HEART FAILURE

Definition, Etiology and

pathophysiology
Definition
Heart failure means simply failure of the heart to pump enough
blood to satisfy the needs of the body (Physiology Guyton)

The situation when the heart is incapable of maintaining a cardiac

output adequate to accommodate metabolic requirements and the
venous return. (E. Braun Wald)

The inability of the heart to pump blood forward at a sufficient

rate to meet the metabolic demands of the body (forward failure),
or the ability to do so only if the cardiac filling pressure are
abnormally high (backward failure), or both. (Pathophysiology of
Heart Disease 4th edition, Lilly, Leonard S)
Definition (ESC 2008 )
HF is a syndrome in which the patients should have the following features:
1. Typical HF symptoms : 3. Objective evidence of an
Breathlessness at rest or on abnormality of the structure or
exercise functional abnormality of the
heart at rest :
Fatigue or tiredness
Cardiomegaly
ankle swelling
3rd heart sound
2. Typical HF sign :
Cardiac murmurs
Tachycardia
Abnormality on echocardiogram
Tachypnoea
Increase natriuretic
Pulmonary rales
concentration
Pleural effusion
Increase JVP
Peripheral oedema
Hepatomegaly
Classification of Heart Failure
Time base:
New onset HF : can be acute or
slow onset
Transient HF : can be recurrent or
episodic
Chronic HF : persistent, stable,
worsening, decompensated
Functional base:
Systolic HF : Inability of the heart
to contract properly
Diastolic HF : inability of the heart
to relax properly (LVEF >40%)
Congestion base:
Left sided HF : Congestion of pulmonary
veins
Right sided HF : Congestion of systemic
veins
Dysfunctional base:
Forward HF : inadequate cardiac output
to body cell needs, causing hypoxemia
and secondary venous distention
Backward HF : Congestion of pulmonary
and systemic
Output base:
High output HF : Normal cardiac output,
extra high demand
Low output HF : Low cardiac output,
normal demand
The Importance of Ejection Fraction in HF Classification
prognostic importance (the lower
the EF the poorer the survival)
most clinical trials selected
patients based upon EF
2 categories of HF:
HF-REF (Heart Failure with Reduced
EF)
Also called systolic HF
EF 35%
HF-PEF (HF with preserved EF)
Also called diastolic HF
EF >50%
More difficult to diagnose
EF in the range 3550% therefore
represent a grey area
Physiology
Acute Effects of
Failure
Immediately, CO curve
becomes greatly lowered
Circulatory reflexes activated
(baroreceptor reflex,
chemoreceptor reflex, CNS
ischemic response) causing:
Strong sympathetic stimulation
The heart becomes a stronger pump
Arterio+venoconstriction
increased blood vessels tone
increases venous return (preload)
increased CO
This stimulation is starterd within a
few seconds and maximally
developed within 30 seconds
Inhibition of parasympathetic
nervous signals
Pathogenesis

(From Mann DL: Mechanisms and models in HF: A combinatorial approach. Circulation 100:99, 1999; and Kaye DM, Krum H:
Drug discovery for heart failure: A new era or the end of the pipeline? Nat Rev Drug Discov 6:127, 2007.)
Pathophysiology
Neurohormonal system activation:
Sympathetic nervous system activation
RAA system activation
Cardiac myocyte remodeling
 Sympathetic Nervous system
Activation

Braunwalds Heart Disease, 9th ed

RAA system activation

(From Nohria A, Cusco JA, Creager MA: Neurohormonal, renal and vascular adjustments in heart failure. In Colucci WS [ed]: Atlas of Heart
Failure. 4th ed. Philadelphia, Current Medicine, 2005, p 107.)
 Cardiac Myocyte Cellular signaling pathways
Remodeling in cardiac hypertrophy
and failure

(From Colucci WS [ed]: Heart Failure: Cardiac Function and Dysfunction. 2nd ed. Philadelphia, Current Medicine, 1999, p 42)
(From Sawyer DB, Colucci WS: Molecular and cellular events in myocardial hypertrophy and failure. In Colucci WS [ed]: Atlas of Heart Failure. 4th
ed.Philadelphia, Current Medicine, 2005, p 62.)
CHRONIC HEART
FAILURE
Diagnosis and treatment
Symptoms
Typical : Atypical :
Breathlessness Nocturnal cough
Orthopneu Wheezing
Paroxysmal Nocturnal dyspneu Weight gain ( >2kg/week )
Reduced exercise tolerance Weight loss
Fatigue, tiredness, increase Bloated feeling
exercise recovery time Loss of appetite
Ankle swelling Confusion
Depression
Palpitation
Syncope
Sign
Specific : Less specific :
Elevated JVP Peripheral oedema
Hepatojugular reflux Pulmonary crepitation
3rd heart sound Pleural effusion
Laterally apical impulse Tachycardia
Cardiac murmur Irregular pulse
Tachypneu
Hepatomegaly
Ascites
Cachexia
Chronic Heart Failure

