Introduction
This chapter describes an anesthetic strategy for a 78-year-old man with Mobitz type II second-degree atrioventricular (AV) block who is scheduled for channel transurethral resection of the prostate (TURP) for an 88-mL prostate. Because of his conduction disease, reduced left ventricular function and diastolic dysfunction, advanced age, and the hemodynamic stresses of TURP, the plan uses a general anesthetic with sevoflurane, a single small dose of cisatracurium (≈4 mg), and an i-gel size 4 airway. Propofol and neuraxial techniques are avoided because of their predictable vasodilatation and negative inotropic effects in this high-risk cardiac patient. The following text integrates relevant pathophysiology, device management, TURP-specific issues, anesthetic rationale, vasopressor choice, expected hemodynamic challenges, fluid-shift management, and practical perioperative steps, with emphasis on molecular, anatomical, and pharmacologic mechanisms.
Patient profile
The patient is a 78-year-old man with Mobitz type II AV block attributed to His-Purkinje system disease (fibrosis or ischemia with sodium-channel—SCN5A—related dysfunction). He is undergoing channel TURP for bladder outlet obstruction caused by an 88-mL prostate. A temporary transvenous pacemaker (Vitatron MEP 3000) was placed preoperatively; device settings were recorded as rate 80 ppm, output 7 mA, sensitivity 3 mV, A/SYNC mode ON. A measured pulse of 51/min in the presence of these settings suggests possible intermittent loss of capture (lead instability, local myocardial changes, threshold elevation, or impending battery/end-of-service issue). Echocardiography shows LVEF ≈40% (mild–moderate systolic impairment), grade II diastolic dysfunction consistent with impaired relaxation and reduced SERCA2a function, bi-atrial enlargement, a sclerotic aortic valve with mild aortic regurgitation, grade I mitral regurgitation, and an estimated RVSP ≈24 mmHg + RAP. Preoperative blood pressure was 106/65 mmHg with SpO2 95% on room air. Advanced age, low baseline blood pressure and conduction disease place him at increased perioperative cardiovascular risk. (Epstein et al. 2013; Issa et al. 2019.)
Cardiovascular considerationsMobitz type II AV block — pathophysiology and perioperative risk
Mobitz type II AV block reflects conduction failure in the His-Purkinje system, commonly from degenerative fibrosis (Lenègre–Lev) or ischemic injury. Because the block is infranodal, vagolytic agents such as atropine are frequently ineffective; the block is strongly associated with progression to complete heart block (annual progression reported in the literature is substantial). Perioperative stimuli (surgical vagal input, electrolyte shifts, ischemia, anesthetic drugs) can precipitate profound bradycardia or asystole in this setting, so reliable pacing is essential. (Kusumoto et al. 2018; Mangrum & DiMarco 2000.)
Systolic and diastolic dysfunction — implications for anesthetic care
Systolic impairment (LVEF ≈40%, fractional shortening reduced) indicates limited contractile reserve. At the cellular level, reduced SERCA2a activity and altered calcium handling decrease contractility and relaxation efficiency. Diastolic dysfunction (grade II) indicates abnormal ventricular filling and increased left-sided filling pressures; small changes in preload or increases in heart rate can precipitate pulmonary congestion. Bi-atrial enlargement signals chronic pressure/volume loading. These physiology facts inform fluid strategy, vasopressor/inotrope selection and the need to avoid precipitous reductions in systemic vascular resistance or sudden tachycardia. (Nagueh et al. 2016; Yancy et al. 2013.)
Valvular and structural disease
A sclerotic aortic valve and mitral annular calcification increase afterload and impede ventricular compliance; even mild aortic regurgitation or mitral regurgitation contributes to volume load. Mild pulmonary hypertension (RVSP ~24 mmHg + RAP) increases right-sided vulnerability during fluid shifts and positive-pressure ventilation. (Nishimura et al. 2014; Baumgartner et al. 2017.)
