Controlled hypotension under rapid ventricular pacing technique in patients with cerebral arteriovenous malformation -a case report-
Article information
Abstract
Background
The transvenous approach to the treatment of cerebral arteriovenous malformation (AVM) is difficult and requires strict blood pressure and blood flow control; however, the cure rate is very high. Appropriate blood pressure control techniques can greatly benefit these patients.
Case
A 55-year-old male patient was found to have an aneurysm complicated with a cerebral AVM (length: 2.0 cm, width: 1.6 cm, height: 1.2 cm). Aneurysm embolization was considered for the first-stage surgery and transvenous AVM embolization for the second-stage surgery. Rapid ventricular pacing (RVP) provided a stable blood flow environment for the surgery, which was completed successfully.
Conclusions
RVP can thus provide an ideal condition for the embolization of cerebral AVM through the transvenous approach and can be a viable surgical option.
Cerebral arteriovenous malformation (AVM) is a rare disease in neurosurgery, with an estimated prevalence of approximately 1.3 cases per 100,000 person-years [1]. Although treatment of AVM using the transvenous approach is challenging, its high cure rate and remarkable efficacy make it a valuable option. The most difficult aspect of this operation is controlling the blood pressure and maintaining a stable blood flow environment so that the embolic agent can solidify quickly. Blood pressure should be controlled at a low level before the embolic agent is injected so that the pressure at both ends of the vascular nest is zero and the embolic agent can enter the vascular nest smoothly. After systemic hypotension, the decrease in blood flow velocity and blood flow to the feeding arteries are correlated to hemorrhaging due to vascular nest rupture. Blood pressure is restored to normal levels after the embolic agent solidifies (generally 30–40 s). Blood pressure can be lowered several times, depending on the intraoperative situation. We present a case in which optimal surgical conditions were achieved by controlling hypotension and maintaining blood pressure at a stable low level using rapid ventricular pacing (RVP) techniques. The patient underwent successful embolization without any postoperative complications.
Case Report
A 55-year-old male patient (height: 158 cm, weight: 61 kg) with an American Society of Anesthesiologists grade II classification was admitted to our hospital after experiencing a sudden headache lasting 6 h. The presenting symptoms included sudden unexplained headaches and walking difficulties. The patient underwent head computed tomography (CT) at a local hospital, which revealed a subarachnoid hemorrhage. Additionally, CT angiography showed an abnormal vascular mass in the right cerebellar horn area suggestive of cerebrovascular malformations (length: 2.0 cm, width: 1.6 cm, height: 1.2 cm). The preliminary diagnosis was a cerebral AVM with subarachnoid hemorrhage. No underlying medical conditions were noted in the patient’s medical history. On physical examination, the patient was conscious and oriented, with bilateral pupils equal and reactive to light without neck tenderness, and muscle strength was normal in all extremities. Electrocardiography (ECG) demonstrated sinus rhythm at a rate of 71 beats/min (bpm). The high-sensitivity cardiac troponin T (hs-cTnT) level was noted at 6.66 ng/L (normal range: 0–14 ng/L), whereas other laboratory tests showed no significant abnormalities. Written informed consent was obtained from the patient for the publication of this case report, and no ethics committee approval was required.
After admission, the digital signature algorithm (DSA) results revealed the presence of an AVM in the right cerebellar hemisphere (Fig. 1A, Supplementary Fig. 1) involving the right superior cerebellar pontine artery and perforating branch artery as well as flow-related aneurysms in the superior cerebellar artery (Fig. 1B). Neither the bilateral internal carotid artery nor external carotid artery were involved in blood supply. The AVM drainage vein comprised a short main drainage vein and three secondary drainage veins (Fig. 1C, Supplementary Fig. 2). The treatment team determined that the first stage would involve treatment of the aneurysms, while the second stage would involve cerebral AVM treatment using a transvenous approach.

(A) Right cerebral angiography. (B) The red line is the right superior cerebellar artery, the yellow line is the perforating branch of the pontine, and the red arrow is a flow-associated aneurysm of the superior cerebellar artery. (C) The red line is the main drainage vein, and the orange, yellow and blue lines are the secondary drainage veins.
