Severe Vasospasm Mimics Hypotension After High-Dose Intrauterine Vasopressin : Anesthesia & Analgesia

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Obstetric Anesthesiology: Case Report

Severe Vasospasm Mimics Hypotension After High-Dose Intrauterine Vasopressin

Riess, Matthias L. MD, PhD*,†,‡; Ulrichs, Jason G. MD§; Pagel, Paul S. MD, PhD; Woehlck, Harvey J. MD*

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Anesthesia & Analgesia 113(5):p 1103-1105, November 2011. | DOI: 10.1213/ANE.0b013e31822cef10

Intramyometrial injection of vasopressin, oxytocin, and epinephrine reduces bleeding during uterine myomectomy.1,2 Vasopressin has the longest clinical effect,3 but its systemic hemodynamic effects may be profound and pose significant challenges for the anesthesiologist.4 Loss of peripheral pulses along with bradycardia, nonmeasurable arterial blood pressure, and cardiac complications have been reported after myometrial injection of vasopressin.511 In most published case reports, these clinical findings were interpreted as global hypotension, despite the fact that vasopressin is a powerful vasoconstrictor, and patients were treated with vasopressors according to Advanced Cardiac Life Support resuscitation protocols.6,9,10 Here, we describe a patient who developed nonmeasurable blood pressure by noninvasive means and loss of peripheral pulses after myometrial administration of vasopressin, with documentation of severe peripheral arterial vasospasm and increased proximal blood pressure. We discuss the pathophysiology of this unusual clinical presentation and emphasize the danger of misinterpreting pulselessness as global hypotension instead of vasospasm in this setting. The authors were unable to obtain patient consent, but the responsible IRB gave explicit permission to publish this report.


A 28-year-old, 124 kg, African American woman was scheduled for an open uterine myomectomy for uterine fibroid tumor removal. Her medical history included asthma, migraine headaches, and a seizure disorder. She denied a history of hypertension. The physical examination was unremarkable. Her baseline arterial blood pressure was 139/89 mm Hg via oscillometry (TRAM® model 450SL from GE healthcare, Waukesha, WI) with a heart rate of 74 beats per minute (bpm).

General anesthesia was induced with propofol (200 mg), fentanyl (100 μg), and rocuronium (60 mg) and maintained with 6% desflurane in an oxygen/air mixture. Approximately 45 minutes after incision, her blood pressure suddenly increased to 165/95 mm Hg. Her heart rate was initially unchanged, but shortly thereafter decreased from 90 to 70 bpm, concomitant with failure to measure blood pressure with the cuff located at the left upper arm. Finger tip pulseoximetry (Masimo SET monitor, Masimo Corporation, Irvine, CA) continued to show an arterial waveform with 100% SPO2, but an oscillometric blood pressure was not detectable on either arm. Peripheral pulses were absent in the radial, brachial, and axillary arteries bilaterally, but carotid arterial pulses were easily palpated. The electrocardiogram showed normal sinus rhythm without ST or T abnormalities. No precipitous decreases in PETCO2 were observed. Capillary refill, flushing, and pallor were difficult to determine because of the patient's dark skin.

Several minutes before the hemodynamic instability occurred, the surgeons had injected a drug whose name resembled “Pitocin” (oxytocin) directly into the uterine muscle and fibroid tumor. As a result, the anesthesia team initially assumed that oxytocin-induced global hypotension was responsible for the clinical events, and IV phenylephrine (150 μg) was administered. Despite this intervention, failure of oscillometry and absence of peripheral arterial pulses persisted. Blood loss was estimated at <150 mL, and intraoperative fluid replacement consisted of 1500 mL of Ringer's lactate solution. An additional 1000 mL of crystalloid was administered during the initial resuscitative effort. The anesthesia team subsequently discovered that a total of 60 U of “Pitressin” (vasopressin) in 33 mL of 0.9% normal saline and not “Pitocin” had been administered into the myometrium, indicating that the patient had received a high dose of an intense vasoconstrictor. According to the surgeon, this drug dose was given intentionally and injected over the course of approximately 1 minute with frequent negative aspirations.

