Intravenous Atropine Research Articles

Inferior ST-Elevation Myocardial Infarction (STEMI) with Heart Block: Can We Always Trust External Pacemakers?

A 65-year-old man called emergency medical service (EMS) because of chest pain and diaphoresis. The EMS team found him hypotensive and bradycardic. His field 3-lead rhythm strip showed inferior ST-elevation myocardial infarction (STEMI) with heart block (Figure 1A). Intravenous atropine was given with no response; therefore, external transcutaneous pacing was initiated, and he was taken to the hospital (Figure 1B). However, he remained hypotensive en route.

193 13 SECONDS OF ASYSTOLE IN YOUNG: IS A PACEMAKER NECESSARY?

Abstract Introduction Cardioinhibitory neurocardiogenic syncope (CNS) is caused by inappropriately trigger-activated cardiac reflex which finally precipitates asystole, sinus bradycardia, or atrioventricular block. In the absence of structural heart disease, the prognosis is excellent, but frequent syncopal episodes can have a significant impact on quality of life. No medical therapy has proved to be really effective and studies concerning pacemaker implantation are often controversial. However, in young individuals, especially those under 40 years of age, implanting a pacemaker may carry more risks than benefits. Thus, alternative techniques such as ablation of the cardiac atrial parasympathetic ganglia (GP) have emerged. Case report A 34-year-old man with frequent episodes of reflex syncope performed a tilt test in March 2022 that diagnosed cardio-inhibitory syncope with 13-second asystole interrupted with external cardiac massage and intravenous atropine. In May 2022 he had an MRI scan showing normal biventricular systolic function and absence of late-gadolinium enhancement and underwent loop recorder implantation. He came to our centre in June 2022 and underwent electrophysiological study and electroanatomical mapping of the right atrium (Carto 3) during general anaesthesia. The anatomical areas of the supero-posterior and infero-posterior GPs of the right atrium were identified by electroanatomical mapping of complex fractionated atrial electrograms (CFAE). Radiofrequency pulses (Thermocool 30 watts) were delivered at these points, resulting in the disappearance of the CFAEs and an increase in basal heart rate. The greatest number of ganglia are allocated on the posterior surface of the right atrium and in particular the supero-posterior GP is the nexus point for vagal input to the GPs before innervating the atria. Therefore, it was decided to localise and ablate exclusively the GPs of the right atrium. The procedure was completed without complications. The patient has not complained of any syncopal episodes since, and the loop has not recorded any significant pauses. Conclusions The anatomic ablation of GP only in the right atrium could represent a feasible method to reduce CNS, to increase the warning symptoms period, and to delay as much as possible pacemaker implant, especially in young patients who have experienced a related physical trauma. This approach significantly decreased the procedural time and risks.

1262: A CURIOUS CASE OF SHOCK AFTER A FALL

Introduction: Neurogenic shock is a rare presentation that follows spinal cord injuries. Bilello et al argued that up to 31% of cervical spine injury patients typically develop this phenomenon (2). However, the diagnosis remains difficult, as patients typically presents following a major injury and hemorrhagic shock cannot be ruled out. Due to its uniqueness and lack of treatment guidelines, it is important to identify neurogenic shock early. Description: A 70-year-old Caucasian female with a past medical history of dementia, recurrent falls, recurrent UTI’s, and well controlled seizures presented to the Emergency Department following an unwitnessed fall. Labs including CBC, lactic acid, BUN/Cr, troponin, and UA were unremarkable. At presentation the patient was hypotensive and bradycardic which progressed despite receiving 6 liters of intravenous fluids and atropine. This prompted an admission to the ICU for IV norepinephrine. Within hours of being on norepinephrine, her blood pressure improved, and she quickly transitioned to oral midodrine. Nonetheless, the bradycardia persisted. Echocardiogram and EKGs were performed and shockingly were without any insight to the persistent bradycardia. CT Head and C-spine, chest X-ray, and MRI-brain w/o contrast were all unremarkable. An MRI of the C-Spine showed cord compression of C3/C4 and C4/C5. It was at this point that neurosurgery was consulted to evaluate the patient for surgery. Discussion: Our case is unique in that the etiology of the shock is unclear. Neurogenic shock is understood to be a product of both primary and secondary spinal cord injury; a direct damage to the axons that often leads to vascular insult or edema, leading to loss of sympathetic tone3. Typically, this is seen following major traumatic accidents or repeated falls. While our patient does have an inciting factor, the imaging findings seem to infer that there was a baseline chronic degenerative disease, exacerbated by the fall, that resulted in cord compression. Management of neurogenic shock centers around ample fluid resuscitation followed by vasopressor as needed with MAP goals 85-904 for 7 days. However, guidelines are less clear on the best agents, with most recommending a drug that targets both alpha and beta receptors1.

