Sympathetic Surge Research Articles

Neuraxial Anesthesia and Analgesia During Cardiothoracic Surgery: A Narrative Review.

The purpose of this review is to synthesize and examine the literature on the use of neuraxial anesthesia and analgesia during cardiothoracic surgery. As cardiothoracic procedures often require systemic anticoagulation, neuraxial techniques are quite often underutilized due to the theoretical risk of epidural hematoma. In this review, we seek to examine the literature to review the indications and contraindications and to explore if neuraxial anesthesia and analgesia has a role in cardiothoracic surgery. Neuraxial techniques have multiple advantages during cardiothoracic surgery including coronary vasodilation, decreased sympathetic surge, and a decreased cortisol level leading to overall reduction in stress response. Multiple studies have shown an improvement in pain scores, reduction in pulmonary complications, faster extubation times, with minimal complications when neuraxial techniques are utilized in cardiothoracic surgeries. Given the numerous advantages and minimal complications of neuraxial techniques in cardiothoracic surgeries, we hope its utilization continues to increase. Moving forward, we hope additional studies continue to reaffirm the benefits of neuraxial anesthesia and analgesia for cardiothoracic surgeries to improve its utilization.

Comparative evaluation between oral gabapentin and oral pregabalin premedication for attenuation of hemodynamic surge to laryngoscopy and endotracheal intubation in elective procedures under general anesthesia

Background: Effective attenuation of the sympathetic surge due to laryngoscopy and endotracheal intubation is needed. We wanted to compare the role of oral gabapentin (600 mg) and oral pregabalin (150 mg) in controlling this sympathetic surge. Aims and Objectives: To compare the role of oral gabapentin (600 mg) and oral pregabalin (150 mg) as premedications for attenuating hemodynamic surge to laryngoscopy and endotracheal intubation. Materials and Methods: 90 patients aged 18–45 years with ASA grade I or II posted for elective surgical procedure under general anesthesia were randomly allocated to two equal groups (45 in each group) to receive either 600 mg oral gabapentin or 150 mg oral pregabalin 1 h prior to surgery. Heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), and rate pressure product (RPP) were recorded after intubation at 1 (T1), 3 (T3), 5 (T5), and 10 (T10) min. Post-operative sedation and post-operative nausea and vomiting (PONV) were recorded and compared. Results: Gabapentin attenuates hemodynamic surge in terms of HR, SBP, DBP, MAP, and RPP better than pregabalin during laryngoscopy and endotracheal intubation at 3, 5, and 10 min after intubation, while there was no significant difference between the two groups at 1 min after intubation. Post-operative sedation score and adverse effects like PONV and SpO2 fluctuations at different points in time were comparable. Conclusion: Oral gabapentin (600 mg) was found to be more effective than oral pregabalin (150 mg) in attenuating the hemodynamic surge to laryngoscopy and intubation.

Abstract 13349: The Effect of Chronic Standard Cigarette Smoke Exposure Compared to Chronic Electronic Cigarette Exposure With or Without Nicotine on Blood Pressure

Background: While the acute exposure to electronic cigarette (e-C) vapor has been associated with an increase in blood pressure, the chronic effect of e-C vapor on blood pressure compared to standard cigarette smoke has not been extensively studied. We determined the effect of chronic e-C exposure versus standard cigarette smoke on blood pressure and other cardiac functional measures. Methods: Sprague Dawley rats (both sexes) were randomly exposed to air (n=34), e-C with nicotine (e-Cn; n=30), e-C without nicotine (e-C; n= 28) or standard cigarette smoke (SCS; n=27) for 12 weeks. After 12 weeks of exposure hemodynamics were determined by Millar catheter, echocardiography, and thermodilution catheter, a few days after their last exposure. Results: As shown in the Table, SCS was associated with higher systolic, diastolic and mean blood pressures and peak LV systolic pressure compared to air or e-Cn or e-C groups. Neither fractional shortening or cardiac output differed among the groups. dp/dt min, a measure of diastolic LV function, was lowest in the e-C group. Tau, a measure of LV relaxation was worse in this group as well. Conclusions: Standard cigarette smoke exposure was associated with an increase in blood pressure when blood pressure was tested at 12 weeks. Neither electronic cigarette smoke with or without nicotine caused an increase in blood pressure compared to air. However, e-C was associated with worse diastolic function. Standard cigarettes may be associated with a greater sympathetic surge causing elevated blood pressure compared to electronic cigarettes.