DIAGNOSTIC TEST
ECG If Normal, <10% is likely tobe systolic dysfunction
Chest X-ray
Normal X-ray HF X-ray
 Pulmonary vein
congestion

Cardiomegaly

Blunt CPA and kerley B

Lines
Enlargement of RA
Blunted Costophrenic Angle Blur pulmonary vasculature

Kerley B lines
CHEST X-RAY
Echocardiography
Provides information about :
- Cardiac anatomy
Volumes, geometry, mass
- Function
LV function
Wall motion
Valvular function
Right ventricular function
Pulmonary artery pressure
Pericardium
Stress Echocardiography

Using exercise or pharmacological stress

echocardiography:
To identify the presence and extent of inducible
ischaemia
Useful in evaluating patients with suspected
severe aortic stenosis, reduced EF, and a low
transvalvular gradient
Exercise testing (treadmill test)
An objective evaluation of exercise capacity and exertional symptoms
The 6-min walk test and a variety of treadmill and bicycle protocols
are available

Cardiac magnetic resonance

Non-invasive technique that provides most of the anatomical and
functional information
High accuracy and reproducibility of volumes, mass, and wall motion
Limitations include lack of availability, high cost and some
patients cannot tolerate because of claustrophobia
Ambulatory ECG monitoring
Assessment of patients with symptoms suggestive of arrhythmia or
bradycardia
Monitoring ventricular rate control in patients with AF
Identifying the type, frequency,and duration of atrial and ventricular
arrhythmias, silent episodes of ischaemia and conduction disturbances,
which may cause/exacerbate HF

Endomyocardial biopsy
Patients with suspected constrictive or restrictive cardiomyopathy
Patients with suspected myocarditis and infiltrative diseases
LABORATORY TEST
Chronic Heart Failure

MANAGEMENT
Goal of treatment
Relieve symptoms and signs (e.g. oedema)
Prevent hospital admission
Improve survival
Slow or prevent progressive worsening of HF
Improvement in quality of life
Increase in functional capacity
Non-Pharmacological

Adherence to treatment - only Alcohol Restriction

20-60% adhere to treatment Weight reduction
(Eur J of HF)
Smoking cessation
Symptoms recognition
Immunization
Weight monitoring Pneumococcal
Diet and nutrition - sodium Influenza
intake
Resistance or endurance
Fluid Restriction - 1.5-2L/day physical training
ACE- Inhibitor
Should be used in all patients with symptomatic HF and LVEF 40%, irrespective of
symptoms
CONSENSUS Mortality RRR 27%
SOLVD Mortality RRR 16%
SOLVD Hospitalization RRR of 26%
SOLVD ARR 4,5% NNT 22 in mild to moderate HF
CONSENSUS 14.6% for ARR and 7 for NNT in severe HF
RCT improve symptoms, exercise tolerance, quality of life, and exercise
performance.
ATLAS lisinopril high dose RRR 15% for mortality and hospitalization
compare to low dose
SOLVD RRR 20% for asymptomatic systolic HF
SAVE, AIRE, TRACE 26% RRR mortality and 27% RRR hospitalization
ACE- I Contraindication
Contraindication:
History of angioedema
Bilateral renal artery stenosis
Serum potassium (K+)concentration .5.0 mmol/L
Serum creatinine >220 mmol/L (~2.5 mg/dL)
Severe aortic stenosis
Side effect :
(creatinine >2.5 mg/dL or eGFR 30 mL/min/1.73 m2)
Abnormal Kalium(K+) level
ACE-I side effect
Worsening renal function
Cr up to 50% from baseline / (~3 mg/dL) --> acceptable
Cr 3.0 mg/dL --3.5 mg/dL) --> halve dose of ACEI and monitor blood chemistry
closely
Cr > 3.5 mg/dL --> stop ACEI immediately and monitor blood chemistry closely
Hyperkalemia
K > 5.5 mmol/L --> halve dose of ACEI and monitor blood chemistry closely
K > 6.0 mmol/L --> stop ACEI immediately and monitor blood chemistry closely
Symptomatic hypotension
Reduce the dose of diuretics and other hypotensive agents (except ARB/b-
blocker/aldosterone antagonist)
Cough
troublesome cough --> switch to an ARB
Beta-Blocker
CIBIS II (Bisoprolol), COPERNICUS (carvedilol), MERIT-HF
(Metoprolol CR/XL) RRR 34% in moratilty and 28-36% in
hospitalization
CIBIS II, MERIT-HF mild to moderate HF ARR in mortality 4.3%,
NNT 23 severe HF
COPERNICUS severe HF ARR 7.1% and NNT 14
SENIORS RRR 14% in cardiac hospitalization
Indication
LVEF 40%
Mild to severe symptoms (NYHA functional class II IV)
Optimal dose level of an ACEI or/and ARB (and aldosterone antagonist, if
indicated)
Patients should be clinically stable