Occlusion of Two Coronary Arteries Simultaneously

A 60-year-old woman with a history of stroke and known hypertension presented to the emergency room after experiencing acute chest pain for an hour. Her blood pressure was 80/55 mmHg, and her pulse rate was 42 beats per minute. An electrocardiogram (ECG) showed first-degree cardiac block and inferior and anteroseptal leads with acute ST-elevation myocardial infarction (STEMI) (Panel A). The patient was promptly moved to the catheterization lab after receiving first care. Early distal left anterior descending (LAD) artery partial blockage with thrombus-containing lesion was found during diagnostic coronary angiography (Panel B). After a challenging engagement of the right coronary artery (RCA), it was discovered that there was a proximal complete blockage with a thrombus-containing lesion (Panel C). Unfortunately, the patient collapsed with severe bradycardia (34 beats per minute) and hypotension (systolic blood pressure = 60 mmHg), which did not react to quick intravenous fluid and atropine ampules. A temporary pacemaker was soon implanted. After the pacing was started, the patient developed ventricular fibrillation, which required cardiopulmonary resuscitation (CPR) and successive DC shocks before the pulse returned to sinus. The RCA was successfully stented quickly, followed by the stenting of the LAD lesion (Panel D and E). The patient rapidly returns to sinus rhythm with great coronary blood flow, and normal blood pressure is recorded after one hour of recovery. Two hours later, echocardiography demonstrated normal systolic function with no aberrant segmental motion. Occlusion of two coronary arteries is a critical disorder that requires immediate detection and treatment to avoid complications such as ventricular arrhythmias and cardiogenic shock. The patient was released with excellent outcomes.

A Couple With False Hellebore Poisoning

Veratrum album is a poisonous plant with steroidal alkaloids. It is often confused with Allium tricoccum (ramps), which is used as an alternative to scallion/spring onions. This is a case series of a 43-year-old woman and a 54-year-old man poisoned after consuming raw and cooked false hellebore (Veratrum album), most likely confused with Allium tricoccum, ramps, or wild scallions/onions. They presented with complaints of nausea and vomiting and were noted to be bradycardic and hypotensive on examination. They received intravenous fluids and atropine but one of the patients required admission to the medical intensive care unit after responding poorly to management.

Paradoxical worsening of bradycardia following atropine administration.

Bradyarrhythmias are a common entity in both emergency and out-of-hospital (OOH) medicine. In unstable bradycardic patients, paramedics will often initiate life-saving therapies in the OOH setting. Clinical guidelines for bradyarrhythmias are largely consistent across the globe, with intravenous (IV) atropine recommended as a first-line therapy, escalating to IV adrenaline or isoprenaline and transcutaneous pacing where atropine is unsuccessful. In this case report, we describe a case in the OOH setting of ventricular standstill following the administration of atropine to a patient with bradycardia and 2:1 heart block. The patient was a 77-year-old female presenting with a symptomatic 2:1 heart block. Following a single dose of 600 micrograms IV atropine, the patient deteriorated into ventricular standstill with a loss of consciousness and decorticate posturing. The patient was successfully managed with an IV infusion of adrenaline and subsequently received an implanted pacemaker in hospital. The paradoxical worsening of this patient's bradycardia following atropine administration may have been related to the location of the heart block. It has been shown that patients with atrioventricular blocks at the level of the His-Purkinje fibres (infranodal) are at an increased risk of adverse events following atropine administration, while those at the nodal level or secondary to increased vagal tone are more likely to respond favourably. Paramedics should be prepared to manage unexpected adverse events secondary to atropine administration in patients with heart block.

