Description

Disclaimer: A quick note — this is AI narration, so you may hear a few mispronounced medical terms. Focus on the science, not the syllables.

Case vignette

A 70-kg adult male presents 10 days after a major crush injury with extensive soft-tissue destruction, internal and external degloving and rhabdomyolysis. He has progressed to sepsis with evolving multiple organ dysfunction, is on norepinephrine, and is planned for further wound debridement.

He arrives intubated on CPAP/pressure support. Preoperative ABG (IMG_8842.JPG):

• pH 7.36

• PaCO₂ 45 mmHg

• PaO₂ 179 mmHg

• Na⁺ 140 mmol/L

• K⁺ 3.5 mmol/L

• Ionized Ca²⁺ 0.90 mmol/L (Ca²⁺(7.4) 0.89)

• Glucose 134 mg/dL

• Lactate 1.4 mmol/L

• Hct 35% (THb 10.9 g/dL)

• HCO₃⁻ 25.4 mmol/L, TcO₂ 26.8 mmol/L, BE 0

He undergoes a 1-hour debridement, receives 1 unit PRBC intraoperatively, appears hemodynamically stable and returns to ICU.

Over the next 12 hours he receives 4 units PRBC, 4 units FFP, 4 units cryoprecipitate, and 20% albumin at 10 mL/h for 5 hours for falling hemoglobin, ongoing oozing and vasopressor-dependent hypotension. Norepinephrine requirements rise and vasopressin 1.2 U/h is added.

Twelve hours post-surgery, a second ABG (IMG_8843.JPG) shows:

• pH 7.47

• PaCO₂ 24 mmHg

• PaO₂ 240 mmHg

• Na⁺ 144 mmol/L

• K⁺ 3.9 mmol/L

• Ionized Ca²⁺ 0.84 mmol/L (Ca²⁺(7.4) 0.86)

• Glucose 88 mg/dL

• Lactate 7.7 mmol/L

• Hct 20% (THb 6.2 g/dL)

• HCO₃⁻ 17.5 mmol/L, TcO₂ 18.2 mmol/L, BE –5.6

• SpO₂ 100%

• Dynamic indices: PPV 14–20%

• Hemodynamics: BP ~130/75 mmHg, HR 127/min, high-dose norepinephrine + vasopressin

At first glance, the preoperative ABG looks “normal” and the postoperative ABG looks “alkalotic yet oxygen-rich”. In reality, they depict progression from tenuous compensatory physiology to cryptic, cellular shock.

This chapter uses these two ABGs to walk through:

1. Core basic sciences that shape ABG patterns in septic trauma.

2. Detailed interpretation of the preoperative ABG.

3. Why the intraoperative period looked deceptively stable.

4. How the postoperative period and massive transfusion precipitated collapse.

5. Deep analysis of the postoperative ABG.

6. An integrated macro–micro–mitochondrial shock model.

7. A management strategy grounded in physics and biochemistry.

8. High-yield clinical pearls, formulas and flow-charts.

INTRODUCTION

Severely injured, septic trauma patients are moving integration tests for every basic science discipline we learn in anesthesia training. In them, oxygen transport physics, mitochondrial biochemistry, microvascular biology, transfusion medicine, acid–base chemistry, and cardiovascular physiology all collide.

In late sepsis with trauma and rhabdomyolysis:

• Macro-hemodynamics (BP, HR) may appear...