Vagus nerve-induced cardiac arrest during percutaneous nephrolithotomy: a clinical challenge

Abstract

Background

Vagal overexcitation is a rare trigger of cardiac arrest during percutaneous nephrolithotomy, and is closely related to the abundant vagal branches in the renal hilum region. When surgical instruments or high-pressure perfusion directly stimulate the vagus nerve, sudden bradycardia or even asystole may be triggered.

Case presentation

A 56-year-old man undergoing percutaneous nephrolithotomy under general anesthesia experienced cardiac arrest due to vagus nerve stimulation following the injection of a small volume of iohexol into the renal calyx. Cardiopulmonary resuscitation was immediately performed, and the patient was transferred to the intensive care unit for further treatment and discharged after full recovery.

Conclusion

This case suggests that cardiovascular events caused by the vagus nerve reflex should be monitored during percutaneous nephrolithotomy, and emergency medicine should be prepared before operations that may stimulate the vagus nerve, such as pyelocentesis or high-pressure perfusion.

Supplementary Information

The online version contains supplementary material available at 10.1186/s12871-025-03592-z.

Introduction

Percutaneous Nephrolithotomy (PCNL) is the first-line treatment for renal stones larger than 2 cm in diameter and staghorn calculi, offering advantages such as minimal invasiveness, rapid recovery, and a high stone clearance rate. However, as an invasive procedure, PCNL carries a risk of complications, among which cardiac arrest (CA) due to vagus nerve stimulation is rare but potentially serious [1]. In our hospital, a patient experienced vagus nerve stimulation, which led to sudden CA during PCNL. Following successful resuscitation, the patient was transferred to the intensive care unit (ICU), where he recovered and was later discharged. This case report aims to explore the pathogenesis, clinical manifestations, and management of vagus nerve stimulation during PCNL, providing a reference for the prevention and treatment of such complications.

Case report

The patient was a 56-year-old male, 160 cm tall, and weighing 66 kg, with a body mass index (BMI) of 26 kg/m². On November 4, 2024, the patient underwent left PCNL laser lithotripsy in the prone position with tracheal intubation under general anesthesia at our hospital. The admission diagnosis was bilateral renal stones, and the preoperative patient’s reports were normal. Upon arrival in the operating room, the patient’s vital signs were as follows: heart rate (HR) 82 beats per minute (bpm), blood pressure (BP) 123/70 mmHg, and pulse oxygen saturation (SpO₂) 98.3%. After establishing an intravenous access, the patient received anesthetic induction with 2 mg midazolam, 0.4 mg glycopyrrolate, 20 mg etomidate, 25 µg sufentanil, 50 mg rocuronium, and 60 mg esketamine. Intubation was performed using direct laryngoscopy with a reinforced endotracheal tube under general anesthesia. Anesthesia was maintained with propofol (4.8 mg/kg/h), remifentanil (0.1 µg/kg/min), and dexmedetomidine (0.4 µg/kg/h). The surgery was initiated 30 min after anesthetic induction. At this point, the patient’s vital signs were as follows: HR 67 bpm, BP 95/71 mmHg, SpO₂ 100% with an inspired oxygen fraction (FiO₂) of 60%, arterial partial pressure of oxygen (PaO₂) was 240 mmHg, and arterial partial pressure of carbon dioxide (PaCO₂) was 39 mmHg. 25 min after the initiation of surgery, during percutaneous puncture of the renal calyx and injection of a small volume of iohexol for residual stone detection, the patient experienced a sudden cardiac arrest (CA). His HR dropped precipitously from 65 bpm to 0, the pulse oximetry waveform was lost and the airway pressure was 19 cmH₂O, the operation was immediately terminated. After a few seconds, the patient’s HR was restored to 50 bpm, however, ST-segment elevation was observed, with no measurable non-invasive blood pressure (NIBP) or SpO₂, additionally, the radial pulse was absent, and the end-tidal carbon dioxide (ETCO₂) was 10 mmHg. Immediately, all anesthetic maintenance infusions were discontinued, and the patient was rapidly repositioned from the prone to the supine position. During rapid repositioning from prone to supine, the anesthesia team maintained endotracheal tube patency, continued mechanical ventilation with FiO₂ 100%, and monitored vital signs in real time while preparing resuscitative medications and equipment. Immediately upon completion of repositioning, the patient suffered recurrent CA. Cardiopulmonary resuscitation (CPR) was initiated promptly. Subsequently, 1 mg epinephrine was administered intravenously, along with 80 mg methylprednisolone and 10 mL of 3% calcium chloride solution. Additionally, an ice cap was applied to the patient’s head, and the pupil diameter was approximately seven mm. After five minutes of resuscitation, the patient’s HR was restored, and the pupil diameter was approximately three mm. Femoral vein catheterization, radial artery catheterization, and bedside transthoracic echocardiography (TTE) were performed simultaneously to rule out pulmonary embolism, massive myocardial infarction, and cardiac tamponade as potential etiologies of CA. TTE showed no significant abnormalities in cardiac anatomy or intracardiac hemodynamics (Supplementary material 1, 2, and 3). Based on the arterial blood gas results, symptomatic treatment was administered with 200 mL of 5% sodium bicarbonate solution. After 20 min of resuscitation, ST-segment elevation had subsided, but the patient continued to experience frequent premature ventricular contractions and tachycardia. Additional treatment measures included a single intravenous bolus of phenylephrine (50 µg), continuous intravenous infusion of dopamine at a dose of 8 µg/kg/min, and intravenous infusion of 10 mL of 15% potassium chloride (KCl) diluted in 500 mL of lactated Ringer’s solution. After 90 min of resuscitation, the patient’s vital signs had stabilized, and he was transferred to the ICU. Upon leaving the operating room, his HR was 95 bpm, BP was 109/86 mmHg, and SpO₂ was 100%. Postoperatively, the patient’s blood samples were tested for immunoglobulin E (IgE) and tryptase, and both markers showed no elevation. No abnormalities were noted on postoperative bedside chest radiography and bedside TTE. Two days postoperatively, the patient was successfully weaned from mechanical ventilation, and on postoperative day 4, he was discharged in good condition. The patient’s intraoperative arterial blood gas results are shown in Table 1, and postoperative arterial blood gas results are presented in Table 2. Dynamic changes in B-type natriuretic peptide (BNP) and myocardial injury markers (high-sensitivity cardiac troponin I (hs-cTnI), myoglobin (Mb), and creatine kinase-MB (CK-MB)) are displayed in Table 3.

