note of acute heart failure

Acute Heart Failure ManagementMy Note of 2016 ESC guideline and books Yuan Chieh Chang, 2016

Acute Heart failure medical management | CYC 2016 Outline

ESC 2016 guideline Tx of acute Heart failurePrognosis and Identify the high riskDischarge checklistOxygen TherapyPharmacology therapy

DiuresisVasodilator Inotropic agents Inodilator Inotropic vasopressor

Acute Heart failure medical management | CYC 2016

ESC 2016 Heart Failure Guideline

Acute Heart failure medical management | CYC 2016 Definition and Classification

Rapid onset or worsening of symptoms and/or signs

CONGESTION

HYP

OPE

RFU

SIO

N

Dry & Warm Wet & Warm

Dry & Cold Wet & Cold


CONGESTION

HYP

OPE

RFU

SIO

N


Dry & Cold Wet & Cold Pulmonary congestionOrthopnea/PNDPeripheral oedemaJugular vein distensionHepatomegalyGuts congestion/ascitesHepatojugular reflux

5% of AHF 95% of AHF


CONGESTION

HYP

OPE

RFU

SIO

N


Dry & Cold Wet & Cold

Cold sweated extremitiesOligouriaMental CongusionDizzinessNarraw Pulse pressure

Acute Heart failure medical management | CYC 2016 Definition of terms

Acute Heart failure medical management | CYC 2016 Elevated BNP ?


Wet

Warm

Cold

Dry

Warm

Cold

Management

Vascular Type Fluid distributionHypertension Predomates

Cardiac Type Fluid distributionCongestion Predomates


Wet

Warm

Cold

Dry

Warm

Cold

Management



Diuresis Vasodilator


Wet

Warm

Cold

Dry

Warm

Cold

Management



Diuresis

VasodilatorUltrafiltration

Acute Heart failure medical management | CYC 2016 Management

Wet

Warm

Cold

Dry

Warm

Cold

SBP < 90mmHg SBP >= 90mmHg

Correct Perfusion

Inotropic

MechanicalIf Medical therapy fail

Diuresis

in refractory caseVasopressor


Wet

Warm

Cold

Dry

Warm

Cold

SBP < 90mmHg SBP >= 90mmHg

in refractory caseInotropic

Diuresis

Vasodilator


Wet

Warm

Cold

Dry

Warm

Cold

Well Compensated ! (Oral Medication)


Wet

Warm

Cold

Dry

Warm

Cold Hypoperfused, HypovolemicConsider Fluid Challenge

If still HypoperfusedInotropic


Identify High Risk Patient

Acute Heart failure medical management | CYC 2016 Risk

Braunwald's heart disease 10th Ed

Acute Heart failure medical management | CYC 2016 Preparing for discharging

persistent clinical congestionassociated elevations of discharge BNP level

High risk for rehospitalization

Acute Heart failure medical management | CYC 2016 Preparing for discharging

Check list



Oxygen Therapy

Acute Heart failure medical management | CYC 2016 Oxygen therapy

Oxygen Therapyin SpO2

Acute Heart failure medical management | CYC 2016 Before Intubation

improvement in dyspnea, heart rate, acidosis, and hypercapnea after 1 hour of therapy

may decrease intubation and mortality rates (Not conclusive)

continuous positive airway pressure (CPAP) noninvasive intermittent positive-pressure ventilation (NIPPV)


Pharmacology Therapy

Acute Heart failure medical management | CYC 2016 Diuresis

clinically evident congestion: 4 to 5 liters of excess volume

greater than 10 L are not uncommon

DiuresisSymptom Relief

Acute Heart failure medical management | CYC 2016 Diuresis

Initial

i.v. dose should be at least equal to the pre-existing oral dose

2.5 x the outpatient dose:

renal dysfunction/severe volume overload

*transient worsening in renal function

Titration should be rapid with doubling

Consider continuous infusion

significant volume overload (>5 to 10 liters) or diuretic resistance

Acute Heart failure medical management | CYC 2016 Volume Management


Acute Heart failure medical management | CYC 2016 Vasodilator

VasodilatorSymptom ReliefReduce Mortality

Acute Heart failure medical management | CYC 2016 Cardiorenal Syndrome



Vasodilator can help!


