A profound case of neurally mediated syncope with asystole after septoplasty

Vasovagal syncope (VVS) is an alarming yet benign condition that may present postoperatively for the first time in otherwise healthy patients. Although VVS is associated anecdotally with nasal manipulation, no data have been found to quantify this incidence with otolaryngology surgeries. We present a case of profound, recurrent syncope and documented asystole with an initial diagnosis of glossopharyngeal neuralgia. We conclude with a discussion of neurally mediated syncope particular to the perioperative setting. It is essential to recognize neurocardiogenic etiology to differentiate it from other more concerning causes of syncope and asystole.     

Evaluation of the relationship between baseline autonomic tone and the vagotonic effect of a bolus dose of remifentanil

Remifentanil stimulates the parasympathetic nervous system, and patients with increased parasympathetic tone may be at greater risk of bradycardia after its administration. We aimed to establish if adult patients with increased baseline parasympathetic tone were at higher risk of bradycardia and hypotension when given a bolus dose of remifentanil. Seventy adults (age 20–60 years and ASA physical status 1 or 2) were given remifentanil 1 μg.kg^?1. A Holter ECG monitor was used to assess heart rate changes. Heart rate variability in the frequency domain during the 5 min after remifentanil administration was analysed. Multivariate analysis demonstrated that baseline heart rate was the only independent predictor of remifentanil‐induced bradycardia [odds ratio (95% CI) 0.877 (0.796–0.966)]. The vagotonic action of remifentanil does not appear to be related to baseline autonomic tone in adult patients.     

Paradoxical bradycardia and hemorrhagic shock]

We report two cases of paradoxical bradycardia associated with acute hemorrhage and hypotension in conscious patients who had no antecedents of myocardial disease. In some cases of massive and rapid hypovolemia the occurrence of bradycardia may constitute a protective reflex directed to improve ventricular filling. This reflex is probably mediated by a vagal mechanism which acts on a previously increased sympathetic nerve tone and tends to maintain systemic vascular resistances and keep a cerebral blood flow high enough to preserve conscience level. We discuss the differential diagnosis with vasovagal syncope which can also occur during the initial phases of acute hemorrhage and during the preterminal bradycardia that develops during the so called "irreversible phase" of shock. Paradoxical bradycardia during hemorrhagic shock is always a sign of important bleeding that requires a rapid reposition of volemia. Administration of vagolytic agents is contraindicated since they can favour the occurrence of severe cardiac arrhythmias.     

Trigeminocardiac reflex during the percutaneous injection of ethylene vinyl alcohol copolymer (Onyx) into a juvenile nasopharyngeal angiofibroma: a report of two cases

The trigeminocardiac reflex (TCR) is a rare but well-described phenomenon encountered during invasive procedures involving the face, orbit, and cranial base. The reflex is characterized by the abrupt onset of hypotension, bradycardia, asystole, and dysrhythmias. With temporary cessation of the surgical procedure, vital signs typically stabilize without the need for further investigation, though anticholinergic drugs are often used to prevent prolonged hypotension and bradycardia. Two separate cases of the TCR were encountered during the percutaneous embolization of a juvenile nasopharyngeal angiofibroma with dimethylsulfoxide (DMSO) before the injection of ethylene vinyl alcohol copolymer (Onyx, ev3, Irvine, California, USA). In both cases, the injection of DMSO precipitated approximately 30 s of bradycardia/asystole, which then resolved after halting the procedure and administering anticholinergic drugs. There were no additional occurrences afterward and the patients underwent tumor excision with good recovery.     

Vasovagal syncope and anaesthetic practice

We surveyed anaesthetists working in North-West England and in North Wales concerning episodes of vasovagal syncope encountered in their practice. Eighty-eight anaesthetists described 109 such events occurring in either patients or their relatives and the estimated frequency of syncope was 1 in 5000 anaesthetic episodes. The patient syncopal episodes were triggered by venous cannulation in 16 instances and regional or local techniques in 20 instances. Thirty-three of the 53 patients were in the upright position when syncope occurred. Thirty-nine of the 56 relatives were male partners of female patients and four of these partners suffered some morbidity. The results of the survey are consistent with our current knowledge of the pathophysiology of vasovagal syncope, which is summarized, and also highlight the common anaesthetic scenarios where fainting is most likely to occur. Given this information anaesthetists will be in a better position to avoid such potentially harmful episodes in the future.     