Ventricular Tachycardia.

This scenario was developed to educate emergency medicine residents on the diagnosis and management of ventricular tachycardia (VT) that is refractory to single dose anti-arrhythmic management. Electrical storm, defined as three or more episodes of sustained VT, ventricular fibrillation, or appropriate shocks from an implantable cardioverter defibrillator within 24 hours,1 has a mortality rate up to 14% in the first 48 hours.2 Ventricular tachycardia may present in a heterogenous fashion, not only with stable versus unstable clinical presentations, but also with different electrocardiographic morphologies and etiologies.1 Understanding how to rapidly diagnose, treat, and utilize second or third-line treatments is vital in the setting of refractory ventricular tachycardia rather than relying on the success of first-line agents. Appreciation for what medications are readily available in your crash cart and medication dispensing cabinet is critical for timely management for refractory ventricular tachycardia. At the conclusion of the simulation session, learners will be able to: 1) identify the different etiologies of VT, including structural heart disease, acute ischemia, and acquired or congenital QT syndrome; 2) describe confounding factors of VT, such as electrolyte abnormalities and sympathetic surge; 3) describe how to troubleshoot an unsuccessful synchronized cardioversion, including checking equipment connections, increasing delivered energy, and changing pad placement; 4) compare and contrast treatments of VT based on suspected underlying etiology; 5) describe reasons to activate the cardiac catheterization lab other than occlusive myocardial infarction; and 6) identify appropriate disposition of the patient to the cardiac catheterization lab. This session was conducted using high-fidelity simulation, followed by a debriefing session and lecture on the diagnosis, differential diagnosis, and management of VT. Debriefing methods may be left to the discretion of participants, but the authors have utilized advocacy-inquiry techniques. This scenario may also be run as an oral board case. Our residents are provided a survey at the completion of the debriefing session so they may rate different aspects of the simulation, as well as provide qualitative feedback on the scenario. The local institution's simulation center's electronic feedback form is based on the Center of Medical Simulation's Debriefing Assessment for Simulation in Healthcare (DASH) Student Version Short Form3 with the inclusion of required qualitative feedback if an element was scored less than a 6 or 7. Twelve learners completed a feedback form. This session received 6 and 7 scores (consistently effective/very good and extremely effective/outstanding, respectively) other than three isolated 5 scores. The lowest average score was 6.67 for "Before the simulation, the instructor set the stage for an engaging learning experience." The highest average score was 7 for "The instructor helped me see how to improve or how to sustain good performance." The form also includes an area for general feedback about the case at the end. Illustrative examples of feedback include: "Excellent care and debrief." Specific scores are available upon request. This is a cost-effective method for reviewing VT diagnosis and management. The case may be modified for appropriate audiences, such as describing what medications may be readily available in a free-standing emergency department or pre-hospital setting. Medical simulation, ventricular tachycardia, cardiac emergencies, dysrhythmias, cardiology, emergency medicine.

Electroconvulsive Therapy in Heart Transplant Patients: To Avoid or Embrace?

Patients with heart disease are at an increased risk of depression. Electroconvulsive therapy (ECT) is a highly effective treatment for severe depressive episodes. However, ECT may increase the risk for adverse outcomes in certain patients because of changes in blood pressure and heart rate secondary to an initial parasympathetic surge followed by a sympathetic surge and peripheral catecholamine release. In post-cardiac transplant patients, these acute hemodynamic changes on a denervated heart may bring clinical challenges. The available data on ECT in heart transplant patients are limited. The authors of this article present a summary of the available literature relating to ECT in heart transplant patients.The authors performed a literature search of 6 online databases yielding 6 English-language case reports of ECT in cardiac transplant patients. All patients experienced changes in hemodynamic variables during and immediately after ECT, ranging from moderate decrease in blood pressure to extreme hypertension. The cases did not report any serious cardiac complications during the course of ECT. In the 5 patients whose psychiatric responses to treatment were detailed, all had improvement in their depressive symptoms. Electroconvulsive therapy may be considered for severe cases of depression in patients with a history of cardiac transplant, but the potential benefit of ECT needs to be weighed against risks. In the limited number of cases reported in the literature, ECT seems to have been relatively safe and effective.

Atracurium Versus Cis-Atracurium for Laryngeal Relaxation and Hemodynamic Stability in Pediatric Patients: A Randomized, Double-Blind Study.

