69 research outputs found

    SCAI SHOCK: Does the Stage Help with Management Decisions?

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    Myocardial Dysfunction and Shock after Cardiac Arrest

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    Postarrest myocardial dysfunction includes the development of low cardiac output or ventricular systolic or diastolic dysfunction after cardiac arrest. Impaired left ventricular systolic function is reported in nearly two-thirds of patients resuscitated after cardiac arrest. Hypotension and shock requiring vasopressor support are similarly common after cardiac arrest. Whereas shock requiring vasopressor support is consistently associated with an adverse outcome after cardiac arrest, the association between myocardial dysfunction and outcomes is less clear. Myocardial dysfunction and shock after cardiac arrest develop as the result of preexisting cardiac pathology with multiple superimposed insults from resuscitation. The pathophysiology involves cardiovascular ischemia/reperfusion injury and cardiovascular toxicity from excessive levels of inflammatory cytokine activation and catecholamines, among other contributing factors. Similar mechanisms occur in myocardial dysfunction after cardiopulmonary bypass, in sepsis, and in stress-induced cardiomyopathy. Hemodynamic stabilization after resuscitation from cardiac arrest involves restoration of preload, vasopressors to support arterial pressure, and inotropic support if needed to reverse the effects of myocardial dysfunction and improve systemic perfusion. Further research is needed to define the role of postarrest myocardial dysfunction on cardiac arrest outcomes and identify therapeutic strategies

    Echocardiographic parameters of patients in the intensive care unit undergoing continuous renal replacement therapy.

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    Main objectivesEchocardiographic parameters have been used to predict outcomes for specific intensive care unit (ICU) populations. We sought to define echocardiographic parameters for ICU patients receiving continuous renal replacement therapy (CRRT).Design, setting, participants, and measurementsThis is a historical cohort study of consecutive ICU patients at Mayo Clinic (Rochester, Minnesota) who received CRRT from December 9, 2006, through November 13, 2015. Only patients with an echocardiographic examination within 7 days of CRRT initiation were considered.ResultsThe study included 1,276 patients. Decreased left ventricular ejection fraction (LVEF; ≤45%) was noted in 361/1,120 (32%) and increased right ventricular systolic pressure (RVSP; ≥40 mm Hg) was noted in 529/798 (66%). Right ventricular systolic dysfunction was observed in 320/820 (39%). The most common valvular abnormality was tricuspid regurgitation (244/1,276 [19%]). Stratification of these parameters by ICU type (medical, surgical, cardiothoracic, cardiac) showed that most echocardiographic abnormalities were significantly more prevalent among cardiac ICU patients: LVEF ≤45% (67/105 [64%]), RVSP ≥40 mm Hg (63/79 [80%]) and tricuspid regurgitation (50/130 [38%]). We compared patients with acute kidney injury (AKI) vs end-stage renal disease and showed that decreased LVEF (284/921 [31%] vs 78/201 [39%]), was significantly less prevalent among patients with AKI, but increased RVSP was more prevalent (445/651 [68%] vs 84/147 [57%]) with AKI.ConclusionsICU patients who required CRRT had increased prevalence of pulmonary hypertension and right and left ventricular systolic dysfunction. Prediction of adverse outcomes with echocardiographic parameters in this patient population can lead to identification of modifiable risk factors

    Sedation and Shivering Management After Cardiac Arrest

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    Management of sedation and shivering during targeted temperature management (TTM) after cardiac arrest is limited by a dearth of high-quality evidence to guide clinicians. Data from general intensive care unit (ICU) populations can likely be extrapolated to post cardiac arrest patients, but clinicians should be mindful of key differences that exist between these populations. Most importantly, the goals of sedation after cardiac arrest are distinct from other ICU patients, and may also involve suppression of shivering during TTM. Drug metabolism and clearance is altered considerably during TTM when a low goal temperature is used, which can delay accurate neuroprognostication. When neuromuscular blockade is used to prevent shivering, sedation should be deep enough to prevent awareness and providers should be aware that this can mask clinical manifestations of seizures. However, excessively deep or prolonged sedation is associated with complications including delirium, infections, increased duration of ventilatory support, prolonged ICU length of stay, and delays in neuroprognostication. In this manuscript, we review sedation and shivering management best practices in the post cardiac arrest patient population

    The Role of Genetic Testing in the Evaluation of Dilated Cardiomyopathies

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    We present an adolescent African American male admitted to the cardiac intensive care unit with cardiogenic shock and acute respiratory failure. Through an overview of his presentation, diagnostic workup, and treatment, we demonstrate the clinical utility of genetic testing in the evaluation of unexplained dilated cardiomyopathies

    Timing of Initiation of Extracorporeal Membrane Oxygenation Support and Outcomes Among Patients With Cardiogenic Shock

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    Background Venoarterial extracorporeal membrane oxygenation (ECMO) provides full hemodynamic support for patients with cardiogenic shock, but optimal timing of ECMO initiation remains uncertain. We sought to determine whether earlier initiation of ECMO is associated with improved survival in cardiogenic shock. Methods and Results We analyzed adult patients with cardiogenic shock who received venoarterial ECMO from the international Extracorporeal Life Support Organization (ELSO) registry from 2009 to 2019, excluding those cannulated following an operation. Multivariable logistic regression evaluated the association between time from admission to ECMO initiation and in‐hospital death. Among 8619 patients (median, 56.7 [range, 44.8–65.6] years; 33.5% women), the median duration from admission to ECMO initiation was 14 (5–32) hours. Patients who had ECMO initiated within 24 hours (n=5882 [68.2%]) differed from those who had ECMO initiated after 24 hours, with younger age, more preceding cardiac arrest, and worse acidosis. After multivariable adjustment, patients with ECMO initiated >24 hours after admission had higher risk of in‐hospital death (adjusted odds ratio, 1.20 [95% CI, 1.06–1.36]; P=0.004). Each 12‐hour increase in the time from admission to ECMO initiation was incrementally associated with higher adjusted in‐hospital mortality rate (adjusted odds ratio, 1.06 [95% CI, 1.03–1.10]; P<0.001). The association between longer time to ECMO and worse outcomes appeared stronger in patients with lower shock severity. Conclusions Longer delays from admission to ECMO initiation were associated with higher a mortality rate in a large‐scale, international registry. Our analysis supports optimization of door‐to‐support time and the avoidance of inappropriately delayed ECMO initiation
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