric suctioning losing gastric hydrochloric acid)
  • Diuretic therapy (loop diuretics such as furosemide, thiazide diuretics causing contraction alkalosis and urinary $\text{H}^+$ loss)
  • Severe hypokalaemia (intracellular potassium shifts out of cells into plasma in exchange for hydrogen ions entering cells)
  • Excessive exogenous administration of intravenous sodium bicarbonate or antacids
• Respiratory Compensation: Hypoventilation (decreased respiratory rate and depth) to retain $\text{CO}_2$, limited by arterial hypoxaemia.

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Type 1 vs Type 2 Respiratory Failure

Respiratory failure is defined as the inability of the respiratory system to maintain adequate pulmonary gas exchange, formally diagnosed on arterial blood gas analysis:

+-----------------------------------------------------------------------------+
|                   RESPIRATORY FAILURE CLASSIFICATION                        |
+---------------------------------------+-------------------------------------+
| TYPE 1: HYPOXAEMIC RESPIRATORY FAILURE| TYPE 2: HYPERCAPNIC (VENTILATORY)   |
+---------------------------------------+-------------------------------------+
| * PaO2 < 8.0 kPa (60 mmHg) on air     | * PaO2 < 8.0 kPa (60 mmHg)          |
| * PaCO2 Normal or Low (< 6.0 kPa)     | * PaCO2 Elevated (> 6.0 kPa / 45 mmHg|
| * Underlying: Lung Parenchyma Failure  | * Underlying: Ventilatory Pump Fail |
| * Mechanisms: V/Q mismatch, shunt,    | * Mechanisms: Alveolar hypoventilat, |
|   alveolar-capillary diffusion barrier|   respiratory muscle exhaustion,    |
| * Examples: Pulmonary embolism, ARDS, |   CNS depressants, AECOPD, severe   |
|   lobar pneumonia, pulmonary edema    |   chest wall trauma, neuromuscular  |
+---------------------------------------+-------------------------------------+

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Arterial Blood Sampling & The Modified Allen's Test

The radial artery is the preferred anatomical site for arterial puncture because it is superficial, readily accessible, easy to compress against the distal radius, and supported by collateral circulation via the ulnar artery and deep palmar arch.

Execution of the Modified Allen's Test

Prior to performing a radial artery puncture or cannulation, the nurse must assess the patency of the ulnar artery to ensure adequate collateral blood flow to the hand in the event of radial artery thrombosis or spasm:

1. Instruct the patient to clench their hand tightly into a fist for approximately 30 seconds.
2. Simultaneously apply firm digital compression over both the radial and ulnar arteries at the wrist to occlude arterial inflow.
3. Instruct the patient to open their hand partially (avoiding hyperextension of digits, which can produce false blanching). The palmar surface appears pale, blanched, and bloodless.
4. Release digital pressure ONLY from the ulnar artery, while maintaining continuous, firm compression over the radial artery.
5. Observe the palm and digits for reperfusion (erythema/blush):
   • Normal (Positive) Allen's Test: Palm and fingertips flush pink within 5 to 10 seconds, confirming robust collateral circulation through the ulnar artery and palmar arches. It is clinically safe to proceed with radial puncture.
   • Abnormal (Negative) Allen's Test: Hand remains pale and blanched for longer than 10 to 14 seconds. Ulnar collateral circulation is inadequate. Radial artery puncture at this site is STRICTLY CONTRAINDICATED, as arterial injury or occlusion risks ischaemic necrosis of the hand. Evaluate the contralateral wrist or consult the medical team for alternative sites.

+-----------------------------------------------------------------------------+
|                        MODIFIED ALLEN'S TEST STEPS                          |
+-----------------------------------------------------------------------------+
| 1. Patient clenches fist tightly                                            |
| 2. Nurse compresses BOTH radial and ulnar arteries firmly                   |
| 3. Patient opens hand partially --> Hand appears blanched / pale            |
| 4. Nurse releases ULNAR artery ONLY (maintains radial compression)          |
| 5. Observe reperfusion time:                                                |
|    * < 10 seconds: NORMAL (Adequate collateral flow -> safe to puncture)     |
|    * > 10 seconds: ABNORMAL (Inadequate collateral -> CONTRAINDICATED!)     |
+-----------------------------------------------------------------------------+

Post-Puncture Nursing Care & Specimen Handling

1. Direct Digital Pressure: Immediately upon needle withdrawal, apply direct, firm pressure over the arterial puncture site with a sterile gauze pad for a minimum of 5 continuous minutes (timed by a clock).
2. Patients on Anticoagulants / Coagulopathies: Extend direct pressure to 10 to 15 minutes if the patient is receiving anticoagulants (heparin, warfarin, DOACs) or has severe thrombocytopenia.
3. Do NOT Delegate Pressure: The registered nurse or practitioner must maintain continuous pressure personally; do not instruct the patient to hold the gauze, as inadequate pressure causes painful pseudoaneurysms or large haematomas.
4. Air Bubble Elimination: Immediately expel any visible air bubbles from the syringe within 5 seconds, cap the syringe with a safety bung, and gently invert/roll the syringe between palms for 10–15 seconds to mix the lyophilized heparin and prevent microclots. Air bubbles cause dissolved oxygen to diffuse into blood, falsely elevating $\text{PaO}_2$ and lowering $\text{PaCO}_2$.
5. Rapid Analysis: Analyze the specimen within 10 to 15 minutes. If analysis must be delayed, place the syringe in an iced water slurry ($0^\circ\text{C}$ to $4^\circ\text{C}$) to arrest cellular metabolism and prevent false lactic acidosis and oxygen consumption.
6. Neurovascular Assessment: Re-evaluate the puncture site for bleeding or swelling, and assess distal neurovascular status: check radial pulse, capillary refill time ($< 2$ seconds), skin temperature, and absence of numbness or paresthesia.

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Diagnostic Matrix of Acid-Base Disorders

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Clinical Traps & Safety Pearls

• Trap 1: Omitting the Allen's Test. Never attempt radial artery puncture without first documenting an Allen's test. Thrombosis of an anatomically isolated radial artery can lead to digital gangrene and hand amputation.
• Trap 2: Venous Sample Misinterpreted as Arterial. If an ABG shows an unexpectedly low $\text{PaO}_2$ ($< 5.0\text{ kPa}$) and low saturation ($< 75%$) in a patient who looks pink and comfortable, suspect an accidental venous puncture rather than catastrophic respiratory failure. Check needle flashback and verify pulse synchronization.
• Trap 3: Overlooking Mixed Acid-Base Disorders. A COPD patient presenting with severe septic shock may exhibit a normal pH because high $\text{PaCO}_2$ (respiratory acidosis) is offset by low $\text{HCO}_3^-$ (metabolic lactic acidosis). Both disorders are lethal despite the "normal" pH.
• Trap 4: Leaving Syringe at Room Temperature. Cellular metabolism by leukocytes and erythrocytes continues after blood sampling. Leaving a sample at room temperature for $> 20$ minutes causes cells to consume oxygen and produce lactic acid, falsely lowering $\text{PaO}_2$ and $\text{pH}$.