|Year : 2016 | Volume
| Issue : 2 | Page : 82-84
Carotid sinus hypersensitivity: Entity warrants a caution in the critical care unit
Sugata Dasgupta1, Soumi Das2, Arunima Chaudhuri3
1 Department of Anaesthesiology, Division of Critical Care Medicine, R. G. Kar Medical College, Kolkata, West Bengal, India
2 Department of Anaesthesiology and Critical Care, R. G. Kar Medical College, Kolkata, West Bengal, India
3 Department of Physiology, Burdwan Medical College, Burdwan, West Bengal, India
|Date of Web Publication||18-May-2016|
Krishnasayar South, Borehat, Burdwan - 713 102
Source of Support: None, Conflict of Interest: None
Carotid sinus hypersensitivity (CSH) syndrome is an entity caused by an overreaction of the carotid sinus baroreceptors to stimulation. Three subtypes of CSH syndrome are recognized according to the response to carotid sinus massage (CSM): Predominantly cardioinhibitory, predominantly vasodepressor and a mixed subtype. We report here the case of a middle-aged female patient admitted in our critical care unit with respiratory failure requiring mechanical ventilation. There were episodes of severe bradycardia whenever her head was rotated to any side, relieved on neutralizing head position and administering intravenous atropine. CSM revealed she had predominantly cardioinhibitory type of CSH syndrome. A cardioinhibitory form of hypersensitive carotid sinus reflex, which is idiopathic in causation, probably explains the severe bradycardia on head rotation seen in our patient. A heightened awareness of this syndrome is necessary for timely diagnosis and management. CSH syndrome results from an overreaction of the carotid sinus baroreceptors to stimulation, manifesting commonly as bradycardia, hypotension and syncope. It is an entity, which warrants caution during routine critical care practices.
Keywords: Airway reflexes, cardiovascular system responses, carotid sinus hypersensitivity
|How to cite this article:|
Dasgupta S, Das S, Chaudhuri A. Carotid sinus hypersensitivity: Entity warrants a caution in the critical care unit. J Sci Soc 2016;43:82-4
| Introduction|| |
Carotid sinus hypersensitivity (CSH) syndrome results from an overreaction of the carotid sinus baroreceptors to stimulation, manifesting commonly as bradycardia, hypotension and syncope. It is detected in approximately one-third of elderly patients who present with either syncope or fall. It may be in asymptomatic elderly patients.  Risk factors include female gender, advanced age (over 50 years), hypertension, vasovagal syncope attacks, , history of previously treated head and neck cancers, head and neck surgery with tight surgical scar.  It is estimated that the number of newly diagnosed cases of CSH associated with syncope or presyncope is 35/million population/year.  We report here a case of cardioinhibitory form of CSH in a young, adult, asymptomatic female patient under mechanical ventilation in our critical care unit.
| Case report|| |
A 42-year-old female patient was admitted to our critical care unit with respiratory failure due to pneumonia requiring mechanical ventilation. However, the head extension during laryngoscopy for endotracheal intubation was accompanied by sudden severe bradycardia with heart rate decreasing to 30 beats/min. Her systolic blood pressure decreased slightly from 110 to 90 mm Hg. Bradycardia subsided on administering intravenous atropine 0.6 mg and repositioning the head. Following this, she was put on mechanical ventilation and was sedated. Another such episode occurred when her head was rotated to one side to reduce drag on the ventilator circuit. On this occasion also, her heart rate reduced to 40 beats/min but her blood pressure remained stable which subsided after neutralizing the head position and administering intravenous atropine. It was found that on subsequent occasions of head turning to either side, she developed similar such episodes. Carotid sinus massage (CSM) on the right and left sides were performed allowing a 30 s interval between stimuli, and it was found that she developed ventricular asystole for about 4 s which was not preceded by a drop in blood pressure. CSM was performed both in supine and upright positions (70° head-up tilt) keeping resuscitative drugs and equipments ready. She had no prior history of syncope or presyncope, history of head and neck surgery and was on no cardiovascular medications. Her transthoracic echocardiography and bilateral Doppler of carotid arteries done subsequently were normal. Development of severe bradycardia with stable blood pressure associated with head extension and rotation in this patient and development of ventricular asystole for ≥3 s not preceded by drop in blood pressure points toward the diagnosis of cardioinhibitory type of CSH syndrome although the patient was asymptomatic before. The patient's head was cautiously maintained in the neutral position till she was weaned from mechanical ventilation. She was educated prior to critical care unit discharge regarding avoidance of maneuvers, which can stimulate the carotid sinus.
| Discussion|| |
The symptoms of the carotid sinus syndrome (CSS) are precipitated by maneuvers, which cause mechanical stimulation of the carotid sinus (for example, head turning in the presence of tight neck wear and straining).  Kenny and Traynor  their study found that in 52% patients symptoms of CSS were precipitated by head movement and in 48% by vagal stimuli.
Carotid sinus massage is essential for the diagnosis and categorization of CSH. There are three subtypes of CSH depending on the response to CSM. Cardioinhibitory CSH (in approximately 80% of affected individuals)  is defined as ventricular asystole exceeding 3 s during CSM, although normal limits have not been definitively established.  In fact, asystole exceeding 3 s during CSM is not common but can occur in asymptomatic patients.  Vasodepressor CSH (in 10% of affected individuals)  is generally defined as a decrease in systolic blood pressure of 50 mm Hg or more without associated cardiac slowing or a decrease in systolic blood pressure exceeding 30 mm Hg when the patient's symptoms are reproduced.  The remaining 10% exhibit components of both reflexes. 
Atropine abolishes cardioinhibitory CSH. However, most symptomatic patients require pacemaker implantation (class I indication). 
A review  of anesthetic management of three patients with hyperactive carotid sinus reflex reported one case of intraoperative cardiac arrest in a patient pretreated with scopolamine who recovered after local anesthesia of the carotid sinus. There is a case report of a 62-year-old woman on oral nifedipine undergoing elective surgery who developed severe bradycardia and electromechanical dissociation from neck manipulation and vasovagal reaction after failed attempt to intubate.  In another case, sudden cardiac arrest developed during robotically assisted endoscopic total thyroidectomy while the dissection near the diseased thyroid.  A recurrent thyroid carcinoma patient previously treated with surgery and radiotherapy developed asystolic periods on two occasions during positioning of the neck in hyperextension during surgery. 
Our patient developed severe bradycardia not associated with a fall in blood pressure whenever her head was extended or rotated to any side for purposes of intubation or position changes, which are integral parts of intensive care management. Her diagnosis of cardioinhibitory CSH was confirmed after performing CSM. However, the patient had given no prior history of syncope or presyncope. A high clinical suspicion led us to the diagnosis and timely management, in this case. Our patient was below 50 years age, non-hypertensive, without coronary artery disease or any history of head and neck tumors or previous surgery. Therefore, the probable cause of CSH in our patient is idiopathic.
In conclusion, the diagnosis of CSH as a cause of severe bradycardia, hypotension or syncope should be suspected even in asymptomatic young patients if it is associated by maneuvers stimulating the carotid sinus.
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