When are arterial blood gas (ABG), venous blood gas (VBG), and lactate measurements indicated, what information do they provide about oxygenation, ventilation, acid‑base balance and tissue hypoperfusion, how should abnormal high or low results be interpreted, and what are the appropriate treatment choices, medication dosages, duration, associated symptoms, and differential diagnoses?

Arterial Blood Gas vs Venous Blood Gas vs Lactate: Clinical Utility and Management

When to Order These Tests

Arterial blood gas (ABG) is indicated for critically ill patients requiring precise assessment of oxygenation, ventilation, and acid-base status, while venous blood gas (VBG) serves as a less invasive alternative for pH and metabolic assessment, and lactate measurement identifies tissue hypoperfusion and guides resuscitation. 1

ABG Indications

• All critically ill patients require ABG testing to assess oxygenation (PaO₂), ventilation (PaCO₂), and acid-base status 2
• Patients with shock or hypotension should have initial blood gas sampling from an arterial source 2
• SpO₂ <94% on room air or supplemental oxygen warrants ABG testing 2
• Acute pulmonary edema or history of COPD requires ABG on admission, especially in cardiogenic shock 1
• Respiratory distress with suspected hypercapnia or need for precise PaCO₂ and PaO₂ measurement 1

VBG Indications

• Initial assessment and resuscitation in emergency and intensive care settings when arterial sampling is unnecessary or impractical 3, 4
• Monitoring therapeutic responses and acid-base status when oxygenation assessment is not required 3
• pH and CO₂ assessment during oxygen titration (venous sample acceptably indicates pH and CO₂) 1

Lactate Indications

• All patients with suspected shock or tissue hypoperfusion require lactate measurement 1
• Major trauma patients for prognostic assessment and resuscitation guidance 1
• Serial measurements to evaluate response to therapy in circulatory shock 1

What These Tests Tell You

ABG Parameters

pH (Normal: 7.35-7.45) 2, 5

• **pH <7.35** = acidemia (respiratory if PaCO₂ >45 mmHg; metabolic if HCO₃⁻ <22 mEq/L)
• pH >7.45 = alkalemia (respiratory if PaCO₂ <35 mmHg; metabolic if HCO₃⁻ >26 mEq/L)

PaO₂ (Normal: >90 mmHg at sea level) 2

• PaO₂ <60 mmHg = severe hypoxemia requiring immediate intervention
• Assesses adequacy of oxygenation and pulmonary gas exchange

PaCO₂ (Normal: 35-45 mmHg or 4.7-6.0 kPa) 2, 5

• PaCO₂ >45 mmHg (>6.0 kPa) = hypoventilation/respiratory acidosis
• PaCO₂ <35 mmHg = hyperventilation/respiratory alkalosis
• Directly reflects ventilation status

HCO₃⁻ (Normal: 22-26 mEq/L) 2

• HCO₃⁻ <22 mEq/L = metabolic acidosis
• HCO₃⁻ >26 mEq/L = metabolic alkalosis
• Reflects metabolic/renal component of acid-base balance

Base Deficit/Excess (Normal: -2 to +2 mEq/L) 1

• Base deficit >10 mEq/L = severe metabolic acidosis correlating with increased mortality in trauma
• Independent predictor of mortality in traumatic-hemorrhagic shock 1

VBG Parameters

Strong correlation with ABG for: 3, 4

• pH (r >0.9) - reliable for acid-base assessment
• HCO₃⁻ and base excess (r >0.9) - good correlation in most cases
• pCO₂ - controversial correlation; venous values typically 4-8 mmHg higher than arterial

Poor correlation for: 3, 4

• pO₂ (r <0.3) - significant difference due to oxygen consumption; VBG cannot assess oxygenation

Lactate Levels

Normal: <2 mmol/L 1

Elevated lactate indicates: 1

• Tissue hypoperfusion and anaerobic metabolism
• Inadequate oxygen delivery to tissues
• Predictor of organ failure and mortality

Prognostic significance in trauma: 1

• Lactate normalizes within 24h = 100% survival
• Lactate normalizes within 48h = 77.8% survival
• Lactate elevated >48h = 13.6% survival

Interpretation of Abnormal Results

High PaCO₂ (Respiratory Acidosis)

pH <7.35 with PaCO₂ >6.0 kPa (45 mmHg) 5

Symptoms: 5

• Dyspnea, respiratory distress
• Confusion, altered mental status
• Headache, drowsiness
• Tachycardia

Differential Diagnosis: 5

• COPD exacerbation
• Neuromuscular disorders (myasthenia gravis, Guillain-Barré)
• Chest wall deformities
• Respiratory depression (opioids, sedatives)
• Severe pneumonia or pulmonary edema

Low PaCO₂ (Respiratory Alkalosis)

pH >7.45 with PaCO₂ <35 mmHg

Symptoms:

• Hyperventilation, dyspnea
• Lightheadedness, paresthesias
• Anxiety, panic

Differential Diagnosis:

