Increase In Cardiac Output Research Articles

Correlación clínica y ecocardiográfica en la disfunción miocárdica en el shock séptico en la Unidad de Cuidados Intensivos Pediátricos Hospital Uyapar, Venezuela

Septic shock is a situation of acute circulatory failure with tissue hypoperfusion and cellular hypoxia that affects anaerobic metabolism. During septic shock, tachycardia, and reduction of afterload increase cardiac output. Sepsis continues to be the main cause of death in the hospital environment, and is more frequent in patients of extreme ages. Materials and methodsThe study was carried out prospectively in a period of 1 year with a sample of 13 patients. The data as regards admission and haemodynamic parameters were recorded. Two-dimensional echocardiography was used to measure left ventricular ejection fraction (LVEF) at the time of admission without use of dobutamine, and subsequently 1, 3, 5, and 7days after the use of dobutamine. The results are presented in frequency distribution tables, the arithmetic mean calculated and the Pearson correlation test was applied. ResultsThe patients included 61.5% infants and the sex most affected was male. A respiratory system infection was observed in 38.5%. Cardiovascular dysfunction was present in 61.5% in the first 72hours after admission, with an initial mean LVEF of 41%. There was a recovery at 72hours after the use of dobutamine (P=.89). The heart rate was the clinical variable that showed the greatest statistical significance (P=.96). ConclusionsEchocardiography is a useful tool for non-invasive monitoring and has a high prognostic value. Objectively, heart rate monitoring offers a direct relationship with the improvement of left ventricular function.

Abstract 257: Unselective Pulmonary Vasodilation is an Important Factor in Sodium Nitroprusside Enhanced Cardiopulmonary Resuscitation Improved Blood Flow

Introduction: Sodium nitroprusside enhanced CPR (SNPeCPR) is a novel CPR method that includes a potent vasodilator, active compression-decompression CPR, an inspiratory impedance threshold device and abdominal binding. SNPeCPR has been shown to improve vital organ flow and functional survival outcomes compared to standard CPR methods in animals. We hypothesize that one of the main effects of SNPeCPR mediated increase in cardiac output during prolonged resuscitation is profound pulmonary artery vasodilation. Methods: After electrically induced VF was left untreated for 3 min, 20 (44-48Kg) pigs were randomized to receive SNPeCPR (10) or standard CPR (10) for a total of 30 min; the first 10 minutes were BLS CPR followed by twenty minutes of ACLS. During ACLS, animals were given IV SNP (1mg bolus) or standard epinephrine (0.5mg) q5 min until ROSC or 45 min total CPR. Shocks were delivered after 30 minutes of CPR at 300J. If ROSC was achieved, animal was monitored until 4-hour endpoint. Ventilations were provided with 10ml/kg at 10/min with a mechanical ventilator. Initially during CPR, room air was used and FiO2 was adjusted q5 minutes to maintain O 2 %saturation &gt 92% based on ABG. Lactic acid was also measured. Aortic, right atrial, and coronary artery pressures and carotid blood flow were recorded continuously. A-a oxygen gradient was measured with standard technique. Results: SNPeCPR animals documented a significantly higher mean CPP, lower lactic acid and 3x higher carotid blood flow over 30 minutes compared to standard CPR as previously documented. A-a oxygen gradient was dramatically increased in the SNPeCPR and coincided with a decreased lactate level (see Figure 1). Discussion: SNPeCPR causes profound pulmonary vasodilation and increases flow through non-ventilated lung areas. Despite that, the overall increase in forward flow leads to higher minute O 2 delivery and improved tissue perfusion. SNPeCPR should be used with 100% oxygen in the first human clinical trial.

Is the New Infant Jarvik 2015 Suitable for Patients

Our aim was to study the feasibility of implanting the Infant Jarvik 2015 in patients weighing less than 8kg. The Infant Jarvik 2015 left ventricular assist device (LVAD) was tested in a hybrid simulator of the cardiovascular system reproducing specific patients' hemodynamics for different patient weights (2-7kg). For each weight, the sensitivity of the pump to different circulatory parameters (peripheral resistance, left ventricular elastance, right ventricular elastance, heart rate, and heart filling characteristics) has been tested repeating for each experiment a pump ramp (10000-18000rpm). The increase in the pump speed causes a decrease (increase) in the left (right) atrial pressure, an increase (decrease) in the arterial systemic (pulmonary) pressure, an increase in the right ventricular pressure, a decrease (increase) in the left (right) ventricular volume, a decrease in the left ventricular cardiac output, an increase in the LVAD output and an increase in the right ventricular cardiac output (total cardiac output). Suction was observed for lower weight patients and for higher pump speed in the case of vasodilation, left ventricular recovery, bradycardia, right ventricular failure, and left ventricular hypertrophy. Backflow was observed in the case of left ventricular recovery at lower pump speed. In the hybrid simulator, the Infant Jarvik 2015 could be suitable for the implantation in patients lower than 8kg because of the stability of the device respect to the cardio/circulatory changes (low frequency of suction and backflow) and because of the capability of the device to maintain adequate patient hemodynamics.