Organophosphate Poisoning in a Paediatric Intensive Care Unit: A Retrospective Analysis Based on Ten Years of Experience.

BackgroundOrganophosphate (OP) poisoning is one of the most common etiologies of poisoning in the pediatric age group.ObjectiveThis study aimed to evaluate the demographic characteristics, clinical features, clinical course, and outcomes of children with toxicity from organophosphates admitted to the pediatric intensive care unit.MethodsA retrospective review of hospital medical records of all children aged 14 years and younger who were admitted to the PICU with a provisional diagnosis of organophosphate poisoning at King Fahad Hospital of the University (KFHU), Alkhobar, Saudi Arabia, between January 1, 2008, and December 31, 2018, was conducted. Patients with incomplete medical record information or with suspicion or evidence of one or more agents other than organophosphate were excluded from the study.ResultsThirty-one patients were enrolled in the study. The median age of the study population was 2 years, and 19 (61%) were males. The majority of patients (68%) had more than one route of organophosphate exposure. Skin exposure was reported in 26 patients (84%). Only three patients (10%) had suicidal organophosphate exposure from organophosphates, while the majority (28 patients; 90%) had accidental poisoning. Bronchorrhea was the most prevalent presenting feature, reported in 28 patients (90%). 17 patients (55%) were treated with intravenous atropine and (45%) were used a combination of pralidoxime with atropine for treatment. Five patients (16%) developed acute respiratory distress syndrome. Twelve patients (39%) needed endotracheal intubation and mechanical ventilation secondary to respiratory failure.ConclusionThe presenting features of organophosphate poisoning differ widely in children. Risk factors for mortality for PICU patients with organophosphate poisoning include delayed hospital arrival by more than 1 hour, inhalational route of exposure, need for mechanical ventilation, and high lactate levels in the first 24 hours post-exposure.

Frequency of vaccine-associated syncope after COVID-19 vaccination in adolescents.

Frequency of vaccine-associated syncope after COVID-19 vaccination in adolescents.

The effect of atropine used in dobutamine stress echocardiography on pupil diameter.

The use of atropine during dobutamine stress echocardiography (DSE) is contraindicated in persons with narrow angle glaucoma though there is limited evidence that low doses of intravenous atropine do not cause pupillary dilation. The aim of this study is to investigate whether atropine when administered in persons without glaucoma during dobutamine stress echocardiography causes pupillary dilation. Out of 144 patients without a history of glaucoma referred for DSE for clinical indications, 105 patients received intravenous atropine doses ranging from 0.1 mg to 1.25 mg (most patients received 0.25-0.75 mg). Pupil diameter of both eyes was measured under the same light conditions before and after the DSE using a CP-30 Optical Digital PD Ruler. For the total of 210 examined eyes pupil diameter remained unaltered after each DSE test (3.65 ± 0.799 mm before vs 3.63 ± 0.766 mm after, p = .737). Similarly, pupil diameter remained unchanged when left and right eyes were assessed separately (right eye: 3.770 ± 0.812 before vs 3.752 ± 0.745 mm after, p = .821 and left eye: 3.521 ± 0.770 before vs 3.499 ± 0.770 mm after, p = .806). Diameter of right and left pupil were also unaltered after grouping patients by sex and iris pigmentation. Age, weight, atropine dose and propranolol dose were not correlated with changes in pupil diameter. Intravenous atropine in usual doses administered in DSE does not cause mydriasis in adults without glaucoma. Future studies need to confirm our findings and expand the investigation regarding safety of atropine use during DSE in patients with narrow angle glaucoma.