Pacemaker considerations and apparent dysfunction
The temporary transvenous pacemaker in place (reported settings: rate 80 ppm, output 7 mA, sensitivity 3 mV, A/SYNC ON) requires careful scrutiny. A slow native pulse (51/min) despite these settings suggests intermittent capture failure or sensing issues. Causes include lead dislodgement, local myocardial edema or injury, elevated pacing threshold (electrolyte abnormalities, ischemia), or hardware/battery problems. Pacemaker dependency or high pacing reliance dramatically raises the stakes for immediate intraoperative troubleshooting and ready external/transcutaneous pacing backup. (Wilkoff et al. 2002; Bernstein et al. 2002.)
Channel TURP — procedural implications for anesthesia
Channel TURP is a tissue-sparing procedure designed to relieve bladder outlet obstruction while minimizing irrigation-fluid absorption and the classic TURP syndrome. Nevertheless, this patient’s large gland (88 mL) can prolong operative time and bleeding risk. Although saline irrigation limits the risk of severe hyponatremia from irrigation fluid, even modest absorption can produce hemodilution, electrolyte disturbances and neurologic or cardiac sequelae. Urethral manipulation during TURP can provoke intense vagal reflexes (muscarinic-mediated), potentially causing sudden bradycardia — a particularly dangerous event in someone with infranodal block. Fluid shifts, bleeding and vagal responses therefore require vigilant monitoring and a low threshold to treat pacing or vasopressor support. (Gravenstein 1997; Mebust et al. 1989.)
Age, comorbidities and additional risks
Advanced age reduces physiologic reserve: baroreceptor sensitivity is blunted, mitochondrial oxidative capacity declines, and anesthetic sensitivity increases. Coexisting coronary disease or diabetes (if present) raises the risk of perioperative ischemia. Chronic medications such as beta-blockers can mask compensatory tachycardia and may worsen conduction disturbances. Electrolyte derangements (especially hyponatremia or hyperkalemia after irrigation or transfusion) may increase pacing thresholds or provoke arrhythmias. (Mangano & Goldman 1995; Fleisher et al. 2014.)
Why spinal or neuraxial anesthesia was avoided
A spinal or high neuraxial block causes sympathetic blockade and a fall in systemic vascular resistance that can produce precipitous hypotension — poorly tolerated in a patient with low LVEF, diastolic dysfunction, and marginal perfusion pressure (baseline MAP is low). Reduced SVR and bradycardia could precipitate loss of coronary perfusion and heart failure; neuraxial bleeding risk in the setting of perioperative anticoagulation or bleeding from TURP further argues against this approach. General anesthesia allows tighter, more gradual control of hemodynamics and rapid intervention for conduction or pacing problems. (Rodgers et al. 2000; Horlocker et al. 2018.)
Why propofol was avoided
Propofol produces dose-dependent vasodilation (partly via nitric oxide pathways) and direct negative inotropy through inhibition of L-type calcium channels. In a patient with LVEF ≈40% and limited hemodynamic reserve, induction with propofol risks profound hypotension and further myocardial depression. Propofol also increases vagal tone in some patients, which is undesirable here. By contrast, a carefully titrated inhalational technique using sevoflurane can permit smoother hemodynamic control. (Sprung et al. 2001; Ebert et al. 1992.)
Anesthetic plan: general anesthesia
Induction and maintenance: Use sevoflurane, titrated to effect (typical target 1–2% end-tidal equivalent to appropriate MAC for his age) while maintaining MAP ≥65 mmHg. Avoid rapid deepening of anesthesia that would cause vasodilatation.
Muscle relaxation: Cisatracurium is chosen for neuromuscular blockade because of Hofmann elimination and minimal direct cardiovascular effects; a small dose (~0.05 mg/kg; approximately 4 mg for an 80-kg patient) provides adequate relaxation with predictable recovery.
Airway: An i-gel size 4 is preferred to minimize airway stimulation and abrupt vagal reflexes during laryngoscopy and insertion; confirm placement with capnography and chest rise.