On the fifth day following the first stage of the operation, the patient sporadically reported experiencing headaches. A CT tomography revealed small infarctions in the right cerebellar hemisphere. The patient remained alert with no notable physical examination findings or new neurological impairments. Cerebral AVM embolization was performed via the transvenous approach on the ninth day after the first stage of surgery under elective general anesthesia with controlled hypotension induced by RVP.
Before surgery, the patient was prohibited from drinking for 4 h and eating for 8 h. On arrival at the operating room, ECG and pulse oxygen saturation level monitoring were initiated. Additionally, defibrillation electrode pads were applied, and a catheter was inserted into the left radial artery under local anesthesia for invasive blood pressure (IBP) monitoring (IBP: 119/63 mmHg, heart rate: 70 bpm, oxygen saturation: 99%). The arterial blood gas analysis (ABGA) results showed the following: pH 7.51, PaCO2 35 mmHg, glucose 5.7 mmol/L, lactic acid 0.7 mmol/L, hematocrit 46%, base excess 4.9 mmol/L, and total hemoglobin 15.2 g/dl. A peripheral venous line was established on the left upper limb and 500 ml lactated Ringer’s solution was infused. Oxygen was administered via face mask at 6 L/min, and anesthesia induction began with 0.5 mg pentahexaquinone hydrochloride, 3 mg midazolam, 18 mg etomidate, 15 mg cisatracurium, and 30 µg sufentanil. After loss of consciousness, assisted ventilation was initiated. The endotracheal tube was inserted under direct laryngoscopy after 3 min, and ventilation was controlled at an oxygen flow rate of 1 L/min and an air flow rate of 1 L/min to maintain an end-tidal CO2 between 30 and 35 mmHg. Anesthesia was maintained during surgery with 5 mg/kg/h propofol, 0.2 µg/kg/min remifentanil, 1 µg/kg/min cisatracurium, 0.5 µg/kg/h dexmedetomidine, and 1% sevoflurane. Cerebral oxygen saturation was continuously monitored throughout the procedure.
In preparation for interventional surgery, the tissue was disinfected. Heparin was administered before puncture to ensure that the activated coagulation time (ACT) remained > 250 s, with additional heparin dosages adjusted based on the ACT throughout the procedure. The right femoral artery and vein were punctured and 6 F catheter sheaths were inserted into both the artery and vein. With the assistance of a cardiovascular physician, an ECG electrode was threaded into the right ventricle through the right femoral vein. Correct positioning was confirmed under DSA guidance, and the pacemaker settings were adjusted to ensure heart capture at minimum levels. Under DSA guidance, the right internal jugular vein was punctured and a 6 F catheter sheath was inserted. Using guidewire assistance, a catheter was then inserted into a suitable drainage vein. After connecting the defibrillation electrode to the defibrillator, rescue drugs, such as esmolol, lidocaine, amiodarone, epinephrine, norepinephrine, and nitroglycerin, were prepared along with a transvenous injection of 100 mg phenobarbital sodium. Room temperature was lowered to 18°C, 300 ml of normal saline at 4°C were injected intravenously, and an ice cap was placed on the head to maintain core temperature around 35°C for brain protection. At this point, the IBP was 87/54 mmHg (Fig. 2A) and cerebral oxygen saturation was 75% on the left and 74% on the right side. The pacing rate was set at 180 bpm and RVP was initiated. When the IBP waveform had flattened, the systolic IBP was maintained between 30 and 40 mmHg (Fig. 2B, Supplementary Video 1). Despite ineffective cardiac contractions, a significant amount of forward blood flow persisted. The surgeon then injected embolic agents at the target site, which quickly coagulated at the lesion. Ventricular pacing ceased after 30 s and IBP returned to 95/50 mmHg within 3 s, with 74% cerebral oxygen saturation on both sides. The same procedure was repeated 3 min later with RVP and the embolic agent injection. Following rapid coagulation, ventricular pacing was discontinued, IBP was restored to 113/62 mmHg, and cerebral oxygen saturation remained at 73% on both sides. The entire procedure lasted 8–10 min and proceeded smoothly. Following two rounds of RVP, repeated multiangle angiography revealed satisfactory embolization (Figs. 3A–C, Supplementary Figs. 3 and 4). Prior to the end of surgery, the ABGA indicated the following: pH 7.44, PaCO2 41 mmHg, glucose 7.6 mmol/L, lactic acid 1.2 mmol/L, hematocrit 40%, base excess 3.6 mmol/L, and total hemoglobin 13.2 g/dl. During the operation, 2,500 ml crystalloid fluid was infused along with 10 mg of furosemide, resulting in a urine output of 950 ml, minor bleeding, and dilated and round bilateral pupils. Postoperatively, cerebral oxygen saturation (left: 75%, right: 75%) was maintained, and the patient was transferred to the neurosurgical intensive care unit with a tracheal catheter for further treatment.

