ABG

Overview of Arterial Blood Gas (ABG) Analysis

• Arterial Blood Gas (ABG) analysis is a vital diagnostic modality in neonatal, pediatric, and intensive care units to evaluate acid-base homeostasis, alveolar ventilation, and tissue oxygenation.
• Maintenance of extracellular $\text{pH}$ within the narrow physiologic window ($7.35\text{ -- }7.45$) is essential for enzymatic catalysis, myocardial contractility, cellular metabolism, and systemic vascular responsiveness.
• While venous blood gases (VBG) or capillary gases serve as practical surrogates for acid-base and ventilation trends, arterial sampling remains the gold standard for accurate assessment of arterial oxygen tension ($p{\text{O}}_2$), alveolar-arterial ($A\text{--}a$) oxygen gradient, and pulmonary shunt.

Normal Physiological Reference Values

Technical Considerations, Sampling Pitfalls, & VBG Correlation

1. Pre-analytical Errors in Blood Gas Sampling

2. Temperature Correction (Alpha-Stat vs pH-Stat)

• Blood gas analyzers warm the sample and measure electrodes strictly at ${37}^{\circ }\text{C}$.
• In hypothermic patients (e.g., therapeutic hypothermia for neonatal HIE, cardiopulmonary bypass):
  • Alpha-Stat Strategy: Sample is analyzed at ${37}^{\circ }\text{C}$ without temperature correction. Preserves intracellular electrochemical neutrality and enzyme activity across changing temperatures. Preferred in post-arrest hypothermia and pediatric cardiac surgery.
  • pH-Stat Strategy: Values are mathematically corrected to the patient's actual core body temperature ($p{\text{CO}}_2$ and $p{\text{O}}_2$ decrease with cooling due to increased gas solubility; $\text{pH}$ rises). ${\text{CO}}_2$ is added during ventilation to maintain $\text{pH }7.40$ at hypothermic temperatures, increasing cerebral blood flow.

3. Venous Blood Gas (VBG) vs Arterial Blood Gas (ABG) Correlation

Fundamental Physicochemical Foundations

1. Henderson-Hasselbalch Equation

The traditional approach models the bicarbonate-carbonic acid buffer system in extracellular fluid:

• Where ${\text{pK}}_a^{\prime }=6.10$ at ${37}^{\circ }\text{C}$ and normal ionic strength.
• $\alpha =0.0307\text{ mmol/L/mmHg}$ (solubility coefficient of ${\text{CO}}_2$ in human plasma).
• At normal baseline:

2. Kassirer-Bleich Equation (Bedside Calculation of $[{\text{H}}^{+}]$)

Linear simplification of the Henderson-Hasselbalch equation avoiding logarithms:

• Validation Rule: At $\text{pH }7.40$, $[{\text{H}}^{+}]=40\text{ nEq/L}$.
• Between $\text{pH }7.20\text{ -- }7.50$, for every $0.01$ unit change in $\text{pH}$, $[{\text{H}}^{+}]$ shifts by $1\text{ nEq/L}$ in the opposite direction:
  • $\text{pH }7.40\to \mathbf{40}\text{ nEq/L}$
  • $\text{pH }7.30\to \mathbf{50}\text{ nEq/L}$
  • $\text{pH }7.20\to \mathbf{60}\text{ nEq/L}$
  • $\text{pH }7.50\to \mathbf{30}\text{ nEq/L}$
  • Rule: $[{\text{H}}^{+}]\approx 80-\text{last two digits of pH}$ (for $\text{pH }7.20\text{ -- }7.50$).

3. Total Body Water ($\text{TBW}$)

• Neonates (Preterm): $F=0.80$
• Neonates (Full Term): $F=0.75$
• Infants & Children: $F=0.65\text{ -- }0.70$
• Adult Males: $F=0.60$
• Adult Females: $F=0.50$

4. Serum Osmolality & Serum Osmolar Gap

(If serum urea is expressed as blood urea in $\text{mg/dL}$, divide by $6.0$; if glucose and urea are measured in $\text{mmol/L}$, sum $[\text{Glucose}]+[\text{Urea}]$ directly without divisors).

• Normal Limit: $<10\text{ mOsm/kg}$.
• Elevated Osmolar Gap ($>10\text{ mOsm/kg}$) points to unmeasured low-molecular-weight solutes:
  • Toxic alcohols: Methanol, Ethylene glycol, Isopropanol.
  • Infusions: Mannitol, Propylene glycol (carrier in continuous IV infusions of lorazepam, diazepam, phenobarbital).
  • Diabetic / Alcoholic ketoacidosis (acetone accumulation).