Table 1.

Intraoperative arterial blood gas results

Time	PH	PCO2 (mmHg)	PO2 (mmHg)	SpO2 %	Hct %	Hb (g/dL)	Na+ (mmol/L)	K+ (mmol/L)	Ca2+ (mmol/L)	Glu (mmol/L)	Lac (mmol/L)	BE (mmol/L)	HCO3- (mmol/L)	AG (mmol/L)	OI (mmHg)	FiO2 %
5 min post-CA	7.26	43.3	112	98	44	13	142	4.4	1.18	11.7	6.5	−7.6	18.5	19.5	112	100
21 min post-CA	7.267	51.4	260	100	21.1	13.5	146	2.7	1.24	12.6	8.1	−3.5	21.5	14.5	260	100
24 min post-CA	7.25	50.7	369	100	39.9	13	145	2.8	1.18	12.3	8.7	−4.8	20.3	21.7	369	100
31 min post-CA	7.247	45.8	418	100	37.5	12.2	145	3.9	1.15	11.6	9.7	−7.3	18.6	24.4	418	100
71 min post-CA	7.29	40	365	100	39.6	12.9	145	3.8	1.11	12.3	9.8	−7.3	18.9	17.1	365	100

CACardiac arrest, PH Potential of Hydrogen, PCO₂ Partial Pressure of Carbon Dioxide, PO₂ Partial Pressure of Oxygen, SpO₂ Oxygen Saturation of Hemoglobin, Hct Hematocrit, Hb Hemoglobin, Na⁺ Sodium Ion, K+ Potassium Ion, Ca²⁺ Calcium Ion, Glu Glucose, Lac Lactate, BE Base Excess, HCO^3- Bicarbonate Ion, AG Anion Gap, OI Oxygenation Index, FiO2 Fraction of Inspired Oxygen

Table 2.

