Primary Care Management of Cario-Renal Syndrome. R. Benjamin C. Grant, MS, PA-S OAPA CME Conference ‘13 October 25, 2013. Increasing Burden of Chronic Disease. Increasing Burden of Chronic Disease. Who is our population?. Obese Diabetes Inactive Smokers Hypertensive Fixed Income
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Primary Care Management of Cario-Renal Syndrome R. Benjamin C. Grant, MS, PA-S OAPA CME Conference ‘13 October 25, 2013
Who is our population? • Obese • Diabetes • Inactive • Smokers • Hypertensive • Fixed Income • Fast Food • LOST!
Cardiorenal Syndrome • Objectives • Define Cardiorenal Syndrome • Classifications • Address pathophysiology • Discuss approach to treatment • Highlight Problems with management • Provide recommendations for screening and management • Generic term • Multiple combinations • Acute and Chronic dysfunction of Cardiovascular and Renal systems • Classification • Type I –Acute CV AKI • Type II – Chronic CV CKD • Type III – AKI Acute CV • Type IV – CKD Chronic CV • Type V – Systemic process (sepsis) AKI & Acute CV
Cardiorenal Physiology Cardiovascular Renal • Systemic Perfusion • Maintained by CO and SR • In HF, perfusion can become compromised • End organ damage • Volume homeostasis • Electrolyte balance • pH • Systemic Resistance via RAAS
Cardiorenal Physiology • Intravascular Volume increases • Diuresis • With CKD this can contribute to volume overload • Kidneys are hypoperfused • Intravascular volume • CO • Vascular disease • Systemic Resistance • Increase RAAS
Cardiorenal Physiology • RAAS • BP • Inflammatory pathways • Renal Perfusion • Sodium Retention • Potassium Loss • Evolutionarily Protective • Harmful in the setting of chronic disease
Chronic Kidney Disease • GFR <60 mL/min (KDOQI) • Stage I – normal >90 • Stage II – mild 89-60 • Stage IIIa – 59-45 • Stage IIIb – 44-30 • Stage IV – 29-15 • Stage V - <15 (ESRD) • Treatment • Control volume status • Salt reduction • Protect remaining renal function • Try to avoid Loop diuretics • Start ACE-I/ARB • Avoid NSAIDS • Control Hypertension • Controlled Diabetes • At Stage IV, d/c ACE-I/ARB • Stage V, restart ACE, hemodialysis
Heart Failure • “a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood” Hunt et al. Circulation 2009 • American Heart Association • Stages A and B have risk factors with no current dysfunction • Stage C – current or past symptoms of Heart Failure • Stage D – symptoms refractory to standard therapy • Treatment • Preventative measures • Eg. HTN control, smoking cessation, Lipid goals… • Reduce workload • ACE/ARB (neurohormonal) • Beta blocker • Possibly diuretics • Aldosterone Antagonist • Inotropes • Manage decompensation • Fluid overload, dysrhythmias
Treatment Problem Volume Overload Effects • Common complication of HF • Impacted by Renal Function • Decrease in GFR due to renal injury (AKI) • Activation of RAAS • Increase in Systemic Resistance and thus Workload • RAAS Activation activates proinflammatory and hypercoaguable state • Modest decrease in GFR (<70) • Sig. increase in mortality for pts with HF • Perspective • In 2003, 4.7% GFR (<60) • 6.3% had persistent albuminuria • With increase in chronic diseases, they may be an underestimation
Treatment Problem Preventing decompensation Furosemide • Maintain Euvolemic state • Salt restriction • Most frequent drug class • Loop Diuretics! • Antagonizes Na/K/Cl symporter in ascending Loop of Henle • Loss of Na and K salts and water • Excreted Renally • Can be nephrotoxic in CKD • Increased RAAS activation • In animal models show progression of renal fibrosis
Potential solutions? • Low dose Loop Diuretic • Sigmoidal response curve thus ineffective until high enough dose reached • RAAS antagonism • Could mitigate negative effects of diuretic use • Despite the negative effects of diuretics on renal function, they are still associated with a lower mortality rate than inotropes in acute decompensated heart failure!
Discussion Treatment of Volume Overload How to monitor • Loop Diuretics • RAAS activation • Worsening renal function • Negatively effects volume status and cardiovascular status • Increased risk of adverse outcome • Traditionally • BNP and EF • Clinical assessment • Smith et al. 2006 • Renal impairment holds equal risk as decreased EF • Combining BNP and GFR more predictive for adverse outcome than either alone • Degree of Renal dysfunction directly associated with HF outcomes
Discussion • Decompensation and hospitalization inevitable • Renal function frequently impacted • Even transient renal damage independently predicts increased risk for death or readmission • Even after excluding pts with cardiogenic shock, renal damage from other causes still very common • Mechanism? • Renal and Hepatic dysfunction • Mullens et al. 2009 identifies venous congestion as significant contributor to renal dysfunction
Recommended Management Types 1 & 3 CRS Types 2 & 4 CRS • Type 1 – Acute HF • Treat underlying cause • PCI, Inotropes, Inpatient • Type 3 – AKI • Euvolemia, electrolytes • Dialysis? • Though different etiologies, uniform treatment • Maintaining Cardiac function is Primary Goal! • Renal Function is secondary but not insignificant • Naturally functioning renal system is best management tool for hemodynamics
Conclusions • Patients with Cardiorenal Syndrome can have many etiologies • Provide an interesting and challenging problem for PCPs • Approach to treatment begins with understanding the pathophysiology
Questions? Benjamin Grant, MS, PA-S email@example.com Contact for a copy of presentation or paper
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