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Bài giảng Managing chronic heart failure patient in chronic kidney disease – BS. Trần Hữu Hiền

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Bài giảng “Managing chronic heart failure patient in chronic kidney disease” trình bày các nội dung: Epidemiology, pathophysiolog, management, modification of risk factors, angiotensin-converting enzyme inhibitors,… Mời các bạn cùng tham khảo nội dung chi tiết.

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Nội dung Text: Bài giảng Managing chronic heart failure patient in chronic kidney disease – BS. Trần Hữu Hiền

  1. 1 Managing Chronic Heart Failure Patient in Chronic Kidney Disease BS TRẦN HỮU HIỀN ĐHYK PHẠM NGỌC THẠCH
  2. INTRODUCTION 2  Epidemiology  Pathophysiology  Management  Modification of risk factors  Diuretic  Angiotensin-converting enzyme inhibitors  Angiotensin II receptor blockers  Beta-blockers  Digoxin  Oxidative stress and hemodialysis patients
  3. 3 EPIDEMIOLOGY
  4. 4 U.S. Renal Data System. USRDS 2012 Annual Data Report: Atlas of ChronicKidney Disease and End-Stage Renal Disease in the United States. Bethesda, MD: National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases; 2012
  5. 5 PATHOPHYSIOLOGY
  6. CARDIO-RENAL SYNDROMES (CRS) GENERAL DEFINITION 6 Disorders of the heart and kidneys whereby acute or chronic dysfunction in one organ may induce acute or chronic dysfunction of the other ACUTE CARDIO-RENAL SYNDROME (TYPE 1) Acute worsening of cardiac function leading to renal dysfunction CHRONIC CARDIO-RENAL SYNDROME (TYPE 2) Chronic abnormalities in cardiac function leading to renal dysfunction ACUTE RENO-CARDIAC SYNDROME (TYPE 3) Acute worsening of renal function causing cardiac dysfunction CHRONIC RENO-CARDIAC SYNDROME (TYPE 4) Chronic abnormalities in renal function leading to cardiac disease SECONDARY CARDIO-RENAL SYNDROMES (TYPE 5) Systemic conditions causing simultaneous dysfunction of the heart and kidney House AA, Anand I, Bellomo R, Cruz D, Bobek I, Anker SD, Acute Dialysis Quality Initiative Consensus Group. Defiition and classifiation of cardio-renal syndromes: workgroup statements from the 7th ADQI consensus conference. Nephrol Dial Transplant 2010;25(5):1416–20
  7. 7
  8. 8 MANEGEMENT
  9. Modification of risk factors* 9 1. Smoking cessation 2. Exercise 3. Weight reduction to optimal targets 4. Lipid modification recognizing 5. Optimal diabetes control HbA1C
  10. Diuretics 10 Major clinical role in reducing fluid overload in patients with chronic HF and pulmonary congestion* *Eur Heart J. 2005 Jun;26(11):1115-40. Epub 2005 May 18.
  11. Diuretics 11  First-line loop diuretics GFR ≤30 mL/min per 1.73 m2  The dosage of the loop diuretic should be progressively increased until the effective dose is reached  Intravenous bolus more effective than oral dose, because bypassing the gastrointestinal tract overcomes impaired drug absorption due to gut edema seen in advanced HF  The effective oral or intravenous dose of loop diuretics should be administered as often as needed to maintain the response World J Cardiol 2010 May 26; 2(5): 112-117
  12. Diuretic Resistance 12  Sequential blockade of sodium reabsorption in the nephron can be instituted by administering a distal-acting diuretic, such as hydrochlorothiazide or metolazone, along with a loop diuretic in a dose determined according to the patient’s renal function  Continuous intravenous infusion of diuretics may be more effective in resistant cases, prevents the post-diuretic salt retention associated with sequential doses* * J Am Coll Cardiol. 1996 Aug;28(2):376-82.
  13. Diuretic Adverse Effects 13  Decrease in renal function  Hypovolemia  Hypokalemia  Hyponatremia
  14. Angiotensin-converting enzyme 14 inhibitors  Patients with chronic HF, mild-to-moderate renal insufficiency should not be viewed as a contraindication to ACE inhibitor therapy, and a mild and nonprogressive worsening of renal function during initiation of therapy should not be considered an indication to discontinue treatment, as the drug may offer the dual benefit of reducing disease progression in both the heart and the kidney. Arch Intern Med. 2000 Mar 13;160(5):685-93.
  15. Angiotensin-converting enzyme 15 inhibitors  In patients with moderate or severe renal insufficiency, therapy with low doses of ACE inhibitors should be initiated and the dose should be increased gradually with careful monitoring of renal function and serum electrolytes. World J Cardiol 2010 May 26; 2(5): 112-117
  16. Angiotensin-converting enzyme 16 inhibitors  When the initiation of ACE inhibitor therapy leads to an increase in serum creatinine levels >30% above baseline  ACE inhibitors should be discontinued,  The patients should be evaluated for conditions causing renal hypoperfusion: excessive depletion of circulating volume due to intensive diuretic treatment, concurrent administration of vasoconstrictor agents [most commonly, nonsteroid anti-inflammatory drugs (NSAIDs)] and severe bilateral renal artery stenosis. Unless renal vascular disease is present, therapy with an ACE inhibitor can be reinstituted after correction of the underlying cause of reduced renal perfusion World J Cardiol 2010 May 26; 2(5): 112-117
  17. Risk of hyperkalemia associated 17 with ACE inhibitors*  Discontinuation of drugs known to interfere with renal potassium excretion (e.g. NSAIDs, including cyclooxygenase-2 inhibitors),  Administration of a low potassium diet  Sodium bicarbonate in patients with metabolic acidosis  A potassium level of >5.5 mEq/L should prompt a reduction in the ACE inhibitor dose. *N Engl J Med. 2004 Aug 5;351(6):585-92.
  18. Angiotensin II receptor blockers 18  Alternative in patients intolerant of ACE inhibitors due to cough,  Combination with ACE inhibitors in patients who remain severely symptomatic on conventional therapy Am Heart J. 2007 Jun;153(6):1064-73.
  19. Beta-blockers 19  Recommended for all patients with stable mild, moderate or severe HF who are on standard treatment including diuretics and ACE inhibitors*  In the SOLVD study, treatment with beta-blockers was associated with a 30% decrease in the risk of worsening renal function, both in the ACE inhibitor and the placebo groups (RR 0.70, 95% CI 0.57- 0.85)** *J Am Coll Cardiol. 2004;44:1587-1592 **Am Heart J. 1999 Nov;138(5 Pt 1):849-55.
  20. Digoxin 20  Not affect survival but led to a 28% reduction in HF hospitalizations.  Used safely in patients with HF and renal insufficiency,  Initiated without a loading dose and maintained at a low dose (0.125 mg), alternating days  Serum digoxin levels should be monitored to maintain a serum concentration in the acceptable range of 0.5-1.0 ng/mL  Monitor carefully for symptoms and signs of digoxin toxicity. N Engl J Med. 1997 Feb 20;336(8):525-33.
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