Intravenous Administration Of Atropine Research Articles

Atropine Prophylaxis before Spinal Anesthesia in Young and Middle Age Males Undergoing Inguinal Hernia Repair

Abstract Background Spinal Anesthesia is a common type of anesthesia used during many surgical procedures. This regional technique can be accomplished by administering an intrathecal dose of hyperbaric local anesthetic solution. The local anesthetic within the subarachnoid space can block sensory, motor and sympathetic pathways. One of the most common complications associated with spinal anesthesia is hypotension with or without bradycardia that can increase risk of perioperative cerebral and cardiovascular events. Aim of the Work to find out the effectiveness of prophylactic administration of intravenous atropine for attenuation of spinal anesthesia induced hypotension in inguinal hernia repair surgeries. Patients and Methods Therefore, A randomized controlled clinical trial was found to be the most suitable design in order to achieve the study objectives. A total of 40 patients males included in the study, aged 15-60 years, and were divided equally into two groups: Group 1 received intravenous injection of 0.01 mg /kg atropine sulphate one minute before spinal anesthesia and fluid preloading 500 ml Ringer solution. Group 2 received the same volume of normal saline intravenous bolus. Results Prophylactic intravenous atropine sulphate 0.01 mg /kg intravenous one minute prior to spinal anesthesia in inguinal hernia repair surgeries was effective in reducing spinal anesthesia induced hypotension, incidence of hypotension was lower in atropine exposed group compared to placebo group. The incidence of ephedrine use and number of boluses of fluids were lower in atropine exposed group compared to placebo group. Conclusion among patients who received spinal anesthesia with bupivacaine for elective inguinal hernia repair, prophylactic intravenous atropine sulphate 0.01 mg /kg prior to spinal anesthesia reduced spinal anesthesia induced hypotension and reduced ephedrine use.

Application of Laryngeal Mask Airway (LMA) in Medium and Short Period Traumatic Orthopedic Surgeries

Objective:Application of Laryngeal Mask Airway (LMA) as a ventilation method has been rarely explored in short and medium period orthopedic operations. In this study, we evaluated ventilatory efficacy of LMA in patients admitted to Ho Chi Minh City Orthopedic and Rehabilitation Hospital, Vietnam via a number of patient indicators including changes of pulse, blood pressure, airway pressure, SpO2 and pressure of CO2 at the end of an exhaled breath (EtCO2).
 Method: A total of 154 emergency and elective surgery cases with anesthesia were selected for the study.
 Result: One minute after LMA insertion to discontinuation of anesthetic, we recorded slower pulse of patients but only twenty-six cases (16.9%) required intravenous administration of atropine. Blood pressure of patients dropped after 1 minute following LMA insertion but then recovered afterward and only nine cases (5.8%) needed administration of ephedrine.
 Conclusion: After surgery, only eleven (7.15%) patients experienced oral mucosal bleeding but no further special treatment was used.
 Bangladesh Journal of Medical Science Vol. 23 No. 01 January’24 Page : 207-213

Transient asystole associated with vasovagal reflex in an oral surgery patient: A case report

The perioperative cardiac events may be brought about by a relative imbalance of autonomic activities due to excessive psychological and physical stress. The present case study focuses on the asystole that can occur as a serious cardiac adverse event associated with vasovagal reflex likely to be triggered by venipuncture for securing an intravenous line during dental care. In addition, we describe and discuss herein the management of intravenous sedation for a dental phobic patient who experienced the vasovagal reflex involved in an unexpected transient asystole. The patient with vasovagal reflex episodes in daily life, who had no past medical history relevant to cardiovascular disorders, was scheduled for dental extraction under intravenous sedation. Immediately after peripheral intravenous catheterization, she complained of discomfort and nausea, and a II-lead electrocardiogram revealed asystole following bradycardia associated with vasovagal reflex. Oxygenation and intravenous fluid loading in the supine position with elevation of the lower extremities restored sinus rhythm and normal hemodynamics without the intervention of cardiopulmonary resuscitation. With administration of intravenous atropine and betamethasone as premedication, she was uneventfully treated in stress-free psychosomatic conditions under optimal sedation with midazolam without any signs of cardiovascular disorders. After administration of flumazenil, the patient satisfactorily recovered from sedation without re-sedation. The present case suggests that an asystole associated with vasovagal reflex can be triggered by venipuncture for intravenous catheterization during dental anxiety likely to affect the imbalance between sympathetic and parasympathetic activities.