5. Serum Anion Gap ($\text{AG}$) & Albumin Correction

• Normal Reference: $12\pm 2\text{ mEq/L}$ (without ${\text{K}}^{+}$).
• Albumin Correction (Figge-Jabor Formula):
  • Albumin carries negative charge at physiologic $\text{pH}$ (each $1\text{ g/dL}$ of albumin provides $\approx 2.5\text{ mEq/L}$ of unmeasured anions).
  • Hypoalbuminemia obscures High Anion Gap Metabolic Acidosis (HAGMA).

Systematic 6-Step Acid-Base Interpretation Method

flowchart TD
    A["Step 1: Check Internal Consistency
[H+] = 24 x (pCO2 / [HCO3-])"] --> B["Step 2: Determine Primary Disorder by pH"]
    
    B --> C{"pH < 7.35
(Acidemia)"}
    B --> D{"pH > 7.45
(Alkalemia)"}
    
    C -->|pCO2 > 45| E["Primary Respiratory Acidosis"]
    C -->|HCO3- < 22| F["Primary Metabolic Acidosis"]
    
    D -->|pCO2 < 35| G["Primary Respiratory Alkalosis"]
    D -->|HCO3- > 26| H["Primary Metabolic Alkalosis"]
    
    E & F & G & H --> I["Step 3: Evaluate Secondary Compensation
(Winter's Formula / Expected Compensation Rules)"]
    
    I --> J["Step 4: Calculate Anion Gap on ALL Blood Gases
AG_corrected = AG + 2.5 x (4.0 - Albumin)"]
    
    J --> K{"Is AG_corr > 12?"}
    K -->|Yes| L["Step 5: Calculate Delta-Delta Ratio
ΔAG / ΔHCO3- to detect mixed metabolic disorders"]
    K -->|No| M["Step 5: Evaluate for NAGMA via Urine Anion Gap (UAG)"]
    
    L & M --> N["Step 6: Assess Oxygenation & Strong Ions
(A-a Gradient, P/F Ratio, OI, SID/SIG)"]

Step 1: Check Internal Consistency

Compute $[{\text{H}}^{+}]=24\times (p{\text{CO}}_2/[{\text{HCO}}_3^{-}])$. Compare with $[{\text{H}}^{+}]\approx 80-\text{last two digits of pH}$. If values diverge significantly, suspect laboratory transcription error, air contamination, or hemolyzed sample.

Step 2: Determine the Primary Acid-Base Disturbance

• $\text{pH}<7.35$ (Acidemia):
  • High $p{\text{CO}}_2$ ($>45\text{ mmHg}$) $\to$ Primary Respiratory Acidosis
  • Low ${\text{HCO}}_3^{-}$ ($<22\text{ mEq/L}$) $\to$ Primary Metabolic Acidosis
• $\text{pH}>7.45$ (Alkalemia):
  • Low $p{\text{CO}}_2$ ($<35\text{ mmHg}$) $\to$ Primary Respiratory Alkalosis
  • High ${\text{HCO}}_3^{-}$ ($>26\text{ mEq/L}$) $\to$ Primary Metabolic Alkalosis

Step 3: Evaluate the Adequacy of Secondary Compensation

Physiologic compensation returns $\text{pH}$ towards, but never past, the normal baseline of $7.40$.

Step 4: Calculate the Corrected Anion Gap

Always compute ${\text{AG}}_{\text{corrected}}=[{\text{Na}}^{+}]-([{\text{Cl}}^{-}]+[{\text{HCO}}_3^{-}])+2.5\times (4.0-\text{Albumin})$.

• An elevated corrected $\text{AG}>12\text{ mEq/L}$ defines HAGMA, even if blood $\text{pH}$ and bicarbonate appear entirely normal due to coexisting alkalosis.

