Cardio Renal Syndrome CRS All types.pptx

Cardio Renal Syndrome the effects of kidney failure on heart and vice versa

1. CARDIORENAL SYNDROME

2. Case 18 Months Female Child. Mother complained of fast breathing since birth. Suck rest suck cycle and feeding diaphoresis present. Non Syndromic. ECHO – ACHD/ Inc Qp / Large Muscular VSD 8mm/ Coarctation of Aorta (Distal to LSCA; ~10mm tight stenosis) – Arch Hypoplasia. Valves Normal. Lved – 20mm/m2; Posterior Wall – 5mm; EF – 65%; LV hypertrophy.

3. Surgery Trans RA Dacron Patch VSD Closure + Pericardial Patch Aortoplasty . On 12 th of October, 2023. Aortic Cross Clamp Time : 103 Minutes. CPB Time : 200 Minutes. Off Clamp; CHB +.

4. Course During ICU Stay. Upon Shifting : Peripheral Temp : 31.8 C Core Temp : 39.8 C Heart Rate : 132 / min on DDD. RA Pressure : 10 IBP : 98/76 mmHg on Inf. Dobutamine @10 Mics but stopped after 2 hours of transfer to ICU and Inf. NTG @2 Mics. Urine Output : 40/20/10. Drains : Minimal.

5. Day 1 Infusion Milrinone @0.5 Mics started (RV Dysfunction +++); TAPSE 3mm Sedation Discontinued. Infusion Albumin + Lasix started @0.3 mg per hour. (Net -83mL) Day 2 Infusion SNP and NTG tapered off. Milrinone and Lasix Continued. Net +84 mL. RV Dysfunction MILD. PASP 45. Child Extubated.

6. Day 3 Net balance + 47 mL. TTE – Severe PAH; Severe TR; PASP 70. Child was reintubated in view of Tachypnoea and Resp Distress. Inf. Dobutamine restarted. ~ 8 Hours of Anuria. Peritoneal Dialysis initiated. Inf Lasix Stopped.

7. EVOLUTION OF DEFINITIONS Cardiorenal Syndrome (CRS) refers to a group of diseases where either the heart or the kidneys are damaged. Understanding how the heart and kidneys interact is crucial for treating these conditions, whether they're acute or chronic. Managing CRS is complex and requires a team of experts who understand the underlying causes. Identifying and understanding the underlying issues in CRS can significantly improve patient outcomes. Working Group of the National Heart, Lung, and Blood Institute in 2004

8. EVOLUTION OF DEFINITIONS Acute Dialysis Quality Initiative in 2008. Classified CRS into 2 major groups, cardiorenal and renocardiac syndromes, based on the primary cause of the disease process. This was further grouped into 5 subtypes based on disease acuity and sequential organ involvement

9. CLASSIFICATION OF CRS BASED ON THE CONSENSUS CONFERENCE OF THE ACUTE DIALYSIS QUALITY INITIATIVE

10. AKI DEFINITION AND STAGING ACCORDING TO KDIGO CRITERIA KIDNEY DISEASE: IMPROVING GLOBAL OUTCOMES

11. AKI DEFINITION AND STAGING ACCORDING TO KDIGO CRITERIA KIDNEY DISEASE: IMPROVING GLOBAL OUTCOMES

12. CAUSES OF ACUTE KIDNEY INJURY: EXPOSURES AND SUSCEPTIBILITIES FOR NONSPECIFIC ACUTE KIDNEY INJURY

13. PATHOPHYSIOLOGICAL MECHANISMS IN CRS Cardiorenal Syndrome : A condition in which there is a dysfunctional interaction between the heart and the kidneys. It can be bidirectional. It can be acute / chronic. It could be reversible / irreversible. How do the heart and kidneys work together normally? What happens if one fails? What happens if both fail?

14. HOW ARE THEY SUPPOSED TO WORK? Pumps Blood Perfuse Organs and Tissues Supply oxygen and nutrients. Regulate Extracellular Fluid Volume. Excrete Metabolic Waste Products. Allows Heart to function with Maximum Efficiency.

