Guillermo Lema

Renal function and cardiopulmonary bypass in pediatric cardiac surgical patients.

We studied prospectively the perioperative changes of renal function in nine children undergoing cardiac surgery with cardiopulmonary bypass (CPB). Glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were measured with inulin and 131I-hippuran clearances before CPB, during hypo and normothermic CPB, following sternal closure and 1 h postoperatively. Urinary alpha glutathione S-transferase (alpha GS-T) was measured pre- and postoperatively as a marker for tubular cellular damage. Plasma and urine creatinine and electrolytes were measured. Free water, osmolal and creatinine clearances, as well as fractional excretion of sodium (FeNa) and potassium transtubular gradient (TTKG) were calculated. GFR was normal before and after surgery. ERPF was low before and after surgery; it increased significantly immediately after CPB. Filtration fraction (FF) was abnormally elevated before and after surgery; however, a significant decrease during normothermic CPB and sternal closure was found. Alpha GS-T presented a moderate, but nonsignificant increase postoperatively. FeNa also increased in this period, but not significantly. Creatinine, osmolal, free water clearances, as well as TTKG, were normal in all patients pre- and postoperatively. We conclude that there is no evidence of clinically significant deterioration of renal function in children undergoing repair of cardiac lesions under CPB. Minor increases of alpha GS-T in urine postoperatively did not confirm cellular tubular damage. There was no tubular dysfunction at that time.

Thermoregulatory vasoconstriction increases the difference between femoral and radial arterial pressures

