fluid management in hf

8/13/2019 Fluid Management in HF

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CLINICAL CARDIOLOGY

Jakarta, 28 April 2012


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Hospitalizations for HF Are Increasing

0

100,000

200,000

300,000

400,000

500,000

600,000

'79

'81

'83

'85

'87

'89

'91

'93

'95

'97

Discharges

Women

Men

CDC/NCHS. AHA Heart Stroke and Statistical Update, 2001.


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Mortality Rates After First Hospitalization for HF

Jong et al.Arch Intern Med. 2002;162:1689-1694.

Age- and Sex-Stratified Case-Fatality Rates 30 Days and 1 YearAfter First Hospitalization for HF

Men Women

Mortality, % Mortality, %

Age Group, y No. of Patients 30-Day 1-Year No. of Patients 30-Day 1-Year

20-49

50-64

65-74

75

All Ages

655

3048

5923

9310

18,936

4.6

5.5

8.6

15.6

11.4

15.0

20.5

28.8

43.1

34.0

375

1892

4412

13,087

19,766

4.3

5.4

6.8

14.7

11.8

10.9

19.5

23.0

37.9

32.3


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Most Admitted Patients Are Volume Overloaded

Any dyspnea89%

Pulmonary congestion (CXR)74%

Rales67%

Dyspnea at rest34%

Peripheral edema65%

ADHERE Registry. 3rdQtr 2003 National Benchmark Report.

At HospitalizationADHERE1


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Over 90% of All Hospitalizations for Acutely

Decompensated Heart Failure (ADHF) Are Due to

Fluid Overload1

The Majority of These Patients Have Failed

Treatment With Oral Diuretics2

1. Aronson.ACC. 2000.

2. Adams et al.Am Heart J.2005;149:209-216.


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Fluid overload in normal heart

- Kidney responsible

for 20% of cardiac

output

- Good heart-kidney

relationship

- Integrity of arterial

circulation

HEART FAILURE :Heart-Kidney

Disintegration


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Fluid overload in heart failure

Arterial Underfilling Hypothesis

Angiotensin IIVasopressin


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Cardiorenal syndrome type 1


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HemodynamicCongestion

Clinicalcongestion

VS

Hemodynamic congestion may occur

earlier than clinical congestion Even when clinical congestion is

relieved, patients may still have

hemodynamic congestion

- LV filling

- intravascular

pressure

- Classic signs

- Symptoms

Diuretics

Challenges in Assessment of Fluid Overload

ACE-I/ARB

Aldosterone

antagonist

Beta blocker


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Fluid overload = worse prognosis

Lucas et al : assessed patients 4 to 6 weeks after hospital

discharge for 5 signs of hypervolemia: orthopnea, peripheral edema,

weight gain, need to increase baseline diuretic dose, and jugular

venous distension.

Patients with any 3 of the 5 signs 6 weeks after discharge had a 3-

fold increase in mortality at 2 years after the index hospitalization.


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...even in non heart failure patients


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Ronco, a renowned

nephrologist :5B approach for fluid overload


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Unfortunately....

Classic symptoms & signs has low sensitivity for the

presence of volume overload

Meaning : they can also present frequently without

actual volume overload


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What can we do ?


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Identify the underlying problems...


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What about BNPs?

Myocardial stretch is not analogue of fluid overload

Increase of BNP can happen in other setting

BNP rise may be slower than change in blood volume


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We need multiple modalities...


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...and consider multiple

compartments


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The Vascular Pedicle

The vascular pedicle is

bordered on the right by

venous structures (right

brachiocephalic vein above

and superior vena cava) and

on the left by an arterial

structure (the left subclavianartery origin).

VPW is the distance between

parallel lines drawn from the

point at which the superiorvena cava intersects the right

main bronchus an a line

drawn at the takeoff of the

left subclavian artery from

the aorta


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Salahuddin et al, Indian J Crit Care Med October-December 2007 Vol 11 Issue 4

VPW correlated closely

with positive fluid

balance, r = + 0.88, P

0.000. ROC demonstrated

that VPW of 86.5 mm

had a 100% sensitivity

and an 80% specificity(AUC 0.823) for

predicting fluid overload

1200 ml


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Echocardiography : measure

intravascular volume with caval index

Caval index(%) = (IVC expiratory diameterIVCinspiratory diameter)/ IVC expiratory diameter 100


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Beyond echocardiography : Lung Ultrasound

B lines correlates with extravascular lung water evaluatio


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BioImpedance Vector Analysis : whole

body fluid volume assessment

ESC id li 2008 I iti l


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ESC guideline 2008 : Initial

treatment of acute HF


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Yes

Stevenson LW. Eur J Heart Fail.1999;1:251

NoWarm & Dry

PCWP normal

CI normal(compensated)

Cold & Wet

PCWP elevatedCI decreased

Cold & Dry

PCWP low/normalCI decreased

Congestion at Rest

Low

Perfusion

at Rest

No

Yes

Warm & WetPCWP elevated

CI normal

Congestion vs. Low perfusion

4 Possible Hemodynamic Profiles of HF


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Narrow fluid tolerance in HF


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Indication of diuretics in HF

Loop diuretics is the first line therapy...

