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an adult who becomes silent or withdrawn without warning,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.

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.

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

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.

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...

Renal transplant recipients with coexisting bronchiectasis and fibro-interstitial lung disease exhibit complex respiratory physiology that fundamentally alters perioperative gas exchange. Arterial blood gas (ABG) interpretation in such patients must integrate basic sciences—alveolar diffusion theory, V/Q matching, dead-space physiology, structural lung disease mechanics, ESRD acid–base chemistry, hemoglobin dissociation kinetics, and cardiopulmonary interactions—together with real-time clinical variables.
This article analyzes three perioperative ABGs (preoperative, intraoperative, and post-extubation) in a 61-year-old male with bronchiectasis, fibrocalcific TB sequelae, ground-glass opacities, pleural thickening, and mild pulmonary hypertension. The analysis highlights how CT-documented structural disease shapes oxygenation, ventilation, diffusion, acid–base status, and metabolic response in renal transplant anesthesia.

Bronchiectasis and ESRD each distort fundamental components of respiratory and acid–base physiology:

1.1 Disrupted Airway Geometry & Dead Space

Bronchiectasis enlarges conducting airways.
These do not participate in gas exchange, increasing physiological dead space (VD):

↑VD/Vt → ↑ wasted ventilation → potential for CO₂ retention, especially after extubation.

1.2 Impaired V/Q Matching

Structural distortion → some regions ventilated but poorly perfused (high V/Q), others perfused but poorly ventilated (low V/Q).
This increases A–a gradient, even on high FiO₂.

1.3 Reduced Diffusion Capacity (DLCO)

Ground-glass opacities and fibro-interstitial changes thicken the alveolar–capillary membrane.
By Fick’s law:

Membrane thickening (↑T) → diffusion limitation → PaO₂ rises suboptimally even on high FiO₂.

1.4 ESRD Acid–Base Constraints

• Chronic metabolic acidosis due to loss of renal bicarbonate regeneration

• Increased chloride retention

• Reduced phosphate/ammonia buffering

• Impaired compensation during acute metabolic stress

1.5 Interaction Between Bronchiectasis and ESRD

ESRD requires hyperventilatory compensation,
but bronchiectasis limits this ability → risk of rapid acidosis under stress.

This fundamental physiology frames all ABG interpretations in this case.

2.1 Fibrocalcific Sequelae of Prior TB

• Loss of alveolar surface area (↓A)

• Formation of noncompliant fibrotic zones

• Contributes to chronic shunt physiology

2.2 Traction Bronchiectasis

• Dilated bronchi = ↑ anatomic dead space

• Turbulent airflow increases resistance (Reynolds number)

• Impaired mucus clearance → mucus plugging risk

• V/Q mismatch is chronic and fixed

2.3 Bilateral Ground-Glass Opacities

• Represent interstitial thickening (↑T in Fick’s law)

• Reduce DLCO

• Create diffusion-limited oxygen transport

• Flatten the PaO₂ vs FiO₂ curve

2.4 Pleural Thickening

• Reduced chest wall compliance

• Lower FRC → collapse of dependent alveoli

• Increased risk of postoperative atelectasis

2.5 Pulmonary Artery Enlargement (32 mm)

• Suggests early pulmonary hypertension

• ↑ RV afterload

• ↓ perfusion to...

Sleep is a biologically essential oscillatory brain state governed by interconnected neural circuits, endocrine rhythms, immune pathways, and autonomic patterns. For anesthesiologists, sleep physiology is directly relevant because anesthesia modifies the very circuits responsible for REM, NREM, circadian regulation, and arousal.

1. Non–Rapid Eye Movement (NREM) Sleep

NREM sleep consists of stages N1, N2, and N3:

N1 – Light Sleep

• Transition between wakefulness and sleep

• Decline in alpha activity (8–12 Hz)

• Increased theta activity (4–7 Hz)

N2 – Thalamocortical Sensory Gating

• Sleep spindles (11–16 Hz) generated by the thalamic reticular nucleus

• K-complexes representing cortical down-states

• Essential for initial memory consolidation and sensory isolation

N3 – Slow-Wave Sleep (SWS)

• Dominated by delta oscillations (0.5–4 Hz)

• Maximal parasympathetic dominance

• Physiologic functions:

  • Growth hormone release

  • Immune recalibration

  • Synaptic downscaling

  • Glymphatic clearance of metabolic waste (β-amyloid)

  
  

2. Rapid Eye Movement (REM) Sleep

REM is generated by activation of REM-on cholinergic nuclei in the pons.

