Management of Congestive

Cardiac Failure

BY
DR ANYAMELE
IBUCHIM
Definition
Epidemiology
Types
Pathophysiology
Clinical Presentation
Diagnosis
Investigations
Treatment
Complications
Follow up
Prognosis
 Introduction

Heart failure is a pathophysiologic state in

which the heart, due to an abnormality of
cardiac function (detectable or not), is unable
to pump blood at rates commensurate with the
needs of metabolising tissues, or does so only
with an elevated diastolic filling pressure.
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.
y be due to myocardial failure

also occur under conditions of high demand

presence of normal or near-normal myocard

mpensatory mechanisms set in to

ncrease blood volume
ncrease cardiac filling pressure
ncrease heart rate
ncrease cardiac muscle mass
these are in an attempt to restore cardiac out
normal.
wever, over time, these responses prove
leterious, with worsening heart failure

ny patients present without evidence of fluid

erload

bsequently, heart failure is preferred over th

der term, congestive heart failure.
 Epidemiology

Burgeoning problem worldwide, with up to 20

million people affected
3% of adults affected in developed countries

Nearly 5.6million Americans affected

Responsible for more hospitalizations than all

forms of cancers combined
valence increases with age- affects 6-10% of th
d 65years and above

t frequent cause of hospitalization in patient

d 65years and above

dence and prevalence higher in blacks, hispa

ive Americans and immigrants

dence and Prevalence remain the same for m

d women
wever, there are important differences:
omen tend to develop heart failure later in li
omen survive longer with heart failure
inical features more pronounced in women
omen develop depression more often
aemic cardiomyopathy commonest cause in
ustrialized nations

ertensive heart disease, Valvular disorders a

gas disease seen more in developing nations

ents tend to present earlier in developing

ons; with worse outcomes
ere is paucity of population-based data from
veloping countries like nigeria

rious studies from different areas in Nigeria h

ntified HTN, DCM, RHD as leading causes

he Abeokuta HF Registry, prevalence was 9%

ong medical admissions; women older than

etrospective study in UPTH from 2001-2005

Onwuchekwa and GE Asekomeh identified
mmonest causes of CCF as HTN-56.3%,CRF-7
rdiomyopathy- 12.3%,RHD-4.3%,IHD- 0.2%
 rall prevalence is increasing as treatment for
derlying heart disorders become more effecti
 Classification of Heart Failure

 Heart failure with reduced ejection fraction

(HFrEF) Ejection fraction < 40%
 Heart failure with preserved ejection fraction
(HFpEF) Ejection fraction > 50%
 Heart failure with mid-range ejection fraction
(HFmEF) Ejection fraction 41-49%
 Acute and chronic Heart Failure
 Right and left Heart Failure
 High Output Heart failure
 Pathophysiology

The pathophysiology of heart failure is

complex, multi-factorial and multi-faceted

Involves an interplay of different

compensatory mechanisms aiming to restore
cardiovascular function to a normal
homeostatic range
he short term, these systems are able to resto
diovascular function to normal/near-norma

wever, activation of these systems over time c

d to secondary end-organ damage within the
ntricles, with worsening cardiac decompensa

us a vicious cycle sets in whereby initial decre

pumping capacity triggers compensatory
chanisms, which when sustained over time a
eterious, resulting in further pump failure, a
en further activation of compensatory actions
an end stage is reached.
me of these mechanisms include:
Adrenergic activation and non-osmotic releas
ginine vasopressin(AVP)
ncreased heart rate and myocardial contract
timulates renin release
Renal vasoconstriction
ncrease in afterload
ncreased myocyte calcium,– arrythmogenic s
AVP effects– fluid retention, vasoconstriction
 Cardiac remodeling
 Primary myocardial response to chronically
increased wall
stress is myocyte hypertrophy, death/apoptosis and
regeneration.
 Leads to remodeling, usually eccentric type

 This worsens the loading conditions on the

remaining
myocytes, perpetuating the deleterious cycle

 Myocytes are replaced in the heart

 However, in HF, rate of loss far exceeds replacement

her vasoactive substances also play a rol
Endothelin 1
Tumor necrotic factor-alpha

P and BNP are released in response to atrial

d ventricular wall stretch
ey promote vasodilation and natriuresis

P also inhibits renin and aldosterone release

els are elevated in heart failure

wever, their effects are usually overwhelmed

 History

Breathlessness, manifesting as
Exertional dyspnoea
Orthopnoea
Paroxysmal nocturnal dyspnoea
Dyspnoea at rest
Acute pulmonary oedema
Other symptoms include

 Chest pain/pressure

 Palpitations

 Fatigue

 Nocturia and oliguria

 Cerebral symptoms
so ask for risk factors
Hypertension
Diabetes mellitus
Previous myocardial infarction
Alcohol abuse
Sleep-disordered breathing
Thyroid disease
Chemotherapy/radiation to the chest
Dyslipidemia
Valvular heart disease/familial heart disease
Myopathy
Substance abuse history
Coronary/peripheral vascular disease
hysical signs include
Respiratory distress
Cachexia
Central cyanosis
Diaphoresis
Peripheral oedema
Tachycardia, pulsus alternans
Raised, normal or low blood pressure
Distended neck veins, raised JVP
Normal or displaced apex
S3 gallop
Murmurs
Hepatomegaly, Ascites
Diagnosis
NYHA Class Symptoms

Cardiac disease, but no symptoms and no

limitation in ordinary physical activity, e.g.
I
no shortness of breath when walking,
climbing stairs etc.

Mild symptoms (mild shortness of breath

II and/or angina) and slight limitation
during ordinary activity.