Background and aim Equipotent dose of atracurium and cis-atracurium has failed to show clinically equi-effective muscle relaxation actions required for laryngoscopy and endotracheal intubation (LETI) in adults. There needs to be more data on children. We aimed to compare the efficacy of equipotent atracurium and cis-atracurium for producing optimal LETI. We also compared the hemodynamic stability and side effects. Methods With approvals and informed consent, 104 children between three and 12 years were enrolled in the present randomized, double-blind, parallel-arm study. Fifty-two participants were recruited in each group and received either 2ED95 atracurium (0.5mg/kg) or 2ED95 cis-atracurium (0.1mg/kg). Three-point scale, i.e., excellent, good, and poor, were assigned based on jaw relaxation, vocal cords, diaphragmatic movement, coughing, and resistance to the laryngoscope blade. Basic hemodynamics and adverse events like flushing, hemodynamic instability, and airway spasms were noted. The groups were compared using Wilcoxon-Mann-Whitney U or Chi-square tests as applicable; a p-value <0.05 was considered significant. Results Entire enrolled participants completed the study. Excellent LETI conditions were significantly higher in the atracurium than in cis-atracurium (53.8% versus 19.2%, p-value <0.001). In the present study, blunted laryngoscopy-related sympathetic surge containing the increase in hemodynamic parameters within 20% from the baseline was noted in both groups, but the blunting and fall back of hemodynamic towards the baseline was rapid in the atracurium (within 7 minutes of LETI) group than cis-atracurium, i.e., 72 minutes; p-value <0.001. Only one flushing was noted in the atracurium group compared to none in the cis-atracurium. Conclusion 2ED95 dose of cis-atracurium (0.1mg/kg), although have minor advantages of maintaining hemodynamic better, has lower adverse events, it provides significantly lower 'Excellent LETI conditions' when compared to 2ED95 dose of atracurium (0.5mg/kg) in children of age three to 12 years.

Effect of Continuous Positive Airway Pressure Therapy in Patient with Obstructive Sleep Apnea and Pulmonary Hypertension: A literature review.

Patients with obstructive sleep apnea (OSA) and pulmonary hypertension (PH) have a reduced functional capacity and potential survival. Continuous positive airway pressure (CPAP) is the primary treatment for OSA, and this improves sleep parameters, functional activity, and possibly pulmonary artery pressures (PAPs). This literature review summarizes the available studies that have measured changes in PAPs in patients with sleep apnea following the institution of CPAP. The PubMed.gov database was searched with a combination of keywords including: "Pulmonary Hypertension," "Obstructive Sleep Apnea," and "Continuous Positive Airway Pressure." Specific inclusion and exclusion criteria were applied to select prospective studies, and data were carefully extracted from each study. Seven unique studies were identified from a list of 272 search results. The studies included a range of CPAP treatments; all showed significant improvement in PAP. The average improvement in PAP across all studies when weighted for a number of participants was 9.33 ± 7.71 mm Hg. This systematic literature review demonstrates that CPAP treatment reduces PAPs in patients with OSA. The study intervals ranged from 48 hours to 6 months to determine the effects of CPAP on PH in these patients. The literature review undertaken during the analysis of these original studies on OSA and PH provides information about vascular remodeling during OSA and the effect of apnea on O2 saturation, intrathoracic pressure swings, and sympathetic surges post apnea. Patients with OSA frequently have significant comorbidity, including hypertension, obesity, and overlap syndromes with other pulmonary disorders and/or cardiac disorders. This comorbidity increases the complexity of management and likely contributes to poor outcomes. The gold standard for making a diagnosis of PH requires right heart catheterization, but practical issues dictate the need for frequent echocardiograms to evaluate right ventricular systolic pressures and right atrial and ventricle chamber sizes. A better understanding of the association between OSA and PH and its treatment with CPAP will require long-term perspective studies.

Investigating the effects of beta-blockers on circadian heart rhythm using heart rate variability in ischemic heart disease with preserved ejection fraction

Heart failure is characterized by sympathetic activation and parasympathetic withdrawal leading to an abnormal autonomic modulation. Beta-blockers (BB) inhibit overstimulation of the sympathetic system and are indicated in heart failure patients with reduced ejection fraction. However, the effect of beta-blocker therapy on heart failure with preserved ejection fraction (HFpEF) is unclear. ECGs of 73 patients with HFpEF > 55% were recruited. There were 56 patients in the BB group and 17 patients in the without BB (NBB) group. The HRV analysis was performed for the 24-h period using a window size of 1,4 and 8-h. HRV measures between day and night for both the groups were also compared. Percentage change in the BB group relative to the NBB group was used as a measure of difference. RMSSD (13.27%), pNN50 (2.44%), HF power (44.25%) and LF power (13.53%) showed an increase in the BB group relative to the NBB group during the day and were statistically significant between the two groups for periods associated with high cardiac risk during the morning hours. LF:HF ratio showed a decrease of 3.59% during the day. The relative increase in vagal modulated RMSSD, pNN50 and HF power with a decrease in LF:HF ratio show an improvement in the parasympathetic tone and an overall decreased risk of a cardiac event especially during the morning hours that is characterized by a sympathetic surge.