Features:

• EEG resembles wakefulness

• Muscle atonia via medullary inhibition

• Active limbic system

• Autonomic variability (tachycardia, arrhythmias, BP swings)

Physiologic roles:

• Emotional integration

• Synaptic stabilization

• Autonomic recalibration

1. Suprachiasmatic Nucleus (SCN)

• Master circadian clock

• Receives retinal light input

• Controls melatonin secretion, cortisol timing, temperature minimum, and sympathetic tone

2. Melatonin

• Secreted at night via SCN → pineal gland pathway

• Primary marker of circadian phase

• Enhances sleep onset and REM sleep

• Suppressed by hospital lighting

3. Cortisol

• Peaks before awakening

• High postoperative cortisol disrupts sleep by stimulating arousal circuits

Homeostatic sleep pressure increases due to:

• Adenosine accumulation

• Activity-dependent metabolic changes

• Neuroinflammation

Key principle: anesthesia does not discharge sleep pressure, hence postoperative recovery may begin with a physiologic “sleep debt.”

References

1. Pace-Schott EF, Hobson JA. The neurobiology of sleep: genetics, cellular physiology and subcortical networks. Nat Rev Neurosci. 2002;3(8):591–605.

2. Brown EN, Lydic R, Schiff ND. General anesthesia, sleep, and coma. N Engl J Med. 2010;363(27):2638–50.

3. Xie L, Kang H, Xu Q, et al. Sleep drives metabolite clearance from the adult brain. Science. 2013;342(6156):373–7.

4. Czeisler CA, Klerman EB. Circadian and sleep-dependent regulation of hormone release in humans. Recent Prog Horm Res. 1999;54:97–130.

5. Borbély AA. A two-process model of sleep regulation. Hum Neurobiol.

Patients with COPD and chronic hypercapnia entering the operating room bring with them a unique neurophysiologic signature: a brain adapted to elevated PaCO₂ and reduced baseline arousal. Their respiratory mechanics—characterized by increased airway resistance, long expiratory time constants, dynamic hyperinflation, elevated intrinsic PEEP, and ventilation–perfusion mismatch—combine with impaired oxygen delivery due to reduced hemoglobin and chronic hypoxemia. This creates a fragile balance that can be rapidly disrupted by sedative–hypnotics.

In contrast, stress cardiomyopathy represents a state of myocardial vulnerability to both sympathetic surges and excessive anesthetic-induced hypotension. These patients frequently display transient LV dysfunction, labile hemodynamics, and abnormal responses to catecholamines. Both cardiac and pulmonary circuits must therefore be supported by precise anesthetic titration.

This chapter centers on a high-stakes clinical scenario:
A 54-year-old female with COPD, chronic CO₂ retention, and previous stress cardiomyopathy undergoing laparoscopic anterior resection + hysterectomy under general anesthesia with sevoflurane, dexmedetomidine, atracurium infusion, and a recently performed ESP block. Ten minutes prior to incision, she received a seemingly innocuous 30 mg propofol bolus—yet this bolus produced near burst suppression on EEG.

COPD + Stress Cardiomyopathy + Laparoscopy =
Highest-risk triad for anesthetic overdose.

COPD lowers EEG “activation tone” due to chronic hypercapnia, making EEG easier to suppress.
Stress cardiomyopathy mandates tight hemodynamic control, with myocardial ischemia risk if anesthesia is either too deep or too light.
Laparoscopy elevates intrathoracic pressure, increasing right heart load and decreasing venous return, amplifying the hemodynamic consequences of anesthetic-induced vasodilation.

Traditional anesthetic signs (BP, HR, MAC) are insufficient in such patients because:

• They cannot mount strong sympathetic responses.

• Opioids and dexmedetomidine blunt physiologic reactions.

• ESP block reduces nociceptive input, masking surgical stimulation.

• CO₂ pneumoperitoneum introduces hemodynamic artifacts.

• Hypothermia alters anesthetic pharmacokinetics and EEG patterns.

EEG-derived parameters such as BIS, SEF, MF, and SR therefore become essential:

• BIS tells you “how deep.”

• SEF tells you “how fast the cortex is firing.”

• MF tells you “where the power is distributed.”

• SR tells you “how suppressed the brain actually is.”

1. Propofol hypersensitivity due to chronic CO₂ retention.
   Even mild CNS depressant exposure can push such patients into suppression-level anesthesia.

2. Magnesium and dexmedetomidine synergy.
   These agents reduce cortical excitability; combined with volatile agents, suppression risk increases dramatically.

3. ESP block’s timing (only 30 minutes pre-incision).
   Partial block maturation reduces nociceptive drive and lowers cortical arousal, mimicking deep anesthesia even when hypnotic levels are normal.

4. Hypothermia at 33–33.2°C.
   Hypothermia decreases MAC, reduces propofol clearance, and increases EEG suppression.

5. Stress cardiomyopathy vulnerability.
   Deep anesthesia → hypotension → myocardial ischemia.
   Light anesthesia →...