The Application of a SaCoVLMTM Visual Intubation Laryngeal Mask for the Management of Difficult Airways in Morbidly Obese Patients: Case Report

We report insertion of the SaCoVLMTM in three awake morbidly obese patients (BMI 46. 7–52.1 kg/m2). The patients were given intravenous atropine and midazolam injections after entering the operating room and then inhaled an anesthetic with 2% lidocaine atomization. After SaCoVLMTM insertion while patients were awake, when the vocal cords were visualized, controlled anesthetic induction commenced with spontaneous ventilation. The entire anesthesia induction and intubation process was completed under visualization, and no adverse events such as hypoxemia occurred. No patient had an unpleasant recall of the procedure. We conclude that the SaCoVLMTM is easy to use, well tolerated and suitable for awake orotracheal intubation in patients with known difficult airways.

Developing a multi-disciplinary program for routine acetylcholine vasoreactivity testing in the cardiac catheterization laboratory

Abstract Background/Introduction Of the patients who are referred for invasive coronary angiography 30–50% are found to have no obstructive coronary artery disease. Current ESC Guidelines for chronic coronary syndromes have a class IIa recommendation for intracoronary provocative testing with acetylcholine in patients with ischemia and no obstructive coronary artery disease (INOCA). However, there is limited guidance for pharmacy and nursing teams for the support of provocative testing in the cardiac catheterization laboratory. Purpose To demonstrate feasibility and safety of acetylcholine vasoreactivity testing in the cardiac catheterization laboratory. Methods The inpatient pharmacy developed an adapted protocol based on available evidence and facilitated a multi-disciplinary operational workflow for the assessment of vasospastic angina. 3mL acetylcholine aliquots of 1mcg/mL, 10 mcg/mL, 25 mcg/mL, 50 mcg/mL, and 100 mcg/mL were prepared by pharmacy following sterile compounding standards. The transition from provider or nursing staff compounding to pharmacy compounding provided quality assurance following United States Pharmacopeia compounding standards for improved sterility and patient safety, especially with a complicated micro-dilution recipe. Pharmacy supported the necessary guidance with optimized clinical decision support in the form of a customized order panel embedded in the electronic health record system and compounding software as another layer of standardization and quality assurance. Syringes were made available to the interventional cardiologist in the cardiac catheterization laboratory suite immediately prior to a scheduled case. Eleven orders of acetylcholine were placed with five dilution syringes per order (total 55 compounded syringes) from the customized acetylcholine provoked coronary vasospasm procedure order panel. Results From January 2020 to March 2021, 11 patients underwent acetylcholine vasoreactivity testing for clinical indications. One patient developed atrial fibrillation with a rapid ventricular rate during provocative testing of the right coronary artery which required elective cardioversion the following day. Of 11 patients, 9 were outpatients and 2 were inpatients. 1 patient received intravenous atropine and ondansetron due to profound bradycardia and nausea after 100mcg acetylcholine administration. No other safety events occurred. Conclusion(s) Provocative testing with intracoronary acetylcholine administration is safe and feasible. For clinical assessment, sterile compounding and customized order panels facilitate routine clinical assessment for patients with suspected vasospastic angina. Nursing protocols should include cardiac monitoring, medications to reverse adverse effects, and possible outcomes of provocative testing. We provide a practical description of our workflow for pharmacists, catheterization laboratory staff, and providers for routine acetylcholine provocation for the evaluation of INOCA. Funding Acknowledgement Type of funding sources: None.

Comparison between Adding Intravenous Neostigmine and Atropine versus Intravenous Hydrocortisone for Conservative Treatment of Postdural Puncture Headache After spinal Anaesthesia For Elective Caesarean Section

Abstract Background Postdural puncture headache (PDPH) lacks a standard evidence-based treat- ment. A patient treated with neostigmine for severe PDPH And anther patient treated with hydrocortisone prompted this study. Objective To assess and compare the efficacy of intravenous neostigmine and atropine versus intravenous hydrocortisone as an adjuvant to conservative treatment of PDPH after spinal anaesthesia for elective caesarean section. Patients and Methods This study was carried out in Ain Shams University hospitals for six months (from February 2019 to August 2019) on 60 patients who presented with post dural puncture headache after elective caesarean section under spinal anaesthesia Results In this study, we compared the efficacy of hydrocortisone and neostigmine with conventional methods. All of the three groups (neostigmine, hydrocortisone and conventional methods) were effective in lowering VAS scores at 24, 48 and 72 h after headache's onset but neostigmine alleviated the pain more effectively and with rapid onset. The mean VAS score was significantly lower in neostigmine group compared with others 2, 6, 24, 48 and 72h after start of medications (p < 0.001 for all of them) and significantly lower in hydrocortisone group compared with Conventional group 6, 24, 48, and 72h (p < 0.001 for all of them). Conclusion neostigmine and hydrocortisone are both useful and safe in management of PDPH but neostigmine is more effective in this regard.