15. WHAT HAPPENS WHEN HEART DOES NOT WORK? Pumps Blood Perfuse Organs and Tissues Supply oxygen and nutrients. Regulate Extracellular Fluid Volume. Excrete Metabolic Waste Products. Allows Heart to function with Maximum Efficiency. Decreased CO. Decreased SV. Decreased Renal Blood Flow. Decreased GFR. Increased Metabolic Waste. Raised Sodium and Water Reabsorption.

16. HEART FAILURE DECREASED CARDIAC OUTPUT DECREASED STROKE VOLUME DECREASED EFFECTIVE CIRCULATING VOLUME (BARORECEPTORS) INCREASED RAA INCREASED SNS INCREASED ADH VASOCONSTRICTION; INCREASED SODIUM REABSORPTION. INCREASED WATER REABSORPTION. DECREASED RENAL SODIUM AND WATER EXCRETION. EDEMA INCREASED CAPILLARY HYDROSTATIC PRESSURE INCREASED INTRAVASCULAR VOLUME INCREASED VENOUS PRESSURE

17. CRS IN THE ACUTE SETTING CRS-I R apid decrease in cardiac function leading to acute kidney injury (AKI). High CVP = Impaired Glomerular Function. High RAAS = Detrimental to Kidneys. Oxidate Stress and Nephrotoxic Drugs CRS - III AKI, ischemia, or glomerulonephritis leading to acute cardiac impairment. Higher risk of heart failure, ACS, cerebrovascular disease. CRS – I ACUTE CARDIO RENAL CRS – III ACUTE RENO CARDIAC

18. CRS IN THE CHRONIC SETTING CRS- II Chronic cardiac dysfunction leading to chronic kidney disease (CKD). Both CKD and heart failure (HF) are chronic inflammatory conditions . HF with preserved or reduced ejection fraction, AF, and IHD contribute to CRS-2. TNF-alpha and IL-6 promotes inflammation in the kidneys. Erythropoietin deficiency . CRS- IV CKD as the cause of cardiac dysfunction . CAD and chronic HF common in end-stage renal disease (ESRD) patients. F ibroblast growth factor-23 (FGF23) progress CKD. CRS – II CHRONIC CARDIO RENAL CRS – IV CHRONIC RENO CARDIAC

19. SYSTEMIC CRS CRS-V Systemic illness simultaneously damages both the heart and the kidneys. CRS-V can be classified into four stages based on the disease's pathophysiological process and severity: hyperacute (0–72 hours), acute (3–7 days), subacute (7–30 days), and chronic (beyond 30 days). Sepsis, connective tissue diseases like lupus, amyloidosis, sarcoidosis, and cirrhosis. Complement factors, inflammatory cytokines, RAAS activation. Septic shock further exacerbates endothelial dysfunction and autoregulation issues.

20. BIOMARKERS USEFUL TO SUPPORT THE DIAGNOSIS OF CRS

21. BIOMARKERS OF GLOMERULAR FUNCTION Creatinine and plasma urea levels to calculate estimated glomerular filtration rate (eGFR). Serum urea = glomerular filtration; tubular reabsorption and neurohormonal activity. Cystatin C = early stages of acute kidney injury (AKI) Cystatin-C may be a better diagnostic marker for renal impairment in early AKI compared to creatinine. Elevated cystatin-C levels ~ coronary artery disease. Cystatin C, alone or in combination with creatinine, improving risk stratification and the prediction of mortality.

22. BIOMARKERS OF TUBULAR FUNCTION KIM-1 kidney injury molecule-1 = PCT damage; elevated following toxic or ischemic renal injury. NGAL neutrophil gelatinase-associated lipocalin (lipocalin-2) = Tubular Cells in response to acute tubular damage. Liver fatty acid-binding protein (L-FABP) marker for tubular function, with higher urine L-FABP concentrations observed in ADHF patients developing AKI.

23. URINARY BIOMARKERS Urinary electrolyte levels and volume. Early natriuretic response decline is linked to HF. While 24-hour urine collection-based glomerular filtration rate (GFR). Creatinine clearance can be employed when GFR predictions based on calculations are uncertain. Albuminuria serves as a useful tool to assess glomerular integrity.

