Rapid Assessment and Treatment of Patients with Acute Decompensated Heart Failure (ADHF)

Nani Hersunarti

Department of Cardiology and Vascular Medicine

Faculty of Medicine, University of Indonesia

Harapan Kita National Cardiac Center

Improve patient hemodynamic status in order to relief symptoms and stabilize organ function– Reduce fluid volume and filling

pressures of the heart– Reduce systemic vascular resistance

(SVR)– Increase cardiac output (CO) – Reduce neurohormones

Therapeutic Goals in ADHF

Therapeutic Goal Parameters

in ADHF

SBP > 80 mm HgNo orthopneaNo peripheral

edemaNo hepatomegaly

or ascitesJVP < 8 cmWarm extremities

SBP > 80 mm Hg PCWP < 15 mm HgRAP < 8 mm HgSVRI < 1200 dyne-

s-cm-5

ClinicalHemodynamic

Oxygenation and ventilatory assist.

– The first priority in ADHF treatment is adequate cellular oxygenation to prevent organ target dysfunction.

– Oxygen saturation is maintained 95-98%.• Airway Patency• Oksigen supply ; Nasal or Mask or CPAP or

non-invasive positive pressure ventilation (NIPPV).

• Ventilator support in case of respiratory failure

ESC guidelines Acute Heart Failure, 2005

Pharmacologic option in ADHF

Diuretics Vasodilators Inotropes

Reducefluid

volume

Decreasepreload

andafterload

Augmentcontractility

Vasodilate; reduce fluid

volume;counteract RAAS/SNS

Natriuretic peptides

RAAS = renin-angiotensin-aldosterone system; SNS = sympathetic nervous system

Ideal Agent for ADHF

• Vasodilator (venous and arterial)• Rapidly decreases ventricular filling

pressures• Rapidly decreases symptoms of

congestion • Does not increase heart rate or directly

increase contractility (decreases myocardial oxygen demand)

• Not proarrhythmic

Fonarow GC. Rev Cardiovasc Med. 2001;2(suppl 2):S7

• Does not induce tachyphylaxis (tolerance)

• Provides neurohormonal suppression

• Promotes diuresis / natriuresis

• Conveniently dosed (can be used with or without pulmonary artery catheterization)

• Able to give in a less monitored setting

Ideal Agent for ADHF

Fonarow GC. Rev Cardiovasc Med. 2001;2(suppl 2):S7

A

L C

B

Congestion at rest

Yes

Yes

No

NoWarm & dry

Cold & WetCold & dry

Warm & wet

Low

perf

usi

on a

t re

st

Sign of low perfusion:

Narrow pulse pressure,cool extremities,sleepy, suspect from ACEI hypotension, low Na, renal worsening

Sign of congestion:

Orthopnea,elevated JVP,edema,pulsatile hepatomegaly, asites, rales,louder S3,P2 radiation left ward, abdomino-jugular reflex, valsava square wave

European Heart Journal of Heart Failure,2005; 7:323-331

Two Minutes Assessment of Two Minutes Assessment of Haemodynamic ProfileHaemodynamic Profile

Patient Treatment Selection

Fonarow GC. Rev Cardiovasc Med. 2001;2(suppl 2):S7–S12.

Congestion at Rest

Lowperfusi

onat Rest

YesNo

Warm & DryPCWP normal

CI normal (compensated)

Cold & WetPCWP elevatedCI decreased

Cold & DryPCWP low/normal

CI decreased

Inotropic DrugsDobutamine

Milrinone

Normal SVR High SVR

No

Yes

Warm & WetPCWP elevated

CI normal MOST PATIENTS

VasodilatorsNitroprussideNitroglycerin

or

Natriuretic Peptides

Acute Heart Failure with Systolic Dysfunction

Oxygen/CPAPFurosemide + vasodilator

Clinical evaluation (leading to mechanistic therapy)

SBP > 100 mmHg SBP 85-100 mmHg SBP <85 mmHg

Vasodilator(NTG, nitroprusside, BNP)

Vasodilator and/orInotropic (dobutamin

PDEI or Levosimendan)

Volume loading ?Inotrope and/or

Dopamin > 5mcg/kg/mntAnd/or norepinephrine

Good responseOral therapy

Furosemide, ACE-I

No respon :Reconside mechanistic

therapyInotropic agent ESC, Acute Heart Failure, 2005

Morphine and its analogues

In patient present with restlessness and dyspnoea

Morphine induces • Venodilatalion • Mild arterial dilatation• Reduce heart rate

Dose : 3 mg IV bolus Repeated if required

ESC guidelines Acute Heart Failure, 2005

Diuretics

•For achieving optimal volume status eliminate or minimize congestion•High doses of i.v diuretics 2-3 times daily •More effective with continous i.v.•Combination diuretics•“Resistent diuretics” is a common problem

Inotropes:Dopamine, Dobutamine, Milrinone

• Improve cardiac output by directly increasing cardiac contractility

• Significant proarrhythmic effects• May precipitate ischemia• Not recommended for routine use in

ADHF, but clearly have a role in specific patients

Felker GM. Am Heart J. 2001;142:393–401.