Effects of Systemic Lidocaine Versus Dexmedetomidine on the Recovery Quality and Analgesia After Thyroid Cancer Surgery: A Randomized Controlled Trial.

Surgical management is commonly used for thyroid cancer. We evaluated the effects of systemic lidocaine versus dexmedetomidine on the recovery quality and analgesia after thyroid cancer surgery. A total of 120 patients with thyroid cancer were randomly allocated to groupL (received lidocaine 1.5mg/kg loading, continuously infused 1.5mg/kg per hour), groupD (received dexmedetomidine 0.5µg/kg loading, continuously infused 0.5µg/kg per hour) and groupC (received normal saline), with 40 cases in each group. Anaesthesia induction and maintenance were performed using target-controlled infusions (TCIs) of propofol and remifentanil. The primary outcome of the quality of recovery-15 (QoR-15) score was recorded on the day before surgery and postoperative day1 (POD1). Secondary outcomes included the consumption of remifentanil during surgery, time to first required rescue analgesia, number of patients requiring rescue analgesia, postoperative cumulative consumption of tramadol, visual analogue scale (VAS) pain score, incidence of postoperative nausea or vomiting (PONV) and side effects. The total score of the QoR-15 at POD1 (median, IQR) was higher in groupL (128.0, 122.0-132.8) and groupD (127.5, 122.5-132.5) compared to groupC (118.5, 113.0-123.5) (P = 0.000). Compared to groupC, systemic lidocaine and dexmedetomidine reduced cumulative consumption of remifentanil and VAS pain score (P = 0.000). The time to first required rescue analgesia (mean, SD) was longer in groupL (8.1h, 1.2h) and groupD (8.5h, 1.9h) than groupC (5.9h, 0.9h) (P = 0.000). The number of patients requiring rescue analgesia was lower in groupL (8/40, 20%) and groupD (6/40, 15%) than groupC (16/40, 40%) (P = 0.029), and cumulative consumption of tramadol (mean, SD) was lower in groupL (44.0mg, 17.1mg) and groupD (51.7mg, 14.1mg) than groupC (73.9mg, 18.4mg) (P = 0.000). The incidence of PONV in groupL (7/40, 17.5%) and groupD (9/40, 22.5%) was lower than groupC (18/40, 45.0%) (P = 0.016). Bradycardia (heart rate less than 50beats/min or lower) was noted in 25 patients (25/40, 62.5%), which was reversed by intravenous administration of atropine 0.5mg. Systemic lidocaine and dexmedetomidine had similar effects on enhancing the quality of recovery, alleviating the intensity of pain and reducing the incidence of PONV after thyroid cancer surgery. However, dexmedetomidine may result in bradycardia. Therefore, lidocaine was superior to dexmedetomidine. ChiCTR.org.cn (ChiCTR2000038442). Registered on September 22, 2020.

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.

Guidelines of the Italian Society of Videosurgery (SIVI) in Infancy for the minimally invasive treatment of Hypertrophic Pyloric Stenosis in neonates and infants.

The most appropriate treatment for the infantile Hypertrophic Pyloric Stenosis (HPS) is still debated. The non-surgical conservative treatment with oral or intravenous administration of atropine does not enjoy a widespread appreciation for several factors (...).

Increased oxygenation in the non-contracting forearm muscle during contralateral skilful hand movement.

