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Cardiorenal Syndrome Yerizal Karani SpPD, SpJP SymCARD 2013 Padang- West Sumatera 27-29 Mei 2013

Cardiorenal Syndrome - Cardiology Update FK UNAND

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Cardiorenal Syndrome

Yerizal Karani SpPD, SpJP

SymCARD 2013 Padang-

West Sumatera 27-29 Mei 2013

• HF affects more than 5 million Americans, almost

one-half of them are rehospitalized for ADHF,

• Each year nearly 1 million pts are hospitalized

specifically for ADHF

• Prevalence of HF in US : 2.3%, 500 cases of HF /

year which can double or triple in the next 20 years

• In most patients with HF, a decrease in cardiac

contractility is associated with subendocardial

myocardial ischemia or renal impairment

SymCARD 2013 Padang-

West Sumatera 27-29 Mei

2013

• Krumholz et al 1997: 41 – 55 % patients admitted for HF are rehospitalized with 6 months of their initial discharge

SymCARD 2013 Padang-West

Sumatera 27-29 Mei 2013

SymCARD 2013 Padang-West

Sumatera 27-29 Mei 2013

SymCARD 2013 Padang-

West Sumatera 27-29 Mei

2013

SymCARD 2013 Padang-West

Sumatera 27-29 Mei 2013

• Cardiorenal

syndrome is the

result of an

interaction between

the renal system

and the

cardiovascular

system

• Pathologies that

affect the organ of

one system can

affect the other

General Cause and Effect of Cardiorenal Syndrome

SymCARD 2013 Padang-West

Sumatera 27-29 Mei 2013

Baig MK, Mahon N, McKeena WJ, et al. The pathophysiology of advanced heart failure. Am

Heart J. 1998;135(part 2 suppl):S216-S230.

SymCARD 2013 Padang-West

Sumatera 27-29 Mei 2013

Cycle of Cardiorenal Syndrome

• Neurohormonal activation triggers a cycle of

interrelated cardiac and renal responses

– SNS activity increases blood pressure,

which can increase renal perfusion but

exacerbate hypertension

– RAAS activity stimulates renal sodium

and fluid retention which increase

cardiac preload and afterload unwanted

stressors in the context of HF

• With chronic neurohormonal secretion cardiac and hemodynamic impairments can

progress and eventually overcome the body’s ability to compensate resulting in a

vicious cardiorenal cycle

SymCARD 2013 Padang-

West Sumatera 27-29 Mei

2013

Tipe SYNDROME PATOFISIOLOGI

I Acute Cardiorenal Penurunan fungsi jantung akut (acute cardiogenic

shock atau ADHF) yang menyebabkan Gangguan

Ginjal Akut (GgGA)

II Chronic Cardiorenal Penurunan fungsi jantung kronis (gagal jantung

kongestif) yang menyebabkan penyakit ginjal kronis

(PGK)

III Acute Renocardiac Penurunan fungsi ginjal akut (iskemi atau

glomerulonefritis) menyebabkan gangguan jantung

akut (aritmia,iskemia,infark)

IV Chronic Renocardiac Penurunan fungsi ginjal kronis (iskemi atau

glomerulonefritis kronikfungsi ) menyebabkan

gangguan jantung kronis ( LVH, gagal jantung, PKV

lainnya)

V Secondary Cardiorenal Kondisi sitemik (diabetes mellitus, sepsis)

menyebabkn gangguan kedua organSymCARD 2013 Padang-West

Sumatera 27-29 Mei 2013

SymCARD 2013 Padang-West

Sumatera 27-29 Mei 2013

Schoolwerth AC, et al. Renal Considerations in Angiotensin Converting Enzyme Inhibitor Therapy: Circulation 2001;104;1985-1991SymCARD 2013 Padang-West

Sumatera 27-29 Mei 2013

SymCARD 2013 Padang-

West Sumatera 27-29 Mei

2013

Common Comorbidity of CKD

• DM

• Poorly controlled hypertension

• Elevated triglyceride levels

• Decreased HDL level

• Increased Lp(a)

• Peripheral Vascular Disease

SymCARD 2013 Padang-West

Sumatera 27-29 Mei 2013

SymCARD 2013 Padang-West

Sumatera 27-29 Mei 2013

Other Clinical Factors to Consider

• In addition to the types of comorbidities present, other general factors to consider are

• Patient age

• Duration of cardiac and renal impairments

• Drug therapies

• Specific factors to consider in cardiorenal syndrome include

– Creatinine level

– Glomerular filtration rate (GFR)

• Clinical studies have shown that creatinine levels and GFR are predictive of ortality risk in patients with HF

SymCARD 2013 Padang-West

Sumatera 27-29 Mei 2013

• Forman DE, Buttler J Wang Y. et al. Incidence, predictors at admissions & impact of worsening renal function among

patients hospitalized with heart failure. JACC 2004;43:61-67

• Krumholz, Chen YT. Correlation and impact on outcoumes of worsening renal functions in patiens >65yo with HF. Am J

