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

Therapeutic Goals in ADHF

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 Goal Parameters in ADHF

Hemodynamic Clinical

SBP > 80 mm Hg PCWP < 15 mm Hg RAP < 8 mm Hg SVRI < 1200 dyne-scm-5

SBP > 80 mm Hg No orthopnea No peripheral edema No hepatomegaly or ascites JVP < 8 cm Warm extremities

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 noninvasive positive pressure ventilation (NIPPV). Ventilator support in case of respiratory failure

ESC guidelines Acute Heart Failure, 2005

Pharmacologic option in ADHF

Diuretics

Vasodilators

Inotropes

Natriuretic peptides

Reduce fluid volume

Decrease preload and afterload

Augment contractility

Vasodilate; reduce fluid volume; counteract RAAS/SNS

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

Ideal Agent for ADHF

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

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

Two Minutes Assessment of Haemodynamic Profile Congestion at rest Low perfusion at rest
Sign of congestion:
Orthopnea,elevated JVP,edema, pulsatile hepatomegaly, asites, rales,louder S3,P2 radiation left ward, abdomino-jugular reflex, valsava square wave

No

Yes

No

A
Warm & dry Cold & dry

B
Warm & wet Cold & Wet

Yes

C
European Heart Journal of Heart Failure,2005; 7:323331

Sign of low perfusion: Narrow pulse pressure,cool ex tremities,sleepy, suspect from ACEI hypotension, low Na, renal worsening

Patient Treatment Selection

Congestion at Rest
No
Warm & Dry

Yes
Warm & Wet
PCWP elevated CI normal
MOST PATIENTS

Low perfusion at Rest Yes

No

PCWP normal CI normal

(compensated)

Vasodilators
Nitroprusside Nitroglycerin

or

Cold & Dry

PCWP low/normal CI decreased

Cold & Wet

PCWP elevated CI decreased
Normal SVR High SVR

Natriuretic Peptides

Inotropic Drugs
Dobutamine Milrinone Fonarow GC. Rev Cardiovasc Med. 2001;2(suppl 2):S7S12.

Acute Heart Failure with Systolic Dysfunction

Oxygen/CPAP Furosemide + vasodilator Clinical evaluation (leading to mechanistic therapy)
SBP > 100 mmHg
Vasodilator (NTG, nitroprusside, BNP)

SBP 85-100 mmHg

Vasodilator and/or Inotropic (dobutamin PDEI or Levosimendan)

SBP <85 mmHg

Volume loading ? Inotrope and/or Dopamin > 5mcg/kg/mnt And/or norepinephrine

Good response Oral therapy Furosemide, ACE-I

No respon : Reconside mechanistic therapy Inotropic 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

Role of Inotropic Therapy in Patients With Heart Failure

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

Felker GM. Am Heart J. 2001;142:393401.

Inotropic Agent
Indication : Peripheral hypoperfusion (hypotension, decrease renal function) with or without congestion There is increasing prevalence of i.v. inotropes infusion that Cannot be weaned without symptomatic hypotension, recurrent renal dysfunction

Dependence on i.v. inotrope can be avoided with wean infusion in 1-2 weeks and reduce or discontinuation other medication that decrease blood pressure and renal function ( Nitrate, Ca++ Channel blocker, NSAID)
ESC guidelines, Acute Heart Failure, 2005

Inotropic Agents
Dopamine
Is dose dependent and they involve in three different receptors. In low dose (< 2 mg/kgBW/min), vasodilatation 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 mg/kgBW/min) stimulates b adrenergic and increase in myocardial contractility and cardiac output. At doses > 5 mg/kgBW/min dopamine will increase peripheral vascular resistance via a adrenergic receptors

ESC, Acute Heart Failure, 2005

Inotropic Agents
Dobutamine

Clinical action is dose dependent positive inotropic and chronotropic effects.

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

ESC, Acute Heart Failure, 2005

Inotropic Agents
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

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

Vasodilators Nitroprusside, 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

 Nitrates
Not evaluated by large scale studies Many studies shown their favorable effect Limitation Side effect Nitrate Resistance Nitrate Tolerance Prevention Intermittent dosing : 12 hour nitrate free interval Escalating dose Concomitant use of hydralazine
Elkayam, The American Journal of Cardiology

Pharmacologic Actions of hBNP

Hemodynamic1,2 (balanced vasodilation)
R I SS D S M S K G R L G H G F R C C S S K V LR G S PK M V Q GS

Veins Arteries Coronary arteries

Neurohumoral2
aldosterone4 endothelin2 norepinephrine5

Cardiac3

Vetricular relaxation (lusitropy) Antifibrotic ( TGFb) Antiremodeling

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

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), 2004

IV Agents for ADHF

Therapy Dopamine (ng/kg/min) Low (<3) Mod (3-7) High (7-15) Dobutamine Milrinone Nitroglycerin
CO PCWP BP HR Arrhythmia Diuresis

? ?

Nesiritide
Nitroprusside

BP = blood pressure; CO = cardiac output; HR = heart rate; PCWP = pulmonary capillary wedge pressure Adapted 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