MAMC Journal of Medical Sciences

: 2022  |  Volume : 8  |  Issue : 1  |  Page : 79--81

A Case Report of Sudden Bradycardia and Impending Cardiac Arrest by Intramyometerial Vassopressin in Laproscopic Myomectomy

Shubhangi Sharma, Sameer Raj 
 ESI Hospital, Maneser, Gurugram, Haryana, India

Correspondence Address:
Dr. Shubhangi Sharma
ESI Hospital, House no. 629, Sector 14, Gurgaon 122001, Haryana


Vasopressin has long been used in myomectomy to decrease blood loss. Its efficacy is beyond doubt. But at the same time, it is known to cause some of the serious cardiovascular side effects. We are here to report a case of severe bradycardia and impending cardiac arrest caused by intramyometerial infiltration of 13 IU of vasopressin.

How to cite this article:
Sharma S, Raj S. A Case Report of Sudden Bradycardia and Impending Cardiac Arrest by Intramyometerial Vassopressin in Laproscopic Myomectomy.MAMC J Med Sci 2022;8:79-81

How to cite this URL:
Sharma S, Raj S. A Case Report of Sudden Bradycardia and Impending Cardiac Arrest by Intramyometerial Vassopressin in Laproscopic Myomectomy. MAMC J Med Sci [serial online] 2022 [cited 2022 Jul 2 ];8:79-81
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Vasopressin, a posterior pituitary hormone, is used to reduce blood loss during myomectomy from more than 60 years. Although intramyometerial vasopressin results in good hemostasis, it may cause adverse cardiac events such as bradycardia, arrhythmia, and cardiac arrest by intramyometerial injection of vasopressin in case of laparoscopic myomectomy.

 Case Report

A 27-year-old nulliparous woman, a case of primary infertility with posterior wall intramyometerial fibroid, was posted for elective hysterolaproscopy. She had no medical or surgical history. All her hematologic, biochemical investigations, and electrocardiogram (ECG) was normal. The woman was American Society of Anaesthesiologist grading (ASA) grade 1 and after thorough evaluation, she was taken for surgery after 6 hours of fasting. She was monitored by five lead ECG, non invasive blood pressure (NIBP), pulse oximeter, and end-tidal CO2 (ETCo2). Baseline vitals were pulse 82/minute, blood pressure (BP) 120/76, O2 saturation 100% on room air with normal sinus rhythm. She was preloaded with 1 L ringer lactate. The choice of anesthesia was regional anesthesia with sedation. Combined spinal epidural was given at L3-4 space with bupivacaine (H) 0.5% 3.5 mL and 25 μg fentanyl and test dose with 45 mg lignocaine with 15 μg adrenaline. Level of spinal anesthesia achieved was T6. Dexmedetomidine infusion was started at the rate of 1 μg/kg/hour for first 10 minutes as loading followed by 0.3 μg/kg/minute along with fentanyl 50 μg before insufflation of pneumoperitoneum.

Intraoperatively all vitals remain stable till hysteroscopy was performed. A large subserosal fibroid measuring 7 by 7 cm was visualized in posterior wall of uterus arising from isthmus. Before starting myomectomy to reduce the blood loss 180 mL of intramyometerial vasopressin injected in dilution of 20 IU in 300 mL (13 IU in total) slowly after negative aspiration. Within 1 minute of vasopressin infiltration patient developed sudden bradycardia with heart rate dropping to 25 bpm, hypotension as evidenced by systolic BP of 70. The patient had normal SpO2 and normal ETCo2 at this time indicating adequate perfusion. Peripheral pulses were feeble and there was facial pallor. Pneumoperitoneum was deflated, injection atropine. Six milligram was given at interval of 30 seconds and 1 minute, respectively. Intravenous crystalloids were given fast with heart rate improving to 80 to 90 bpm and BP values improving to 90/60 mmHg, SpO2, and ETCo2 were normal throughout the surgery. Although patient was in regional anesthesia, we could not assess the consciousness level of patient as she was on dexmedetomidine infusion. Half an hour after resuscitation open myomectomy was started and successfully completed with stable vitals. Postoperatively patient was shifted in HDU in stable condition with normal vitals. The patient was discharged on fifth postoperative day.