Central Sleep Apnea in Adults: Diagnosis and Treatment

While the literature has demonstrated a higher prevalence of moderate-to-severe obstructive sleep apnea (OSA) in the general population compared with central sleep apnea (CSA), more evidence is needed on the long-term clinical impact of and optimal treatment strategies for CSA. CSA is overrepresented among certain clinical populations, such as those with heart failure, stroke, neuromuscular disorders, and opioid use. The clinical concerns with CSA parallel those of OSA. The absence of respiration (apneas and hypopneas due to lack of effort) results in sympathetic surge, compromise of oxygenation and ventilation, sleep fragmentation, and elevation in blood pressure. Symptoms such as excessive daytime sleepiness, morning headaches, witnessed apneas, and nocturnal arrhythmias are shared between the 2 disorders. A systematic clinical approach should be used to identify and treat CSA. The purpose of this review is to familiarize the primary care community with CSA to aid in the identification and management of this breathing disturbance.

Abstract 12757: Competing Neurotrophic and Anti-Neurotrophic Remodeling Processes in PVC-Induced Cardiomyopathy

Introduction: We previously demonstrated evidence of pro-arrhythmic sympathetic hyperinnervation and hyperactivity of the stellate ganglia in Premature Ventricular Contraction-induced Cardiomyopathy (PVC-CM). However, the presence of neural remodeling within the myocardium remains unclear. Methods: In a canine model of PVC-CM induced by a novel premature pacing algorithm with 12-weeks of bigeminal short-coupled (200ms) PVC exposure, we performed ELISA of serial plasma norepinephrine levels at baseline vs PVC-CM (N=7), and western blotting of neural proteins and beta-adrenoreceptors using snap-frozen left ventricular free wall myocardium in 6 sham controls and 7 PVC-CM hearts. Results: We found increased trans-cardiac norepinephrine (NE) levels in PVC-CM vs controls (Fig. 1A), increased LV myocardial sympathetic nerve protein Tyrosine Hydroxylase (TH) (Fig.1B) but interestingly, decreased Growth Associated Protein (GAP) 43 (Fig.1C), a marker of sprouting nerve cones. There was no change in synaptophysin (SYN), a neural synapse protein, or Choline acetyltransferase (ChAT), a parasympathetic nerve marker (Fig.1D). Further downstream, we found reduced ß-1 receptor levels similar to other forms of heart failure but markedly increased ß-2 receptor levels (Fig.1E), a finding unique to PVC-CM. Functionally, ß-2 effects are known to oppose the ß-1 inotropic and pro-apoptotic effects in the human myocardium Conclusions: There are competing neurotrophic vs anti-neurotrophic processes occurring within the LV myocardium, along with downstream beta-receptor changes. We hypothesize that these changes are a chronic adaptive response to PVC-induced chronic sympathetic surge, that ultimately protect against sympathetic excess and its consequent downstream effects on myocardial calcium handling and inotropy. These changes may have implications for the pathogenesis of PVC-CM and its pro-arrhythmic consequences. !