Contraindication:
Asthma [COPD is not a contraindication]
Second or third-degree heart block, sick sinus syndrome (in the absence of
a permanent pacemaker), sinus bradycardia (<50 b.p.m.)
Beta-blocker side effect
Asymptomatic hypotension
Doesnt require intervention
Symptomatic hypotension
Often improve with time. Consider reducing dose of other
hypotensive agents (except ACEI/ARB)
Worsening HF
Increase dose of diuretic (temporary) and continue blocker
(lower dose) if possible
Excessive bradycardia
Record ECG to exclude heart block. Stop digitalis if
administered. Dose of blocker may need to be reduced or
discontinued
MRA (mineralcorticoid Antagonis)
RALES RRR 30% in mortality, 35% in hospitalization
RALES ARR 14,1% in mortalityt, NNT 9
EMPHASIS-HF RRR 37% in mortality and hospitalization
EMPHASIS-HF ARR 7,7% in mortality-morbidity, NNT 13
EPHESUS (diabetes) RRR 15% in mortality
MRA
Indications :
LVEF 35%
Moderate to severe symptoms (NYHA functional class III IV)
Optimal dose of a b-blocker and an ACEI or an ARB (but not an ACEI and
an ARB)
Contraindications :
K > 5.0 mmol/L
Cr > 2.5 mg/dL
Concomitant potassium sparing diuretic or potassium supplements
Combination of an ACEI and ARB
 Potential adverse effect
Hyperkalemia
K > 5.5 --> halve dose
K > 6.0 --> stop
Worsening renal function
Cr > 2.5 mg/dl --> halve dose
Cr > 3.5 mg/dl --> stop
Breast tenderness and/ enlargement
Switch from spironolactone to eplerenone
ARBs

Contraindications
As with ACEIs, with the exception of angioedema
Patients treated with an ACEI and an aldosterone antagonist
ARB should only be used in patients with adequate renal function and a
normal serum potassium concentration
Potential adverse effect
As with ACEIs except for cough
Ivabradine

