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Ventricular tachycardia [keywords]
- Obstructive Sleep Apnea Hypopnea Syndrome in Egyptian Patients With Tachyarrhythmia. [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):948A.
Sleep Posters IISESSION TYPE: Original Investigation PosterPRESENTED ON: Wednesday, October 29, 2014 at 01:30 PM - 02:30 PMPURPOSE: The aim of the study was to assess the occurrence of OSAHS in Egyptian patients with tachyarrhythmia, and to describe characteristics of patients with concomitant OSAHS and tachyarrhythmia.METHODS: We enrolled 32 patients with tachyarrhythmia. In addition to standard examination, investigations and echocardiography to exclude possible causes for arrhythmia all patients underwent an over-night sleep study (level III) to diagnose OSAHS. Manual scoring was performed by two specialists according to criteria established by the American Academy of Sleep Medicine 2012. We considered AHI of 15/hour as a cutoff point for diagnosing OSAHSRESULTS: Of the 32 patients: seventeen had rapid atrial fibrillation (AF), eight had premature ventricular contractions, five had persistent sinus tachycardia and three had paroxysmal supraventricular tachycardia. OSAHS was present in 27 patients (84.4%), three patients of them had obesity hypoventilation also. Dividing OSAHS patients according to the disease severity showed that moderate OSAHS in 29.6% patients, and severe OSAHS in 70.4% patients. Studying characteristics of patients with OSAHS revealed that the mean ± SD of neck circumference (NC) was 39.9± 2.47 cm, BMI was 36.3± 9.17 kg/m2, Waist/hip ratio was 0.91±0.08, Epworth Sleepiness Scale (ESS) was 10.85±4.5, Mallampati score (MS) was 2.11± 0.84, clinical apnea score was 2.8± 1.5, and STOP BANG score was 4.03±1.99. Apnea hypopnea index (AHI) was 49.3±33.2, oxygen desaturation index [3%] (ODI) was 39.9±31, mean O2 saturation was 93.6±8.84 and minimal O2 saturation was 7.9±14.49. Nocturnal bradytachyarrhythmia was found in most of patients, the minimal pulse rate during sleep ranges from 22 to 82/minute while the maximal pulse rate ranges from 77 to 254/ minute. Both AHI and ODI were found to be significantly directly correlated with each of BMI, NC, waist/hip ratio, clinical apnea score, STOP BANG score, ESS, MS and mean pulse rate. Linear regression analysis of potential predictors of increased apnea hypopnea index revealed that triglyceride level is the highest predictor followed by NC then BMICONCLUSIONS: OSAHS is highly prevalent in patients with tachyarrhythmia. High triglyceride, NC and BMI are the most predictors of presence of OSAHS. AF is the most common form of the arrhythmia in patients with OSAHS.CLINICAL IMPLICATIONS: OSAHS should be considered as part of the workup of patients with tachyarrhythmia. Both clinical apnea score and STOP BANG are good screening questionnaire to choose patients who need sleep study.DISCLOSURE: The following authors have nothing to disclose: Sahar Mourad, Nashwa AbdelWahab, Akram Fayed, Abeer Kassem, Hebatullah AlsayedNo Product/Research Disclosure Information.
- Management of Cardiac Tamponade in Severe Pulmonary Hypertension. [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):881A.