A SYMPATHETIC CASE OF MULTIPLE INHALER INTOLERANCES

<h3>Introduction</h3> Drug reactions account for a large proportion of complaints evaluated in allergy/immunology clinic. Determining the cause for these drug reactions can often be difficult. In this case, we discuss a rare cause for repeated adverse reactions to multiple inhalers. <h3>Case Description</h3> A 57-year-old male veteran with COPD presented for evaluation of drug allergy. His COPD was previously well-controlled with ipratropium and albuterol inhalers. Over the last several weeks, he has experienced flushing, lightheadedness, and shortness of breath following use of both inhalers. He tolerated inhaled fluticasone and cromolyn for several days before having the same symptoms following each use. Initial testing included skin prick testing to the offending agents, which was negative (Table 1). Drug challenge with budesonide, omalizumab, and albuterol revealed intense flushing, hypertension, and sense of doom within 30 mins. Serum catecholamines, urine metanephrines, urine 5-HIAA, and serum tryptase were normal. 24hr urine cortisol was slightly elevated. Dexamethasone suppression test was normal. In collaboration with endocrinology, he was diagnosed with <i>pseudopheochromocytoma</i> and advised to start an SSRI given the frequency of his paroxysms, which he declined. <h3>Discussion</h3> Non-immunologic drug reactions are suspected when drugs from multiple drug classes incite symptoms. Determining the underlying process is important to allow patients to continue taking life-saving medications. Pseudopheochromocytoma is a rare but important cause of drug reactions that present with paroxysms of hypertension, headache, palpitations, lightheadedness, flushing, and diaphoresis due to somatic sympathetic surges. Treatment includes antidepressants and biofeedback therapy.

A Case of Intractable Hyperhidrosis in Spinal Cord Injury: Role of Stellate Ganglion Block

Objective: Autonomic dysreflexia (AD) in spinal cord injury (SCI) can present as hyperhidrosis due to sudomotor dysfunction. Hyperhidrosis can also occur without an identifiable etiology. There are no standard treatment guidelines for refractory hyperhidrosis in the setting of persistent noxious stimulation. Stellate ganglion blockade may prevent hyperhidrosis by inhibiting profound sympathetic surge and vasoconstriction. Case: 58-year-old female with C7 ASIA-A quadriplegia was admitted to the hospital for episodes of profuse sweating in the setting of autonomic dysreflexia secondary to underlying T7-8 discitis. Despite conservative treatment of discitis, patient continued experience 50-60 episodes of profuse sweating daily. Stellate ganglion block was performed under ultrasound guidance to reduce sympathetic surge. Patient underwent serial stellate ganglion blocks under ultrasound guidance with >75% improvement in her hyperhidrosis episodes. Discussion: Stellate ganglion block is a safe interventional which can be considered for sympathetically mediated refractory hyperhidrosis. It may also be used as a treatment alternative in certain cases of refractory AD in SCI patients.

0723 Elucidation of Obstructive Sleep Apnea-Related Heart Rate Response Using a Novel Continuous Beat to Beat Blood Pressure Monitoring Technology

Abstract Introduction Obstructive sleep apnea (OSA) episode related sympathetic surge may mediate the association of OSA with cardiovascular disease. Heart rate (HR) response (HRR) to OSA events may reflect magnitude of sympathetic surge but is expected to be variable between individuals. We investigated the variability of HRR to OSA events and its relation to degree of oxygen desaturation. Methods We included patients undergoing clinically-indicated polysomnography (PSG). We calculated HRR by deriving inter-beat interval (IBI) from a novel continuous beat-to-beat (b-b) blood pressure (BP) monitoring technology (Caretaker™) that was concurrently recorded during PSG.HRR from respiratory (apnea, hypopnea and desaturation alone events) and non-respiratory events (spontaneous or leg movement-related arousals) were compared. We also examined the association of degree of oxygen desaturation with HRR in a given respiratory event combining all events accounting for the counts of the number of events. In the sub-cohort who underwent split night sleep study, we compared the hourly HR surge events (HRR&amp;gt; 20 pm) between diagnostic and CPAP phases. Results A total of 17 patients(12 men, mean 52 years old, 9 diagnostic and 8 split night PSGs) were included after excluding one patient with poor signal quality due to excessive movement. The device was well tolerated by patients and IBI and BP data were successfully aligned with PSG data. Mean respiratory HRR ranged from 1.0 to 44.0 (Median [IQR]= 11.00[2.0, 20.0]) mmHg. Mean HRR was more pronounced during the non-respiratory events than respiratory events (12.5[7.2] vs. 11.9[6.6] mmHg, p=0.034).Accounting for the count distribution of desaturation/HRR data pair events, there was a moderately positive correlation between the degree of oxygen desaturation and HRR(R=0.63). Hourly HR surge events were significantly reduced during CPAP phase compared to diagnostic phase (11 events/hr vs 126 events/hr, p=0.032). Conclusion We demonstrated highly variable OSA-related HRR patterns between individuals with OSA. There was moderate correlation between degree of oxygen desaturation and HRR to respiratory events. HRR to non- respiratory events was more pronounced than to respiratory events. Future studies should evaluate the clinical implications of the OSA specific HRR. Support (If Any)

