Congestive heart failure

Elias S. (MD+)
March 2015
DBU

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 Introduction
CHF is a clinical syndrome in which the heart fails to
pump adequate blood to meet the metabolic demands
of the body.
It can result from structural or functional disorder of
the heart that impairs the ability of the ventricle to fill
or eject blood.
It represents an end stage of a number of different
diseases.

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 Etiology
 ischemic heart disease

 valvular heart disease

 cardiomyopathy

 hypertensive heart disease

 congenital heart disease

 pericardial diseases

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 Precipitating factors
These are relatively acute disturbances which place
additional work load on the myocardium which is
chronically and excessively burdened

They usually don’t cause CHF by themselves but unmask

an asymptomatic cardiac dysfunction and make patients
symptomatic

Knowing these factors is important because most are

treatable and cardiac function improves when they are
relieved
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 Precipitaing factors Contd…
H – hypertension
E – infective endocarditis
A – anemia
R – recurrent rheumatic fever and myocarditis
T – thyrotoxicosis and pregnancy
F – fever ( infections)
A – arrhythmia
I – infarction
L – lung infection
E – embolism ( pulmonary)
S – stress ( psychological , physical , dietary)

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 Pathophysiology of
chronic CHF
1 . The frank starling mechanism :
- increased preload ( adaptive )
-increased EDV
-stretching of sarcomeres
- increased contractility
- increased preload ( maladaptive)
-excessive strethcing of sarcomeres
-decreased contractility

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 Pathophysiology contd..
2. increased after load(adaptive)
-hypertrophy
- increased contractility
- increased after load ( maladaptive )
- impaired ventricular filling

3. Neurohormonal mechanisms :
A. Adrenergic nervous system
- increased myocardial contractility
(adaptive mechanism)
-but also increases afterload and increases the work load on the
ventricles(maladaptive )

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 Pathophysiology Contd..
B. The rennin angiotensin aldosterone
system(RAAS)
- increased salt and water retention
-maintains cardiac out put ( adaptive )
-but this in the long run results in increased preload
to the heart and contributes to CHF
-also contributes to the occurrence of edema
-angiotensin is also vasoconstrictor and it contributes
to the increase In the afterload(maladaptive)

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 Pathophysiology Contd…
 These neurohormonal mechanisms are initially adaptive
responses to the cardiac dysfunction which results from
any of the etiologic agents listed above.
 But in the long run these adaptive mechanisms further
increase the cardiac work load to increase the cardiac
output
 These results in hypertrophy , dilation and remodelling
of the ventricles which finally damages the myocytes
and worsens the failure state
 Treatment to prevent progression of CHF is directed in
antagonizing these neurohormonal mechanisms.
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 Forms of CHF
1. Systolic versus diastolic :
systolic failure :inability of ventricles to pump sufficient
blood
eg. dCMP , IHD
-presents primarily with weakness and decreased exercise
tolerance
diastolic failure : inability of ventricles to relax normally
during diastole and decreased filling of blood
eg. hCMP , r CMP , constrictive pericarditis , IHD
-primarily present with edema
NB. Most CHF results from combination of the two forms

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 Forms CHF contd..
2. Right sided versus left sided :
left sided failure : dyspnea , orthopnea , PND
right sided failure: peripheral edema ,
hepatomegally , ascites

NB. -Right sided failure usually results from leftsided

failure.
- isolated right sided failure which results from
pulmonary hypertension is called cor pulmonale

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 Forms CHF contd..
3. High output vs low out put failure :
high output : thyrotoxicosis , anemia , AR
low out put : IHD , d CMP , r CMP
4. Acute vs chronic failure :
acute : extensive MI , rupture of valves , myocarditis ,
massive PE
-predominantly systolic abnormality
-pulmonary edema or hypotension ( cardiogenic shock )
with out peripheral edema
chronic : d CMP, VHD
-BP is usually maintained , edema is common

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 Approach to patients with CHF
History:
Symptoms of CHF :
- progressive exertional dyspnea
-orthopnea
-paroxysmal nocturnal dyspnea
-cough productive of pink frothy sputum
-wheezing (cardiac asthma)
-peripheral edema , abdominal distension (ascites)
- right upper quadrant abdominal pain (congested liver)
non specific symptoms : fatigue , light headdness , malaise

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 Approach contd..
Risk factors suggestive of etiology :
-history of rheumatic fever : sore throat , migratory
joint pain , abnormal body movt
-history of HTN and DM
- history of angina and intermittent claudication
- smoking and alcoholism
-family history of heart disease , and sudden death

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 Approach contd..
Risk factors suggestive of precipitating factors:
- tooth extraction , GIT , GUT instrumentation
fever, reddish urine (for IE)
-new onset palpitation ( for arrhythmia)
-symptoms of anemia
-symptoms of thyrotoxicosis
-pregnancy
-drug discontinuation

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 Approach contd..
Physical examination :
signs of reduced CO
- tachycardia
-cool and pale or cyanotic extremities
-diaphoresis
signs of volume overload :
-basal rales
-peripheral edema
-ascites, tender hepatomegaly , splenomegaly
-raised JVP
-hepatojugular reflex

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 Approach contd..
signs of cardiac enlargment :
-displaced apical impulse
-heaves
other signs of CHF :
- S3 gallop
signs of underlying etiology :
-murmurs of VHD
-distant heart sounds in pericardial effusion or pericardial
friction rub or knock in pericarditis
signs of precipitating factors :
anemia , arrythmias , thyrotoxicosis

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 Approach contd..
Investigations :
chest x ray : findings suggestive of CHF
- cardiomegally ( cardiothoracic ratio > 50%)
- cephalization
- pulmonary edema
- pleural effusion
ECG ( electrocardiogram) : shows findings that suggest specific
etiologies
- identifies arrythmia
Echocardiography : provides important information about ventricular
size , function and valvular abnormalities
Other investigations to identify precipitating factors should also be done.
They are discussed In the respective chapters.

