Seizure-Like Episode During Pacemaker Surgery Points to Rare Air Embolism Danger

A routine heart procedure took a dramatic turn when a 78-year-old man suddenly stiffened and began seizure-like movements on the operating table, his oxygen levels plummeting within seconds. The culprit, his medical team concluded, was not a stroke or a drug reaction but something far less expected: air that had slipped into his veins during the implantation of a permanent pacemaker. The case, published in Clinical Case Reports, offers a vivid reminder that even the most familiar procedures can hide rare and easily missed dangers, and that a sudden, unexplained drop in oxygen should set alarm bells ringing long before blood pressure falls.

Venous air embolism, the condition at the heart of this report, occurs when atmospheric air enters the venous circulation and travels toward the right side of the heart and the pulmonary arteries. Once there, bubbles can physically obstruct blood flow through the lungs, raising pressure in the pulmonary vessels and creating a ventilation-perfusion mismatch, a technical term for the situation where parts of the lung receive air but no blood, or blood but no air. The result is an abrupt fall in the oxygen content of the blood leaving the heart. The condition is well documented in neurosurgery, obstetrics, and procedures involving central venous catheters, where large veins are opened to atmospheric pressure. During cardiac device implantation, however, it remains under-reported and frequently under-recognized, partly because the episodes are often transient and partly because registries of device complications focus on more common problems such as pneumothorax, lead dislodgement, infection, and vascular injury.

The mechanics of how air gains entry during a pacemaker implantation are deceptively simple. The procedure requires venous access, usually through the axillary, subclavian, or cephalic veins, and introducer sheaths through which thin insulated pacing leads are threaded toward the heart. Every moment that a sheath hub stands open to air is an opportunity for entrainment, particularly because spontaneously breathing patients generate negative pressure inside the chest with each inspiration, effectively sucking air inward. Hypovolemia, which lowers venous pressure and weakens the natural resistance to inflow, and careless handling of the access system compound the risk. Once inside, the volume and rate of air entry determine the clinical picture. Large, rapid injections of air can cause cardiovascular collapse, while smaller volumes may produce only fleeting symptoms that are easy to attribute to sedation, anxiety, or the patient’s underlying lung disease.

What makes the new case striking is the neurological mask the event wore. The patient, admitted electively for treatment of complete heart block, was stable at baseline with an oxygen saturation of 98 percent on room air and no history of neurological disease. Under local anesthesia, with continuous electrocardiographic and pulse oximetry monitoring, the team obtained left axillary venous access and began advancing the pacing lead without difficulty. Then, during lead manipulation, the patient developed generalized body stiffness with involuntary, seizure-like movements, immediately followed by a sudden drop in oxygen saturation to 70 percent. Crucially, there was no hypotension and no arrhythmia on the monitors. Classical descriptions of venous air embolism emphasize dyspnea, chest pain, cough, hypotension, and, in severe cases, circulatory collapse. This patient showed none of the circulatory features, illustrating that even modest volumes of entrained air can produce hypoxia severe enough to cause transient cerebral dysfunction without overt hemodynamic compromise.

Neurological manifestations of venous air embolism can arise in two ways. The more common route is indirect: air obstructing pulmonary blood flow impairs gas exchange, and the resulting cerebral hypoxia can produce confusion, agitation, or frank seizure-like activity. Less frequently, air crosses directly into the arterial circulation through an intracardiac shunt such as a patent foramen ovale, a phenomenon known as paradoxical embolization, and lodges in the cerebral vessels themselves. Either pathway can mimic a primary neurological disorder or other procedural complications, a diagnostic trap that is especially hazardous in electrophysiology laboratories where patients are typically under conscious sedation and cannot report early symptoms. In this case, the seizure-like activity was almost certainly secondary to acute hypoxia rather than a primary brain event, a distinction with immediate consequences for treatment.

