Pulseless Electrical Activity Cardiac Arrest Research Articles

Association Between QRS Characteristics in Pulseless Electrical Activity and Survival Outcome in Cardiac Arrest Patients: A Systematic Review and Meta-Analysis

Objective Recent studies have shown inconsistent results regarding the association between QRS characteristics and survival outcomes in patients with cardiac arrest and pulseless electrical activity (PEA) rhythms. This meta-analysis aimed to identify the usefulness of QRS width and frequency as prognostic tools for outcomes in patients with cardiac arrest and PEA rhythm. Methods Extensive searches were conducted using Medline, Embase, and the Cochrane Library to find articles published from database inception to 4 June 2023. Studies that assessed the association between the QRS characteristics of cardiac arrest patients with PEA rhythm and survival outcomes were included. The Newcastle-Ottawa Scale was used to assess the methodological quality of the included studies. Results A total of 9727 patients from seven observational studies were included in this systematic review and meta-analysis. The wide QRS group (QRS ≥ 120 ms) was associated with significantly higher odds of mortality than the narrow QRS group (QRS < 120 ms) (odds ratio (OR) = 1.86, 95% confidence interval (CI) = 1.11–3.11, I 2 = 58%). The pooled OR for mortality was significantly higher in patients with a QRS frequency of < 60/min than in those with a QRS frequency of ≥ 60/min (OR = 1.90, 95% CI = 1.19–3.02, I 2 = 65%). Conclusions Wide QRS width or low QRS frequency is associated with increased odds of mortality in patients with PEA cardiac arrest. These findings may be beneficial to guide the disposition of cardiac arrest patients with PEA during resuscitation.

Intraoperative Pulseless Electrical Activity Cardiac Arrest during Intracranial Aneurysm Clipping: Case Report

Cardiac arrest is a rare intraoperative complication with few cases reported during neurosurgery. Proposed causes of PEA cardiac arrest in this setting include medications, irrigation, coronary vasospasm, and elicitation of the trigeminocardiac reflex.

Abstract 11227: A Rare Case of Echo Contrast Anaphylaxis Complicated by Acute Coronary Syndrome

Introduction: Contrast agents in echocardiography are used frequently to enhance endocardial border visualization and assessment of structural heart disease. Sulfur hexafluoride lipid type A injectable suspension is a generally well-tolerated class of contrast. Anaphylaxis to these agents is exceedingly rare. We now report the first case of acute coronary syndrome in the setting of echo contrast anaphylactic shock. Case: A 49-year-old woman was hospitalized for an ST-elevation myocardial infarction (STEMI) for which a drug-eluting stent had been placed in the left anterior descending artery (LAD). An echocardiogram was performed to evaluate for structural heart disease. Shortly after administration of echo contrast the patient developed sudden-onset tachypnea and suffered a pulseless electrical activity cardiac arrest. She was treated for anaphylactic shock with epinephrine and high-dose steroids and achieved return of spontaneous circulation. Following the arrest an electrocardiogram revealed an anterolateral STEMI. The patient immediately underwent repeat angiography which revealed a 100% in-stent thrombosis of the LAD. The occlusion was successfully revascularized with a drug eluting stent with an Impella CP (Abiomed, Danvers MA) support. Subsequent laboratory exam demonstrated an elevated blood tryptase level consistent with an anaphylactic event. Discussion: We present a unique case of anaphylactic shock with acute coronary syndrome following administration of sulfur hexafluoride echo contrast. The incidence of anaphylaxis to echo contrast is less than one per million, and therefore it may not be immediately recognized as a mechanism of shock. Any prior reactions to polyethylene glycol should be noted before using these agents as this ingredient is thought to be the cause of anaphylaxis. In our case, diagnosis of anaphylaxis was confirmed by measuring the serum tryptase level. Tryptase is released from mast cells during allergic events, so this laboratory test with high specificity for anaphylaxis can be a useful tool in challenging cases such as this. Additionally, mast cell and platelet activation secondary to anaphylaxis may be an important mechanism of acute coronary syndrome with in-stent thrombosis.

