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From ArmandGirbes.com Fellows Introduction
The discovery and recognition of the pronounced effects of dopamine on renal function, now more than thirty years ago by the group of Goldberg [1], has contributed to the current extensive use of dopamine Intensive Care Unit (ICU). Particularly in a low-dose, dopamine is administered in the ICU for it’s presumed renal protective effects. According to a recent audit of 93 ICU’s in the UK, 50% of all patients at risk for developing renal failure were on low-dose dopamine. Forty-three ICU’s had a protocol for the use of dopamine in patients at risk [2]. The properties ascribed to the infusion of low-dose dopamine, i.e. enhancement of renal blood flow or preservation of renal blood flow, with an increase in urine output have made it attractive for internists, anesthesiologists, cardiologists and intensivists to prescribe dopamine to the critically-ill patient. Additionally, dopamine is used to reverse the effects of positive pressure ventilation with positive end expiratory pressures, which are a decrease in cardiac output and a decrease in renal blood flow with a concomitant fall in diuresis. And the positive inotropic properties of dopamine reverse the negative inotropic effects of anesthetics. Since the (hourly) diuresis of the critically-ill patient and the patient in the ICU is considered as a very good marker of (peripheral) tissue perfusion, the diuretic properties of dopamine are more than cherished by the clinician. On the contrary, the effect of norepinephrine on renal function is appraised with fear of inducing a deterioration of renal function. This is mainly based on early reports in the seventies of experimental studies with - intra-arterial - norepinephrine-induced acute renal failure [3,4]. Moreover, relatively high doses of norepinephrine were used: up to 1.5 g/kg/min. However, this cannot and should not be extrapolated to the human pathophysiological situation, e.g. in septic shock, and does not take sufficiently into account the importance of restoring perfusion pressure for the kidney in patients with hypotension. Additionally, several recent reports on the use of norepinephrine in patients with sepsis make that norepinephrine is increasingly recognized as a valuable agent in the treatment of septic shock and can improve renal function [5,6]. In this review we will appraise the available data from the literature on the use of dopamine and norepinephrine in the critically-ill patient, focusing on renal function.
Physiology of renal hemodynamics Arterial blood enters the kidney at the hilus through the renal artery, which divides into interlobar arteries, which serially branch into arcuate and interlobular arteries. The interlobular arteries subdivide into numerous afferent arterioles, which deliver blood into the capillary networks: the glomeruli. Here the filtration takes place and the blood remaining in the glomerulus leaves through an efferent arteriole into sequentially the peritubular capillaries, interlobular veins, arcuate veins, interlobar veins and finally the renal vein. The peritubular capillaries run in apposition to the adjacent tubules and the constitution of the fluid contained in these tubules is a determinant for the reabsorption. As will be explained later this is related to the filtration fraction. Branches of the juxtamedullary glomeruli enter the medulla constituting the vasa recta capillaries. The glomerular capsule surrounds the glomerulus, like an inflated chewing gum ball, wrapping up the glomerulus. In this "chewing gum ball", the capsular space, the (glomerular) ultrafiltrate is received: the primary urine, flowing down into the tubules. The amount of ultrafiltrate of plasma across the glomerulus is dependent on (i) the permeability of the membrane and the net effect of (ii) hydraulic pressure and (iii) oncotic pressure gradients. Changes in the glomerular filtration rate (GFR) can therefore be produced by alterations in these factors or by the rate of renal plasma flow (RPF). A constriction of the afferent arteriole will decrease both RPF and GFR. A constriction of the efferent arteriole will tend to increase the GFR through a rise in intraglomerular pressure (Figure 1). In this case the fraction of the amount of RPF that is filtrated into the capsular space is increased: the filtration fraction (FF=GFR/RPF) is increased. A high filtration fraction, as seen in situations with a stimulated Renin-Angiotensin-Aldosterone (RAAS) - and Sympathetic Nervous System (SNS) activity, such as hypotension, the hydrostatic pressure of the peritubular capillaries will fall and the oncotic pressure will rise. This results in an augmented tubular reabsorption. I.e. sodium and water retention occurs. Renal vasodilation per se however, as induced by low doses of dopamine, induces natriuresis. The balance of afferent and efferent vascular tone with concomitant effects on renal hemodynamics and water- and sodium retention, is determined by the SNS and counteracting neurohumoral systems (table 1). Prostaglandins are produced at various sites in the kidney and possess important local functions but little systemic activity. Renal prostaglandins act as vasodilators, antagonize the water-retaining effect of ADH and increase sodium excretion. The deleterious effects of prostaglandin synthesis inhibition by non-steroidal anti-inflammatory drugs in patients with shock can easily be derived from the actions of prostaglandins. However, although the intraglomerular pressure is an important determinant of GFR, under physiological circumstances the GFR and RPF remain approximately constant, through so called autoregulation, despite fluctuations of arterial pressures, provided the perfusion pressure - i.e. the mean arterial pressure - is sufficient. This underscores the importance of perfusion pressure in the maintenance of renal function, i.e. GFR.