Contraindication :
severe heart disease
hypersensitivity.
It should not be administered along with calcium channel blockers.
Ivabradine
Side effect:
Heart - Slow heart rate, palpitations, heart block, abnormal heart
rhythm, difficulty in breathing and fainting.
Central Nervous System - Headache, and dizziness.
Eye - Blurred vision.
Gastrointestinal - Nausea, vomiting and constipation.
Blood - Eosinophilia.
Musculoskeletal - Muscle cramps and muscle weakness.
Diuretics
Indications
HF and clinical signs or symptoms of
congestion
Initiations
Check renal function and serum
electrolytes
Most patients are prescribed loop
diuretics rather than thiazides (higher
efciency of induced diuresis and
natriuresis)
Dose up-titration
Start with a low dosage and increase until
clinical improvement of the symptoms and
signs of congestion
Hydralazine-ISDN
Functions
improves ventricular function and patient well-being
reduces hospital admission for worsening HF
Indications
An alternative to an ACEI/ARB when both of the latter are not tolerated
As add-on therapy to an ACEI if an ARB or aldosterone antagonist is not
tolerated
Contraindications
Symptomatic hypotension
Lupus syndrome
Severe renal failure
 Initiations
Starting dose: hydralazine 37.5 mg and ISDN 20 mg t.i.d
Dose up-titrations
Consider dose up-titration after 2 4 weeks
aim for evidence-based target dose
hydralazine 75 mg and ISDN 40 mg t.i.d or maximum tolerated dose
Potential adverse effect
Symptomatic hypotension
Arthralgia/muscle aches, joint pain or swelling, pericarditis/ pleuritis,
rash or fever
consider drug-induced lupus-like syndrome
check ANA
Discontinue H-ISDN
Digoxin
Functions
improves ventricular function and patient well-being
reduces hospital admission for worsening HF
No effect in survival
Indications
AF
With ventricular rate at rest > 80 b.p.m, at exercise > 110120 b.p.m
SR
LV systolic dysfunction (LVEF 40%)
Mild to severe symptoms (NYHA functional class IIIV)
Optimal dose of ACEI or/and an ARB, b-blocker and aldoster-one antagonist, if indicated
Contraindications
Second or third-degree heart block (without a permanent pacemaker); caution if
suspected sick sinus syndrome
Pre-excitation syndrome
Previous evidence of digoxin intolerance
 Initiations
Starting dose
Adult with normal renal function : 0.25 mg o.d
elderly and in those with renal impairment : 0.125 or 0.0625 mg o.d
Potential adverse effect
Sinoatrial and AV block
Atrial and ventricular arrhythmias, especially in the presence of
hypokalaemia
Signs of toxicity
Confusion
Nausea
disturbance of colour vision
Other drugs used to treat cardiovascular co-
morbidity
Anticoagulants (vitamin K antagonists)
recommended in patients with HF and permanent, persistent, or
paroxysmal AF without contraindications to anticoagulation
Antiplatelets agents
Antiplatelet agents are not as effective as warfarin in reducing the risk
of thromboembolism in patients with AF
There is no evidence that antiplatelet agents reduce athero-sclerotic
risk in patients with HF
HMG CoA reductase inhibitors (statins)
In elderly patients with symptomatic chronic HF and systolic
dysfunction caused by CAD -> reduce cardiovascular hospitalization
Patient with symptomatic (NYHA II-IV) systolic HF
Common Factors That Precipitate
Hospitalization forHeart Failure
Noncompliance with medical regimen, sodium and/or fluid restriction
Acute myocardial ischemia
Uncorrected high blood pressure
Atrial fibrillation and other arrhythmias
Recent addition of negative inotropic drugs (e.g., verapamil, nifedipine,
diltiazem, beta blockers)
Pulmonary embolus
Nonsteroidal anti-inflammatory drugs
Excessive alcohol or illicit drug use
Endocrine abnormalities (e.g., diabetes mellitus, hyperthyroidism,
hypothyroidism)
Concurrent infections (e.g., pneumonia, viral illnesses)

may be associated with a staggering degree of morbidity and mortality,

particularly in the elderly population
2009 Focused Update: ACCF/AHA Guidelines for the Diagnosis and
Management of Heart Failure in Adults
Surgical
Revascularization (CABG / PCI)
co-morbidities
Procedural risk
Coronary anatomy and evidence of the extent of viable myocardium in
the area to be revascularized
LV function
presence of haemodynamically signicant valvular disease
Valvular Heart Surgery
Aortic valve
AS
recommended in eligible patients with HF symptoms and severe AS
AR
recommended in all eligible patients with severe AR who have symptoms of HF
 Mitral Valve
MR
Organic
development of HF symptoms is a strong indication for surgery
recommended for patients with LVEF >= 30% (valve repair if possible)
Functional
severe functional MR and severely depressed LV function, who remain symptomatic
despite optimal medical therapy
Ischaemic
recommended in patients with severe MR and LVEF >= 30% when CABG is planned
Tricuspid Valve
TR
Right-sided HF with systemic congestion respond poorly to aggressive diuretic
therapy
Surgery for isolated functional TR is not indicated
 Left ventricular aneurysmectomy
in symptomatic patients with large, discrete LV aneurysms
Cardiomyoplasty and partial left ventriculectomy (batista op)
not recommended for the treatment of HF
External ventricular restoration
not recommended for the treatment of HF
Device management
CRT
NYHA III IV class who are
symptomatic despite optimal
medical therapy
Reduced EF (LVEF <=35%)
QRS prolongation (QRS width >=
120 ms)
ICD
Primary Prevention
at least 40 days post-MI
LVEF <= 35%
NYHA functional class II or III,
receiving optimal medical therapy
have a reasonable expectation of
survival with good functional status
for > 1 year
Secondary Prevention
survivors of ventricullar brillation
(VF)
documented haemodynamically
unstable VT and/or VT with syncope
LVEF <= 40%
on optimal medical therapy
expectation of survival with good
functional status for >= 1 year
Heart Transplant

