Download Unexplained asystole during thoracotomy irrigation: A case report

Unexplained asystole during thoracotomy
irrigation: A case report
MARK WELLIVER, CRNA, MS
RONALD KUMOR, CRNA, MS
Philadelphia,Pennsylvania
This case presentationinvolves a 76-year-old
man with a 60-year history of smoking one
and a halfpacks of cigarettesper day, who
presentedfor a transurethralresection of the
prostate (TURP). A preadmission chest x-ray
revealed a left upper lobe lung lesion that
was suggestive of carcinoma by subsequent
computerizedaxial tomography. The TURP
procedurewas postponed, and the patient
was advised to undergo an open thoracotomy
biopsy with possible left upper lobectomy.
The patient consented, and an open
thoracotomy biopsy confirmed carcinoma.
A left upper lobectomy was then performed.
The operativeprocedure was significantfor a
12-second acute episode of atrioventricular
standstill duringpost-thoracotomy thoracic
irrigationwith warm saline. Return of sinus
rhythm occurredspontaneously after
cessation of irrigation.The operativefield
was closed, and the patient's recovery was
unremarkable.Postoperative evaluation was
unremarkable, and the patient was
discharged1 week later.Anatomic and
physiologic vagal mechanisms are reviewed,
and applicationto this case presentation is
discussed.
Key words: Asystole, baroreceptor reflex,
lobectomy, parasympathetic
innervation, thoracotomy, vagus.
October 1998/ Vol. 66/No. 5
Case summary
A 76-year-old man with a 60-year history of smoking one and a half packs of cigarettes per day presented for a transurethral resection of the prostate
(TURP). On preadmission evaluation, a chest x-ray
revealed a left upper lobe lesion. Computerized
axial tomography further revealed a left upper lobe
"ill-defined" density that was suggestive of carcinoma. No hilar, mediastinal, or para-aortic adenopathy was found.
Subsequently, the patient was scheduled for a
left upper lobectomy. Preoperative pulmonary
function tests were performed and revealed mild
restrictive lung disease with moderate impairment
of gas transfer. The patient's cardiovascular assessment was significant for a fourth heart sound (S4)
with a grade I/VI systolic murmur and suggested
mild atherosclerotic cardiovascular disease. His
electrocardiogram (ECG) revealed a normal sinus
rhythm with left atrial hypertrophy. The patient
denied further history of cardiovascular disease.
Upon arrival to the cardiovascular/cardiothoracic operating suite, the standard routine was
begun. This included ECG, pulse oximetry, intravenous access, and central venous access, and an
arterial line and a thoracic epidural catheter were
inserted. General anesthesia was then induced with
thiopental sodium, fentanyl, and vecuronium. The
patient was intubated with a 37 French doublelumen endobronchial tube. Placement was verified by fiberoptic bronchoscopy. After the patient
was moved to the right lateral decubitus position,
451
proper tube placement was reconfirmed by fiberoptic bronchoscopy. General anesthesia was maintained with isoflurane and fentanyl, 9.0 pg/kg,
which was titrated intravenously before incision.
Muscle relaxation was maintained with vecuronium.
A left upper lobe open lung biopsy was performed. Carcinoma was confirmed, and a left upper
lobectomy followed without incident. After lobectomy, warm (approximately 38 0 C) normal saline
irrigation of the pleural cavity by the surgeon was
associated with an 8- to 12-second acute episode of
asystole. The patient's baseline heart rate was a
sinus bradycardia of 50 beats per minute. Irrigation was immediately discontinued, and manual
compression of the pericardium was performed by
the surgeon. Return of the patient's bradycardia
occurred without pharmocologic intervention.
Blood pressure was maintained after asystole at
140/60 mmHg without further intervention. Glycopyrrolate, 0.2 mg, was given intravenously to attenuate vagal tone. The vital signs remained stable
throughout surgical closure. Before the end of
closure, the patient was given a bolus of 5 mg of
morphine sulfate and 100/ g of fentanyl via the
epidural catheter for postoperative pain management. At the conclusion of surgery, neostigmine,
4.0 mg, and glycopyrrolate, 0.6 mg, was given intravenously over 5 minutes for muscle relaxant reversal. Before extubation, the patient was awake
and met all extubation criteria.
