Postoperative respiratory deterioration is a critical situation that demands rapid, structured evaluation. Among all tools available to the anesthesiologist—clinical examination, pulse oximetry, lung ultrasound, chest radiography, CT scan, and laboratory markers—arterial blood gas (ABG) analysis remains the single most informative and immediate diagnostic investigation.
This chapter analyzes a striking example: a patient with a stable postoperative course and a normal POD-1 ABG who, after mobilization on POD-4, developed sudden dyspnea requiring high-flow oxygen support. Despite SpO₂ of 98% on 10 L/min, the ABG revealed severe hypoxemia (PaO₂ of 46 mmHg), profound respiratory alkalosis (PaCO₂ 25 mmHg), and an A–a gradient >350 mmHg—findings diagnostic of acute shunt physiology long before CT confirmed pulmonary edema.
For anesthesiologists, the core lesson is clear:
ABG identifies life-threatening physiologic collapse earlier than chest imaging, SpO₂, or hemodynamic monitoring.
This chapter is written with a strong emphasis on physiology and clinical reasoning relevant to anesthesia practice. Using this case as a template, we explain:
How ABGs reveal shunt physiology before imaging does
Why SpO₂ may appear normal despite catastrophic hypoxemia
How diastolic dysfunction and pulmonary hypertension produce flash pulmonary edema
The bedside decision pathway an anesthesiologist should follow
How POCUS complements ABG interpretation
Why the A–a gradient is essential for differentiating postoperative causes of dyspnea
The pitfalls to avoid, including misinterpreting respiratory alkalosis as anxiety or overlooking pulmonary edema in HFpEF
The chapter integrates respiratory physiology, cardiac mechanics, renal function, oxygen transport physics, and clinical anesthesia decision-making into a unified framework.
Arterial blood gas (ABG) analysis remains one of the most powerful, time-critical, and physiologically rich investigations available to an anesthesiologist. In postoperative deterioration, the ABG provides a real-time map of respiratory, metabolic, and cardiovascular status, revealing abnormalities long before radiology or routine clinical signs become obvious.
Unlike other investigations, an ABG simultaneously informs:
Ventilation (PaCO₂, pH)
Oxygenation (PaO₂, A–a gradient)
Diffusion impairment (Alveolar–arterial gradient)
Shunt physiology (PaO₂ unresponsive to FiO₂)
Metabolic compensation (HCO₃⁻, base excess)
Perfusion adequacy (lactate)
Cardiorenal interaction (electrolytes, acid–base trends)
In the postoperative setting—where pain, opioids, atelectasis, fluid shifts, sepsis, cardiac dysfunction, embolism, and pulmonary edema are all possible—ABG interpretation becomes a cornerstone of anesthesia-level clinical reasoning.
Pulse oximetry is a saturation-based measurement:
Saturation plateaus at PaO₂ > 80 mmHg
SpO₂ stays falsely normal even when alveolar oxygenation is collapsing
It gives no information about:
PaCO₂
A–a gradient
Ventilation
Shunt fraction
Alveolar collapse
Diffusion limitation
For example:
In this case, SpO₂ = 98% on 10 L/min O₂, yet PaO₂ = 46 mmHg, revealing...
