Definition Acute heart failure

Acute heart failure is defined as the rapid

onset of symptoms and signs secondary to
abnormal cardiac function. AHF can present
itself as acute de novo (new onset of acute
heart failure in a patient without previously
known cardiac dysfunction) or acute
decompensation of chronic heart failure.
It is often life threatening and requires
urgent treatment.
Classification EF (%) Description

I. Heart failure with

Also referred to as
reduced ejection 40
systolic HF.
fraction (HFrEF)

II. Heart failure with

Also referred to as
preserved ejection 50
diastolic HF.
fraction (HFpEF)

These patients fall into

a. HFpEF, borderline 41 to 49 a borderline or
intermediate group.

It has been recognized

that a subset of
b. HFpEF, improved >40
patients with HFpEF
previously had HFrEF.
 Scope of the Problem
- More than 1,000,000 annual hospital
admission (increased 50% in past 10 years)
- Most common admission diagnosis in
patients older than 65 years.
- 6.5 million hospital days per year.
- Annual hospital costs: $15 billion.

AHA 2002 / Heart and Stroke Statistical Update

 Aetiology of AHF
1- Acute decompensation of CHF.
2- ACS :
a- AMI/UAP/Ischemic dysfunction.
b- Mechanical complications of AMI.
c- RV infarction.
3- Hypertensive crisis.
4- Acute arrhythmia ( VT,VF,AF,SVT ).
5- Acute severe myocarditis.
6- Acute valvular regurgitation.
7- Cardiac tamponade.
8- Aortic dissection.
9- Post partum CM.
10-Severe aortic valve stenosis.
 ACC/AHA Stages of Heart Failure

A: At high risk for HF but without structural heart

disease or symptoms of HF
B: Structural heart disease but without signs or
symptoms of HF
C: Structural heart disease with prior or current
symptoms of HF
D: Refractory HF requiring specialized
interventions
 Clinical syndromes of AHF
1- Acute decompensation of CHF:
( mild symptoms & signs).
2- AHF with pulmonary oedema :
(severe respiratory distress + pul. Rales +SaO2<90%).
3- Low output syndrome :
( SBP<90mmHg & 0r MBP by >30mmHg, urine
output <0.5ml/kg/h , tissue hypoperfusion ).
4- Severe cardiogenic shock :
( BP,anurea,organ hypoperfusion ).
5- Hypertensive HF :
( S & S of AHF, BP, preserved LVEF % ).
6- High output HF :
( HR, worm periphery, pul congestion ).
7- RV failure :
( Low output syndrome + JVP+tender hepatomegaly ).
 Goals of therapy in AHF
1- Clinical stabilization.
2- Stabilization of haemodynamics
( PCWP, COP, BNP )
3- Avoidance / Limitation of myocardial damage .
4- Favorable effects on pt outcome
* stay in ICU.
* readmission rate.
* mortality
Heart Failure Society Meeting;2001 : Washington DC
 I- Initial management
* Instrumentation and choice of therapy are
carried out according to clinical situation.
* Resuscitation may be required with life
threatening complications.
* IV line & arterial line may be useful for
monitoring.
* Correct hypoxia & COP, renal perfusion,
Na excretion and urine output.
* Ultrafiltration or dialysis may be requried.
 Initial management (cont)
* Devices may be indicated (IABP, assisted ventilation,
LVAD) as temporary measures or as a bridge for heart
transplantation.
* Invasive monitoring as (Pulmonary artery catheter) PAC
may assist in decision
making with volume loading during use of diuretics
and/or vocative agents in severe AHF.
* Pts with ACS or severe mechanical cardiac disorders
should do CA +/- PCI or surgery.
* Meticulous glycaemic & infection control and close
monitoring of renal function are mandatory.
* O2 by face mask or CPAP. SaO2 target is > 95%.
* IV morphine (2.5-5 mg)
J Card Fail 2004, 10(suppl) :120.
II-Conventional Treatments of
Acute Heart FailureI
Diuretics Vasodilators Inotropes

