• Rezūm is a short, minimally invasive procedure for BPH that avoids major risks of TURP (fluid overload, TUR syndrome, bleeding).
• In elderly, anticoagulated patients with AF and comorbidities, neuraxial anesthesia may be contraindicated; short general anesthesia with spontaneous ventilation is a safe alternative.
• Careful titration of propofol and sevoflurane with adjuncts (fentanyl, dexmedetomidine, glycopyrrolate) minimizes hemodynamic swings and movement.
• Lithotomy positioning, risk of patient movement, and the surgical learning curve demand vigilance from the anesthesia team.
• Anticoagulation resumption and catheter care remain essential parts of postoperative planning.

References

1. McVary KT, Roehrborn CG, et al. Rezūm water vapor thermal therapy for lower urinary tract symptoms secondary to BPH: 2-year results. J Urol. 2019;202(3):601-609.
2. Gilling PJ, Barber N, Bidair M, Anderson P, Sutton M, Roehrborn C. Rezūm water vapor thermal therapy: 4-year results and safety profile. Urology. 2021;147:154-161.

Case Description

Patient: An 89-year-old male with recurrent UTIs and indwelling catheter due to obstructive BPH was scheduled for Rezūm therapy.

Comorbidities:

• Chronic atrial fibrillation on apixaban 5 mg, stopped 48 h prior.
• Recovered from left frontoparietal acute infarct.
• Hypertension on nebivolol 2.5 mg BD, sacubitril-valsartan 50 mg OD, rosuvastatin 10 mg HS.
• ECHO: Bilateral atrial enlargement, EF 55%, pulmonary artery pressure 44 mmHg.
• Renal function: Creatinine 1.6 mg/dL.
• Vitals: HR 88/min (irregular), BP 140/90 mmHg.

References

3. Yates J, Barham CP, Perry M. Perioperative risk assessment in the elderly patient. Anaesthesia. 2020;75(S1):e83-e92.

4. Weitz JI, Pollack CV. Practical management of anticoagulation in patients with atrial fibrillation. Circulation. 2017;135(7):648-651.

Anesthetic ManagementPreoperative Considerations

• High-risk profile due to advanced age, anticoagulation, AF with pulmonary hypertension, and prior stroke.
• Spinal anesthesia avoided because apixaban was stopped only 48 h earlier and renal clearance was impaired.
• Planned for short GA with spontaneous breathing to maintain safety, hemodynamic stability, and airway control.

References

5. Narouze SN, Benzon HT, Provenzano DA, et al. Interventional spine and pain procedures in patients on antiplatelet and anticoagulant medications (ASRA guidelines). Reg Anesth Pain Med. 2018;43(3):225–262.

6. Kirchhof P, Benussi S, Kotecha D, et al. 2016 ESC guidelines for the management of atrial fibrillation. Eur Heart J. 2016;37(38):2893-2962.

Intraoperative Course

• Premedication/Induction:
• Fentanyl 100 mcg IV
• Glycopyrrolate 0.2 mg IV
• Dexmedetomidine 25 mcg IV over 15 min
• Propofol 40 mg IV
• Airway: Mask ventilation with oxygen and air.
• Maintenance: Sevoflurane in oxygen-air mixture, spontaneous breathing.
• Duration: 10 minutes.
• Course: Hemodynamically stable, no adverse airway or cardiovascular events.

References

7. Weerink MAS, Struys MMRF, Hannivoort LN, et al. Clinical pharmacokinetics and pharmacodynamics of dexmedetomidine. Clin Pharmacokinet. 2017;56(8):893–913.

8. Miller RD, Eriksson LI, Fleisher LA, Wiener-Kronish JP, Cohen NH, Young WL. Miller’s Anesthesia. 9th ed. Philadelphia: Elsevier; 2020.

Postoperative

• Aldrete score 10 at 15 minutes. Pain score <3. Stable vitals, no desaturation or arrhythmia.
• Catheter left in situ.
• Pain managed with paracetamol; NSAIDs avoided due to CKD.
• Apixaban resumption planned after 24–48 h based on surgical advice.

References

9. Polderman JAW, Farhang-Razi V, Van Dieren S, et al. Adverse side effects of dexamethasone in surgical patients. Cochrane Database Syst Rev. 2018;2018(8):CD011940.

10. Douketis JD, Spyropoulos AC, Murad MH, Arcelus JI, Dager WE, Dunn AS, et al. Perioperative management of antithrombotic therapy. Chest. 2022;162(5):e207-e243.