The falcine trigeminocardiac reflex: case report and review of the literature

BACKGROUND: Trigeminocardiac reflex (TCR), the reproducible hypotension and bradycardia upon stimulation of the trigeminal nerve, has been reported during craniofacial surgery and during surgery within the cerebellopontine angle, petrosal sinus, orbit, and trigeminal ganglion. Whereas the falx cerebri is known to be innervated by the nervus tentorii, a recurrent branch of V1, there have been no reports to date of this response upon mechanical stimulation of the falx. CASE DESCRIPTION: We report a case of immediate, reproducible, and reflexive response of asystole upon stimulation of the falx cerebri during operative resection of a parafalcine meningioma in a 53-year-old woman. Upon recognition of the reproducible relationship between falcine stimulation and increased vagal tone, the patient was given glycopyrrolate in an effort to block cholinergic hyperactivity. After glycopyrrolate was given, no further dysrhythmias occurred. CONCLUSION: In this patient, mechanical stimulation of the falx likely resulted in the hyperactivity of the trigeminal ganglion, thereby triggering TCR. The dorsal region of the spinal trigeminal tract includes neurons from hypoglossal and vagus nerves, and projections have been seen between the vagus and trigeminal nuclei. The vagus provides parasympathetic innervation to the heart, vascular smooth muscle, and abdominal viscera. Vagal stimulation via these connections after trigeminal nerve activation likely accounts for the reflexive response of asystole seen in this patient. This is confirmed by the observation that the reflex was inhibited by the anticholinergic effects of glycopyrrolate. Awareness of TCR allows for early detection and appropriate treatment.     

Non-drug related asystole associated with anaesthetic induction

A patient is presented where routine venepuncture associated with anaesthetic induction resulted in bradycardia and asystole. The case highlights the need for special caution with, and ECG monitoring throughout induction for, patients with a history of syncope. It also demonstrates the need for caution when attributing cardiovascular events during induction to the effect of the induction agents used.     

Asystole during inadvertent high spinal anesthesia in a high risk patient without morbidity

Sudden cardiac arrest following high spinal anesthesia (SA) in young and healthy patients with poor outcome has been reported. Extreme bradycardia, hypotension and/or asystole during SA has recently received worldwide attention. We report a high risk patient who developed cardiac arrest associated with two other episodes of extreme bradycardia, hypotension and verbal unresponsiveness during SA without adverse outcome.     

Prevention of carotid angioplasty-induced bradycardia and hypotension with temporary venous pacemakers

OBJECTIVE: Carotid angioplasty with stent placement is becoming an established treatment modality for patients with high-risk carotid stenosis. Unlike carotid endarterectomy, angioplasty causes direct mechanical dilation of the stenotic carotid artery and bulb. Stimulation of the sinus baroreceptors induces a reflexive response that consists of increased parasympathetic discharge and inhibition of sympathetic tone, which results in bradycardia and subsequent cardiogenic hypotension. METHODS: At a single institution, the experience with 43 patients treated from November 1994 to January 2000 with 47 angioplasty and stent procedures for occlusive carotid artery disease was retrospectively reviewed. Prophylactic temporary venous pacemakers were used to prevent hypotension from possible angioplasty-induced bradycardia. Pacemakers were set to capture a heart rate decrease below 60 beats per minute. Variables analyzed included demographics, etiology of disease, side of the lesion, the presence of symptoms, history of coronary artery disease, percent stenosis, type of stent used, number of dilations, pressure of dilation, and angioplasty balloon diameter. RESULTS: Ten patients were excluded because pacemakers were not used during their angioplasty procedures, and these included three emergencies and a lesion that was unrelated anatomically to the carotid sinus (petrous carotid). The remaining 37 procedures were performed in 33 patients with a mean age of 67 years, and consisted of 17 men, 16 women, 20 right and 17 left-sided lesions. The pacemakers maintained a cardiac rhythm in 23 (62%) of the 37 procedures and in no case did the pacemaker fail to respond when activated. Recurrent (56%; 10 of 18), radiation-induced (78%; 7 of 9), and medically refractory carotid stenosis (67%; 6 of 9) required intraprocedural pacing. Two patients with recurrent stenosis became hypotensive despite the aid of the pacing device but were not symptomatic. Seventy-nine percent (15 of 19) of symptomatic lesions and 57% (8 of 14) of nonsymptomatic lesions required pacing, which was statistically significant (P = 0.049). No patient experienced an operative morbidity or mortality as a consequence of the temporary pacing devices. CONCLUSION: Angioplasty-induced bradycardia is a common condition, and it is more prevalent in radiation-induced stenosis and with symptomatic lesions. Temporary venous demand pacing is a safe procedure and may prevent life-threatening, baroreceptor-induced hypotension.     