In Vitro Examination of the VentriFlo True Pulse Pump for Failing Fontan Support.

The current methodology of Fontan palliation results in a one "pump" circulatory system with passive flow to the lungs. Inherent hemodynamic differences exist between a biventricular circulatory system and this modified physiology, leading to a host of long-term complications. Mechanical circulatory support (MCS) is a potential option to combat these pathophysiological conditions. In this study, we examine the VentriFlo True Pulse Pump as a MCS option to support a failing Fontan patient. An in vitro circulatory loop was used to model a failing Fontan patient, reproducing pathophysiological pressures and flow rates. The VentriFlo True Pulse Pump was positioned as a right sided support, testing multiple cannulation and baffle restriction strategies, as well as various pumping parameters including flow rate, frequency, stroke volume and the ejection to filling time ratio. A 10 mmHg decrease in IVC pressure and 0.75L/min increase in cardiac output were achieved using a complete baffle restriction strategy. Additional cannulation and banding strategies were not as successful. Pump flow rate and frequency significantly impacted hemodynamics, while the ejection to filling time ratio did not. Though not ideal, complete baffle restriction was necessary to achieve successful support. The ability to tune individual pumping parameters for a given MCS device will have a substantial impact on the pressures and flow augmentation seen in a Fontan circulation. Both future pump design and off-label VADs for Fontan use should consider the pump configuration and parameter combinations presented here, which offered successful support.

Changing views on the common physiologic abnormality that mediates salt sensitivity and initiation of salt-induced hypertension: Japanese research underpinning the vasodysfunction theory of salt sensitivity.

High-salt intake is one of the major dietary determinants of increased blood pressure and cardiovascular disease. Thus, there is scientific and medical interest in understanding the mechanistic abnormalities mediating the pressor effects of salt (salt sensitivity). According to historical theory, salt sensitivity stems from an impairment in renal function (referred to as "abnormal pressure natriuresis" or a "natriuretic handicap"), which causes salt-sensitive subjects to excrete a sodium load more slowly, and retain more of it than salt-resistant normotensive controls. However, this historical view has come under intense scrutiny because of growing awareness that in salt-sensitive subjects, acute salt loading does not usually induce greater increases in sodium balance and cardiac output than those induced by salt loading in salt-resistant normotensive controls. Here we highlight pioneering studies from Japan that challenge the historical thinking and provide insights into a contemporary theory of salt sensitivity termed the "vasodysfunction theory." According to this theory, initiation of salt-induced hypertension usually involves abnormal vascular resistance responses to increased salt intake, not greater renal retention of a salt load in salt-sensitive subjects than in normal subjects. By shifting the focus from the historical theory to a contemporary final common pathway for the pathogenesis of salt sensitivity, research from Japan is building the scientific foundation for more effective approaches to the prevention and treatment of salt-induced hypertension. Among the most promising approaches are dietary strategies for reducing the risk for salt-induced hypertension that do not depend on reducing salt consumption in the population.

The Sudden Infant Death Syndrome mechanism of death may be a non-septic hyper-dynamic shock

BackgroundSudden Infant Death Syndrome (SIDS) mechanisms of death remains obscured. SIDS' Triple Risk Model assumed coexistence of individual subtle vulnerability, critical developmental period and stressors. Prone sleeping is a major risk factor but provide no clues regarding the mechanism of death. The leading assumed mechanisms of death are either an acute respiratory crisis or arrhythmias but neither one is supported with evidence, hence both are eventually speculations. Postmortem findings do exist but are inconclusive to identify the mechanism of death. What does the proposed hypothesis based on?1. The stressors (suggested by the triple risk model) share a unified compensatory physiological response of decrease in systemic vascular resistant (SVR) to facilitate a compensatory increase in cardiac output (CO). 2. The cardiovascular/cardiorespiratory control of the vulnerable infant during a critical developmental period may be impaired. 3. A severe decrease in SVR is associated with hyper-dynamic state, high output failure and distributive shock. The hypothesisInfant who is exposed to one or more stressors responds normally by decrease in SVR which increases CO. In normal circumstances once the needs are met both SVR and CO are stabilized on a new steady state. The incompetent cardiovascular control of the vulnerable infant fails to stabilize SVR which decreases in an uncontrolled manner. Accordingly CO increases above the needs to hyper-dynamic state, high output heart failure and hyper-dynamic shock. ConclusionsThe proposed hypothesis provides an appropriate alternative to either respiratory crises or arrhythmia though both speculations cannot be entirely excluded.