Objective. Thermoregulatory vasoconstriction locally increases arterial wall tension and arteriolar resistance, thereby altering physical properties of the arteries. The arterial pressure waveform is an oscillatory phenomenon related to those physical characteristics; accordingly, we studied the effects of thermoregulatory vasomotion on central and distal arterial pressures, using three hydraulic coupling systems having different dynamic responses.Methods. We studied 7 healthy volunteers. Central arterial pressure was measured from the femoral artery and distal pressure was measured from the radial artery, using 10.8-cm long, 20-gauge catheters. Three hydraulic coupling systems were used: (1) a 10-cm-long, 2-mm internal diameter connector; (2) a 150-cm-long, 1-mm internal diameter connector (Combidyn 520-5689, B. Braun, Melsungen, Germany); (3) a 180-cm long, 2-mm internal diameter connector (Medex MX564 and MX562, Medex Inc., Hillard, OH). Brachial artery pressure was measured oscillometrically. Core temperature was measured at the tympanic membrane. The vasomotor index, defined as finger temperature minus room temperature, divided by core temperature minus room temperature, was used to estimate the degree of vasoconstriction. Constriction was considered near maximal when the index was less than 0.1, and minimal when it exceeded 0.75. Measurements were taken every 3 min. Baseline readings were obtained when subjects were warm. They then were cooled by exposure to 20°C to 22°C room air and a circulating-water mattress set at 4°C until 4 index was less than 0.1. They then were rewarmed by increasing water temperature to 42°C and adding a forced-air warmer until the vasomotor index exceeded 0.75. Data were analyzed by ANOVA and linear regression.Results. Thermoregulatory vasoconstriction was associated with marked arterial pressure waveform changes. Radial pressure showed, in lieu of a dicrotic notch, large oscillations of decreasing amplitude. Femoral pressure showed a single diastolic oscillation of smaller amplitude. The waveforms appeared different, depending on the hydraulic coupling system used, artifact being more marked with the longer connectors. On the average, radial systolic pressure exceeded femoral systolic pressure during vasoconstriction; however, during vasodilatation, femoral systolic pressure exceeded radial systolic pressure (p < 0.05). Oscillometric measurements underestimated systolic pressure, and did so more markedly during vasoconstriction. There were no differences in the values of mean and diastolic pressures.Conclusion. Thermoregulatory vasoconstriction alters radial arterial pressure waveform, artifactually increasing its peak systolic pressure compared with the femoral artery. Poor dynamic responses of recording systems further distort the waveforms. Consequently, radial artery pressure may be misleading in vasoconstricted patients.RésuméObjectifs. La vasoconstriction due à la thermorégulation augmente localement la tension transmurale artérielle et la résistance artériolaire; de ce fait les propriétés physiques des artéres sont modifiees. La forme de la courbe de pression artérielle est un phénoméne oscillatoire lié a ces caractéristiques physiques; en conséquence, nous avons étudié les effets de la vasomotricité due à la thermorégulation sur les pressions artérielles centrales et distales en utilisant 3 systemes de liaisons hydrauliques ay ant des réponses dynamiques différentes.Méthodes. Nous avons étudié 7 volontaires sains. La pression artérielle centrale a été mesurée à l’aide d’un cathéter fémoral et la pression artérielle distale par un cathéter radial (longueur 10.8 cm, diamétre externe 20 G). Trois systémes de liaison hydraulique ont été utilisés: a) un prolongateur de 10 cm de long, 2 mm diamétre interne; b) un prolongateur de 150 cm de long, 1 mm diametre interne (Combidyn(r) 520-5689, B Braun); c) un prolongateur de 180 cm de long, 2 mm diamétre interne (Medex MX 564 et MX 562). La pression de l’artére humérale a été mesurée par oscillométrie. La température centrale a été mesurée au niveau de la membrane tympanique. L’index vasomoteur, défini comme la température au doigt moins la température de la piéce, divisée par la température centrale moins la température de la piéce, a été utilisé pour estimer le degré de vasoconstriction. La vasoconstriction a été considérée comme maximale quand l’index était inférieur à 0.1 et minimale quand il était supérieur à 0.75. Les mesures ont été faites toutes les 3 minutes. Les relevés de base ont été faits quand les sujets étaient chauds. Ensuite, ils ont été refroidis par exposition à une température ambiante de 20-22 °C et par matelas à circulation d’eau froide à 4°C jusqu’à atteindre une valeur d’index inférieure a 0.1. Ils ont, ensuite, été réchauffés par augmentation de la température de l’eau à 42°C et ajoûtant d’un diffuseur d’air chaud jusqu’à ce que l’index vasomoteur ait dépassé 0.75. Les données ont été analysées par