Decrease
Reduce
Preload
Fluid
And/or Augment
volume
After load Contractility

Rev Cardiovasc Med. 2001:2:7

 1) Diuretics
(Class I Level of evedence B)
* To treat pulmonary & peripheral congestion
secondary to fluid retention.
* IV administration in acute phase.
* Enhance water & Na excretion + loop diuretics
exert VD effect.
* In moderate fluid retention furosemide
(20 40 mg IV ).
* In severe fluid retention furosemide
infusion (5 - 40mg/h) better than high bolus dose (>1mg/kg).
* High bolus doses risk of reflex VC.
* In ACS, diuretics should be given in low dose
NB: VDs are better.
* Spironolactone with loop diuretics in low doses are more effective.
Demadex Tablets, 20 mg (Roche)
 1- Electrolyte abnormalities.
2- Metabolic alkalosis.
Potential 3- Activation of RAAS & SNS.
risk with
IV diuretics 4- Worsening of renal function.
5- Diuretic resistance.
6- Potential risk of mortality.
 1- Restrict Na/water.
2- Follow electrolytes.
3- Volume repletion in hypovolemia.
Diuretics 4- Combined loop diuretic +
(cont) Treatment
spironolactone +/- Dopamine
of diuretic
resistance renal dose.
5- Consider ultrafiltration.
6- Nesiritide +low dose loop diuretic
is beneficial.
 III- Novel strategies for
management of ADHF
A- Neurohormonal aquaretic therapy:
1-Vasopressin RA(tolvaptan) = Samsca (trade name)
used for treatment of hyponatremia.
2-Adenosine type-1 RA .
B- Vasoactive therapy:
1-BNP (Nesiritide)
= Natrecor (trade name).
C- Inotropic therapy:
1-Calcium Sensitizers/PDEI(Levosimendan)
= Simdax (trade name).
D- Mechanical therapy:
1-Ultrafiltration.
2-Aortic Flow Augmentation Device.
Current Cardiology Review 2005;1:1-5.
 2) Vasodilators
* Indicated as first line therapy,if hypoperfusion is
associated with adequate BP and signs of
congestion with low diuresis to lower preload.

* NTG relieves pulmonary congestion without SV &

myocardial Vo2 in AHF especially in pts with ACS.
(Class I Level of evidence B)

* SNP in AHF with predominantly afterload such as

hypertensive HF or MR.
(Class I Level of evidence C)

* In AHF due to ACS, NTG is favoured over SNP

coronary steal.
 Potential risk with IV Vasodilators
1- Tachyphylaxis
Nitroglycerin 2- Hypotension
3- Reflex tachycardia
4- Headache

1- Toxic metabolites
Nitoprusside 2- Hypotension
3- Reflex tachycardia
4- Coronary steal

1- Hypotension
Nesiritide 2- Not associated with proarrhythmia
3- ??worsening of renal function
 3) Inotropic Agents
Indications
1- Peripheral hypoperfusion with :
* hypotension
* decrease renal function.
2- With or without congestion.
3- Refractory HF to diuretics & VDs at
optimal doses.
 1- Hypotension:
(milrinone > dobutamine > dopamine)
2- Tachycardia :
Potential
risk with IV (dopamine > dobutamine > milrinone)
Inotropes 3- Proarrhythmia :
(dopamine > dobutamine > milrinone)
4- Mortality.
5- Tachyphylaxis.
 4) Beta blocking agents
* Overt AHF is considered a contraindication for BB use.
* Consider IV metoprolol if there is ongoing ischemia or
tachycardia.
(Class IIb Level of evidence C)
* Pts with AMI who stabilize after AHF start early
BB Rx.
(Class IIa Level of evidence B)
* Pts with chronic HF , start BB after AHF stabilization
( usually after 4 days )
(Class I Level of evidence A)
 Does It Matter How
Congestion Is Relieved?
- Inotropic Therapy
. Increases mortality
-Diuretic Therapy
. Worsens neurohormonal activation
-Vasodilator Therapy
. Limits renal perfusion pressure.
JAMA 2002;287 :1541
 III- Novel strategies for
management of ADHF
A- Neurohormonal aquaretic therapy:
1-Vasopressin RA(tolvaptan) = Samsca (trade name)
used for treatment of hyponatremia.
2-Adenosine type-1 RA .
B- Vasoactive therapy:
1-BNP (Nesiritide)
= Natrecor (trade name).
C- Inotropic therapy:
1-Calcium Sensitizers/PDEI(Levosimendan)
= Simdax (trade name).
D- Mechanical therapy:
1-Ultrafiltration.
2-Aortic Flow Augmentation Device.
Current Cardiology Review 2005;1:1-5.
 Nesiritide
VMAC trial
(Vasodilatation in the Management of Acute Congestive heart failure)

1- Nesiritide is more effective than NTG in decline of CVP.