Preservation of myocardial contractility during acute hypoxia with OMX-CV, a novel oxygen delivery biotherapeutic.

The heart exhibits the highest basal oxygen (O2) consumption per tissue mass of any organ in the body and is uniquely dependent on aerobic metabolism to sustain contractile function. During acute hypoxic states, the body responds with a compensatory increase in cardiac output that further increases myocardial O2 demand, predisposing the heart to ischemic stress and myocardial dysfunction. Here, we test the utility of a novel engineered protein derived from the heme-based nitric oxide (NO)/oxygen (H-NOX) family of bacterial proteins as an O2 delivery biotherapeutic (Omniox-cardiovascular [OMX-CV]) for the hypoxic myocardium. Because of their unique binding characteristics, H-NOX–based variants effectively deliver O2 to hypoxic tissues, but not those at physiologic O2 tension. Additionally, H-NOX–based variants exhibit tunable binding that is specific for O2 with subphysiologic reactivity towards NO, circumventing a significant toxicity exhibited by hemoglobin (Hb)-based O2 carriers (HBOCs). Juvenile lambs were sedated, mechanically ventilated, and instrumented to measure cardiovascular parameters. Biventricular admittance catheters were inserted to perform pressure-volume (PV) analyses. Systemic hypoxia was induced by ventilation with 10% O2. Following 15 minutes of hypoxia, the lambs were treated with OMX-CV (200 mg/kg IV) or vehicle. Acute hypoxia induced significant increases in heart rate (HR), pulmonary blood flow (PBF), and pulmonary vascular resistance (PVR) (p < 0.05). At 1 hour, vehicle-treated lambs exhibited severe hypoxia and a significant decrease in biventricular contractile function. However, in OMX-CV–treated animals, myocardial oxygenation was improved without negatively impacting systemic or PVR, and both right ventricle (RV) and left ventricle (LV) contractile function were maintained at pre-hypoxic baseline levels. These data suggest that OMX-CV is a promising and safe O2 delivery biotherapeutic for the preservation of myocardial contractility in the setting of acute hypoxia.

Monitorización de la variación de la presión de pulso durante la cirugía de resección pulmonar

Background and objectiveAlthough pulse pressure variation (PPV) is an effective dynamic parameter widely used to predict the increase in cardiac output after the administration of fluids in abdominal surgery, its use in thoracic surgery is controversial. A study was designed to describe the behaviour of PPV during lung resection surgery. Patients and methodsA prospective observational study was conducted on adult patients scheduled for lung resection surgery. Patients with bleeding greater than 200cc, or those who required vasopressors during data collection, were excluded. The PPV values were collected during different phases: in bipulmonary ventilation (T1), after the start of single lung ventilation, and the opening of the thorax (T2), at the end of the procedure prior to the restoration of the bipulmonary ventilation (T3), and after the closure of the thorax in bipulmonary ventilation (T4). The correlation coefficient of the PPV values at the different times was calculated. ResultsThe study included 50 consecutive patients. The mean values and standard deviations of PPV in the different phases were: T1, 11.14% (6.67); T2 6.24% (3.21, T3 5.68% (3.19), and T4 7.84% (4.61). The repeated ANOVA measurements found significant differences between the mean values of PPV in the different phases (P<.001).The correlation between the PPV values during T1 and T2 (PPVT1 and PPVT2) was r=0.868 ([P<.001], r2=0.753), while between T3 and T4 (PPVT3 and PPVT4) the correlation was r=0.616 ([P<.001], r2=0.379) between the PPV values in T3 and T4. ConclusionsPPV presents a predictable behaviour in the course of lung resection surgery, characterised by a decrease of almost half at the beginning of the unipulmonary ventilation and opening of the thorax. It then remains stable throughout the surgery when there are no changes in the intravascular blood volume.

PO-286 The research about the evaluation index on cardiac reserve of female athletes

PO-286 The research about the evaluation index on cardiac reserve of female athletes

Características eletrocardiográficas de éguas da raça Crioula em diferentes fases do período gestacional

Pregnancy can cause several physiologic changes in mares, including modifications in cardiac output and heart positioning. Therefore, these changes could influence electrocardiographic parameters in various stages of pregnancy. This study aimed to evaluate the electrocardiogram of Crioulo mares in different pregnancy stages. Nine non pregnant mares (G0), 11 mares at three months (G3), 11 mares at six months (G6) and 11 mares at 10 months of pregnancy (G10) were submitted to electrocardiographic evaluation. There was higher (P= 0,002) heart rate of G10 (60.45±12.16bpm) when compared to other groups (G0=45.67±10.75bpm; G3=44.91±7.91bpm; G6=46.91±9.12bpm), probably because of an increase in cardiac output to uterine perfusion at the end of pregnancy. Normal sinus rhythm was predominant in most of mares of groups G0, G3 and G6, and sinus tachycardia in most of G10 mares. In conclusion, changes in hemodynamics and in cardiac position can influence on the electrocardiogram of pregnant Crioulo mares, but do not cause relevant rhythm or conduction disturbs.

