Adverse cardiac events during catecholamine vasopressor therapy: a prospective observational study

Purpose: To determine the incidence of and risk factors for adverse cardiac events during catecholamine vasopressor therapy in surgical intensive care unit patients with cardiovascular failure. Methods: The occurrence of any of seven predefined adverse cardiac events (prolonged elevated heart rate, tachyarrhythmia, myocardial cell damage, acute cardiac arrest or death, pulmonary hypertension-induced right heart dysfunction, reduction of systemic blood flow) was prospectively recorded during catecholamine vasopressor therapy lasting at least 12h. Results: Fifty-four of 112 study patients developed a total of 114 adverse cardiac events, an incidence of 48.2% (95% CI, 38.8-57.6%). New-onset tachyarrhythmia (49.1%), prolonged elevated heart rate (23.7%), and myocardial cell damage (17.5%) occurred most frequently. Aside from chronic liver diseases, factors independently associated with the occurrence of adverse cardiac events included need for renal replacement therapy, disease severity (assessed by the Simplified Acute Physiology Score II), number of catecholamine vasopressors (OR, 1.73; 95% CI, 1.08-2.77; p=0.02) and duration of catecholamine vasopressor therapy (OR, 1.01; 95% CI, 1-1.01; p=0.002). Patients developing adverse cardiac events were on catecholamine vasopressors (p<0.001) and mechanical ventilation (p<0.001) for longer and had longer intensive care unit stays (p<0.001) and greater mortality (25.9 vs. 1.7%; p<0.001) than patients who did not. Conclusions: Adverse cardiac events occurred in 48.2% of surgical intensive care unit patients with cardiovascular failure and were related to morbidity and mortality. The extent and duration of catecholamine vasopressor therapy were independently associated with and may contribute to the pathogenesis of adverse cardiac event

Concomitant arginine-vasopressin and hydrocortisone therapy in severe septic shock: association with mortality

Purpose: To evaluate the association between concomitant arginine-vasopressin (AVP)/hydrocortisone therapy and mortality in severe septic shock patients. Methods: This retrospective study included severe septic shock patients treated with supplementary AVP. To test the association between concomitant AVP/hydrocortisone use and mortality, a multivariate regression and Cox model (adjusted for admission year, initial AVP dosage and the Sepsis-related Organ Failure Assessment score before AVP) as well as a propensity score-based analysis were used. In both models, intensive care unit (ICU) and 28-day mortality served as outcome variables. Results: One hundred fifty-nine patients were included. Hydrocortisone was administered to 76 (47.8%) at a median daily dosage of 300 (200-300)mg. In the multivariate logistic regression model, concomitant use of AVP and hydrocortisone was associated with a trend towards lower ICU (OR, 0.51; CI 95%, 0.24-1.08; p=0.08) and 28-day (HR, 0.69; CI 95%, 0.43-1.08; p=0.11) mortality. The probability of survival at day 28, as predicted by the regression model, was significantly higher in patients treated with concomitant AVP and hydrocortisone compared to those receiving AVP without hydrocortisone (p=0.001). In a propensity score-based analysis, ICU (45 vs. 65%; OR, 0.69; CI 95% 0.38-1.26; p=0.23) and 28-day mortality (35.5 vs. 55%; OR, 0.59; CI 95%, 0.27-1.29; p=0.18) was not different between patients treated with (n=40) or without concomitant hydrocortisone (n=40). Conclusion: Concomitant AVP and hydrocortisone therapy may be associated with a survival benefit in septic shock. An adequately powered, randomised controlled trial appears warranted to confirm these preliminary, hypothesis-generating result

Space matters: incorporating mechanistically determined spatial patterns into projected impacts of climate change on stream temperature

River temperatures are increasing as a results of climate change, and combined with decreased summertime flows, coldwater species are becoming increasingly stressed. In order to conserve sensitive species, managers need an estimate of how the availability of summertime thermal refuges in rivers will change in the future. Here, we applied the DHSVM-RBM, an existing process-based water temperature model that has been shown to accurately represent temporal variance in water temperature over hours to years. We calibrated this model to empirical data for two case study watersheds (Siletz River, Oregon and Snoqualmie River, Washington) to also ensure representation of observed spatial heterogeneity during summer. We used the model to predict future spatiotemporal patterns in water temperature that may arise as a result of climate change and to assess Pacific salmon vulnerability. We then compared our predictions to those made by statistical models to assess the unique benefits and constraints of a process-based approach. We found that a substantial decrease of snowmelt, and subsequently summer flow, will drive increases in water temperature and spatial variability in future summers. Our vulnerability analysis suggested that for salmon and steelhead exposed to warm August temperatures, conditions are already stressful in lower portions of the case study watersheds, and unlikely to become better in the future. All models predicted generally similar spatial patterns of water temperature in the future; across models, future cool patches will be reduced in number and located farther upstream. However, projected increases in water temperature were strikingly different among models, ranging from about +5 oC in the Snoqualmie River as predicted by DHSVM-RBM, to a negligible change in both watersheds as predicted by statistical methods. This information can be used to identify locations where protection and restoration of coolwater habitats may be most important into the future