ANOVA et régression linéaire.Résultats. La vasoconstriction due à la thermorégulation était associée à des modifications nettes de la forme de la courbe de pression artérielle. La pression radiale montrait, à la place de l’onde dicrote, de grandes oscillations d’amplitude décroissante. La pression fémorale montrait une oscillation diastolique unique de plus faible amplitude. La forme des courbes est apparue différente, dépendant du systeme de liaison hydraulique utilisé, les artefacts étant plus marqués avec les prolongateurs les plus longs. En moyenne, la pression systolique radiale dépassait la pression systolique fémorale pendant la vasoconstriction; cependant, la pression systolique fémorale dépassait la pression systolique radiale pendant la vasodilatation (P < 0.05). Les mesures oscillométriques sous-estimaient la pression systolique, et ce, encore plus pendant la vasoconstriction. II n’y avait pas de différences dans les valeurs de pressions moyenne et diastolique.Conclusions. La vasoconstriction due à la thermorégulation modifie la forme de la courbe de pression radiale, son pic de pression systolique est faussement augmenté comparé à celui de la pression fémorale. Les médiocres réponses dynamiques des systémes d’enregistrement déforment davantage encore la forme des courbes de pression. En conséquence, la pression de l’artére radiale peut être cause d’erreurs chez les patients vasoconstrictés.AbstraktHintergrund. Thermoregulatonsche Vasokonstriktion erhoht lokal die artenelle Wandspannung und den Widerstand in den Artenolen, wodurch sich die physikallschen Eigenschaften der Artenen verandern Die artenelle Druckkurve stellt ein oszillatorisches Phanomen dar, das auf diese physikahschen Eigenschaften zuruckzufiihren ist Dementsprechend untersuchten wir die Wirkungen thermoregulatorischer Vasomotonk auf den zentralen und distalen arterlellen Blutdruck unter Verwendung von drei hydraulischen Verbindungssystemen mit verschiedenen dynamischen ReaktionsartenMethodik. Wir untersuchten sieben gesunde Freiwillige Der zentrale artenelle Druck wurde in der Femoralartene gemessen, der distale Druck in der A radiahs Dabei verwendeten wir 10,8 cm lange 20-G-Katheter Drei hydraulische Verbindungssysteme wurden verwendet, a) ein 10 cm langer Konnektor mit einem Innendurchmesser von 2 mm, b) em 150 cm langer Konnektor (Innendurchmesser 1 mm) (Combidyn?p004,041? 520-5689, B Braun) sowie, c) ein Konnektor mit 180 cm Lange und einem Innendurchmesser von 2 mm (Medex MX564 und MX562) Der Druck in der A brachialis wurde oszillometnsch gemessen Die Kerntemperatur wurde am Trommelfell abgenommen Der Vasomotoren-Index, definiert als der Quotient aus der Differenz von Fingertemperatur minus Raumtemperatur geteilt durch die Differenz von Kerntemperatur minus Raumtemperatur, war das Maβ, um den Grad der Vasokonstnktion zu erfassen Die Konstriktion wurde als fast maximal betrachtet, wenn der Index weniger als 0,1 betrug und als minimal, wenn er 0,75 uberschntt Alle drei Minuten fand eine Messung statt Die Eichung der Null-Lime erfolgte, solange die Probanden noch warm waren Danach wurden sie einer Zimmertemperatur von 20-22°C ausgesetzt und lagen auf einer Matratze mit zirkulierendem Wasser, dessen Temperatur 4°C betrug Die Abkuhlung wurde solange durchgefuhrt, bis der Index wemger als 0,1 betrug Danach wurden die Probanden wieder aufgewarmt, indem die Wassertemperature bis 42°C angehoben und zusatzlich warme Luft zugefuhrt wurde bis der Index 0,75 uberschritt Die statistische Analyse bestand aus ANOVA und der Methodik der linearen RegressionErgebnisse. Die thermoregulatorische Vasokonstriktion war mit deutlichen Veranderungen der artenellen Druckkurve verbunden Der Druck in der A radiahs zeigte, anstatt einer dikrotischen Einkerbung, weitlaufige Oszillationen von abnehmender Amplitude Der Druck in der A femorahs zeigte eine einzige diastohsche Oszillation mit kleiner Amplitude Die Druckkurven erschienen unterschiedlich, abhangig vom verwendeten hydrauhschen Verbindungssystem, Artefakte traten bei Verwendung der langeren Konnektoren deutlicher auf Im Durchschnitt uberschntt der systolische Druck in der A radialis den systolischen Femoraldruck wahrend der Vasokonstriktion; während der Vasodilatation allerdings war es umgekehrt (p < 0,05). Oszillometrische Messungen unterschätzten den systolischen Druck und taten dies deutlicher während der Vasokonstnktion. Zwischen den Werten des Mitteldruckes und des diastolischen Druckes ergaben sich keine Differenzen.Schluβfolgerung. Thermoregulatorische Vasokonstnktion verändert die Form der arteriellen Druckkurve in der A. radialis; artefaktbedingt kommt es zu einem Anstieg der systolischen Druckspitze im Vergleich zur Femoralarterie. Schlechtes dynamisches Verhalten des Registrierungssystems verändert ebenfalls die Wellenform. Folglich kann die Messung des Radialisdruckes bei Patienten mit Vasokonstnktion irreführende Werte erzielen.ResumenObjetivos. La vasoconstricción termorreguladora aumen