Effects of norepinephrine Norepinephrine (NE), the effector component of the SNS, stimulates both - and -receptors (table 2). After its release from the terminal nerve endings of the SNS, NE acts in an autocrine fashion on local adrenoceptors, while at the same time small amounts leak into the circulation [7]. This spilled-over NE is not an inert circulating neurotransmitter, but a hormonally active substance [8]. NE has a high binding affinity for 1-adrenoceptors that cause vasocontriction in many vascular beds. The kidney is richly innervated by sympathetic nerves that terminate on both renal vasculature and discrete segments of the nephron [9]. Accordingly, 1-adrenoceptors have been located along the interlobular, afferent and efferent glomerular arterioles, mesangial cells and tubular segments [10]. This distribution pattern suggests that NE may control glomerular blood flow, glomerular capillary pressure and renal sodium handling [7,11]. Experimental studies on renal sympathetic nerves have shown that low frequency stimulation results in sodium retention and renin release and high frequency stimulation in a fall in RPF and some decline in glomerular filtration rate (GFR) [7,12]. Exogenous NE infusions have been documented to markedly reduce RPF without much change in GFR in animals [13]. These renal haemodynamic effects of NE are likely mediated via changes in glomerular arteriolar tone [11,13-15]. Studies of isolated renal vessels of rats and rabbits have shown that NE causes vasoconstriction of the interlobular renal arteries and of the afferent and efferent glomerular arterioles [14,15]. The latter vessels are the major sites of flow resistance in the kidney and thus importantly determine renal blood flow, whereas they are also involved in the control of intraglomerular pressure [11]. According to the equation GFR= kf(Pc-p), glomerular ultrafiltration is determined by net hydraulic pressure (Pc), net oncotic pressure (), filtration surface area and hydraulic permeability (kf) [11]. Under conditions of pressure equilibrium like in the hydropenic rat, changes in GFR are linearly related to changes in RPF [11]. This indicates that any decrease in RPF by NE will reduce GFR unless other factors like an increase in net hydraulic e.g. intraglomerular pressure compensates for a fall in GFR. Indeed, early micropuncture studies in the rat documented that the NE induced fall in RPF was accompanied by an increase in intraglomerular pressure. The lack of change in GFR during NE infusion was explained by the increase in intraglomerular pressure offsetting the fall in RPF [13]. Interestingly, the prevailing blood pressure was found to determine the glomerular vessel response. There was a predominant increase in efferent tone when blood pressure was kept unchanged, whereas both afferent and efferent glomerular resistance increased when blood pressure was allowed to increase [13]. Thus, in experimental studies exogenous NE has been recognized as an important renal vasoconstrictor that decreases RPF but without much change in GFR due to a rise of intraglomerular pressure. In the human situation the precise effects of NE on afferent and efferent glomerular vasoconstriction and intraglomerular pressure are unknown, and it is uncertain to what extent intrarenal -adrenoceptor distribution differs from species like rats and rabbits. Nonetheless, renal hemodynamic responses to NE infusion show obvious similarities with animal data. Intravenous infusion of NE lowers RPF but has little effect on GFR [16-21]. Even with high NE infusion rates that decreased RPF up to 40 to 50% in healthy volunteers, we have previously not noted any deteriorating effect