Influenza A(H1N1) infection and severe cardiac dysfunction in adults: A case series

Zusammenfassung: HINTERGRUND: Während die virale Myokarditis und das Herzversagen anerkannte und gefürchtete Komplikationen einer saisonalen Influenza A Infektion sind, liegen bislang nur wenig Informationen über ein durch das 2009 Influenza A(H1N1) Virus induziertes Herzversagen vor. METHODEN UND HAUPTERGEBNISSE: Diese Fallsammlung fasst den Krankheitsverlauf von vier Patienten mit 2009 Influenza A(H1N1) Infektion zusammen, welche an unserer Klinik im Zeitraum von November 2009 bis September 2010 behandelt wurden. Alle Patienten präsentierten sich mit einer schweren kardialen Funktionsstörung (akutes Herzversagen, kardiogener Schock oder Herzkreislaufstillstand im Rahmen eines Kammerflimmerns) als das führende Symptom einer Influenza A(H1N1) Infektion. Zwei Patienten waren mit hoher Wahrscheinlichkeit kardial vorerkrankt, und drei benötigten eine Katecholamintherapie, um die hämodynamische Funktion zu stabilisieren. Mit Ausnahme eines Patienten der vor der Diagnosestellung der Influenza A(H1N1) Infektion verstarb, wurden alle Patienten mit einer antiviralen Therapie mit Oseltamivir und supportiver Intensivtherapie behandelt. Ein Acute Respiratory Distress Syndrom infolge der Influenza A(H1N1) Infektion trat bei einem Patienten auf. Die Herzfunktion normalisierte sich bei zwei Patienten und war bei einem Patienten noch bei Krankenhausentlassung eingeschränkt. SCHLUSSFOLGERUNG: Eine Influenza A(H1N1) Infektion kann mit einer schweren kardialen Funktionseinschränkung assoziiert sein. Diese kann sich sogar als führendes klinisches Symptom darstellen. Während einer Influenza Pandemie kann eine genaue Anamneseerhebung Grippeähnliche Symptome hervorbringen und sollte auch bei kritisch kranken Patienten mit akutem Herzversagen eine Diagnostik auf H1N1 Infektion veranlasse

Hemodynamic variables and mortality in cardiogenic shock: a retrospective cohort study

INTRODUCTION: Despite the key role of hemodynamic goals, there are few data addressing the question as to which hemodynamic variables are associated with outcome or should be targeted in cardiogenic shock patients. The aim of this study was to investigate the association between hemodynamic variables and cardiogenic shock mortality. METHODS: Medical records and the patient data management system of a multidisciplinary intensive care unit (ICU) were reviewed for patients admitted because of cardiogenic shock. In all patients, the hourly variable time integral of hemodynamic variables during the first 24 hours after ICU admission was calculated. If hemodynamic variables were associated with 28-day mortality, the hourly variable time integral of drops below clinically relevant threshold levels was computed. Regression models and receiver operator characteristic analyses were calculated. All statistical models were adjusted for age, admission year, mean catecholamine doses and the Simplified Acute Physiology Score II (excluding hemodynamic counts) in order to account for the influence of age, changes in therapies during the observation period, the severity of cardiovascular failure and the severity of the underlying disease on 28-day mortality. RESULTS: One-hundred and nineteen patients were included. Cardiac index (CI) (P = 0.01) and cardiac power index (CPI) (P = 0.03) were the only hemodynamic variables separately associated with mortality. The hourly time integral of CI drops 0.05). The hourly time integral of CPI drops 0.05). CONCLUSIONS: During the first 24 hours after intensive care unit admission, CI and CPI are the most important hemodynamic variables separately associated with 28-day mortality in patients with cardiogenic shock. A CI of 3 L/min/m2 and a CPI of 0.8 W/m2 were most predictive of 28-day mortality. Since our results must be considered hypothesis-generating, randomized controlled trials are required to evaluate whether targeting these levels as early resuscitation endpoints can improve mortality in cardiogenic shock

Association of arterial blood pressure and vasopressor load with septic shock mortality: a post hoc analysis of a multicenter trial

