Heart-failure or Kidney Failure?

Transcription

1 Heart-failure or Kidney Failure? Dr Ajith James Consultant Nephrologist Barts Health and BHRUT Mr AR 65 yrs Case Type 2 DM, IHD-MI 1998, PCI x 3. CABG 2008, HT CCF with LVEF 30% NYHA Class 2 Heart-Failure. Has had 2 admissions to hospital with decompensated HF in the last year. Progressive worsening of dyspnoea over the past 2-3 weeks, currently symptomatic at less than ordinary activities of life. On Aspirin 75mg od, Bisoprolol 5mg od, Amlodipine 10mg od, Ramipril 5mg od, Frusemide 40mg od, Spironolactone 25mg od, Simvastatin 40mg od. Case O/E BP 105/65 HR 95/min JVP elevated 8cms. Sats 93% on air. Oedema upto knees Loud PSM in the left sternal border Few crackles in the lung bases Oliguric ~20mls/hr Electro-Cardiogram Sinus Rhythm at 95bpm Poor R wave progression in Chest leads Lateral and inferior ST depression (II, III, AVF,V3-V6) 1

2 Blood tests Hb 10.8 cca 2.23 WCC 8.2 Phos 1.92 PLT 180 Echocardiogram LVH. Moderate LV systolic dysfunction with EF 25% Dialated LA with normal mitral valve function Dialated RV with severe TR Na 133 Bil 22 K 4.5 ALT 32 Urea 23.5 (15.2) Alk P 252 Creat 232 (165) Alb 40 Urine dipstick- NAD Renal Investigations Renal US: Normal sized symmetrical and un-obstructed kidneys. What would you do next? Fluid restrict to 1.5L/day and salt restrict Weight monitoring Increase Frusemide progressively to achieve a weight-loss of 1-1.5kgs/day Look for causes of acute decompensation- arrhythmias, ischemia, infection, poor compliance with medications and fluid-restriction. Close monitoring of clinical condition, electrolytes and renal function. 2

3 Acute decompensated CCF Type 2 Diagnosis Stop Diuretics? Stop Ramipril? Stop Amlodipine? Stop Bisoprolol? What would you do next? Give IV Fluids? What would you do next? Fluid restrict to 1L/day and salt restrict. Do not give IV Fluids! Stop Ramipril Stop Amlodipine and reduce Bisoprolol (BP 105/65) Increase Frusemide to 80mg bd Weight monitoring Close monitoring of clinical condition, electrolytes and renal function Look for causes of acute decompensation- arrhythmias, ischemia, infection, poor compliance with medications and fluid-restriction. (CRS) Patients with HF and worsening renal functions have a poor prognosis. Patients with CKD have associated coronary artery disease and HF. CKD causes salt & fluid retention. Complications of CKD predisposes to HF- eg Anemia, BMD, Salt and Water overload. Decompensating HF and worsening renal functions may be a reason to escalate HF therapy. Eg Device therapies like CRT. 3

4 ACEI intolerance in low CO, low SVR states (CRS) GFR Maintained GFR Declines A pathophysiological disorder of the heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction in the other organ. Circulation 2001:104:1985 CRS has five subtypes: Type I, acute CardioRenal Syndrome Type II, chronic CardioRenal Syndrome Type III, acute RenoCardiac Syndrome Type IV, chronic RenoCardiac Syndrome Type V, secondary CRS, meaning systemic diseases such as diabetes, sepsis and amyloidosis causing simultaneous cardiac and renal dysfunction. Background Pathophysiology Management Options Congestive Heart Failure Epidemiology changing from acute management to managing the chronicity of cardiac dysfunction Incidence: 1 in 1000 population per year; increasing by about 10% every year. In >85y incidence is 10 cases per 1000 [DH, 2000]. Prevalence: ranges from 3-20 cases per 1000 population, increasing to at least 80 cases per 1000 in people aged 75 years and over [DH, 2000]. Morbidity & Mortality: Responsible for about 100,000 yearly hospitalizations in the UK (mean LOS 12 days) 40% die within the first year of diagnosis 24,000 deaths annually BHF Heart Failure Supp

5 Percent of Population 3/17/2017 Prevalence of Congestive Heart Failure by Age and Sex NHANES: Prevalence is rising Ages Men Women Source: CDC/NCHS and NHLBI. Survival after diagnosis of cancer or heart disease 100 Survival % Men: MI Bladder Ca Prostate Ca Bowel Ca Heart Failure 0 Lung Ca Months from diagnosis Levy, NEJM 2002; 347: Stewart S, EJHF 2001; 3: Survival after diagnosis of cancer or heart disease in women: Where does breast cancer lie? Cardiovascular Outcomes with renal dysfunction Stratified by GFR 100 Survival % Breast cancer Ca MI Ovarian Ca Bowel Ca Heart Failure Cumulative incidence Cardiovascular death Unplanned ADHF admission reduced LVEF (LVEF<=40%) Stratified by GFR Lung Ca LV systolic function (LVEF>40%) Months from diagnosis Hillege, H. L. et al. Circulation 2006;113:

6 CHF patients at increased risk for CRS: ohypertension odiabetes osevere Vascular Disease oelderly Comorbid Conditions... Associated with a worse prognosis Anemia (Hb < 10.0) Cirrhosis Peripheral Vascular Disease Hyponatremia (<135) Renal failure N Engl J Med 2006; 355: July 20, 2006 Background Pathophysiology Causes Management Conclusions Pathophysiology Neurohormonal Factors: SNS, RAAS, AVP System Hemodynamics: Loss of Cardiac Output Transrenal perfusion pressure Intrarenal hemodynamics Neurohormonal Axis Adenosine 6

7 CVP and Heart Failure Kaplan-Meier Analysis of Event-Free Survival According to Tertiles of CVP Damman, K. et al. J Am Coll Cardiol 2009;53: Curvilinear Relationship Between CVP and egfr According to Different Cardiac Index Values Solid line = cardiac index <2.5 dashed line = cardiac index 2.5 to 3.2 dotted line = cardiac index >3.2 Transrenal perfusion pressure TRPP = MAP - CVP CVP influenced: PAP -- Oxygenation, Valve Dysfunction, CO Volume Status MAP -- Perfusion Pressure Cardiac Output Systemic Vascular Resistance Renal Hemodynamics p = Central Venous Pressure Damman, K. et al. J Am Coll Cardiol 2009;53:

8 Renal Hemodynamics Ultimately lack of adequate transrenal perfusion pressure: Renal Hypoxia Inflammation / Cytokine Release Progressive loss of nephron function and structural Activation of the Neurohormonal cascade Background Pathophysiology Causes Management Conclusions Background Pathophysiology Causes Management Options ACA/AHA Guidelines on HF- Goals of therapy Eliminate Clinical Evidence of fluid retention Peripheral and Pulmonary Oedema and elevated JVP Improve patients subjective assessment of symptoms Improve prognosis: ACE/ARB, B Blockers, Aldosterone Antagonists, CRT, ICD Improve survival Reduce Hospital admissions Assessment of fluid status by daily weights 8

9 Diuretics Treatment Goals: Removal of excess fluid volume Optimizing Hemodynamics Management of complications of CKD Optimising Anemia, Acidosis & Mineral-Bone Disease Use of Prognostic medications & therapies Reduced filling pressure: Reduced pre-load and CO leading to increase release of Neuro-Humoral factors Worsening renal function: A marker of renal perfusion and indicates worse prognosis if this happens before euvolemia is achieved. Could also be due to a rate of diuresis that exceed mobilisation of interstitial fluid. Increased congestion of Splanchnic veins from increased intraabdominal pressure in ~ 60% of patients admitted with advanced HF. Aims of treatment Optimise fluid balance by reducing fluid and salt intake and increasing diuresis. Combinations of diuretics eg: Frusemide + Spironolactone +/- Thiazide diuretics. Remember diuresis alone will reduce BP. Often there may be temporary worsening of renal functions, but it may even improve when euvolemia is achieved. Optimise rhythm abnormalities. Optimise HF management- Optimise dose of ACE-I or ARBs, Optimise use of Beta-Blockers. Improve blood flow to the kidneys- Stop other antihypertensives if MAP low and high CVP. Consider device therapies - CRT. Canadian Cardiovascular Society consensus recommendations on heart failure and concomitant renal dysfunction Recommendations Heart failure patients with stable renal function (serum creatinine levels less than 200 μmol/l) should be monitored for serum potassium and creatinine if combination therapy is used or in the presence of potential dehydration (class I, level B). Patients with heart failure with increasing serum creatinine should be assessed for reversible causes such as concomitant medications (eg, nonsteroidal anti-inflammatory drugs), hypovolemia, hypotension, urinary tract obstruction or infection (class I, level C). In oliguric heart failure patients who are hemodynamically stable, diuretics, ACE inhibitors, ARBs, spironolactone and nonheart failure drugs that can impair renal function should be reviewed daily (class I, level C). In stable heart failure patients who are not oliguric but have increasing serum creatinine levels of more than 30% from a previous stable baseline, the dose of diuretics, ACE inhibitors, ARBs and spironolactone may be reduced until renal function stabilizes (class 1, level C). In heart failure patients not responding adequately to more than 240 mg intravenous furosemide daily, treatment options include: More frequent or higher doses of intravenous boluses of diuretic (class IIb, level C); Combination with thiazide diuretic, eg, hydrochlorothiazide or metolazone (class IIA, level B); or Continuous intravenous furosemide infusion (class IIa, level B). MANAGING DIURETIC RESISTANCE/CRS Ultrafiltration Strict fluid and salt restriction IV Frusemide: Work out a Celling dose. Use divided doses. Bolus or Continuous infusion Titrate dose of diuretics up and use combination of diuretics Stop BP lowering agents and ACE temporarily. blockers may be beneficial Drain tense ascites and large pleural effusions?hypoalbuminemia: IV HAS + Frusemide.?Ultrafiltration/Peritoneal Dialysis?Dobutamine rescue 9

10 Peritoneal Dialysis Summary CRS is the result of a complex interaction between the heart and the kidneys. Diuretics are not toxic to the kidneys. Diuresis-related worsening of renal functions is reversible and often improve functions when the circulation improves. Nephrologists can help with volume over-load, treatment of Anemia Erythropetin and consider RRT in patients with relatively preserved LV function. Further treatment aimed at optimising QOL Summary CRS has a high mortality. When the cardiac function is poor, they tolerate treatments like dialysis poorly. Palliative/End-of-life care is important and should be instituted early. At this stage treatment aim should be to preserve/improve QOL. 10