A SEVER CASE OF CALCIUM CHANNEL BLOCKER TOXICITY REQUIRING HYPERINSULINEMIA EUGLYCEMIA AND LIPID EMULSION TREATMENT

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Calcium channel blocker (CCB) is a significant drug exposure reported to the American Association of Poison centers (1). Medical care of patients poisoned with CCBs can be complex as profound bradycardia and hypotension might be challenging to control, with insufficient evidence on which medical therapy is best (2). Calcium channel blockers directly block calcium L-type channels in the heart and blood vessels leading to hypotension and circulatory collapse in overdose cases. Dihydropyridines are generally less notorious for causing bradycardia than non-dihydropyridine. Amlodipine has a relatively long half-life, and therefore toxicity with amlodipine tends to cause prolonged circulatory collapse (3).This case was particularly challenging since calcium channel blockers were combined with three additional medications, including a benzodiazepine and a GABA receptor agonist (zolpidem). This combination made cardiopulmonary collapse an inevitable consequence. CASE PRESENTATION: A 32-year-old man presented to the emergency department in a stable clinical condition about an hour after intentionally ingesting a total of 300 mg of amlodipine, 1500 mg of bupropion, 3 mg alprazolam, and an unknown amount of zolpidem in a suicidal attempt. Soon after arriving at the emergency room, he started to have slurred speech, and his blood pressure started dropping—treatment initiated with activated charcoal. Subsequently, the patient became more lethargic, requiring emergent sedation, intubation, and mechanical ventilation for airway protection. Additional treatments included hyperinsulinemia euglycemia treatment (HIET), calcium gluconate, sodium bicarbonate, and lipid emulsion.The patient quickly became hemodynamically unstable with a refractory distributive shock requiring high doses of four different vasopressors (norepinephrine, vasopressin, phenylephrine, and epinephrine). Initial laboratory results showed metabolic acidosis (pH of 7.14). Complete blood count and chemistry were unremarkable. Chest x-ray, electrocardiogram, and echocardiogram were essentially normal. After stabilization in the intensive care unit, all vasopressors were successfully weaned off, and the patient was extubated on day 4 of admission. He was transferred out to an inpatient psychiatric unit on day 8 of admission. DISCUSSION: Aside from the initial therapy with intravenous fluids and atropine for bradycardia, there is no agreed-upon algorithms for CCBs toxicity treatment.Hyperinsulinemia euglycemia treatment (HIET) was originally shown to improve survival in dogs poisoned with verapamil in a controlled environment. CONCLUSIONS: Management of calcium channel blocker toxicity is based on maintaining adequate circulation with the use of IV fluids, vasopressors, calcium, high-dose insulin, glucagon, and other therapies that have been documented. REFERENCE #1: Kent R. Olson, Andrew R. Erdman, Alan D. Woolf, Elizabeth J. Scharman, Gwenn Christianson, E. Martin Caravati, Paul M. Wax, Lisa L. Booze, Anthony S. Manoguerra, Daniel C. Keyes, Peter A. Chyka & William G. Troutman (2005) Calcium Channel Blocker Ingestion: An Evidence-Based Consensus Guideline for Out-of-Hospital Management, Clinical Toxicology, 43:7, 797-822. REFERENCE #2: DeWitt CR, Waksman JC. Pharmacology, pathophysiology and management of calcium channel blocker and beta-blocker toxicity. Toxicol Rev. 2004;23(4):223-38. REFERENCE #3: Vimal Upreti, V. R. Ratheesh, Pawan Dhull, and Ajay Handa.Shock due to amlodipine overdose. Indian J Crit Care Med. 2013 Nov-Dec; 17(6): 375–377. DISCLOSURES: No relevant relationships by Matthew Apedo, source=Web Response no disclosure on file for Setana Idriss; No relevant relationships by Mazin Shaikhoun, source=Web Response

Regulation of Coronary Blood Flow by the Carotid Body Chemoreceptors in Ovine Heart Failure.