DiscussionNeurophysiology of Pain in Rezūm

The prostate and prostatic urethra receive innervation via pelvic splanchnic nerves (parasympathetic S2–S4) and sympathetic fibers via the hypogastric plexus. Transurethral manipulation stimulates these afferents, producing visceral pain. Systemic sedation/GA blunts this; peri-prostatic infiltration can also block local nociceptive transmission.

References

11. Lang RJ, Tonta MA, Zolfaghari P, Hashitani H, Parkington HC. Contractile and electrical properties of smooth muscle in the prostate. BJU Int. 2006;97(6):1144–1153.

Pulmonary Hypertension Physiology

In this patient, pulmonary artery systolic pressure 44 mmHg indicates moderate PH. Hypoxia, hypercarbia, and acidosis all increase pulmonary vascular resistance, risking RV strain. Hence, sevoflurane was chosen for smooth control, with careful ventilation to maintain normoxia/normocapnia.

References

12. Muñoz R, Gómez-Ruiz M, et al. Anesthetic management of elderly patients with pulmonary hypertension. Curr Opin Anaesthesiol. 2021;34(1):43-50.

13. Ghofrani HA, Humbert M. The role of combination therapy in managing pulmonary arterial hypertension. Eur Respir Rev. 2014;23(134):469–475.

Pharmacology Rationale

• Fentanyl 100 mcg: Short-acting, synergistic with sevoflurane, minimal renal excretion.
• Glycopyrrolate 0.2 mg: Reduces vagal tone, prevents bradycardia in AF, decreases airway secretions.
• Dexmedetomidine 25 mcg: Provides anxiolysis, analgesia, and stable hemodynamics in frail elderly.
• Propofol 40 mg: Low-dose induction, minimizing hypotension, used in conjunction with sevoflurane.

References

14. Shafer SL, Flood P. Pharmacology of anesthetic drugs. In: Miller RD, ed. Miller’s Anesthesia. 9th ed. Philadelphia: Elsevier; 2020.

15. Fragen RJ. Pharmacology of fentanyl and its derivatives. Br J Anaesth. 1984;56(Suppl 1):3S–14S.

Clinical Relevance

Positioning Risks: Lithotomy in elderly can precipitate hip pain, neuropathy (peroneal nerve), DVT, and pressure sores. Padding and short duration reduce risks.

Risk of Movement: Even under GA, movement may compromise probe placement, risking urethral/bladder trauma. Hence titration of volatile anesthetic was critical.

Surgical Learning Curve: Early Rezūm procedures may last 20–25 min. Anesthesiologists should anticipate this variability and avoid under-dosing sedation or volatile agents.

References

16. Warner MA, Martin JT, Schroeder DR, Offord KP, Chute CG. Lower-extremity motor neuropathy associated with lithotomy positions. Anesthesiology. 1994;81(1):6–12.

17. Gilling PJ, Barber N, Bidair M, Anderson P, Sutton M, Roehrborn C. Rezūm therapy outcomes in a multi-institutional cohort. Urology. 2021;147:154–161.

Box 1: Clinical Pearls

• Short GA with mask ventilation is safe in frail elderly Rezūm patients when neuraxial is contraindicated.
• Always anticipate movement; titrate sevoflurane carefully.
• Lithotomy positioning risks increase with age—pad carefully, minimize duration.
• Early learning curve may prolong procedures → anticipate anesthetic adjustments.
• Resume anticoagulation cautiously post-procedure in collaboration with urology.

1. Introduction

Monitoring of end-tidal carbon dioxide is a cornerstone of modern anesthetic practice. It serves as a non-invasive, continuous surrogate for arterial partial pressure of carbon dioxide, reflecting the integration of cellular metabolism, cardiovascular delivery, and pulmonary ventilation. A sudden fall in end-tidal carbon dioxide during anesthesia often signals a critical intraoperative event, ranging from benign sampling errors to life-threatening pulmonary embolism.

In renal transplant recipients, intraoperative physiology is further complicated by fluid shifts, electrolyte derangements, and immunosuppressive therapies. Anesthetic vigilance in this population requires an understanding of both molecular physiology and clinical interpretation of monitoring changes.

This chapter expands upon a clinical scenario: a 31-year-old male undergoing renal transplantation, 2 hours into the procedure, experiencing a sudden end-tidal carbon dioxide drop from 27 millimeters of mercury to 18 millimeters of mercury, while remaining hemodynamically stable. Through this lens, we explore the molecular, physiological, and clinical mechanisms underlying end-tidal carbon dioxide changes, with an evidence-based algorithm for management.

References:

1. Miller RD, Cohen NH, Eriksson LI, Fleisher LA, Wiener-Kronish JP, Young WL. Miller’s Anesthesia. 9th edition. Philadelphia: Elsevier; 2020.
2. Barash PG, Cullen BF, Stoelting RK, Cahalan MK, Stock MC, Ortega R. Clinical Anesthesia. 9th edition. Philadelphia: Wolters Kluwer; 2021.