Naloxone hydrochloride, 60.0 pg intravenously, was given to increase the respiratory rate
from 12 per minute to 16 per minute, and the patient was successfully extubated. He was transferred
and maintained on full monitoring in the recovery
room and intensive care without incident. Postoperative evaluation found no pathological irregularities of cardiac function.
Physiological considerations
A review of thoracic parasympathetic innervation is helpful in understanding possible causes of
this intraoperative asystole. The vagus nerve is the
most extensive of all cranial nerves, and it is the
primary nerve of the parasympathetic system. The
origin of the vagus nerve is the nucleus tractus
solitarius in the medulla located at the base of the
fourth ventricle. As the vagus nerve descends between the jugular vein and the carotid artery, it
begins to branch (Table).
The heart is innervated by parasympathetic
and sympathetic nerve fibers. The parasympathetic
innervation to the heart is via the vagus nerve
which sends branches to the conduction system,
especially the sinoatrial (SA) and atrioventricular
(AV) nodes and, to a lesser extent, the myocardium
452
Table
Branches of the vagus nerve'
Anatomic location of
vagus nerve
v
Branches
Jugular fossa
Meningeal
Auricular
Neck
Pharyngeal
Superior laryngeal
Recurrent laryngeal
Cervical cardiac
Thoracic cardiac
Anterior pulmonary
Posterior pulmonary
Esophageal
Gastric
Thorax
Abdomen
itself. Parasympathetic innervation to the myocardium is primarily in the atrial tissue with very few
fibers in the ventricular muscle. The parasympathetic nervous system harbors the ability to set the
: 24
'
tone for cardiac function.'(P
Afferent impulses are carried centrally primarily by the glossopharyngeal and vagus nerves, and
cranial nerves IX and X, respectively. Stimulation
of the cardiac vagal nerve fibers causes the release
of acetylcholine (Ach). Among the effects of Ach
release is an increase in the permeability of the
cardiac conductive cell membranes to potassium.
The increase in permeability allows potassium to
flow more easily out of the cell causing the cell to
become more electronegative. The lower membrane
potential will require a greater stimuli to propagate an action potential or a longer period for spontaneous depolarization to occur. The net result is a
slower heart rate. In addition, stimulating cardiac
muscarinic receptors inhibits norepinephrine release from adrenergic receptors, preventing normal sympathetic derived cardiac tone and, thus,
furthering the vagotonic effects.3
It is well known that vagal stimulation can
cause severe bradycardia and, in rare .rcumstances,
asystole. The Valsalva maneuver, carotid sinus massage, diving reflex, occulocardiac reflex, and visceral traction all cause vagally medicated bradycardia. Berk et al tested several vag.ly mediated
reflexes: diving reflex, Valsalva maneuver, carotid
massage, ocular compression, and Muller maneuver (inspiration against a closed glottis) and found
the diving reflex produces the greatest slowing of
heart rate.
Cervical and thoracic cardiac branches terminate as a cardiac plexus surrounding the aorta.
Specific receptors of the cardiac plexus along the
aortic arch respond to longitudinal and circumferential stretch of the vessel and send afferent vagal
Journalof the American Association of Nurse Anesthetists
impulses to the vasomotor center (nucleus tractus
solitarius) in the medulla." Efferent vagal impulses
.travel back from the vasomotor center to the heart
to slow firing of the SA and AV nodes and also
cause vasodilatation. This is known as the baroreceptor reflex.
If these baroreceptors, found in abundance in
the aortic arch and carotid arteries, receive strong
enough stimulation, complete cessation of heart
rate can occur. The cardiac vagal plexus tissue itself may be stimulated mechanically. An impulse
can be generated with a stimulus anywhere along a
nerve fiber: at the dendrite, cell body, or axon.