Pulmonary Vascular Disease Student/Resident Case Report Posters ISESSION TYPE: Medical Student/Resident Case ReportPRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PMINTRODUCTION: The incidence of Pericardial effusion (PCE) in Pulmonary Artery Hypertension (PAH) is 15-65% Compared to PCE from other conditions, presence of PAH significantly alters the echocardiographic and hemodynamic manifestations of cardiac tamponade1,2. Furthermore, drainage of PCE in the presence of severe PAH, is associated with a high mortality due to right ventricular decompensation3.CASE PRESENTATION: A 33-year-old Caucasian female with Class 1 Idiopathic PAH managed on tadalafil, ambrisentan, treposteionil, digoxin and diuretics presented with progressive dyspnea and orthopnea of two-week duration. Cardiac examination revealed hypotension, tachycardia, pulsus paradoxus, jugular venous distension, muffled heart sounds, loud P2 and holo-systolic murmur at left-lower sternal border. TTE demonstrated a large circumferential PCE with diastolic left atrial (LA) collapse and uncollapsed right atrium (RA). Right Ventricle (RV) was dilated with systolic dysfunction and severe tricuspid regurgitation. RV systolic pressure was 170 mmHg and inferior vena cava was dilated without respiratory variation. Urgent pigtail catheter placement and drainage of 200mL provided hemodynamic improvement. Concerns for RV decompensation precluded rapid drainage, with 2.3L drained over 15 days with gradual LA filling improvement. Serological and microbiological studies were unrevealing and patient was referred for pulmonary rehabilitation, pending heart-lung transplantation.DISCUSSION: Postulated etiopathogenic mechanisms of PCE in PAH include venous/lymphatic obstruction due to elevated RA/RV pressures with consequent cytokine release1,3. Large PCE present with atypical TTE signs of tamponade due to high RA pressures and can demonstrate isolated LA/LV collapse. Respiratory variation in trans-mitral and trans-tricuspid flows can be unreliable2. Rapid drainage can result in RV ballooning, hemodynamic instability and death1,3,4. Despite high mortality with drainage, isolated reports suggest that gradual drainage may be safer, resulting in hemodynamic improvement.CONCLUSIONS: This report highlights that gradual drainage of PCE in severe PAH using a pericardial catheter can be hemodynamically well tolerated and should be the preferred method in patients with cardiac tamponade and severe PAH.Reference #1: 1. Shimony A, Fox BD, Langleben D et al. Incidence and significance of pericardial effusion in patients with pulmonary arterial hypertension. Can J Cardiol. 2013 Jun;29(6):678-82.Reference #2: 2. Habib G, Torbicki A. The role of echocardiography in the diagnosis and management of patients with pulmonary hypertension. Eur Respir Rev. 2010 Dec;19(118):288-99Reference #3: 3. Hemnes AR, Gaine SP, Wiener CM. Poor outcomes associated with drainage of pericardial effusions in patients with pulmonary arterial hypertension. South Med J. 2008 May;101(5):490-4. 4. Honeycutt GR, Safdar Z. Pulmonary hypertension complicated by pericardial effusion: a single center experience. Ther Adv Respir Dis. 2013 Jun;7(3):151-9.DISCLOSURE: The following authors have nothing to disclose: Saraschandra Vallabhajosyula, Swapna Kanuri, Pranathi Sundaragiri, Venkata AllaNo Product/Research Disclosure Information.
- Rapidly Rising Pressure to Make a Diagnosis. [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):349A.
Miscellaneous Case Report Posters IIISESSION TYPE: Affiliate Case Report PosterPRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PMINTRODUCTION: Pulmonary hypertension (PH) is the final common pathway for a number of small vessel pulmonary vascular disorders. Defining the underlying mechanism is essential to guide therapies.CASE PRESENTATION: A 43 year old woman with a past medical history of recurrent left breast carcinoma was noted to have an insidious cough, hypoxemia and rapid progression of dyspnea on exertion prompting emergency evaluation. Initial vital signs were significant for tachycardia (HR 117 bpm) and tachypnea (RR 28). Cardiac examination was remarkable for an accentuated pulmonary component to the second heart sound, pulmonary auscultation was normal. Contrast enhanced CT chest showed no acute pulmonary emboli. There were scattered bilateral ground-glass opacities and nodules. Transthoracic echocardiogram demonstrated right ventricular (RV) systolic pressure estimated at 79 mmHg with severe RV enlargement and mild decrease in function. Left ventricular function was preserved. Ventilation perfusion scan showed heterogeneous perfusion throughout both lungs concerning for chronic thromboembolic disease, pulmonary vascular disease, or possible microangiopathy. Right heart catheterization (RHC) was performed with concomitant pulmonary capillary wedge (PCW) fluid cytology. Mean PA pressure 49 mmHg; pulmonary vascular resistance index 18 WU. Concurrent bronchoscopy with trans-bronchial biopsy was obtained. Biopsy results confirmed pulmonary lymphangitic carcinomatosis (PLC) on transbronchial biopsy and wedge blood cytology. Our patient rapidly declined with increased work of breathing over the next several days. Given the results and poor prognosis associated with this she requested comfort measures only and passed away 24 hours after diagnosis.DISCUSSION: The mechanism for PH should be evaluated in all patients to guide prognosis and therapies. PLC is an uncommon cause of PH requiring a tissue diagnosis typically obtained via lung biopsy or post-mortem examination. This case illustrates the utility of PCW cytology to aid in the diagnosis of PLC. PCW cytology was first described in 1985 but remains infrequently used. Diagnostic yield has not been extensively studied. It may be particularly useful in patients deemed too high risk for transbronchial biopsy.CONCLUSIONS: PLC should be considered as a cause of PH in patients with metastatic disease.Reference #1: Pulmonary microvascular cytology. Chest 1985:88(6)908-914.DISCLOSURE: The following authors have nothing to disclose: Rachel Le, Sherry-Ann Brown, Omar Abou-Ezzedine, Darlene NelsonNo Product/Research Disclosure Information.