(A) Basic vital signs of the patient before RVP initiation. (B) Patient's vital signs at a ventricular rate of 180 beats/min. RVP: rapid ventricular pacing.

(A) Total cerebral angiography after embolization. (B) AVM did not appear at all after embolization. (C) The main drainage vein, secondary drainage vein and AVM vascular mass were completely embolized. AVM: arteriovenous malformation.
On the first postoperative day, CT showed no evidence of a new infarction or hemorrhage. The patient regained consciousness, was able to follow commands, had normal muscle strength with stable vital signs, and had an hs-cTnT level of 5.57 ng/L. Blood, liver, and kidney function tests were normal. The endotracheal tube was removed under sedation. On the fifth postoperative day, the patient occasionally reported headaches that improved compared to first few days after surgery. Before discharge on the fifth postoperative day, the patient was alert, oriented, had a normal mental status, equal and reactive pupils, normal neck movement, and normal limb movements.
Discussion
Cerebral AVM is a rare form of cerebrovascular malformation in which the arteries and veins in the brain are directly connected and have irregular and fragile clumps of blood vessels that form lesions. These plexiform vessels are prone to rupture due to a lack of normal smooth muscle structure and abnormal angiogenesis, resulting in life-threatening bleeding [2]. AVM may be caused by the abnormal development of fetal angiogenesis and is an important cause of cerebral hemorrhage in young people. Clinical manifestations include hemorrhages, seizures, headaches, and progressive neurological impairment secondary to the “steal phenomenon.” The risk of hemorrhage is doubled after the first bleeding event [3,4]. Various treatment options for AVM are available, including conservative treatment, surgical resection under a microscope, neurointerventional therapy, and stereotactic radiation therapy. Depending on the patient’s condition and the location and size of the AVM, these methods can be used alone or in combination for a complete cure.
With the continuous innovation of neurointerventional techniques and embolic materials, interventional treatment of AVM has developed rapidly and is now widely used. Interventional therapy is usually performed via an arterial approach. AVM embolization using this approach can be performed as an independent treatment or as an adjunct before surgical resection under a microscope or stereotactic radiation therapy. However, for a small AVM (diameter ≤ 3 cm) with a single drainage vein, transarterial embolization is not feasible due to the lack of clear arterial pedicles and the presence of multiple small feeding arteries or tiny perforated arteries that supply blood; thus, transvenous embolization becomes an appropriate treatment method [5]. In 1994, Mullan [6] first proposed transvenous embolization as an independent treatment for AVM. Radical embolization of AVM may be easier to achieve using a transvenous approach than a transarterial approach. Several studies have demonstrated the safety and feasibility of this technique [2,5,7] in sharp contrast to the low cure rate of transarterial embolization. However, transvenous embolization is a very challenging procedure because the lesion is mainly located between the arteriole and venule and the guidewire placement path is curved, making it difficult to insert the drainage venous catheter and deliver the embolic agent retrogradely into the lesion without causing venous rupture and bleeding. In addition, it is associated with a high risk of remote migration of the embolic agent, which can accidentally lead to blocked venous discharge or pulmonary embolism with catastrophic consequences.
