A Rare Case of Coronary Artery and Cerebral Air Embolism Associated with Catheterization and General Anesthesia

doi:10.21203/rs.3.rs-8378024/v1

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Case Report

A Rare Case of Coronary Artery and Cerebral Air Embolism Associated with Catheterization and General Anesthesia

https://doi.org/10.21203/rs.3.rs-8378024/v1

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We report a rare case of coronary and cerebral air embolism (AE) following radiofrequency ablation (RFA) for ventricular premature beats (VPBs) combined with patent foramen ovale (PFO) closure. This study aims to highlight the role of anesthesia-induced negative pressure in the pathogenesis of AE.

Case Presentation: A 67-year-old male was admitted due to palpitations. Twenty-four-hour Holter monitoring revealed 10,469 VPBs. Transthoracic and transesophageal echocardiography confirmed PFO with severe right-to-left shunt. The patient first underwent RFA under local anesthesia, followed by planned PFO closure under general anesthesia. After induction of general anesthesia, the patient developed bradycardia, junctional escape rhythm, and ST-segment elevation in leads Ⅱ and Ⅲ. Transesophageal echocardiography detected massive air bubbles in the left atrium, aorta, and inferior vena cava. Intraoperative monitoring showed a sudden decrease in end-tidal carbon dioxide (ETCO₂) from 35 mmHg to 28 mmHg (a reduction of 7 mmHg) and a drop in jugular bulb pressure (JBP) to -2 mmHg. Postoperative brain computed tomography (CT) and magnetic resonance imaging (MRI) demonstrated cerebral air accumulation and multiple small infarcts. Postoperative myocardial enzymes were significantly elevated. The patient was managed with antiepileptic drugs, neuroprotective agents, and supportive care.

Discussion: AE is a life-threatening complication of cardiac interventional procedures. In this case, the key pathogenic factor was anesthesia-induced negative pressure: general anesthesia caused decreased central venous pressure (CVP) due to relative hypovolemia and increased intrathoracic negative pressure during laryngeal mask ventilation, creating a pressure gradient between the atmosphere and the vascular system ^1,2. Additionally, the SL1 sheath with an indwelling guidewire exhibited reduced airtightness—when negative pressure falls below − 13.4 mmHg, air leakage may occur between the catheter sheath and guidewire, enabling air entry ³. Our in vitro pressure testing of the SL1 sheath (conducted under standard laboratory conditions: 25°C, simulated physiological saline environment, n = 5 replicates) confirmed that the sheath-end cap assembly maintained integrity under negative pressure up to 54 kPa without a guidewire (exceeding the YY0450.1-2020 standard of 42 kPa), but only tolerated 16 kPa when a 0.035-inch guidewire (Biosense Webster) was inserted non-coaxially. PFO and iatrogenic atrial septal defect further facilitated paradoxical air embolism into the systemic circulation, leading to coronary and cerebral ischemia⁴. Anesthesia-induced negative pressure is closely associated with AE pathogenesis: changes in sympathetic tone after anesthesia induction (causing a mean 6.9 mmHg reduction in left atrial pressure³, switching from mechanical ventilation to spontaneous breathing, and body position adjustments during recovery can all expand the pressure gradient between veins and the atmosphere, promoting air aspiration^2,3.

Conclusion: Anesthesia-induced negative pressure is a critical driver of AE in cardiac interventional procedures. Perioperative management should focus on maintaining CVP (5–15 cm H₂O) ^1,5, optimizing sheath sealing (ensuring guidewire-catheter coaxiality), and closely monitoring for AE using transesophageal echocardiography (TEE) or precordial Doppler (PCD) with simultaneous tracking of JBP (> 0 mmHg) and ETCO₂ in patients with right-to-left shunts ^5,6.