- A Rare Case of Fatal Thyroid Storm (TS) Resulting in DIC and Multiorgan Failure. [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):302A.
Critical Care Student/Resident Case Report Posters IISESSION TYPE: Medical Student/Resident Case ReportPRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PMINTRODUCTION: We describe a case of atypical TS; normotensive, normothermic, without any signs of CNS or GI symptoms, leading to multi-organ-dysfunction-syndrome (MODS), including disseminated intravascular coagulation (DIC).CASE PRESENTATION: A 64-year-old female with questionable thyroid disorder on kelp, presented with progressively increasing dyspnea. On exam, she was a cachectic woman weighing 46.6 kg with moderate respiratory distress, BP 153/102 mmHg. She had an enlarged, irregular thyroid gland, irregular tachycardia with a systolic murmur, marked jugular venous distention and diminished breath sounds bilaterally at lung bases. Labs included elevated BNPT (1557) and TSH <0.01 mcIU/ml. Chest x-ray showed cardiomegaly with bilateral pleural effusions. She was placed on Venturi mask, heparin by weight, propranolol and hydrocortisone for the new onset Afib and TS. The night of admission, she developed PEA and was successfully resuscitated, placed on mechanical ventilation and noted to be hypotensive and bradycardic requiring norepinephrine and vasopressin infusion. After 24 hours, she had MODS with respiratory failure, anion gap metabolic acidosis, hepatic failure, renal failure, lactic acidosis and melena with drop in Hb, platelets and fibrinogen indicating DIC. Labs revealed elevated free and total T3, T4. Transthoracic echocardiogram showed a left ventricular EF of 25%. Endocrinologist initiated her on propylthiouracil and potassium iodide for TS. Despite aggressive resuscitation, the patient deteriorated and died 36 hours after presentation.DISCUSSION: TS is a rare disorder with sudden onset, rapid progression and high mortality. We witnessed a case of TS with a devastating course leading to MODS, DIC and eventually death, despite early recognition and aggressive resuscitation. Very few cases of TS with DIC have been reported. The diagnostic criteria for TS used worldwide were established by Burch, et al; a score of > 45 suggests TS. Our patient scored 60. More recently, Japan Thyroid Association and Japan Endocrine Society came up with additional criteria. As per these criteria, our patient had elevated FT3, FT4 and had two of the five symptoms. TS is precipitated by an acute critical condition. In our patient, the cause of TS was multifactorial, including acute onset congestive failure, consumption of kelp, medical noncompliance and/ or clinical palpation of her thyroid gland.CONCLUSIONS: TS is a medical emergency. Early diagnosis based on the criteria and intervention is critical for survival.Reference #1: Akamizu T et al. Diagnostic criteria and clinico-epidemiological features of thyroid storm based on a nationwide survey. Thyroid 22 (7): 661-679, 2012.DISCLOSURE: The following authors have nothing to disclose: Amareshwar Podugu, Khulood Rizvi, Chandra Dasari, Asha Chakka, Nihad BoutrosNo Product/Research Disclosure Information.
- Multiorgan Dysfunction Triggered by Acute Thyroid Storm. [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):271A.