Indications
motivated patients with end-stage HF
Severe symptoms
no serious co-morbidity
no alternative treatment option
 Contraindications
current alcohol and/or drug abuse
Lack of proper cooperation
serious mental disease not properly controlled
Treated cancer with remission and < 5 years follow-up
Systemic disease with multiorgan involvement
active infection
signicant renal failure (creatinine clearance < 50 mL/min)
irreversible high pulmonary vascular resistance (68 Wood units and
mean trans-pulmonary gradient > 15 mmHg)
Recent thromboembolic complications
unhealed peptic ulcer
evidence of signicant liver impairment
other serious co-morbidity with a poor prognosis
Left Ventricle Assist Device (LVAD) &
Artificial Heart
limited documentation from randomized clinical trials - class of
recommendation II, level of evidence C
bridging to transplantation
managing patients with acute, severe myocarditis
Ultrafiltration
Reduce uid overload (pulmonary and/or peripheral oedema)
Correct hyponatraemia in symptomatic patients refractory to
diuretics
ACUTE HEART
FAILURE
Pathophysiology, diagnosis, and
treatment
Definition
Acute heart failure (AHF) is defined as a rapid onset or change in
the signs and symptoms of HF, resulting in the need for urgent
therapy.
AHF may be either new HF or worsening of pre-existing chronic HF.
Patients may present as a medical emergency such as acute
pulmonary oedema.

ESC Guidelines for the Diagnosis and Treatment of Acute and Chronic Heart Failure ,2008
Causes and precipitating factors of acute heart
failure
Ischaemic heart disease Circulatory failure
Acute coronary syndromes Septicaemia
Thyrotoxicosis
Mechanical complications of acute MI
Anaemia
Right ventricular infarction Shunts
Valvular Tamponade
Valve stenosis Pulmonary embolism
Valvular regurgitation Decompensation of pre-exiting chronic
HF
Endocarditis Lack of adherence
Aortic dissection Volume overload
Myopathies Infections,especially pneumonia
Cerebrovascular insult
Postpartum cardiomyopathy
Surgery
Acute myocarditis Renal dysfunction
Hypertension/arrhythmia Asthma, COPD
Hypertension Drug abuse
Acute arrhythmia Alcohol abuse

ESC Guidelines for the Diagnosis and Treatment of Acute and Chronic Heart Failure ,2008
Pathophysiology
Initial phase Amplification phase

Myocardial stunning
Vicious Cycle
Hibernation

Cotter G et al. AHF: nomenclature. Pathophysiology, and outcome measures. In OConnor et al, Managing
Acute Decompensated Heart Failure, Taylor & Francis 2005.
Clinical presentation

Hypertensive AHF

Acutely
Decompensated
Chronic HF
PULMONARY
OEDEMA
ACS and
HF

Cardiogenic Right HF
shock
Clinical presentation
Worsening or decompensated chronic HF (peripheral
oedema/congestion)
there is usually a history of progressive worsening of known chronic HF on
treatment, and evidence of systemic and pulmonary congestion.
Low BP on admission is associated with a poor prognosis.
Pulmonary oedema
patients present with severe respiratory distress, tachypnoea, and
orthopnoea with rales over the lung fields.
Arterial O2 saturation is usually ,90% on room air prior to treatment with
oxygen.
Clinical presentation
Hypertensive HF
signs and symptoms of HF accompanied by high BP and usually relatively preserved LV
systolic function.
There is evidence of increased sympathetic tone with tachycardia and vasoconstriction.
The patients may be euvolaemic or only mildly hypervolaemic, and present frequently
with signs of pulmonary congestion without signs of systemic congestion.
The response to appropriate therapy is rapid, and hospital mortality is low.

Cardiogenic shock
evidence of tissue hypoperfusion induced by HF after adequate correction of preload
and major arrhythmia.
no diagnostic haemodynamic parameters cardiogenic shock is characterizedby
reduced systolic blood pressure (SBP < 90 mmHg or a drop of mean arterial pressure >
30 mmHg) and absent or low urine output < 0.5 mL/kg/h).
Rhythm disturbance are common.
Evidence of organ hypoperfusion and pulmonary congestion develop rapidly.
Clinical presentation
Isolated right HF
characterized by a low output syndrome in the absence of pulmonary
congestion with increased jugular venous pressure, with or without
hepatomegaly, and low LV filling pressures.