Continuous heart rate dynamics preceding in-hospital pulseless electrical activity or asystolic cardiac arrest of respiratory etiology

IntroductionRespiratory failure is a common cause of pulseless electrical activity (PEA) and asystolic cardiac arrest, but the changes in heart rate (HR) pre-arrest are not well described. We describe HR dynamics prior to in-hospital cardiac arrest (IHCA) among PEA/asystole arrest patients with respiratory etiology. MethodsIn this retrospective study, we evaluated 139 patients with 3–24 hours of continuous electrocardiogram data recorded preceding PEA/asystole IHCA from 2010-2017. We identified respiratory failure cases by chart review and evaluated electrocardiogram data to identify patterns of HR changes, sinus bradycardia or sinus arrest, escape rhythms, and development right ventricular strain prior to IHCA. ResultsA higher proportion of respiratory cases (58/73, 79 %) fit a model of HR response characterized by tachycardia followed by rapid HR decrease prior to arrest, compared to non-respiratory cases (30/66, 45 %, p < 0.001). Among the 58 respiratory cases fitting this model, 36 (62 %) had abrupt increase in HR occurring 64 (IQR 23–191) minutes prior to arrest, while 22 (38 %) had stable tachycardia until time of HR decrease. Mean peak HR was 123 ± 21 bpm. HR decrease occurred 3.0 (IQR 2.0–7.0) minutes prior to arrest. Sinus arrest occurred during the bradycardic phase in 42/58 of cases; escape rhythms were present in all but 2/42 (5 %) cases. Right ventricular strain ECG pattern, when present, occurred at a median of 2.2 (IQR −0.05–17) minutes prior to onset of HR decrease. ConclusionIHCAs of respiratory etiology follow a model of HR increase from physiologic compensation to hypoxia, followed by rapid HR decrease prior to arrest.

Woman With Cardiac Arrest

A 44-year-old woman presented to the emergency department (ED) in cardiac arrest. Thirty minutes before arrival, she developed shortness of breath and called emergency medical services. En route to the hospital, she suffered a pulseless electrical activity cardiac arrest and arrived at the ED with chest compressions ongoing. Physical examination revealed no signs of life. A transesophageal echocardiogram was performed by the emergency physician (Figure 1 and Video E1 [available at http://www.annemergmed.com]).

P430 TUMORAL THROMBOTIC MICROANGIOPATHY: A RARE CAUSE OF ACUTE PULMONARY HYPERTENSION

Abstract Introduction Among the causes of acute pulmonary hypertension, the occlusion of the little pulmonary vessels caused by tumoral microemboli, even from an unknown neoplasm, is an infrequent condition with a very poor prognosis. Clinical Case A 55–years old woman with no relevant past medical history presented to the Emergency Department with dyspnea at rest, desaturation, palpitations and a brief episode of chest pain, after several days of fatigue and exertional dyspnea. ECG showed sinus tachycardia and signs of right ventricle pressure overload with inverted T waves in V3–V4 and in the inferior leads (Fig. 1). On laboratory tests there were high D–dimer values and a slightly elevated TnI. Blood gas analysis showed hypoxemic hypocapnic respirstory alkalosis. An Echocardiogram revealed severe dilatation and dysfunction of the right ventricle and signs of high probability of pulmonary hypertension (Fig. 2). Pulmonary CT scan ruled out embolism and showed irregular thickening of the interstitium and mediastinal lymphoadenopathy. Then, a rapid clinical deterioration happened, refractory to inotropes infusion and larger volumes of oxygen. The programmed diagnostic pathway cannot be pursued. On day 4, there was respiratory distress and pulseless electrical activity cardiac arrest during endotracheal intubation. ECMO mechanical support was positioned but on day 7 the patient died. Autopsy, made to discover the cause of pulmonary hypertension, revealed the presence of a colonic invasive adenocarcinoma with micropapillary pattern and thoracic and pelvic lymph–nodal metastases. Microscopic evaluation of the lungs showed a widespread neoplastic vascular invasion with microthromboemboli (Fig. 3). Discussion Tumoral thrombotic microangiopathy is a cause of pulmonary hypertension of multifactorial origin and should be suspected in cases of pulmonary hypertension without pulmonary embolism or interstitial lung disease. The rarity of this condition and the absence of an oncological medical history make difficult the diagnostic hypothesis. Besides, the lacking of an effective therapy makes the prognosis poor.