Critical Care Cases ISESSION TYPE: Affiliate Case Report SlidePRESENTED ON: Monday, October 27, 2014 at 11:00 AM - 12:00 PMINTRODUCTION: Thyroid storm is a life-threatening complication of thyrotoxicosis characterized by tachycardia, hyperpyrexia, central nervous system dysfunction, and gastrointestinal symptoms. Multi-system organ failure is rare but accounts for the approximately 10% mortality of thyroid storm1.CASE PRESENTATION: A 29 year old male presented to the emergency room complaining of abdominal distention and vitiligo. He was febrile (39.2 C) and in atrial fibrillation with rapid ventricular response (148 bpm). Thyroid stimulating hormone (TSH) was <0.01 uIU/mL (0.45-4.50 uIU/mL) and free T4 was >6.00 ng/dL (0.7-1.5 ng/dL). Thyroid stimulating antibody was 5.5 (<= 1.3) consistent with Grave's disease. Initial management included metoprolol, propylthiouracil (PTU), and hydrocortisone. While in the ED, his mental status acutely declined and he became hemodynamically unstable. During the following 12 hours his transaminases rose from previously normal to AST 5265 U/L (<35 U/L) and ALT 2716 U/L (<55 U/L) with coagulopathy (INR 5.6). He developed acute renal failure (Cr 0.6 to 2.6 with oliguria) requiring continuous renal replacement therapy. Transthoracic echocardiogram revealed biventricular heart failure with right ventricle dilation and left ventricle ejection fraction 30-35%. This was confirmed by right heart catheterization (PCWP 25 mmHg, CI 1.9 L/min/m2).DISCUSSION: Given the contraindication of methimazole and PTU in acute liver failure, an alternative strategy of plasma exchange followed by thyroidectomy was pursued. After plasma exchange on hospital day 1, free T3 declined from >30.0 to 14.3 pg/mL (2.3-4.2 pg/mL) and total T3 declined from 741 to 299 ng/dL (58-159 ng/dL) associated with improvement in vital signs and vasopressor requirement. Despite his critical illness and coagulopathy, he was taken for emergent thyroidectomy on hospital day 2. Post-operatively he had rapid decline in his circulating thyroid hormones associated with improved hemodynamics and liver enzymes. He required levothyroxine supplementation on hospital day 4. Currently the patient is improving with normalization of liver and cardiac function. Likewise, his mental status is improving and he is weaning from mechanical ventilation. He remains on renal replacement therapy as of this submission.CONCLUSIONS: This case highlights a novel and multi-disciplinary approach of pharmacotherapy in conjunction with plasma exchange followed by thyroidectomy to successfully control severe thyrotoxicosis.Reference #1: Thyroid. 2012 Sep;22(9):979.DISCLOSURE: The following authors have nothing to disclose: Elaine Cagnina, Ramya Embar-Srinivasan, Sue Brown, Kyle EnfieldNo Product/Research Disclosure Information.
- Ventricular Bigeminy During Cryopreserved Autologous Hematopoietic Stem Cell Infusion. [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):265A.
Critical Care Case Report Posters IIISESSION TYPE: Affiliate Case Report PosterPRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PMINTRODUCTION: Cryopreserved hematopoietic stem cell transfusions are sometimes associated with transient and benign reactions like nausea, flushing and bradycardia. We present a patient who developed ventricular bigeminy during the infusion of peripheral blood stem cell transplant (PBSCT).CASE PRESENTATION: A 69-year-old man with a history of multiple myeloma, peripheral neuropathy and intermittent palpitations presented for autologous PBSCT after receiving two days of melphalan conditioning. Two months prior, he received 9 cycles of lenalidomide, dexamethasone and bortezomib. For his history of palpitations, he had undergone 24-hour Holter monitoring a day prior to presentation, which showed 2133 (1.76%) supraventricular ectopics, 2 supraventricular tachycardia runs, 773 (0.64%) ventricular ectopics and 9 ventricular bigeminy runs. A recent echocardiogram was only positive for grade 1/4 diastolic dysfunction. A baseline ECG showed sinus rhythm with 1st degree atrioventricular (AV) block. During PBSCT infusion, the patient was noted to be bradycardic on the pulse oximeter, but was asymptomatic. Vital signs were: temperature 36.2 C, pulse 47/min, blood pressure 137/78 mmHg, respirations 16/min, and oxygen saturation 99% on room air. Aside from a regular, bradycardic pulse, physical exam was unrevealing. The ECG showed new ventricular bigeminy (Figure 1) and a critical care consult was called. Serum potassium and magnesium were normal. A dimethyl sulfoxide (DMSO) reaction was suspected and the infusion was paused. About 1 minute later, the bigeminy reverted to sinus rhythm. The infusion was resumed at a slower rate and bigeminy soon recurred. The patient remained asymptomatic and the infusion was completed. An ECG repeated several hours later was similar to baseline (Figure 2). The patient was discharged after an in-patient cardiac evaluation.DISCUSSION: DMSO is used as a cryopreservative for PBSCT. Infusion-related nausea, headaches and vomiting are common and transient reactions reported in association with DMSO-containing PBSCT (1). Cardiac events, such as arrhythmias (2), cardiac arrest (3) or coronary spasm are rare. Our case highlights the arrhythmogenic potential of cryopreserved PBSCT products, most likely resulting from DMSO.CONCLUSIONS: Patients with pre-existing rhythm abnormalities may benefit from cardiac monitoring during cryopreserved PBSCT infusions.Reference #1: Cox MA et al. Cell Tissue Bank. 2012;13:203-15.Reference #2: Zenhausern R et al. Ann Hematol. 2000;79:523-6.Reference #3: Rapoport AP et al. Bone Marrow Transplant. 1991;7:401-3.DISCLOSURE: The following authors have nothing to disclose: Sumedh Hoskote, James OnigkeitDimethyl sulfoxide (DMSO) is commonly used as a cryopreservative for hematopoietic stem cells. However, the US FDA has not approved it for this purpose. Our case describes a potential adverse effect that may be related to DMSO.
