Effects of norepinephrine on renal perfusion, filtration and oxygenation in vasodilatory shock and acute kidney injury

Redfors, Bengt; Bragadottir, Gudrun; Sellgren, Johan; Swärd, Kristina; Ricksten, Sven‐Erik

doi:10.1007/s00134-010-2057-4

Cited by 126 publications

(96 citation statements)

References 39 publications

(48 reference statements)

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“…On the other hand, too low a dose of norepinephrine may result in an arterial blood pressure that may be below the limit of renal autoregulation, i. e., when renal blood fl ow becomes pressure-dependent. In a recent study in post-cardiac surgery patients with norpinephrine-dependent vasoplegia and concomitant AKI, the eff ects of norepinephrine on renal perfusion, fi ltration and oxygenation were evaluated [47]. Nor epineph rine infusion rate was randomly and sequentially titrated to target a mean arterial pressures (MAP) of 60, 75 and 90 mm Hg.…”

Section: Vasodilatory Shock and Aki: Role Of Norepinephrinementioning

confidence: 99%

Renal Oxygenation in Clinical Acute Kidney Injury

Ricksten¹,

Bragadottir²,

Redfors³

2013

Annual Update in Intensive Care and Emergency Medicine 2013

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Renal oxygenation is defi ned as the relationship between renal oxygen delivery (DO 2 ) and renal oxygen consumption (VO 2 ) and it can easily be shown that the inverse of this relationship is equivalent to renal extraction of O 2 (O 2 Ex). An increase in renal O 2 Ex means that renal DO 2 has decreased in relation to renal VO 2 , i. e., renal oxygenation is impaired, and vice versa. When compared to other major organs, renal VO 2 is relatively high, second only to the heart. In sedated, mechanically ventilated patients, renal VO 2 is two-thirds (10 ml/min) that of myocardial oxygen consumption (15 ml/min) (Table 1) [1,2]. Renal blo od fl ow, w hich accounts for approximately 20 % of cardiac output, is three times higher than myocardial blood fl ow in this group of patients. Renal O 2 Ex in the non-failing kidney is therefore low, 10 %, compared with, e.g., the heart, in which O 2 E X is 55 % (Table 1). Determin a nts of renal oxygenationIt is well known from experimental studies that tubular sodium reabsorption is the major determinant of renal VO 2 [3] and tha t under normal physiological conditions, approximately 80 % is used to drive active tubular transport of particularly sodium, but also glucose, amino acids and other solutes. Tubular transport processes are highly load-dependent and it has been shown in experimental studies [4] and in p atients [2,[5][6][7] that the re i s a close linear correlation between glomerular fi ltration rate (GFR), renal sodium reabsorption and renal VO 2 (Fig. 1). Th e fi l tered load of sodium is, thus, an important determi nant of renal VO 2 and maneuvers that decrease GFR and the tubular sodium load act to decrease tubular sodium reabsorption and renal VO 2 , and vice versa [8]. It has b een shown that renal O 2 Ex remains stable over a wide range of renal blood fl ows, which means that changes in renal DO 2 , caused by changes in renal blood fl ow, are directly off set by changes in renal VO 2 [9], i. e., r enal VO 2 is fl ow-dependent. Th us, unlike other organs where increases in blood fl ow will improve oxygenation, increased renal blood fl ow augments GFR and the fi ltered load of sodium, which will increase renal VO 2 . Due to this fl ow-dependency of renal VO 2 , renal oxygenation will re main constant, as long as renal blood fl ow and GFR change in parallel. Regional intrarenal oxygenation and medullary hypoxiaTh e relatively high renal blood fl ow is directed preferentially to the cortex to optimize the fi ltration process and solute reabsorption. In contrast, blood fl ow in the outer medulla is less than 50 % of the cortical blood fl ow to preserve osmotic gradients and to enhance urinary concentration [10]. Th e combi nation of low me dullary perfusion, high oxygen consumption of the medullary thick ascending limbs (mTAL) and the countercurrent exchange of oxygen within the vasa recta, results in a poorly oxygenated outer medulla [11]. Oxygen av ailability is, therefore, low in the outer medulla, which has an oxygen tissue partial pressure (PO 2 ) of 10-20 mm Hg ...

