Bài giảng managing chronic heart failure patient in chronic kidney disease – BS trần hữu hiền

Managing
Chronic Heart Failure Patient
in Chronic Kidney Disease
BS TRẦN HỮU HIỀN
ĐHYK PHẠM NGỌC THẠCH
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INTRODUCTION

Epidemiology

Pathophysiology

Management
 Modification of risk factors

Diuretic

Angiotensin-converting enzyme inhibitors

Angiotensin II receptor blockers
 Beta-blockers

Digoxin

Oxidative stress and
hemodialysis patients
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EPIDEMIOLOGY
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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
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PATHOPHYSIOLOGY
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CARDIO-RENAL SYNDROMES (CRS) GENERAL DEFINITION
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
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MANEGEMENT
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Modification of risk factors
*
1. Smoking cessation
2. Exercise
3. Weight reduction to optimal targets
4. Lipid modification recognizing
5. Optimal diabetes control HbA1C <7% (53 mmol/mol)

6. Optimal BP control <130/80 mm Hg
7. Aspirin is indicated for secondary prevention but not primary prevention
8. Correction of anemia to individualized targets
* KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease
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Diuretics
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.
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Diuretics

First-line loop diuretics GFR ≤30 mL/min per 1.73 m
2

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
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Diuretic Resistance

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.
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Diuretic Adverse Effects

Decrease in renal function

Hypovolemia

Hypokalemia

Hyponatremia
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Angiotensin-converting enzyme
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.
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Angiotensin-converting enzyme
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
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Angiotensin-converting enzyme
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
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World J Cardiol 2010 May 26; 2(5): 112-117
Risk of hyperkalemia associated
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.
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Angiotensin II receptor blockers

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.
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Beta-blockers

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.

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Digoxin

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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Oxidative stress and
hemodialysis patients

Supplementation with 800 IU/day vitamin E reduces
composite cardiovascular disease endpoints and myocardial infarction*

Treatment with acetylcysteine (600 mg
BID) reduces composite cardiovascular end points**
**Circulation. 2003 Feb 25;107(7):992-5.*Lancet. 2000;356:1213-1218.
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HOME MESSAGE

Modification of risk factors


ACE inhibitors, ARBs, and β-blockers are the fist-line drugs treat HF in
CKD

Loop diuretics are the first line treat fluid overload

Digoxin use low dose (0.125mg) and close monitoring

Oxidative stress and hemodialysis patients: vitamin E
and acetylcysteine
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THANKS FOR LISTENING
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