The use of inotropes as a treatment of :

• cardiogenic shock

• diuretic/ACE inhibitor– refractory heart failure decompensations

• a short-term bridge to definitive treatment, such as revascularization or cardiac transplantation, is potentially appropriate

Role of Inotropic Therapy in Patients With Heart Failure

Inotropic AgentIndication :

Peripheral hypoperfusion (hypotension, decrease renal function) with or without congestion

ESC guidelines, Acute Heart Failure, 2005

There is increasing prevalence of i.v. inotropes infusion that Cannot be Cannot be weaned without symptomaticweaned without symptomatic hypotension, recurrent renal dysfunction

!

Dependence on i.v. inotropeDependence on i.v. inotrope can be avoidedcan be avoided with wean infusion in 1-2 weekswean infusion in 1-2 weeks and reduce or discontinuation other medication that decrease discontinuation other medication that decrease blood pressure and renal functionblood pressure and renal function ( Nitrate, Ca++ Channel blocker, NSAID)

Inotropic AgentsDopamine• Is dose dependent and they involve in

three different receptors.

• In low dose (< 2 In low dose (< 2 g/kgBW/min), g/kgBW/min), vasodilatationvasodilatation occurs predominantly in renal, coronary, and cerebral vascular beds.

• However if no response is seen in diuresis the therapy should be terminated (Level of evidence C, class IIb)ESC, Acute Heart Failure, 2005

Inotropic Agents

Dopamine (cont.)• At higher doses (> 2 g/kgBW/min)

stimulates adrenergic and increase in myocardial contractility and cardiac output.

• At doses > 5 g/kgBW/min dopamine will increase peripheral vascular resistance via adrenergic receptors

ESC, Acute Heart Failure, 2005

DobutamineDobutamine

• Clinical action is dose dependent positive inotropic and chronotropic effects.

• In low dose induce arterial vasodilatation and in higher induce arterial vasoconstriction

Inotropic Agents

ESC, Acute Heart Failure, 2005

Phosphodiesterase inhibitors

• Block the breakdown of cyclic AMP into AMP (milrinone, enoximone)

• In advance HF, associated with inotropic, lusitropic, vasodilating effects

• Intermediate between vasodilator and predominant inotrope

Inotropic Agents

ESC, Acute Heart Failure, 2005

Treat the rhythm disturbance

AF or Atrial Flutter;

Cardiovert if possible, or digoxin 0.125-0.25 mg IV or B blocker or amiodarone

ST or SVT;

B bloker when clinically and hemodimanically tolerated - metoprolol 5 mg iv as slow bolus

VF or pulseless VT; Defibrilate 200J

ESC, Acute Heart Failure, 2005

VasodilatorsNitroprusside, Nitroglycerin, Nitrate family

• Work by cGMP mediated smooth muscle relaxation -> vasodilation

• Decrease myocardial work by afterload and preload reduction

• May cause hypotension• May cause headache

• NitratesNitrates

– Not evaluated by large scale studies– Many studies shown their favorable effectLimitationLimitation– Side effect– Nitrate ResistanceNitrate Resistance– Nitrate ToleranceNitrate Tolerance

Prevention• Intermittent dosing : 12 hour nitrate free

interval• Escalating dose• Concomitant use of hydralazine

Elkayam, The American Journal of Cardiology

DR I

MKRG

S SS

SGLG

FC CS SG

SGQVMK V L R

RH

KPS

Cardiac3

Vetricular relaxation (lusitropy) Antifibrotic ( TGF) Antiremodeling

Hemodynamic1,2

(balanced vasodilation) Veins Arteries Coronary arteries

Neurohumoral2

aldosterone4

endothelin2

norepinephrine5

Renal1,5

Diuresis Natriuresis

1Marcus LS et al. Circulation. 1996;94:3184; 2Zellner C et al. Am J Physiol. 1999;276(3 pt 2):H1049;3Tamura N et al. Proc Natl Acad Sci U S A. 2000;97:4239; 4Abraham WT et al. J Card Fail. 1998;4:37;5Clemens LE et al. J Pharmacol Exp Ther. 1998;287:67

Pharmacologic Actions of hBNP

Nesiritide Dosing and Administration

• IV bolus of 2 mcg/kg followed by a continuous infusion of 0.01 mcg/kg/min.

• Natrecor should not be initiated at a dose above the recommended dose.

• The infusion dose can be increased by 0.005 mcg/kg/min no more frequently than every 3 hours up to a maximum dose of 0.03 mcg/kg/min.

Natrecor Prescribing Information (PI), 2004Natrecor Prescribing Information (PI), 2004

IV Agents for ADHF

Nitroprusside

Nesiritide

Nitroglycerin

Milrinone

Dobutamine

??

Dopamine (ng/kg/min)Low (<3)Mod (3-7)High (7-15)

DiuresisArrhythmiaHRBPPCWPCOTherapy

BP = blood pressure; CO = cardiac output; HR = heart rate; PCWP = pulmonary capillary wedge pressureAdapted from Young JB. Rev Cardiovasc Med. 2001;2(suppl 2):S19-S24.

P0415400

Conclusion

• Rapid assessment and treatment of ADHF could decreased mortality and morbidity rate

• Management strategies including – Ensure oxygenation– Reduce pain– Reduce fluid volume– Reduce preload and or afterload – Increase cardiac output– Identify and treat the cause of CHF

Rapid assessment and prompt treatment result in a good outcome for ADHF patients