Plasma levels of potassium and magnessium after modified ultrafiltration in pediatric cardiac surgery with cardiopulmonary bypass

Objective: Modified ultrafiltration (MUF) reduces some of the complications associated with cardiopulmonary bypass (CPB) in pediatric cardiac surgery. However, we have observed hypokalemia and hypomagnesemia in children when MUF is used. Such alterations may elicit severe arrhythmias in the postoperative period. To date, no studies have focused on the effects MUF may have in plasma levels of potassium (K) and magnesium (Mg). The objective of our study was to determine if there is any variation in plasma levels of K (plK) and Mg (plMg) after MUF in children undergoing cardiac surgery with CPB. Patients: Sixteen children scheduled for cardiac surgery with CBP and MUF were prospectively studied. Anesthetic, CPB and MUF management were standardized for all patients, the latter lasting for 10 minutes. Results: Plasma K average levels before and after MUF were 4.16 mmol/L and 3.58 mmol/L, respectively. The average plasma Mg levels before and after MUF were 4.82 mmol/L and 4.81 mmol/L, respectively. Conclusions: The plasma level of K is reduced by 13.7% after MUF (p<0.0001). The reduction in Mg at the same period of time was not statistically significant (p<0.970).

Aortic Stenosis and Acquired von Willebrand Disease: Lack of Association

OBJECTIVES The association between aortic stenosis (AS) and acquired von Willebrand disease type 2A has been described. It may be present in up to 90% of patients with AS. Shear stress has been proposed as the underlying mechanism; however, the physiopathology of this condition is not completely understood. No specific treatment has been studied in this specific population besides aortic valve replacement (AVR). As a coadjuvant therapy, some cardiac surgery centers use desmopressin routinely. The authors report the first stage of an ongoing study designed to compare the effects of desmopressin versus placebo in patients with severe AS scheduled for AVR. Because of the different incidences of the acquired von Willebrand type 2A reported in the literature, the first stage was conducted to describe the incidence of this clinical association in the present population, allowing the sample size for the second stage of the study to be obtained. DESIGN A prospective cohort study. SETTING A single academic medical center. PARTICIPANTS Thirteen patients with severe AS scheduled for AVR. INTERVENTION None. MEASUREMENTS AND MAIN RESULTS Patients with severe AS scheduled for AVR were studied preoperatively with a von Willebrand laboratory panel. Results were negative for acquired von Willebrand disease type 2A in all patients. The second stage of the trial was stopped. CONCLUSION Contrary to previous reports, no correlation was found between AS and acquired von Willebrand disease type 2A. Further studies are needed to ascertain whether this lack of association is caused by a specific characteristic of the present population, the small sample size, or other factors.

Ulinastatin treatment and renal injury in patients undergoing aortic valve replacement with cardiopulmonary bypass. A note of aution

We appreciate the constructive comments by Dr. Guillermo Lema regarding our article. Undoubtedly, patients with pre-existing renal dysfunction would be more prone to aggravation of the renal dysfunction after cardiac surgery. Theoretically, these patients would benefit the most from therapeutic measures aimed at reducing the postoperative kidney injury, yet it would also require a harder clinical endpoint such as the requirement of renal replacement therapy for validation. As the incidence of renal replacement therapy after cardiac surgery is low, this would require a substantial number of patients. In our study, we used differences in renal biomarkers as the primary endpoint in a relatively homogenous group of patients undergoing aortic valve replacement. Compared to other valvular procedures, aortic valve surgery is associated with relatively higher incidence of acute kidney injury [1]. As with the assessment of postoperative myocardial infarction using cardiac enzymes, the correlation between renal dysfunction and changes in renal biomarkers, especially creatinine, has been well validated [2]. Even transient elevations in the postoperative serum creatinine concentrations have been shown to be associated with adverse outcome following cardiac surgery. As this was the first study to address the reno-protective effect of ulinastatin, we tried to avoid the introduction of confounding factors as much as possible. In patients with pre-existing renal dysfunction, however, the concentrations of renal biomarkers would be already increased and diverse, which could act as a major confounder. Thus, to efficiently assess the potential reno-protective effect of ulinastatin using a small sample size, we had excluded patients with pre-existing renal dysfunction. This in turn, however, invariably confronts generalization of the observed results as was commented by Dr. Guillermo Lema. Notwithstanding the complex relationship between preoperative patients co-morbid diseases and postoperative renal dysfunction and clinical outcome, we do acknowledge that a further study with a large sample size involving a heterogeneous group of patients would be necessary to draw a more definite conclusion adding value to the literature. We hope that our study would draw many attentions in that regard.

Aortic Valve Stenosis and von Willebrand Disease: A Clinical Condition Without Full Explanation

However, no clear explanation has been found so far. It hasbeen hypothesized that this association could be related to flowalteration with exposure of blood to high shear stress, thusincreasing proteolytic degradation of von Willebrand factors byADAMTS13 (a metalloprotease), or the increased interactionbetween von Willebrand factor and platelets caused by theshear stress, which could lead to a higher clearance of thelargest multimers, among others.

Renal Protection: What Should We Aim For?