Right Sided Stellate Ganglion Block before Pneumoperitoneum in Laparoscopic Surgeries. Does it Balance Hemodynamics? A Case Series

The laparoscopic technique is currently used for many types of surgery because it is painless, has less nociceptive stimulus from the skin and tissues, has fewer wound complications, and allows for a faster and smoother postoperative recovery. Institution of capnoperitoneum to visualize the viscera inside is the need in these cases. However, capnoperitoneum can cause many side effects including a significant rise in heart rate and blood pressure. Stellate ganglion block (SGB) is a sympathetic block for the head, neck, chest, and upper limbs. Hence, we hypothesized that blocking the same, especially right-sided, will decrease a sympathetic surge after capnoperitoneum. We conducted three such cases with administration of ultrasound-guided SGB in the right side 10 min before capnoperitoneum and found that there was no surge in hemodynamics. We postulate that right-sided SGB can be added to the armamentarium of countless techniques to blunt the response. We admit that this is a very small primitive report with only three cases. As ultrasound was used in all the cases, the deposition of local anesthetic drug was precise.

Sympatho-adrenergic mechanisms in heart failure: new insights into pathophysiology.

The sympathetic nervous system is activated in the setting of heart failure (HF) to compensate for hemodynamic instability. However, acute sympathetic surge or sustained high neuronal firing rates activates β-adrenergic receptor (βAR) signaling contributing to myocardial remodeling, dysfunction and electrical instability. Thus, sympatho-βAR activation is regarded as a hallmark of HF and forms pathophysiological basis for β-blocking therapy. Building upon earlier research findings, studies conducted in the recent decades have significantly advanced our understanding on the sympatho-adrenergic mechanism in HF, which forms the focus of this article. This review notes recent research progress regarding the roles of cardiac β2AR or α1AR in the failing heart, significance of β1AR-autoantibodies, and βAR signaling through G-protein independent signaling pathways. Sympatho-βAR regulation of immune cells or fibroblasts is specifically discussed. On the neuronal aspects, knowledge is assembled on the remodeling of sympathetic nerves of the failing heart, regulation by presynaptic α2AR of NE release, and findings on device-based neuromodulation of the sympathetic nervous system. The review ends with highlighting areas where significant knowledge gaps exist but hold promise for new breakthroughs.

Morning sympathetic activity after evening binge alcohol consumption.

Binge alcohol consumption elicits acute and robust increases of muscle sympathetic nerve activity (MSNA), yet the impact of evening binge drinking on morning-after MSNA is unknown. The present study examined the effects of evening binge alcohol consumption on polysomnographic sleep and morning-after MSNA. We hypothesized that evening binge drinking (i.e. 4-5 drink equivalent in <2 h) would reduce sleep quality and increase morning-after blood pressure (BP) and MSNA. Following a familiarization night within the sleep laboratory, 22 participants (12 men, 10 women; 25 ± 1 yr) were examined after simulated binge drinking or fluid control (randomized, crossover design). Morning MSNA was successfully recorded across both conditions in 16 participants (8 men, 8 women) during a 10-min baseline and three Valsalva's maneuvers (VM). Binge drinking reduced rapid eye movement (REM) sleep (15 ± 1 vs. 20 ± 1%, P = 0.003), increased stage II sleep (54 ± 1 vs. 51 ± 1%, P = 0.002), and increased total urine output (2.9 ± 0.2 vs. 2.1 ± 0.1 liters, P < 0.001) but did not alter morning-after urine specific gravity. Binge drinking increased morning-after heart rate [65 (54-72) vs. 58 (51-67) beats/min, P = 0.013] but not resting BP or MSNA. Binge drinking elicited greater sympathoexcitation during VM (38 ± 3 vs. 43 ± 3 bursts/min, P = 0.036). Binge drinking augmented heart rate (P = 0.002), systolic BP (P = 0.022), and diastolic BP (P = 0.037) reactivity to VM phase IV and blunted cardiovagal baroreflex sensitivity during VM phases II (P = 0.028) and IV (P = 0.043). In conclusion, evening binge alcohol consumption disrupted REM sleep and morning-after autonomic function. These findings provide new mechanistic insight into the potential role of binge drinking on cardiovascular risk.NEW & NOTEWORTHY Chronic binge alcohol consumption is associated with future cardiovascular disease (CVD) risk in both men and women. In addition, binge alcohol consumption is known to disrupt normal sleep quality during the early morning hours, coinciding with the morning sympathetic surge. In the present study, an evening of binge alcohol consumption increased baseline morning heart rate and cardiovascular reactivity during the Valsalva maneuver (VM) strain. Specifically, muscle sympathetic nerve activity and phase IV hemodynamic responses increased during VM the morning after binge alcohol consumption. The autonomic dysfunction and increased cardiovascular reactivity during VM suggests a contributing mechanism to CVD risk present in individuals who binge drink.