Vasopressin is an antidiuretic hormone and has a strong vasoconstrictive effect on smooth muscles. It is a direct vasoconstrictor and also acts by stimulating contraction of myometrial cells in the uterus via its action on V2 receptors. The half-life of vasopressin is 24 minutes[1] when compared with a very short half-life of epinephrine (2 minutes)[2] and oxytocin (10 minutes),[3] making it superior agent for achieving hemostasis.

Various studies have demonstrated proven efficacy of vasopressin in varied dosages in decreasing blood loss during myomectomy.

It was first reported by Dillon et al.[4] almost 60 years ago on 20 patients in whom vasopressin was used to decrease blood loss associated with gynecologic surgery. They used 4 IU as the total maximum dose diluted in 20 mL of saline (0.2/mL). They injected 5 to 10 mL (1–2 IU) at the beginning of surgery, repeated the injections as needed, but did not exceed a total cutoff of 4 IU. The authors monitored the ECG and vital signs and found no evidence of abnormalities or untoward events while still noting a marked decrease in blood loss. The latest Cochrane database review showed that vasopressin use is associated with a reduction in blood loss of between 392.51 and 507.49 mL during abdominal myomectomy and between 121.73 and 172.17 mL during laparoscopic myomectomy.[5]

Although vasopressin is a very good hemostatic agent but at the same time, there are published reports of adverse cardiac effects by vasopressin such as bradycardia, hypotension, arrhythmias, atrioventricular block, pulmonary edema, and even cardiac arrest.

Barcroft et al.[6] reported a case of acute pulmonary edema which developed in a case of laparoscopic myomectomy after infiltration of 20 IU of vasopressin. This case initially developed bradycardia and hypotension which was managed with glycopyrrolate, ephedrine, and crystalloids. The patient settled down but at extubation was found to have pink frothy sputum and desaturated to 89%, suggesting that she developed acute pulmonary edema. She was managed with intravenous furosemide and diamorphine and recovered after stay in ICU.

Hobo et al.[7] reported a case of bradycardia and cardiac arrest caused by infiltration of 56 mL of 20 IU of vasopressin diluted in 200 mL saline (0.2 IU/mL). The patient was managed with ephedrine, atropine, and cardiac massage and had uneventful recovery.

Hung et al.[8] described two cases of bradycardia followed by cardiac arrest and pulmonary edema after local infiltration of 6 to 10 mL of dilute vasopressin (2 IU/mL) during an open myomectomy.

Lee et al.[9] reported a case of severe bradycardia and cardiac arrest during robotic-assisted myomectomy after infiltration of vasopressin in doses of 20 IU (20 IU diluted in 40 mL of normal saline). The patient was successfully revived with atropine 0.5 mg, reversal of Trendelenburg position, and supportive care. They attributed bradycardia to physiologic effects of vasopressin, pneumoperitoneum in steep Trendelenburg position for laparoscopy, shoulder braces for robotic surgery which add to carotid sinus compression and lowered sympathetic activity leading to bradycardia.

There are three kinds of vasopressin receptors V1, V2, and V3. V1 and V2 receptors are located in the periphery, whereas V3 receptors are found in central nervous system. Vasopressin produces generalized constriction of most blood vessels including coronary vessels resulting in increase in blood pressure. This sudden hypertension induces sympathoinhibitory reflex by activating baroreceptors in aortic arch and carotid sinus, resulting in lowering of cardiac contractility and heart rate. In the collecting tubules vasopressin acts on V2 receptors, causing water retention and it also acts on area postrema of brain to decrease cardiac output. Thus, there is a decrease in heart rate and cardiac output as a result of coronary vasoconstriction, decreased blood flow, altered sympathetic tone, and potentiated baroreflex in response to generalized vasoconstriction, which results in bradycardia, global hypotension, and in severe cases cardiac arrest.

