Nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroids are both frequently employed for pain management and anti-inflammatory purposes in perioperative care. However, their renal safety profiles differ significantly, especially in at-risk populations such as the elderly, diabetics, and patients with pre-existing renal compromise. Understanding the basic science behind their mechanisms and the clinical implications of their use can help anesthesiologists make evidence-based decisions for safer patient care.

References

Kellum JA, Lameire N. Diagnosis, evaluation, and management of acute kidney injury: a KDIGO summary. Crit Care. 2013.

Lee A, Cooper MG, Craig JC, et al. Effects of non-steroidal anti-inflammatory drugs on postoperative renal function in adults with normal renal function. Cochrane Database. 2007.

NSAIDs inhibit cyclooxygenase (COX) enzymes, primarily COX-1 and COX-2. This inhibition reduces renal prostaglandin synthesis, particularly prostaglandin E2 (PGE2) and prostacyclin (PGI2). These prostaglandins normally mediate afferent arteriolar vasodilation, preserving renal blood flow during physiological stress. By suppressing these mediators, NSAIDs induce afferent vasoconstriction, which may reduce glomerular filtration rate (GFR). This effect is particularly deleterious in hypovolemic patients or those with existing renal compromise.

Corticosteroids act more upstream in the inflammatory cascade by inhibiting phospholipase A2 (PLA2) through induction of annexin-1 (lipocortin). This reduces the availability of arachidonic acid, thereby inhibiting both the cyclooxygenase and lipoxygenase pathways. Despite this broad inhibition, renal prostaglandins appear to be relatively spared. This may be due to differential tissue sensitivity or indirect steroid effects on nitric oxide production and renal hemodynamics. As a result, steroids are generally associated with less acute renal vasoconstriction compared to NSAIDs.

References

Harris RC. Cyclooxygenase-2 in the kidney. J Am Soc Nephrol. 2000.

Flower RJ. Lipocortin and the mechanism of action of the glucocorticoids. Br J Pharmacol. 1988.

NSAIDs directly target COX-1 and COX-2, resulting in reduced prostaglandin synthesis and afferent arteriolar vasoconstriction, leading to reduced renal blood flow. Their most common renal risk is acute kidney injury, especially in the setting of hypovolemia or pre-existing renal disease.

Corticosteroids target phospholipase A2, indirectly suppressing prostaglandins. Their effect on afferent arteriolar tone is minimal, and renal blood flow is relatively preserved. However, steroids carry other risks such as sodium and water retention, hypokalemia, long-term nephrocalcinosis, and hypertension.

References

Nolph KD, Moore HL. Acute renal failure induced by NSAIDs. Clin Nephrol. 1982.

Perazella MA. Drug-induced acute kidney injury: diverse mechanisms of tubular injury. Curr Opin Crit Care. 2019.

Monitoring renal function is essential when NSAIDs are used perioperatively. Traditional markers include serum creatinine, blood urea nitrogen (BUN), and urine output expressed in milliliters per kilogram per hour. However, these indicators may rise only after significant renal injury has occurred.

Emerging biomarkers such as urinary neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), and interleukin-18 (IL-18) offer earlier detection of acute kidney injury. Functional indices including fractional excretion of sodium (FeNa) and urine osmolality provide further insights into renal handling of electrolytes and water balance.

References

Haase M, Bellomo R, Devarajan P, et al. Accuracy of neutrophil gelatinase-associated lipocalin (NGAL) in diagnosis and prognosis in acute kidney injury: a systematic review. Am J Kidney Dis. 2009.

Vaidya VS, Ferguson MA, Bonventre JV. Biomarkers of acute kidney injury. Annu Rev Pharmacol Toxicol. 2008.

Perioperative renal protection requires a multifactorial approach, particularly in high-risk surgeries. Continuous urine output monitoring remains a cornerstone. Goal-directed fluid therapy, using pulse pressure variation or stroke volume optimization, helps maintain adequate intravascular volume without fluid overload.

Avoidance of intraoperative hypotension is critical, with mean arterial pressure maintained above 65 mmHg, especially in patients with chronic hypertension. Invasive monitoring, including arterial lines for beat-to-beat blood pressure and central venous pressure (CVP) or dynamic fluid indices, is indicated in major surgeries or in patients with significant renal risk.

References

Futier E, Constantin JM, Paugam-Burtz C, et al. A trial of goal-directed fluid therapy in major abdominal surgery. N Engl J Med. 2017.

Bijker JB, van Klei WA, Kappen TH, et al. Incidence of intraoperative hypotension as a function of the chosen definition. Anesthesiology. 2007.

Corticosteroids vary in their anti-inflammatory potency, mineralocorticoid activity, and duration of action. Hydrocortisone has high mineralocorticoid activity and a relatively short duration of action (8–12 hours), making it less suitable in patients with renal or cardiac compromise due to fluid retention. Prednisolone has moderate mineralocorticoid activity and an intermediate duration (12–36 hours), often preferred for chronic inflammatory conditions. Dexamethasone, with a very high anti-inflammatory potency, minimal mineralocorticoid activity, and a long duration (36–72 hours), is favored in perioperative settings for its efficacy in preventing postoperative nausea and vomiting without significant fluid retention.

References

Czock D, Keller F, Rasche FM, Häussler U. Pharmacokinetics and pharmacodynamics of systemic glucocorticoids. Clin Pharmacokinet. 2005.

Heney D, Turney JH, Clarke J, et al. Dexamethasone-induced renal dysfunction. Br Med J. 1983.

NSAIDs are widely incorporated into Enhanced Recovery After Surgery (ERAS) protocols because of their opioid-sparing properties. They reduce opioid-related adverse effects such as ileus, nausea, and sedation, contributing to faster recovery and mobilization.

However, NSAID-related renal risks must be considered, particularly in the elderly, dehydrated patients, or those with chronic kidney disease. The risk increases when combined with angiotensin-converting enzyme inhibitors and diuretics—the so-called “triple whammy.”

Best practice recommendations include using the lowest effective dose for the shortest duration, avoiding NSAIDs in patients with estimated GFR below 60 mL/min/1.73 m², and considering alternatives such as paracetamol or low-dose ketamine when renal risk is significant.

References

Wick EC, Grant MC, Wu CL. Postoperative multimodal analgesia and ERAS pathways. Anesthesiol Clin. 2015.

Khanna A, English SW, Wang XS, et al. Angiotensin-converting enzyme inhibitors and risk of AKI: systemic review. Clin J Am Soc Nephrol. 2014.

The KDIGO 2012 guidelines for acute kidney injury recommend avoiding nephrotoxic drugs where possible and closely monitoring serum creatinine and urine output in perioperative patients.

The ASA Practice Guidelines emphasize tailoring anesthetic and analgesic plans based on renal risk while encouraging multimodal analgesia that balances pain control with renal safety.

The ESAIC also cautions against NSAID use in high-risk groups and advocates for individualized ERAS implementation that accounts for renal considerations.

References

KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Int Suppl. 2012.

Apfelbaum JL, et al. Practice Guidelines for Acute Pain Management in the Perioperative Setting. Anesthesiology. 2012.

A structured protocol can guide safe perioperative use of anti-inflammatory agents:

1. Assess preoperative renal function: Serum creatinine, eGFR, urinalysis, and if available, biomarkers such as NGAL and KIM-1.
2. Identify risk factors: Diabetes, advanced age, congestive heart failure, and concurrent nephrotoxic drugs.
3. Classify surgical stress and inflammatory burden: Major abdominal or orthopedic procedures may warrant steroid use if prolonged inflammation is anticipated.
4. Evaluate analgesic needs and ERAS protocol: NSAIDs may be appropriate in patients with low renal risk, whereas steroids or acetaminophen are preferable in high-risk patients.
5. Monitor intraoperative and postoperative course: Track urine output, mean arterial pressure, and renal biomarkers. Adjust analgesia if renal function shows signs of decline.