24. CARDIAC BIOMARKERS Cardiac troponin T ( cTnT ) - predictive potential - AKI following heart surgery Subjects who developed AKI had significantly higher cTnT concentrations compared to those without AKI. Elevated concentrations of natriuretic peptides have relevance in various types of cardiorenal syndrome (CRS). Copeptin, soluble ST2 (sST2), and Galectin-3 have been explored in the context of cardiac stress, remodeling, and fibrosis in CRS.

25. OTHER BIOMARKERS IN CRS PATIENTS Elevated levels of aldosterone and plasma renin-activity (PRA) are strongly associated with worsening renal function (WRF) in ADHF. In subjects who experienced myocardial damage from sudden cardiac arrest (SCA), higher levels of cardiac troponin I ( TnI ), interleukins (IL-1 and IL-10), and endothelin-1 (ET-1) are linked to the development of acute kidney injury (AKI), with IL-6 and ET-1 playing a significant role in the interaction between cardiac and renal impairment in this context.

26. MANAGEMENT AND THERAPEUTIC APPROACH

27. CRS IN THE ACUTE SETTING. In CRS-1, regular kidney function assessment. Focus on assessing worsening renal function (WRF) onset, causes, diuretic response, and functional status. Complete decongestion. Up-titration of diuretic dosage. Reinitiating and up-titrating RAAS blockers. Vasodilators for hemodynamically stable ADHF patients, and ultrafiltration – last resort. The use of vasopressors, inotropes, or mechanical assistance should be evaluated for those with hypotension and inadequate diuretic response.

28. In CRS-3, the treatment approach depends on the cause and severity of acute kidney injury (AKI) and the type of acute cardiac damage. Loop diuretics. Renal replacement therapy (RRT) non-recoverable AKI with complications like hyperkalemia, acidemia, and fluid overload. Negative daily fluid balance with RRT is associated with a better prognosis in subjects with oliguric AKI and critical fluid overload.

29. OCCURANCE OF WRF DURING TREATMENT DECONGESTIVE THERAPY IN AHF YES CHECK DIURETIC RESPONSE NO NO WRF CONTINUE DECEONGESTIVE THERAPY TILL DRY GOOD PSEUDO WRF CONTINUE DECEONGESTIVE THERAPY TILL DRY MONITOR CREAT AND ELECTROLYTES RE EVALUATE DECONGESTION DAILY POOR CHECK FOR CONGESTION ABSENT ASSESS CVP CONSIDER TTE MEASURE IAP IF INCREASED IAP; CONSIDER PARACENTESIS PRESENT PSEUDO WRF / WRF MONITOR CREAT AND ELECTROLYTES IF HYPOPERFUSION; CONSIDER INOTROPES; MCS CHECK FOR HYPOPERFUSION AND HYPOTENSION ABSENT INCREASE DIURETIC INTENSITY AND CONSIDER IV VASODILATORS DISCONTINUE / REDUCE BP LOWERING AGENTS AND CONSIDER INOTROPES AND VASOPRESSORS IN CARDIAC OUTPUT IS LOW WRF DUE TO CONGESTION ACHIEVE DECONGESTION. REDUCE DIURETIC DOSE WHEN DRY. RECHECK LABS FREQUENTLY THERAPY RESISTANT WRF. ICU ADMISSION CONSIDER INVASIVE HD GUIDED THERAPY (MCS) CONSIDER ULTRAFILTRATION. WRF DUE TO HYPOPERFUSION / HYPOTENSION. INVASIVE HD MONITORING. ICU ADMISSION RECHECK LABS FREQUNTLY. AVOID HIGH DOSE INOTROPES CONSIDER REDUCING DOSES GDMT IMPROVEMENT NO IMPROVEMENT IMPROVEMENT PRESENT

