A 70-kg male with a 10-day-old crush injury, extensive internal and external degloving, rhabdomyolysis, and sepsis underwent wound debridement under general anesthesia. Despite apparently stable macrocirculatory parameters, he developed severe postoperative oxygen-delivery failure, progressive hypocalcemia after transfusion and albumin therapy, distributive–cytopathic septic shock, and microcirculatory collapse masked by vasopressor support. Serial ABGs revealed rapid transition from compensated physiology to metabolic–mitochondrial failure (lactate 7.7 mmol/L) despite normal SpO₂ and MAP. Thromboelastography normalized following blood products, but tissue perfusion deteriorated. BNP increased to 545 pg/mL with negative troponin and unchanged echocardiography. This case underscores that blood pressure, oxygen saturation, and coagulation normalization cannot be equated with cellular perfusion and metabolic rescue. Lactate kinetics, ionized calcium, and oxygen-delivery physics provide superior physiologic insight for anesthetic decision-making.

Late-phase crush injury complicated by sepsis creates a uniquely hostile landscape for anesthetic management. These patients exhibit simultaneous:

• profound vasoplegia

• disordered venous capacitance

• coagulation–fibrinolysis imbalance

• mitochondrial dysfunction

• microvascular shunting

• transfusion-related biochemical derangements

• calcium–catecholamine uncoupling

Anesthesiologists are often misled by stabilization of MAP and SpO₂, especially in patients supported by norepinephrine and vasopressin. However, macrocirculatory stability provides no assurance of microcirculatory adequacy. Tissue hypoxia and mitochondrial paralysis may progress silently, manifesting only as rising lactate and base deficit.

This case illustrates the principle of hemodynamic incoherence—a state in which blood pressure and organ flow dissociate from capillary perfusion and oxygen utilization.

Preoperative Status

A previously healthy 70-kg male presented 10 days after a major crush injury with internal and external degloving and rhabdomyolysis. He had undergone multiple surgeries elsewhere and arrived with:

• septic physiology

• increasing bilirubin

• hypoalbuminemia

• evolving MODS

• intubated on CPAP

• requiring norepinephrine

Ventilation

• FiO₂: 35%

• PEEP: 5 cmH₂O

• PS: 10 cmH₂O

Hemodynamic Support

• Norepinephrine: 8 mg/50 mL dilution

Preoperative ABG

1. Normal ABG ≠ Normal Physiology

pH normalization reflects buffering, not physiologic health. In sepsis, early maintenance of lactate often precedes abrupt mitochondrial collapse. Ionized calcium was already low, impairing vascular tone and adrenergic signaling.

2. Oxygen Delivery Physics

Calculated CaO₂ ≈ 14.6 mL/100 mL — barely sufficient for a hypermetabolic septic state.

3. Ventilatory Masking

Pressure support temporarily concealed:

• muscular fatigue

• increased CO₂ production

• rising oxygen debt

References

1. West JB. Respiratory physiology: the essentials. 9th ed. Philadelphia: LWW; 2012.

2. Walsh BK, Smallwood CD. Use of noninvasive ventilation. Respir Care. 2017;62:932-950.

3. Marino PL. The ICU Book. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 2014.

A 41-year-old male with end-stage renal disease (ESRD), thrice-weekly dialysis, hemoglobin 9 g/dL, post-dialysis potassium 5–6 mmol/L, creatinine 8–9 mg/dL, and urea 110–150 mg/dL undergoes preoperative echocardiographic assessment before renal transplantation. He demonstrates classical uremic cardiac remodeling: severe LV hypertrophy, diastolic dysfunction, pulmonary hypertension, and right heart dilation.

The purpose of this chapter is to integrate echo findings → physiology → physics → anatomy → anesthesia strategy, forming a complete, mechanistic, clinically relevant approach.

The LV has:

• Thick muscular myocardium (especially septum and posterior wall)

• Helico-spiral fiber orientation, allowing torsion and recoil

• A relatively small cavity in severe concentric LVH

• IVSd = 20 mm, PWd = 18 mm
  (Normal: ~9–11 mm)

This is pathological concentric hypertrophy with significantly altered chamber compliance.

Laplace’s Law (Wall Stress = (Pressure × Radius) / (2 × Wall Thickness))

• When wall thickness increases, wall stress drops.

• The LV adapts to chronic hypertension by thickening its walls to reduce wall stress.

But this comes at a cost:

• Reduced compliance

• Higher diastolic pressures

• More oxygen consumption

• More dependence on slow filling

This fundamentally changes anesthetic goals:

A hypertrophied LV can generate pressure but cannot accept volume.

The RV has:

• Thin free wall

• Crescent-shaped geometry

• Greater sensitivity to afterload than preload

• RV dilated

• TR Grade II

• RVSP = 57 + RAP mmHg
  → Moderate–severe pulmonary hypertension

RV afterload is primarily determined by PVR (pulmonary vascular resistance).
PVR ∝ (Mean PAP – LAP) / CO

Any increase in:

• Hypoxia

• Hypercarbia

• Acidosis

• High PEEP
  → increases PVR → RV failure.

• Reflects diastolic dysfunction and volume overload

• LA contraction becomes essential for LV filling

In Grade II diastolic dysfunction:

• Up to 40% of LV stroke volume is dependent on atrial contraction
  Loss of atrial kick (AF, junctional rhythm) = sudden drop in CO.

The LV pressure-volume relationship becomes:

• Steep early diastolic slope

• Small increase in volume → large increase in pressure
  (Physics: ∂P/∂V greatly increased)

Clinical anesthesia relevance:
Small fluid boluses → FLASH PULMONARY EDEMA.