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Case Reports  |   May 2003
Complete Vasomotor Collapse: An Unusual Manifestation of the Carotid Sinus Reflex
Author Affiliations & Notes
  • James R. Boyce, M.D., F.R.C.P.C.
    *
  • Glenn E. Peters, M.D., F.A.C.S.
  • * Professor and Division Director, Department of Anesthesiology. † John S. Odess Professor of Surgery and Division Director, Department of Surgery, Division of Otolaryngology Head and Neck Surgery.
  • From the Department of Anesthesiology, University of Alabama at Birmingham, Birmingham, Alabama.
Article Information
Case Reports
Case Reports   |   May 2003
Complete Vasomotor Collapse: An Unusual Manifestation of the Carotid Sinus Reflex
Anesthesiology 5 2003, Vol.98, 1285-1287. doi:
Anesthesiology 5 2003, Vol.98, 1285-1287. doi:
THE carotid sinus is a major part of the arterial baroreceptor reflex system. 1,2 When the arterial vessel wall of the sinus is deformed during rapid pressure changes in the systemic arteries, the stretch receptors in the right and left carotid sinuses and aortic arch are activated, which elicits the threefold response of bradycardia, hypotension, and apnea. 2 Usually bradycardia is the most common response associated with the reflex. 3 This case report describes sudden intraoperative hypotension without bradycardia, which we think was an unusual manifestation of the carotid sinus reflex.
Case Report
A 45-yr-old white man presented with recurrence of a right carotid body tumor. One year earlier, a carotid body tumor was removed, at which time the right internal jugular vein and right vagus nerve were excised due to tumor involvement. The tumor recurrence involved the right carotid artery, necessitating excision and replacement with an autologous vein graft. The preoperative assessment revealed normal electrocardiographic results and no history of dysrhythmias or syncope.
In addition to the standard monitors, an intraarterial catheter and electroencephalogram leads were placed. Anesthesia was induced using 250 μg fentanyl, 150 mg propofol, and 14 mg cisatracurium. Tracheal intubation was accomplished without difficulty and without significant variations in heart rate and blood pressure. Isoflurane and oxygen were administered for maintenance anesthesia. When the right carotid artery was cross-clamped below the tumor at the common carotid artery bifurcation, the EEG indicated adequate collateral flow and the blood pressure and pulse were stable. During resection of the isolated portion of the carotid artery, the blood pressure suddenly decreased to 0 mmHg. The absence of any systemic pressure was confirmed by absent heart sounds from the precordial stethoscope, loss of waveform on the pulse oximeter, and absence of any palpable femoral or left carotid pulsation. The EEG that had been normal for the 15 min after cross-clamping displayed evidence of global ischemia. However, the electrocardiogram was unchanged, showing normal sinus rhythm at 76 beats/min. Cardiopulmonary resuscitation was instituted and 0.5 ml epinephrine (1:10,000) was administered intravenously. During chest compressions, the arterial catheter showed systolic pressures of 30–40 mmHg, then rapidly increased to 260/140 mmHg with a tachycardia of 150 beats/min at 45 s after epinephrine administration. Soon the blood pressure, heart rate, and EEG returned to baseline values. Arterial blood gas and chemistry measurements were normal as was follow-up electrocardiogram and cardiac enzyme studies. The subsequent surgical and postanesthetic course was uneventful.
Discussion
We believe that, during surgical dissection and excision of the recurrent tumor, the surgical instruments perturbed the right nerve of Hering and produced supramaximal stimulation of the afferent limb of the baroreceptor reflex. The noteworthy features of this event were the absence of bradycardia and the extent of the vasomotor collapse.
The afferent limb of the baroreceptor reflex is composed of two separate nerves. One nerve, the nerve of Hering, carries impulses from both the carotid sinus and the carotid body. 2 It is a branch of the glossopharyngeal (IX) cranial nerve. The other nerve is the aortic depressor nerve, a branch of the vagus, which carries impulses from stretch receptors in the aortic arch. The receptors in the vessel wall of the carotid sinus and the aortic arch are composed of mechanosensitive ion channels, 4 which respond to deformation of the vessel wall with changes in blood pressure. The generated impulses are carried in the afferent fibers to synapse with secondary neurons in the nucleus tractus solitarius of the dorsal medulla. The efferent limb of the reflex is also twofold: one part is the vagus nerve with predominant innervation of the sinoatrial node in the right atrium 5; the other part is the sympathetic innervation to the blood vessels.
When the baroreceptor reflex is activated, usually by increases in blood pressure, impulses in the vagal efferent component of the reflex are increased, releasing acetylcholine at the muscarinic receptors in the sinoatrial node, slowing the heart rate. However, impulses in the sympathetic efferent component are decreased and the reduced release of norepinephrine causes arteriolar and venous dilation with resultant hypotension. During surgical procedures in the neck (e.g.  , carotid endarterectomy), mechanical stimulation of the carotid sinus commonly elicits the baroreceptor reflex with bradycardia and occasionally hypotension. Administration of a muscarinic blocker such as atropine or field application of a local anesthetic typically eliminates further reflex activity.
The mechanosensitive ion channels are normally responsive to vessel wall stretching in the pressure range of 60–200 mmHg, 1,2 and they are most affected by the rate of pressure change (i.e.  , the rate of increase of left ventricular pressure, dP/dt), and the diastolic blood pressure. 6 In our patient, the blood pressure initially was stable, fluctuating in a small range with normal values. Probably, the mechanical stimulation of the carotid sinus or the nerve of Hering itself provided the afferent input necessary for a maximal response from the sympathetic component of the reflex, namely complete cessation of sympathetic activity to the vasculature. Experiments in animals have demonstrated cessation of postganglionic sympathetic nerve activity in response to electrical stimulation of the carotid sinus nerve. 7 Human experiments using pharmacologic manipulation of systemic blood pressure to elicit the baroreceptor reflex have also demonstrated sympathetic ablation in response to acute blood pressure elevation. 8,9 Shoukas et al.  10 contend that the reduction of sympathetic activity is equally manifested in both arterial and venous components of the vascular tree. In our patient, the sudden decrease in pressure from normal levels to 0 suggests both reduction in afterload by arteriolar dilatation and reduction in preload by an increase in venous capacitance.
