new insights into an old problem
Introduction
The main indication for renal replacement therapy in critically ill patients is ischemic acute tubular necrosis associated with multiple organ failure requiring mechan- ical ventilation and catecholamine administration. The kind of renal replacement therapy offering the best he- modynamic tolerance remains debated. Intermittent he- modialysis (IHD) is often viewed by many ICU physi- cians as inducing hemodynamic instability. The applica- tion of recent concepts regarding hemodialysis modali- ties is able to solve part of this old problem [1]. A major problem with IHD is the direct application of chronic he- modialysis concepts in the management of acute renal failure. This approach is responsible for much of the ob- served hemodynamic instability and can be minimized by thoughtful planning prior to IHD in the critically ill patient.
What are the mechanisms of hypotension during hemodialysis?
In critically ill patients intradialytic hypotension results from the underlying process and is exacerbated by the
technique itself. Systemic blood pressure is determined by the interaction of blood flow and peripheral vasomo- tor tone, both of which may be altered by critical illness and hemodialysis. Vasomotor tone is the complex result of interactions between autonomic tone, metabolic de- mand, blood flow distribution, and the responsiveness of the vascular smooth muscle to vasoactive stimuli, such as ionized calcium, mediators of sepsis, and their vaso- active by-products (e.g., prostaglandin F
2_, prostacy- clin). Blood flow, on the other hand, is the result of an- other complex interaction between the determinants of both venous return and ventricular pump function. Im- portantly, venous return is determined by the pressure gradient from the periphery to the heart, such that either loss of circulating blood volume (hypovolemia) or loss of vasomotor tone (functional hypovolemia) decreases venous return. The main pathogenesis of intradialytic hy- potension is a decrease in absolute or relative blood vol- ume. Adaptation to this hypovolemic state includes fluid shift from the extra- to the intravascular space and in- creases in vascular resistance and myocardial contractili- ty (Fig. 1). Although changes in cardiac contractility may also occur, these appear to less important. Hemodi- alysis settings have a direct impact on these adaptive mechanisms, and hemodynamic stability requires hemo- dialysis procedures to be optimized to facilitate plasma refilling and cardiovascular reactivity.
How to preserve blood volume?
Role of ultrafiltration
The volume of ultrafiltration ordered must be based on
the patient’s intravascular volume status (volemia) and
not on the patient’s dry weight. In contrast to chronic he-
modialysis, where patients are always hypervolemic be-
fore starting IHD session, hypervolemia is rarely present
in critically ill patients, except in the case of congestive
heart failure. Patients needing renal replacement therapy in the ICU are typically treated in the context of septic shock complicated by oliguric acute tubular necrosis de- spite aggressive fluid loading and administration of va- soactive drugs. They often present interstitial edemas with a positive weight gain, whereas their plasma vol- ume may not be yet fully restored, and vasopressor per- fusions are still needed. During the acute phase of sepsis or hypovolemic shock the indication for ultrafiltration must be addressed cautiously. Fluid removal may be beneficial only in the case of acute respiratory distress syndrome with severe hypoxemia, where the removal of extravascular lung water is expected to improve oxygen- ation [1].
At the beginning of the hemodialysis session intravas- cular blood volume decreases due to ultrafiltration but usually remains stable thereafter despite continuous fluid removal because of the plasma refilling process (Fig. 2).
Intravascular space filling comes at first from interstitial and then from intracellular fluids. The use of high ultra- filtration rates, approx. 1 l/h, promotes a high incidence of intradialytic hypotensions in critically ill patients [2].
Because plasma refilling is time dependent, a high rate of blood volume decrease must be avoided in the nonhy-
pervolemic patient. To provide clinically effect dialysis and, if indicated, fluid removal without inducing hypo- tension, patients with acute renal failure require a longer hemodialysis run than that required for chronic IHD.
Thus to receive an adequate dialysis dose, patients suf- fering from acute renal failure need prolonged (>4 to 6 h) or iterative (daily or every other day) IHD sessions, which allows the ultrafiltration rate per hour to be re- duced [1, 2].
Role of osmolality
During hemodialysis solute removal is achieved by dif- fusion according to concentrations gradient across the membrane. Solute movements are independent of sol- vent shift and may occur in either direction between blood and dialysate depending on the respective solute concentrations in the dialysate and the blood. This dis- sociation between solute and solvent shifts may be re- sponsible for changes in blood osmolality during the session. Removal of sodium, which represents the main osmotic agent during hemodialysis, decreases osmolali- ty. Decrease in blood osmolality during IHD has been shown to be a risk factor for hemodynamic worsening [3]. Indeed, fall in plasma osmolality promotes water displacement into the cells and impedes plasma refilling (Fig. 2).
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Fig. 1 Main mechanisms of hemodynamic stability during inter-
mittent hemodialysis
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Increasing sodium concentration in the dialysate above the plasma concentration permits sodium shift from the dialysate to the patient’s blood. Increase in plasma and interstitial osmolality facilitates adequate fluid movements for plasma refilling (i.e., from intracel- lular to vascular space through the interstitium; Fig. 2).
In comparison to the usual sodium concentration used in chronic hemodialysis patients (i.e., 138–140 mmol/l), the use of high concentration of sodium in the dialysate, 145–150 mmol/l, limits blood volume reduction despite a higher volume of ultrafiltration and reduces the inci- dence of hypotensions needing therapeutic intervention [1, 4]. In the absence of ultrafiltration the use of a high concentration of sodium in the dialysate is useful to in- crease blood volume, similarly to the use of hypertonic saline perfusion.
How to preserve vascular reactivity?
Improving adaptation of peripheral vascular resistances to volume depletion may reduce the risk of intradialytic hypotension. According to the Starling law, precapillary
vasoconstriction can decrease intravascular hydrostatic pressure and facilitate plasma refilling. The main initiat- ing factor for vasodilatation during IHD session is the in- crease in body temperature.
Role of thermal balance
An increase in core temperature is observed during a standard hemodialysis session (dialysate temperature 37°–37°5 C), which is associated with vasodilatation and impairment of vascular response to the decrease in blood volume. In chronic hemodialysis patients cardiovascular tolerance to IHD is improved when the dialysate temper- ature is adjusted to the range of 35°–35°5 C [5]. More important than the absolute dialysate temperature, a bet- ter hemodynamic tolerance is achieved if the dialysate temperature setting prevents any increase in core temper- ature and heat accumulation in the body [6]. To maintain the body temperature unchanged in chronic hemodialysis patient the dialysate temperature must be set 1°–2°C be- low the baseline body temperature recorded before con- nection. The level of the dialysate temperature setting avoiding increase in body temperature, however, has not been specifically studied in patients with acute renal fail- ure.
Fig. 2 Principle of plasma refilling during intermittent hemodialy-