- Delayed Recurrent Effect of Pentamidine: Polymorphic Ventricular Tachycardia. [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):262A.
Critical Care Case Report Posters IIISESSION TYPE: Affiliate Case Report PosterPRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PMINTRODUCTION: Pentamidine is used for treating Pneumocystis jiroveci pneumonia (PCP) in patients with intolerance or no response to Trimethoprim-Sulphamethoxazole. QT prolongation and Polymorphic Ventricular Tachycardia (VT) have been observed temporally following IV administration (1). Delayed occurrence of VT after discontinuation of Pentamidine is rare. We present such a rare case.CASE PRESENTATION: 53 years old African-American female with HIV noncompliant to antiretrovirals was admitted to ICU with acute respiratory failure from PCP. Pentamidine IV was started due to intolerance to Trimethoprim-Sulphamethoxazole. Baseline QTc,echocardiogram,electrolytes, renal, hepatic functions were normal. Patient improved and was successfully extubated. On day fifteen of Pentamidine therapy, patient suffered a cardiac arrest from VT and was revived within two minutes after 200 Joule(J )cardioversion. QTc had prolonged to 549 msec(ms). Blood sugar, electrolytes including magnesium, potassium were normal. Pentamidine was immediately discontinued. Acute coronary syndrome was ruled out. Review of medications revealed no other QTc prolonging agents. QTc increased to 810ms two days after discontinuation of Pentamidine. Isoproterenol drip was started as per cardiology, QTc decreased to 530ms. Eight days after discontinuation of Pentamidine, patient again developed VT and revived after 200J cardioversion. QTc was noted to be 616 ms. Electrolytes and renal functions were normal. Patient was constantly monitored during her further stay and QTc normalized. No further ventricular arrhythmias occurred and patient was discharged after full recovery.DISCUSSION: The mechanism with which Pentamidine induces VT is not well known. However its proarrythmogenic properties may be due to similarity of its structure to Procainamide. Prolonged effect on QTc many days after its discontinuation could be due to tissue binding(2).CONCLUSIONS: Serum magnesium, potassium,creatinine, QTc should be monitored closely(2). Our patient developed VT seven days after discontinuation of Pentamidine. Patients treated recently with Pentamidine should be closely monitored for prolonged period to prevent this deadly complication. Required duration of monitoring is arbitrary.Reference #1: Recurrent Ventricular Tachycardia Due to Pentamidine-Induced Cardiotoxicity Mark R. Bibler M.D; Te-Chuan Chou M.D; Robert J Toltzis M.D; Patricia A Wade MD Reference #2: Prolonged recurrence of pentamidine-induced torsades de pointes Cortese LM, Gasser RA Jr, Bjornson DC, Dacey MJ, Oster CNDISCLOSURE: The following authors have nothing to disclose: Vikram Oke, Rakesh Vadde, Saurav Pokharel, Bikash Bhattarai, Prajakta Mungikar, Joseph Quist, Danilo Enriquez, Francis SchmidtNo Product/Research Disclosure Information.
