What are the characteristic arterial blood gas (ABG) findings for patients with diabetic ketoacidosis (DKA), renal failure, trauma, shock, sepsis, chronic anemia, chronic obstructive pulmonary disease (COPD), and hypercapnia?

Arterial Blood Gas Findings in Critical Conditions

Diabetic Ketoacidosis (DKA)

DKA presents with high anion gap metabolic acidosis (pH <7.3, bicarbonate <18 mEq/L, anion gap >10-12 mEq/L) with compensatory respiratory alkalosis, though up to 23% of cases can paradoxically present with alkalemia (pH >7.4) due to mixed acid-base disorders. 1, 2

Classic ABG Pattern:

• pH: <7.3 (mild DKA), <7.0 (moderate), <6.9 (severe) 3, 1, 4
• Bicarbonate: <18 mEq/L (mild), <10 mEq/L (moderate to severe) 1, 5
• Anion gap: >10 mEq/L (mild), >12 mEq/L (moderate to severe), can exceed 30 mEq/L in very severe cases 1, 4
• PaCO2: Typically low due to compensatory hyperventilation (Kussmaul respirations) 6
• PaO2: Usually normal unless complicated by pulmonary edema 3

Important Caveats:

• Euglycemic DKA (glucose <250 mg/dL) is increasingly common with SGLT-2 inhibitor use, making hyperglycemia no longer a required diagnostic criterion 5
• Diabetic ketoalkalosis (pH >7.4) occurs in 23% of DKA cases due to concurrent metabolic alkalosis and/or respiratory alkalosis, yet 34% of these patients still have severe ketoacidosis requiring standard DKA treatment 2
• Venous pH (typically 0.03 units lower than arterial) is adequate for monitoring; repeat arterial blood gases are generally unnecessary 3, 7
• The nitroprusside method for ketone measurement only detects acetoacetate and acetone, not beta-hydroxybutyrate (the predominant ketoacid), and may falsely suggest worsening ketosis during treatment 3

Key Signs and Symptoms:

• Polyuria, polydipsia, nausea, vomiting, abdominal pain 5
• Kussmaul respirations (deep, rapid breathing) 6
• Fruity breath odor (acetone) 6
• Altered mental status, lethargy (especially with pH <7.0) 3
• Dehydration signs (poor skin turgor, dry mucous membranes) 6

Resolution Criteria:

• Glucose <200 mg/dL, bicarbonate ≥18 mEq/L, venous pH >7.3 3, 1

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Renal Failure (Chronic Kidney Disease/Uremia)

Chronic renal failure produces non-anion gap metabolic acidosis early in disease, progressing to high anion gap metabolic acidosis (uremic acidosis) in advanced stages due to accumulation of organic acids and phosphates.

ABG Pattern:

• pH: 7.25-7.35 (mild to moderate acidosis)
• Bicarbonate: 12-20 mEq/L (progressively decreases with worsening renal function)
• Anion gap: Normal (10-12 mEq/L) in early CKD; elevated (>12 mEq/L) in advanced uremia 1
• PaCO2: Low-normal due to compensatory hyperventilation
• Base excess: Negative

Key Signs and Symptoms:

• Uremic symptoms: nausea, vomiting, anorexia, altered mental status
• Pruritus, uremic frost (severe cases)
• Pericardial friction rub (uremic pericarditis)
• Asterixis, myoclonus
• Oliguria or anuria in advanced disease

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Trauma and Shock (Hemorrhagic/Hypovolemic)

Shock states produce lactic acidosis with high anion gap metabolic acidosis (pH <7.35, elevated lactate >2-4 mmol/L, anion gap >12 mEq/L) due to tissue hypoperfusion and anaerobic metabolism.

ABG Pattern:

• pH: 7.20-7.35 (mild shock) to <7.10 (severe shock)
• Bicarbonate: 10-18 mEq/L (decreases with severity)
• Anion gap: >12-16 mEq/L (elevated lactate is the primary contributor)
• Lactate: >2 mmol/L (mild), >4 mmol/L (severe), >8 mmol/L (critical)
• PaCO2: Initially low (compensatory hyperventilation), may rise with respiratory fatigue
• PaO2: May be low if concurrent lung injury or ARDS
• Base deficit: >-6 mEq/L (correlates with shock severity and mortality)

Key Signs and Symptoms:

• Hypotension, tachycardia, weak pulses
• Cool, clammy, mottled skin
• Delayed capillary refill (>2 seconds)
• Altered mental status, confusion, agitation
• Oliguria (<0.5 mL/kg/hr)
• Tachypnea (compensatory)

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Sepsis/Septic Shock

Sepsis produces mixed acid-base disorders: high anion gap metabolic acidosis from lactic acidosis combined with respiratory alkalosis (early) or respiratory acidosis (late with ARDS/respiratory failure).