Marked limitation in activity due to

symptoms, even during less-than-ordinary
III activity, e.g. walking short distances (20–
100 m).
Comfortable only at rest.

Severe limitations. Experiences symptoms

IV even while at rest. Mostly bedbound
patients.
 Investigations

The ACC/AHA, HFSA, and ESC recommend the

following basic laboratory studies in the initial
evaluation of patients with suspected HF

 FBC- may indicate anaemia or infection

 E/U/Cr- may be normal or abnormal
 FBG
 Liver function tests
 BNP and NT-proBNP
 Lipid profile
 ECG
Imaging tests include

 Chest radiography

 2-D echocardiographic and Doppler flow studies

 Coronary arteriography if ischaemic left

ventricular dysfunction is suspected

 Cardiac CT, MRI as indicated

er investigations include

hyroid stimulating hormone

roponin I if acute coronary syndrome is susp
IV screening
aemochromatosis screening
olter monitoring
ests for amyloidosis, rheumatological disord
rine and serum protein electrophoresis
enetic testing for at-risk patients
 Treatment

The goals of treatment are

 Alleviate symptoms

 Address the underlying conditions

 Slow/reverse cardiac remodelling

 Prolong life
is important to address certain
o-morbidities including

Coronary artery disease

Sleep apnoea

Anaemia

Atrial fibrillation

Cardio-renal syndrome
Medical care of CCF include

 Non-pharmacological

 Pharmacological

 Invasive therapies

When progressive end-stage HF occurs despite

Maximal medical therapy; when prognosis is
Poor, and when there`re no viable therapeutic
alternatives, standard for therapy is cardiac
transplantation
However, ventricular assist devices(VADs), and
total artificial hearts(TAH) serve as a bridge to
surgery

Ventricular assist devices are increasingly being used

as a permanent therapy
 Non-Pharmacological care

 Sodium and water restriction

 Sodium restriction to 2-3g/day

 Water restriction to 2L/day, especially if
hyponatremic

 Diet and lifestyle modifications

 Encourage physical activity as tolerated
 Attention to weight gain– ensure daily weighing
 Advise on regular drug compliance
 Pharmacological Therapies

The 2013 ACC/AHA guidelines, the 2010 HFSA

guidelines, and the 2008 ESC guidelines
recommend the following drug groups

 Diuretics - for symptomatic relief

 ACEIs – neurohormonal modification, vaso-

dilatation, improvement in LVEF and survival
benefit
Angiotensin receptor blockers – survival ben

Hydralazine and nittrates -- survival benefit

ẞ-adrenergic blockers -- survival benefit

Aldosterone antagonists – survival benefit

Digoxin – improved symptoms and reduced

hospitalization
Anticoagulants –reduce risk of thromboembo

Inotropic agents – restore organ perfusion

Newer therapeutic interventions include
 Ivabradine, approved in April 2015 following
the SHIFT trial. It blocks the HCN channel res-
ponsible for the cardiac pacemaker current, I(f)
which regulates heart rate without any effect
on ventricular repolarization or myocardial
contractility.

 Sacubitril/Valsartan, approved in July 2015

following the PARADIGM-HF trial. It belongs to
the Angiotensin receptor neprilysin inhibitor
class.
 Nesiritide, a human natriuretic peptide analogue
It reduces
 Pulmonary capillary wedge pressure
 Right atrial pressure
 Systemic vascular resistance
A vasodilator that was initially thought to alleviate
dyspnoea faster than nitroglycerin when combined
with diuretics

 Aliskiren, a direct renin inhibitor. However, it

does not replace ACE-Is or ARBs in Management
protocols
From: 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failureThe Task Force
for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology
(ESC)Developed with the special contribution of the Heart Failure Association (HFA) of the ESC
Eur Heart J. 2016;37(27):2129-2200. doi:10.1093/eurheartj/ehw128
Eur Heart J | The article has been co-published with permission in European Heart Journaland European Journal of Heart
Failure.All rights reserved in respect of European Heart Journal. © European Society of Cardiology 2016. All rights reserved. For
 Device Therapies

These are used for electrophysiologic interven-

tions in heart failure. They include
 Pacemakers

 Cardiac resynchronisation therapy devices

 Implantable cardioverter-defibrillators
Pacemakers could be temporary or permanent.

If there`re indications for permanent pacing, a

cardiac resynchronisation therapy is used.

They are usually used to maintain a normal

chronotropic response and AV synchrony

ICDs remarkably reduce the risk of sudden deaths

from ischaemic and non-ischaemic sustained
ventricular tachyarrhthmias in HF patients.

Recommended in all patients with LVEF < 35%

Cardiac resynchronisation therapy aims to improve
cardiac performance by restoring the heart`s
interventricular septal electrical and mechanical
synchrony

It reduces presystolic mitral regurgitation and

optimizes diastolic function
Ventricular assist devices are also available.

 Left ventricular assist device

 Right ventricular assist device

 Biventricular assist device

They`re superior to medical therapy in terms

quality and quantity of life in refractory heart
failure patients
Cardiac transplantation
 Preferred therapy in refractory, end stage
heart failure with poor prognosis and when
no other feasible therapy is available

 Limited by donor availability and long

waiting lists
 Prognosis

Prognosis is poor, despite advances in

therapy
 Mortality after hospitalization
 10.4% at one month
 22% at one year
 42.3% at 5 years
Poor prognostic factors include anaemia,
hyponatremia, advanced stage, elevated BNP and
NT-proBNP, poor socioeconomic status etc
 Follow up

Regular follow up visits are very important

Home calls and support staff visits also

important
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