What is the central question of this study? When performing skilful hand movement, motor command descends especially towards distal arm muscles. Does central command evoke a vascular response selectively in the distal arm muscles during skilful hand movement? What is the main finding and its importance? We found, using near-infrared spectroscopy, that unilateral skilful hand movement evoked a greater increase in oxygenation of the contralateral forearm muscle compared with that of the upper arm muscles. Mental imagery of the hand movement also increased oxygenation of the forearm muscle. These findings suggest that central command might contribute to the vasodilator response in the non-contracting forearm muscle during contralateral skilful hand movement. The human hand is a special organ to perform skilful movement in daily life. To meet metabolic demands of the working distal arm muscles, central command might evoke neurogenic vasodilatation in the muscles. Based on our previous demonstration that a centrally generated vasodilator signal is transmitted bilaterally to skeletal muscles during exercise, centrally induced vasodilatation might occur in the non-contracting distal arm muscles during contralateral skilful hand movement. To examine this possibility, we used near-infrared spectroscopy to measure the relative concentrations of oxygenated haemoglobin (Oxy-Hb; as an index of regional blood flow) in the non-contracting arm muscles during skilful hand movement (two-ball rotation) in 22 subjects. Two-ball rotation increased Oxy-Hb of both forearm and upper arm muscles, with little changes in perfusion pressure and cardiac output. The increased Oxy-Hb was greater in the forearm muscle than in the upper arm muscles. The increased Oxy-Hb of the forearm muscle during two-ball rotation was greater than that during one-armed cranking performed with no load. Mental imagery of two-ball rotation increased Oxy-Hb of the forearm and biceps muscles. The increases in Oxy-Hb of both forearm and upper arm muscles during two-ball rotation were reduced by decreasing the level of task difficulty. Intravenous administration of atropine attenuated the increases in Oxy-Hb of the arm muscles during two-ball rotation. It is likely that contralateral skilful hand movement evokes a selective increase in Oxy-Hb of the non-contracting forearm muscle via a sympathetic cholinergic mechanism and that the increase in oxygenation might be mediated, at least in part, by central command.

Urethral dysfunction and therapeutic effects of a PDE 5 inhibitor (tadalafil) in a rat model of detrusor underactivity induced by pelvic nerve crush injury.

The urethral dysfunction produced by a rat model of peripheral neurogenic detrusor underactivity (DU) using pelvic nerve crush (PNC) injury was characterized and then tested with the administration of tadalafil, a phosphodiesterase type 5 (PDE 5) inhibitor. Ten days after producing PNC rats, awake cystometrograms (CMGs) and isovolumetric cystometrograms with urethral perfusion pressure (IC-UPP) measurements were performed. Also, in control rats, IC-UPP was recorded before and after intravenous atropine administration to determine if the reduction of bladder contraction pressure affects urethral relaxation during voiding. Then, CMG and IC-UPP measurements in PNC rats were recorded after intravenous administration of tadalafil. Lastly, real-time polymerase chain reaction was used to measure transcript levels of neuronal nitric oxide synthases (nNOS), endothelial nitric oxide synthases, and PDE 5 in urethral specimens from PNC and control rats. PNC rats demonstrated the characteristics of DU in CMG. Also, PNC rats exhibited significant decreases in isovolumetric bladder contraction amplitudes and urethral relaxation. Atropine attenuated the amplitude of isovolumetric bladder contractions; however, atropine did not affect urethral relaxation in control rats. Tadalafil decreased postvoid residual and increased voiding efficiency without changing bladder contraction amplitude in PNC rats. Also, tadalafil improved the amplitude of urethral relaxation during bladder contraction in PNC rats. Urethral nNOS transcript levels were upregulated in PNC rats compared to control rats. PNC rats revealed both DU and impaired urethral relaxation. PDE 5 inhibition in PNC rats enhanced urethral relaxation during voiding, resulting in improved voiding efficiency. Thus, urethral dysfunction could be a potential target for the treatment of inefficient voiding associated with neurogenic DU.

Investigating the Efficacy of Dexmedetomidine as an Adjuvant to Local Anesthesia in Brachial Plexus Block: A Systematic Review and Meta-Analysis of 18 Randomized Controlled Trials.

Dexmedetomidine has been thought to be an effective adjuvant to local anesthetics in brachial plexus blockade. We sought to clarify the uncertainty that still exists as to its true efficacy. A meta-analysis of randomized controlled trials was conducted to assess the ability of dexmedetomidine to prolong the duration and hasten the onset of motor and sensory blockade when used as an adjuvant to local anesthesia for brachial plexus blockade versus using local anesthesia alone (control). A search strategy was created to identify eligible articles in MEDLINE, EMBASE, and The Cochrane Library. The methodological quality for each included study was evaluated using the Cochrane Tool for Risk of Bias. Eighteen randomized controlled trials were included in this meta-analysis (n = 1092 patients). The addition of dexmedetomidine significantly reduced sensory block time onset time by 3.19 minutes (95% confidence interval [CI], -4.60 to -1.78 minutes; I = 95%; P < 0.00001), prolonged sensory block duration by 261.41 minutes (95% CI, 145.20-377.61 minutes; I = 100%; P < 0.0001), reduced the onset of motor blockade by 2.92 minutes (95% CI, -4.37 to -1.46 minutes; I = 96%, P < 0.0001), and prolonged motor block duration by 200.90 minutes (CI, 99.24-302.56 minutes; I = 99%; P = 0.0001) as compared with control. Dexmedetomidine also significantly prolonged the duration of analgesia by 289.31 minutes (95% CI, 185.97-392.64 minutes; I = 99%; P < 0.00001). Significantly more patients experienced intraoperative bradycardia with dexmedetomidine (risk difference [RD], 0.06; 95% CI, 0.00-0.11; I = 72%; P = 0.03); however, there was no difference in the incidence of intraoperative hypotension (RD, 0.01; 95% CI, -0.02 to 0.04; I = 3%; P = 0.45). It is important to note that all studies reported that intraoperative bradycardia was either transient in nature or reversible, when needed, with the administration of intravenous atropine. Dexmedetomidine has the ability to hasten the onset and prolong the duration of blockade when used as an adjuvant to local anesthesia for brachial plexus blockade. Considering an analgesic effect to be either decreased pain, a longer duration of analgesic block, or decreased opioid consumption, the addition of dexmedetomidine to local anesthetics for brachial plexus blockade was found to significantly improve analgesia in all 18 included studies. However, patients receiving dexmedetomidine should be continuously monitored for the potentially harmful but reversible adverse effect of intraoperative bradycardia. Therapeutic, level I.