Adjuncts: Fentanyl (1–2 µg/kg) for analgesia; neuromuscular reversal with neostigmine (0.04–0.07 mg/kg) plus glycopyrrolate (≈0.01 mg/kg) if needed. All drugs are titrated to effect with continuous hemodynamic monitoring. (Eger 1994; Lien et al. 1995.)
Pacemaker management protocol — perioperative steps
- Preoperative verification: Immediate preoperative interrogation by cardiology/arrhythmia team to confirm lead integrity, battery status, and capture/sensing thresholds. Document programmed mode and thresholds.
- Monitoring: Continuous 5-lead ECG and invasive arterial pressure monitoring are mandatory. Consider TEE or at least arterial waveform analysis in the event of unexplained hypotension. Maintain SpO2 monitoring and have transcutaneous pacing pads placed and ready.
- Programming and adjustments: If capture failure is suspected, increase pacing output (to 10–15 mA as needed) and consider a higher backup rate (90–100 ppm) if bradycardia produces hypotension. Sensitivity settings may be adjusted to avoid over- or under-sensing (typical adjustments depend on device behavior; examples: lower to 2–2.5 mV for oversensing or increase sensitivity threshold for undersensing depending on the situation).
- Intraoperative management of bradycardia/asystole: At the first sign of loss of capture or sustained bradycardia, maximize output and rate, initiate transcutaneous pacing if transvenous capture cannot be immediately restored, and treat reversible causes (electrolytes, ischemia, drug effects). Atropine is unlikely to be effective for infranodal block but may be used if an additional vagal component is suspected.
- Electrolyte and metabolic control: Monitor and promptly correct sodium, potassium and acid-base disturbances that can raise pacing thresholds.
- Consultation and documentation: Keep cardiology/electrophysiology involved for reprogramming and decisions about lead revision or device replacement. Document all adjustments and patient responses in the chart. (Atlee & Bernstein 2001; Rozner 2012.)
Management during common hemodynamic changes
- Hypotension: First consider increasing pacing rate/output if hypotension is rate-dependent; initiate vasopressor support (norepinephrine preferred) and correct volume status carefully.
- Bradycardia/asystole: Maximize device output and perform transcutaneous pacing if necessary; treat reversible causes.
- Tachyarrhythmia: Adjust pacing parameters downward and address precipitating causes.
- Fluid shifts: Be prepared to alter pacing output if thresholds change with electrolyte or volume status.
Vasopressor and inotrope selection
Choice of vasoactive drugs should match the hemodynamic derangement and myocardial reserve:
- Norepinephrine (α-1 and β-1 agonist) is the vasopressor of choice for hypotension with relative vasodilation and provides some inotropy. Typical infusion: 0.01–0.05 µg/kg/min titrated to effect.
- Phenylephrine (pure α-1 agonist) raises systemic vascular resistance and can be used as boluses (50–100 µg) or infusions (0.5–2 µg/kg/min) when reflex tachycardia is undesirable; caution in low-output states because afterload increase can reduce stroke volume.
- Dobutamine (predominant β-1 agonist) may be needed to augment contractility (2–5 µg/kg/min) if systolic dysfunction limits cardiac output.
- Dopamine is generally avoided in this context because of greater chronotropic and myocardial oxygen consumption effects. (Overgaard & Dzavík 2008; De Backer et al. 2010.)
Predicted hemodynamic challenges
Expect episodes of hypotension and low forward output related to baseline cardiomyopathy and vasodilatant elements of anesthesia, and an increased risk of pulmonary edema from diastolic dysfunction if intravascular volume is not tightly controlled. Pacemaker dependency and intermittent capture failure raise the risk of sudden asystole. Even small intraoperative fluid shifts or bleeding may produce clinically significant changes in perfusion. Careful titration of anesthetic depth, proactive pacing adjustments and prompt vasoactive support will be required. (Vincent & De Backer 2013; Zile & Brutsaert 2002.)