2- It provides a synergistic diuretic effect to loop diuretics.
3-Rapidly improves symptoms of congestion.
4-Symptomatic hypotension is as low as 4% & no evidence of tachycardia.

PRECEDENT trial
(Prospective Randomized Evaluation of Cardiac Ectopywith
DobutaminE or Nesiritide Therapy)

* Nesiritide,unlike Dobutamine, is not proarrhythmogenic.

FUSION-1 study
(Follow Up Serial Infusions Of Nesiritide)

* The mortality rate is not significantly different from

standard therapy.
VMAC Investigators. JAMA 2002;287:1531.
VMAC Investigators. JAMA 2002;287:1531
Circulation 2004 ;109:630.
J Am Coll Cardiol 2005 ;46:57.
VMAC Investigators. JAMA 2002;287:1531.
Am J Cardiol 2004;93:237.
Am J Cardiol 2001;88:35-8.
 Levosimendan
LIDO study
(Levosimendan Infusion vs Dobutanine in severe
low Output heart failure)
* Better hemodynamic &clinical response than Dobutamine.
* Has the potential to challenge Dobutamine in :
# ischemic HF
# BB treated pts
* Mortality rate than IV dobutamine (6.8% vs 17% at 31 days, 26%
vs 38% at 6 months).

CASINO study
(Calcium Senitizer or Inotropic or None in low
Output heart failere)
* Mortality rate than dobutamine & placebo (15.3% vs 24.7% vs
39.6% at 6 months).
Lancet2002;360:196-202.
Lancet 2002;360:196-202.
Lancet 2002;360:196-202.
J Am Coll Cardiol 2004;43:206.
Treatment of arrhythmias in AHF.
1- VF or pulseless VT :
*Defibrilation (360 J).
* If refractory inject Epinephrine (1mg) or Vasopressin (40 IU )
and/or Amiodarone (150-300 mg ).

2- VT :
* If pt is unstable C.V.
* IF pt is stable inject Amiodarone or Lidocaine ( medical C.V).

3- SVT :
* Use BB when pt is stable ( Metoprolol 5mg as slow IV bolus ).
* Adenosine may be used to slow AV conduction or to cardiovert
re-entry tachycardia.
Treatment of arrhythmias in AHF ( cont )
4- AF or A flutter :
* Pts with AHF& AF should be anticoagulated
* Paroxysmal AF medical or electrical C.V.
* If AF is > 48h pt should be anticoagulated + Optimal rate
control for 3 weeks before C.V ( by Amiodarone and BB ).
* If pt is unstable urgent C.V is mandatory ( LA thrombus
should be excluded by TEE ).
* Verapamil and Diltiazem should be avoided (they may worsen
HF and cause third degree HB).

5- Bradycardia :
* Atropine (o.25- o.5mg) IV to total 1-2mg.
* Theophylline may be used with Atropine resistant bradicardia
( bolus of o.25-o.5mg/kg & then infusion of o.2-o.4mg/kg/h ).
* If bradycardia persists Pacing.
 Cardiac disorders and AHF
requiring surgical treatment
1- Cardiogenic shock after AMI in pts with MVD.
2- Post infarction VSD.
3- Free wall rupture.
4- Acute decompensation of pre-existing valve disease.
5- Prosthetic valve failure or thrombosis.
6- Ao aneurysm or dissection rupture into pericardial sac.
7-Acute MR or AR .
8-Rupture aneurysm of sinus of valsalva .
9- Acute decompensation of chronic CM requiring support
by VADs .