There are further risk factors associated with laparoscopy. Pneumoperitoneum with CO2 stretches the peritoneum which induces the vagal-mediated cardiovascular reflex leading to bradycardia. Trendelenberg position leads to increased venous return resulting in increase in stroke volume, and cardiac output thereby activating baroreceptors further which may lower the heart rate by diminishing sympathetic activity.

Our patient exhibited similar manifestations as pallor, sudden bradycardia, and hypotension just after intramyometrial injection of vasopressin. Pale conjunctiva may be due to cutaneous vasoconstriction, whereas bradycardia is due to potentiated baroreflex and altered sympathetic tone. Hypotension may be due to decrease cardiac output, heart rate, altered sympathetic tone, or because of peripheral vasopressin mimicking hypotension.

Treatment includes identification of this situation and cardiac life support measures oxygenation and atropine for bradycardia. Vasopressin has short half life so early recognition and correct resuscitation results in successful outcome. Failure to identify this will lead to treatment with vasopressors which will worsen cardiac complications.

There are some previous case reports of vasopressin overdose, resulting in bradycardia and apparent hypotension that was treated with anticholinergic, inotropic, and vasoconstrictor drugs. Many of these cases subsequently developed pulmonary edema and acute ST-segment changes suggestive of myocardial injury. These complications point to the fact that caution is required when using vasopressors in the treatment of vasopressin-induced vasospasm. Treatment of bradycardia or hypotension after high-dose vasopressin with additional vasopressors and inotropes may be deleterious. Vasodilators such as nitroglycerine, atropine or increasing depth of anesthesia may theoretically have benefits in these situations. Noninvasive BP measurement based on oscillometric waveform of blood flow may not be truly applicable in the setting of peripheral vasospasm and can lead to administration of additional inotropic drugs that can contribute to iatrogenic cardiovascular morbidity. It has also been proposed to measure central BP using preoperative placement of central arterial catheter as peripheral vasospasm with central hypertension may give misleading clinical signs.[10]

In case invasive cardiac monitoring is not performed, palpable carotid pulses, and normal value of PET CO2 can help in differentiating peripheral vasospasm from global hypotension.

Contrary to all the above case reports, a study of the effects of vasopressin during laparoscopic myomectomy has shown that it has less effect on larger and more central vessels. Although the study was conducted on nine patients, the concentration of vasopressin used was 4 IU (20 IU diluted in 100 mL saline) and uterine blood flow was measured using transvaginal ultrasound evaluating arcuate artery and ascending branch of uterine artery, whereas systemic blood flow was measured using transesophageal Doppler evaluating aorta and measuring urine output.[11]

Another randomized controlled trial by Cohen et al., comparing different dilutions of vasopressin − 200 mL of diluted vasopressin solution (20 IU in 400 mL saline), and 30 mL of concentrated vasopressin solution (20 IU in 60 mL NS) found no significant difference in blood loss or change in hematocrit levels in both the groups.[12]


To summarize, vasopressin is cost-effective agent in reducing blood loss during myomectomy the efficacy of which has been proven in well-designed randomized controlled trials. But cardiovascular complications may occur with vasopressin use in varied dosages. The safe dose and concentration of vasopressin still needs to be determined. The amount of blood loss saved during myomectomy using vasopressin and the rare but potentially serious cardiovascular complications caused by its use needs to be weighed using risk–benefit analysis in larger well-randomized controlled trials. Whether we may consider invasive monitoring using central arterial line in women undergoing myomectomy with vasopressin use also needs to be addressed in future.

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Conflicts of interest

There are no conflicts of interest.


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