References

Goren A, Matot I. Perioperative acute kidney injury. Br J Anaesth. 2015.

Forget P, Cata JP. Stable intraoperative hemodynamics and renal protection. Curr Opin Anaesthesiol. 2017.

While NSAIDs and corticosteroids both play roles in perioperative analgesia and inflammation control, their renal safety profiles diverge due to distinct molecular mechanisms. NSAIDs increase the risk of acute kidney injury by suppressing prostaglandin-mediated vasodilation and reducing renal perfusion. Corticosteroids, despite broader upstream inhibition of inflammatory pathways, often preserve renal blood flow and may represent a safer option in at-risk patients.

For anesthesiologists, understanding these mechanistic differences and integrating them into perioperative decision-making allows for safer, individualized patient care.

Obesity affects more than 650 million adults worldwide, with its prevalence continuing to rise according to the World Health Organization in 2020. In anesthesia practice, obesity introduces multifaceted challenges such as altered drug metabolism, difficult airway management, and cardiovascular instability. These difficulties are further compounded by common comorbidities including hypertension, diabetes, and obstructive sleep apnea, which add complexity to perioperative care. Importantly, obesity is not simply an issue of excess adipose tissue but a neurohumoral disorder characterized by chronic sympathetic nervous system (SNS) overactivation. This sympathetic overdrive influences blood pressure regulation, cardiac performance, renal physiology, and thermoregulation, thereby increasing perioperative risk.

The SNS is centrally regulated by the hypothalamus, which integrates stress and metabolic signals before relaying them to the rostral ventrolateral medulla (RVLM). Preganglionic neurons in the intermediolateral cell column of the spinal cord (T1–L2) project to the sympathetic chain ganglia, which then connect to postganglionic fibers innervating target organs. These fibers influence the heart by increasing rate and contractility, constrict vascular smooth muscle to elevate systemic blood pressure, stimulate renal renin release, and promote lipolysis in adipose tissue.

Norepinephrine is the principal neurotransmitter of postganglionic sympathetic fibers, while epinephrine is released from the adrenal medulla in response to stress. Different receptor subtypes mediate distinct effects: alpha-1 receptors cause vasoconstriction in vascular smooth muscle; beta-1 receptors increase heart rate and contractility in cardiac tissue; beta-2 receptors mediate bronchodilation and vasodilation in skeletal muscle; and alpha-2 receptors, found both presynaptically and centrally, inhibit norepinephrine release and dampen sympathetic tone.

Baroreceptors in the carotid sinus and aortic arch detect blood pressure changes and transmit signals to the nucleus tractus solitarius in the medulla. Sympathetic efferent output modulates both muscle sympathetic nerve activity (MSNA), which governs vascular tone, and renal sympathetic nerve activity (RSNA), which regulates sodium balance and renin secretion. In obesity, baroreflex sensitivity is diminished, perpetuating sympathetic overactivity.

Several mechanisms contribute to the persistent sympathetic activation observed in obesity:

Leptin-mediated activation: Leptin, secreted by adipocytes, normally regulates appetite and sympathetic activity. In obesity, leptin resistance blunts appetite suppression but paradoxically sustains sympathetic stimulation. Leptin crosses the blood-brain barrier to activate the RVLM, increasing MSNA and RSNA, which promotes hypertension and cardiovascular strain.

Insulin resistance and hyperinsulinemia: In healthy states, insulin induces vasodilation through nitric oxide release. In obesity, insulin resistance impairs this vasodilatory effect but its sympathoexcitatory influence on the RVLM persists. Elevated insulin levels also enhance renal sodium retention, contributing to hypertension.

Adipokines and cytokines: Adiponectin, normally anti-inflammatory and vasodilatory, is reduced in obesity. Conversely, pro-inflammatory cytokines such as TNF-α and IL-6 activate hypothalamic pathways that drive SNS activity, causing vascular dysfunction and stiffness. Visceral fat serves as a major source of these inflammatory mediators.

Sleep-disordered breathing: Obstructive sleep apnea, affecting the majority of morbidly obese patients, triggers intermittent hypoxia that stimulates carotid body chemoreceptors and diminishes baroreflex function. The result is nocturnal surges in blood pressure and a sustained increase in daytime sympathetic activity.

RAAS-SNS interactions: Sympathetic stimulation promotes renin release, and angiotensin II further activates RVLM neurons, amplifying SNS output. This reciprocal activation exacerbates vasoconstriction, hypertension, and sodium retention.

Chronic SNS overactivity in obese individuals has several cardiovascular consequences. Persistent beta-1 receptor stimulation leads to resting tachycardia, while elevated MSNA raises systemic blood pressure. Heart rate variability is reduced, reflecting autonomic imbalance and limited adaptive reserve. Structural changes include left ventricular hypertrophy due to pressure overload, increasing myocardial oxygen consumption and the risk of ischemia. Diastolic dysfunction is common, impairing ventricular filling and predisposing patients to heart failure, particularly in the hemodynamically labile perioperative environment. Excess sympathetic tone also enhances catecholamine sensitivity, creating a substrate for arrhythmias such as atrial fibrillation, ventricular ectopy, and QT prolongation. Surgical stressors, including laryngoscopy and intubation, may precipitate life-threatening rhythm disturbances in such patients.

Preoperative evaluation should identify common comorbidities associated with sympathetic overactivity, including hypertension, diabetes, and obstructive sleep apnea. A focused history should cover snoring, witnessed apneas, and use of CPAP. Physical examination should assess resting heart rate, blood pressure, neck circumference, and Mallampati score to anticipate airway challenges. Investigations include ECG to detect left ventricular hypertrophy or arrhythmias and echocardiography to evaluate diastolic dysfunction and pulmonary pressures. The STOP-BANG questionnaire is a practical screening tool for OSA. Risk stratification should incorporate airway indices, cardiac risk scores such as the Revised Cardiac Risk Index, and markers of autonomic dysfunction such as postural hypotension.

Induction is often accompanied by exaggerated sympathetic responses to laryngoscopy and intubation. These may be attenuated with opioids (e.g., fentanyl or remifentanil), beta-blockers such as esmolol, or alpha-2 agonists such as dexmedetomidine. Regional anesthesia techniques can further reduce sympathetic outflow.

During maintenance, volatile anesthetics help suppress sympathetic tone, although obese patients may require higher MAC values. Alternatively, total intravenous anesthesia with propofol and remifentanil offers stable hemodynamics. Invasive arterial pressure monitoring is advisable for patients with BMI greater than 35 or those at risk of cardiovascular instability. Depth of anesthesia monitoring and advanced hemodynamic monitoring (e.g., cardiac output devices) are valuable in high-risk cases. Neuromuscular blockade should avoid succinylcholine where possible due to risks of hyperkalemia and SNS stimulation; rocuronium, dosed on ideal body weight, is often preferred. Ventilation strategies should prevent hypoxia and hypercarbia, which otherwise trigger sympathetic surges, by applying lung-protective settings with adequate PEEP and FiO₂.