Diuretic Strategy in ADHF


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Diuretic Strategy in ADHF

THE DOSE study : 300 patients, double blind randomized study

High dose : 2,5 x previous oral dose

Low dose : equivalent to previous oral dose

HIGH DOSEvs LOW DOSE ?

BOLUS vs CONTINUOUS ?


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No significant differences in patients global assessment of

symptoms or in the change in renal function when diuretic therapy

was administered by bolus as compared with continuous infusion

or at a high dose as compared with a low dose


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PROBLEM #1 : Diuretic Resistance

Can be described as a clinical state in which the

diuretic response is diminished or lost before the

therapeutic goal of relief from edema has been

reached

1

Affects 20%30% of patients with HF2

1. Kramer et al. Nephrol Dial Transplant. 1999;14(suppl 4):39-42.

2. Ellison. Cardiology. 2001;96:132-143.


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Diuretic Resistance: Two Types

Braking phenomenon

A decrease in response to a diuretic after the first dose has been

administered

Long-term tolerance

Tubular hypertrophy to compensate for salt loss

Brater. N Engl J Med. 1998;339:387.

C f Di ti R i t i HF1 3


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Causes of Diuretic Resistance in HF1-3

Decreased renal function and distal Na+ delivery

Variability in diuretic absorption (bioavailability)

Neurohormonal activation (RAAS/SNS) Drugs/dietincreased sodium intake

Noncompliance with medications

Infrequent dosing

1. Neuberg et al.Am Heart J. 2002;144:31-38.

2. Brater. N Engl J Med. 1998;339:387-395.

3. Wilcox. J Am Soc Nephrol. 2002;13:798-805.

Overcoming Diuretic Resistence in HF


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Restrict daily fluid intake (1.01.5 L)

Moderate restriction of daily salt intake (2 g)

Avoid NSAIDs

Institute and uptitrate ACE inhibitors and/or angiotensin receptorblocker

Give short-acting loop diuretic orally in several divided(and increasing) doses, bolus, or continuous intravenousadministration

Use sequential nephron blockade via combination loop diuretic andthiazide diuretic

Add small doses of spironolactone (12.525 mg)

Consider short-term acetazolamide in selected patients

Overcoming Diuretic Resistence in HF


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Bayliss et al. Br Heart J.1987;57:17

Before

(n=12)

PlasmaReninActivity

(ng/mL/h)

50

10

2.5

0.5

PlasmaAldosterone

(pmol/L)

Mean, 95%

ConfidenceInterval

1000

600

200

100 P =.0007P =.0002After

Diuretic

(n=11)

Diuretics Activate Neurohormonal Systems in HF?

Before

(n=12)

After

Diuretic

(n=11)


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PROBLEM #2 : Hyponatremia


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When to treat ?

Serum sodium < 120 meq/L or

symptomatic

How to treat ?


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Tolvaptan in Heart Failure : quite

promising


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PROBLEM #3 : Oliguria and or increasing

Serum Creatinine Level

S l i Ul fil i i HF


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Solution : Ultrafiltration in HF

European and North American practice guidelines state

that UF is reasonable for patients with refractory congestion

not responding to medical therapy and assign to this

recommendation a class IIa, level of evidence: B.


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Ultrafiltration Initiation ?

- Neither practice guidelines nor clinical trial data provide guidance as

to which clinical variables should trigger initiation of extracorporeal

therapies

- The expert consensus suggests that a congestion grade higher than

12 together with low urine output (1,000 mL/24 h) should trigger the

use of extracorporeal fluid removal.


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Possible Contraindications to Ultrafiltration inPatients With HF

Inadequate venous access

Hypotension

Hypercoagulable states

Stage V chronic kidney disease; requirementfor hemodialysis

Patients responsive to diuretics


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Comparison to Continuous Venovenous

Hemofiltration

Aquapheresis CVVH

Patient Fluid overload Renal

Prescriber Any who have received training

(cardiologist, hospitalist,nephrologist, surgeon, etc)

Nephrologist

Treatment venue Inpatient/Outpatient ICU

Blood withdrawal rates 1040 mL/min 100300 mL/min

Extracorporeal volumes 33 mL 100300 mL

Venous access Peripheral or central CentralReported adverse events

since June 2002

Aquadex 6 (0.12% MDR

event per patient, 5000

patients) 0 device malfunctions

Prisma 812

(patient numbers not available)

NxStage 230 (23% MDR event

per patient, 1000 patients)


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TAKE HOME MESSAGE

1. Fluid overload is predictor of worse

prognosis in HF

2. Assessment is not always easy so

we must use multiple modalities3. Diuretics is firstline therapy, but

watch out for :- Diuretic resistance

- Hyponatremia

- Oliguria/worsening renal function

4. Consider ultrafiltration in the future


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fluid management in hf

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