PULMONARY HYPERTENSION AND ISOLATED RIGHT HEART FAILURE: AN UNUSUAL PRESENTATION OF THYROID STORM

SESSION TITLE: Pulmonary Manifestations of Systemic Disease 1 SESSION TYPE: Med Student/Res Case Report PRESENTED ON: 10/09/2018 03:45 PM - 04:45 PM INTRODUCTION: Graves' disease and other hyperthyroid states are known to have significant effects on the cardiovascular system. These may include increase in heart rate, increase in cardiac output, and decrease in systemic vascular resistance[1]. When heart failure is present, left ventricular dysfunction is frequently reported[2,3]. Thyrotoxicosis rarely presents with pulmonary hypertension and isolated right heart failure. CASE PRESENTATION: A 42-year-old African-American female with no past medical history was sent into the hospital by her outpatient physician for tachycardia. History revealed unintentional 70-pound weight loss over one year. Vital signs were notable for tachycardia identified as atrial fibrillation with rapid ventricular response(>150bpm) on ECG[Figure 1]. Physical exam revealed exophthalmos, symmetrically enlarged and non-tender thyroid, JVD 11 cm, irregularly-irregular tachycardia, decreased breath sounds right lung base, bilateral 2+ pitting edema of lower extremities, and hyperreflexia. Laboratory values indicated suppressed TSH(<0.004 uIU/mL) with elevated T3 Total, T4, and TSH-receptor antibody(494ng/dL, 23.14ug/dL, 111.10IU/L respectively). Diagnosis of Graves' disease was made. Burch-Wartofsky Point Scale of 55 suggesting thyroid storm. Treatment initiated with propranolol, methimazole, glucocorticoids. Chest x-ray showed right pleural effusion, cardiomegaly, and mediastinal widening[Figure 2]. Ultrasound thyroid showed enlarged, heterogeneous, hypervascular gland. Radioactive iodine scan showed diffuse uptake. Echocardiogram showed severe pulmonary hypertension(PASP 88mmHg), right ventricular systolic dysfunction, severe tricuspid regurgitation, left ventricular ejection fraction of 60%. Workup for causes of pulmonary hypertension negative for HIV, connective tissue disease, drugs, toxins, underlying pulmonary disease, and thromboembolic disease. Patient discharged after radioiodine ablation of thyroid gland. Follow up echocardiogram approximately six months after treatment showed significant improvement of both pulmonary hypertension (PASP 35 mmHg) and right heart systolic function. DISCUSSION: This case demonstrates that thyrotoxicosis can induce pulmonary hypertension and right-sided heart failure independent of left-heart disease. Proposed mechanisms of pulmonary hypertension in thyrotoxicosis include autoimmune endothelial dysfunction, endothelial damage from high cardiac output, changes in metabolism of vasodilators or vasoconstrictors, and sympathetic pulmonary vasoconstriction. CONCLUSIONS: It is important to consider thyrotoxicosis in patients with pulmonary hypertension and right heart failure since normalizing thyroid hormones can reverse even severe cardiopulmonary disease. Reference #1: Klein, I., & Ojamaa, K. (2001). Thyroid hormone and the cardiovascular system. The New England Journal of Medicine, 344(7), 501-509. https://doi.org/10.1056/NEJM200102153440707 Reference #2: Klein, I., & Danzi, S. (2007). Thyroid Disease and the Heart. Circulation, 116(15), 1725-1735. https://doi.org/10.1161/CIRCULATIONAHA.106.678326 Reference #3: Siu, C.-W., Yeung, C.-Y., Lau, C.-P., Kung, A. W. C., & Tse, H.-F. (2007). Incidence, clinical characteristics and outcome of congestive heart failure as the initial presentation in patients with primary hyperthyroidism. Heart (British Cardiac Society), 93(4), 483-487. https://doi.org/10.1136/hrt.2006.100628 DISCLOSURES: No relevant relationships by Mina Bushra, source=Admin input No relevant relationships by Kevin Rabii, source=Web Response No relevant relationships by Sally Ziatabar, source=Web Response

Early Paracentesis-Induced Thrombocytopenia (EPIT): A Retrospective Study With Novel Insights Regarding Splenic Hemodynamics

