Epinephrine and short-term survival in cardiogenic shock: an individual data meta-analysis of 2583 patients

Léopold, Valentine; Gayat, Étienne; Pirracchio, Romain; Špinar, Jindřich; Pařenica, Jiří; Tarvasmäki, Tuukka; Lassus, Johan; Harjola, Veli Pekka; Champion, Sébastien; Zannad, Faı̈ez; Valente, Serafina; Urban, Philip; Chua, Horng Ruey; Bellomo, Rinaldo; Popovic, Batric; Ouweneel, Dagmar M.; Henriques, José P.S.; Simonis, Gregor; Lévy, Bruno; Kimmoun, Antoine; Gaudard, Philippe; Basir, Mir B.; Markota, Andrej; Adler, Christoph; Reuter, Hannes; Mebazaa, Alexandre; Chouihed, Tahar

doi:10.1007/s00134-018-5222-9

Cited by 129 publications

(87 citation statements)

References 37 publications

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“…Furthermore, a recent meta-analysis with more than 2500 patients found that epinephrine use for hemodynamic management of CS patients was associated with a threefold increase in risk of death (Léopold et al, 2018a(Léopold et al, , 2018b. However, the proportion of post CA patients was only 45%.…”

Section: Discussionmentioning

confidence: 99%

Malignant Arrhythmias During Induction of Target Temperature Management After Cardiac Arrest

Adler

Schregel

Heller

et al. 2020

Therapeutic Hypothermia and Temperature Management

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The aim of this study was to evaluate the incidence and determinants of malignant arrhythmias (MA) in patients with shock following out-of-hospital cardiac arrest (OHCA) treated with targeted temperature management. Risk factors for the development of MA were prospectively analyzed in patients after OHCA. MA were defined as ventricular tachycardia or fibrillation with a duration >30 seconds, which had to be terminated by defibrillation. All patients were treated with therapeutic hypothermia for 24 hours. Demographics, OHCA details, interventions, and intensive care unit (ICU) treatment were recorded. A total of 55 patients were included, 11 (20%) of whom developed MA during the ICU stay. All MA occurred within the first 18 hours after admission. Patients who developed MA showed a stronger decrease in body temperature (D-2.4°C-0.8°C vs. D-1.3°C-1.3°C; p = 0.016) and in serum potassium levels (D-0.9-1 mmol/L vs. D-0.3-0.6 mmol/L; p = 0.037) during the cooling period compared with patients without MA. In the multivariable analysis, fast temperature decline as well as lower potassium levels were associated with MA. In addition, higher number of shocks during resuscitation and higher ICU epinephrine use were independent predictors of MA in patients with OHCA. The use of epinephrine as well as hypokalemia in context with intense cooling may increase the incidence of MA in patients with shock after cardiac arrest. Therefore, these therapeutic strategies should be applied with caution in this vulnerable group of patients.

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Section: Discussionmentioning

confidence: 99%

Malignant Arrhythmias During Induction of Target Temperature Management After Cardiac Arrest

Adler

Schregel

Heller

et al. 2020

Therapeutic Hypothermia and Temperature Management

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“…3 The combination of adrenaline with dobutamine, however, portends a particular risk for adverse outcome. 53 In a recent meta-analysis, adrenaline was associated with a three-fold increase in mortality, 54 and in patients with cardiogenic shock after acute myocardial infarction, refractory shock was five-fold more frequent with adrenaline than with NA. 55 For a similar effect on blood pressure, adrenaline (but not NA) increased heart rate (due to its strong b 2 -AR activation; Table 1) and myocardial oxygen consumption (derived from the cardiac double product), increasing lactate as a sign of metabolic compromise.…”

Section: Catecholaminesmentioning

confidence: 99%

Treatments targeting inotropy

Maack

Eschenhagen

Hamdani

et al. 2018

European Heart Journal

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Acute heart failure (HF) and in particular, cardiogenic shock are associated with high morbidity and mortality. A therapeutic dilemma is that the use of positive inotropic agents, such as catecholamines or phosphodiesterase-inhibitors, is associated with increased mortality. Newer drugs, such as levosimendan or omecamtiv mecarbil, target sarcomeres to improve systolic function putatively without elevating intracellular Ca2+. Although meta-analyses of smaller trials suggested that levosimendan is associated with a better outcome than dobutamine, larger comparative trials failed to confirm this observation. For omecamtiv mecarbil, Phase II clinical trials suggest a favourable haemodynamic profile in patients with acute and chronic HF, and a Phase III morbidity/mortality trial in patients with chronic HF has recently begun. Here, we review the pathophysiological basis of systolic dysfunction in patients with HF and the mechanisms through which different inotropic agents improve cardiac function. Since adenosine triphosphate and reactive oxygen species production in mitochondria are intimately linked to the processes of excitation–contraction coupling, we also discuss the impact of inotropic agents on mitochondrial bioenergetics and redox regulation. Therefore, this position paper should help identify novel targets for treatments that could not only safely improve systolic and diastolic function acutely, but potentially also myocardial structure and function over a longer-term.

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“…However, there is a lack of robust outcome data. Evidence for the use of epinephrine in RV failure is equally sparse, however, its use in cardiogenic shock has come under scrutiny as it was recently shown in a large meta-analysis to be associated with increased short-term mortality [70]. One meta-analysis found significant hemodynamic improvements with levosimendan [71], perhaps suggesting an indication in selected patients, but here too there is a paucity of longer-term outcome data.…”

Section: Support Of Inotropy In Rv Failurementioning

confidence: 99%

The Right Ventricle—You May Forget It, But It Will Not Forget You

Wanner

Filipovic

2020

JCM

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Right ventricular (RV) dysfunction and failure are common and often overlooked causes of perioperative deterioration and adverse outcomes. Due to its unique pathophysiologic underpinnings, RV failure often does not respond to typical therapeutic measures such as volume resuscitation and often worsens when therapy is escalated and mechanical ventilation is begun, with a danger of irreversible cardiovascular collapse and death. The single most important factor in improving outcomes in the context of RV failure is anticipating and recognizing it. Once established, a vicious circle of systemic hypotension, and RV ischemia and dilation is set in motion, rapidly spiraling down into a state of shock culminating in multi-organ failure and ultimately death. Therapy of RV failure must focus on rapidly reestablishing RV coronary perfusion, lowering pulmonary vascular resistance and optimizing volemia. In parallel, underlying reversible causes should be sought and if possible treated. In all stages of diagnostics and therapy, echocardiography plays a central role. In severe cases of RV dysfunction there remains a role for the use of the pulmonary artery catheter. When these mostly simple measures are undertaken in a timely fashion, the spiral of death of RV failure can often be broken or even prevented altogether.

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Epinephrine and short-term survival in cardiogenic shock: an individual data meta-analysis of 2583 patients

Abstract: In this very large cohort, epinephrine use for hemodynamic management of CS patients is associated with a threefold increase of risk of death.

Cited by 129 publications

References 37 publications

Malignant Arrhythmias During Induction of Target Temperature Management After Cardiac Arrest

Malignant Arrhythmias During Induction of Target Temperature Management After Cardiac Arrest

Treatments targeting inotropy

The Right Ventricle—You May Forget It, But It Will Not Forget You

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