Use of vasodilators was superior to ultraltration with regard to preserving renal function and decongestion

Vasodilator Ultrafiltration


Preload Afterload

Venous Arterial

PCWP/Pulmonary edema

Nitrates

Coronary artery

Nitroprusside

High dose

stealing phenomenon

Nesiritide

Myocardial O2 Consumption

CCB


Nitroprusside

stealing phenomenon

Vasodilator

Nesiritide

CCBNitrates

High dose

Preload Afterload

Venous Arterial


Coronary artery


Acute Heart failure medical management | CYC 2016 Vasodilator effect (Nitrates)

ALARM-HF registry Braunwald's heart disease 10th Ed

Acute Heart failure medical management | CYC 2016 Vasodilator effect (Nitrates)

ALARM-HF registry

SBP100-120mmHg

Acute Heart failure medical management | CYC 2016 Nitrates

Increased coronary blood flow

Relatively selective for epicardial, (>intramyocardial, coronary arteries)

Goal

immediate symptom relief

MAP reduction > 10 mm Hg , SBP > 100 mm Hg

dose may need to be reduced if SBP is 90 to 100 mm Hg and often will need to be discontinued with SBP below 90 mm Hg

Acute Heart failure medical management | CYC 2016 Nitrates

Recent use of phosphodiesterase-5 inhibitors (sildenafil, tadalafil, and vardenafil) should be ruled out


Nitrates

High dose

Vasodilator

Nesiritide

CCB

Preload Afterload

Venous Arterial


Coronary artery


Nitroprusside

stealing phenomenon

Acute Heart failure medical management | CYC 2016 Sodium Nitroprusside

a very short half-life (seconds to a few minutes)

SBP 90 to 100 mmHg are typical goals

Tapering the dose of before discontinuation

Cyanide toxicity:

as low and as short as possible

no longer than 10 minutes at top dose in the treatment of severe hypertension

contraindicated in hepatic or real failure

Acute Heart failure medical management | CYC 2016 Sodium Nitroprusside

Being replaced in.

severe acute-on-chronic heart failure by nitrates

hypertensive crises by intravenous nicardipine, fenoldopam, or labetalol


Coronary artery

CCBNitrates

High dose

Nitroprusside

stealing phenomenon

Vasodilator

Nesiritide

Preload Afterload

Venous Arterial



Acute Heart failure medical management | CYC 2016 Nesiritide

ASCEND-HF)

minimal improvement in dyspnea

as VMAC trial revealed reduced PCWP

no beneficial effect on hospitalizations for HF or death within 30 days.

increased incidence of symptomatic hypotension

no differences in the rates of worsening renal function5

Recombinant human B-type [brain] natriuretic peptide

Acute Heart failure medical management | CYC 2016 Sympathomimetic Inotropes and inotropic dilators

InotropicSymptom Relief

Maintain end-organ functionIncrease Hemodynamic profile

Acute Heart failure medical management | CYC 2016 Inotropes

Drugs for the Heart, 8th Edition

Acute Heart failure medical management | CYC 2016 Inotropes

VasocontrictionVasodilation

Inotropic

DobutamineDopamine

Norepinephrine

Epinephrine

()

Chonotropic ++ Arrhythmia risk+++

Arrhythmia risk++ Arrhythmia risk+ (high dose)

Arrhythmia risk+ Milrinone

Arrhythmia risk+ Hypotension


Inotropic

Vasodilator


Inotropic

Vasodilator

/ -

cAMP-mediated inotropy and reduce PCWP through vasodilation


Inotropic

Vasodilator

/ -

cAMP-mediated inotropy and reduce PCWP through vasodilation

Limited to dilated ventricles + reduced EF + SBP

Acute Heart failure medical management | CYC 2016 Dobutamine

Beta2 Increase CO via afterload reduction in low dose

decreased aortic impedance and systemic vascular resistance

Tachyphylaxis : infusions longer than 24 to 48 hrs

long-term mortality may be increased,as well as increasing cardiac sympathetic activity in heart failure patients


Acute Heart failure medical management | CYC 2016 Dobutamine

Side effect:

tachycardia, increasing ventricular response to Af, atrial and ventricular arrhythmias, myocardial ischemia

possibly cardiomyocyte necrosis (direct toxic effects and induction of apoptosis)


Acute Heart failure medical management | CYC 2016 Dopamine

precursor of norepinephrine and releases norepinephrine

Periphery this effect is overridden by the activity of the prejunctional dopaminergic-2 receptors, inhibiting norepinephrine release and thereby helping to vasodilate



Low-dose (2 g/kg/min)

selective dilation of renal, splanchnic, and cerebral arteries (DA1R)

Low dose Dopamine + low dose furosemide

may improved renal function profile and potassium homeostasis compared with high-dose furosemide (not conclusive!)