Trigemino-Cardiac Reflex: A Phenomenon Neglected in Maxillofacial Surgery?

Trigemino-cardiac reflex is a physiologic response of the body to pressure effects in the region of distribution of the trigeminal nerve. Oral and maxillofacial surgical procedures can induce the development of this reflex, which leads to significant changes in the heart rate and sinus rhythms. This study intends to evaluate the effects of this reflex in patients with facial fractures and its subsequent management. A total of thirty-seven patients with facial fractures who reported to the Department of Oral and Maxillofacial Surgery at Basaveswar Teaching and General Hospital, Gulbarga during a period from July 2015-March 2016 were considered for the study. A male preponderance is observed with the most susceptible age group being 21-30years. Twenty-three patients sustained mid-facial fractures alone, nine patients had isolated mandible fractures and five patients had fractures of both the mid-face and mandible. A relative bradycardia was observed in the patients with mid-facial trauma, both at the time of presentation and also during the surgical reduction of midfacial fractures which improved after completion of procedure in most of the patients. However, in two patients, the bradycardia progressed to a cardiac asystole during midface manipulation which required immediate halt of the procedure and intravenous administration of atropine. Trigeminocardiac reflex though physiologic, which usually tends to subside without complications is not to be neglected in the surgeries of the maxillofacial skeleton. A propensity for unforeseen complications due to this reflex has to be avoided by meticulous monitoring of the ECG.

Role played by periaqueductal gray neurons in parasympathetically mediated fear bradycardia in consciousrats.

Freezing, a characteristic pattern of defensive behavior elicited by fear, is associated with a decrease in the heart rate. Central mechanisms underlying fear bradycardia are poorly understood. The periaqueductal gray (PAG) in the midbrain is known to contribute to autonomic cardiovascular adjustments associated with various emotional behaviors observed during active or passive defense reactions. The purpose of this study was to elucidate the role played by PAG neurons in eliciting fear bradycardia. White noise sound (WNS) exposure at 90 dB induced freezing behavior and elicited bradycardia in conscious rats. The WNS exposure‐elicited bradycardia was mediated parasympathetically because intravenous administration of atropine abolished the bradycardia (P < 0.05). Moreover, WNS exposure‐elicited bradycardia was mediated by neuronal activation of the lateral/ventrolateral PAG (l/vlPAG) because bilateral microinjection of muscimol, a GABAA agonist, into the l/vlPAG significantly suppressed the bradycardia. It is noted that muscimol microinjected bilaterally into the dorsolateral PAG had no effect on WNS exposure‐elicited bradycardia. Furthermore, retrograde neuronal tracing experiments combined with immunohistochemistry demonstrated that a number of l/vlPAG neurons that send direct projections to the nucleus ambiguus (NA) in the medulla, a major origin of parasympathetic preganglionic neurons to the heart, were activated by WNS exposure. Based on these findings, we propose that the l/vlPAG‐NA monosynaptic pathway transmits fear‐driven central signals, which elicit bradycardia through parasympathetic outflow.

Origins of the vagal drive controlling left ventricular contractility.

