Heart Failure

Heart failure is present when the heart is unable to

pump blood forward at a sufficient rate to meet the
metabolic demands of the body (forward failure)
Or
Is able to do so only if the cardiac filling pressures are
abnormally high (backward failure)
Or
Both.

Lilly. 2011. Pathophysiology of heart disease 5th Edition

 HF is a clinical syndrome characterized by
typical symptoms(e.g. breathlessness, ankle
swelling and fatigue) that may be
accompanied by signs (e.g. elevated jugular
venous pressure, pulmonary crackles and
peripheral oedema) caused by a structural
and/or functional cardiac abnormality,
resulting in a reduced cardiac output and/ or
elevated intracardiac pressures at rest or
during stress.

ESC guideline acute and chronic HF 2016

Key mediators of cardiac output. Determinants
of the stroke volume include contractility, preload, and
afterload. Cardiac output Heart rate Stroke volume
Preload

Left ventricular (LV) performance (FrankStarling) curves relate preload, measured as LV end-diastolic volume
(EDV) or pressure (EDP), to cardiac performance, measured as ventricular stroke volume or cardiac output.

On the curve of a normal heart (middle line), cardiac performance continuously increases as a function of
preload. States of increased contractility (e.g., norepinephrine infusion) are characterized by an augmented
stroke volume at any level of preload (upper line). Conversely, decreased LV contractility (commonly associated
with heart failure) is characterized by a curve that is shifted downward (lower line). Point a is an example of a
normal person at rest. Point b represents the same person after developing systolic dysfunction and heart
failure (e.g., after a large myocardial infarction): stroke volume has fallen, and the decreased LV emptying
results in elevation of the EDV. Because point b is on the ascending portion of the curve, the elevated EDV
serves a compensatory role because it results in an increase in subsequent stroke volume, albeit much less
than if operating on the normal curve. Further augmentation of LV fi lling (e.g., increased circulating volume) in
the heart failure patient is represented by point c, which resides on the relatively fl at part of the curve: stroke
volume is only slightly augmented, but the signifi cantly increased EDP results in pulmonary congestion.

Afterload the ventricular wall stress ( ) that develops
during systolic ejection.

Where P is ventricular pressure,

r is ventricular chamber radius, and
h is ventricular wall thickness.
ETIOLOGY OF HEART FAILURE:
Conditions that cause left-sided heart
failure through impairment of
ventricular systolic or diastolic function.

A Note that in chronic stable stages the

conditions in this box may instead result
in heart failure with preserved EF, due
to compensatory ventricular hypertrophy
and increased diastolic stiffness
(diastolic dysfunction).
Right-Sided Heart Failure
Examples of Conditions That Cause
Right-Sided Heart Failure
CLASSIFYING HEART FAILURE:
TERMINOLOGY AND STAGING
TYPES OF HEART FAILURE

Systolic Dysfunction
Coronary Artery Disease
Hypertension
Valvular Heart Disease
Diastolic Dysfunction
Hypertension
Coronary artery disease
Hypertrophic obstructive cardiomyopathy
(HCM)
Restrictive cardiomyopathy
EJECTION FRACTION

ESC guideline acute and chronic HF 2016

 CLASSIFICATION OF HF: COMPARISON
BETWEEN ACC/AHA HF STAGE AND NYHA
FUNCTIONAL CLASS
ACC/AHA HF Stage1 NYHA Functional Class2

A At high risk for heart failure but without None

structural heart disease or symptoms
of heart failure (eg, patients with
hypertension or coronary artery disease)
I Asymptomatic
B Structural heart disease but without
symptoms of heart failure

II Symptomatic with moderate exertion

C Structural heart disease with prior or
current symptoms of heart failure
III Symptomatic with minimal exertion

D Refractory heart failure requiring IV Symptomatic at rest

specialized interventions

1Hunt SA et al. J Am Coll Cardiol. 2001;38:21012113.

2New York Heart Association/Little Brown and Company, 1964. Adapted from: Farrell MH et al. JAMA. 2002;287:890897.
PATHOPHYSIOLOGY HEART FAILURE:
COMPENSATORY MECHANISMS
1. The FrankStarling mechanism,
2. Neurohormonal alterations, and
3. The development of ventricular hypertrophy and
remodeling

Compensatory mechanisms in heart failure.