on GFR [20]. Consequently, NE raises the filtration fraction (i.e. the quotient of GFR and RPF), which may reflect a change in pressure profile along glomerular arterioles. Moreover, NE infusion augments proteinuria in nephrotic patients [19] and increases microproteinuria in healthy subjects and diabetic patients in conjunction with a large rise in blood pressure [20,21]. Taken together the rise in filtration fraction and the proteinuria promoting effects of NE, it is plausible that NE also increases intraglomerular pressure in man. The finding that GFR is independent from a wide range of NE-induced reductions in RPF, could also implicate that glomerular blood flow is not the most important determinant of human ultrafiltration. It therefore seems that the dependency of GFR on RPF is not operative in adequately hydrated humans, unlike the hydropenic rat [11]. The notion that RPF is a determinant of human GFR is in fact only based on observations that GFR is highly correlated with RPF in man [22]. Moreover, it has been outlined that an increase in filtration fraction concomitantly with a fall in RPF does not necessarily reflect a predominant increase in efferent over afferent glomerular arteriolar resistance and thus an increase in intraglomerular pressure [23]. In fact, the filtration rises to some extent with a proportional increase in afferent and efferent glomerular arteriolar tone. Thus, the lack of a decrease of GFR during NE infusion in humans could also indicate a large functional reserve of RPF in man. NE infusions are in most but not all studies associated with an antinatriuretic effect in healthy subjects, which is in accordance with experimental nerve stimulation studies [7,16-18]. The sodium retaining effect of NE is ascribed to direct stimulation of proximal tubular sodium reabsorption. In addition, intrarenal angiotensin II generation by NE has been proposed to play a contributory role. This is supported by the finding that angiotensin-converting-enzyme inhibitors blunt NE-induced anti-natriuresis in healthy man [24]. The physiological importance of the NE effects of renal sodium handling under normal circumstances are not well known, but it is evident that pressure natriuresis is not a feature of NE-induced rises in blood pressure. This indicates that exogenous infusions NE may reset renal sodium handling towards sodium retention. NE is a potent vasoconstrictor substance that is increasingly reported to be a very effective agent to restore blood pressure and tissue perfusion in patients with septic shock [5,6,25]. However, fear of renal function loss with NE infusions is widely distributed. This is in fact only based on studies in animals in which relatively high doses of intra-arterially administered NE produce renal ischemia and insufficiency [3,4]. No data are available on the exact renal haemodynamic effects as measured with appropriate clearance methods in the critically ill. Only with indirect measures as urine output and/or creatinine values, it has been shown that NE is able to quickly reverse oliguria in septic patients [5,6,25,26]. From these observations it can be inferred that the benefits of NE are due to restoration of perfusion pressure e.g. intraglomerular pressure, which is generally conceived to be the driving force of the human glomerular ultrafiltration process [22]. It suggested, therefore, that the NE-induced reduction in RPF is of limited importance in patients with septic shock and does not deteriorate renal function. In contrast, renal vasoconstriction by NE may increase perfusion pressure and thus improve renal function (i.e. GFR), provided adequate fluid resuscitation has been established.