ABG Pattern:

• pH: Variable (7.30-7.50) depending on dominant disorder
• Bicarbonate: 12-20 mEq/L (metabolic acidosis component)
• Anion gap: >12 mEq/L (elevated lactate)
• Lactate: >2 mmol/L (sepsis), >4 mmol/L (septic shock)
• PaCO2: <35 mmHg (early hyperventilation) or >45 mmHg (late respiratory failure)
• PaO2: Often low (<80 mmHg) with widened A-a gradient

Key Signs and Symptoms:

• Fever (>38°C) or hypothermia (<36°C)
• Tachycardia (>90 bpm), tachypnea (>20/min)
• Hypotension (SBP <90 mmHg or MAP <65 mmHg)
• Altered mental status
• Warm, vasodilated peripheries (early) vs. cold, vasoconstricted (late)
• Oliguria, elevated creatinine

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Chronic Anemia

Chronic anemia itself does not directly cause acid-base disturbances; ABGs are typically normal unless complicated by tissue hypoxia, cardiac failure, or underlying disease.

ABG Pattern:

• pH: 7.35-7.45 (normal)
• Bicarbonate: 22-26 mEq/L (normal)
• PaCO2: 35-45 mmHg (normal)
• PaO2: Normal (oxygen content is reduced due to low hemoglobin, but PaO2 reflects dissolved oxygen)
• SaO2: Normal (>95%) unless concurrent lung disease

Key Signs and Symptoms:

• Fatigue, weakness, dyspnea on exertion
• Pallor (conjunctiva, palmar creases)
• Tachycardia, flow murmurs
• Angina (if severe anemia with coronary disease)
• High-output heart failure (severe chronic anemia)

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COPD (Chronic Obstructive Pulmonary Disease)

Stable COPD produces chronic compensated respiratory acidosis (elevated PaCO2 with near-normal pH due to metabolic compensation with elevated bicarbonate); acute exacerbations cause acute-on-chronic respiratory acidosis with pH drop.

Stable COPD ABG Pattern:

• pH: 7.35-7.40 (compensated)
• PaCO2: 50-70 mmHg (chronic hypercapnia)
• Bicarbonate: 28-35 mEq/L (renal compensation)
• PaO2: 55-70 mmHg (chronic hypoxemia)
• Base excess: +4 to +8 mEq/L

Acute COPD Exacerbation ABG Pattern:

• pH: <7.35 (acute respiratory acidosis)
• PaCO2: >70-80 mmHg (acute rise from baseline)
• Bicarbonate: Elevated but insufficient compensation
• PaO2: <55 mmHg (worsening hypoxemia)

Key Signs and Symptoms:

• Chronic productive cough, dyspnea
• Barrel chest, prolonged expiratory phase
• Pursed-lip breathing
• Use of accessory muscles
• Cyanosis (central if severe hypoxemia)
• Acute exacerbation: increased dyspnea, sputum production, confusion (CO2 narcosis)

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Hypercapnia (Acute Respiratory Acidosis)

Acute hypercapnia from any cause (neuromuscular weakness, CNS depression, airway obstruction) produces uncompensated respiratory acidosis with rapid pH decline before renal compensation occurs.

ABG Pattern:

• pH: <7.35 (drops 0.08 units per 10 mmHg PaCO2 rise acutely)
• PaCO2: >45 mmHg (can exceed 80-100 mmHg in severe cases)
• Bicarbonate: Normal to slightly elevated acutely (24-28 mEq/L); takes 3-5 days for full renal compensation
• PaO2: Often low (<60 mmHg) unless supplemental oxygen provided
• Base excess: Normal acutely, becomes positive with chronic compensation

Key Signs and Symptoms:

• Dyspnea, tachypnea or bradypnea (depending on cause)
• Confusion, somnolence, asterixis (CO2 narcosis)
• Headache (cerebral vasodilation)
• Papilledema (severe cases)
• Diaphoresis, flushed skin
• Hypertension, bounding pulses (catecholamine release)
• Respiratory arrest (severe hypercapnia >100 mmHg)

Common Pitfall:

• Administering high-flow oxygen to COPD patients with chronic hypercapnia can worsen CO2 retention by removing hypoxic respiratory drive; target SpO2 88-92% in these patients