Carotid bodies (CBs) are peripheral chemoreceptors, which are primary sensors of systemic hypoxia and their activation produces respiratory, autonomic, and cardiovascular adjustments critical for body homeostasis. We have previously shown that carotid chemoreceptor stimulation increases directly recorded cardiac sympathetic nerve activity (cardiac SNA) which increases coronary blood flow (CoBF) in conscious normal sheep. Previous studies have shown that chemoreflex sensitivity is augmented in heart failure (HF). We hypothesized that carotid chemoreceptor stimulation would increase CoBF to a greater extent in HF than control sheep. Experiments were conducted in conscious HF sheep and control sheep (n = 6/group) implanted with electrodes to record diaphragmatic electromyography (dEMG), flow probes to record CoBF as well as arterial pressure. There was a significant increase in mean arterial pressure (MAP), CoBF and coronary vascular conductance (CVC) in response to potassium cyanide (KCN) in both groups of sheep. To eliminate the effects of metabolic vasodilation, the KCN was repeated while the heart was paced at a constant level. In this paradigm, the increase in CoBF and CVC was augmented in the HF group compared to the control group. Pre-treatment with propranolol did not alter the CoBF or the CVC increase in the HF group indicating this was not mediated by an increase in cardiac sympathetic drive. The pressor response to CB activation was abolished by pre-treatment with intravenous atropine in both groups, but there was no change in the CoBF and vascular conductance responses. Our data suggest that in an ovine model of HF, carotid body (CB) mediated increases in CoBF and CVC are augmented compared to control animals. This increase in CoBF is mediated by an increase in cardiac SNA in the control group but not the HF group.

IS EMERGENCY ROOM OBSERVATION SUFFICIENT FOR MAD HONEY POISONING? A CASE REPORT

Grayanotoxin poisoning is most commonly seen in the East Black Sea Region of Turkey due to consumption of mad honey, which is made by bees from the flowers of the rhododendron plant. Mad honey poisoning is dose dependent. In low doses, it causes dizziness, hypotension and bradycardia. In high doses, it can cause unconsciousness, seizures and atrioventricular blocks. Local people are well aware of mad honey poisoning and generally do not go to the hospital for mild symptoms. In clinical practice, patients with mad honey poisoning are kept under coronary intensive care observation for at least 12-24 hours. As seen in this case report as well as in some publications in the literature, stable patients who respond to atropine and fluid therapy may not need to be hospitalized. In this case report, we present a patient with sinus bradycardia due to mad honey poisoning from the East Black Sea Region of Turkey, who responded to intravenous fluid and atropine treatment in a short time.

Assessment of effect of propofol and ketamine in electroconvulsive therapy anesthesia

Background: Ketamine is in clinical use since 1970. It is a unique intravenous (IV) anesthetic that produces a wide spectrum of pharmacological effects including sedation, catalepsy, somatic analgesia, bronchodilation, and sympathetic nervous system stimulation. Materials and Methods: The present study was conducted in the Department of Anesthesiology of MGM Medical College, Navi Mumbai. 100 patients who were scheduled for ECT treatment were enrolled. The study population was randomly assigned to receive one of three anesthetic agents (Ketamine, Propofol, or Ketofol). After premedication with intravenous atropine sulfate (0.25 mg), propofol (10 mg/ml), ketamine (10 mg/ml), or ketofol was administered slowly (20 mg/10 s) until the patient no longer responded to his/her name being called loudly and showed loss of the eyelash reflex. Results: We found that both ketamine and Ketofol have an increased mean seizure duration compared to propofol.Conclusion:We found that both Ketamine and Ketofol have an increased mean seizure duration compared to propofol.