Key points The strength, functional significance and origins of parasympathetic innervation of the left ventricle remain controversial.This study tested the hypothesis that parasympathetic control of left ventricular contractility is provided by vagal preganglionic neurones of the dorsal motor nucleus (DVMN).Under β‐adrenoceptor blockade combined with spinal cord (C1) transection (to remove sympathetic influences), systemic administration of atropine increased left ventricular contractility in rats anaesthetized with urethane, confirming the existence of a tonic inhibitory muscarinic influence on cardiac inotropy.Increased left ventricular contractility in anaesthetized rats was observed when DVMN neurones were silenced.Functional neuroanatomical mapping revealed that vagal preganglionic neurones that have an impact on left ventricular contractility are located in the caudal region of the left DVMN.These neurones provide functionally significant parasympathetic control of left ventricular inotropy. The strength, functional significance and origins of direct parasympathetic innervation of the left ventricle (LV) remain controversial. In the present study we used an anaesthetized rat model to first confirm the presence of tonic inhibitory vagal influence on LV inotropy. Using genetic neuronal targeting and functional neuroanatomical mapping we tested the hypothesis that parasympathetic control of LV contractility is provided by vagal preganglionic neurones located in the dorsal motor nucleus (DVMN). It was found that under systemic β‐adrenoceptor blockade (atenolol) combined with spinal cord (C1) transection (to remove sympathetic influences), intravenous administration of atropine increases LV contractility in rats anaesthetized with urethane, but not in animals anaesthetized with pentobarbital. Increased LV contractility in rats anaesthetized with urethane was also observed when DVMN neurones targeted bilaterally to express an inhibitory Drosophila allatostatin receptor were silenced by application of an insect peptide allatostatin. Microinjections of glutamate and muscimol to activate or inhibit neuronal cell bodies in distinct locations along the rostro‐caudal extent of the left and right DVMN revealed that vagal preganglionic neurones, which have an impact on LV contractility, are located in the caudal region of the left DVMN. Changes in LV contractility were only observed when this subpopulation of DVMN neurones was activated or inhibited. These data confirm the existence of a tonic inhibitory muscarinic influence on LV contractility. Activity of a subpopulation of DVMN neurones provides functionally significant parasympathetic control of LV contractile function.

Extrinsic ghrelin in the paraventricular nucleus increases small intestinal motility in rats by activating central growth hormone secretagogue and enteric cholinergic receptors

Background/ObjectivesGhrelin is a brain-gut peptide that regulates gastrointestinal (GI) motility. We hypothesized that the excitatory effect of ghrelin on the paraventricular nucleus (PVN) increases GI motility by activating the central growth hormone secretagogue receptor (GHSR) and central neuropeptide Y (NPY) signaling pathways, leading to increased enteric cholinergic activity. MethodsThirty-six male Sprague Dawley rats were maintained on duodenal catheterization and PVN cannulation. Small intestinal transit (SIT) was observed and rats were divided as follows: experimental animals received ghrelin injections in the PVN (0.03, 0.08, or 0.24nM); 1nM GHSR antagonist D-Lys3-GHRP6 alone; 1nM D-Lys3-GHRP6 before ghrelin injection in the PVN, respectively. Electrophysiologic parameters of the interdigestive myoelectric complex (IMC) were examined by administration of 0.24nM ghrelin in the PVN after small intestinal electrode implantation and PVN cannulation. GI cholinergic pathway activation was analyzed after intravenous atropine administration. The involvement of central NPY signaling was evaluated by injecting an anti-NPY immunoglobulin (IgG) in the PVN. Neuronal expression of c-Fos in the brain and GI tract was examined using immunohistochemistry. ResultsInjection of ghrelin in the PVN dose-dependently accelerated SIT, and this excitatory effect was competitively inhibited by a GHSR antagonist. The excitatory effect of ghrelin on IMC activity was diminished by GHSR antagonism and NPY neutralization, as well as by blockade of peripheral muscarinic acetylcholine receptors. Extrinsic ghrelin significantly upregulated c-Fos expression in the PVN and other central nuclei, as well as in the enteric nervous plexuses of the stomach, duodenum, and proximal colon. The ghrelin-induced upregulation of central and enteric c-Fos expression was also dependent on central GHSR activation. ConclusionsGhrelin positively regulates GI motility by exciting both central and enteric neurons, including those of the PVN, by activating GHSR and NPY pathways, and peripheral muscarinic acetylcholine receptors.

Severe iatrogenic bradycardia related to the combined use of beta-blocking agents and sodium channel blockers.