Cardiac radiofrequency ablation

Patent foramen ovale

Air embolism

General anesthesia

Iatrogenic complications

Radiofrequency ablation (RFA) is a first-line treatment for symptomatic ventricular premature beats (VPBs) refractory to medical therapy¹. Patent foramen ovale (PFO), a common congenital cardiac defect with a prevalence of 20–30% in adults⁶, is frequently associated with paradoxical embolism, which increases the risk of stroke and systemic ischemia⁷. Although RFA and PFO closure are generally safe, rare but fatal complications such as air embolism (AE) may occur⁸. AE develops when air enters the vascular system, resulting in obstruction of blood flow to vital organs. The pathogenesis of AE involves two core conditions: communication between air and the vascular system, and a pressure gradient driving air entry². Previous studies have identified iatrogenic factors (e.g., catheter manipulation, sheath disconnection) as major causes of AE⁹. However, the role of anesthesia-induced negative pressure in AE has not been fully emphasized, especially in the setting of combined RFA and PFO closure. Anesthesia-related negative pressure can arise from multiple mechanisms relevant to this case: general anesthesia-induced reduction in CVP, increased intrathoracic negative pressure during spontaneous breathing phases of laryngeal mask ventilation, and relative hypovolemia from preoperative fasting³. These factors expand the pressure gradient between the vascular system and the atmosphere, creating favorable conditions for air aspiration.^2,3

In specific cardiac interventional scenarios, the risk of AE is further elevated. For example, semi-sitting neurosurgical procedures (with similar venous negative pressure mechanisms) have an overall venous air embolism (VAE) incidence of 0%-76%, with clinically significant VAE (requiring intervention) occurring in 0%-14%¹. The anesthetic recovery period (5–15 minutes after extubation) is a high-risk window for AE, as demonstrated by case reports of sudden hypotension (120→40 mmHg), decreased oxygen saturation (80%), and massive air bubbles in the right heart and pulmonary arteries detected by TEE ².

Herein, we report a case of coronary and cerebral AE following RFA and planned PFO closure, with a focus on the mechanistic role of anesthesia-induced negative pressure. We also review relevant literature and compare with similar cases to provide insights into the prevention and management of this complication.

A 67-year-old male was admitted to our hospital with "recurrent palpitations for 2 years, aggravated for 1 month". He had a history of recurrent unexplained migraines, characterized by intermittent headaches accompanied by visual disturbances, which worsened during the Valsalva maneuver. PFO-related migraine was highly suspected. He had no underlying diseases such as hypertension, diabetes mellitus, or coronary artery disease.

Preoperative Examinations

Holter Monitor: Twenty-four-hour Holter monitoring recorded a total of 85,703 heartbeats with 10,469 VPBs (12.2% burden), showing a right bundle branch block pattern in lead V1, suggesting a possible left-heart origin.
Head CT: Multiple lacunar cerebral infarctions were detected.
Echocardiography: PFO with grade Ⅱ right-to-left shunt at rest, which aggravated to grade Ⅲ during the Valsalva maneuver (Fig. 1a, b); left atrial diameter was 36 mm, left ventricular ejection fraction was 62%, and no pericardial effusion was noted.
Laboratory Indicators: Cardiac enzymes (myoglobin, CK-MB, high-sensitivity troponin) and NT-pro BNP were within the normal range.

Surgical Procedure

After the patient signed the informed consent form, "radiofrequency ablation for VPBs + PFO closure" was performed concurrently:

Surface and intracardiac electrograms were recorded using the system from Sichuan Jinjiang Electronic Medical Device Technology Co, Ltd., and mapping was conducted with the CARTO 3 three-dimensional electroanatomic mapping system (Biosense Webster). Right femoral vein puncture was performed to place an 8.5Fr (2.83mm) SL1 sheath, followed by advancement of a ThermoCool SmartTouch Surround Flow ablation catheter (Biosense Webster) into the left atrium. A second right femoral vein puncture was performed, and a 6Fr sheath (for 10-pole mapping electrodes) was inserted via the left femoral vein. Through 3D mapping with the CARTO system, the origin of VPBs was localized at the 3 o'clock position of the right tricuspid annulus, 20 ms ahead of the surface electrocardiogram. Ablation was delivered at the right coronary sinus (35 W, 55°C, irrigated saline flow rate 20 ml/min); VPB frequency decreased after 5 seconds of ablation, and VPBs disappeared completely after RFA.