Extubation should be carefully managed to avoid sympathetic surges, using agents such as intravenous lidocaine, esmolol, or dexmedetomidine. Postoperative pain management should emphasize multimodal regimens combining acetaminophen, NSAIDs, and regional blocks to reduce opioid reliance, particularly in patients with OSA. Monitoring must detect hypertension, arrhythmias, and respiratory depression, with consideration for ICU or HDU admission in patients with severe OSA, BMI greater than 40 with comorbidities, or perioperative hemodynamic instability.

Several pharmacologic agents are used perioperatively to counteract sympathetic overactivity in obese patients. Esmolol, a selective beta-1 antagonist, provides short-acting control of tachycardia during intubation or extubation. Dexmedetomidine, an alpha-2 agonist, reduces norepinephrine release, providing both sedation and sympatholysis. Magnesium sulfate acts as an NMDA antagonist and calcium channel blocker, blunting SNS activity while offering analgesic benefit. Labetalol, with combined alpha and beta antagonism, is particularly useful for managing emergence hypertension. Clonidine, another alpha-2 agonist, may be administered preoperatively for anxiolysis and intraoperative sympatholysis.

Obstructive Sleep Apnea: Intermittent hypoxia in OSA exacerbates sympathetic activity. Postoperative opioid minimization, CPAP therapy, and continuous oximetry with capnography are essential components of care.

Bariatric Surgery: Enhanced Recovery After Surgery protocols are particularly beneficial in this population, emphasizing multimodal analgesia, regional techniques such as TAP blocks, and early mobilization.

Diabetic Autonomic Neuropathy: This condition reduces sympathetic reserve and baroreflex function, predisposing to intraoperative hypotension. Invasive arterial monitoring and careful vasopressor titration with agents such as phenylephrine or norepinephrine are recommended.

Heart rate variability has potential as a non-invasive predictor of perioperative risk, though validation in anesthesia-specific settings remains limited. Novel tools such as pupillometry and skin conductance may allow real-time monitoring of sympathetic activity and guide sympatholytic therapy. Prehabilitation strategies—structured exercise, weight loss, and OSA optimization—may reduce sympathetic overactivity prior to surgery. Pharmacogenomic approaches investigating adrenergic receptor polymorphisms could eventually tailor perioperative drug therapy to individual patients.

Obesity drives chronic sympathetic nervous system overactivity through mechanisms involving leptin, insulin resistance, inflammation, and sleep-disordered breathing. This sympathetic burden contributes to hypertension, arrhythmias, and perioperative instability. Preoperative assessment should emphasize screening for OSA, cardiac dysfunction, and autonomic imbalance. Intraoperative care should focus on sympatholytic strategies using agents such as esmolol and dexmedetomidine, supplemented by regional anesthesia and advanced monitoring in high-risk patients. Postoperatively, smooth extubation, multimodal analgesia, and vigilant monitoring are critical to reducing complications. Special populations—including those with OSA, undergoing bariatric procedures, or with diabetic autonomic neuropathy—require tailored management strategies.

Vagus Nerve Stimulation (VNS) is a neuromodulation therapy used in patients with treatment-resistant conditions such as epilepsy and depression. The anesthesiologist’s role is central to ensuring safe perioperative management, given the vagus nerve’s complex anatomy and physiology. This chapter reviews anesthetic considerations, with emphasis on differences between right- and left-sided stimulation.

VNS involves implantation of an electrode around the cervical vagus nerve, connected to a pulse generator implanted subcutaneously in the chest. The device delivers programmed electrical impulses to modulate neural activity.

• Pharmacoresistant epilepsy: Reduces seizure frequency in refractory cases.
• Treatment-resistant depression: Improves mood in patients failing conventional therapies.
• Cluster headaches: Provides relief in refractory cases.

• Post-traumatic stress disorder (PTSD)
• Inflammatory diseases (rheumatoid arthritis, Crohn’s disease)
• Heart failure
• Tinnitus
• Obesity
• Modulation of inflammatory pathways in ongoing trials

References: Groves DA, Brown VJ. Neurosci Biobehav Rev. 2005;29(3):493-500.

Ben-Menachem E. Lancet Neurol. 2002;1(8):477-82.

Johnson RL, Wilson CG. Front Neurosci. 2018;12:897.

• Standard and preferred site for VNS implantation.
• Primarily influences the atrioventricular (AV) node rather than the sinoatrial node.
• Carries a lower risk of bradycardia and asystole.
• Associated with a safer perioperative profile.

• Provides dominant innervation to the sinoatrial (SA) node.
• Increases risk of severe bradyarrhythmias, asystole, or cardiac arrest.
• Rarely used, reserved for cases where left-sided access is not feasible.
• Requires preoperative cardiology evaluation and intraoperative cardiac monitoring.

References: Ardell JL, et al. J Physiol. 2016;594(14):3877-3909.

Yuan H, Silberstein SD. Headache. 2016;56(1):71–78.

• The vagus nerve (cranial nerve X) is a mixed nerve with motor, sensory, and parasympathetic fibers.
• Exits the medulla via the jugular foramen.
• Contributes to the cardiopulmonary and abdominal plexuses.
• Left vagus nerve: Mainly supplies the AV node and thoraco-abdominal viscera.
• Right vagus nerve: Dominantly supplies the SA node, with stronger cardiac effects.

• Approximately 80% of fibers are afferent, projecting to the nucleus tractus solitarius (NTS).
• The NTS integrates inputs to higher centers, influencing the amygdala, hypothalamus, and locus coeruleus.
• Stimulation enhances GABAergic and noradrenergic activity, suppressing hyperexcitability in epilepsy and mood disorders.

References: Kandel ER, et al. Principles of Neural Science. 5th ed. McGraw-Hill; 2013.

Bonaz B, et al. Neuron. 2016;89(6):1131-1146.

• Cardiac assessment: Review arrhythmias, conduction abnormalities, or pacemakers.
• Neurological status: Assess seizure control, antiepileptic drug (AED) levels.
• Psychiatric medications: Consider interactions with anesthetics (SSRIs, TCAs, antipsychotics).
• Device history: Confirm previous implant details, need for battery replacement or revision.
• Diagnostics: Baseline ECG for all patients; mandatory cardiology consult for right-sided VNS.

Reference: DeGiorgio CM, et al. Seizure. 2000;9(7):448–451.

• General anesthesia: Standard, with endotracheal intubation for airway protection. Short-acting agents (propofol, remifentanil) favored.
• Monitored anesthesia care (MAC): Limited to minor procedures (e.g., generator replacement) in stable, cooperative patients.

• Avoid agents that lower seizure threshold (ketamine, enflurane).
• TIVA with propofol preferred for stable hemodynamics.
• Be prepared for sudden bradycardia; atropine or glycopyrrolate should be immediately available.

• Supine, with head rotated for surgical exposure.
• Avoid hyperextension to minimize venous congestion.
• Endotracheal intubation ensures airway security.

• Standard ASA monitors plus continuous ECG.
• External defibrillator/pacing pads must be available.
• NIM endotracheal tubes may help monitor recurrent laryngeal nerve function.

• Electrocautery: Prefer bipolar; monopolar used with caution, away from generator.
• Magnet usage: Surgeons may test or disable the device intraoperatively; anesthesiologists must monitor hemodynamic effects.

Reference: Rychlicki F, et al. Paediatr Anaesth. 2006;16(2):143–149.

• Vagal manipulation can induce bradycardia, hypotension, or asystole.
• Treat bradycardia with atropine (0.5–1 mg IV) or glycopyrrolate (0.2–0.4 mg IV).
• Asystole requires immediate cessation of stimulation and ACLS protocols.
• Hemodynamic instability: Optimize fluids and use vasopressors as required.
• Airway complications: Recurrent laryngeal nerve stretch may cause postoperative hoarseness or laryngospasm.
• Device testing: Coordinate with surgeons; stop testing if significant bradycardia or hypotension occurs.