Fluid-shift recognition and management
Preoperative baseline assessment: Look for signs of volume overload (jugular venous distension, peripheral edema) and obtain baseline laboratory values including sodium and hematocrit.
Intraoperative monitoring: Continuous arterial pressure, urine output goals (>0.5 mL/kg/hr as a minimum), and CVP (if used) in the range of 8–12 mmHg for guidance in this patient with diastolic dysfunction. SpO2 falling below 90% or new crackles should trigger evaluation for pulmonary edema.
Indicators of fluid events: Confusion or hypotension may suggest absorption; a falling hematocrit suggests hemorrhage; rising airway pressures, hypoxia or pink frothy sputum suggest pulmonary edema.
Management principles:
- Give judicious isotonic crystalloid (0.9% NaCl) in boluses appropriate to the clinical context (e.g., 5–10 mL/kg as guided by hemodynamics).
- For symptomatic hyponatremia from irrigation absorption, use small boluses of hypertonic saline (3% NaCl, 1–2 mL/kg) with neurology and electrolyte guidance.
- Use loop diuretics (e.g., furosemide 10–20 mg IV) for pulmonary edema once perfusion is supported and if intravascular volume is judged excessive.
- Management must weigh the risk of under-filling (worsening hypotension) against precipitating pulmonary edema in a patient with impaired relaxation. (Hahn 2006; Myburgh & Mythen 2013.)
Perioperative management plan
Preoperative optimization
- Obtain cardiology review and formal device interrogation; arrange reprogramming or battery/lead management as indicated.
- Baseline ECG, echocardiogram review, and correction of electrolyte abnormalities.
- Prepare transcutaneous pacing pads and confirm availability of pacing/defibrillation equipment.
Intraoperative management
- Monitoring: continuous ECG, invasive arterial pressure, SpO2, and consideration of TEE if hemodynamics become unstable.
- Anesthetic technique: sevoflurane titrated to effect, fentanyl for analgesia, cisatracurium for neuromuscular relaxation, airway managed with i-gel size 4 if appropriate.
- Pacemaker: follow the device protocol above with readiness to increase output, raise rate, or convert to external pacing. Keep cardiology on call.
- Vasopressors/inotropes: norepinephrine first-line for hypotension; add dobutamine if contractility support is required.
- Fluids: tight, goal-directed crystalloid therapy; treat clinically significant hyponatremia or volume overload per guidelines.
Postoperative care
- Postoperative monitoring in a high-dependency or ICU setting for 24–48 hours given pacemaker dependency, borderline cardiac function, and TURP-related risks.
- Immediate postoperative device interrogation and reassessment of thresholds; plan for definitive lead/device management or replacement if indicated.
- Continue close electrolyte and fluid management; monitor for neurologic changes and signs of TURP syndrome despite the lower risk with channel TURP. (Fleisher et al. 2014; Apfelbaum et al. 2011.)
Conclusion
A patient with Mobitz type II AV block, reduced LV systolic function, diastolic dysfunction and a temporary transvenous pacemaker undergoing channel TURP is best managed with a carefully titrated general anesthetic that minimizes myocardial depression and avoids sudden sympathetic withdrawal. Sevoflurane, cisatracurium, an i-gel airway and judicious opioid use provide a balanced technique. Continuous invasive monitoring, proactive pacemaker management (including the ability to increase output and rate or institute external pacing), and norepinephrine-based hemodynamic support form the backbone of intraoperative management. Judicious fluid therapy and early postoperative ICU monitoring complete the perioperative strategy. Multidisciplinary coordination with cardiology/electrophysiology is essential.
Correction and disclaimer: an earlier podcast statement that this patient had a permanently implanted pacemaker was incorrect. In fact, the patient had Mobitz type II AV block for which a temporary transvenous pacemaker was inserted by the cardiology team prior to surgery. The earlier wording resulted from an editing oversight during AI-assisted audio processing; we regret the error and have provided this clarification.