- Acetaminophen Myocardial Toxicity: An Underrecognized Entity. [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):247A.
Critical Care Case Report Posters ISESSION TYPE: Affiliate Case Report PosterPRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PMINTRODUCTION: We present two cases of acetaminophen (APAP) overdose which, in addition to hepatic failure, also caused direct myocardial injury.CASE PRESENTATION: The first patient is a 29 yo woman who presented with an APAP overdose. Initial labs revealed AST > 14,000 units/L, ALT > 8,000units/L, lactate 5.8mmol/L, creatinine 4.57mg/dL, INR 8.3 and acetaminophen 115mg/L. Initial, electrocardiogram revealed ST elevation in the inferior leads and ST depression in V2/V3. Echocardiogram revealed mildly depressed systolic function but no wall motion abnormalities. Serum cardiac biomarkers were elevated with CK 10,000units/L, CK-MB 163ng/mL and troponin > 50ng/mL. Coronary angiography was deferred due to her acute illness. The patient recovered and was discharged. An echocardiogram two weeks later, continued to show some dysfunction. The second patient is a 31 yo woman who presented with APAP overdose and was found to be in fulminant hepatic failure. Initial labs revealed AST/ALT > 5,000units/L, creatinine 1.78mg/dL, INR 10, acetaminophen 160mg/L and bicarbonate < 6mmol/L. The patient developed wide complex tachycardia and subsequent electrocardiogram revealed inferior and anterolateral ST elevation. The echocardiogram revealed abnormal interventricular septal thickness without wall motion abnormality. Serum cardiac biomarkers revealed CK 811units/L, CK-MB 65ng/mL and troponin 32ng/mL. Coronary angiography was deferred due to her acute illness. The patient subsequently developed ventricular fibrillation and died.DISCUSSION: Hepatology in 2004 reported that APAP overdose was the leading cause of calls to Poison Control, accounted for > 56,000 Emergency Department visits, 2,600 hospitalizations/year and approximately 458 deaths secondary to hepatic failure. The mechanism of injury in hepatic failure due to APAP is well known. The first documented case of cardiac toxicity due to APAP was in 1969. It was not until 1991 that further documentation of direct toxicity of acetaminophen to the myocytes was postulated after a failed heart transplant from an APAP overdose donor revealed myocyte necrosis at explant, not related to rejection.CONCLUSIONS: This is an important but not yet completely understood consequence of APAP toxicity and can cause long term cardiac disability in those that survive, thus should not be missed in work-up of these patients. Reference #1: Price L:Fatal Acetaminophen Poisoning with Evidence of Subendocardial Necrosis of the Heart.Journal of Forensic Science.1991;36(3):930-935DISCLOSURE: The following authors have nothing to disclose: Rebecca Potfay, George Mueller, Sammy PedramNo Product/Research Disclosure Information.
- Therapeutic Hypothermia: Implementation and Disposition Outcomes at a Tertiary Care Institution. [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):121A.
CAD/Coronary Syndromes PostersSESSION TYPE: Original Investigation PosterPRESENTED ON: Wednesday, October 29, 2014 at 01:30 PM - 02:30 PMPURPOSE: Cardiac arrest is a common cause of in hospital and out of hospital mortality. It commonly causes severe neurological impairment leading to high mortality rates. Hypothermia has been shown to improve neurological recovery and decrease mortality in out of hospital ventricular fibrillation and ventricular tachycardia patients. The purpose of our study is to review the implementation of hypothermia at a tertiary care facility. Data was collected to determine the benefit of hypothermia protocol, compliance with the inclusion and exclusion criteria, difference in mortality rates for in-hospital versus out-of-hospital arrests, and mortality rates in shockable versus non-shockable rhythms.METHODS: This is a single center systematic review of data collected from 2011-2013 on patients admitted with cardiac arrest and considered as potential candidates for therapeutic hypothermia (TH). Audits were performed on all patients who presented to the emergency department after cardiac arrest and were considered for hypothermia protocol. Audits were also performed on in-hospital cardiac arrests who required mechanical ventilation.RESULTS: Three hundred and fifty three patient charts were reviewed and 67(18.9%) were initiated on TH. Of those, 26 patients had V-tach/V-fib arrest while 39 patients had PEA/asystole. Of the V-tach/V-fib patients, 69% expired, 23% went home, and 7.7% were sent to SNF. Of the PEA/asystole patients 89.7% expired, 7.6% went home and 2.5% went to SNF. Interestingly, 43% of patients cooled met the inclusion criteria while 57% did not. The most common inclusion criteria that cooled patients failed to meet was hypotension defined as systolic blood pressure (SBP) <90mmHg.CONCLUSIONS: Hypothermia protocol improves neurological outcome (defined as discharge to SNF or home). Further education and exposure is needed for the physicians and nursing staff to increase the implementation of the hypothermia protocol. Compliance is difficult to measure as it is unknown how many patients were never considered for TH.CLINICAL IMPLICATIONS: There was no statistical significance seen in outcomes with therapeutic hypothermia between V-tach/V-fib versus PEA/asystole patients. No statistical significance was seen between in hospital and out of hospital cardiac arrest outcome either. Further randomized controlled trials need to be performed to determine efficacy of TH in patients with PEA/asystole. Despite proven efficacy in numerous studies, compliance remains low.The following authors have nothing to disclose: Aasim Afzal, Jamil Alsahhar, Adam MoraNo Product/Research Disclosure Information.