Abstract #1182972: Euglycemic PEA

Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes mellitus (DM). DKA is more commonly seen in patients with type 1 DM rather than type 2 DM. Though in recent years the incidence of DKA in patients with type 2 DM has increased, including euglycemic DKA (EDKA), with frequent use of sodium glucose transporter 2 (SGLT2) inhibitors. We present a case of severe EDKA leading to pulseless electrical activity (PEA) cardiac arrest.

Pulseless electrical activity and asystolic cardiac arrest in infants: identifying factors that influence outcomes.

There is limited information on pulseless electrical activity (PEA)/asystolic cardiac arrest (CA) in the infant population. The aim is to describe the incidence and factors associated with outcomes in infants with PEA/asystolic CA. Single-center retrospective chart review study of infants less than one year of age who suffer in-hospital PEA/asystolic CA from January 1 2011 to June 30 2019. The primary outcome was the return of spontaneous circulation. The secondary outcome was survival to discharge. CA occurred in 148 infants and PEA/asystolic was found in 38 (26%). Of those 29 (76%) achieved ROSC, and 12 (32%) survived to discharge. Infants on inotrope support or receiving longer duration of chest compressions and epinephrine had increase mortality. All infants with respiratory etiology of arrest survived to hospital discharge. PEA/asystolic CAs are uncommon. Poor prognostic indicators include the need for pre-arrest inotrope support and increased duration of chest compressions.

October 2021 Critical Care Case of the Month: Unexpected Post-Operative Shock

No abstract available. Article truncated after 150 words. History of Present Illness: A 55-year-old man with a past medical history significant for endocarditis secondary to intravenous drug use, osteomyelitis of the right lower extremity was admitted for ankle debridement. Pre-operative assessment revealed no acute illness complaints and no significant findings on physical examination except for the ongoing right lower extremity wound. He did well during the approximate one-hour “incision and drainage of the right lower extremity wound”, but became severely hypotensive just after the removal of the tourniquet placed on his right lower extremity. Soon thereafter he experienced pulseless electrical activity (PEA) cardiac arrest and was intubated with return of spontaneous circulation being achieved rapidly after the addition of vasopressors. He remained intubated and on pressors when transferred to the intensive care unit for further management. PMH, PSH, SH, and FH: • S/P Right lower extremity incision and drainage for suspected osteomyelitis as above • Distant history of endocarditis related …

Association between wide QRS pulseless electrical activity and hyperkalemia in cardiac arrest patients.

We evaluated the relationship between hyperkalemia and wide QRS complex in patients with pulseless electrical activity (PEA) cardiac arrest. This was a single-center, retrospective observational study of patients over the age of 18 treated for cardiac arrest at a tertiary referral hospital whose initial electrocardiogram rhythm was PEA from February 2010 to December 2019. Wide QRS PEA was defined as a QRS interval of 120ms or more. Hyperkalemia was defined as serum potassium level>5.5mmol/L. The primary outcome was hyperkalemia. Multivariable logistic regression analysis was used to evaluate the relationship between wide QRS and hyperkalemia. Among 617 patients, we analyzed 111 episodes in the wide QRS group and 506 episodes in the narrow QRS group. The potassium level in the wide QRS group was significantly higher than in the narrow QRS group (5.4mmol/L, IQR 4.4-6.7 vs. 4.6mmol/L, IQR 4.0-5.6, P<0.001). Among all patients, 49.6% (n=55/111) in the wide QRS group had hyperkalemia, which was significantly higher than the 26.7% (n=135/506) in the narrow QRS group (P<0.001). In multivariable logistic regression analysis, wide QRS PEA was significantly associated with hyperkalemia (odds ratio=2.86, 95% confidence interval: 1.80-4.53, P<0.001). Wide QRS PEA as an initial cardiac rhythm was significantly associated with hyperkalemia in cardiac arrest patients.