30. OLIGURIA ? ACUTE KIDNEY INJURY (AKI) YES MEASURE URINARY AND SERUM SODIUM; SR. UREA AND SR. CREAT. NO ELIMINATE OFFENDING DRUGS GLUCOCORTICOIDS OTHER RENAL ULTRASONOGRAPHY. URINARY SODIUM <30 mEq /L Sr. UREA/ Sr. CREAT RATIO >20/1 PRE RENAL AKI VOLUME DEPLETION ADMINISTER FLUIDS. AHF. DECONGESTIVE THERAPY HYDRONEPHROSIS BILATERAL SMALL KIDNEYS NORMAL SIZE KIDNEYS POST RENAL AKI REMOVE OBSTRUCTION. PARENCHYMAL DISEASE CKD. URINE ANALYSIS; RENAL BIOPSY INTERSTITIAL NEPHRITIS ACUTE TUBULAR NECROSIS GLOMERULONEPHRITIS AND VASCULITIS ELIMINATE NEPHROTOXINS TREAT UNDERLYING CAUSE IMMUNOSUPPRESSANTS

31. CRS IN THE CHRONIC SETTING OPTIONS : ACEI, ARBs, ARNI, MRA, SGLT2i. RAAS blockers can decrease GFR in baseline CKD patients. Sacubitril/valsartan has shown a more favorable impact on GFR reduction compared to enalapril and maintains its positive effects on mortality rates even in individuals with severe CKD. MRA introduction and SGLT2 inhibitors can also result in an acute decrease in GFR, with SGLT2 inhibitors showing long-term stability in eGFR compared to placebo.

32. CHRONIC HEART FAILURE WITH WRF DURING FOLLOWUP YES DURING UPTITRATION OF RAAS INHIBITOR NO NO WRF NO ACTION NEEDED CHECK KFT AND ELECTROLYTES EVERY 4 MONTHS. PRESENCE OF CONGESTION DISCONTINUE RAAS BLOCKERS, CONSIDER OTHER FORMS OF AFTERLOAD REDUCTION HYPER K >5 MEQ/L S.CR >100% INCREASE PSEUDO WRF. TOLERATE CHANGES IN RENAL FUNCITON. CHECK KFT AND ELECTROLYTES EVERY 4 MONTHS. YES S.CR <50% INCREASE + S.CR <3 MG AND GFR STILL >25 ML/MIN YES NO NO YES IMPROVEMENT PSEUDO WRF. CONSIDER RECHALLENGE CONSIDER REDUCING LOOP DIURETIC DOSE. NO YES TREAT CONGESTION TRUE WRF STOP OTHER NEPHROTOXINS. CONSIDER RENAL ARTERY STENOSIS. CONSIDER OTHER CAUSES. NEPHROLOGY CONSULT. NO IMPROVEMENT IMPROVEMENT TRUE WRF DUE TO CONGESTION . ACHIEVE DECONGESTION. REDUCE DIURETICS IF DRY RECHECK LABS FREQUENTLY. CHECK FOR HYPOPERFUSION OR HYPOTENSION. REDUCE DIURETICS / RAASI/ ANTIHYPERTENSIVES. PRESENT TRUE WRF OR INTRINSIC RENAL DISEASE INTRAGLOMERULAR HYPERTENSION CANDIDATE FOR SGLT 2 INHIBITORS NEPHROLOGY CONSULT NO IMPROVEMENT THERAPY RESISTANT WRF . ICU ADMISSION. HD GUIDED THERAPY. CONSIDER MCS AND TRANSPLANT CONSIDER MHD. IMPROVEMENT TRUE WRF. STOP NEPHROTOXINS. CONSIDER CONTINUOUS OR INTERMITTENT INOTROPIC SUPPORT. CONSIDER THERAPIES OF CRT, MCS, TRANSPLANT IF APPROPRIATE. NO

33. SYSTEMIC CRS In CRS-5 - manage the underlying systemic condition. For septic CRS-5, - eradicating the infection, administering antibiotics, and providing supportive care. Intravenous fluid management and the use of vasopressors or inotropic medications. If renal damage persists despite fluid optimization and hemodynamic interventions, renal replacement therapy (RRT) may be recommended as a treatment option.

34. CONCLUSION Understanding the intricate relationship between the heart and the kidney is essential. Multidisciplinary approach focused on understanding the underlying causes and mechanisms. Recognizing and characterizing the pathophysiology of CRS. Comprehensive knowledge of CRS.

35. THANK YOU

36. CKD is defined as kidney damage or glomerular filtration rate (GFR) <60 mL/min/1.73 m(2) for 3 months or more, irrespective of cause.