THE COMPANY YOU KEEP: A CASE OF REFRACTORY HYPOXEMIC RESPIRATORY FAILURE, THYROID STORM, AND SYSTOLIC HEART FAILURE IN THE POSTPARTUM PERIOD

SESSION TITLE: Medical Student/Resident Critical Care Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: We present a case of acute hypoxemic respiratory failure from flash pulmonary edema in a new mother with Graves’ disease. CASE PRESENTATION: A 36 year old woman, four days postpartum with history of Graves’ disease and pre-eclampsia presented in acute respiratory distress. On admission, she had a systolic BP > 200 mmHg, sinus tachycardia to 150 BPM, bilateral patchy pulmonary infiltrates, and profound hypoxemia requiring intubation. Severe hypoxemia persisted despite paralysis and lung recruitment maneuvers, therefore airway pressure release ventilation (APRV) was used as a rescue strategy. Thyroid studies suggested evidence of thyroid storm (low TSH, high free T3, normal free T4 and a Burch-Wartofsky score of 70). Intravenous esmolol was initiated to achieve peripheral beta blockade but was complicated by PEA arrest. Return of spontaneous circulation was achieved after five minutes of CPR. An echocardiogram showed biventricular failure and ejection fraction of 30%. Hydrocortisone, propylthiouracil, and iodine were initiated for thyroid storm and eventually she was extubated. Repeat echocardiogram revealed recovered ejection fraction of 60%. She was discharged in stable condition on methimazole with close follow-up. DISCUSSION: Therapies invariably consist of both positive and negative effects. The role of an intensivist is to weigh these risks and benefits, make sound judgement, and adapt to unintended consequences. This patient presented in extremis with hypoxemic respiratory failure from flash pulmonary edema. Her history of Graves’ disease combined with laboratory and clinical data pointed strongly to thyroid storm. The best evidence suggests that early treatment of thyroid storm is crucial and mortality rates rise to 75% with delays in therapy. While beta-blockade is considered first line therapy to treat the effects of uncontrolled thyroid hormone, in this case it undoubtedly led to cardiac arrest. Following the successful resuscitation, it was clear that RV dysfunction paired with high intrathoracic pressures generated by APRV mode should be seen as a death knell if paired with beta blockade. Opposing the sympathetic surge and tachycardia required to maintain cardiac output, our patient quickly decompensated, with loss of chronotropy and RV failure leading to cardiac arrest. Rapid removal of the short-acting agent esmolol, along with resuscitative efforts were able to quickly correct the untoward effects and the patient made a full recovery. CONCLUSIONS: This case offers a unique presentation of thyroid storm and highlights the duality of therapies. A high level of suspicion is required for timely diagnosis of thyroid storm and early treatment is critical. Despite this, the benefits of therapy cannot be seen in a vacuum and we must strive to understand the potential negative consequences in our quest to provide exceptional critical care. Reference #1: Chiha M, Samarasinghe S, Kabaker AS. Thyroid Storm: An Updated Review. Journal of Intensive Care Medicine. August 5, 2013. Volume: 30 issue: 3, page(s): 131-140. Reference #2: Karger S, Führer D. Thyroid storm--thyrotoxic crisis: an update. Dtsch Med Wochenschr. 2008;133(10):479-484. doi:10.1055/s-2008-1046737 DISCLOSURES: No relevant relationships by Paul Cooper, source=Web Response No relevant relationships by Dustin Fraidenburg, source=Web Response No relevant relationships by Janae Gonzales, source=Web Response No relevant relationships by Malvika Kaul, source=Web Response No relevant relationships by Shuvani Sanyal, source=Web Response No relevant relationships by Christen Vagts, source=Web Response

Impact of Adding Midazolam to Bupivacaine 0.5% in Regional Spinal Anesthesia on Maternal Middle Cerebral Artery Velocimetry in Parturients with Severe Preeclampsia