Mechanisms behind and treatment of sudden, unexpected circulatory collapse during central neuraxis blockade

Judging from the number of cases reported in the literature, severe bradycardia and/or asystole in association with central neuraxis blockade fortunately seems a rare complication. However, short periods of extreme bradycardia may go unnoticed and manifest cases, especially when outcome is favourable, may go unreported, and thus the real incidence may be much higher. Although the decrease in systemic blood pressure as a result of central neuraxis blockade is caused by various mechanisms, the most important factor causing severe hypotension, bradycardia and circulatory collapse is decreased venous return, and both prevention and treatment are aimed at preserving or restoring adequate venous return to the heart. Correction of preoperative hypovolaemia, limiting the extent of sensory blockade and positioning the patient so that gravity promotes venous return are the most significant preventive measures. Although a widespread custom, controversy exists regarding the efficacy of a preload; for certain categories of patients intravenous volume loading may be deleterious, and rather than a routine measure, the decision to administer a preload should be based on the clinical situation and the condition of the individual patient. For the treatment of mild bradycardia, anticholinergic drugs are the first choice. Hypotension may be treated by promoting venous return using gravity, by intravenous fluid infusion, by intravenous administration of sympathomimetic drugs, or by a combination of all three measures. In the event of sudden circulatory collapse, the first therapeutic measure that is usually immediately effective is elevation of the legs, thus promoting venous return.     

Carotid Sinus Syndrome: Treatment by Carotid Sinus Denervation

Hypersensitive carotid sinus is a rare cause of spontaneous syncopal attacks. It must be differentiated from the other more common causes, such as intrinsic cardiac disease, vasovagal responses, postural hypotension and cerebrovascular insufficiency, although it may accompany these conditions. The definition of carotid sinus syncope is syncope elicited by stimulation of a hypersensitive carotid sinus.Nineteen patients with carotid sinus syncope were treated by carotid sinus denervation. Ages ranged from 48 to 83 with a mean of 65.5 years. Symptoms of marked dizziness or syncope were reproduced by gentle compression over the carotid bifurcation, while ECG monitoring revealed bradycardia or transient asystole. Seventeen patients had carotid arteriograms, eleven of which were normal. One patient had stenosis of the external carotid artery, while five had stenosis of the internal carotid. The right carotid sinus was involved in ten patients, the left in three and both sides in six. All patients underwent unilateral or bilateral carotid sinus denervation. Five patients with internal carotid stenosis had concomitant carotid endarterectomy. Complete relief of symptoms or marked improvement was noted in all but one patient. Postoperative follow-up ranged up to 15 years. Carotid sinus denervation is a simple, effective method of treating this disorder.     

Asystole during successive electroconvulsive therapy sessions: a report of two cases

Intense vagal discharge often follows stimulus application during electroconvulsive therapy (ECT). Related periods of asystole during ECT have been reported sporadically in psychiatric journals, but to date not in the anesthesia literature. We report here two cases of prolonged asystole that occurred in our facility in spite of the fact that published suggestions for its prevention were followed. With careful monitoring of these patients--including echocardiography for one patient--we document the onset of asystole at the exact time of ECT stimulus application. With these data, we discuss why asystole is likely to result from a direct central pathway rather than via a baroreceptor reflex, and discuss a neuroanatomic pathway potentially responsible for our findings. We also demonstrate that high-dose atropine (0.8 mg) can effectively prevent most cases of asystole in susceptible patients, and that administration of esmolol following cessation of seizures effectively reduces the elevated heart rate without causing asystole or bradycardia.     