2. Physiology and Molecular Basis of Carbon Dioxide Transport2.1 Production of Carbon Dioxide

Carbon dioxide is the final metabolic product of aerobic metabolism. At the cellular level, carbon dioxide originates primarily in the tricarboxylic acid cycle during oxidative decarboxylation reactions (isocitrate to alpha-ketoglutarate, alpha-ketoglutarate to succinyl-CoA). Each glucose molecule metabolized via oxidative phosphorylation generates approximately six molecules of carbon dioxide.

Molecularly, the rate of carbon dioxide production is tightly coupled to adenosine triphosphate demand. Hypothermia or pharmacological metabolic suppression (for example: anesthetics, muscle relaxants) reduce enzymatic activity through the Q₁₀ effect, lowering carbon dioxide production.

2.2 Transport of Carbon Dioxide in Blood

• Bicarbonate (90 percent): Carbon dioxide diffuses into erythrocytes, where carbonic anhydrase II catalyzes hydration to carbonic acid → hydrogen ion + bicarbonate. Chloride shift maintains electroneutrality.
• Carbamino compounds (5 percent): Carbon dioxide binds terminal amine groups of hemoglobin to form carbaminohemoglobin.
• Dissolved carbon dioxide (5 percent): According to Henry’s law, proportional to arterial partial pressure of carbon dioxide.

2.3 Alveolar Exchange

Diffusion across the alveolar-capillary membrane is governed by Fick’s law, influenced by surface area, membrane thickness, diffusion constant, and partial pressure gradient. Carbon dioxide diffuses approximately 20 times faster than oxygen due to higher solubility.

2.4 End-Tidal Carbon Dioxide–Arterial Partial Pressure of Carbon Dioxide Gradient

Under normal conditions, end-tidal carbon dioxide is 2–5 millimeters of mercury lower than arterial partial pressure of carbon dioxide, due to alveolar dead space ventilation. This gradient widens with increased dead space (for example: pulmonary embolism, low perfusion states).

References:

3. West JB. Respiratory Physiology: The Essentials. 11th edition. Philadelphia: Wolters Kluwer; 2021.

4. Ward JP, Clarke R. An Introduction to Human Disease. 10th edition. Jones & Bartlett; 2019.

5. Lumb AB. Nunn’s Applied Respiratory Physiology. 9th edition. Philadelphia: Elsevier; 2021.

3. Capnography: Physics and Technology3.1 Principle of Infrared Absorption

Capnography is based on infrared absorption spectroscopy. Carbon dioxide has a characteristic absorption peak at 4.3 micrometers due to vibrational transitions of the carbon-oxygen double bond. The degree of infrared light absorbed is proportional to the concentration of carbon dioxide molecules in the gas stream.

3.2 Mainstream versus Sidestream Systems

• Mainstream: sensor placed directly in airway; immediate response, but adds dead space.
• Sidestream: gas sampled via tubing to an analyzer; more versatile but prone to leaks, condensation, and delay.

3.3 Common Artifacts

• Kinked sampling line → reduced carbon dioxide delivery to analyzer.
• Water trap condensation → absorption interference.
• Excessive fresh gas flow → dilutional effect.
• Analyzer pump malfunction → inadequate sample aspiration.

References:

6. Bhavani-Shankar K, Moseley H, Kumar AY, Delph Y. Capnometry and anaesthesia. Canadian Journal of Anaesthesia. 1992;39(6):617–32.

7. Kodali BS. Capnography: a comprehensive review. Anesthesiology Clinics. 2012;30(1):45–62.

4. Clinical Case Analysis: Sudden Fall in End-Tidal Carbon Dioxide4.1 Case Correlation

• Respiratory rate, tidal volume, minute ventilation, positive end-expiratory pressure unchanged → no ventilator-induced hyperventilation.
• End-tidal carbon dioxide waveform persists at lower amplitude → not total disconnection.
• Hemodynamics stable → rules out major embolism or cardiac arrest.

Interpretation: most consistent with technical artifact rather than physiological catastrophe.

References:

8. Eipe N, Doherty DR. A physiological approach to capnography. British Journal of Anaesthesia Education. 2010;10(5):161–7.

5. Differential Diagnosis of Sudden End-Tidal Carbon Dioxide Drop5.1 Technical Causes

• Sampling line leak or kink.
• Water condensation in trap.
• Analyzer malfunction.
• Dilution from high fresh gas flows.