PurposeDrug-induced bradycardia is common during antiarrhythmic therapy; the major culprits are beta-blockers. However, whether other antiarrhythmic drugs are also a significant cause of this, alone or in combination with beta-blockers, is not well known.MethodsWe retrospectively investigated the records of all patients hospitalized at our institution for drug-related bradycardia from the years 2004 to 2012. Patients with cardiac disease and electrolytic or hormonal abnormalities that could cause bradyarrhythmias were excluded.ResultsEight patients were identified (mean age, 79±5 years; range, 71–85 years; 6 women). Three patients were taking only beta-blockers (hereafter referred to as the BB group), while five patients were on both beta-blockers and Na channel blockers (hereafter referred to as the BB + Na group). Heart rates ranged from 20∼49 beats/minute on arrival. The initial electrocardiogram showed sinus bradycardia (n=6) or sinus arrest with escape beats (n=2). QRS duration was 80–100 ms. The clinical presentation of the BB + Na group was considerably worse than that of the BB group, and included cardiogenic shock and heart failure. Four of the BB + Na patients had been on their medications for over 300 days. The BB group recovered solely with drug discontinuation, while 4 of the 5 patients in the BB + Na group needed additional treatments, such as intravenous administration of atropine or adrenergic agonist and temporary pacing. Bradycardia did not recur during follow-up (median, 687 days).ConclusionAlthough wide QRS ventricular tachyarrhythmia is a better known proarrhythmic effect of Na channel blockers, life-threatening bradycardia may also occur in combination with beta-blockers in the elderly, even months after the start of medication, and at plasma concentrations that do not prolong QRS width.

Prevention of Spinal Anesthesia Induced Hypotension in Elderly: Comparison of Prophylactic Atropine with Ephedrine

Background: Spinal anesthesia induced hypotension is more common and hazardous in elderly, as they have decreased physiological reserve and compromised blood supply to various vital organs. Reversal of the blunted reflexes of tachycardia following hypotension in elderly with atropine or ephedrine may help in prevention of hypotension. Methodology: Present study is a prospective, randomized, double blind, controlled trial where sixty ASAPS I-II patients undergoing urological surgeries were assigned to receive either IV normal saline (placebo) or IV atropine 0.6 mg or IV ephedrine 12 mg one minute after induction of spinal anesthesia. Heart rate (HR), mean arterial pressure (MAP), requirement mephentermine and phenylephrine and side effects profile were studied were studied. Hemodynamic parameters were compared with baseline in each and among the groups. Results: The patients were comparable with demographic data, baseline hemodynamic parameters and duration of surgery. Compared to baseline, trend of mean HR and MAP significantly dropped in placebo in most of the times (p group (5%)]. Conclusion: Administration of intravenous atropine 0.6 mg or IV ephedrine (12 mg) one min after induction of spinal anesthesia in elderly patient is safe and effective in the prevention of spinal anesthesia induced hypotension and bradycardia, requirement of vasopressors decreased without clinically significant side effects.

Anaphylaxis following atropine administration during general anesthesia: a case report.

Anaphylaxis is an acute, potentially lethal, multisystem syndrome resulting from the sudden release of mast-cell- and basophile-derived mediators into the circulation. Common manifestations of anaphylactic reactions include urticaria, angioedema, nausea, vomiting, hypotension and cardiovascular collapse. Cardiovascular collapse is the first detected manifestation in up to 50% of cases in perioperative anaphylaxis, because patients are anesthetized and unable to report symptoms. A 25-year-old male presented with severe hypotension and erythema after intravenous atropine administration during general anesthesia. Postoperative laboratory findings demonstrated elevated serum tryptase and total immunoglobulin E. An intradermal test showed atropine sensitivity. Although atropine is used widely as a perioperative anticholinergic agent, it is a potential risk factor for a severe anaphylactic reaction. Therefore, prompt recognition and adequate therapeutic measures are necessary to avoid fatal consequences.

Pulmonary effects of intravenous atropine induce ventilation perfusion mismatch.