Prophylactic efficacy of intravenous atropine with crystalloid co-loading for hemodynamic stability in parturient undergoing cesarean delivery at Dilla University Referral Hospital. A randomized controlled trial

BackgroundThe main objective of this study is to assess the prophylactic efficacy of intravenous atropine for the prevention of hypotension after spinal anesthesia in a parturient who underwent cesarean delivery under spinal anesthesia. MethodA randomized controlled trial study was conducted at Dilla University hospital. Pregnant women scheduled for elective cesarean section were randomized to either atropine prophylaxis (n = 33) or active prophylaxis (n = 33) for prevention of post-spinal hypotension. Sample sizes were calculated using a G-power version 3.1.9.2 getting a total of 66 participants. Intraoperative blood pressure, heart rate, and incidence of postoperative nausea and vomiting were assessed. Paired sample t-test was used to compare each group change from baseline. Independent t-test and Manny Whitney tests were used based on the distribution of data. A statistically significant difference was determined at a p-value of ≤05. ResultBoth systolic and diastolic blood pressure declined from the baseline in both groups after spinal anesthesia. Atropine didn't prevent a decline in blood pressure from the baseline during the first 60 min of initiation of spinal anesthesia (p > 0.05). Heart rates at the 15th and 20th minute were higher in the atropine group (p < 0.05). There is no statistically significant difference between groups regarding mean Apgar score, and neonatal outcome. The total crystalloid fluid given during the perioperative period is higher in the active prophylaxis group with a mean of 2151.5 ml compared to 1651.52 ml in the atropine group p = 0.002. The incidence of intraoperative nausea and vomiting was higher in the active prophylaxis group compared to the atropine group but the difference is not statistically significant p > 0.05 as it was shown in the figure below. ConclusionProphylactic administration of atropine didn't prevent a decline in blood pressure from baseline. The incidence of nausea and vomiting was lower in the atropine group with no statistically significant difference.

Intramyometrial injection of vasopressin resulting in severe bradycardia during myomectomy.

To the Editor: Myomectomy is an important treatment option for removing a hysteromyoma, along with intramyometrial vasopressin to reduce intraoperative bleeding.[1,2] Sometimes, however, it results in life-threatening complications.[3] We report two rare cases of sudden severe bradycardia after intramyometrial injection of vasopressin during myomectomy. The two patients were diagnosed with uterine leiomyomas. The preoperative laboratory studies, chest radiography, electrocardiography, and blood pressure were normal in both patients. The first case was a 36-year-old woman who underwent laparoscopically assisted myomectomy under general anesthesia. After anesthesia induction, endotracheal intubation, and ensuring that mechanical ventilation was established, laparoscopic myomectomy was performed at 12 mmHg abdominal pressure in the Trendelenburg position. After trocar insertion, the abdominal cavity appeared smooth, and multiple uterine myomas were found covering the entire uterine wall. After negative aspiration, 10 mL of diluted vasopressin (0.6 U/mL) was injected into the myometrium using a 16-gauge needle. Approximately 2 min after the injection of the diluted vasopressin, sudden severe bradycardia was developed. The heart rate (HR) suddenly decreased from 68, to 47, to 25 beats/min. Both the operation and anesthesia were immediately discontinued, and the operative bed was adjusted to a supine position. The patient's HR returned to 55 beats/min and then, within 30 s, dropped to 30 beats/min, and then 25 beats/min. Intravenous atropine (0.5 mg) was administered immediately. Approximately 2 min later, the patient's HR gradually returned to baseline levels. After 10 min of observation, the operation continued and went smoothly. The patient recovered uneventfully and was discharged 4 days later. The second case was a 38-year-old woman who underwent abdominal myomectomy under combined spinal-epidural anesthesia. The operation commenced after anesthesia induction. Bleeding occurred during excision of the myoma, and 10 mL of diluted vasopressin (0.6 U/mL) was injected into the myometrium to relieve bleeding. Approximately 3 min after the injection, the patient's HR dropped suddenly from 70, to 50, to 25 beats/min. One minute later, her blood pressure was 70/40 mmHg. Intravenous atropine sulfate (0.5 mg) was administered. Severe bradycardia (30 beats/min) lasted for nearly 2 min. The patient was ventilated with 100% oxygen. Intravenous ephedrine (6 mg) was also administered immediately, resulting in the HR returning to 108 beats/min and the blood pressure to 125/80 mmHg 3 min later. The operation went smoothly. No more vasoactive drugs were administered. The patient recovered uneventfully and was discharged 6 days later. Vasopressin, an extremely potent vasoconstrictor, is widely used to control acute hemorrhage during myomectomy. The vasopressor effect of vasopressin is primarily mediated by the VIa receptors in vascular smooth muscle, resulting in increased vascular resistance and slowing of the HR. Our two patients showed that intramyometrial injection of vasopressin may result in severe bradycardia, regardless of whether general anesthesia or combined spinal–epidural anesthesia had been used or whether laparoscopically assisted myomectomy or abdominal myomectomy was performed. Anesthesiologists should be vigilant while injecting vasopressin during surgery. Severe bradycardia may be the first symptom. If left untreated, it may lead to life-threatening complications, including cardiac arrest.[4] Stopping the surgical procedure and ejecting carbon dioxide gas from the abdominal cavity to reduce abdominal pressure does not completely relieve this severe bradycardia. Early use of atropine alone may be an appropriate choice for alleviating the severe bradycardia associated with vasopressin and preventing it from progressing to cardiac arrest. We strongly recommend early cardiopulmonary resuscitation if atropine is not effective and the severe bradycardia deteriorates to <25 beats/min. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form, the patients have given their consent for their images and other clinical information to be reported in the article. The patients understands that their names and initials will not be published and due efforts will be made to conceal the identity of the patients, although anonymity cannot be guaranteed. Conflicts of interest None.