Direct nerve stimulation could mimic massive baroreceptor discharge by utilizing the same nerve pathway but with an axonal or cell body origin. Vagally
mediated asystole, even with strong continued stimulation, is not sustainable due to the little vagal
and high sympathetic innervation of the ventricles.;
The asystole usually lasts 5 to 20 seconds until ventricular escape beats or a higher pacemaker takes
over.
There are two main types of pulmonary vagal
nerve receptors: stretch and irritant. The HeringBreuer reflex is a stretch receptor reflex carried by
the vagus nerve centrally that causes a reflex to
end inspiration. Irritant receptor stimulation also
travels centrally to the medulla, and vagal efferent
impulses cause coughing.t It is possible for stimulation of vagal nerve fibers in the respiratory tract
to cause reflex bradycardia and hypotension. Visceral traction and rectal distention may also elicit
'1
the celiac reflex. nia
Discussion
In this case study, we have discussed several
likely mechanisms of the bradycardia: the celiac or
baroreceptor reflex and direct cardiac vagal plexus
stimulation. Pulmonary vagal afferent impulses
may cause cardiac asystole. This mechanism is not
likely as the irrigant was poured into a pleural
space devoid of the upper lobe lung tissue and its
innervation. Ligated tissues or the lower lobe may
have been stimulated by the irrigant, but the direction of the irrigant flow was downward onto the
October 1998/ Vol. 66/No. 5
mediastinal pleura. We have postulated that the
mechanical stimulation of the falling irrigant onto
the arotic arch, immediately inferior to the exposed
pleura, caused massive baroreceptor discharge or
direct nerve tissue stimulation and resulted in the
asystole. The pressure, caused by the falling irrigant
from approximately 5 inches above the open chest
cavity, is suggested to be enough to cause direct
nerve stimulation and likely baroreceptor firing.
The asystole is not felt to be related to the
temperature of the irrigation fluid as the temperature was approximately 38 0 C. Lingaraju et al found
that mean heart rate actually increased with pericardial warm irrigation (44 0 C ± 5°C) in postcardiopulmonary bypass patients." Questions left
unanswered include the following: Does narcoticinduced bradycardia accentuate vagotonic effects
thus predisposing patients to heightened vagal reflexes? Was this asystole mediated by an unidentified reflex similar to the celiac, baroreceptor, and
other reflexes?
In the light of this case experience, we believe
gentle irrigation of the thoracic cavity may decrease
the likelihood of asystole from occurring. Thoracic
irrigation-induced asystole needs to be investigated
further to identify a definitive cause. We are unable to offer any specific suggestions for preventing another occurrence of this event until a definitive cause is identified.
REFERENCES
(1)
;ray H. Gray sAnatomy. 15th ed. New York: Bounty Books. 1995:
1252.
(2) Barasch PG, Cullen BF, Stoelting RK. Clinical Anesthesia. 2nd ed.
Philadelphia: JB Lippincott. 1990.
(3) (;uyton AC, Hall JE. 7extbook of Medical lPhsiology. 9th ed. Philadelphia: WB Saunders. 1996:126.
(4) Berk WA, Shea MJ, Crevey MI). Bradvcardic responses to vagally
mediated bedside maneuvers in healthy volunteers. Am / Med.
1991;90:725-728.
(5) Assef SJ. Carotid sinus and carotid body physiology. In: Faust Rj.
ed. Anesthesiology Review. New York: Churchill Livingstone. 1994:214-216.
(6) Lingaraju N, Horrow JC, Colonna-Romano P, Strong MI).
Haemodynamic consequences of warm cardiac irrigation during cardiac surgery. Can J Anaesth. 1994;41:384-386.
AUTHOR
Mark Welliver, CRNA, MS, is a stall nurse anesthetist at 'Thomas
Jefferson University IHosp)ital. Philadelphia, Pennsylvania.
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