Severe preeclampsia is a challenging issue facing both intensivist and anesthetic team carrying both maternal and fetal morbidity and mortality. Termination of pregnancy after blood pressure control is the golden key in management. Cerebral complications due to diffuse cerebral vasospasm are most common and serious. Intrathecal midazolam with its gamma amino butyric action may antidote glutamate mediated sympathetic surge and decreasing cerebral vasospasm. Temporal view transcranial Doppler imaging maternal middle cerebral artery is used to examine blood flow indices namely pulsatility index and resistive index. One hundred ladies with severe preeclampsia scheduled for urgent caesarian section were recruited in 2 groups, both received 10 mg bupivacaine 0.5%, Midazolam group received 1 mg midazolam and the other group received 0.2 ml sterile saline 0.9% NaCl. All vascular indices were significantly better in midazolam group, less ICU stay.

R-From-T as a Common Mechanism of Arrhythmia Initiation in Long QT Syndromes.

Long QT syndromes (LQTS) arise from many genetic and nongenetic causes with certain characteristic ECG features preceding polymorphic ventricular tachyarrhythmias (PVTs). However, how the many molecular causes result in these characteristic ECG patterns and how these patterns are mechanistically linked to the spontaneous initiation of PVT remain poorly understood. Anatomic human ventricle and simplified tissue models were used to investigate the mechanisms of spontaneous initiation of PVT in LQTS. Spontaneous initiation of PVT was elicited by gradually ramping up ICa,L to simulate the initial phase of a sympathetic surge or by changing the heart rate, reproducing the different genotype-dependent clinical ECG features. In LQTS type 2 (LQT2) and LQTS type 3 (LQT3), T-wave alternans was observed followed by premature ventricular complexes (PVCs). Compensatory pauses occurred resulting in short-long-short sequences. As ICa,L increased further, PVT episodes occurred, always preceded by a short-long-short sequence. However, in LQTS type 1 (LQT1), once a PVC occurred, it always immediately led to an episode of PVT. Arrhythmias in LQT2 and LQT3 were bradycardia dependent, whereas those in LQT1 were not. In all 3 genotypes, PVCs always originated spontaneously from the steep repolarization gradient region and manifested on ECG as R-on-T. We call this mechanism R-from-T, to distinguish it from the classic explanation of R-on-T arrhythmogenesis in which an exogenous PVC coincidentally encounters a repolarizing region. In R-from-T, the PVC and the T wave are causally related, where steep repolarization gradients combined with enhanced ICa,L lead to PVCs emerging from the T wave. Since enhanced ICa,L was required for R-from-T to occur, suppressing window ICa,L effectively prevented arrhythmias in all 3 genotypes. Despite the complex molecular causes, these results suggest that R-from-T is likely a common mechanism for PVT initiation in LQTS. Targeting ICa,L properties, such as suppressing window ICa,L or preventing excessive ICa,L increase, could be an effective unified therapy for arrhythmia prevention in LQTS.

P5698What predicts the inefficiency of stellate ganglion block in the treatment of electrical storm?

Abstract Introduction Electrical storm (ES) is an emergent condition which requires a sofisticated approach. Massive sympathetic surge almost always connected with ES precipitates recurrent ventricular arrhythmias. Performing stellate ganglion block (SGB) to alleviate the sympathetic activity on myocardium is becoming a standard of care in many centers. However, there is no clear data to predict in which patients the SGB will be ineffective. Purpose To identify predictors of SGB failure in patients with ES. Methods We analyzed our case series of SGB – the procedure was performed in 31 patients with ES in our center from March 2017 to December 2018. Results Mean left ventricular ejection fraction was 27% (±9%), 74% of patients had ischaemic cardiomyopathy. The most frequent type of arrhythmia was monomorphic ventricular tachycardia (VT), occurring in 71% of patients, followed by polymorphic VT in 13% of cases. After SGB, the burden of ventricular arrhythmias failed to decrease by at least 50% in 10% of cases - these patients were marked as non-responders. Slow monomorphic VT (under 160/min) was observed in all of these patients. On the other hand, fast monomorphic VT or polymorphic VT seemed to respond very well to SGB. We also observed, that patients with ES after acute coronary syndromes were good responders as well. The effect of SGB was not related to age, gender, EF LK or the etiology of cardiomyopathy. Conclusions According to our experience, the failure of SGB in the treatment of ES is not frequent. It typically occurs in patients with slow monomorphic VT. It is probable that such arrhythmias are sustained primarily due to the extensive myocardial substrate, and not because of the sympathetic surge. The situation is quite the opposite in patients with fast VT and acute ischemia.