Introduction: Thrombocytopenia is commonly observed in patients with advanced liver disease. The occurrence of a temporary reduction in platelet count after paracentesis has not been described in the literature. An acute drop in platelet count after paracentesis often leads to unnecessary tests to search for causes such as heparin-induced thrombocytopenia (HIT). The primary purpose of this study is to document this phenomenon occurring in the early post-paracentesis period and test the hypothesis that this is related to a temporary reduction in intra-abdominal pressure and increase in splenic arterial flow leading to splenic congestion and increased splenic sequestration of platelets. Methods: A retrospective review of patients who underwent inpatient paracentesis was performed. The primary outcome was an acute reduction in platelet count post-paracentesis. The secondary outcome was a concomitant drop in WBC and RBC counts. Using multiple regressions, we examined variables including etiology of the liver disease, amount of ascitic fluid removed, presence of infection, splenomegaly, use of antibiotics, intravenous fluids (IVF), steroid use, and venous thromboembolism prophylaxis that may independently predict changes in platelet, WBC and RBC counts after paracentesis. Results: Out of 220 patients who underwent inpatient paracentesis, 190 (86.4%) patients had a reduction in platelet count (p < .001). Reductions in Platelet, WBC and RBC after paracentesis were 14.5% (p < .001), 14.2% (p < .001) and 5.9%, respectively (p < .001). Among multiple predictors of a drop in platelet count in the early post-paracentesis period, only the amount of fluid removed was a significant predictor (p < .001). Conclusion: We coined this phenomenon of acute drop in platelet count after paracentesis - Early paracentesis induced thrombocytopenia (EPIT) - that represents an absolutely new mechanism of thrombocytopenia in patients with advanced liver disease. This phenomenon is related temporary mechanical alteration in splenic hemodynamics due to reduction in intra-abdominal pressure (IAP) post-paracentesis and increase in cardiac output with subsequent increase in splenic congestion and platelet sequestration. Physicians and other practitioners caring for patients with chronic liver disease need to be aware of this condition and pathophysiological phenomenon to reduce unnecessary testing, patient aggravation, and reduce healthcare costs.915_A Figure 1. Platelet counts pre- and post-paracentesis.915_B Figure 2. Patient Characteristics:915_C Figure 3. Variable affecting change in Platelet count.

PARADOXICAL WORSENING HYPOXEMIA WITH MECHANICAL VENTILATION IN A PATIENT WITH BILATERAL PNEUMONIA

SESSION TITLE: Medical Student/Resident Pulmonary Physiology SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/09/2018 01:15 PM - 02:15 PM INTRODUCTION: Chronic obstructive pulmonary disease (COPD) is associated with chronic hypoxemia due to right-to-left shunting. We present a patient with a history of COPD and adenocarcinoma with bilateral pneumonia who developed severe hypoxemia on mechanical ventilation. CASE PRESENTATION: A 64-year-old male with a history of COPD and Stage IIIA adenocarcinoma presented in respiratory distress. Chest x-ray (CXR) revealed bilateral opacities. Arterial blood gas (ABG) on a non-rebreather mask with a fraction of inspired oxygen (FiO2) 100% was pH of 7.42, pCO2 40.9, and PaO2 of 79.3. He was started on broad spectrum antibiotics. CT chest angiogram was negative for a pulmonary embolism, but showed a 2.8 cm spiculated mass in the right upper lobe, and extensive bilateral ground glass opacities. Echocardiography confirmed right-to-left intrapulmonary shunting with normal right ventricular function. With worsening hypoxemia, despite noninvasive-positive-pressure support, the patient was intubated with etomidate and rocuronium and placed on volume-control ventilation (VCV) with positive-end-expiratory pressure (PEEP) 5 cmH2O; respiratory rate 16, and FiO2 100%. His SpO2 dropped to 60% and was switched to pressure-control ventilation. He subsequently became hypotensive and bradycardic with a PEA arrest. A code blue was initiated with ROSC after several minutes. Repeat ABG showed: pH 7.154, pCO2 52, PaO2 63.7; and SaO2 76.4. Patient was changed back to VCV with PEEP 10 cmH2O; respiratory rate 24, and FiO2 100% that improved SpO2 to 80-82% temporarily. Despite trials of escalating PEEP and mode changes, the SpO2 declined to 50-60%. After an aborted recruitment maneuver, a second episode of PEA arrest occurred with ROSC, but he continued to have low SpO2 values, which was confirmed with ABG. Repeat CXR showed worsening bilateral infiltrates. A bedside ultrasound showed forceful cardiac contractions, which reduced the likelihood of cardiogenic pulmonary edema. Blood pressure continued to fall despite increasing doses of vasopressors. Family decided no further intervention and the patient expired. DISCUSSION: Pneumonia causes increased pulmonary vascular resistance; PEEP can improve oxygenation by recruiting alveoli, but at the expense of elevated intrathoracic pressures (ITP). In focal pathologies, PEEP paradoxically worsens ventilation-perfusion ratios and gas exchange.1 No set recommendations for ventilator management with worsening hypoxemia in right-to-left intrapulmonary shunting have been established.2 Airway pressure release ventilation decreases shunt fraction has been shown to improve V/Q matching, increase cardiac output, and decrease right atrial pressure by facilitating low airway pressure. Our patient’s rapid clinical decline prevented such attempts. CONCLUSIONS: When hypoxemia worsens paradoxically to increasing oxygenation maneuvers, clinicians should consider the possibility of right-to-left shunt. Reference #1: Annals of American Thoracic Society 11:2014 Reference #2: Respiratory Care 57:2012 DISCLOSURES: No relevant relationships by Sravya Brahmandam, source=Web Response no disclosure on file for Timothy Janz