ACS and HF
many patients with AHF present with a clinical picture and laboratory
evidence of an ACS.
Approximately 15% of patients with an ACS have signs and symptoms of HF.
Episodes of acute HF are frequently associated with or precipitated by an
arrhythmia (bradycardia, AF, VT).
Acute Heart Failure

DIAGNOSIS
Initial assessment and monitoring of patients
Does the patient have HF or is there an alternative cause for their
symptoms and signs (e.g. chronic lung disease, anaemia, kidney
failure, or pulmonary embolism)?
If the patient does have HF, is there a precipitant and does it
require immediate treatment or correction (e.g. an arrhythmia or
acute coronary syndrome)?
Is the patients condition immediately life-threatening because of
hypoxaemia or hypotension leading to underperfusion of the vital
organs (heart, kidneys, and brain)?
Acute Heart Failure

HEMODYNAMIC
PROFILE
A B

2 minutes

L C
Acute Heart Failure

TREATMENT
Goals of treatment in acute heart failure
Treatment

ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
European Heart Journal, 2008
 Congestion at rest?
No Yes Diuretics
Low perfusion at rest
Vasodilator(nitrat)

ADHF

No A B
Acute pulmonary
edema
Hypertensive HF
Warm & dry Warm & wet

Cold & Wet

Cold & dry

L C
Yes

European Heart Journal of Heart Failure,2005;

March. Vol 7:323-331
 Congestion at rest?
Yes
Diuretic
No
Low perfusion at rest
Vasodilator

No A B
Warm & dry Warm & wet

Cold & Wet

Cold & dry

L C
Syok Kardiogenik
STEMI akut Killip 4
Yes
Inotropic drugs :
Dobutamine
Milrinone
Levosimendan

European Heart Journal of Heart Failure,2005;

March. Vol 7:323-331
 Congestion at rest?
No Yes
Low perfusion at rest

No A B
Warm & dry Warm & wet

Cold & Wet

Cold & dry

L
Right heart failure
Dehydration C
Yes
Excessive diuretics Fluid loading

European Heart Journal of Heart Failure,2005;

March. Vol 7:323-331
Oxygen
As early as possible in hypoxaemic patients to achieve O 2
saturation 95% (> 90% in COPD).
Class I, level C
NIV with PEEP as soon as possible in every patient with
acute cardiogenic pulmonary oedema
Contraindication:
- unconscious patients
- anxiety
- immediate need ET intubation
- severe obstructive airway disease
- severe Right HF
ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
European Heart Journal, 2008
Morphine

Morphine should be considered in the early stage of severe

AHF with restlessness, dyspnoea, anxiety, chest pain.
Respiration should be monitored
Caution: hypotension, bradycardia, advanced AV block, CO 2
retention

ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
European Heart Journal, 2008
Loop diuretics

Diuretics are recommended in AHF patients with

congestion and volume overload.
Class I, level B
Adverse effect:
- hypokalaemia, hyponatraemia
- hyperuricaemia
- hypovolaemia and dehydration
- neurohormonal activation
- may increase hypotension following ACEI/ARB therapy

ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
European Heart Journal, 2008
ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
European Heart Journal, 2008
Vasodilators

Vasodilators are recommended at an early stage for AHF

without hypotension or serious obstructive valvular
disease.
Class I, level B
Adverse effect:
- headache (nitrat)
- tachyphylaxis (nitrat)
- hypotension (NTG or nesiritide infusion)

ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
European Heart Journal, 2008
ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
European Heart Journal, 2012
Inotropic agents

Inotropic agents should be considered in low output

states, in the presence of hypoperfusion or congestion.
Dobutamine (class IIa, level B)
Dopamine (class IIb, level C)
Milrinone and enoximone (class IIb,level B)
Levosimendan (class IIa, level B)
Norepinephrine (class IIb, level C)
Cardiac glycoside (class IIb, level C)

ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
European Heart Journal, 2008
Non pharmacological/non-device therapy
Restrict sodium and fluid intake
Ventilation
Non-invasive ventilation: CPAP, NIPPV
Endotracheal intubation and invasive ventilation
Mechanical circulatory support
Intra-aorticballoon pump
Ventricular assist devices
Ultrafiltration
THANK YOU