INTRODUCTION: It is unclear to which level mean arterial blood pressure (MAP) should be increased during septic shock in order to improve outcome. In this study we investigated the association between MAP values of 70 mmHg or higher, vasopressor load, 28-day mortality and disease-related events in septic shock. METHODS: This is a post hoc analysis of data of the control group of a multicenter trial and includes 290 septic shock patients in whom a mean MAP > or = 70 mmHg could be maintained during shock. Demographic and clinical data, MAP, vasopressor requirements during the shock period, disease-related events and 28-day mortality were documented. Logistic regression models adjusted for the geographic region of the study center, age, presence of chronic arterial hypertension, simplified acute physiology score (SAPS) II and the mean vasopressor load during the shock period was calculated to investigate the association between MAP or MAP quartiles > or = 70 mmHg and mortality or the frequency and occurrence of disease-related events. RESULTS: There was no association between MAP or MAP quartiles and mortality or the occurrence of disease-related events. These associations were not influenced by age or pre-existent arterial hypertension (all P > 0.05). The mean vasopressor load was associated with mortality (relative risk (RR), 1.83; confidence interval (CI) 95%, 1.4-2.38; P 70 mmHg by augmenting vasopressor dosages may increase mortality. Future trials are needed to identify the lowest acceptable MAP level to ensure tissue perfusion and avoid unnecessary high catecholamine infusions

The association between body-mass index and patient outcome in septic shock: a retrospective cohort study

Zusammenfassung: HINTERGRUND: Es bestehen keine Daten über die Assoziation zwischen dem Body Mass Index (BMI) bzw. BMI Kategorien und der Mortalität von septischen Schock-patienten. METHODEN: Die Datenbank einer interdisziplinären Intensivstation wurde retrospektiv nach erwachsenen Patienten mit septischem Schock durchsucht. Von allen Patienten wurde der BMI, demographische, klinische und laborchemische Parameter gemeinsam mit Outcomevariabeln dokumentiert. Die Studienpatienten wurden wie folgt anhand des BMI kategorisiert: BMI 30 kg/m2, Fettleibigkeit. Bivariate und multivariate logistische Regressionsmodelle wurden verwendet, um den Zusammenhang zwischen dem BMI und Outcome-variabeln zu untersuchen. RESULTATE: 301 septische Schockpatienten wurden identifiziert. Der BMI war bivariat mit der Mortalität auf der Intensivstation assoziiert (OR, 0,91; 95% CI, 0,86-0,98; p = 0,007). Es gab keine signifikante Assoziation zwischen dem BMI und der Mortalität auf der Intensivstation. Allerdings waren höhere BMI Werte trendmässig mit einer niedrigeren Intensivstations-mortalität assoziiert (OR, 0,93; 95% CI, 0,86-1,01; p = 0,09). Während übergewichtige (OR, 0,43; 95% CI, 0,19-0,98; p = 0,04) und fettleibige (OR, 0,28; 95% CI, 0,08-0,93; p = 0,04) Patienten ein unabhängig niedrigeres Risiko auf der Intensivstation zu versterben hatten als normalgewichtige Patienten, gab es keinen Unterschied im Sterberisiko zwischen normal- und untergewichtigen Patienten (p = 0,22). Ein hoher BMI war unabhängig mit einer geringen Häufigkeit eines akutem Deliriums (p = 0,04) und einer geringeren Intensivwieder-aufnahmerate (p = 0,001), aber mit mehr Harnwegsinfektionen (p = 0,02) assoziiert. SCHLUSSFOLGERUNG: Bis zu einem BMI von 50 kg/m2 scheint keine Assoziation zwischen BMI und schlechterem Überleben auf der Intensivstation oder im Krankenhaus bei septischen Schockpatienten zu bestehen. Im Gegenteil, hohe BMI Werte könnten sogar das Risiko am septischen Schock zu versterben reduziere

Comparing two different arginine vasopressin doses in advanced vasodilatory shock: a randomized, controlled, open-label trial

Purpose: To compare the effects of two arginine vasopressin (AVP) dose regimens on the hemodynamic response, catecholamine requirements, AVP plasma concentrations, organ function and adverse events in advanced vasodilatory shock. Methods: In this prospective, controlled, open-label trial, patients with vasodilatory shock due to sepsis, systemic inflammatory response syndrome or after cardiac surgery requiring norepinephrine >0.6μg/kg/min were randomized to receive a supplementary AVP infusion either at 0.033IU/min (n=25) or 0.067IU/min (n=25). The hemodynamic response, catecholamine doses, laboratory and organ function variables as well as adverse events (decrease in cardiac index or platelet count, increase in liver enzymes or bilirubin) were recorded before, 1, 12, 24 and 48h after randomization. A linear mixed effects model was used for statistical analysis in order to account for drop-outs during the observation period. Results: Heart rate and norepinephrine requirements decreased while MAP increased in both groups. Patients receiving AVP at 0.067IU/min required less norepinephrine (P=0.006) than those infused with AVP at 0.033IU/min. Arterial lactate and base deficit decreased while arterial pH increased in both groups. During the observation period, AVP plasma levels increased in both groups (both P<0.001), but were higher in the 0.067IU/min group (P<0.001) and in patients on concomitant hydrocortisone. The rate of adverse events and intensive care unit mortality was comparable between groups (0.033IU/min, 52%; 0.067IU/min, 52%; P=1). Conclusions: A supplementary AVP infusion of 0.067IU/min restores cardiovascular function in patients with advanced vasodilatory shock more effectively than AVP at 0.033IU/mi