The Effect of Preoperative Anemia on Patients Undergoing Cardiac Surgery: A Propensity-Matched Analysis

It is unknown if anemia in the absence of transfusions is an independent risk factor for adverse outcomes in cardiac surgery, and if correction to higher hemoglobin targets impacts these outcomes. This is a retrospective review of 3848 cardiac surgery patients. Propensity matching was completed using 41 covariates. Intraoperative Anemia Analysis matched patients with or without anemia who did not receive intraoperative transfusions (n = 392/group), while Intraoperative Transfusion Analysis matched anemic patients treated conventionally with intraoperative transfusions to end cardiopulmonary bypass hemoglobin greater or less than 95 g/L (n = 261/group). Outcomes of death, renal failure, and 2 composite outcomes were assessed using paired analysis techniques. Study composite 1 consisted of prolonged ventilation, renal failure, myocardial infarction, stroke, or deep sternal wound infection, while composite 2 was the TRICS-III composite. In the Intraoperative Anemia Analysis, anemia was associated with mortality (P = 0.034), stroke (P = 0.021), renal failure (P = 0.015), and a significant increase in the composite measure (control 8.7% vs anemia 16.1%, P = 0.002). These findings were unchanged in patients who did not receive any postoperative transfusions. The Intraoperative Transfusion Analysis showed no difference in mortality or the composite outcome between groups. There was a significant increase in low cardiac output in the lower threshold group (P = 0.001). There were no differences in outcomes between those who did and did not receive postoperative transfusions (P > 0.05). Preoperative anemia in the absence of transfusions is a risk factor for morbidity and mortality after cardiac surgery, and there is no evidence that transfusion to higher end cardiopulmonary bypass hemoglobin levels impacted this risk.

Warm water immersion in patients with chronic heart failure: a pilot study

BackgroundPatients with chronic conditions, such as heart failure, swim regularly and most rehabilitation exercises are conducted in warm hydrotherapy pools. However, little is known about the acute effects of warm water immersion (WWI) on cardiac haemodynamics in patients with chronic heart failure (CHF).MethodsSeventeen patients with CHF (NYHA I and II; mean age 67 years, 88% male, mean left ventricular ejection fraction 33%) and 10 age-matched normal subjects were immersed up to the neck in a hydrotherapy pool (33–35 °C). Cardiac haemodynamics were measured non-invasively, and echocardiography was performed at baseline, during WWI, 3 min after kicking in the supine position and after emerging.ResultsIn patients with CHF, compared to baseline, WWI immediately increased stroke volume (SV, mean ± standard deviation; from 65 ± 21 to 82 ± 22 mL, p < 0.001), cardiac output (CO, from 4.4 ± 1.4 to 5.7 ± 1.6 L/min, p < 0.001) and cardiac index (CI, from 2.3 ± 0.6 to 2.9 ± 0.70 L/min/m², p < 0.001) with decreased systemic vascular resistance (from 1881 ± 582 to 1258 ± 332 dynes/s/cm5, p < 0.001) and systolic blood pressure (132 ± 21 to 115 ± 23 mmHg, p < 0.001). The haemodynamic changes persisted for 15 min of WWI. In normal subjects, compared to baseline, WWI increased SV (from 68 ± 11 to 80 ± 18 mL, p < 0.001), CO (from 5.1 ± 1.9 to 5.7 ± 1.8 L/min, p < 0.001) and CI (from 2.7 ± 0.9 to 2.9 ± 1.0 L/min/m², p < 0.001).In patients with CHF, compared to baseline, WWI caused an increase in left atrial volume (from 57 ± 44 to 72 ± 46 mL, p = 0.04), without any changes in left ventricular size or function or amino terminal pro B-type natriuretic peptide.ConclusionsIn patients with CHF, WWI causes an acute increase in cardiac output and a fall in systemic vascular resistance.Clinical trial registrationClinicalTrials.gov (Identifier: NCT02949544) https://clinicaltrials.gov/ct2/show/NCT02949544?cond=NCT02949544&rank=1.