Postoperative arterial blood gas results

Time	PH	PCO2 (mmHg)	PO2 (mmHg)	SpO2 %	Hb (g/dL)	Na+ (mmol/L)	K+ (mmol/L)	Ca2+ (mmol/L)	Glu (mmol/L)	Lac (mmol/L)	BE (mmol/L)	HCO3- (mmol/L)	AG (mmol/L)	OI (mmHg)	FiO2 %
0.25 h post-ICU transfer	7.318	38.7	114.7	98	14.4	144.5	4.2	1.14	13.5	8.8	−5	20.3	16.4	191.2	60
2.05 h post-ICU transfer	7.278	42.4	61.9	87.5	14.8	144.4	4.2	1.13	16.1	8.6	−6	19.4	17.1	296.2	20.9
3.35 h post-ICU transfer	7.387	33.4	133.9	98.9	13	142.2	4.2	1.14	14.7	6.2	−3.3	21.7	13.2	334.6	40
7.55 h post-ICU transfer	7.437	30.9	154.4	98.4	8.7	142	3.7	1.17	11.7	4.8	−2	22.8	10.3	385.9	40
POD 1, 5:40	7.424	29.8	157.3	99.2	12.2	141.1	3.6	1.17	9	3.1	−3	21.9	9.8	393.2	40
POD 1, 12:36	7.397	35.6	143.2	99	11.9	143.2	3.9	1.15	6.1	1.6	1.7	23	9.4	358	40
POD 1, 21:06	7.454	32.8	155.7	99.2	11.8	141.5	3.9	1.18	7.5	1.2	0.5	24.9	8	389.2	40
POD 2, 6:11	7.461	30.6	139.9	99	12.1	142.2	3.8	1.19	6.6	0.9	−0.4	24.1	9.9	349.8	40
POD 2, 9:39	7.451	32.8	144.8	99.1	12.2	141.9	3.9	1.19	7.2	1.2	0.3	24.7	8.5	362	40
POD 2, 15:12	7.425	37.4	82.9	96	11.6	141.6	4	1.19	7.2	0.6	1.1	25.4	7.3	251.3	33
POD 2, 20:40	7.446	35.5	118.3	98.6	12.2	141.9	3.9	1.2	6.2	0.5	1.5	25.7	8.4	358.5	33
POD 3, 5:13	7.440	32	119.1	98.6	12.1	140.3	4	1.18	5.5	0.5	−0.9	23.7	7.7	360.9	33

ICU Intensive Care Unit, POD Postoperative Day, PH Potential of Hydrogen, PCO₂ Partial Pressure of Carbon Dioxide, PO₂ Partial Pressure of Oxygen, SpO₂ Oxygen Saturation of Hemoglobin, Hb Hemoglobin, Na⁺ Sodium Ion

Table 3.

Dynamic changes in B-Type natriuretic peptide and myocardial injury markers

Time	BNP (pg/ml)	hs-cTnI (pg/ml)	MB (ng/ml)	CK-MB (ng/ml)
3 days preoperatively	31	4.3	39.7	3
0.25 h post-ICU transfer	20	15.0	29.5	1.4
9.00 h post-ICU transfer	68	400.0	154.6	3.9
POD 1, 10:52	83	389.5	169.9	5.5
POD 2, 9:54	21	227.5	87.4	1.7
POD 3, 6:16	42	121.5	52	1.5
POD 4, 6:52	18	44.1	57.7	2.3

ICU Intensive Care Unit, BNP B-type natriuretic peptide, hs-cTnI High-sensitivity cardiac troponin I, MB Myoglobin, CK-MB Creatine kinase-MB

Discussion

PCNL is a well-established technique, with common complications including bleeding, infection, drainage tube displacement, perirenal hematoma, and adjacent organ injury. Reports of events induced by the vagal nerve reflex are rare. Current literature on the causes of CA during nephroscopic surgery includes the following:

1. Inadvertent damage to the pleura during the procedure, where large volumes of irrigation fluid enter the pleural cavity through the pleural injury, can result in amassive pleural effusion. This can lead to acute respiratory dysfunction and circulatory failure, ultimately resulting in CA.

2. Excessive perfusion pressure during irrigation causes the irrigating fluid to passthrough the perirenal space into the retroperitoneal cavity and potentially into the mediastinum via potential channels. Even small amounts of fluid can lead to mediastinal compression and superior vena cava syndrome, resulting in acute circulatory failure and CA [2].

3. The injection of air into the renal pelvis through a ureteral catheter for pyelography can lead to an air embolism [3].

4. The release of stone fragments into the bloodstream during lithotripsy can trigger disseminated intravascular coagulation (DIC) [4]. A review of the existing literature revealed that vagal nerve reflexes most commonly occur in laparoscopic surgeries or situations involving visceral traction, such as during the establishment of pneumoperitoneum [5].

In these cases, traction on the peritoneum is considered the most common cause of bradycardia triggered by the vagal nerve reflex; in this case, the triggering factor was direct stimulation of the urinary organs. The abdominal branch of the vagus nerve courses caudally and posteriorly to join the celiac plexus. It runs along the renal artery with sympathetic fibers, enters the renal parenchyma, and forms a network of nerve endings in the glomeruli and renal tubules, thereby regulating renal function. When the surgeon injected a small volume of iohexol into the renal calyx, it directly stimulated the vagus nerve. The regulation of systemic BP involves both afferent and efferent fibers of the vagus nerve. When the vagus nerve is compressed or stimulated, afferent impulses are transmitted to the central nervous system, which can reflexively inhibit the heart through parasympathetic fibers, ultimately leading to CA. This highlights the need for anesthesiologists to be vigilant regarding the occurrence of vagal reflexes during these procedures.