Cardiol 2000:85 (9):1110-3

Specific Factor : Creatinine Level

• In a prospective study of 412 patients hospitalized for HF,

– 75% had creatinine elevations of >0.1 mg/dL

– 24% had creatinine elevations of > 0.5 mg/dL

• Large Creatinine increases predicted the highest mortality risks

– However, even minor changes were associated with adverse

outcomes

– Large elevations were more important predictors than single

baseline measures

• In clinical practice, definitions of worsening renal function differ

– Absolute creatintie increase form >0.1 to >0.5 mg/dL

– Increase of 25% from baseline creatinine values

How we define worsening renal function will affect the number of

patients we identify as being at risk for mortality

SymCARD 2013 Padang-West

Sumatera 27-29 Mei 2013

SymCARD 2013 Padang-West

Sumatera 27-29 Mei 2013

SymCARD 2013 Padang-West

Sumatera 27-29 Mei 2013

Treatment of Patients with Cardiorenal Syndrome

• No evidence from clinical HF trials.

• Inhibitors of RAAS are cornerstone of management of LVs dysfnction, prevent progressive renal dysfunction in diabetic.

• ACE inhibitors elevations in creatinine, potasium

Rise in creatinine levels after initiation of ACE achieve the greatest benefit from their use

Discontinuation of ACE inh because of renal dysfunction high mortality risk (57% over an 8.5 month of study)

Continue ACE I despite a rise in creatinine, as long as renal dysfunction does not steadily deteriorate and severe hyperkalemia dos not develop

SymCARD 2013 Padang-West

Sumatera 27-29 Mei 2013

Diuretics

• Aggressive diuresis associated with worsening renal

function

• High diuretic dosis have been associated with

increased mortality rates

Diuretic resistance and concomitant worsening renal

dysfunction necessitate high doses of diuretics,

marker rather than a mechanism for poor outcome

• Positive inotropic agents facilitate diuresis

• Dopamine effect is severely limited in advance

heart failure

• Intravenous vasodilators improve hemodynamics,

less improve renal function

SymCARD 2013 Padang-West

Sumatera 27-29 Mei 2013

poor

perfusion

VOLUME

OVERLOAD

LOW

COP

INCREASED

BP

HEART

FAILURE

Clamping down

Sodium retention

RENAL

FAILURE

CARDIO-RENAL SYNDROME

TARGET OF TREATMENT

ANURI

OLIGOURI

(VOLUME OVERLOAD)

INFLAMMATION

R A S

ALDOSTERONE

SNS ACTIVITY

NO-ROS dysbalance

DIURETICS ULTRAFILTRATION

ANTI-INFLAMMATION

ANTI- RAAS

SymCARD 2013 Padang-West

Sumatera 27-29 Mei 2013

TARGET OF TREATMENT

VOLUME OVERLOAD

DIURETICS

LOOP DIURETICS

(furosemide)

ORAL

DRIP

(recommended)BOLUS

Diuretic Resistance

-Inadequate dose

-Excess sodium

-Delayed absorption

-NSAID

-Renal or Heart failure

THIAZIDES

(HCT)

LFG < 30 cc/mnt

Note : diuretics therapy can worsen renal function

Change to other LD

(bumetanide/torsemide)

Use ß-type Natriuretic Peptide

(BNP=nesiritides)

Increased oncotic pressure with :

Albumin/Mannitol/ColloidLow-dose Dopamin:

Not recommended

Effect :

-reduce pre/after-load

-natriuresis/diuresis

-suppress norepinephrine, endotelin,

and aldosterone

may increased risk of renal failure

In heart failure patients

NEED MORE INVESTIGATION

SymCARD 2013 Padang-West

Sumatera 27-29 Mei 2013

TARGET OF TREATMENT

ULTRAFILTRATION

SEVERE VOLUME OVERLOAD

iv DIURETICSDIURETIC

RESISTANCE ULTRAFILTRATION

CRRT SLEDD

The UNLOAD trial : early UF

SymCARD 2013 Padang-West

Sumatera 27-29 Mei 2013

TARGET OF TREATMENT

INREASED RAAS

Use of ACE-I OR ARB

Start with low dose

Patient not dehydrated

Avoid using NSAID

When using of ACE-I OR ARB beware of : increased creatinin and potassium

BETTER OUTCOME(SOLVD,PRIME-2,CONSENSUS,ELITE)

increased

potassium

increased

creatinine

Combination with

CCB

Combination with

DIURETICS

If contra-

indicated

Hydralazine/

Isosorbid-dinitrates

ISORDIL

SymCARD 2013 Padang-West

Sumatera 27-29 Mei 2013