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Section: Vasodilatory Shock and Aki: Role Of Norepinephrinementioning

confidence: 99%

Renal Oxygenation in Clinical Acute Kidney Injury

Ricksten¹,

Bragadottir²,

Redfors³

2013

Annual Update in Intensive Care and Emergency Medicine 2013

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“…The major cause for the emergence of acute kidney injury after cardiac surgery is surely ischemia secondary to renal hypoperfusion. (26) Scientific research shows that a higher time of mechanical ventilation significantly exposes patients to the occurrence of acute kidney injury after cardiac surgery. (19) In this study, despite the high incidence of acute kidney injury, the invasive ventilation strategy employed an average positive end-expiratory pressure of 5.4±0.9cmH 2 O.…”

Section: Discussionmentioning

confidence: 99%

Lesão renal aguda no pós-operatório de cirurgia cardíaca

Nascimento

Aguiar²,

Silva

et al. 2015

Acta paul. enferm.

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Objective: To identify the occurrence of acute kidney injury (AKI) in the postoperative period of cardiac surgery. Methods: A prospective cohort study including 51 patients exposed to coronary artery bypass surgery, valve replacement, or combined surgery (bypass surgery and valve replacement) without history of kidney disease and kidney transplant, and who were followed from the preoperative period until 72 hours after surgery. Acute renal failure was defined as baseline creatinine increase of 0.3 mg/dL in 48 hours or less, or its increase from 1.5 to 1.9-fold, or a reduction in urine flow <0.5mL/kg/h for 6 hours. The Kidney Disease: Improving Global Outcomes (KDIGO) classification was used. Results: The KDIGO classification showed that 92.2% of patients had renal impairment. The urinary flow criterion of this classification alone showed that 31.4% of patients had renal dysfunction in stage of risk, 33.3% in stage of renal injury, and 21.6% in stage of renal failure. By the serum creatinine criterion, 27.5% were identified in the stage of risk, 3.9% in stage of injury and another 3.9% in stage of kidney failure. Conclusion: A high percentage of patients in the postoperative period of cardiac surgery (coronary artery bypass surgery and valve replacement) progressed to acute kidney injury. ResumoObjetivo: Identificar a ocorrência de lesão renal aguda em pós-operatório de cirurgia cardíaca. Métodos: Estudo de coorte prospectivo que incluiu 51 pacientes expostos a cirurgia de revascularização do miocárdio, troca valvar ou cirurgia combinada (revascularização do miocárdio e troca valvar), sem antecedentes de doença renal e de transplante renal e que foram acompanhados desde o pré-operatório até 72 horas de pós-operatório. Foi definido como lesão renal aguda o aumento de 0,3mg/dL em tempo menor ou igual a 48 horas ou aumento de 1,5 a 1,9 vez da creatinina basal, ou ainda redução do fluxo urinário <0,5mL/kg/h por 6 horas. Foi utilizada a classificação Kidney Disease: Improving Global Outcomes (KDIGO). Resultados: A classificação KDIGO sinalizou 92,2% dos pacientes com disfunção renal. O critério fluxo urinário dessa classificação isoladamente mostrou que 31,4% dos pacientes apresentaram disfunção renal no estágio de risco, 33,3% no estágio de lesão renal, e 21,6% no estágio de falência renal. Pelo critério creatinina sérica, foram identificados 27,5% no estágio de risco e, nos estágios de lesão e falência renal, foram identificados 3,9% pacientes em cada. Conclusão: Um percentual elevado de pacientes em pós-operatório de cirurgia cardíaca (revascularização miocárdica e troca valvar) progrediu com lesão renal aguda.