To proceed with PFO closure, the SL1 sheath (with an indwelling 0.035-inch guidewire) was retained in the left atrium, and the mapping electrode was placed in the coronary sinus (Fig. 2). General anesthesia was induced with intravenous fentanyl citrate (5 µg), 0.2% remifentanil hydrochloride (5 ml/h), midazolam (0.5 mg), etomidate (5 mg), dexmedetomidine (10 ml/h) and remimazolam (5 mg). No endotracheal intubation was performed, and anesthesia was maintained with laryngeal mask airway (LMA) ventilation and pure oxygen inhalation. Intraoperative ventilation parameters: tidal volume 400 ml, respiratory rate 12 breaths/min, volume-controlled ventilation mode, inspiratory/expiratory (I:E) ratio 1:2, positive end-expiratory pressure (PEEP) 3 cmH₂O. Intraoperative monitoring included pulse oxygen saturation (SpO₂) and radial artery pressure、ugular bulb pressure (JBP)、end-tidal carbon dioxide(ETCO₂).

Intraoperative Complications and Management

Ten minutes after anesthesia induction, the patient's blood pressure dropped to 85/60 mmHg, heart rate decreased to 50 beats per minute, and electrocardiography showed junctional escape rhythm (Fig. 4a) and ST-segment elevation in leads Ⅱ/Ⅲ (Fig. 4b). Concurrently, ETCO₂ decreased suddenly from 35 mmHg to 28 mmHg (a reduction of 7 mmHg), JBP dropped to -2 mmHg, and SpO₂ decreased to 91%.
Emergency TEE: The echo of the SL1 sheath was visualized in the left atrium, with a small number of microbubbles in the left atrium and aortic root, and no obvious microbubbles in the right atrium (Fig. 3a); after withdrawing the SL1 sheath into the right heart, a large number of microbubbles appeared in the right atrium and inferior vena cava (Fig. 3b, c). TEE is the gold standard for AE detection, capable of identifying bubbles as small as 0.02 mL/kg and confirming their source [4].
Atropine 0.5 mg was immediately administered intravenously, and the heart rate increased to 65 beats per minute; a temporary pacemaker was implanted (pacing frequency: 60 beats per minute), and the ST segment gradually returned to normal. PFO closure was terminated, and coronary angiography was not performed.

Postoperative Condition

Conscious State: Two hours after discontinuing anesthesia, the patient remained drowsy, could respond to verbal stimuli but had slurred speech, and experienced limb convulsions (lasting approximately 10 seconds), with SpO₂ maintaining at 92% under oxygen inhalation. A sudden decrease in SpO₂ is an early sign of AE, particularly in anesthesia-related negative pressure scenarios ^1,9.
Imaging Re-examination: Head CT showed vesicular gas shadows in the posterior brain and retention of intracranial contrast agent (Fig. 5a); brain DWI + MRI revealed decreased ADC signals in the cortex of the bilateral frontal, parietal, and occipital lobes, suggesting cortical infarction (Fig. 6).
Laboratory Indicators: Six hours after surgery, cardiac enzymes were significantly elevated (myoglobin: 461.6 ng/ml, high-sensitivity troponin: 3441 pg/ml, CK-MB: 31.20 ng/ml, NT-pro BNP: 2990 pg/ml).
Treatment and Outcome: After transfer to the intensive care unit (ICU), the patient received hyperbaric oxygen therapy (2.5 ATA, once daily for 10 days, 90 minutes per session)—a recognized gold standard for AE treatment that shrinks bubbles and improves oxygen delivery to ischemic tissues^4,10—antiepileptic treatment (sodium valproate 0.5 g, twice daily), and myocardial nutritional support (trimetazidine 20 mg, three times daily). Tracheal intubation was removed 2 months after surgery. Limb function was not fully recovered, with upper and lower limb muscle strength only grade Ⅲ and increased muscle tone. Language function was also impaired, and the patient could only express simple words, phrases, and cry. After discharge from the ICU, the patient continued rehabilitation treatment in the Department of Rehabilitation Medicine. Full recovery of limb function has not been achieved.