Reference: Wheless JW, et al. Epilepsy Res. 2001;46(1):1–10.

• Monitor in PACU for:
• Recurrent laryngeal nerve dysfunction (hoarseness, dysphagia).
• Respiratory compromise (rare, requires urgent evaluation).
• Resume AEDs and psychiatric medications promptly.
• Provide patient education on wound care, device titration, and expected sensations.

Reference: Handforth A, et al. Neurology. 1998;51(1):48–55.

• Indicated only if left vagus access is not possible.
• Requires preoperative cardiology evaluation.
• Intraoperative precautions:
• Continuous ECG monitoring.
• Immediate availability of pacing and defibrillation.
• Greater vigilance needed due to high arrhythmia risk.

Reference: Engineer ND, et al. Nature. 2011;470(7332):101–104.

• Baseline ECG and cardiac assessment.
• Confirm AED and psychiatric medication status.
• Cardiology consult for right-sided VNS.

• TIVA or balanced anesthesia, avoid seizure-threshold-lowering drugs.
• Continuous ECG, atropine/glycopyrrolate ready.
• Use bipolar cautery when possible.
• Coordinate with surgeons during device testing.

• Monitor for laryngeal nerve complications and respiratory compromise.
• Resume AEDs and psychiatric medications promptly.
• Educate patient on device function and wound care.

BIS 95 at MAC 1.2 — awareness or artifact? In this episode, we cut through the noise with a stepwise framework to decode BIS anomalies and sharpen safe decision-making.

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• 51-year-old female undergoing surgery.
• Anesthesia maintained at MAC 1.2, corresponding to 1.2 times the alveolar concentration of an inhalational anesthetic such as sevoflurane.
• Intended depth: sufficient to prevent movement and maintain unconsciousness.

• BIS: 95 (expected 40–60 under general anesthesia).
• SQI: 56 (normal >70).
• EMG: 37 (normal <30).
• Heart rate: 58 bpm (normal 60–100 bpm).
• Blood pressure: 72/45 mmHg (normal 90/60–120/80 mmHg).
• SpO₂: 100% (normal >95%).
• Arterial pressure: 72/43 mmHg.

• Date/Time: August 1, 2025, at 11:54 AM IST.
• Electrode Placement: Around the articular (temporomandibular joint) area, increasing risk of artifact contamination.
• Observation: Significant discrepancy between BIS (95) and hemodynamic stability, suggesting artifacts rather than inadequate anesthesia.

• EMG 37 exceeded normal range (<30), indicating substantial muscle activity.
• Muscle activity contaminates EEG signals, falsely elevating BIS values.
• Articular electrode placement increases exposure to muscular and joint movement artifacts.
• Literature shows EMG >30 µV can increase BIS by 10–20 units depending on contraction intensity.

• SQI 56 was below the acceptable range (>70).
• Low SQI suggests poor electrode contact or noise contamination.
• Articular proximity increases susceptibility to motion artifacts.
• SQI <70 is associated with 15–25% error rates in BIS interpretation.

• At MAC 1.2, expected BIS range is 40–60.
• A BIS of 95 strongly indicates artifact rather than insufficient anesthetic depth.
• Non-standard electrode placement (articular site) increases artifact susceptibility by 30–40% compared to frontal Fp1–Fp2 placement.

• BIS 95 may falsely suggest intraoperative awareness.
• True incidence of awareness: approximately 0.1–0.2%.
• Stable hemodynamics (bradycardia, hypotension, normoxia) are inconsistent with awareness, which is often accompanied by tachycardia and hypertension.

• Over-reliance on BIS alone may result in unnecessary deepening of anesthesia.
• Consequences of excessive anesthetic dosing include hypotension, prolonged emergence, and postoperative cognitive dysfunction.
• Conversely, failure to address artifact-related discrepancies risks inadequate monitoring fidelity.

• Articular region placement amplifies EMG and motion artifacts.
• Proper frontal electrode placement remains critical for reliable BIS data.

• Continuously monitor EMG, SQI, and BIS values.
• Recognize thresholds: EMG <30, SQI >70, BIS 40–60.
• Use automated alerts where available.

• Reassess electrode positioning when BIS values deviate from expected ranges.
• Avoid articular sites; preferentially use frontal placements (Fp1–Fp2).
• Proper placement reduces artifact incidence by 20–30%.

• Consider neuromuscular blocking agents if excessive EMG persists.
• Reposition electrodes away from active muscle regions.
• These interventions reduce EMG-related interference by 15–20%.

• Always integrate BIS values with clinical signs, hemodynamic parameters, and anesthetic concentration.
• Cross-checking minimizes false positives and improves anesthetic titration accuracy.

• Record electrode location, BIS artifacts, and corrective actions.
• Documentation supports postoperative review and quality assurance.

• A 51-year-old female patient demonstrated a BIS of 95 despite MAC 1.2 and stable hemodynamics.
• Artifact sources included elevated EMG (37), low SQI (56), and articular electrode placement.
• These factors likely explain the elevated BIS, rather than true light anesthesia or awareness.
• Optimal practice involves proper electrode placement, vigilant artifact recognition, and correlation with clinical parameters.
• Integration of BIS with clinical judgment ensures safe and effective anesthesia management.

Vocal cord assessment after surgery is critical in anesthesia, as intubation and airway management can affect vocal cord integrity. This review integrates anatomy, physiology, clinical practice, and diagnostic tools, emphasizing diverse patient populations and resource-limited settings.

• Vocal Cord Structure
• Mucosal folds covering the thyroarytenoid muscles
• Supported by cricoid and thyroid cartilages
• Innervation
• Recurrent laryngeal nerve (RLN): motor control of most intrinsic laryngeal muscles
• Superior laryngeal nerve (SLN): sensation and cricothyroid function
• Function
• Vibration produces sound
• Controlled by airflow from lungs and intrinsic laryngeal muscles
• Anesthesia Relevance
• Intubation may cause trauma, edema, or nerve injury
• Special risk groups: pediatric (smaller airways), geriatric (reduced elasticity), neurological patients
• Basic Science Integration
• RLN vulnerability during thyroidectomy and neck surgeries
• Anatomical variations across age and comorbidities affect intubation strategies

• Key Signs
• Hoarseness or dysphonia: may indicate RLN/SLN dysfunction
• Stridor or breathing difficulty: suggests obstruction or bilateral paralysis
• Weak cough: impaired glottic closure and airway protection
• Dysphagia: SLN injury increasing aspiration risk
• Clinical Integration
• Assess voice quality 1–2 hours post-extubation
• Pediatric patients: monitor for stridor or weak cry
• Geriatric/neurological patients: bedside swallow test for aspiration
• Documentation: note symptoms (e.g., hoarse voice, weak cough) in chart
• Resource-limited settings: rely on visual inspection and early ENT referral

• Patient-Reported Complaints
• Hoarseness, vocal fatigue, difficulty projecting voice
• Acute vs delayed onset of symptoms
• Daily communication and cultural impact
• Clinical Integration
• Structured questions (“Does your voice tire after speaking?”)
• Conduct interviews within 24 hours post-surgery
• Professional voice users: ask about pitch range and stamina
• Use translated questionnaires for multilingual patients
• Repeat interviews at 48–72 hours if symptoms persist