Despite lack of Doppler capability, ultrasonography was able to reveal pulsating radial and ulnar arteries measuring approximately 1 mm in external diameter at the wrist. Radial artery catheter placement under ultrasound guidance was nevertheless unsuccessful. The brachial arteries measured 1.2 to 1.4 mm. A 22-gauge needle was briefly inserted into the lumen of the right brachial artery, and an arterial blood pressure of 135/80 mm Hg was recorded, yet it was impossible to cannulate either brachial artery directly or by using the Seldinger technique. The oscillometric blood pressure cuff remained nonfunctional throughout these events.

Approximately 90 minutes later, ultrasonography revealed a modest increase in radial artery diameters, and each had a clearly visible lumen. The left radial artery was successfully cannulated, and arterial blood pressure ranged between 120/80 and 150/100 mm Hg. The remainder of the operation was uneventful. Arterial blood pressure remained approximately 140 to 160 over 90 to 100 mm Hg. More than 2 hours after the oscillometric blood pressure cuff had failed, it began to record blood pressure readings that were similar to those obtained using the arterial cannula. Emergence from anesthesia and the patient's postoperative course were uneventful. Laboratory analysis did not reveal evidence of myocardial injury. Two days after surgery, the radial and brachial artery diameters were measured by ultrasound at 1.7 to 2 mm and 4.5 mm, respectively.


The anesthesia team first presumed that the patient's lack of peripheral pulses and failure of the oscillometric blood pressure measurement was due to oxytocin-induced global hypotension. The similarity of the brand names Pitocin and Pitressin led to initial confusion, especially because both drugs are used to reduce uterine bleeding, but exhibit vastly different hemodynamic effects. Therefore, these misleading clinical signs were initially misinterpreted as global hypotension. However, subsequently it became clear that the patient had received sufficient vasopressin to cause severe peripheral arterial vasospasm, rendering oscillometric blood pressure measurements unobtainable; only carotid pulses were palpable.

Ultrasonography demonstrated severe vasospasm of both brachial and radial arteries. In conjunction with the documented presence of a normal to moderately increased invasive blood pressure at the level of the brachial artery, these findings suggest lack of oscillometric peripheral blood pressure and pulse represented peripheral arterial vasospasm. If placed preoperatively, an axillary or femoral arterial catheter may have facilitated the measurement of a more central arterial blood pressure in our patient, but cannulating these sites intraoperatively was complicated by the patient's obesity and advanced stage of surgery.

Continued functionality of the Masimo SET pulse oximeter, which has been reported to detect pulsatile flow at perfusion levels 4 or more times below that of an arterial line,12,13 as well as continued presence of ETCO2 excluded pulseless electrical activity and cardiovascular collapse. In addition, unchanged PETCO2 excluded global hypoperfusion and clinically significant air embolism through uterine vessels from the differential diagnosis.

Because the operation was well advanced by the time the sequence and cause–effect relationship of events had become clear, cancellation of the surgical procedure was not possible. Therefore, it was decided to continue the operation as planned and to allow the vasopressin effects to wear off without further treatment.

Although low doses of intrauterine vasopressin have been used safely,3 hemodynamic complications during uterine myomectomy have been reported with doses exceeding 5 U.511 Frishman suggested a routine intramyometrial dose of 2 U, with a maximum of 4 to 6 U to avoid hemodynamic complications.14 The dose of vasopressin administered to our patient substantially exceeded these recommended limits.