Effects of dopamine Dopamine exerts a complicated influence on the cardiovascular and renal system. This is due to the fact that dopamine stimulates different types of adrenergic receptors: not only - and ß-adrenergic but also specific dopamine receptors [27,28]. And each of these receptors can be divided in two subtypes according to the effects exerted by their stimulation (table 2). Dopamine is used for various indications depending on the given dose. This is due to the amount of stimulation and the change of balance of these receptor effects for different doses. Dopamine receptors are present at various sites of the body, not only in the Central Nervous System (CNS), but also outside the CNS, the so called peripheral dopamine receptors. These receptors are currently divided in two types: postsynaptic D1-like, and (presynaptic) D2-like receptors. D1-like receptors are located in blood vessels and in the (mainly proximal) tubule of the kidney [29]. Stimulation induces vasodilation and natriuresis. The D2-like receptors are situated prejunctionally on sympathetic nerve terminals and in the adrenal gland. Stimulation of D2-like receptors results in inhibition of norepinephrine release and inhibition of aldosterone secretion [28,29]. Dopamine is known to increase cardiac output already at lower doses due to ß - and a- receptor stimulation, without changes or slight fall in systemic vascular resistance [27,30,31]. In patients with low or depressed cardiac output dopamine can be used to increase the cardiac output. In case of conditions with total body fluid overload the diuretic properties (mainly D1-like receptor stimulation) of dopamine are of additional value [32]. At higher doses (>10 g/kg/min) systemic vascular resistance will increase. For this reason dopamine is often used in critically-ill patients with septic (hyperdynamic) shock, which is in the early phase characterized by a high cardiac output and low systemic vascular resistance. Low-dose dopamine (<4 g/kg/min), still wrongly nicknamed by many clinicians as "renal dose" suggesting only renal effects, increases renal bloodflow by preferential postglomerular vasodilation, and increases cardiac output [29,31]. The renal vasodilation together with direct tubular effects will lead to an increase of natriuresis and diuresis [28]. In a recent study we demonstrated also a decrease in plasma aldosterone concentration in postoperative mechanically ventilated patients, which will contribute to the natriuretic effect of dopamine [31]. However, the effects of dopamine on renal plasma flow are dependent on the GFR. Effects are significantly blunted or even absent in case of a low GFR [33]. An increase in mesenteric flow has been observed in anesthetized preoperative patients at a dose of 4 g/kg/min [34] and in patients undergoing elective spinal cord surgery [35]. Additionally, in animal studies an improved oxygenation of the jejunal mucosa has been observed [36]. The different studies describing the effects of dopamine on the systemic- and local circulation make it attractive for use in the ICU and theater. Since effects on bloodflow are considered to be beneficial, dopamine is often used as a drug for preservation of regional bloodflow and is given for prophylaxis of impairment of cardio-renal function and protection of splanchnic flow. Additionally, dopamine is in this context suitable for different types of shock and the effects of dopamine can be modified by simply increasing the dose. However, the studies on splanchnic flow are not conclusive: a study by Segal et al. showed an indication of earlier onset of gut ischemia in a porcine model of hemorrhagic shock [37]. Hemmer & Suter demonstrated that the 20% fall in cardiac output and oxygen delivery (DO2) and the 47% decrease of creatinine clearance during mechanical ventilation with 20 cm PEEP could be reversed by dopamine [38]. Similarly, the cardiovascular depression by anesthetics is counteracted by dopamine [30,39]. Furthermore, the hypertension as observed in patients undergoing general anesthesia without thoracic epidural analgesia, was neutralized by dopamine, making the patient more "stable" during anesthesia [40]. In a study by Flancbaum it was shown that some critically-ill oliguric patients respond with a >50% increase of diuresis upon dopamine administration [41]. However, prospective controlled studies on outcome using more appropriate endpoints are scarce and disappointing for those who expect a demonstrable favorable effect of dopamine. In a prospective double-blind placebo controlled study by Myles et al. the effect of 3 g/kg/min dopamine on renal function following cardiac surgery was examined in 49 patients with a previous serum creatinine value < 300 mmol/l. Dopamine did not improve renal creatinine clearance, although systemic hemodynamics were ameliorated by dopamine during the operation [42]. In a prospective double-blind placebo controlled study in sixty patients undergoing renal transplantation, with pair-wise randomization of both kidneys of one donor, no beneficial effect of 3 g/kg/min of dopamine could be detected. Dopamine was started 10 minutes before release of the vascular clamps and continued until 48 hours after the transplantation. Outcome after 3 months was identical in both groups [43]. The need for application of dopamine in septic patients becomes also questionable since several studies now show that norepinephrine is more efficacious in restoring blood pressure, thereby establishing a better perfusion pressure [6]. Furthermore, it has been suggested that dopamine causes an uncompensated increase in splanchnic oxygen requirements in septic patients [43]. Cardiac failure with extensive fluid retention might remain a special indication for dopamine since it both increases cardiac output and renal bloodflow and sodium excretion, which will result in relief of the symptoms of dyspnea. However, studies comparing treatment with diuretics and dobutamine versus dopamine are lacking. But, in general improvement of complaints in a short time in such patients is beyond doubt, as any clinician can indicate.