Refractory pelvic fracture-associated hemorrhage after preperitoneal packing: now what?

A male patient in his 50s presented after a high-speed motorcycle crash. On arrival to the trauma bay, his primary survey was intact with normal vital signs. He had an...

Brain MR Spectroscopic Findings in 3 Consecutive Patients with COVID-19: Preliminary Observations.

Brain multivoxel MR spectroscopic imaging was performed in 3 consecutive patients with coronavirus disease 2019 (COVID-19). These included 1 patient with COVID-19-associated necrotizing leukoencephalopathy, another patient who had a recent pulseless electrical activity cardiac arrest with subtle white matter changes, and a patient without frank encephalopathy or a recent severe hypoxic episode. The MR spectroscopic imaging findings were compared with those of 2 patients with white matter pathology not related to Severe Acute Respiratory Syndrome coronavirus 2 infection and a healthy control subject. The NAA reduction, choline elevation, and glutamate/glutamine elevation found in the patient with COVID-19-associated necrotizing leukoencephalopathy and, to a lesser degree, the patient with COVID-19 postcardiac arrest, follow a similar pattern as seen with the patient with delayed posthypoxic leukoencephalopathy. Lactate elevation was most pronounced in the patient with COVID-19 necrotizing leukoencephalopathy.

QRS complex characteristics and patient outcomes in out-of-hospital pulseless electrical activity cardiac arrest

BackgroundPulseless electrical activity (PEA) is increasingly observed in out-of-hospital cardiac arrest (OHCA), but outcomes are still poor. We aimed to assess the relationship between QRS characteristics and outcomes of patients...

PRESUMED CATASTROPHIC ANTIPHOSPHOLIPID SYNDROME

SESSION TITLE: Fellows Critical Care Posters SESSION TYPE: Fellow Case Report Posters PRESENTED ON: October 18-21, 2020 INTRODUCTION: Antiphospholipid antibodies (aPLs) are associated with recurrent early pregnancy loss and arterial as well as venous thrombosis. A small subset of patients develop a life-threatening form of the disease with widespread thrombosis and multiorgan failure, called catastrophic antiphospholipid syndrome (CAPS). CASE PRESENTATION: A 26-year-old female, 10 weeks pregnant, with a history of 2 prior miscarriages presented with hyperemesis gravidarum. She had a pulseless electrical activity cardiac arrest in the ER with return of spontaneous circulation after 15 minutes of advanced cardiovascular life support (ACLS). Left heart catheterization showed no evidence of coronary artery disease. Transthoracic echocardiogram showed preserved ejection fraction and no other abnormality. CT angiogram of the chest ruled out pulmonary emboli but showed diffuse bilateral airspace opacities, concerning for acute respiratory distress syndrome (ARDS). Patient developed acute kidney injury, acute right lower extremity arterial thrombosis and compartment syndrome requiring fasciotomy, upper extremities superficial venous thrombi, fetal loss and spontaneous abortion. Working diagnosis of CAPS was made; aPLs, anti-cardiolipin and anti-beta2 glycoprotien-1 antibodies levels ordered and patient started on IV heparin infusion, IV glucocorticoids and plasmapheresis followed by IV immunoglobulins (IVIG). Anticoagulation was held intermittently due to acutely worsening thrombocytopenia with low fibrinogen levels concerning for disseminated intravascular coagulation (DIC), and bleeding around the fasciotomy site, hematuria and vaginal bleeding (workup for heparin induced thrombocytopenia remained negative). Cryoprecipitate and blood transfusions were required. Acute respiratory failure resolved with low tidal volume ventilation, prone positioning and aggressive diuresis. Tissue biopsies for histopathology were deferred. Patient was discharged to inpatient rehab after prolonged hospital stay. DISCUSSION: Approximately 1% of antiphospholipid syndrome patients develop CAPS. Lungs are the second most common organs involved with ARDS being the most common complication. Mortality was 37% in a cohort of 500 patients. Management of CAPS includes aPL testing including lupus anticoagulant, antibeta-2 glycoprotein-1 and anticardiolipin antibodies without delaying empiric treatment. Combination therapy with glucocorticoid, heparin, and plasmapheresis or IVIG rather than single agents is recommended. CONCLUSIONS: Differential diagnosis of CAPS includes DIC which usually presents with small vessel thrombosis but has been reported to cause arterial thrombosis as well, and for which the patient was treated once the platelet counts dropped later. However, with the patient’s history and clinical presentation and given the high mortality rate, we decided to start aggressive empiric therapy after having sent aPL testing. Reference #1: Cervera R.: Antiphospholipid syndrome. Thromb. Res. 2017; 151: pp. S43-S47 Reference #2: Cervera R., Piette J.-C., Font J., Khamashta M.A., Shoenfeld Y., Camps M.T., et al: Antiphospholipid syndrome: clinical and immunologic manifestations and patterns of disease expression in a cohort of 1,000 patients. Arthritis Rheum. 2002; 46: pp. 1019-1027 Reference #3: Bucciarelli S., Espinosa G., Cervera R., Erkan D., Gómez-Puerta J.A., Ramos-Casals M., et al: Mortality in the catastrophic antiphospholipid syndrome: causes of death and prognostic factors in a series of 250 patients. Arthritis Rheum. 2006; 54: pp. 2568-2576 DISCLOSURES: No relevant relationships by Priyanka Bhat, source=Web Response no disclosure on file for Shafaq Ejaz; No relevant relationships by Ahmed Qadir, source=Web Response No relevant relationships by karan Singh, source=Web Response No relevant relationships by Rodney Steff, source=Web Response

