Bradycardia during cold ocular irrigation under general anaesthesia: an example of the diving reflex
George A. Arndt
0
1
M. Christine Stock ~
0
0
From the Departments of Anesthesiology,Universityof WisconsinClinical ScienceCenter
1
Madison
,
Wisconsinand Emory UniversitySchool of Medicine
,l"Atlanta,
Georgia
. Department of Anesthesiology
,
Universityof Wisconsin Clinical ScienceCenter
, B6/387 CSC, 600 Highland Avenue,
Madison
,
WI 53792
. Acceptedfor publication 22nd February
, 1993
A case o f bradycardia is reported which was precipitated by cold normal saline applied to the eye during general anaesthesia. The history and physiology o f the diving reflex is discussed and we believe that these data suggest that this patient's bradycardia was induced by the diving reflex, and not by the oculocardiac reflex. Nous rapportons un cas bradycardie provoquOepar l'application oculaire de solut~ physiologique froid. La discussion porte sur I'histoire et la physiologie du r~flexe de plongke. Nous croyons que ces donn~es supportent notre hypoth~se d'un bradycardie provoqu~e par le r~flexe de plong~e et non par le rdflexe oculocardiaque.
-
The oculocardiac reflex, well-described in the anaesthesia
literature, results from a variety of stimuli including
traction on the extraocular muscles, ocular manipulation,
pressure or traction on the globe, or pressure applied to
an empty orbit. I-5 However, even in the absence of these
stimuli, cold ocular irrigation may elicit bradycardia
induced by the diving reflex. The oculocardiac reflex is
active in awake and anaesthetized subjects and is
manifested by a variety of dysrhythmias, which include
bradycardia, bigeminy, ectopic beats, nodal rhythm, and
asystole. 6-8 The diving reflex may have similar physiological
mechanisms and clinical significance.
Case report
A 60-yr-old woman was scheduled for left scleral buckle.
Her past medical history was unremarkable, with no
history of cardiovascular, neurological, renal, haematopoetic,
endocrinological, or pulmonary disease. She did not
smoke or use alcohol or take medications. Previously she
had undergone two gynaecological operations during
uncomplicated general anaesthesia. Physical examination
was normal and there was no syncopal history. The
preoperative laboratory results were normal, with
haemoglobin and haematocrit 13.7 gin. dl-I and 39.7%,
respectively. The preoperative 12-lead electrocardiograph
(ECG) showed normal sinus rhythm with no suggestion
of ischaemia. The vital signs the day before surgery were
blood pressure 140/80 mmHg, pulse 88 beats, min -I and
respirations 18 breaths, min -x. She weighed 55.7 kg and
was 155 cm tall. Sixty minutes before her operation, the
patient received diazepam I0 mg po, and a peripheral
/v infusion of lactated Ringer's solution with 5% dextrose.
Intraoperative monitoring included a fivedead
continuous ECG which displayed limb lead II. After
preoxygenation, anaesthesia was induced with thiopentone 275
mg and lidocaine 100 mg /v. Tracheal intubation was
facilitated with succinylcholine 80 mg/v, and was easily
accomplished. Anaesthesia was maintained with 1%
isoflurane and 50% nitrous oxide in oxygen. Ventilation was
controlled so that end-tidal carbon dioxide concentration
was 36 mmHg. Relaxation was maintained with 5 mg
/v vecuronium bromide. Vital signs did not vary by more
than 5% during anaesthetic induction and maintenance
up to this point.
Fifteen minutes after induction, a watertight drape was
placed around the left eye and the surgeon began to
irrigate the eye liberally with sterile, room-temperature,
normal saline. The temperature of the saline was 19.7~
The heart rate promptly decreased from 78 beats, min -1
with normal sinus rhythm to a sinus bradycardia of 30
beats, min-l. The surgeon stopped the irrigation and
atropine 0.4 mg was given/v. The heart rate increased to
90 beats- min -I with normal sinus rhythm. The episode
of bradycardia was short-lived (lasting approximately 20
sec), and quickly returned to an acceptable rate with
atropine administration and cessation of irrigation. During
the episode, no ocular stimulus was present other than
application of cold saline; the surgeon had placed no
retractors, instruments, retracted the eye muscles or placed
pressure on the eye. Pulse oximetry revealed that the
patient was not hypoxic during the episode, neither did
she become hypotensive, the blood pressure remaining
at 110/80 as measured by auscultation before, during and
after the episode. After the heart rate stabilized, the
surgeon proceeded cautiously with ocular irrigation which
caused no further change in vital signs. We were unable
to record a rhythm strip during the episode. The drape
was found to form a watertight seal, preventing the
irrigation solution escaping from the field.
The remainder of anaesthesia was uneventful. The vital
signs remained stable. At the end of the procedure muscle
relaxation was reversed with glycopyrrolate and
neostigmine with no change in heart rate. Emergence was
uncomplicated and the tracheal tube was removed when
the patient opened her (...truncated)