• Anxiety/panic disorder
• Pulmonary embolism
• Pneumonia
• Sepsis
• Salicylate toxicity

High Lactate (Lactic Acidosis)

Lactate >2 mmol/L 1

Symptoms:

• Tachypnea, dyspnea
• Altered mental status
• Hypotension, shock
• Cool, clammy extremities

Differential Diagnosis: 1

• Septic shock
• Hypovolemic shock
• Cardiogenic shock
• Tissue ischemia (mesenteric, limb)
• Severe heart failure
• Mitochondrial myopathy
• Severe deconditioning

Low Lactate Response to Exercise

Failure to elevate lactate during exercise testing 6

Causes: 6

• Exercise intensity below lactate threshold (most common)
• Myophosphorylase deficiency (McArdle disease) - markedly decreased lactate with exercise cramps and potential myoglobinuria
• Poor effort during testing

Treatment Choices, Dosages, and Duration

Respiratory Acidosis (pH <7.35, PaCO₂ >6.0 kPa)

Immediate Management - Controlled Oxygen Therapy: 5

• Target SpO₂ 88-92% for COPD and hypercapnic respiratory failure
• Start at 1 L/min, titrate up in 1 L/min increments until SpO₂ >90%
• Recheck ABG within 60 minutes after initiating or changing oxygen
• Uncontrolled high-flow oxygen increases mortality by 58% in COPD 5

Medical Therapy (First-Line): 5

Bronchodilators:

• Salbutamol 2.5-5 mg nebulized every 4-6 hours OR
• Ipratropium bromide 0.25-0.5 mg nebulized every 4-6 hours
• Drive nebulizers with compressed air (not oxygen) if PaCO₂ elevated, while continuing supplemental oxygen at 1-2 L/min via nasal prongs 5

Corticosteroids:

• Prednisolone 30 mg PO daily for 7-14 days OR
• Hydrocortisone 100 mg IV for 7-14 days 5

Antibiotics (if infection present):

• Amoxicillin (first-line) or tetracycline if increased sputum purulence, volume, or dyspnea 5

Non-Invasive Ventilation (NIV): 5

• Initiate BiPAP when pH <7.35 persists after optimal medical therapy and controlled oxygen
• Especially urgent if pH <7.26 or respiratory distress continues
• British Thoracic Society criteria: pH <7.35 with PaCO₂ >6.5 kPa (49 mmHg) and respiratory rate >23 breaths/min despite optimal treatment 5
• Start NIV promptly—delays worsen outcomes 5

Invasive Mechanical Ventilation: 5

• Consider intubation if pH <7.26 with rising PaCO₂ despite NIV and optimal medical therapy
• Factors favoring intubation: reversible cause, first episode, acceptable baseline quality of life 5

Alternative Pharmacologic Support: 5

• Doxapram IV (respiratory stimulant) as temporizing measure for 24-36 hours in patients with pH <7.26 who are not candidates for immediate NIV or intubation

Severe Acidosis in Cardiac Arrest

Sodium Bicarbonate: 1

• Judicious use limited to severe acidosis: arterial pH <7.1 and base deficit <10
• Special circumstances: hyperkalemia or tricyclic antidepressant overdose
• No clinical evidence that any buffer increases survival rates after cardiac arrest 1
• Best method of reversing acidosis is to restore spontaneous circulation 1

Shock with Elevated Lactate

Resuscitation Goals: 1

• Serial lactate measurements to guide resuscitation
• Target lactate normalization (<2 mmol/L) within 24 hours for optimal survival 1
• Lactate clearance provides early, objective evaluation of response to therapy 1

Treatment priorities:

• Restore tissue perfusion (fluid resuscitation, vasopressors as needed)
• Treat underlying cause (sepsis, hemorrhage, cardiac dysfunction)
• Monitor base deficit alongside lactate for comprehensive assessment 1

Critical Pitfalls to Avoid

• Normal SpO₂ does not rule out significant acid-base disturbances or hypercapnia 2
• Failing to repeat ABG after oxygen therapy changes in patients at risk for CO₂ retention is a common management error 2
• ABG alone may be misleading for acid-base status; even simultaneous arterial and central venous samples may not estimate myocardial/cerebral intracellular acid-base status 1
• Routine ABG is not needed in most acute heart failure cases except when hemodynamic instability is present 1
• VBG cannot assess oxygenation due to poor pO₂ correlation 3, 4
• Lactate reliability may be lower in alcohol-associated trauma; base deficit may be better predictor 1
• Rise in PaCO₂ >1 kPa (7.5 mmHg) during oxygen titration indicates clinically unstable disease requiring further optimization 2

Monitoring During Recovery

• Measure ABG on room air before discharge to guide long-term oxygen therapy assessment 5
• Record FEV₁ before discharge 5
• Monitor peak flow twice daily until clinically stable 5
• Repeat blood gases if clinical deterioration occurs at any time 5