FA05.03: EFFECT OF EPHEDRINE ON GASTRIC CONDUIT PERFUSION MEASURED BY LASER SPECKLE CONTRAST IMAGING (LSCO) AFTER ESOPHAGECTOMY: A PROSPECTIVE IN-VIVO COHORT STUDY

Abstract Background Compromised perfusion due to ligation of arteries and veins in esophagectomy with gastric tube reconstruction often (5–20%) results in necrosis and anastomotic leakage, which relate to high morbidity and mortality (3–4%). Ephedrine is used widely in anesthesia to treat intra-operative hypotension and may improve perfusion by the increase of cardiac output (CO) and mean arterial pressure (MAP). This study tests the effect of ephedrine on perfusion of the future anastomotic site of the gastric conduit, measured by Laser Speckle Contrast Imaging (LSCI). Methods This prospective, observational, in-vivo pilot study includes 26 patients undergoing esophagectomy with gastric tube reconstruction from October 2015 to June 2016 in the Academic Medical Center (Amsterdam). Perfusion of the gastric conduit was measured with LSCI directly after reconstruction and after an increase of MAP by ephedrine 5 mg. Perfusion was quantified in flux (LSPU) in four perfusion locations, from good perfusion (base of the gastric tube) towards decreased perfusion (fundus). Intra-patient differences before and after ephedrine in terms flux were statistically tested for significance with a paired t-test. Results LSCI was feasible to image gastric microcirculation in all patients. Flux (LSPU) was significantly higher in the base of the gastric tube (791 ± 442) compared to the fundus (328 ± 187) (P &lt; 0.001). After administration of ephedrine, flux increased significantly in the fundus (P &lt; 0·05) measured intra-patients. Three patients developed anastomotic leakage. In these patients, the difference between measured flux in the fundus compared to the base of the gastric tube was high. Conclusion This study presents the effect of ephedrine on perfusion of the gastric tissue measured with LSCI in terms of flux (LSPU) after esophagectomy with gastric tube reconstruction. We show a small but significant difference between flux measured before and after administration of ephedrine in the future anastomotic tissue (313 ± 178 vs. 397 ± 290). We also show a significant decrease of flux towards the fundus. Disclosure All authors have declared no conflicts of interest.

Effect of anticipation and cuff inflation on blood pressure during self-measurement.

Self-measurement of blood pressure (BP) is increasingly being used for the diagnosis of hypertension and to monitor BP at home. Whenever compared with ambulatory BP measurements, home BP values are frequently higher and less predictive for incident cardiovascular events. We hypothesized that this could be caused by a pressor response elicited by the self-measurement of BP. A total of 50 patients (mean age 62.0 ± 11.2 years, 44% women) were included, 25 with and 25 without at least 10/5 mmHg higher home BP compared with daytime ambulatory BP. All patients performed 10 consecutive oscillometric BP measurements after 10 min of rest, followed by another resting period of 10 min, while continuously monitoring BP and central hemodynamics using finger photoplethysmography. Baseline BP before the start of the self-measurements was compared with the average BP during the first 10 s of inflation of the cuff. In both groups, we observed a significant increase in SBP and DBP during cuff inflation. The mean rise in average BP was 6.9 ± 6.3/4.5 ± 4.3 mmHg in the group with and 4.4 ± 9.4/2.7 ± 5.3 mmHg in the group without a BP difference between home and daytime ambulatory BP compared with baseline, whereas the maximum increase in average BP was 17.4/8.4 mmHg and 17.7/7.5 mmHg (P < 0 01). The increase in BP coincided with an increase in heart rate and cardiac output. BP differences attenuated after multiple readings, but did not disappear. Our results support the existence of a pressor response during self-BP measurement that remains present after multiple BP readings.

Intravenous Levosimendan and Vasopressin in New-Onset Acute Pulmonary Hypertension After Weaning from Cardiopulmonary Bypass

A novel treatment with intravenous levosimendan and vasopressin for new-onset acute pulmonary hypertension after weaning from cardiopulmonary bypass is described. Retrospective analysis of a case series. Single-center study. Nineteen patients undergoing cardiac surgery exhibited new-onset acute pulmonary hypertension with acute right ventricular dysfunction after cardiopulmonary bypass. Pulmonary hypertension with acute right heart dysfunction was treated with levosimendan as inodilator therapy and vasopressin combined with norepinephrine for systemic vasopressor therapy. Mean pulmonary artery pressure decreased from 32 ± 9 to 26 ± 6 mmHg (p = 0.039) in the first 24 hours along with an increase in cardiac output (3.2 ± 1 to 4.2 ± 1.1 L/min; p = 0.012) and resolution of lactic acidosis. The ratio between mean pulmonary artery pressure and mean arterial pressure decreased from 1:2 to 1:3, and Wood units decreased from 3 ± 1 to 1.5 ± 2 (p = 0.042). At 30 days after intervention, 3 patients died. The combination of levosimendan for inotropic support of the right ventricle in conjunction with its vasodilatory effect on the pulmonary circulation, along with the combination of vasopressin and norepinephrine for systemic vasopressor therapy, may be an effective alternative for the treatment of acute new-onset pulmonary hypertension and acute right heart dysfunction after cardiopulmonary bypass. Although there are many confounding variables in this case series, these findings justify additional sufficiently powered trials.