Step 5: Calculate the Delta-Delta Ratio ($\mathrm{\Delta }\text{AG}/\mathrm{\Delta }{\text{HCO}}_3^{-}$)

In the presence of HAGMA, calculate the Delta Ratio ($\mathrm{\Delta }/\mathrm{\Delta }$) to uncover occult mixed metabolic processes:

Urine Indices & Evaluation of NAGMA

When evaluation reveals Normal Anion Gap (Hyperchloremic) Metabolic Acidosis (NAGMA), calculate urine electrolytes to determine whether the defect is Gastrointestinal (intact renal acid excretion) or Renal (impaired tubular acidification).

flowchart TD
    A["Normal Anion Gap Metabolic Acidosis (NAGMA)
AG_corr = 8-12 mEq/L, Hyperchloremia"] --> B["Calculate Urine Anion Gap
UAG = (Na+_u + K+_u) - Cl-_u"]
    
    B --> C{"UAG Negative
(-20 to -50 mEq/L)"}
    B --> D{"UAG Positive
(+10 to +40 mEq/L)"}
    B --> E{"Unmeasured Urine Anions Present?
(DKA, Toluene, Penicillins)"}
    
    C --> F["Intact Renal NH4+ Excretion
• Diarrhea / GI loss
• 0.9% Normal Saline dilution
• Proximal RTA (Type 2, distal intact)"]
    
    D --> G["Impaired Renal Acid Excretion (RTA)"]
    G --> H{"Serum Potassium (K+)"}
    H -->|Hypokalemia / Normal| I["Type 1 Distal RTA
(Urine pH > 5.5, Nephrocalcinosis)"]
    H -->|Hyperkalemia| J["Type 4 RTA
(Hypoaldosteronism / Resistance, CAH)"]
    
    E --> K["Calculate Urine Osmolal Gap (UOG)
UOG = Measured U_Osm - Calc U_Osm
U_NH4+ ≈ UOG / 2"]
    K -->|UOG > 150 mOsm/kg| F
    K -->|UOG < 100 mOsm/kg| G

1. Urine Anion Gap ($\text{UAG}$)

• The kidney excretes acid primarily as ammonium (${\text{NH}}_4^{+}$) paired with chloride (${\text{Cl}}^{-}$). As ${\text{NH}}_4^{+}$ excretion increases, urine $[{\text{Cl}}^{-}]$ exceeds $([{\text{Na}}^{+}]+[{\text{K}}^{+}])$.
• Negative UAG ($-20\text{ to }-50\text{ mEq/L}$):
  • Confirms robust, appropriate renal ${\text{NH}}_4^{+}$ excretion.
  • Causes: Gastrointestinal ${\text{HCO}}_3^{-}$ loss (acute diarrhea, enterocutaneous fistula), post-saline dilution, proximal RTA (distal acidification intact).
• Positive UAG ($+10\text{ to }+40\text{ mEq/L}$):
  • Indicates defective distal renal ${\text{NH}}_4^{+}$ excretion.
  • Causes: Distal RTA (Type 1), Type 4 RTA, advanced renal impairment.

2. Urine Osmolal Gap ($\text{UOG}$) & Urine Ammonium

When urine contains unmeasured non-chloride anions (e.g., ketoacids in DKA, hippurate from toluene/glue sniffing, high-dose carbenicillin/ampicillin), cations (${\text{Na}}^{+},{\text{K}}^{+}$) are excreted with these anions. This makes UAG spuriously positive despite high ${\text{NH}}_4^{+}$. In these cases, calculate the Urine Osmolal Gap:

• $\text{UOG}>150\text{ mOsm/kg}$ (or urine ${\text{NH}}_4^{+}>75\text{ mEq/L}$): Appropriate renal response (GI loss).
• $\text{UOG}<100\text{ mOsm/kg}$ (or urine ${\text{NH}}_4^{+}<40\text{ mEq/L}$): Impaired renal response (Renal Tubular Acidosis).

3. Comparison of Renal Tubular Acidosis (RTA) Subtypes

Stewart Physicochemical (Strong Ion) Approach

The Stewart physicochemical model explains complex acid-base pathophysiology in critically ill pediatric patients where classical Henderson-Hasselbalch equations oversimplify the interactions between water, plasma proteins, and non-volatile buffers.

In Stewart's system, $\text{pH}$ and $[{\text{H}}^{+}]$ are dependent variables governed by three independent variables:

1. Strong Ion Difference ($\text{SID}$)
2. Total Weak Non-Volatile Acids ($A_{\text{TOT}}$) (Albumin and Phosphate)
3. Partial Pressure of Carbon Dioxide ($p{\text{CO}}_2$)

flowchart LR
    subgraph Independent Variables
        A["Strong Ion Difference (SID)
[Strong Cations] - [Strong Anions]"]
        B["Total Weak Acids (ATOT)
Albumin + Inorganic Phosphate"]
        C["pCO2
Alveolar Ventilation"]
    end
    
    subgraph Dependent Variables
        D["pH / [H+]"]
        E["[HCO3-]"]
    end
    
    A --> D & E
    B --> D & E
    C --> D & E

1. Apparent Strong Ion Difference (${\text{SID}}_a$)

Strong ions are fully dissociated at biological $\text{pH}$. ${\text{SID}}_a$ represents the net electrical charge of all measured strong cations minus strong anions:

(Bedside approximation: ${\text{SID}}_a\approx [{\text{Na}}^{+}]-[{\text{Cl}}^{-}]$)

• Normal ${\text{SID}}_a$: $40\pm 2\text{ mEq/L}$.
• Decreased ${\text{SID}}_a$ ($<38\text{ mEq/L}$): Drives water dissociation (${\text{H}}_2\text{O}\to {\text{H}}^{+}+{\text{OH}}^{-}$) to balance negative charge $\to$ Acidosis (e.g., Hyperchloremic acidosis after large-volume $0.9\mathrm{\%}$ Normal Saline infusions, which have a $\text{SID}=154-154=0$).
• Increased ${\text{SID}}_a$ ($>42\text{ mEq/L}$): Consumes ${\text{H}}^{+}$ ions $\to$ Alkalosis (e.g., Hypochloremia from loop diuretics or upper GI losses).

2. Effective Strong Ion Difference (${\text{SID}}_e$)

${\text{SID}}_e$ represents the balancing electrical charge from weak non-volatile buffers ($A_{\text{TOT}}$: Albumin, Phosphate) and volatile bicarbonate:

3. Strong Ion Gap ($\text{SIG}$)

• Normal SIG: $0\pm 2\text{ mEq/L}$.
• $\text{SIG}>2\text{ mEq/L}$: Proves the presence of circulating unmeasured strong anions (ketoacids, sulfates, urate, exogenous toxic anions, organic acids in septic shock).
• Unlike the traditional Anion Gap, $\text{SIG}$ is mathematically independent of fluctuations in serum albumin and phosphate.

Standard Base Excess ($\text{SBE}$) & Van Slyke Physiology

• Actual Base Excess ($\text{ABE}$): Titratable base in whole blood in vitro at $p{\text{CO}}_2=40\text{ mmHg}$ and ${37}^{\circ }\text{C}$. Heavily influenced by hemoglobin concentration.
• Standard Base Excess ($\text{SBE}$ / in vivo Base Excess): Standardized to extracellular fluid by modeling hemoglobin at $[\text{Hb}]=5\text{ g/dL}$ (representing whole-body extracellular buffering capacity):

(Simplified bedside estimation: $\text{SBE}\approx \mathrm{\Delta }[{\text{HCO}}_3^{-}]+[10\times (\text{pH}-7.4)]$)

• Clinical Significance:
  • $\text{SBE}<-5\text{ mEq/L}$ in pediatric trauma, shock, or sepsis correlates with severe occult tissue hypoperfusion, high transfusion requirements, and elevated mortality.
  • Normalization of SBE during fluid resuscitation serves as an objective resuscitation endpoint.

Etiological Classifications & Differentials

1. High Anion Gap Metabolic Acidosis (HAGMA)

Commonly recalled by the pediatric mnemonic GOLD MARK or MUDPILES:

• G — Glycols (Ethylene glycol, Propylene glycol infusions)
• O — Oxoproline ($5$-oxoproline / pyroglutamic acidosis in malnourished children on chronic paracetamol)
• L — L-Lactate (Tissue hypoperfusion, septic shock, cardiogenic shock, severe hypoxemia)
• D — D-Lactate (Short bowel syndrome with carbohydrate malabsorption and bacterial overgrowth)
• M — Methanol (Toxic alcohol ingestion)
• A — Aspirin / Salicylates (Salicylate intoxication causing mixed respiratory alkalosis and HAGMA)
• R — Renal Failure / Uremia (Phosphate, sulfate, and organic anion retention in acute or chronic kidney injury)
• K — Ketoacidosis (Diabetic Ketoacidosis, Starvation ketosis, Inborn Errors of Metabolism such as Methylmalonic / Propionic acidemia, MSUD)

2. Normal Anion Gap Metabolic Acidosis (NAGMA / Hyperchloremic)

Mnemonic USED CARP:

• U — Ureterostomy / Urinary diversions (ileal conduits, ureterosigmoidostomy)
• S — Saline resuscitation (Large-volume $0.9\mathrm{\%}\text{ NaCl}$ leading to hyperchloremic dilution of $\text{SID}$)
• E — Early renal failure / Enterocutaneous fistulas
• D — Diarrhea (Gastrointestinal bicarbonate loss)
• C — Carbonic anhydrase inhibitors (Acetazolamide, Topiramate)
• A — Acid ingestions / TPN (${\text{NH}}_4\text{Cl}$, ${\text{CaCl}}_2$, amino acid-rich parenteral nutrition)
• R — Renal Tubular Acidosis (Types 1, 2, and 4)
• P — Pancreatic fistulas / biliary drainage

3. Metabolic Alkalosis (Urine Chloride Classification)

Oxygenation Metrics, Alveolar-Arterial Gradient, & Shunt

1. Alveolar Gas Equation

• At sea level: $P_{\text{atm}}=760\text{ mmHg}$, $P_{{\text{H}}_2\text{O}}=47\text{ mmHg}$ at ${37}^{\circ }\text{C}$, $R\approx 0.8$.

2. Alveolar-Arterial Oxygen Gradient ($A\text{--}a\text{ Gradient}$)

• Normal Range on Room Air ($Fi{\text{O}}_2=0.21$):
  • Children: $<10\text{ mmHg}$
  • Age-estimated formula: $\text{Normal }A\text{--}a\text{ Gradient}\approx \frac{\text{Age in years}}{4}+4$
• Diagnostic Differentiation of Hypoxemia:
  • Normal $A\text{--}a\text{ Gradient}$: Hypoventilation (CNS depression, neuromuscular disease, airway obstruction) or Low ambient $Fi{\text{O}}_2$ (high altitude).
  • Elevated $A\text{--}a\text{ Gradient}$: $V/Q$ mismatch, Intrapulmonary/Intracardiac Right-to-Left Shunt, or Alveolar-capillary diffusion impairment (ARDS, severe pneumonia, pulmonary edema).

3. Oxygenation Index ($\text{OI}$) & Oxygen Saturation Index ($\text{OSI}$)

Standard severity markers for Pediatric & Neonatal Acute Respiratory Distress Syndrome (PARDS/PALICC-2) and Persistent Pulmonary Hypertension of the Newborn (PPHN):

Sodium Bicarbonate Therapy in Pediatric Acidosis

1. Calculation of Bicarbonate Deficit

• Target ${\text{HCO}}_3^{-}$: Aim for a safe intermediate level of $12\text{ -- }15\text{ mEq/L}$ (or target $\text{pH }\approx 7.20$), not full normalization to $24\text{ mEq/L}$.
• Administer half of the calculated deficit slowly over $1\text{ -- }2\text{ hours}$, then reassess with repeat ABG.

2. Evidence-Based Indications vs Hazards

High-Yield Pediatric Worked Clinical Cases

Case 1: Neonate with Lethargy and Suspected IEM

• ABG & Labs: $\text{pH }7.18$, $p{\text{CO}}_{2}18\text{ mmHg}$, $p{\text{O}}_{2}92\text{ mmHg}$, ${\text{HCO}}_3^{-}6.5\text{ mEq/L}$, ${\text{Na}}^{+}138\text{ mEq/L}$, ${\text{Cl}}^{-}98\text{ mEq/L}$, Albumin $4.0\text{ g/dL}$, Ammonia $420\mu \text{mol/L}$.
• Stepwise Breakdown:
  1. $\text{pH }7.18\to$ Severe Acidemia.
  2. ${\text{HCO}}_3^{-}6.5\text{ mEq/L}\to$ Primary Metabolic Acidosis.
  3. Winter's Formula: $\text{Expected }p{\text{CO}}_2=(1.5\times 6.5)+8\pm 2=9.75+8=17.75\pm 2\text{ mmHg}$ ($15.8\text{ -- }19.8\text{ mmHg}$). Measured $p{\text{CO}}_2=18\text{ mmHg}$ (Adequate respiratory compensation).
  4. Anion Gap: $\text{AG}=138-(98+6.5)=33.5\text{ mEq/L}$ (Markedly elevated $\to$ HAGMA).
  5. Delta Ratio: $\mathrm{\Delta }\text{AG}/\mathrm{\Delta }{\text{HCO}}_3^{-}=(33.5-12)/(24-6.5)=21.5/17.5=1.23$ (Pure HAGMA).
• Diagnosis: High Anion Gap Metabolic Acidosis with hyperammonemia consistent with an Organic Acidemia (Methylmalonic / Propionic acidemia) or Inborn Error of Metabolism.