- Group B Streptococcal Endocarditis After Cesarean Section Presenting as Multifocal Pneumonia. [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):109A.
Cardiovascular Student/Resident Case Report Posters ISESSION TYPE: Medical Student/Resident Case ReportPRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PMINTRODUCTION: We report a case and review 34 other instances of Group B streptococcus (GBS) endocarditis since the last review in 2006. Till date this is the only case of tricuspid valve GBS endocarditis reported after a caesarean section procedure.Thirty seven year old female with history of uncomplicated caesarean section 18 days ago comes in with dry cough, fever and dyspnea 4 days prior to presentation. No recent cough, cold, sick contacts and travel. Examination was significant for sinus tachycardia, fever, bilateral lower zone lung crackles and bilateral pitting pedal edema. A complete blood count revealed white cell count of 16.4, erythrocyte sedimentation rate 125 and C-reactive protein was 37. Chest X-ray showed bilateral fluffy infiltrates. Computerized tomography chest showed patchy consolidations and ground glass opacities in bilateral upper, lower and right middle lobes consistent with multifocal pneumonia (image:1). Ultrasound pelvis was negative for any focus of infection in genitourinary tract. Culture of vaginal secretions was negative for GBS. Blood culture was positive for GBS. Echocardiogram showed multiple large mobile masses attached to the tricuspid valve largest measuring 22.5 cm in length, normal right and left ventricular size and function with moderate tricuspid regurgitation. Patient was started on penicillin G and repeat echocardiogram revealed significant reduction in the size of tricuspid valve mass. Subsequent blood cultures were negative. Patient completed 6 weeks course of antibiotics uneventfully.DISCUSSION: Till date 34 cases of pregnancy associated GBS endocarditis have been reported of which 8 cases involved tricuspid valve.1,2,3 None of the cases have occurred after Caesarean section. All other cases like our patient had no apparent tricuspid valve disease.1,2,3 The course for our patient is typical of other 8 cases with major complication being septic pulmonary emboli. The case is unique because of the uncertainty of source of GBS bacteremia due to lack of detectable vaginal colonization, central venous catheters and complications during surgery. This raises further questions on the already existing controversial guidelines for GBS screening and treatment of asymptomatic carriers during pregnancy.CONCLUSIONS: GBS tricuspid endocarditis is the most common cause of pregnancy related endocarditis in absence of risk factors. This case emphasis the importance of blood cultures and echocardiography in post-partum patients with persistent fever.Reference #1: Crespo A, Retter AS, Lorber B. Group B streptococcal endocarditis in obstetric and gynecologic practice. Infect Dis Obstet Gynecol 2003;11:109-15. Reference #2: Shimoni Z, Ben David M, Niven MJ. Postpartum group B streptococcal tricuspid valve endocarditis. Isr Med Assoc J. 2006 Dec; 8(12):883-4. Reference #3: Salih H, Guellab D, Zoubidi M, Bennis A. Postpartum group B streptococcal endocarditis of the tricuspid valve. Ann Cardiol Angeiol (Paris). 2012 Apr;61(2):121-4.The following authors have nothing to disclose: Amit Kachalia, Kinjal Kachalia, Erik Perez, Sethu MuralidharanNo Product/Research Disclosure Information.