Introduction

Every anesthesiologist has encountered a patient whose reactions appear “disproportionate” to the situation—
a child who fights the mask with surprising strength,
an adult who becomes silent or withdrawn without warning,
a teenager whose pain expression feels puzzlingly out of sync with clinical findings.

These are not behavioral quirks. These are neurobiological signatures of the autistic brain.

Autism Spectrum Disorder (ASD) represents a distinct neurodevelopmental configuration. Its sensory pathways, predictive systems, autonomic responses, and neurochemical networks follow patterns that differ from neurotypical physiology. For anesthesia practice, this means that the perioperative environment, transitions, communication, and drug effects interact differently with this neurobiology.

The goal of this chapter is to integrate basic science, clinical fundamentals, and compassionate practice into a coherent framework that is academically rigorous yet deeply human-centered.

1. Predictive Coding: The Architecture That Governs Stress and Cooperation

The brain is fundamentally a prediction engine. It continually attempts to minimize “prediction error”—the mismatch between expected and actual sensory input.

In ASD:

• Predictions are narrower and more precise.

• Incoming sensory data carries more weight.

• Small mismatches produce disproportionately large autonomic responses.

Clinical meaning

Unannounced touch, sudden mask placement, or abrupt movement triggers limbic activation, cortisol release, and sympathetic surges—not because the patient is “difficult,” but because the predictive model has been violated.

Understanding this transforms clinical care:
the anesthesiologist’s greatest asset is not pharmacology, but predictability.

2. Sensory Hyperacuity: High-Gain Input in a Low-Noise System

Many autistic individuals experience an amplified sensory world:

• Visual cortex shows stronger responses to light.

• Auditory cortex exhibits heightened gain for sudden sounds.

• Tactile pathways show reduced habituation.

• Thalamic filtering is less efficient.

This creates a bandwidth–noise imbalance: the sensory system receives too much high-fidelity data and too little suppression.

CLINICAL CONSEQUENCES

• A cold stethoscope feels disproportionately painful.

• The OR’s beeping monitors accumulate into overwhelming auditory load.

• Bright overhead lights “flood” visual cortex and increase stress.

• Light touch (mask, ECG electrodes) may be perceived as intrusive or threatening.

This is why sensory-adapted anesthetic care is not a courtesy—it is physiology-driven medicine.

3. Autonomic Nervous System: The Fragile Symmetry of Arousal

Autonomic instability is one of the most clinically relevant aspects of ASD.

Neurophysiological studies reveal:

• Lower baseline vagal tone

• Exaggerated sympathetic surges

• Slower return to autonomic baseline after distress

• Heightened amygdala–locus coeruleus signaling loops

CLINICAL RELEVANCE

Expect:

• Tachycardia during mask induction

• Hypertension with environmental overstimulation

• Movement in response to unexpected touch

• Prolonged agitation during...

Morbid obesity is not merely an excess of body weight. It represents a chronic cardiometabolic disease state that exerts continuous stress on the cardiovascular system, leading to structural remodeling, functional impairment, and altered physiological reserve. For anesthesiologists, this distinction is critical: patients with extreme obesity and no “comorbidities” may already have advanced yet silent myocardial disease.

Echocardiography has emerged as the most comprehensive perioperative cardiovascular assessment tool in bariatric anesthesia. It does not simply identify pathology; it quantifies functional reserve, reveals preload dependence, assesses pulmonary vascular physiology, and predicts vulnerability to anesthetic stress. Unlike electrocardiography or chest radiography, echocardiography delivers dynamic insight into ventricular compliance, atrial pressure burden, right heart mechanics, and volume responsiveness—variables that directly influence anesthetic management.

This chapter applies echocardiographic interpretation to a typical bariatric surgery patient and translates imaging findings into practical anesthetic strategy.

A 50-year-old male with body mass index (BMI) of 50 kg/m² is scheduled for laparoscopic sleeve gastrectomy. He has no documented hypertension, diabetes, coronary disease, or heart failure. However, he reports poor exercise tolerance, loud snoring, and daytime somnolence suggesting undiagnosed obstructive sleep apnea.

Given his extreme obesity and reduced functional capacity, preoperative transthoracic echocardiography was obtained in anticipation of cardiopulmonary stress from general anesthesia, pneumoperitoneum, and reverse Trendelenburg positioning.

Despite the lack of overt cardiovascular disease, obesity itself imposes chronic hemodynamic stress leading to silent structural and functional cardiac remodeling.

Structural and Functional Summary

Two-dimensional measurements:

• Left ventricular end-diastolic diameter: 51 mm

• Left ventricular end-systolic diameter: 34 mm

• Interventricular septum thickness: 16 mm

• Posterior wall thickness: 16 mm

• Left atrial diameter: 49 mm

• Inferior vena cava diameter: 15 mm with respiratory collapse

Functional data:

• Ejection fraction: 60%

• Fractional shortening: 32%

• Right ventricular size: normal

Doppler parameters:

• Mitral E/A ratio ≈ 0.7

• Reduced tissue Doppler e′ velocity

• Grade I diastolic dysfunction

Valve assessment:

• Aortic sclerosis without stenosis

• Trivial mitral, tricuspid, and aortic regurgitation

Integrated Impression

Moderate concentric left ventricular hypertrophy, dilated left atrium, preserved systolic function, impaired relaxation, no pulmonary hypertension, and normal right ventricular size.

Obesity imposes a sustained high-output circulatory state through increased metabolic demand and blood volume expansion. Over time, this results in:

• Increased left ventricular wall stress

• Elevated systemic vascular resistance

• Endothelial dysfunction

• Neurohormonal activation

• Pulmonary vascular remodeling

At the cellular level, obesity leads to lipid infiltration of cardiomyocytes, interstitial fibrosis, impaired calcium cycling, and mitochondrial dysfunction. These mechanisms collectively reduce ventricular compliance and impair myocardial relaxation.

This evolution produces an obesity cardiomyopathy phenotype characterized by concentric hypertrophy, left atrial...

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.