The article by Cogliati et al1 focuses on a subject not completely understood that carries high morbidity and mortality. Several rugs and techniques have been used to prevent renal dysfunction after cardiac surgery. Similar strategies repeatedly have been used n other critical care patients. The different studies have failed to show robust positive results.2-4 The term “renal protection” has been used extensively, but no “magic drug or therapy” can be said to be a renal protective agent. ogliati et al used fenoldopam as a possible renoprotective agent, with positive findings in the fenoldopam-treated group. However, ther studies have not found beneficial effects with the same drug in cardiac and noncardiac patients.2-4 Fenoldopam works by vasodilating renal blood vessels, thus increasing renal blood flow. Renal blood flow, contrary to many eliefs, is increased during cardiopulmonary bypass.5 We do not know, however, if the increases in flow go to the cortex or the edulla. Normally renal flow goes predominantly to the cortex and there is no reason to think that the increase of flow produced y fenoldopam is diverted to other areas, specifically the medulla, within the kidney. Oxygen consumption is higher in the medulla and unless the flow can be redirected to this portion of the kidney, all the high xygen consumption metabolic processes will occur without changes; ischemic insults of any kind (low blood pressure, low cardiac utput, nephrotoxic drugs) affect this portion more than any other. This complex situation may explain, in part, why vasodilating gents have not shown beneficial effects in all patients. Renoprotective drugs or techniques have been difficult to find, and this may be because we are choosing the wrong method of rotection. The goal has been to use a drug that can keep the renal function normal. A new hypothesis is to find a drug that may, s in other organs (the heart and brain), reduce the metabolic processes in the medulla, allowing the kidney to “preserve function” y reducing the oxygen consumption; in that case, it would not be necessary to vasodilate the renal blood vessels. Normal flow ould be enough to meet all requirements. If this is the case, then we should not use normal renal function tests as early outcome easures in this situation; other cellular markers will be needed to assess renal protection.

Renal outcome following on- and off-pump coronary artery bypass graft surgery: few patients, cautious conclusions.

In the introduction, the authors implicate the use of CPB as one of the main causes of postoperative renal failure. ‘‘Inadequate or nonpulsatile renal perfusion, macroand microembolic loads on the renal vasculature, and the inflammatory response to CPB have been implicated as potential etiologic factors for postoperative renal dysfunction and renal failure’’. This statement could be misleading. There are a great numbers of clinical conditions that can deteriorate the function of the kidneys, including: low hematocrit, low cardiac output, vasoconstriction associated to inotropic support, bleeding, blood transfusions, haemodilution, among others.

Función renal en cirugía cardíaca con circulación extracorpórea: Pacientes valvulares y coronarios

BACKGROUND Patients with valvular heart disease are at high risk of acute renal failure after surgery with extracorporeal circulation. AIM To describe changes in renal function parameters during surgery with extracorporeal circulation in patients with valvular heart disease and compare them with those found in patients undergoing elective coronary surgery. MATERIAL AND METHODS Two groups of patients were studied. Group 1 was composed by twelve patients undergoing elective coronary surgery and group 2 was composed by eleven patients undergoing surgery for heart valve replacement. Glomerular filtration rate and effective renal plasma now were estimated from inulin and the 131 I-hippuran clearance respectively, at five different times, during surgery and the postoperative period. Sodium filtration fraction and fractional excretion were calculated. Alpha and pi-glutathione s-transferase in urine were measured as markers of tubular damage in the pre and postoperative periods. RESULTS Effective renal plasma flow was reduced in both groups before induction of anesthesia, did not change during surgery and decreased significantly in patients with valvular disease in the postoperative period. Glomerular filtration rates were normal during all the study period. There was a non significant reduction of filtration fraction during extracorporeal circulation. Alpha and pi glutathione s-transferases were normal and did not change. Fractional excretion of sodium increased significantly postoperatively. CONCLUSIONS In patients with valvular disease undergoing surgery with extracorporeal circulation, renal function does not deteriorate. No significant difference was found when compared with patients undergoing coronary surgery. No evidence of functional and cellular renal disfunction or damage was found in both study groups.

HANP on renal damage during cardiac surgery

1. Many research groups are looking for a therapy that can protect kidneys during surgery with cardiopulmonary bypass. Strategies involving the use of mannitol, fenoldopam, dexmedetomidina, high hematocrit, pulsatile flow, perfusion pressure, human natriuretic peptide, among others have been described, but none of these have shown benefits in patients at risk [1, 2]. 2. A plasma creatinine concentration of ≥1.5 mg/dl is the cut-off reported in most published studies. Therefore, I disagree with the plasma creatinine level on which the authors use to base their conclusions. In order to study renal protection in the population described, we may need a much larger number of patients, as the authors mentioned [1, 2]. 3. Plasma creatinine does not show any benefit of the protective drug used during treatment. The increase in enzyme levels also does not show any protective effects. Enzymes are released by the renal tubules due to injury. It has yet to be seen whether that injury becomes renal dysfunction [2]. 4. Is cardiopulmonary bypass the main factor for renal failure? The incidence of renal failure in high-risk renal patients among patients undergoing off-pump surgery compared to those undergoing on-pump surgery is comparable [3]. Thus, a reno-protective strategy should include the peri-operative period. However, such a study would be almost impossible due to the type of patients and the diversity of therapies used in the post-operative period.