The heart rate response pattern to dialysis hypotension in haemodialysis patients

BACKGROUND: Hypotension during haemodialysis may be caused by the activation of a cardiovascular reflex causing abrupt sympathetic withdrawal, vasodilatation and bradycardia (bradycardic hypotension). However, the frequency of this type of hypotension is undefined and it is unclear whether or not it underlies a peculiar predisposition to vasodepressor syncope. OBJECTIVE: To assess the prevalence of bradycardic hypotension and to test the hypothesis that dialysis patients are predisposed to vasodepressor syncope. RESULTS: Sixty hypotensive episodes were recorded in 20 patients (> or = 2 episodes in 15 patients). Heart rate increased in 35 episodes, did not change in 19 episodes and decreased in six episodes. The HR response pattern to hypotension was reproducible in 10 patients (always tachycardia, 6; always unchanged heart rate 4). Patients developing bradycardic hypotension (n = 5) all had an erratic HR response to hypotension (i.e. bradycardia preceded or followed by tachycardia or by no HR change) and were characterized either by the typical haemodynamic pattern of hypovolaemia (predialysis hypotension, tachycardia and low TBW) or by being treated with a very high UF rate (> 0.3 ml/kg/min). Post-dialysis echocardiography showed that the LVEDD was less (one-tailed P = 0.055) in patients with bradycardic hypotension than in those with tachycardic responses or with unchanged HR. On tilt testing (after dialysis) three of 11 (27%) dialysis hypotensive patients developed bradycardic hypotension. This proportion was identical to that expected in healthy subjects and in control patients without syncope. CONCLUSIONS: Tachycardia is the more frequent heart rate response to dialysis hypotension in uraemic patients. Bradycardic hypotension in dialysis patients is associated with a haemodynamic profile indicating a more severe degree of cardiovascular underfilling. Bradycardic hypotension probably represents a physiological response to hypovolaemia rather than the expression of a peculiar predisposition to vasodepressor syncope.      

Glossopharyngeal neuralgia with syncope and cervical mass

GPN syndrome with syncope, hypotension, and bradycardia is rare. The association of this syndrome with neck masses mandates that these patients undergo a search for such tumors. A review of the literature and our experience revealed 12 cases of this syndrome associated with neck masses. The majority (60%) of the patients did not respond to medical therapy and eventually required a neurosurgical procedure to cure symptoms. However, medical therapy, including high-dose carbamazepine, should be tried first, particularly in individuals who represent a high operative risk.     

Decreased bispectral index as an indicator of syncope before hypotension and bradycardia in two patients with needle phobia

We report two cases who exhibited a decrease in their bispectralindex (BIS^TM) score, associated with syncope during venipuncturein patients with suspected needle phobia. In case 1, the reductionin BIS score occurred during the development of hypotensionand bradycardia and may well have been caused by cerebral hypoperfusion.In case 2, the patient lost consciousness with decreasing BISscore before hypotension and bradycardia; this patient’scondition could not be completely explained by cerebral hypoperfusionas a result of a vasovagal reflex because the patient’sblood pressure and heart rate remained normal during the syncopalepisode. Br J Anaesth 2003; 91: 749–52     

Case of Vasovagal Syncope With Asystole Associated With Propofol Sedation

Few cases of bradycardic complications occurring under intravenous sedation have been reported. Here, we report a case of vasovagal syncope with asystole (7.2 seconds) associated with propofol sedation.Key Words: Vasovagal syncope, Propofol sedationThe vasovagal response can be triggered by stress, prolonged standing, extreme emotions, or severe pain.¹ It is caused by reduced arterial pressure and blood supply to the brain and is mediated through neural mechanisms rather than primary cardiac dysfunction.² Most modern anesthetic agents do not have anticholinergic or sympathomimetic side effects. Simple vasovagal reflexes with bradycardia and transient asystole are more common.³ Bradycardic complications have been reported to occur after induction, during, or at the end of propofol-induced anesthesia. Abrupt, unpredictable, or progressive decreases in heart rate, as well as cases of sudden cardiac arrest, under general anesthesia have been reported.^4,5 However, few cases of bradycardic complications occurring under intravenous sedation have been reported. Here, we report a case of vasovagal syncope with asystole (7.2 seconds) associated with propofol sedation.     