Posthypoxic action myoclonus (the Lance-Adams syndrome)

A 62-year-old man was resuscitated after an in-hospital pulseless electrical activity (PEA) cardiac arrest. He awakened after 24 hours but after another 24-hour interval, he had worsening action and stimulus-induced...

Bradycardia at the onset of pulseless electrical activity arrests in hospitalized patients is associated with improved survival to discharge

BackgroundRecent studies have suggested that the incidence of in-hospital pulseless electrical activity (PEA) arrests is increasing. Bradycardia in patients with in-hospital PEA is common but it is unknown if it is associated with respiratory arrest or patient outcomes. ObjectiveTo determine risk factors and outcomes associated with bradycardic-PEA arrests, and relationship between bradycardia and respiratory arrest. MethodsThis was a retrospective cohort study of all inpatient cardiac arrests at an academic medical center over a four-year period. Patient demographics, comorbidities, vital signs, arrest event data, and outcomes were abstracted from the medical record. PEA arrest was defined as a non-shockable rhythm with loss of pulse requiring cardiopulmonary resuscitation and having organized electrocardiographic activity. Bradycardia was classified as a HR < 60 bpm at the time of pulse loss. The primary outcomes were survival of arrest and survival to hospital discharge. ResultsBetween July 2013 and August 2017, there were 176 in-hospital patients with PEA arrests. While 105 (59.7%) survived the arrest, only 38 (21.6%) survived to discharge. A total of 66 (37.5%) were bradycardic-PEA arrests. Patients with bradycardic PEA arrests were no more likely to have their arrest precipitated by respiratory failure than non-bradycardic PEA patients (36.4% vs 27.3%, P = 0.24), but patients with non-bradycardic PEA arrests were more likely to have a CIED than non-bradycardic PEA patients (14.5% vs 3.0%, P = 0.02). On multivariate analysis, bradycardic PEA was associated with improved survival to hospital discharge (OR = 3.31, 95% CI: 1.41–7.79, p = 0.006), but not survival of arrest (OR 1.45, 95% CI: 0.68–3.09, p = 0.34). Respiratory arrest was an independent predictor of survival of code (OR 2.62, 95% CI: 1.36–5.47, P = 0.01) and to hospital discharge (OR 3.47, 95% CI: 1.35–8.91, P = 0.01). Other predictors of survival to discharge include history of coronary artery disease, and non-use of epinephrine, atropine, and sodium bicarbonate. ConclusionIn a retrospective study of hospitalized patients in the intensive care unit and non-intensive care, bradycardia at the time of PEA cardiac arrest was associated with improved survival to hospital discharge but not survival of arrest. Respiratory arrest was an independent predictor of survival, but there was no association between respiratory arrest and bradycardic PEA arrest.