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“…Renal blood fl ow calculation is based on measured changes in te mper ature of the renal vein blood after injection of a bolus of isotonic saline at room temperature [19]. Using such methods, Ricksten et al have conducted several elegant studies of global renal perfusion in cardiac surgery patients [20][21][22]. For example, they demonstrated that restoring mean arterial pressure (MAP) from 60 to 75 mm Hg improved the renal oxygen supply/demand relationship after cardiac surgery in patients with vasodilatory shock and AKI [21].…”

Section: Renal Vein T Hermodilution Methodsmentioning

confidence: 99%

“…Using such methods, Ricksten et al have conducted several elegant studies of global renal perfusion in cardiac surgery patients [20][21][22]. For example, they demonstrated that restoring mean arterial pressure (MAP) from 60 to 75 mm Hg improved the renal oxygen supply/demand relationship after cardiac surgery in patients with vasodilatory shock and AKI [21]. Th is technique, however, remains highly invasive and, because of the risk of renal vein thrombosis, can only be applied for a limited period of time.…”

Section: Renal Vein T Hermodilution Methodsmentioning

confidence: 99%

Measurement of Kidney Perfusion in Critically Ill Patients

Schneider

Goodwin

Bellomo

2013

Annual Update in Intensive Care and Emergency Medicine 2013

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Acute kidney injury (AKI) is a major complication of critical illness [1] occurring in 30 to 40 % of all critically ill patients and in its sev ere form requires renal replacement therapy (RRT), in approximately 5 % of patients [2]. AKI has been s hown to be an independent predictor for mortality [3] and is associated with invasive therapy and substantial costs [4].Despite its impor tance, the pathoph ysiology of AKI is still poorly understood. AKI is most commonly associated with systemic diseases, such as septic shock, major surgery and cardiogenic shock [1], but a specifi c mechanism causing AKI to develop in specifi c patients can rarely be determined. Since the early description of an "acute uremia syndrome" in crush injury victims during World War II [5,6] and its association with histopathological fi ndings similar to those found in experimental renal artery ligation, ischemia or some form of alteration in renal blood fl ow has been thought to play a pivotal role in the pathogenesis of AKI. Th is paradigm that essentially all AKI in critically ill patients is the result of some form or degree of ischemia remains of continuing conceptual dominanc e to this day [7]. Despite such dominance, there are only very limited data supporting this concept. In a recent systematic review, Prowle et al. [8] highlighted the extraordinary fact that renal blood fl ow measurement, irrespective of the technique used, has only been reported in 46 critically ill patients (fi ve studies) within the last sixty years. Th us, our knowledge, understanding, and theoretical constructs regarding global renal perfu sion in critically ill patients with RRT-treated AKI (an estimated 5 % of all ICU admissions for a total of approximately a quarter of a million such patients each year in developed countries alone) is, like an inverted pyramid, based on extremely weak evidence.Furthermore, given the complex and heterogeneous nature of the renal vasculature, evaluating the fl ow in the main renal arteries (macrocirculation) might not provide suffi cient information to adequately understand perfusion alterations in complex diseases, such as septic or cardio genic shock. Indeed, some pathophysiological processes may be associated with increased global renal blood fl ow [9,10] despite loss of f un ction. In such instances, there is experimental evidence that, at least in sepsis, this phenomenon may be caused by intra-renal shunting [11]. Hence, correlation between macroscopic renal blood fl ow and function is far from linear. Th erefore, techniques allowing the study of microcircu latory parameters, such as cortico-med ullary perfusion ratio and regional tissue oxygenation measurement, and assessment of their relative change over time may be more valuable in increasing our understanding of the pathophysiology of AKI.In this state-of-the art review, we discuss the value, challenges, limitations, safety and feasibility of diff erent techniques for the measurement of kidney perfusion in critically ill patients. Th e advantages of each technique wi...

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Effects of norepinephrine on renal perfusion, filtration and oxygenation in vasodilatory shock and acute kidney injury

Cited by 126 publications

References 39 publications

Renal Oxygenation in Clinical Acute Kidney Injury

Renal Oxygenation in Clinical Acute Kidney Injury

Lesão renal aguda no pós-operatório de cirurgia cardíaca

Measurement of Kidney Perfusion in Critically Ill Patients

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