5.2 Physiological Causes

• Pulmonary embolism (air or thrombus): sudden increase in dead space → decreased end-tidal carbon dioxide, often with hemodynamic collapse.
• Pneumothorax: decreased alveolar ventilation on one side, increased dead space.
• Hyperventilation: decreased arterial partial pressure of carbon dioxide → decreased end-tidal carbon dioxide.
• Metabolic suppression: decreased carbon dioxide production (hypothermia, anesthetic depression).

5.3 Prioritization

• Most likely: Technical artifact.
• Dangerous but less likely: Embolism, pneumothorax.
• Rare: Metabolic suppression.

References:

9. Bhavani-Shankar K, Kumar AY, Moseley H. Terminology and limitations of time capnography. Journal of Clinical Monitoring and Computing. 1995;11(3):175–82.

10. Wood KE. Major pulmonary embolism: pathophysiology. Chest. 2002;121(3):877–905.

6. Renal Transplant Context6.1 Fluid Balance

Large intraoperative volume shifts may alter pulmonary perfusion, influencing end-tidal carbon dioxide.

6.2 Electrolyte Abnormalities

• Hyperkalemia → membrane depolarization → impaired respiratory muscle function.
• Hypocalcemia → lower threshold potential → muscle irritability.

6.3 Immunosuppressants

• Calcineurin inhibitors impair mitochondrial oxidative phosphorylation, altering carbon dioxide production.
• Steroids increase gluconeogenesis, increasing carbon dioxide generation.

6.4 Surgical Risks

During vascular anastomosis, venous air entrainment is possible → risk of air embolism, presenting as sudden end-tidal carbon dioxide fall.

References:

11. O’Malley CM, Moriarty DC, Wong K. Anaesthesia for renal transplantation. British Journal of Anaesthesia Education. 2017;17(12):401–8.

12. Verma A, Prasad G. Anaesthesia for renal transplantation: Current perspectives. Indian Journal of Anaesthesia. 2016;60(11):757–64.

13. Naesens M, Kuypers DR, Sarwal M. Calcineurin inhibitor nephrotoxicity. Clinical Journal of the American Society of Nephrology. 2009;4(2):481–508.

7. Stepwise Management AlgorithmStep 1: Patient Check

• Oxygen saturation, chest movement, auscultation, airway pressures.
• Molecular: hemoglobin–oxygen affinity (Bohr effect) ensures rapid detection of ventilatory compromise.

Step 2: Monitor and Circuit Check

• Inspect sampling line, connectors, and water trap.
• Replace defective tubing.
• Check fresh gas flows.

Step 3: Physiological Consideration

• Hyperventilation? (check ventilator settings).
• Embolism? (sudden desaturation, hypotension).
• Hypothermia? (temperature, metabolic rate).

Step 4: Confirm with Arterial Blood Gas

• Arterial partial pressure of carbon dioxide–end-tidal carbon dioxide gap helps differentiate artifact versus true physiology.

Step 5: Management

• Artifact → replace line or trap.
• Hyperventilation → reduce minute ventilation.
• Embolism → notify surgical team, flood field, support hemodynamics, aspirate via central line if possible.

Step 6: Document and Communicate

Essential for safety and medico-legal protection.

References:

14. Hartmann T, Fiamoncini J, Grafetstätter M, Verstraeten S. Molecular basis of metabolic rate regulation. Molecular and Cellular Biochemistry. 2019;454(1–2):1–15.

15. American Society of Anesthesiologists. Standards for Basic Anesthetic Monitoring. ASA Guidelines. 2020.

8. Practical Mnemonic — C-A-M-E-L

• Check patient (clinical assessment plus oxygenation).
• Alter ventilator (minute ventilation).
• Monitor sampling line (integrity).
• Evaluate embolism or dead space.
• Log and communicate.

References:

16. Sinha PK, Singh B. Capnography in anaesthesia and intensive care. Indian Journal of Anaesthesia. 2003;47(6):437–46.

9. Conclusion

A sudden drop in end-tidal carbon dioxide during anesthesia demands immediate attention. In this case, a stable 31-year-old renal transplant recipient experiencing a fall from 27 millimeters of mercury to 18 millimeters of mercury most likely represents capnography artifact. However, the differential includes serious pathologies such as embolism and pneumothorax. Understanding the molecular physiology of carbon dioxide transport, the physics of capnography, and renal transplant-specific risks enables anesthesiologists to respond rapidly and appropriately.

References:

17. West JB, Luks AM. West’s Pulmonary Pathophysiology: The Essentials. 10th edition. Wolters Kluwer; 2021.

18. Nunn JF. Nunn’s Applied Respiratory Physiology. 9th edition. Elsevier; 2021.