The team’s response illustrates the management principles that experts emphasize. The procedure was halted at once and 100 percent high-flow oxygen was administered. Oxygen therapy does more than correct hypoxemia; it also accelerates the washout of nitrogen from intravascular bubbles, since breathing pure oxygen creates a steep diffusion gradient that shrinks the embolus and restores pulmonary perfusion. Trendelenburg positioning, the head-down posture traditionally recommended to trap air in the venous system and prevent its migration, could not be used because the patient depended on temporary pacing support, a real-world constraint the authors highlight. No additional drugs were required. A fluoroscopic X-ray taken during the episode showed no air in the pulmonary arteries, but imaging in such situations is often unrevealing, and the diagnosis remained clinical. The patient improved rapidly, his oxygen saturation normalized, his neurological signs resolved completely, and the implantation was resumed and finished without further complications.

The differential diagnosis in such an event is broad, and working through it clarifies why air embolism fit best. Local anesthetic systemic toxicity typically announces itself with perioral numbness, tinnitus, or altered mental status before progressing to seizures and, critically, cardiovascular instability, none of which appeared here. A vasovagal reaction produces bradycardia, hypotension, and sweating rather than isolated hypoxia with neurological signs. An acute exacerbation of the patient’s chronic obstructive pulmonary disease was a genuine consideration given his age and history, but the abrupt onset immediately following venous manipulation argued against it. Continuous electrocardiography excluded malignant arrhythmias and ischemic changes, and repeated fluoroscopy ruled out pneumothorax. What remained was the tight temporal link between lead advancement and symptom onset, the absence of circulatory collapse, and the rapid response to oxygen, a combination the authors judged most consistent with venous air embolism. Because the episode was acute and self-limiting, further tests such as echocardiography or arterial blood gas analysis were not performed.

The broader lesson the authors draw is a simple but powerful rule: any sudden, unexplained desaturation during pacemaker implantation should be presumed to be air embolism until proven otherwise. Continuous pulse oximetry proved decisive in this case, catching the desaturation before the full clinical picture emerged, and the authors argue that early hypoxia may sometimes be the only warning sign an operator receives. Prevention, meanwhile, rests on meticulous technique: careful handling of venous sheaths, minimizing the time the hub remains open to air, and maintaining adequate venous pressure, particularly in spontaneously breathing patients where every inspiration generates suction. Standardized response protocols, they suggest, would help operators avoid misreading seizure-like activity as a primary neurological or drug-related event and losing precious minutes.

The outcome in this instance was favorable. The patient remained stable afterward, showed no recurrence of symptoms, was discharged without neurological deficit, and follow-up evaluation revealed no delayed complications. But the case carries a message that extends well beyond one operating room. Cardiac implantable electronic devices are implanted in enormous numbers worldwide for bradyarrhythmias such as complete heart block, and the safety record of the procedure is excellent, which is precisely why rare events like venous air embolism can slip beneath the radar of large complication registries. Awareness, the authors conclude, is the most effective safeguard: recognizing that air embolism can present atypically, with isolated hypoxia and transient neurological symptoms even in a hemodynamically stable patient, allows for immediate intervention that can convert a potentially life-threatening complication into a fully reversible episode with no lasting harm.

Subject of Research: Venous air embolism presenting as seizure-like activity and acute hypoxia during permanent pacemaker implantation

Article Title: Seizure Like Activity During Permanent Pacemaker Implantation: A Case of Suspected Venous Air Embolism With Acute Hypoxia

Article References: Ansari, S., & Dhungana, M. (2026). Seizure Like Activity During Permanent Pacemaker Implantation: A Case of Suspected Venous Air Embolism With Acute Hypoxia. Clinical Case Reports, 14(10), Article e73689. https://doi.org/10.1002/ccr3.73689

Image Credits: AI Generated

DOI: 10.1002/ccr3.73689

Keywords: venous air embolism, pacemaker implantation, hypoxia, seizure-like activity, cardiac implantable electronic devices, pulmonary circulation, oxygen therapy, patient safety, electrophysiology, case report, COPD, procedural complications