• Definition and Procedure
• Duration of sustained vowel (/a/) on one breath
• Normal values: 25–35 sec (males), 15–25 sec (females), 10–15 sec (children)
• <10 seconds in adults suggests dysfunction
• Clinical Integration
• Bedside test with stopwatch post-extubation
• Pediatric adaptation: shorter phonation tasks
• Adjust expectations in COPD or Parkinson’s disease
• <10 seconds requires ENT referral
• Document values in anesthesia record

• Description
• Perceptual rating: Grade, Roughness, Breathiness, Asthenia, Strain
• Each parameter scored 0–3; ≥2 indicates dysfunction
• Clinical Integration
• Requires brief training for anesthesiologists
• Apply during postoperative checks
• Adjust for age-related changes or neurological tremor
• In resource-limited settings: reliable screening tool
• Referral for score ≥2

• Overview
• 30-item questionnaire (0–120 total score)

• Clinical Integration
• Use pre- and post-surgery in professional voice users
• Repeat within 24–48 hours, and at 1 week if persistent
• Use validated translations for multilingual patients
• Scores >30 trigger speech pathology referral
• Document in chart

• Purpose
• 10-item tool focusing on quality of life impacts
• Scored 0–100; <75 indicates significant impact
• Clinical Integration
• Short, suitable for busy recovery units
• Administer within 48 hours post-surgery; repeat at 1–2 weeks
• Use translated versions for tonal languages
• Scores <75 prompt referral

• Parameters
• Jitter (<1%), shimmer (<3%), noise-to-harmonics ratio (<0.2)
• Tools
• Software (e.g., Praat, MDVP) for voice recordings
• Clinical Integration
• Performed 48–72 hours post-surgery for persistent hoarseness
• Collaborate with speech pathologists
• Adjust interpretation for neurological baseline voice changes
• Best suited to tertiary centers

• Types
• Direct, indirect, flexible fiberoptic
• Findings
• Detects edema, hematoma, paralysis, granulomas
• Clinical Integration
• Indicated for abnormal MPT/GRBAS or high-risk patients
• ENT collaboration within 24–48 hours if persistent
• Pediatric: flexible fiberoptic preferred
• In low-resource settings: reserve for severe cases

• Technique
• Non-invasive ultrasound to visualize vocal fold movement
• Clinical Integration
• Bedside use post-extubation
• Safe for pediatric and geriatric patients
• Repeat at 48 hours if abnormal
• Especially useful in resource-limited environments

• Purpose
• Visualizes larynx and subglottis with high resolution
• Clinical Integration
• Intraoperative use for trauma assessment
• Postoperative use for stridor or severe hoarseness
• Pediatric scopes minimize trauma
• Reserved for severe or unclear cases in resource-limited centers

• Method
• Mirror or endoscope via oral cavity
• Clinical Integration
• Bedside screening within 24 hours
• Suitable for geriatric or neurological patients
• Rapid assessment with phonation task (/e/)
• Abnormal findings prompt ENT referral

• Intraoperative Neuromonitoring (IONM)
• Electromyography monitoring of RLN during high-risk surgery
• AI-Based Voice Analysis
• Detects subtle pitch or quality changes via machine learning
• High-Resolution Imaging
• Narrow-band imaging and advanced endoscopy improve detection of lesions
• Clinical Integration
• IONM during thyroidectomy and neurosurgery
• AI analysis for professional voice users
• Advanced imaging in tertiary centers

• Pediatric: Small cords, higher risk of trauma; use smaller tubes and early stridor monitoring
• Geriatric: Reduced elasticity, aspiration risk; perform bedside swallow tests
• Professional Voice Users: Baseline VHI/V-RQOL critical; coordinate rehabilitation with speech therapy
• Neurological Conditions: Pre-existing weakness may compound injury; document baseline voice
• Multilingual Patients: Use culturally adapted and translated questionnaires

• Preoperative Assessment
• Baseline evaluation using MPT, GRBAS, or VHI/V-RQOL
• Identify high-risk patients (prior neck surgery, neurological disease)
• Document baseline for postoperative comparison
• Intraoperative Care
• Use video laryngoscopy to minimize trauma
• Select appropriate ETT sizes; maintain cuff pressure <20–30 cmH₂O
• Consider IONM in high-risk surgeries
• Postoperative Evaluation
• Bedside MPT and GRBAS within 1–2 hours
• Repeat at 24–48 hours if abnormal
• Use ultrasonography in low-resource settings
• ENT referral for persistent abnormalities
• Collaboration
• ENT for structural and functional assessment
• Speech pathology for rehabilitation planning
• Patient Education
• Inform about risk of voice changes
• Encourage reporting of hoarseness, swallowing difficulty
• Provide follow-up details
• Documentation
• Record MPT, GRBAS, VHI/V-RQOL, ultrasonography, or laryngoscopy findings
• Ensure clear follow-up and referral notes

Anesthesiologists are central to the early detection and management of postoperative vocal cord dysfunction. A multimodal strategy—combining bedside screening tools (MPT, GRBAS), patient-reported measures (VHI, V-RQOL), and advanced diagnostics (ultrasonography, laryngoscopy, acoustic analysis)—ensures timely intervention. Integration of clinical vigilance, patient education, and multidisciplinary collaboration optimizes outcomes across all patient groups, including pediatric, geriatric, professional voice users, neurological, and multilingual populations, even in resource-limited settings.

The pre-anesthesia clinic is bustling with preparations for a diverse surgical roster, including orthopedic joint replacements, oncologic resections, and cardiac procedures. Regional anesthesia (RA) offers significant advantages—opioid-sparing analgesia, faster recovery, and reduced hospital stays. However, many patients are on antithrombotic therapy, which raises the risk of catastrophic complications such as epidural hematomas or deep plexus hemorrhages. These bleeding events, if not decompressed promptly, may result in irreversible neurologic injury such as paraplegia.

Examples of patients commonly encountered include:

• A 78-year-old on apixaban for atrial fibrillation, requiring a femoral nerve block for knee replacement.
• A 65-year-old on enoxaparin (LMWH) for DVT prophylaxis after orthopedic surgery, planned for a paravertebral block for mastectomy.
• A 55-year-old on dual antiplatelet therapy (clopidogrel and aspirin) following coronary stenting, awaiting hip fracture repair, where a lumbar plexus block is being considered.

For each case, the indication, dose, half-life, clearance (especially renal), and reversibility of the antithrombotic must be evaluated. Renal impairment or polypharmacy may prolong effects unpredictably. Bleeding into closed or non-compressible spaces, particularly around the spinal canal or deep plexus structures, poses a devastating risk.

• Reduces opioid use.
• Improves postoperative recovery.
• Shortens hospital stay.

• Catastrophic complications: Epidural or spinal hematomas may cause paralysis unless decompressed within 6–12 hours. Deep plexus blocks (lumbar plexus, paravertebral) also carry high bleeding risks.
• Critical timing: Antithrombotics vary in half-life, clearance, reversibility, and renal dependence. Regional anesthesia must coincide with minimal drug activity.
• Increasing prevalence: Widespread use of DOACs, DAPT, and LMWH requires careful drug-specific planning.
• Medico-legal responsibility: ASRA-ESRA guidelines form the standard of care. Documentation, informed consent, and risk discussion are mandatory.