Adverse Cardiovascular Effects of Phenylephrine Eye Drops Combined With Intravenous Atropine.

Background: Phenylephrine and atropine can cause serious adverse effects when applied in combination. We investigated the effect of phenylephrine eye drops combined with intravenous atropine on the cardiovascular system in patients under general anesthesia undergoing intraocular surgery. Methods: The effects of the drugs were observed through clinical study. Thirteen patients undergoing intraocular surgery under general anesthesia were observed in this study; all were injected intravenously with atropine due to the oculocardiac reflex during surgery. To study the combination of drugs, an in vivo study was performed on rats. Seventy-two standard deviation rats that received phenylephrine eye drops and intravenous atropine treatment under general anesthesia were assessed, of which 18 treated with these drugs simultaneously were administered normal saline, neostigmine or esmolol. Blood pressure and heart rate were recorded and analyzed. Findings: The age of the patients ranged from seven to 14 years old with an average age of 10.7 years old, and 11 patients were male. In patients, 5% phenylephrine eye drops combined with intravenous atropine led to a significant heart rate increase and the increase lasted 20 min. The significant increase in diastolic blood pressure and systolic blood pressure lasted for 15 and 25 min, respectively. From five to 25 min after intravenous atropine treatment, the systolic blood pressure and diastolic blood pressure were both more than 20% higher than that at baseline. In rats, the changes in blood pressure and heart rate were independent of the phenylephrine and atropine administration sequence but were related to the administration time interval. The neostigmine group showed a significant decrease in blood pressure after the increase from the administration of phenylephrine and atropine. Interpretation: Phenylephrine eye drops combined with intravenous atropine have obvious cardiovascular effects that can be reversed by neostigmine. This drug combination should be used carefully for ophthalmic surgery, especially in patients with cardio-cerebrovascular diseases.

ST-Segment Elevation Associated with Mobitz II Atrioventricular Block During Transseptal Puncture for Atrial Fibrillation Ablation

Pulmonary veins electrical isolation as an invasive treatment of atrial fibrillation has been widely used in electrophysiology laboratories. This case report presents a rare and transient complication, during transseptal puncture for atrial fibrillation ablation. ST-segment elevation, hypotension and bradyarrhythmia related to catheterization were observed despite cineangiocoronariography without obstructive lesions. Clinical stability was achieved after administration of intravenous atropine and saline solution. It is speculated that the phenomenon is attributed to an increased vagal tone after the mechanical effect of transseptal puncture in the interatrial vagal network. The procedure was completed despite the phenomenon.