Trigeminocardiac reflexes: maxillary and mandibular variants of the oculocardiac reflex

Three case reports are presented to illustrate the existence and importance of reflex bradycardic responses that can occur during maxillofacial surgical procedures. All three patients were healthy young adults undergoing operations which did not include any manipulation of orbital structures. After the patients had been anaesthetized for some time and were haemodynamically stable, profound bradycardia or ventricular asystole occurred suddenly in response to manipulations of the bony structures of the maxilla or mandible, or dissection of, or traction on, the attached soft tissue structures. The parasympathetic supply to the face is carried in the trigeminal nerve. Alternative afferent pathways must exist via the maxillary and/or mandibular divisions, in addition to the commonly reported pathway via the ophthalmic division of the trigeminal nerve in the classic oculocardiac reflex. The efferent arc involves the vagus, regardless of which branch of the trigeminal nerve transmits the afferent impulses. All patients undergoing maxillofacial procedures should be monitored carefully for reflex bradycardia and ventricular asystole.     

Bradycardia leading to asystole during dexmedetomidine infusion in an 18 year-old double-lung transplant recipient

The case of an 18 year-old double-lung transplant recipient recovering from acute respiratory distress syndrome who developed repeated episodes of bradycardia and asystole (maximum duration: 10 sec) during dexmedetomidine administration is presented. Increased baseline vagal tone, paroxysmal coughing spells, and opioid administration were likely contributors to the episodes. Discontinuation of the drug restored regular sinus rhythm. Double-lung transplant recipients may be at especially increased risk for this phenomenon as a result of changes in the autonomic innervation of the heart.     

Cardiovascular autonomic function in patients with hemodynamic instability at induction of capnoperitoneum: a case–control study

Background This study hypothesized that patients in whom bradycardia and hypotension develop with induction of positive-pressure capnoperitoneum have an underlying autonomic cardiovascular dysfunction.Methods A case–control study was conducted to examine the baseline autonomic function of patients in whom bradycardia and hypotension develop with induction of positive-pressure capnoperitoneum. The control group consisted of patients who maintained normal cardiac rhythm and blood pressure during the same procedure. Two groups of tests were performed: bedside stress tests of cardiovascular autonomic function (response graded 1 (normal) to 4 (severely abnormal) and heart rate variability analysis (spectral and time domain components).Results The study evaluated 6 patients in the bradycardia group and 10 in the control group. The group in whom bradycardia had developed scored significantly worse on the bedside stress tests than the control group (for grades I to IV: ² = 6.5, p = 0.022; for trend: ² = 5.6, p = 0.018). In contrast, both groups had similar baseline autonomic tone, as measured by heart rate variability.Conclusions Patients in whom bradycardia and hypotension develop with induction of positive-pressure capnoperitoneum have cardiovascular autonomic dysfunction, which is identifiable by bedside stress tests of autonomic function.     

Head-upright tilt-table testing: a useful tool in the evaluation and management of recurrent vertigo of unknown origin associated with near-syncope or syncope.

Recurrent idiopathic vertigo associated with near-syncope and syncope is a common perplexing problem, some cases of which are considered autonomically mediated (vasovagal). Upright-tilt-table testing has emerged as a potential method to test for vasovagal episodes. This study evaluated the use of this technique in the evaluation and management of patients with recurrent idiopathic vertigo associated with near-syncope or syncope. Twenty-one patients with recurrent unexplained vertigo and syncope/near-syncope and 11 control subjects were evaluated by use of an upright-tilt-table test for 30 minutes, with or without a graded isoproterenol infusion (1 to 4 micrograms/min given intravenously), in an attempt to provoke hypotension, bradycardia, or both, which reproduced the patient's symptoms. The patients included 10 men and 11 women (mean age, 51 +/- 16 years). Eleven controls with no history of vertigo were also studied. Transcranial Doppler sonography was used to assess cerebral arteriolar blood flow during tilt. All tilt-positive patients were placed on therapy with either beta-blockers, disopyramide, or transdermal scopolamine, the effectiveness of which was determined with another tilt-table study. Symptoms occurred in seven patients (33%) during the baseline tilt and in eight patients (38%) during isoproterenol infusion (total positives, 71%). Transcranial Doppler sonography demonstrated a 225% +/- 192% increase in pulsatility index and a 70% +/- 29% increase in resistance index (indicative of cerebral arteriolar vasoconstriction) at the time of vertigo. No control subject experienced syncope during this test. Each tilt-positive patient eventually became tilt-negative with therapy, and over a mean follow-up period of 26 months, no further episodes have occurred.(ABSTRACT TRUNCATED AT 250 WORDS)