The 5th Edition of the ASRA-ESRA Guidelines (2025) provides a structured framework:

• Timing: Hold times depend on half-life, renal clearance, and drug reversibility.
• Risk stratification of block types:
• High risk: neuraxial, lumbar plexus, paravertebral.
• Intermediate risk: femoral, adductor canal.
• Low risk: superficial fascial plane blocks (e.g., TAP, ESP, SCB).
• Interdisciplinary input: Coordination with cardiologists, surgeons, and hematologists is essential.
• Documentation and consent: Explicit records protect against medico-legal risks.
• Lab monitoring: Drug-specific assays (e.g., anti-Xa, thrombin time, platelet counts) are emphasized.

Key updates compared with 2018 include:

• Dosing terminology: Shift from “prophylactic vs therapeutic” to “low-dose vs high-dose.”
• DOAC timing: Hold 72–120 hours, adjusted for renal function.
• LMWH: Emphasis on anti-Xa monitoring in renal dysfunction.
• Laboratory use: Encouragement of assays for DOACs and renal impairment cases.
• Block stratification: Explicit risk-based classification.
• Reversal agents: Guidance on antidotes such as idarucizumab (dabigatran) and andexanet alfa (Xa inhibitors).
• Catheter removal: Based on anti-Xa thresholds (<0.1 IU/mL for LMWH).

• aPTT: Delay RA if >35 seconds; safe 4–6 hours after last dose.
• Platelets: Monitor for HIT if <100,000/µL.
• Anti-Xa: Safe when <0.1 IU/mL.

• Platelets: Stop LMWH and investigate HIT if <100,000/µL.
• Creatinine/eGFR: Extend hold times if <30 mL/min.
• Anti-Xa: Delay RA until <0.1 IU/mL.

• INR: Safe when ≤1.4.
• Management: Hold 5–7 days; use vitamin K or FFP if urgent reversal required.

• Creatinine clearance: Extend hold times if <50 mL/min.
• Anti-Xa levels: Safe when <30 ng/mL.
• PT/INR/aPTT: Not reliable.

• Renal clearance critical: Hold 72–120 hours depending on CrCl.
• Thrombin time or ecarin clotting time: Confirm absence of activity before RA.
• Idarucizumab available for reversal.

• Aspirin: Safe alone.
• Clopidogrel/Ticagrelor/Prasugrel: Require 5–10 day hold before RA, depending on drug.
• Platelet function testing: Useful in high-risk cases.

• Aspirin/NSAIDs: No delay needed.
• Clopidogrel: Hold 5–7 days.
• Prasugrel: Hold 7–10 days.
• Ticagrelor: Hold 10 days.
• UFH: Wait 4–6 hours after last dose.
• LMWH: Hold 12 hours (low dose), 24 hours (high dose).
• Fondaparinux: Hold 36–105 hours depending on renal function.
• DOACs: Hold ≥72 hours, longer in renal impairment.
• Dabigatran: 72–120 hours depending on renal clearance.
• Thrombolytics: Avoid RA within 48 hours.

• Recent DOAC ingestion: Avoid neuraxial; consider GA or superficial blocks; reversal with andexanet alfa or idarucizumab.
• Mechanical valve with LMWH bridging: Delay until anti-Xa <0.1 IU/mL; avoid catheters.
• Post-stenting on DAPT: Avoid neuraxial; consider superficial blocks such as ESP or TAP.
• CKD patients: Extend DOAC hold; confirm with drug levels.
• Emergency surgery: GA or superficial blocks safer; coordinate reversal if urgent.

• Elderly: Reduced clearance; favor superficial blocks with lab confirmation.
• Neurosurgical patients: Avoid neuraxial; strict LMWH protocols.
• CKD: Extended hold times; anti-Xa monitoring essential.
• Obese patients: Ultrasound guidance preferred.
• Pediatric: Individualize; confirm drug clearance before RA.

Documentation should include:

1. Patient and procedure details (demographics, surgery, planned block).
2. Antithrombotic details (drug, dose, indication, last dose timing, renal function, lab values).
3. Risk assessment (block category, hold times, lab monitoring, catheter plan).
4. Multidisciplinary input (surgeon, cardiologist, hematologist, nephrologist).
5. Patient counseling and consent (verbal and written, bleeding risks explained).
6. Final anesthesia plan (chosen block, precautions, antithrombotic restart timing).

• Perform RA only when antithrombotic activity is minimal (anti-Xa <0.1 IU/mL, INR ≤1.4).
• Tailor decisions to drug type, block risk, renal clearance, and laboratory results.
• Avoid high-risk blocks in anticoagulated patients unless drug effect is absent.
• Laboratory monitoring is critical in DOACs, renal impairment, and high-risk procedures.
• Fixed hold times are not sufficient; context and patient-specific factors must guide decisions.
• Interdisciplinary coordination is essential.
• Comprehensive documentation ensures both patient safety and medico-legal protection.

Kaplan’s lesion is a rare but surgically complex traumatic injury involving disruption of digital neurovascular bundles and flexor tendons, often on the volar aspect of the index finger or hand. Because repair requires precise exposure and neurovascular reconstruction, the anesthetic plan must be comprehensive. A wrist block alone fails to provide complete surgical anesthesia, compromising exposure, pain control, and hemostasis.

This article explains the limitations of a wrist block in this context and highlights preferred anesthesia options.

• Involves simultaneous injury to flexor digitorum profundus (FDP), flexor digitorum superficialis (FDS), digital nerves, and arteries.
• Typically occurs at the MCP joint or proximal phalanx.
• Mechanism: lacerations from sharp objects (knives, glass) or crush injuries.
• Classified within flexor tendon Zone II or III, which are challenging areas for tendon repair and functional recovery.

• Requires magnification for neurovascular repair.
• Demands deep field exposure and tendon retraction.
• Commonly performed under an arm tourniquet for hemostasis.

References: Doyle JR (1988); Tang JB (2019); Green DP et al. (2010).

• Targets median, ulnar, and superficial radial nerves at or distal to the wrist crease.
• Provides cutaneous anesthesia but has limited motor and autonomic blockade.
• Commonly chosen for minor hand procedures because of technical simplicity and safety.

• Does not provide tolerance to an arm tourniquet.
• Produces incomplete motor block.
• Fails to anesthetize the palmar cutaneous branch of the median nerve.

References: Hadzic A (2017); Neal JM et al. (2009).

• The palmar cutaneous branch of the median nerve arises ~5 cm proximal to the wrist, escaping wrist-level blockade.
• Kaplan’s lesion repair may require incisions extending proximally beyond wrist block coverage.

References: Fabregas N et al. (1996); Sunderland S (1978).

• Tourniquet pain arises from unmyelinated C fibers and A-delta fibers.
• Involves proximal nerves such as the medial cutaneous nerve of the arm and intercostobrachial nerve.
• Wrist block does not anesthetize these fibers, making it inadequate when a tourniquet is required.

References: Flamer D, Peng PWH (2011); McCartney CJ et al. (2007).

• Wrist block does not cover anterior interosseous nerve fibers, which supply FDP and FDS.
• Preserved motor activity may hinder tendon exposure and surgical manipulation.

References: Tubbs RS et al. (2007); Franco CD, Vieira ZE (2000).

• Variations such as Martin-Gruber anastomosis (median–ulnar crossover) and Berrettini anastomosis (ulnar–median digital communication) compromise the predictability of wrist block.
• Such cross-innervations may leave unblocked sensory zones.

References: Roy J et al. (2016); Cannie M et al. (2006).

• Provides dense anesthesia of median, ulnar, radial, and musculocutaneous nerves.
• Offers reliable tourniquet tolerance and motor relaxation.
• Suitable for surgeries below the mid-humerus.

References: Neal JM et al. (2002); Delaunay L et al. (2008).

• Particularly effective in obese patients or trauma cases.
• Produces dense plexus anesthesia while minimizing risk of phrenic nerve palsy.