Air embolism can occur during numerous clinical procedures, such as endoscopy, hemodialysis, thoracentesis, tissue biopsy, angiography, and the insertion and removal of central and peripheral venous lines—these have surpassed surgery and trauma as common causes³. A study involving over 11,000 central venous catheter placements reported an incidence of 1 in 772 ⁵.

Mechanism of Air Embolism in This Case

1. Catheter-related Factors

During the procedure, the sheath and guidewire were positioned in the left atrium. Although there is a hemostatic valve at the tip of the sheath, the presence of an indwelling guidewire can compromise the seal if the guidewire's tip is not coaxial with the catheter. This reduction in seal integrity potentially allows air to communicate with the vascular system.

The end cap of the SL1 extended sheath used in the surgery exhibited excellent negative pressure sealing performance in our in vitro testing (conducted under standard laboratory conditions: 25°C, simulated physiological saline environment, n = 5 replicates). Without a guidewire, it maintained integrity under negative pressures of up to 54 kPa without leakage—exceeding the standard requirement of 42 kPa (YY0450.1-2020). However, when a 0.035-inch guidewire (Biosense Webster) was inserted non-coaxially, the assembly could only withstand a negative pressure of 16 kPa. Consequently, when the pressure difference between atmospheric pressure and central venous pressure exceeded 16 kPa (consistent with the critical threshold of -13.4 mmHg reported in previous studies ³), a negative pressure gradient was established within the catheter, potentially drawing external air into the vascular system through the catheter.

2. General Anesthesia-related Factors

In this case, passive deep inhalation (a spontaneous Valsalva maneuver) induced by general anesthesia generated substantial negative intrathoracic pressure and significant reductions in intravascular pressure. The patient had fasted overnight before surgery, leading to relative hypovolemia. Combined with decreased blood pressure after induction of general anesthesia and a notable drop in CVP (from 8 cm H₂O to 2 cm H₂O), cardiac chamber pressures fell below atmospheric pressure. When this pressure difference exceeded 16 kPa, a small amount of ambient air was aspirated into the heart via the SL1 extended sheath containing the guidewire.

Anesthesia-induced negative pressure is a well-documented driver of AE: propofol sedation can reduce left atrial pressure by a mean of 6.9 mmHg³, and switching from mechanical ventilation to spontaneous breathing (a common transition in laryngeal mask ventilation) increases intrathoracic negative pressure, lowering right atrial pressure and expanding the venous-atmospheric pressure gradient². Additionally, body position adjustments during the recovery period (e.g., transfer from the operating table) can displace static venous bubbles, exacerbating embolism². Although laparoscopic surgery was not involved in this case, the principle of pressure gradient management (low pressure reducing embolism risk) ⁹ further supports the critical role of maintaining balanced vascular pressures in AE prevention.

3. Role of PFO and Iatrogenic Atrial Septal Defect

Venous air emboli often lead to pulmonary embolism, but this patient had PFO. Additionally, atrial septal puncture was performed during VPB radiofrequency ablation, resulting in an iatrogenic atrial septal defect. The coexistence of these two conditions allowed air to migrate from the right atrium to the left cardiac system. PFO is a major risk factor for paradoxical AE, as it enables air to bypass the pulmonary filter and enter the systemic circulation, causing coronary and cerebral ischemia⁴. Massive air entry into the pulmonary circulation can also increase pulmonary vascular resistance and pulmonary hypertension, leading to right heart failure and decreased cardiac output ².

Comparison with Similar Cases

Table 1

summarizes the key features of previously reported AE cases related to cardiac interventional procedures and anesthesia, compared with the current case.
Reference	Procedure	Anesthesia Type	AE Mechanism	Involved Organs	Outcome
¹¹	Atrial fibrillation ablation (dextrocardia)	General anesthesia	Catheter-related air entry	Left atrium	Improved
⁴	Upper endoscopy	Conscious sedation	Mucosal injury + pressure gradient	Brain	Improved
²	General surgery	General anesthesia	Recovery position change	Right heart, lungs	Fatal
Current case	RFA + PFO closure	General anesthesia (laryngeal mask)	Anesthesia-induced negative pressure + sheath leakage + PFO	Coronary artery, brain	Persistent neurological deficit

Compared with previous reports, the current case is unique in its triple pathogenic mechanism (anesthesia-induced negative pressure, catheter sheath sealing defect, and PFO-related right-to-left shunt) and simultaneous involvement of coronary and cerebral circulation. Most similar cases focus on single mechanisms (e.g., catheter manipulation ¹¹ or position change ) or single-organ involvement, highlighting the novelty of this report in demonstrating the synergistic effect of multiple risk factors.