Pulseless Electrical Activity Cardiac Arrest.

This simulation-based scenario is appropriate for senior level emergency medicine residents. Pulseless electrical activity (PEA) accounts for up to 25% of sudden cardiac arrest;1 therefore the ability to recognize and care for this condition is an essential skill of emergency medicine physicians. Management of PEA arrest in the emergency department centers on Advanced Cardiac Life Support (ACLS) algorithms and the identification and treatment of potentially reversible causes. Massive pulmonary embolism (PE) is one of several causes of PEA cardiac arrest.2 However, diagnosis by CT-angiographic or nuclear imaging may not be obtainable in the hemodynamically unstable patient, requiring physicians to have a high index of suspicion. Systemic thrombolytic therapy is indicated in cardiac arrest due to known or presumed massive pulmonary embolism.3,4,5. After competing this simulation-based session, the learner will be able to:Identify PEA arrestReview the ACLS commonly recognized PEA arrest etiologies via the H &T mnemonicReview and discuss the risks and benefits of tissue plasminogen activator (tPA) for massive PE. This is a high-fidelity simulation that allows learners to evaluate and treat a PEA arrest secondary to massive PE in a safe environment. The learners will demonstrate their ability to recognize a PEA arrest, sort through possible etiologies, and demonstrate treatment of a massive PE with tPA. Debriefing will focus on diagnosis and management of the PEA arrest. This case was piloted with 12 PGY-2 and PGY-3 residents. Group and individual debriefing occurred post-case. Post-simulation feedback from the faculty suggested two potential issues. First was fidelity, which we increased by using our ultrasound simulator. Second, the elevated presenting glucose with lactic acidosis could be a poor cue, leading some towards diabetic ketoacidosis (DKA). Learners felt more confident about running a PEA arrest. The simulation improved resident awareness of the value of point of care ultrasound (POCUS) in cardiac arrest. It also clarified the dosing of tPA in massive PE. Faculty felt simulating the actual US without breaking simulation would be more challenging without our US simulator. Although there was concern about results pointing towards possible DKA, this did not occur in any of the pilot simulations. The presenting glucose was reduced to make this less likely in future simulations. Pulseless electrical activity (PEA), syncope, cardiac arrest, Hs and Ts from ACLS PEA instruction, tPA for massive PE, critical care medicine, simulation.