Conclusion The widespread use of dopamine in the ICU is by no means supported by the literature. Till present all studies on low-dose dopamine have failed to demonstrate a renal protective effect of low-dose dopamine in any patient group. Clinicians mix-up an increase in diuresis with preservation or improvement of renal function. So why do clinicians still administer low-dose dopamine to mechanically ventilated, but otherwise stable patients? Is it only because they feel happier with a patient with a diuresis of 100 ml/hr than with the same patient with a diuresis of 30 ml/hr? But the question should be of course whether this patient is better off at the end with a (temporary) increase of diuresis. Low-dose dopamine does increase cardiac output and exerts positive inotropy and chronotropism by ß1-receptor agonist activity. It therefore increases intracellular Ca2+ which can lead to arrhythmias. Vasoactive drugs should never be considered harmless and only be given whenever an indication is present. The fear of the use of norepinephrine comes from animal studies with high doses of intra-arterial norepinephrine administration or dehydrated animals getting norepinephrine. Also the misconception that renal blood flow is equal to renal function contributes to this fear. GFR is the most important determinant of renal function and is independent within a wide range of renal blood flow. Evidence now exists that norepinephrine improves renal function in patients with septic shock, provided adequate fluid resuscitation has been achieved [5,25]. Additionally, studies have now shown that norepinephrine is more efficacious to restore the blood pressure of septic patients after fluid resuscitation than dopamine [6]. Prevention of renal failure with low-dose dopamine is even more disappointing, since no human study has shown evidence. However, it should be acknowledged that in clinical practice dopamine can be used in patients with shock in whom the diagnosis is not yet established, if it improves the hemodynamics. We should accept of course that well controlled prospective studies are not always available and even not always necessary. Although a prospective controlled study of the efficacy of a parachute is lacking, no one would doubt it's usefulness... But it can be concluded that routine administration of low-dose dopamine should be banned and the role of dopamine in the ICU should be reassessed. Norepinephrine is a pharmacologically rational choice in patients with septic shock and can be safely given provided an adequate fluid status is present.
Vasoconstriction * Renin-Angiotensin-Aldosterone-System + * Activation Sympathetic Nervous System Water/sodium retention * ADH (vasopressin) * Endothelin
Vasodilation * Atrial Natriuretic Peptide + * Endogenous dopamine Natriuresis * PGE2 (metabolites) * EDRF (NO)
Table 1 Counteracting systems on renal function.
Table 2 The effects of dopamine and norepinephrine on adrenergic receptors. The amount of stimulation is indicated by a number, where 0 indicates absent stimulation and 2 potent stimulation. An asterisk indicates dose dependent effects, mainly observed at higher doses.
Figure 1 Simplified representation of a glomerulus with afferent and efferent arteriole. A preglomerular vasal constriction will result in a decrease of RPF and a fall in intraglomerular pressure (igP) and a subsequent fall of GFR. A postglomerular vasa constriction will result in a rise of igP and a (relative) rise of GFR.
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