Abstract 303: Fast Skeletal Myosin Binding Protein-c Expression in Heart Failure

Background: Heart failure is a devastating disease affecting nearly 5 million Americans. We recently identified the upregulation of fast skeletal myosin binding protein-C (fsMyBP-C) in models of heart failure. fsMyBP-C is a homologue of cardiac MyBP-C, which is normally expressed in the heart. This family of proteins regulate contractility by modulating thick and thin filament interactions. However, the functional role(s) of fsMyBP-C expression in the heart is unknown. Methods: To understand the role of fsMyBP-C expression in the heart, we generated cardiac specific transgenic mice expressing fsMyBP-C under the control of the alpha myosin heavy chain promoter. Mice underwent serial echocardiography to monitor cardiac function. Western blotting and qRT-PCR were performed to determine transgene expression levels. Additionally, fsMyBP-C localization in cardiomyocytes was established by immunofluorescence. Furthermore, to understand the temporal expression profiles of the MyBP-C homologues, we performed qRT-PCR on 9 muscle groups at different developmental stages in healthy mice. Results: qRT-PCR demonstrated an upregulation of the slow MyBP-C transcript in the developing heart, while fsMyBP-C transcript levels increased steadily following birth in WT mice. At 3 months of age, transgenic mice displayed a significant increase in ventricular dimensions compared to NTG littermates by echocardiography (LVID d : 3.72 ± 0.07 vs. 4.17 ± 0.09 mm, p&lt;0.01; LVID s : 2.44 ± 0.09 vs. 2.81 ± 0.09, p&lt;0.05), with no changes in wall thickness. This was accompanied by a 25% increase in stroke volume (p&lt;0.01) and a 30% increase in cardiac output (p&lt;0.05). fsMyBP-C correctly localized to the C-zone of the sarcomere. Furthermore, protein levels showed mild expression of fsMyBP-C, in line with the small upregulation seen in diseased hearts, while qRT-PCR confirmed overexpression of fsMyBP-C in the ventricles. Conclusion: Mice expressing fsMyBP-C in the heart display a mild hypertrophic phenotype at 3 months, with preserved function, possibly indicating compensated hypertrophy. Ongoing studies investigate cardiac function at later stages and cardiac specific conditional knockout of fsMyBP-C to determine the long-term effect of fsMyBP-C regulation in the heart.

Altered arterial baroreflex-muscle metaboreflex interaction in heart failure.

Two powerful reflexes controlling cardiovascular function during exercise are the muscle metaboreflex and arterial baroreflex. In heart failure (HF), the strength and mechanisms of these reflexes are altered. Muscle metaboreflex activation (MMA) in normal subjects increases mean arterial pressure (MAP) primarily via increases in cardiac output (CO), whereas in HF the mechanism shifts to peripheral vasoconstriction. Baroreceptor unloading increases MAP via peripheral vasoconstriction, and this pressor response is blunted in HF. Baroreceptor unloading during MMA in normal animals elicits an enormous pressor response via combined increases in CO and peripheral vasoconstriction. The mode of interaction between these reflexes is intimately dependent on the parameter (e.g., MAP and CO) being investigated. The interaction between the two reflexes when activated simultaneously during dynamic exercise in HF is unknown. We activated the muscle metaboreflex in chronically instrumented dogs during mild exercise (via graded reductions in hindlimb blood flow) followed by baroreceptor unloading [via bilateral carotid occlusion (BCO)] before and after induction of HF. We hypothesized that BCO during MMA in HF would cause a smaller increase in MAP and a larger vasoconstriction of ischemic hindlimb vasculature, which would attenuate the restoration of blood flow to ischemic muscle observed in normal dogs. We observed that BCO during MMA in HF increases MAP by substantial vasoconstriction of all vascular beds, including ischemic active muscle, and that all cardiovascular responses, except ventricular function, exhibit occlusive interaction. We conclude that vasoconstriction of ischemic active skeletal muscle in response to baroreceptor unloading during MMA attenuates restoration of hindlimb blood flow. NEW & NOTEWORTHY We found that baroreceptor unloading during the muscle metaboreflex in heart failure results in occlusive interaction (except for ventricular function) with significant vasoconstriction of all vascular beds. In addition, restoration of blood flow to ischemic active muscle, via preferentially larger vasoconstriction of nonischemic beds, is significantly attenuated in heart failure.