MISSED INTRA-ABDOMINAL HEMATOMA FROM INTERCOSTAL ARTERY LACERATION DURING THORACENTESIS

SESSION TITLE: Tuesday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/22/2019 01:00 PM - 02:00 PM INTRODUCTION: Hemorrhagic complications of thoracentesis are rare but life-threatening. We report a fatal case of intercostal artery (ICA) laceration during percutaneous thoracentesis, presenting as intra-abdominal hematoma diagnosed on bedside sonogram (US). CASE PRESENTATION: A 49-year-old female with end-stage renal disease, coronary artery bypass grafting on dual anti-platelet therapy (DAPT) was admitted for pneumonia. Despite 7 days of inpatient antibiotic treatment she remained hypoxic. Chest radiograph (CXR) showed complete opacification of left hemithorax. Bedside left percutaneous US guided thoracentesis was done which revealed fluid consistent with empyema. Post procedure CXR showed left lung re-expansion with no pneumothorax. Approximately 3 hours after procedure patient had a pulseless electrical activity cardiac arrest. After 3 minutes of resuscitation she was awake, responsive and transferred to the medical ICU. Initial laboratory values including hemoglobin (Hb), troponin and a repeat CXR were unchanged from prior. She remained hypotensive despite aggressive fluid resuscitation and maximal vasopressor support. A chest tube was inserted which drained 50ml of sero-sanguinous fluid. Repeat Hb approximately 6 hours after thoracentesis, revealed drop from 12 to 5gm/dl, requiring massive transfusion. On re-examination, her abdomen appeared distended and firm. Bedside US revealed a 19cm hypoechoic mass in left abdomen concerning for hematoma. Emergent CT angiogram showed contrast extravasation from left 10th ICA which was successfully embolized. Hemodynamics improved. Shortly after she developed abdominal compartment syndrome and DIC and unfortunately passed away. DISCUSSION: : Thoracentesis is a common procedure and considered low risk. Hemorrhage is usually from ICA laceration, and manifests as hemothorax, rarely as abdominal wall hematoma, but intra-abdominal hematoma have not been reported. Patients at risk are those with INR > 1.5-2, platelets <50,000/µl, advanced renal disease; anti-platelets are generally considered safe, though some studies report higher chest tube outputs especially with DAPT. ICA typically runs along the subcostal groove, however studies demonstrate increased exposure and tortuosity with advanced age, previous sternotomy, and caudal intercostal spaces. Some studies have noted utility of thoracic US in identifying ICA. Recent reports suggest the use of vascular US with color Doppler to visualize the ICA and its collaterals. These are yet to be universally adopted in clinical practice. US is helpful in quick bedside evaluation for location of bleed which is critical in unstable patients. CONCLUSIONS: Clinicians should be mindful of anatomical variations of ICA even in US guided thoracentesis. They should also consider abdominal bleeding and appropriately use the bedside US in suspected cases. Reference #1: Helm EJ, Rahman NM, Talakoub O, Fox DL. Course and Variation of the Intercostal Artery by CT Scan. Chest. 2013;143(3):634-639. https://doi.org/10.1378/chest.12-1285 Reference #2: Patel IJ, Davidson JC, Nikolic B, et al. Consensus Guidelines for Periprocedural Management of Coagulation Status and Hemostasis Risk in Percutaneous Image-guided Interventions. JVIR. 23(6):727-736. https://doi.org/10.1016/j.jvir.2012.02.012 Reference #3: Kanai M, Sekiguchi H. Avoiding Vessel Laceration in Thoracentesis A Role of Vascular Ultrasound With Color Doppler. Chest. 2015;147(1):e5-e7. https://doi.org/10.1378/chest.14-0814. DISCLOSURES: No relevant relationships by Jayashri Bhaskar, source=Web Response No relevant relationships by Jyotirmayee Lenka, source=Web Response No relevant relationships by Laurie Lerner, source=Web Response No relevant relationships by Yetunde Ogunsesan, source=Web Response No relevant relationships by Naman Sharma, source=Web Response No relevant relationships by Qiu Tong, source=Web Response

Severe Venlafaxine Intoxication with Refractory Pulseless Electrical Activity Cardiac Arrest Successfully Treated with Intravenous Lipid Emulsion

Severe Venlafaxine Intoxication with Refractory Pulseless Electrical Activity Cardiac Arrest Successfully Treated with Intravenous Lipid Emulsion

Cardiac arrest and pulmonary hypertension in scurvy: a case report.

We report a case of a six-year-old boy who presented after a cardiac arrest, likely due to a pulmonary hypertensive crisis in the setting of vitamin C deficiency. After initially presenting with subacute multifocal bone lesions of unknown etiology, he experienced a pulseless electrical activity cardiac arrest while undergoing a diagnostic procedure under sedation. During his post-arrest convalescence, he developed persistent tachycardia and peripheral edema. An echocardiogram revealed findings consistent with significant pulmonary arterial hypertension, which was found to be responsive to inhaled nitric oxide. Laboratory investigation revealed undetectable levels of vitamin C, resulting in disclosure of a history of severe restrictive eating behavior. With ascorbate supplementation, the patient’s pulmonary vasodilators were weaned and discontinued. Given his complete recovery, we suspect that the cardiac arrest and pulmonary hypertension were the consequence of a rare, but reversible, complication of scurvy.