The absence of bradycardia in association with the hypotension made the diagnosis difficult. Anaphylaxis and venous air embolism were other considerations; however, no recent medications or blood products had been given and, though the end tidal CO2decreased to near 0, no mill-wheel murmur was detected when listening for heart sounds. Because the sinoatrial node is innervated primarily by the right vagus nerve with little involvement from the left vagus nerve, 5 the predominant source of cholinergic-induced bradycardia associated with the baroreceptor reflex was missing because the right vagus nerve was excised during the previous surgery (fig. 1).
Fig. 1. Stimulation of the carotid sinus and the aortic arch produces afferent impulses in the glossopharyngeal and vagal depressor nerves. The efferent limbs are the vagus to the sinoatrial node and the decrease in sympathetic activity to the vasculature. In our case the vagal component was absent due to previous surgical excision.
Fig. 1. Stimulation of the carotid sinus and the aortic arch produces afferent impulses in the glossopharyngeal and vagal depressor nerves. The efferent limbs are the vagus to the sinoatrial node and the decrease in sympathetic activity to the vasculature. In our case the vagal component was absent due to previous surgical excision.
Fig. 1. Stimulation of the carotid sinus and the aortic arch produces afferent impulses in the glossopharyngeal and vagal depressor nerves. The efferent limbs are the vagus to the sinoatrial node and the decrease in sympathetic activity to the vasculature. In our case the vagal component was absent due to previous surgical excision.
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Exactly how the nerve of Hering was stimulated to elicit such a profound hypotensive response is unclear. In experimental animals, the stimuli used in baroreflex studies include electrical stimulation of the carotid sinus and aortic depressor nerves, with supramaximal intensity for 0.1 ms at 1–200 Hz. 7 Perhaps the use of electrocautery was the precipitating stimulus in our case. It is also possible that simple mechanical stimulation, often seen in carotid surgery, was the cause.
Anesthetic agents can have a profound effect on the baroreceptor reflex. Propofol at infusion rates of 200 μg · kg−1· min−1, but not 100 μg · kg−1· min−1, will block sympathetic nervous system–mediated responses when baroreceptors are stimulated experimentally, but it has no effect on the vagal component. 11 The propofol we used on induction could cause initial hypotension by a baroreceptor reflex–related sympathetic block, but it would be an unlikely etiologic factor an hour after induction. The isoflurane we used for maintenance of anesthesia could have contributed to the hypotension. McCallum et al.  12 showed that 1.5% isoflurane abolished all sympathetic reflex responses to bilateral carotid artery occlusion. Prior to the vascular collapse, our patient was stable with a 1.1% end-tidal concentration of isoflurane, but it can be surmised that this inhalational agent exacerbated the hypotensive response to carotid sinus stimulation.
Early animal experiments by Glick and Braunwald 13 indicated that the heart rate response to baroreceptor stimulation was mediated both vagally (increased efferent activity) and sympathetically (decreased efferent activity). If such were the case in humans, our patient would have manifested at least partial reduction of heart rate by the cessation in sympathetic activity at the sinoatrial node. However Leon et al.  14 observed that humans, adrenergically blocked with 10 mg propranolol intravenously, responded with both bradycardia and tachycardia to pharmacologically induced hypertension and hypotension, respectively. These investigator concluded that although β-adrenergic activity may influence basal heart rate, it exerts little if any influence on baroreflex heart rate control. This conclusion is consistent with our case because the hypothesized supramaximal carotid sinus nerve stimulation produced profound vascular collapse, presumably through reflex sympathectomy, but the heart rate was unchanged due to vagal denervation of the sinoatrial node.
In summary, we present a case of acute vasomotor collapse, which resulted from intraoperative dissection of recurrent carotid body tumor. Prior excision of the right vagus nerve prevented any heart rate response, namely bradycardia.
The authors thank David H. Chestnut, M.D. (Chairman, Department of Anesthesiology, University of Alabama at Birmingham, Birmingham, Alabama) for his review of this manuscript prior to submission.
References
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Zipes DP: Genesis of cardiac arrhythmias: electrophysiological considerations, Heart disease, 2nd edition. Edited by Braunwald E. Philadelphia: WB Saunders Company, 1984, pp 605–6
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Fig. 1. Stimulation of the carotid sinus and the aortic arch produces afferent impulses in the glossopharyngeal and vagal depressor nerves. The efferent limbs are the vagus to the sinoatrial node and the decrease in sympathetic activity to the vasculature. In our case the vagal component was absent due to previous surgical excision.
Fig. 1. Stimulation of the carotid sinus and the aortic arch produces afferent impulses in the glossopharyngeal and vagal depressor nerves. The efferent limbs are the vagus to the sinoatrial node and the decrease in sympathetic activity to the vasculature. In our case the vagal component was absent due to previous surgical excision.
Fig. 1. Stimulation of the carotid sinus and the aortic arch produces afferent impulses in the glossopharyngeal and vagal depressor nerves. The efferent limbs are the vagus to the sinoatrial node and the decrease in sympathetic activity to the vasculature. In our case the vagal component was absent due to previous surgical excision.
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