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

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


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


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


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


Thank you for your attention!

intern seminar: severe bradycardia during cesarean section ri 黃哲南 & ri 陳雅茹

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