Prevention and Management Insights

When air embolism is clinically suspected, aspiration of air through a catheter at the site of bubble accumulation may be an effective intervention to reduce air volume ¹². Hyperbaric oxygen therapy shrinks pathological bubbles, delivers oxygen to ischemic organs, and promotes the conversion of nitrogen from the gaseous to the liquid phase, thereby reducing bubble size. Essentially, it decreases gas volume, alleviates cerebral edema, and increases the partial pressure of dissolved oxygen in the blood, making it widely recognized as the gold standard for treatment⁴. A study by Blanc et al. found that patients achieved the best treatment outcomes when hyperbaric oxygen therapy was administered within 6 hours¹⁰; however, treatment within 30 hours may still be beneficial ¹³.

Preventive strategies should focus on:

Maintaining venous positive pressure: Adequate preoperative fluid resuscitation (20 mL/kg crystalloid) and intraoperative CVP monitoring (target 5–15 cm H₂O) to avoid excessive dehydration-induced hypotension⁵. Continuous JBP monitoring is recommended to maintain JBP > 0 mmHg, as negative JBP is a key predictive indicator for VAE ⁵.

Optimizing catheter and sheath management: Ensuring guidewire-catheter coaxiality to maintain seal integrity, avoiding unnecessary sheath indwelling, and selecting sheaths with proven sealing performance under negative pressure³.

Enhancing perioperative monitoring: Using TEE or PCD for real-time AE detection, especially during anesthesia induction, position adjustments, and recovery⁸. Continuous ETCO₂ monitoring is critical, as a sudden decrease ≥ 3 mmHg is an early warning sign ⁹

Avoiding high-risk anesthesia practices: Minimizing nitrous oxide use (which can expand bubble volume) and ensuring a smooth transition between mechanical and spontaneous breathing to prevent abrupt changes in intrathoracic pressure ¹.

Paradoxical embolism leading to systemic air embolism should be prevented, especially in patients with congenital or acquired intracardiac right-to-left shunts ¹¹. The mechanism of air embolism in this case involves multiple factors, including anesthesia-induced negative pressure, catheter-related air leakage, and cardiac anatomy (PFO), which is relatively unique and clinically significant. This case provides valuable experience for preventing and managing the recurrence of such adverse events. Even with appropriate treatment, recent data suggest that the overall 1-year mortality rate may be approximately 21%¹⁴. Interventional cardiologists and anesthesiologists should maintain a high index of suspicion for air embolism, implement comprehensive monitoring strategies, and initiate timely hyperbaric oxygen therapy to reduce morbidity and mortality.

Authors’ contributions

XIUYU WANG wrote the main manuscript text and provided the idea for the manuscript. SHEN HUANG provided the idea for the manuscript, FENGKUN prepared figures1 and figures .

CHUAN HE and JIAFA JIN reviewed the manuscript.

Competing interests

The authors declare that they have no competing interests.

Consent for publication

Written informed consent was obtained from the patient for publication of

this case report including clinical data and any accompanying images.

Ethics approval and consent to participate

No ethics approval was required in this case.

The article is not supported by any funding.

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No competing interests reported.

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You are reading this latest preprint version

A Rare Case of Coronary Artery and Cerebral Air Embolism Associated with Catheterization and General Anesthesia

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Abstract

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Introduction

Case Presentation

Discussion

1. Catheter-related Factors

2. General Anesthesia-related Factors

3. Role of PFO and Iatrogenic Atrial Septal Defect

Conclusion

Declarations

References

Additional Declarations

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