Atropine is used for a number of medical conditions, predominantly for its cardiovascular effects. Cholinergic nerves that innervate pulmonary smooth muscle, glands, and vasculature may be affected by anticholinergic medications. We hypothesized that atropine causes alterations in pulmonary gas exchange. We conducted a prospective interventional study with detailed physiologic recordings in anesthetized, spontaneously breathing rats (n = 8). Animals breathing a normoxic gas mixture titrated to a partial arterial pressure of oxygen of 110-120 were exposed to an escalating dose of intravenous atropine (0.001, 0.01, 0.1, 5.0, and 20.0 mg/kg body mass). Arterial blood gas measurements were recorded every 2 min (×5) at baseline, and following each of the 5 doses of atropine. In addition, the animals regional pulmonary blood flow was measured using neutron-activated microspheres. Oxygenation decreased immediately following intravenous administration of atropine, despite a small increase in the volume of inspired air with no change in respiratory rate. Arterial blood gas analysis showed an increase in pulmonary dysfunction, characterized by a widening of the alveolar-arteriole gradient (p < 0.003 all groups except for the lowest dose of atropine). The microsphere data demonstrates an abrupt and marked heterogeneity of pulmonary blood flow following atropine treatment. In conclusion, atropine was found to decrease pulmonary gas exchange in a dose-dependent fashion in this rat model.

Evidence for centrally induced cholinergic vasodilatation in skeletal muscle during voluntary one-legged cycling and motor imagery in humans

We have recently reported that central command contributes to increased blood flow in both noncontracting and contracting vastus lateralis (VL) muscles at the early period of voluntary one-legged cycling. The purpose of this study was to examine whether sympathetic cholinergic vasodilatation mediates the increases in blood flows of both muscles during one-legged exercise. Following intravenous administration of atropine (10 μg/kg), eight subjects performed voluntary 1-min one-legged cycling (at 35% of maximal voluntary effort) and mental imagery of the exercise. The relative concentrations of oxygenated- and deoxygenated-hemoglobin (Oxy- and Deoxy-Hb) in the bilateral VL were measured as an index of muscle tissue blood flow with near-infrared spectroscopy (NIRS). The Oxy-Hb in both noncontracting and contracting VL increased at the early period of one-legged cycling, whereas the Deoxy-Hb did not alter at that period. Atropine blunted (P < 0.05) the Oxy-Hb responses of both VL muscles but did not affect the Deoxy-Hb responses. The time course and magnitude of the atropine-sensitive component in the Oxy-Hb response were quite similar between the noncontracting and contracting VL muscles. With no changes in the Deoxy-Hb and hemodynamics, imagery of one-legged cycling induced the bilateral increases in the Oxy-Hb, which were completely abolished by atropine. In contrast, imagery of a circle (with no relation to exercise) did not alter the NIRS signals, irrespective of the presence or absence of atropine. It is concluded that central command evokes cholinergic vasodilatation equally in bilateral VL muscles during voluntary one-legged cycling and motor imagery.

Severe bradycardia and prolonged hypotension in ciguatera

Ciguatera results when ciguatoxin-contaminated coral reef fish from tropical or subtropical waters are consumed. The clinical features that present in affected persons are mainly gastrointestinal, neurological, general, and much less commonly, cardiovascular. We report the case of a 50-year-old man who developed the characteristic combination of acute gastrointestinal and neurological symptoms after the consumption of an unidentified coral reef fish head. In addition to those symptoms, he developed dizziness, severe bradycardia (46 bpm) and prolonged hypotension, which required the administration of intravenous atropine and over three days of intravenous fluid replacement with dopamine infusion. Patients with ciguatera can develop severe bradycardia and prolonged hypotension. Physicians should recognise the possible cardiovascular complications of ciguatera and promptly initiate treatment with intravenous atropine, intravenous fluid replacement and inotropic therapy if such complications are observed.

Cardiac arrest after spinal anesthesia in a patient with neurally mediated syncope

We present the case of cardiac arrest in a patient with neurally mediated syncope (NMS). A 66-year-old male patient was scheduled to undergo right inguinal hernioplasty. He had a history of syncope, which occurred a few times a year in childhood and once a year recently. One minute after the second spinal injection, cardiac arrest (asystole) developed. Sinus rhythm was restored by cardiac massage and intravenous administration of atropine and ephedrine. The operation was cancelled. The patient was diagnosed as NMS by a cardiologist. Four months later, right inguinal hernioplasty was performed, uneventfully, under general anesthesia. High sympathetic blockade due to spinal anesthesia and transient withdrawal of sympathetic tone and increase in vagal discharge due to NMS could be the main causes of the cardiac arrest. If the patient has any possibility of NMS, anesthesiologists should consider the possibility of cardiac arrest after spinal anesthesia.