INTERN SEMINAR: Severe Bradycardia During Cesarean Section Ri 黃哲南 & Ri 陳雅茹.
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Transcript of INTERN SEMINAR: Severe Bradycardia During Cesarean Section Ri 黃哲南 & Ri 陳雅茹.
INTERN SEMINAR: Severe Bradycardia During Cesarean Section
Ri 黃哲南 & Ri 陳雅茹
Brief History 36-year-old Korean woman Height: 165cm Weight: 83.6kg GA 37 weeks, admitted for scheduled C/S Regular examination revealed a healthy
pregnancyno hypertensionno gestational diabetes mellitus (GDM)
Obs / Gyn History
G5 P3 SA1P1: NSDP2: C/S due to placenta previaP3: C/S due to prior C/S
Menarche: 13 y/o Interval / Duration: 28 days / 4days LMP: 93/8/24 EDC: 94/5/25
Past History
Deny any systemic disease Previous OP history: C/S X 2, both were
uneventful Smoking: nil Alcohol consumption: nil Drug or food allergy: denied
Physical Examination Consciousness: clear and alert T/P/R: 36.4 / 100 / 20℃ HEENT: grossly normal
Conjunctiva: not pale Sclera: anicteric Neck: supple, no LAP, JVE or goiter Chest: symmetrical expansion, clear BS Heart: RHB, no audible murmur Abdomen: ovoid, normoactive BoS Extremities: freely movable, no cyanosis
Laboratory Examination
Date RBC Hb PLT WBC Band Seg Eos
5/3 4.38 11.1 274 7.57 0 71.7 3.3
Date BUN Cre Alb AST ALT
3/16 10.1 0.7 3.93 23 6
Date Na K Cl Ca
3/16 136 4.1 105 1.95
Date PT INR PTT
3/16 11.6 0.98 29.2
Clinical Course Pre-anesthetic evaluation was unremarkable Classified as ASA class 1
Clinical Course
C/S was performed on May 4 under spinal anesthesia
A male baby, weighed 3114 gm, was delivered smoothly
Uterus was pulled out, and a huge myoma was noted at the fundus of uterus
Clinical Course Progressive bradycardia and loss of consci
ousness were noted (slowest HR was 20/min)
NIBP was un-measurable CPR was started Near-asystole had been shown by ECG dur
ing resuscitation
Clinical Course Atropine (1mg) and epinephrine (0.05mg) w
ere given intravenously Vital signs became stable within minutes, a
nd consciousness was regained gradually No more hemodynamic unstability develope
d during the remained operation ABG
pH=7.461 PaCO2=22.4 PaO2=284.2
HCO3=16.0 BE=5.6 Estimated blood loss was 400 mL
Clinical Course Sent to 4FI for further close observation Cardiologist was consulted
Clinical Course Cardiologist consultation
PE: same as admission evaluationEKG:
Sinus tachycardia (HR=104/min) Non-specific ST-T change at lead III and aVF
Echocardiography: Good LV contractility (LVEF=72%) Mild TR (PG=28mmHg) Mild MR No chamber dilatation
Impression: Vasovagal reflex
Clinical Course
No cardiac event occurred in 4FI, so she was transferred to 5B on May 5
The following admission course was uneventful, and she discharged on May 9 (Post OP Day 5)
Discussion
Differential Diagnosis
High spinal block and spinal induced sympathectomy
Massive hemorrhage Amniotic fluid embolism Pulmonary embolism Myocardial infarction Bezold-Jarisch reflex & Vasovagal reflex
Bezold-Jarisch Reflex
Anesthesiology 2003; 98:1250–60Clinical Relevance of the Bezold–Jarisch Reflex
1867: Bezold and HirtVeratrum alkaloid Hypotension, bradycardia, apnea
Definition of Bezold-Jarisch reflex:By Dawes in 1947Hypotension, bradycardia, peripheral vasodilation
Clinical Relevance of the Bezold–Jarisch ReflexAnesthesiology 2003; 98:1250–60
Anesthesiology 2003; 98:1250–60
Anesthesiology 2003; 98:1250–60
Anesthesiology 2003; 98:1250–60
Anesthesiology 2003; 98:1250–60
Vasovagal Reflex
Stimulus Afferent pathway Efferent response
Higher centers
Medullary vasomotor center
Pain, Emotion
Carotid sinus sensitivity
Carotid sinus
Aortic baroreceptors
Ventricular afferents
Vagus
Decreased Venous return Unmyelinated ‘c’ fibers.
Respond to chemical and mechanical stimuli. Enhanced activation by β2 receptor stimulation.
Other viscera e.g. bladder
Pancreatic polypeptide
Bradycardia
+
Vagus nerve
NEVasodilation in resistance vessels
Adrenal gland
Epinephrine-vasodilation in skeletal muscles
+
Sympathetic
British Journal of Anaesthesia 86(6):859-68 (2001)
+
IX
CausesHemorrhageOrthostasisCompression of inferior vena cava during pre
gnancyRegional anesthesia
British Journal of Anaesthesia 86(6):859-68 (2001)
The current pathophysiological hypothesis for such vasovagal episodes holds that a rapid preload reduction causes an abnormally elevated inotropic response, due to an exaggerated catecholamine release.
Chest Volume 117(6) June 2000; pp 1801-1803
Stroke Volume 29(11) November 1998 ; pp 2347-2351
The increase in myocardial contractility in the setting of a preload reduction activates cardiac mechanoceptors, mediating via the brain stem an abnormal enhancement of parasympathetic activity, together with a sympathetic withdrawal.
Chest Volume 117(6) June 2000; pp 1801-1803
Stroke Volume 29(11) November 1998 ; pp 2347-2351
Management
Restoration of venous return
Head-down tilt or leg elevation Compression of the vena cava should be r
elieved in obstetric cases If hypovolemia was considered, IVF shoul
d be given
British Journal of Anaesthesia 86(6):859-68 (2001)
Medication:
Anticholinergic drugs: Atropine
Not be the best single agent if bradycardia is suspected to be accompanied by vasodilation
Sympathomimetic drugs: Ephedrine
Direct sympathetic effects on the heart rateEpinephrine
British Journal of Anaesthesia 86(6):859-68 (2001)
Thump pacing for asystolePrompt treatment with epinephrine has been em
phasized as crucial for successful recoveryEpinephrine may be necessary during cardiac arr
est in association with high spinal anesthesiaFor asystole or persistent severe bradycardia, ep
inephrine should be used early
British Journal of Anaesthesia 86(6):859-68 (2001)
Thank you for your attention!