Individually Optimized Hemodynamic Therapy Reduces Complications and Length of Stay in the Intensive Care Unit

Goepfert, Matthias S.; Richter, Hans Peter; Eulenburg, Christine zu; Gruetzmacher, Janna; Rafflenbeul, E.; Röher, Katharina; Sandersleben, Alexandra von; Diedrichs, Stefan; Reichenspurner, Hermann; Goetz, Alwin E.; Reuter, Daniel A.

doi:10.1097/01.sa.0000450916.06503.48

Cited by 17 publications

(14 citation statements)

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“…Our data show that both hemodynamic monitoring and therapy are clinically important in order to increase CI, since it has been shown that they reduce the length of the stay on intensive care units [12]. The effects of hemodynamic treatments are similar to other studies [13]; in other studies lower dosages of catecholamines were applied [14,15]; targeted MAP levels were accomplished to 92% of monitoring time.…”

Section: Discussionsupporting

confidence: 81%

Is mean arterial pressure the best parameter in ischemic stroke?

Fuhrer

Weiller

Niesen

2016

Clinical Case Reports

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Section: Discussionsupporting

confidence: 81%

Is mean arterial pressure the best parameter in ischemic stroke?

Fuhrer

Weiller

Niesen

2016

Clinical Case Reports

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“…A more recent GDT trial in patients undergoing cardiac surgery showed a reduction in length of stay and complications in the group with fluids management that was guided by stroke volume variation (173). Although this study was not powered to detect changes in the incidence of AKI, there was a trend toward reduced AKI in the protocol group (three versus eight; P=0.20).…”

Section: Prevention Of Aki Nonpharmacologic Strategiesmentioning

confidence: 54%

AKI Associated with Cardiac Surgery

Thiele¹,

Isbell²,

Rosner

2015

Clinical Journal of the American Society of Nephrology

254

211

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Approximately 18% of patients undergoing cardiac surgery experience AKI (on the basis of modern standardized definitions of AKI), and approximately 2%-6% will require hemodialysis. The development of AKI after cardiac surgery portends poor short-and long-term prognoses, with those developing RIFLE failure or AKI Network stage III having an almost 2-fold increase in the risk of death. AKI is caused by a variety of factors, including nephrotoxins, hypoxia, mechanical trauma, inflammation, cardiopulmonary bypass, and hemodynamic instability, and it may be affected by the clinician's choice of fluids and vasoactive agents as well as the transfusion strategy used. The risk of AKI may be ameliorated by avoidance of nephrotoxins, achievement of adequate glucose control preoperatively, and use of goal-directed therapy hemodynamic strategies. Remote ischemic preconditioning is an exciting future strategy, but more work is needed before widespread implementation. Unfortunately, there are no pharmacologic agents known to reduce the risk of AKI or treat established AKI.

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“…This type of personalized therapy based on a step-by-step analysis of the determinants of organ perfusion has been shown to reduce length of stay in selective populations with CS. 79 In other types of shock, rapid hemodynamic stabilization based on oxygenation targets or lactate clearance has also increased survival. 29,80 However, there is no clinical evidence showing the superiority of a flowdirected approach relative to a pressure-based strategy.…”

Section: Maximum Vasoconstrictionmentioning

confidence: 99%

Reconsidering Vasopressors for Cardiogenic Shock

Squara

Hollenberg

Payen

2019

Chest

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Scientific statements and publications have recommended the use of vasoconstrictors as the first-line pharmacologic choice for most cases of cardiogenic shock (CS), without the abundance of strong clinical evidence. One challenge of guidelines is that the way recommendations are stated can potentially lead to oversimplification of complex situations. Except for acute coronary syndrome with CS, in which maintenance of coronary perfusion pressure seems logical prior to revascularization, physiologic consequences of increasing afterload by use of vasoconstrictors should be analyzed. Changing the CS conceptual frame, emphasizing inflammation and other vasodilating consequences of prolonged CS, mixes causes and consequences.Moreover, the considerable interpatient differences regarding the initial cause of CS and subsequent consequences on both macro-and microcirculation, argue for a dynamic, step-by-step, personalized therapeutic strategy. In CS, vasoconstrictors should be used only after a reasoning process, a review of other possible options, and then should be titrated to reach a reasonable pressure target, while checking cardiac output and organ perfusion. CHEST 2019; 156(2):392-401 KEY WORDS: cardiogenic shock; inotropes; norepinephrine; vasoconstrictorsCardiogenic shock (CS) is a low cardiac output (CO) state due to heart failure, resulting in life-threatening end-organ hypoperfusion and hypoxia. 1,2 In the setting of acute myocardial infarction, support of coronary perfusion pressure with vasoconstrictor agents as an initial step prior to revascularization seems reasonable. CS, however, occurs in many other settings, including decompensation of chronic heart failure, fulminant myocarditis, post-cardiac arrest, severe valvular heart disease, right ventricular failure, and as a component of mixed shock in lung injury, sepsis, and other inflammatory conditions. In these settings, application of an early vasoconstricting approach intended for BP support may not always be the best course of action.In the classic pathophysiologic model of CS, early compensatory systemic vasoconstriction occurs in order to maintain BP and organ perfusion. Persistence of tissue hypoxia, however, may induce inflammation with subsequent altered vasoreactivity, 3 ABBREVIATIONS: CO = cardiac output; CP = cardiac power; CS = cardiogenic shock; Ea = arterial elastance; LV = left ventricle; RV = right ventricle; VO 2 = oxygen consumption AFFILIATIONS:

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Individually Optimized Hemodynamic Therapy Reduces Complications and Length of Stay in the Intensive Care Unit

Cited by 17 publications

References 0 publications

Is mean arterial pressure the best parameter in ischemic stroke?

Is mean arterial pressure the best parameter in ischemic stroke?

AKI Associated with Cardiac Surgery

Reconsidering Vasopressors for Cardiogenic Shock

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