Intermediate-dose dopamine (2 to 10 g/kg/min)

enhanced NE release, stimulating cardiac receptors with an increase in inotropy and mild stimulation of peripheral vasoconstricting receptors

dependent on myocardial catecholamine stores (ineffective in advance stage )

Dosing should be gradually decreased from to 3 to 5 g/kg/min and then discontinued, avoid potential hypotensive effects of low-dose dopamine



High-dose dopamine (10 to 20 g/kg/min)

peripheral and pulmonary artery vasoconstriction (direct agonist effects on alpha1-adrenergic receptors)



Cardiogenic shock or AMI

5 mcg/kg/min is enough to give a maximum increase in stroke volume

Renal flow reaches a peak at 7.5 mcg/kg/min

Arrhythmias may appear at 10 mcg/kg/min



In septic shock

Dopamine has an inotropic effect and increases urine volume

Dopamine is widely used after cardiac surgery

In critically ill hypoxic patients

may depression of ventilation and increased pulmonary shunting



Contraindication in ventricular arrhythmias, and pheochromocytoma

MAO inhibitor


Acute Heart failure medical management | CYC 2016 Dopamine or Dobutamine

Dopamine is preferred if the patient requires

pressor effect (high-dose-effect) +

increase in cardiac output+

No marked tachycardia or ventricular irritability

Cardiogenic shock infusion of equal concentrations may afford more advantages than either drug singly

Acute Heart failure medical management | CYC 2016 Epinephrine

Full beta receptor agonist

inotropy independent of myocardial catecholamine stores ( denervative )

Potent inotropic agent

balanced vasodilator and vasoconstrictor effects

Contraindications : late pregnancy


Acute Heart failure medical management | CYC 2016 Epinephrine

A low physiologic infusion rate ( 0.01 mcg/kg/min)

decreases BP (vasodilator effect)

Cardiac arrest: combined inotropic-chronotropic stimulation

High Dose: Alfa stimulation > Beta


Acute Heart failure medical management | CYC 2016 Phosphodiesterase Inhibitors - Milrinone

Inhibition cAMP degraded

increases inotropy, chronotropy, and lusitropy in cardiomyocytes

vasorelaxation in vascular smooth muscle

Peripheral and pulmonary vasodilation

ESC: may be considered to reverse the effect of beta-blockade

Decrease Afterload and Preload and is Inotropic


Acute Heart failure medical management | CYC 2016 Mechanism

World J Cardiol 2016 July 26; 8(7): 401-412


Ca SERCA Sarcoplasmic reticulum SRCaSystolic phase CytoplasmCa Diastolic phase

PDEI Ca

cAMP

Acute Heart failure medical management | CYC 2016 Vasodilation in smooth muscle

Elvebak, R. L., Eisenach, J. H., Joyner, M. J. and Nicholson, W. T. The Function of Vascular Smooth Muscle Phosphodiesterase III is Preserved in Healthy Human Aging

Acute Heart failure medical management | CYC 2016 Vasodilation in smooth muscle

Nitrate


Subcellular localization

possibility to stimulate inotropy without increasing heart rate

Bypasses receptor downregulation

Acute Heart failure medical management | CYC 2016 Attention

Extremely long duration

elimination half-life of 2.5 hours pharmacodynamic half-life > 6 hours

Renally excreted

Hypotension and atrial and ventricular arrhythmias

OPTIME-HF (2002) N = 951 Compare with Placebo No change in Days with CV-related hospitalization excess sustained hypotension (P = .004), new atrial fibrillation/flutter (P

< .001), VT/VF (P = .06)

Acute Heart failure medical management | CYC 2016 Levosimendan

Anesthesiology 3 2006, Vol.104, 556-569

Anesthesiology 3 2006, Vol.104, 556-569


Increases myocardial contractility

Cardiac myofilament calcium sensitization by calcium-dependent (systolic) troponin C binding

Peripheral vasodilation

activation of vascular smooth muscle potassium channels

Some in vitro PDEI activity


Benefit on mortality?

SURVIVE (2007) N = 1327 Compare with Dobutamine

No change in dyspnea at 24 hr, days alive out of hospital at 180 days, all-cause mortality at 31 days, CV mortality at 180 days

REVIVE-2 (2013) N = 600 Compare with Placebo

More frequent hypotension and cardiac arrhythmias during infusion period;

numerically higher risk of death, 90 days (REVIVE-1,-2: Levo, 49 deaths/350 pts. vs. placebo, 40/350, P = .29)


Inotropic

Vasopressor

Acute Heart failure medical management | CYC 2016 Vasopressor

Vasopressor (norepinephrine preferably)

considered in cardiogenic shock+ treatment with another inotrope

to increase blood pressure and vital organ perfusion

increase in LV afterload

Norepinephrine > Dopamine (fewer side effects and lower mortality)

Epinephrine : restricted to persistent hypotension

despite adequate cardiac filling pressures and the use of other vasoactive agents

Acute Heart failure medical management | CYC 2016 Norepinephrine

Logically, should be of most use:shock-like state + peripheral vasodilation (warm shock)

Combination with PDE inhibitors helps to avoid the hypotensive effects of the PDE inhibitors

Contraindications :late pregnancy and preexisting excess vasoconstriction


Acute Heart failure medical management | CYC 2016 Recommend Dosing


note of acute heart failure

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