References: Kilka HG et al. (1995); Tran DQH et al. (2015).

• Can be used for distal surgeries but is less reliable due to variation in musculocutaneous nerve location.
• Inadequate for controlling proximal tourniquet pain.

References: Urban MK, Urquhart B (1994).

• Pressure: 100–150 mmHg above systolic blood pressure.
• Maximum recommended time: 90 minutes.
• Block choice must account for deep ischemic pain pathways.

• Light sedation with agents such as dexmedetomidine can improve comfort.
• Over-sedation should be avoided to allow neurological monitoring.

References: Brull R et al. (2007); Marhofer P et al. (2010).

• Long-acting local anesthetics such as bupivacaine or ropivacaine provide 12–18 hours of relief.
• Adjuvants such as dexamethasone or clonidine can further extend duration.

• Paracetamol, NSAIDs, and rescue opioids as required.
• Cryotherapy and limb elevation aid in pain and edema reduction.

References: Ilfeld BM (2011); Mariano ER et al. (2010).

Wrist block alone is insufficient for Kaplan’s lesion repair because it does not address proximal innervation, tourniquet pain, or motor requirements and is subject to anatomical variability. Supraclavicular or infraclavicular brachial plexus blocks provide superior anesthesia and surgical conditions. The anesthesiologist must individualize the regional anesthesia plan to surgical field, expected duration, and tourniquet use, ensuring optimal outcomes through a combination of anatomical knowledge and pharmacologic expertise.

• Glomus tumors are rare, benign neoplasms arising from the glomus body, a neuro-myo-arterial structure specialized for thermoregulation.
• They are typically exquisitely painful, particularly when located in subungual or digital regions.
• Surgery often requires meticulous anesthetic planning due to:
• High vascularity
• Neuropathic pain profile
• Potential need for reconstructive flap coverage, especially in recurrent or large tumors
• This article discusses perioperative anesthetic management of a 29-year-old female undergoing excision of a glomus tumor in the right ring finger with abdominal flap reconstruction.

• Derived from modified smooth muscle cells of the Sucquet-Hoyer canal, a dermal arteriovenous shunt.
• Rich innervation:
• Unmyelinated C-fibers (nociceptive)
• Sympathetic vasoconstrictor fibers
• Molecular features:
• Overexpression of TRPV1 and ASIC3 channels
• Increased nociceptor firing → hypersensitivity to cold and mechanical stimuli

• Histology: numerous dilated capillary-sized vessels surrounded by glomus cells.
• Immunohistochemistry: overexpression of VEGF-A and angiopoietins.
• Clinical implication:
• High bleeding risk intraoperatively
• Hemodynamic stability critical during anesthesia

• Triggered by inflammatory mediators:
• Bradykinin
• Substance P
• Prostaglandin E2
• Leads to:
• Upregulation of Nav1.7 sodium channels
• Increased TRPV1 activity
• Lower nociceptor threshold

• Persistent peripheral input → hyperexcitable dorsal horn neurons.
• Key molecular changes:
• NMDA receptor upregulation
• Reduced GABAergic inhibition
• Clinical relevance:
• Pain may persist even after tumor removal.
• Requires preemptive analgesia.

• DN4 questionnaire: identifies neuropathic pain component.
• Pharmacologic strategies:
• Gabapentinoids (gabapentin, pregabalin)
• NMDA antagonists (ketamine)

• Patient: cold-induced focal pain in right ring finger.
• Impact: disturbed sleep, impaired dominant-hand function.
• Goal: optimize recovery while minimizing neuropathic recurrence.

• MRI (contrast-enhanced): hyperintense T2 lesion, strong gadolinium enhancement.
• Histopathology: positive staining for SMA, vimentin, and nestin.

• Ultrasound-guided supraclavicular block with 0.5% ropivacaine.
• Ropivacaine selected for:
• Lower cardiotoxicity vs. bupivacaine
• High sensory selectivity
• Perineural dexmedetomidine added:
• Prolongs block duration via α2-adrenoceptor activity
• Enhances analgesia and reduces sympathetic tone

• TIVA with propofol + remifentanil:
• Propofol: GABA-A receptor agonist, reduces cortical arousal
• Remifentanil: ultra-short acting µ-opioid agonist for titratable analgesia
• Avoided inhalational agents due to vasodilation effects on flap perfusion

• Multimodal regimen:
• Paracetamol (1 g IV q6h)
• IV ketorolac (if renal function intact)
• Gabapentin (300 mg PO, pre-op, continued 5–7 days)
• Rescue: tramadol or low-dose morphine
• Supraclavicular block: provided 18–24 hours analgesia
• Early physiotherapy to prevent stiffness

• Monitored parameters:
• Color (pink vs. dusky)
• Temperature (>35°C)
• Capillary refill time
• Doppler flow over pedicle
• Perioperative strategies:
• Avoided vasopressors
• Maintained ambient temperature
• Active warming with forced-air devices

• Limited to <90 minutes to reduce ischemia-reperfusion risk.
• Prior to release:
• Optimized IV fluids
• Considered antioxidants (e.g., vitamin C)

• Central venous catheter (CVC) placement is essential in perioperative and critical care for hemodynamic monitoring, fluid therapy, and drug delivery.
• The procedure carries potential complications, notably cardiac arrhythmias arising from mechanical irritation of cardiac structures.
• Arrhythmias commonly result from contact with the coronary sinus and right heart due to the anatomical relationship of central veins to the heart.
• This chapter examines the basic science (anatomy, electrophysiology, procedural mechanics) and integrates those principles into practical anesthetic strategies to anticipate, prevent, and manage arrhythmias during CVC placement.

• Coronary sinus
• Large venous sinus in the posterior atrioventricular groove.
• Drains approximately 70% of myocardial venous blood (great, middle, small cardiac veins; posterior vein of the left ventricle).
• Empties into the right atrium via the coronary sinus ostium; may be guarded by a Thebesian valve.
• Other venous structures
• Thebesian veins: small veins draining directly into the right atrium or ventricle.
• Anterior cardiac veins: empty directly into the right atrium.
• Spatial relationships relevant to CVC placement
• Coronary sinus lies ~2–3 cm from the superior vena cava–right atrial junction.
• Proximity to typical CVC insertion paths (right internal jugular and subclavian veins) predisposes to inadvertent catheter or guidewire entry.

• Coronary sinus contains myocardial tissue and is electrically active; mechanical contact can trigger ectopic activity.
• Right atrium and ventricle house conduction structures (SA node, AV node, Purkinje fibers) that are susceptible to mechanical disruption.
• Anatomical variants (e.g., persistent left superior vena cava [PLSVC], dilated coronary sinus) increase the risk of misplacement and arrhythmias.
• Awareness of these anatomical nuances aids in planning access site choice and insertion technique.

• Conduction system components: sinoatrial (SA) node, atrioventricular (AV) node, bundle of His, Purkinje fibers.
• SA node generates spontaneous action potentials that propagate through the atria to the AV node and ventricles.
• Myocardial cell properties: automaticity, excitability, conductivity — governed by sodium, potassium, and calcium ion channels.
• Myocardial sleeves (including those in the coronary sinus) can act as ectopic foci when irritated.