Case 2: 4-Week-Old Infant with Projectile Non-Bilious Vomiting

• ABG & Labs: $\text{pH }7.56$, $p{\text{CO}}_{2}48\text{ mmHg}$, $p{\text{O}}_{2}85\text{ mmHg}$, ${\text{HCO}}_3^{-}42\text{ mEq/L}$, ${\text{Na}}^{+}132\text{ mEq/L}$, ${\text{K}}^{+}2.8\text{ mEq/L}$, ${\text{Cl}}^{-}80\text{ mEq/L}$, Urine $\text{pH }5.0$, Urine ${\text{Cl}}^{-}8\text{ mEq/L}$.
• Stepwise Breakdown:
  1. $\text{pH }7.56\to$ Severe Alkalemia.
  2. ${\text{HCO}}_3^{-}42\text{ mEq/L}\to$ Primary Metabolic Alkalosis.
  3. Compensation: $\text{Expected }p{\text{CO}}_2=40+[0.7\times (42-24)]=40+12.6=52.6\pm 2\text{ mmHg}$. Measured $p{\text{CO}}_2=48\text{ mmHg}$ (Appropriate compensatory hypoventilation).
  4. Urine ${\text{Cl}}^{-}<15\text{ mEq/L}$: Chloride-responsive metabolic alkalosis.
• Pathophysiology Note (Paradoxical Aciduria): As volume and ${\text{Cl}}^{-}$ become depleted, the kidney prioritizes ${\text{Na}}^{+}$ reabsorption in the distal nephron. Due to profound hypokalemia, aldosterone promotes ${\text{Na}}^{+}$ reabsorption in exchange for ${\text{H}}^{+}$ secretion rather than ${\text{K}}^{+}$, producing acid urine ($\text{pH }5.0$) despite systemic alkalemia.
• Diagnosis: Hypertrophic Pyloric Stenosis with classic hypochloremic, hypokalemic metabolic alkalosis and paradoxical aciduria.

Case 3: 7-Year-Old with Acute Severe Status Asthmaticus

• Scenario Evolution:
  • Initial Gas (Early Attack): $\text{pH }7.48$, $p{\text{CO}}_{2}28\text{ mmHg}$, ${\text{HCO}}_3^{-}22\text{ mEq/L}$ $\to$ Acute Respiratory Alkalosis secondary to tachypnea and hyperventilation.
  • Repeat Gas (2 Hours Later, Tiring Child): $\text{pH }7.39$, $p{\text{CO}}_{2}40\text{ mmHg}$, ${\text{HCO}}_3^{-}24\text{ mEq/L}$.
• Critical Clinical Interpretation:
  • A "normal" $p{\text{CO}}_2$ of $40\text{ mmHg}$ in a tachypneic asthmatic child is NOT normal—it is an ominous warning of respiratory muscle exhaustion, loss of hyperventilation, and impending respiratory failure requiring urgent escalation (PICU transfer, magnesium sulfate, non-invasive or invasive mechanical ventilation).

Case 4: Ventilated Child with Septic Shock and Gastric Suction

• ABG & Labs: $\text{pH }7.32$, $p{\text{CO}}_{2}52\text{ mmHg}$, ${\text{HCO}}_3^{-}26\text{ mEq/L}$, ${\text{Na}}^{+}140\text{ mEq/L}$, ${\text{Cl}}^{-}92\text{ mEq/L}$, Albumin $2.0\text{ g/dL}$, Lactate $6.0\text{ mmol/L}$.
• Stepwise Breakdown:
  1. $\text{pH }7.32\to$ Acidemia.
  2. $p{\text{CO}}_{2}52\text{ mmHg}\to$ Respiratory Acidosis (hypoventilation / lung pathology).
  3. Corrected Anion Gap: ${\text{AG}}_{\text{obs}}=140-(92+26)=22\text{ mEq/L}$. ${\text{AG}}_{\text{corr}}=22+2.5\times (4.0-2.0)=27\text{ mEq/L}$ (Severe HAGMA).
  4. Delta Ratio: $\mathrm{\Delta }\text{AG}=27-12=15$. $\mathrm{\Delta }{\text{HCO}}_3^{-}=24-26=-2$. Ratio is strongly positive and ${\text{HCO}}_3^{-}$ is higher than expected $\to$ Coexisting Metabolic Alkalosis (due to continuous nasogastric drainage).
• Diagnosis: Triple Mixed Acid-Base Disorder (HAGMA due to septic lactic acidosis + Metabolic Alkalosis from NG losses + Respiratory Acidosis from lung injury/hypoventilation).