The key to successful transvenous embolization lies in the temporary stagnation of arterial blood flow, which enables the embolic agent to penetrate deeper into the lesion. Massoud and Hademenos [8] proposed transvenous retrograde therapy (TRENSH) using a controlled hypotension technique, that is, the temporary use of systemic hypotension with or without temporary occlusion of the supporting artery. The transvenous approach enables better penetration of embolic agents into the lesion through retrograde blood flow, which contributes to the temporary stagnation of arterial flow and reduces the risk of ischemic complications. Techniques for controlling hypotension depend on both pharmacological and non-pharmacological approaches. Pharmacological approaches include sodium nitroprusside, esmolol, and adenosine, whereas non-pharmacological approaches include temporary balloon blocking of the arterial flow and RVP. Most controlled hypotension in neurointerventional surgery involves the use of drugs; however, conventional drugs take effect slowly and patient recovery takes time, with large individual differences between patients. For the treatment of high-flow AVM, reducing the target IBP is difficult and repeated drug administration is required. Currently, the mainstream practice is to use adenosine-induced cardiac arrest technology; however, this approach may lead to long-term hypotension and heart-related complications such as increased troponin, ventricular tachyarrhythmia, atrial fibrillation, and chronic arrhythmia [9].
RVP is a cardiac electrophysiological examination method widely used in cardiac interventional surgery, especially for transcatheter aortic valve replacement (TAVR). RVP induces ventricular tachycardia, resulting in a significantly reduced ventricular filling time, stroke output, and cardiac output, thereby controlling the reduction in IBP [10–12]. First, the patient had undergone most of the malformation embolization procedures, and the remaining malformation was small and suitable for curative embolization through the transvenous approach. Second, the RVP provides slow and stable blood flow, creating the best conditions for this surgery. Compared to antihypertensive drugs, the benefits of RVP are as follows: precise control of the onset and duration of decreased blood flow, quick establishment of a stable and continuous advection low-pressure environment, and quick recovery to the previous IBP level after embolization, making the management of IBP convenient and precise. RVP thus meets surgeons’ requirements for IBP and allows for effective embolization of AVM and rapid recovery of IBP [13]. However, persistent hypotension inevitably increases the risk of brain, myocardial, and kidney injury. Therefore, we used hypothermic brain protection and brain function monitoring to monitor changes in myocardial markers and renal function. In this patient, no related injuries were noted.
Reducing the frequency of RVP use may also improve patient outcomes. In terms of the incidence of postoperative kidney injury, although no studies on neural intervention have been conducted, the risk of postoperative kidney injury in patients who underwent RVP three or more times during TAVR surgery was 1.5 times higher (28% vs. 18%) than in those who underwent RVP two or fewer times. Additionally, no difference in the incidence of kidney injury was found (18% vs. 18%) for those who underwent RVP 1–2 times compared to no RVP use [14]. Although RVP is widely used in cardiac interventional surgery, its use in neurointerventional surgery is rarely reported in China, and few studies [5,14] have been conducted on the protection of relevant organs. Due to the complexity and associated risks of this surgery, highly specialized multidisciplinary teams that include anesthesiologists, neurosurgeons, and cardiologists are required for efficient and effective communication and for careful protection of multiorgan function.
Notes
Funding
None.
Conflicts of Interest
No potential conflict of interest relevant to this article was reported.
Data Availability
Data sharing not applicable to this article as no datasets were generated or analyzed during the current study.
Author Contributions
Zijian Zhao (Conceptualization; Writing – original draft)
Hang Wang (Investigation)
Xinxu Min (Project administration; Resources)
Zheng Li (Project administration; Validation)
Feng Feng (Supervision; Visualization; Writing – review & editing)
Supplementary Materials
Blood vessels in the right cerebral hemisphere.
Supplying artery of AVM.
Total cerebral angiography after embolization.
The AVM did not appear after embolization.
Supplementary Video 1.
Rapid ventricular pacing.