• Coronary sinus irritation
• Mechanical stimulation of myocardial sleeve can produce premature atrial contractions (PACs), atrial flutter, or atrial fibrillation.
• Mechanical disturbance can trigger early afterdepolarizations (EADs) or delayed afterdepolarizations (DADs).
• Proximity to AV nodal tissue increases risk of re-entrant arrhythmias if conduction pathways are disrupted.
• Right heart stimulation
• Catheter or guidewire contact with endocardium or conduction tissue may provoke sinus tachycardia, supraventricular tachycardia (SVT), or ventricular tachycardia (VT).
• Localized mechanical stress can precipitate ischemia, altering ion channel function and excitability.
• Guidewire-induced arrhythmias
• J-tipped or straight guidewires advanced into the right heart can transiently irritate myocardium and Purkinje fibers, causing PACs or premature ventricular contractions (PVCs).
• Phase 4 depolarization in Purkinje fibers may be induced by mechanical contact, producing ventricular ectopy.
• Electrolyte and hemodynamic effects
• Rapid or maldirected infusion (e.g., into coronary sinus) can create localized electrolyte shifts (hyperkalemia, hypocalcemia) and increase irritability.
• Direct infusion of vasoactive drugs into sensitive myocardial regions can exacerbate arrhythmogenesis.

• Reported arrhythmia rates during CVC insertion are approximately 1–2%, with higher rates when imaging guidance is not used.
• Right internal jugular access carries heightened risk due to its direct trajectory toward the superior vena cava and right atrium.

• Seldinger technique steps: venous needle access, guidewire insertion, dilation, catheter advancement.
• Procedural risk factors
• Lack of imaging guidance (blind landmark approach) increases misplacement risk.
• Over-advancement of guidewire (beyond ~20–25 cm) increases probability of entering the right atrium or ventricle.
• Catheter tip positioned too low (within right atrium/coronary sinus) increases arrhythmia risk.

• Anatomical variations
• PLSVC or inherently dilated coronary sinus elevates misplacement risk particularly with left-sided access.
• Cardiac disease
• Atrial enlargement, pulmonary hypertension, ischemic heart disease increase myocardial irritability.
• Metabolic factors
• Pre-existing electrolyte abnormalities (hypokalemia, hypomagnesemia, hyperkalemia) potentiate arrhythmogenesis.

• Cardiac history
• Document prior arrhythmias, heart failure, congenital variants (e.g., PLSVC).
• Electrolyte optimization
• Correct hypokalemia and hypomagnesemia before elective central access when feasible.
• Imaging review
• Inspect prior chest radiographs and echocardiography for right heart enlargement or venous anomalies.

• Continuous ECG monitoring
• Use multi-lead monitoring (e.g., 5-lead) to detect PACs, PVCs, atrial fibrillation, and ischemic ST changes in real time.
• Ultrasound guidance
• Real-time ultrasound for vessel localization and needle guidance reduces complication rates compared with landmark techniques.
• Visualize guidewire within the vessel when possible prior to dilatation and catheter advancement.
• Guidewire and catheter positioning
• Limit guidewire advancement to approximately 20–25 cm to minimize right heart entry.
• ECG-guided technique: connect guidewire to an ECG lead and monitor for P-wave amplitude changes that indicate right atrial entry; withdraw if marked increase occurs.
• Advanced imaging in high-risk cases
• Use fluoroscopy or transesophageal echocardiography (TEE) to confirm tip location when anatomical variants are suspected or in cardiac surgery settings.
• TEE allows visualization of the coronary sinus ostium and catheter position in real time.

• Initial steps
• Halt wire/catheter advancement and withdraw slightly (1–2 cm) to reduce mechanical irritation.
• Reassess ECG to classify arrhythmia (PAC, PVC, SVT, VT, atrial fibrillation).
• Pharmacologic therapy
• Supraventricular arrhythmias: consider rate control or antiarrhythmics per ACLS (e.g., esmolol for acute rate control; amiodarone for sustained or unstable SVT/AF).
• Ventricular arrhythmias: amiodarone or lidocaine for sustained VT; defibrillation if unstable.
• Electrolyte repletion: magnesium sulfate (e.g., 2 g IV) for torsades de pointes or polymorphic VT; correct potassium and calcium as indicated.
• Confirm and correct catheter position
• Obtain chest radiograph, fluoroscopy, or TEE to confirm tip location and reposition catheter into the superior vena cava if misplaced.
• Avoid large or rapid infusions until correct placement is assured.

• Chest X-ray confirmation
• Verify that the catheter tip lies in the superior vena cava, approximately 1–2 cm above the right atrial junction.
• Continued monitoring
• Maintain ECG monitoring for 24–48 hours post-insertion when clinically appropriate due to risk of delayed arrhythmias from migration or thrombosis.
• Patient education and follow-up
• Inform patients about signs of complications (palpitations, chest pain, syncope); arrange prompt reassessment and imaging if symptoms appear.

• Recognizing the coronary sinus as an electrically active structure explains why direct mechanical contact induces ectopy and arrhythmias.
• Appreciating proximity of conduction tissues in the right heart supports conservative guidewire advancement and tip positioning.
• Selecting insertion sites (e.g., right internal jugular vs left-sided access) should incorporate anatomical risks such as PLSVC.

• Anesthetic agents influence arrhythmia risk:
• Propofol: may exhibit antiarrhythmic properties but causes hypotension that can worsen myocardial ischemia in vulnerable patients.
• Volatile anesthetics (isoflurane, sevoflurane): generally minimal direct conduction effects but require careful hemodynamic titration.
• Local anesthetic systemic toxicity: inadvertent intravascular injection of significant lidocaine doses can cause cardiac conduction disturbances and should be avoided.

• Fluid dynamics and vessel selection
• Principles such as Poiseuille’s law support choosing larger, straighter veins for central access to minimize turbulence and mechanical stress.
• Avoiding rapid infusion through malpositioned catheters
• Understanding how localized electrolyte concentration affects membrane potentials informs conservative infusion practices until placement is confirmed.

• Clinical vignette
• A 65-year-old male with atrial fibrillation and heart failure requires CVC placement for coronary artery bypass grafting.
• During right internal jugular cannulation, new-onset PVCs appear on ECG.
• Management
• Guidewire advancement is stopped and the guidewire is withdrawn 2 cm.
• Ultrasound confirms intravascular position; transesophageal echocardiography verifies catheter tip in the superior vena cava, not the coronary sinus.
• PVCs resolve after slight withdrawal and confirmation of correct tip placement.
• Takeaway
• Real-time monitoring, imaging guidance, and prompt withdrawal of the irritant effectively manage most procedure-related arrhythmias.

• Imaging and device innovations
• Magnetic-tipped guidewires and real-time navigation systems may improve accuracy of catheter placement and reduce arrhythmia risk.
• AI-enhanced ultrasound could increase vein visualization quality and operator detection of misplacement.
• Biomarker research
• Investigation into biomarkers of myocardial irritation (e.g., procedural troponin release) may help stratify risk and guide monitoring strategies.
• Procedural protocols
• Further evidence may refine guidelines on monitoring duration post-insertion and standardize ECG-guided techniques across institutions.

• Arrhythmias during CVC placement stem from anatomical proximity and electrophysiological sensitivity of the coronary sinus and right heart structures.
• Integration of anatomy, electrophysiology, and procedural mechanics permits anticipation and prevention of most arrhythmias.
• Critical preventive measures include pre-procedural assessment and correction of electrolytes, real-time ultrasound guidance, continuous ECG monitoring, conservative guidewire advancement, and immediate withdrawal when irritation occurs.
• Persistent or unstable rhythms require pharmacologic or advanced resuscitative measures and confirmation of correct catheter position before continuing infusions.
• Advances in imaging, device design, and AI hold promise to further reduce arrhythmia incidence and improve procedural safety.