MANAGEMENT OF CARDIORENAL SYNDROME IN INTENSIVE CARE PATIENTS

Abstract

SUMMARY he heart, by regulating the systemic circulation, and the kidneys, through their effect on extracellular fluid volume, share responsibility for the hemodynamic balance in the body. Disorders of the heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other. It is called Cardiorenal Syndrome (CRS) and is classified into 5 specific subtypes. There are a variety of neurohormonal mediators associated with the deterioration of kidney function in Acute decompansated heart failure. These agents have receptors in the heart, kidneys, and the vasculature that affect volume status, vascular tone, cardiac output and inotropy. A change in the performance of one of these organs elicits a cascade of mediators that affects the other. Understanding these-mediators and effectors yields insight into the diagnosis and therapy of CRS. There are several pathways through which the kidney and the heart cross-talk to each other: the main ones are hemodynamic imbalance and neurohormonal and paracrine signalling activation. On one side, pressure, fluid overload, sodium retention, altered electrolyte levels and academia (due T Summary Management of Cardiorenal Syndrome in Intensive Care Patients 102 to renal failure) may contribute to enhance ventricular dysfunction, accelerating cardiac remodelling and so increasing the risk of arrhythmias. On the other, myocardial dysfunction promotes the worsening of kidney function, so that a vicious circle is triggered: hypervolemia, rennin-angiotensinaldosterone system activation, inflammatory cytokines, nitric oxide dysregulation, oxidative and mechanical stress and increase in myocardial oxygen consumption are all factors that lead to myocytes injury and death. Serum creatinine (sCr) is an insensitive and unreliable biomarker during acute changes in kidney function as it is a marker of function rather than injury, and its concentration does not increase until about half of the kidney function is lost. Urinary biomarkers early predictive biomarkers indicating renal structural damage at an earlier stage may potentially allow timely intervention in high-risk patients at a point when damage is still reversible may be able to identify renal injury more quickly and specifically than serum creatinine. It is important to ensure optimal fluid status and perfusion pressure to prevent kidney injury from low perfusion. So volume depletion should be corrected. A vasopressor may be added after adequate volume resuscitation in hypotensive patients to maintain mean arterial pressure. However, volume overload should be avoided and, if it occurs, requires prompt treatment. So strict monitoring of fluid balance is essential and volume loading should be avoided in patients who have Summary Management of Cardiorenal Syndrome in Intensive Care Patients 103 increased preload even if they manifest evidence of acute kidney injury (AKI), as continued fluid administration to fluidoverloaded AKI patients is an important mechanism of CRS type 3. Fluid removal is the mainstay of therapy in ADHF and the same is true for CRS type 3. However, although reducing fluid overload with diuretic therapy can improve symptoms, there is also concern about potential injury to the kidney in the setting of AKI. Diuretic use in AKI patients has been associated with an increased risk of death and has shown no benefit in recovery of kidney function. Diuretic resistance is the inability to decongest a patient with ADHF with escalating doses of diuretics, and has been attributed to renal insufficiency, mesenteric edema and increased distal tubular sodium reabsorption. Continuous infusion of a loop diuretic avoids the enhanced sodium reabsorption during the intra-diuretic period from which both oral and intravenous bolus loop diuretics suffer, thereby facilitating a slow and gradual diuresis that limits renal injury.