Both the FrankStarling mechanism (which is invoked by the rise in ventricular end-
diastolic volume) and myocardial hypertrophy (in response to pressure or volume
overload) serve to maintain forward stroke volume (dashed lines). However, the chronic
rise in EDV by the former and increased ventricular stiffness by the latter passively
augment atrial pressure, which may in turn result in clinical manifestations of heart
failure (e.g., pulmonary congestion in the case of left-sided heart failure).
 Neurohormonal Alterations
Adrenergic Nervous System
Sympathetic outflow to the heart and peripheral circulation is increased, and
parasympathetic tone is diminished. There are three immediate consequences :
1. An increase in heart rate,
2. Augmentation of ventricular contractility, and
3. Vasoconstriction caused by stimulation of -receptors on the systemic veins and
arteries.

ReninAngiotensinAldosterone System
The main stimuli for renin secretion from the juxtaglomerular cells of the kidney in heart
failure patients :
1. Decreased renal artery perfusion pressure secondary to low cardiac output,
2. Decreased salt delivery to the macula densa of the kidney owing to alterations in
intrarenal hemo dynamics, and
3. Direct stimulation of juxtaglomerular 2-receptors by the activated adrenergic
nervous system.
 Neurohormonal Alterations

Antidiuretic Hormone
Secretion of this hormone (also termed vasopressin) by the posterior pituitary is
increased in many patients with heart failure, presumably mediated through arterial
baroreceptors, and by increased levels of AII. ADH contributes to increased
intravascular volume because it promotes water retention in the distal nephron.

Natriuretic Peptides
Atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP).
They result in excretion of sodium and water, vasodilatation, inhibition of renin
secretion, and antagonism of the effects of AII on aldosterone and vasopressin levels.
COMPENSATORY MECHANISMS

Neurohormonal Alterations
Compensatory neurohormonal
stimulation develops in response to the
reduced forward cardiac output and
blood pressure of heart failure.
ReninAngiotensinAldosterone System
PRECIPITATING FACTORS
HOW HEART FAILURE IS DIAGNOSED

Medical history is taken to reveal symptoms

Physical exam is done
Tests
Chest X-ray
Blood tests
Electrical tracing of heart (Electrocardiogram or ECG)
Ultrasound of heart (Echocardiogram or Echo)
X-ray of the inside of blood vessels (Angiogram)
Common Symptoms and Physical Findings in Heart Failure
HOW HEART FAILURE IS DIAGNOSED

Framingham Criteria for Congestive Heart Failure

Diagnosis of CHF requires the simultaneous

presence of at least 2 major criteria or 1 major
criterion in conjunction with 2 minor criteria.

The Framingham Heart Study criteria are 100%

sensitive and 78% specific for identifying
persons with definite congestive heart failure.
 SYMPTOMS
Major symptoms Minor symptoms
Paroxysmal nocturnal dyspnea Bilateral ankle edema
Neck vein distention Nocturnal cough
Rales Dyspnea on ordinary exertion
Radiographic cardiomegaly (increasing Hepatomegaly
heart size on chest radiography) Pleural effusion
Acute pulmonary edema Decrease in vital capacity by one third
S3 gallop from maximum recorded
Increased central venous pressure (>16 Tachycardia (heart rate>120 beats/min.)
cm H2O at right atrium)
Hepatojugular reflux
Weight loss >4.5 kg in 5 days in
response to treatment
CARDIOMEGALY
KERLEY B LINES
PULMONARY VESSEL CONGESTION
 ECHOCARDIOGRAPHY (CONT.)

Systolic dysfunction:
Reduced LVEF (<45%)

Enlarged left ventricle

Thin LV wall

Eccentric LV remodeling

Mild or moderate mitral regurgitation

Pulmonary hypertension

Reduced mitral filling

Signs of increased filling pressure

 ECHOCARDIOGRAPHY (CONT.)