Intraoperative vagal nerve reflex is mostly triggered by mechanical stimuli (traction, compression) and hypovolemia, which leads to abnormally increased vagal nerve excitability. This increase in excitability causes bradycardia and peripheral vasodilation, resulting in clinical symptoms involving multiple systems, including the circulatory, respiratory, neurological, and digestive systems. In severe cases, it can even lead to CA.

This condition should be differentiated from hypoglycemia, anaphylactic shock, hemorrhagic shock, septic shock, myocardial infarction, cardiac tamponade, pulmonary embolism, and pneumothorax. In the present case, preoperative examinations revealed no significant abnormalities, and no notable intraoperative blood loss was observed. Additionally, bedside TTE, bedside chest radiography, IgE levels, and tryptase levels all showed no abnormalities. CA occurred immediately after the injection of a small volume of iohexol into the renal calyx, with a clear trigger: percutaneous puncture of the renal calyx stimulating the vagus nerve and causing CA. This should be differentiated from an allergic reaction. As a low-osmolar iodinated contrast agent, iohexol has a relatively low overall incidence of allergic reactions, ranging from 0.3% to 1.4%, and the majority of these reactions are mild to moderate in severity [6]. Allergic reactions typically present with the classic triad of erythema, elevated airway pressure, and cardiovascular abnormalities, as well as elevated levels of IgE and tryptase [7]. The patient had no history of allergy prior to surgery. After iohexol injection, the patient’s HR dropped from 65 bpm to 0 within seconds, BP was undetectable, airway pressure showed no significant changes, and no erythema was observed on the skin, additionally, no elevation was noted in the levels of IgE and tryptase. Therefore, an allergic reaction can be excluded from the differential diagnoses.

During surgery, when a vagal nerve reflex occurs, it is crucial to closely monitor vital signs such as BP, HR, respiration, and blood glucose levels. If the HR is < 60 bpm and systolic blood pressure (SBP) is < 90 mmHg, and after excluding shock, atropine can be administered to relieve bradycardia, diazepam for sedation, and dopamine for vasopressor support until the patient’s hemodynamic status stabilizes [8]. This case provides a detailed review of the treatment process for CA caused by the vagal nerve reflex, exploring the underlying mechanisms, clinical manifestations, and management strategies, and offers valuable experience and insights into related fields.

This case report presents an instance of sudden CA during general anesthesia with endotracheal intubation for PCNL, which was successfully resuscitated. The patient experienced CA due to direct stimulation of the renal vagus nerve during the surgery. After CPR and pharmacological intervention, the patient fully recovered and was subsequently discharged. This case emphasizes the potential for serious complications, such as CA, during renal surgery, particularly when the procedures stimulate the vagus nerve. This case report provides a detailed review of the treatment process for CA caused by the vagal nerve reflex, exploring the underlying mechanisms, clinical manifestations, and management strategies. It offers valuable experience and highlights the importance of vigilance for such rare but critical events during PCNL.

Abbreviations

PCNL

Percutaneous Nephrolithotomy

CA

Cardiac Arrest

ICU

Intensive Care Unit

BMI

Body Mass Index

HR

Heart Rate

bpm

Beats Per Minute

BP

Blood Pressure

SpO₂

Oxygen Saturation of Hemoglobin

FiO₂

Fraction of Inspired Oxygen

PO₂

Partial Pressure of Oxygen

PCO₂

Partial Pressure of Carbon Dioxide

NIBP

Non-Invasive Blood Pressure

ETCO₂

End-Tidal Carbon Dioxide

CPR

Cardiopulmonary Resuscitation

TTE

Transthoracic Echocardiography

KCl

Potassium Chloride

IgE

Immunoglobulin E

hs-cTnI

High-Sensitivity Cardiac Troponin I

Mb

Myoglobin

CK-MB

Creatine Kinase-MB

DIC

Disseminated intravascular coagulation

SBP

Systolic Blood Pressure

Authors’ contributions

Bingyi Wang: Case management, manuscript drafting.Xiaodan Wang, Chen Wang, Zitian Chen, Qiaoyu Han: Data collection, literature review.Yi Feng, Ran Zhang, Luyang Jiang: Critical revision, final approval.

Funding

This work was supported by the Research and Development Foundation of Peking University People’s Hospital (Project Number: RDL2024-11).

Data availability

The datasets used and/or analyzed during the current study are available from the corresponding author upon reasonable request.

Declarations

Ethics approval and consent to participate

Not applicable.

Consent for publication

Written informed consent was obtained from the patient for the publication of this case report and any accompanying images. A copy of the consent form is available for review by the editor of this journal.

Competing interests

The authors declare no competing interests.