Kraft et al. previously reported paradoxical hypotension and bradycardia during a vasopressin infusion in a patient with cirrhosis, although the method and location of blood pressure measurement was not described in their report.15 No accepted explanation for paradoxical global hypotension after vasopressin administration has been proposed, but peripheral vasospasm and artifacts of blood pressure measurement when measured distal to a vasospastic vessel are consistent with these findings. There are other reports of patients presenting with initial bradycardia, especially in combination with spinal or epidural anesthesia.6,7,911 Although it is not possible to extrapolate with certainty to other published reports, it appears likely in these cases that reflex bradycardia mediated by a strong vagal tone was caused by central hypertension,9 despite the absence of peripheral pulses. Some cases even progressed to cardiac arrest, possibly with asytole as an extreme of reflex bradycardia. Another possible explanation could be acute heart failure due to a sudden high afterload in response to high-dose systemic vasopressin, especially when followed by administration of additional α-agonists to treat the “paradoxical hypotension” without a sufficient increase in cardiac inotropy. Moreover, when combined with high neuraxial anesthesia, reflex bradycardia may occur faster and progress to more extreme values.

Cohn demonstrated that an infusion of the vasoconstrictors angiotensin amide and levarterenol reduces and may eliminate Korotkoff sounds despite normal or increased blood pressure, thereby falsely indicating global hypotension.16 Arterial bloodflow, not merely pressure, is required for Korotkoff sounds to be produced, and vasodilators or other maneuvers that increase bloodflow enhance the amplitude of Korotkoff sounds.1618 Oscillometric arterial blood pressure measurement is the current standard method used in clinical anesthesia, but algorithms for interpretation of raw oscillometric data may not be validated in unusual clinical situations associated with severe vasospasm. These algorithms are typically proprietary and may vary substantially among manufacturers and devices.19 In fact, there is an acknowledged need for “new research into the largely unknown physiological basis of oscillometric blood pressure measurement.”20 The current case suggests that despite technological advances, modern oscillometric blood pressure devices are subject to similar limitations as Korotkoff sounds, and peripheral vasospasm with central hypertension may give misleading clinical signs.

Several previous reports of vasopressin overdose described apparent hypotension that was treated with Advanced Cardiac Life Support protocols for asystole or pulseless electrical activity, including anticholinergic, inotropic, and vasoconstrictor drugs; many of these patients subsequently developed pulmonary edema, acute ST-segment changes, or evidence of myocardial injury.6,7,9,10 These observations emphasize that caution is required when contemplating treatment of vasopressin-induced vasospasm. Review of prior case reports suggests that treatment of pulselessness or nonmeasurable blood pressure after high-dose vasopressin with additional vasopressors and inotropes may be deleterious. Uterine myomectomy patients receiving 5 or more units of vasopressin may require proximal invasive arterial blood pressure monitoring to measure central blood pressure in the presence of peripheral vasospasm. Vasodilators such as nitroglycerine21 or increasing depth of anesthesia8 may theoretically have benefits in the setting of exogenous vasoconstrictor administration if used cautiously and if hypovolemic or cardiogenic shock is eliminated as a primary cause for a vasoconstrictor response.

In summary, we have documented that the administration of high-dose vasopressin during myomectomy may cause peripheral vasospasm and artifacts suggestive of global hypotension despite centrally maintained or increased arterial blood pressure. Noninvasive blood pressure measurement may become unreliable in this setting and trigger inappropriate and potentially deleterious administration of additional inotropic or vasoconstrictor drugs that can contribute to iatrogenic cardiovascular morbidity. If the use of large doses of vasopressin is anticipated to control local bleeding, the authors recommend preoperative placement of a proximal arterial catheter for blood pressure measurement. In the absence of invasive cardiac output monitoring, palpable carotid pulses and maintenance of normal PETCO2 may differentiate peripheral vasospasm from global hypotension.


Name: Matthias L. Riess, MD, PhD.

Contribution: This author helped write the manuscript.

Attestation: Matthias L. Riess approved the final manuscript.

Name: Jason G. Ulrichs, MD.

Contribution: This author helped write the manuscript.

Attestation: Jason G. Ulrichs approved the final manuscript.

Name: Paul S. Pagel, MD, PhD.

Contribution: This author helped write the manuscript.

Attestation: Paul S. Pagel approved the final manuscript.

Name: Harvey J. Woehlck, MD.

Contribution: This author helped write the manuscript.

Attestation: Harvey J. Woehlck approved the final manuscript.

This manuscript was handled by: Cynthia A. Wong, MD.


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