Diastolic dysfunction:
Normal LVEF (45%-50%)

Normal LV size

Thick LV wall, dilated atria

Concentric LV remodeling

No or minimal mitral regurgitation

Pulmonary hypertension

Abnormal mitral filling pattern

Signs of increased filling pressure

 TREATING CONGESTIVE HEART FAILURE

Upright position
Nitrates
Lasix
Oxygen
ACE inhibitors
Digoxin

Fluids(decrease)
After load (decrease)
Sodium retention
Test (Dig level, ABGs, Potassium level)
THERAPEUTIC ALGORITHM HFREF
 Acute Heart Failure
Rapid onset of symptoms and signs secondary to
abnormal cardiac function
Can present as new onset and without previously known
cardiac dysfunction or ADHF
Often life threatening and requires urgent treatment

AHF may present with one or several clinical

conditions:
1. Worsening or Decompensated Chronic Heart Failure
2. Hypertensive Heart Failure
3. Pulmonary Oedema
4. Cardiogenic Shock
5. Isolated Right HF
6. ACS and HF
CLINICAL CLASSIFICATIONS

Pulmonary congestion

ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
European Heart Journal, 2016
 CAUSES AND PRECIPITATING FACTORS
Ischaemic heart disease
Acute coronary syndrome
Mechanical complications of acute MI
RV infarction
Valvular
Valve stenosis
Valvular regurgitation
Endocarditis
Aortic dissection
Myopathies
Postpartum cardiomyopathy
Acute myocarditis
Hypertension/arrhythmias
Circulatory failure
Septicaemia
Thyrotoxicosis
Anaemia
Tamponade
Pulmonary embolism
Decompensation of pre-existing CHF
Volume overload
Infection
Cerebrovascular insult
Surgery
Renal dysfunction
Asthma, COPD
Drug and alcohol abuse
DIAGNOSTIC OF ACUTE HEART FAILURE
Based on presenting symptoms and clinical
findings
History
Physical examination
ECG
Chest X-ray
Echocardiography
Laboratory (BGA, etc)

ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure
European Heart Journal, 2008
FLUID OVERLOAD > Acute Decompensated Heart
Failure (ADHF)/Pulmonary Edema

>Medical Emergency!
 MONITORING
Non invasive:
Vital Sign
Oxygenation
Urine output
ECG
Invasive:
Arterial line (haemodynamic unstable)
Central venous lines
Pulmonary artery catheter
Coronary angiography
 GOALS OF TREATMENT
Immediate (ED/ICU/ICCU)
Improved symptom

Restore oxygenation and improve organ perfusion

Limit cardiac/renal damage

Minimize ICU length of stay

Intermediate (hospital)
Stabilize patient & optimize treatment strategy

Initiate appropriate pharmacology therapy

Consider device therapy

Minimize hospital length of stay

Long term and pre discharge management

Plan follow up strategy

Education

Prevention

Quality of life
 MANAGEMENT

Immediate symptomatic treatment

Patient distressed or in pain >> analgesia,
sedation
Pulmonary congestion >> diuretic, vasodilator
Arterial oxygen saturation < 95% >> increase FiO2,
consider CPAP, NIPPV, mechanical ventilation
Heart rate and rhythm disorder >> pacing,
antiarrhythmics, electroversion

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

As early as possible in hypoxaemic patients to achieve O2

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, CO2
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
 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
 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
PATIENT COUNSELING

Lifestyle changes

Monitoring for changes

Medications

Surgery
PATIENT COUNSELING

Lifestyle changes
Stop smoking
Loose weight
Avoid or limit alcohol
Avoid or limit caffeine
Eat a low-fat, low-sodium diet
Exercise
PATIENT COUNSELING

Reduce stress
Keep track of symptoms and weight
and report any changes or concern to
the doctor
Limit fluid intake
See the doctor more frequently
HEART FAILURE
COMPLICATIONS
Pleural effusion
Atrial fibrillation (most common
dysrhythmia)
Loss of atrial contraction (kick) -reduce CO by
10% to 20%
Promotes thrombus/embolus formation inc.
risk for stroke
Treatment may include cardioversion,
antidysrhythmics, and/or anticoagulants
HEART FAILURE
COMPLICATIONS
**High risk of fatal dysrhythmias (e.g., sudden
cardiac death, ventricular tachycardia) with HF
and an EF <35%

HF lead to severe hepatomegaly, especially

with RV failure
Fibrosis and cirrhosis - develop over time
Renal insufficiency or failure
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