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 Modified Framinghams criteria for
diagnosis of CHF
diagnosis requires 2 major or 1 major and two minor
criteria not attributed to other medical conditions

Major criteria
Paroxysmal nocturnal dyspnea
Orthopnea
Elevated JVP
Third heart sound
Pulmonary rales
Cardiomegally on chest x ray
Pulmonary edema on chest x ray
Weight loss >= 4.5 kg in five days in response to treatment of presumed CHF
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 Framingham contd..
Minor criteria
Bilateral leg edema
Nocturnal cough
Dyspnea on ordinary exertion
Hepatomegaly
Pleural effusion
Tachycardia ( HR >= 120 bpm)
Weight loss > = 4.5 kg in five days

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 NYHA functional classification of severity
Functional Objective assessment
capacity
Class 1 No limitation of physical activity , ordinary physical
activity doesn’t cause symptoms
Class 2 Slight limitation of physical activity , ordinary physical
activity results in dyspnea and fatigue
Class 3 Marked limitation of physical activity , less than ordinary
activity causes dyspnea and fatigue
Class 4 Symptomatic at rest

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 Staging of heart disease
Stage A : those who are at high risk to develop heart failure but with
out structural heart disease ( eg. DM , HTN )

Stage B : those who have structural heart disease but with out
symptoms ( eg. previous MI )

Stage C : those who have structural heart disease and who have
developed symptoms

Stage D : those who have refractory HF requiring special

interventions like cardiac transplantation

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 Writing complete diagnosis of
CHF
1. The severity of the failure state as NYHA class
2. The stage of the disease
3. The failure state as CHF
4. The underlying etiology
5. The anatomic abnormality( eg. Valve abnormalities
as MR , MS etc
6. The precipitating factor

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 Management of CHF
Principles of management
1. identify and treat the precipitating factor
2. control the congestive state
3. prevention of deterioration of myocardial function
4. treat the underlying cause

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 A. General measures
Dietary sodium restriction : less than 2gm per day

Activity and life style modifications :

-small and frequent meals
-reduce anxiety and emotional stress
- avoid excess physical exercise
-weight loss for obese patients
-cessation of smoking
-avoid other CVD risk factors

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 B. Control of the congestive state
1.Reduction of cardiac work load :
- those general measures stated

2. Control of excess fluid :

-salt restriction
Diuretics :
a. loop diuretics : furosemide( lassix)
- potent diuretics useful in all forms of CHF
-started at lower dose like 20 – 40 mg po or 20 mg iv and increased if
there is no response to doses as high as 400 mg po daily or 160 mg iv per day
Side effects : hypokalemia , hypovolemia , hyperuricemia, hyperglycemia

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 Control of congestive state contd..
b. thiazides : hydrochlorthiazide , chlorthiazide
-weaker diuretic agents useful in mild CHF alone
or used in combination with loop diuretics in CHF
which doesn't respond to high dose lasix
- Dose hydrochlorthiazide 25 mg per day
increased up to 100 mg per day.
Side effects : hypotension , hypokalemia

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 Control of congestive state contd..
c. potassium sparing diuretics : spironolactone
are aldosterone antagonists
-weak diuretics , usually used with other diuretics
for their potassium sparing property
-spironolactone dose: initiall dose is 25 mg po per
day increased up to 100 mg BID
side effects: hyperkalemia , gynecomastia
since hyperkalemia is a life threatening side effect
of spironolactone it is contraindiacated in ptients with
renal failure

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 Control of congestive state contd..
3. enhancement of myocardial contractility(inotropic
agents) :
cardiac glycosides : digoxin and digitoxin
digoxin is less toxic than digitoxin it is the commonly used
effects :- positive inotropic effect (increase myocardial
contractility)
-increased authomaticity(arrythmia)
-delays AV node conduction
uses :- in systolic heart failure not responding to
diuretic therapy
- particularly when atrial fibrillation co exists with
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CHF
 Control of congestive state contd..
dose : 0.25 mg per day
- it is excreted via the kidneys and therfore dose should be reduced to
0.125 mg per day in patients with renal failure and elderly.
Toxicity of digoxin :
early non cardiac : anorexia , nausea ,
vomiting,
chronic toxicity : weight loss , neuralgia , worsening of CHF, intractable
vomiting
treatment of toxicity :
-discontinue digoxin
-treat the arrhythmia
-supplement potassium if hypokalemic
-anti digoxin antibodies
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 C. Prevention of deterioration of
myocardial function
The following drugs prevent deterioration in myocardial function by antagonizing the
neurohormonal mechanisms which cause cardiac remodelling and progression of failure state
1.Angiotensin converting enzyme inhibitors (ACEIs) : captopril ,
enalapril
-inhibit the RAAS
-start at low dose : captopril 6.25 mg po per day , enalapril
2.5 mg per day and increase dose
to maximum of captopril 50 – 100 mg po qid and enalapril 20 mg
po bid
side effects : angioedema , cough
acute renal failure , hyperkalemia
contraindications : angioedema , renal failure
hypotension
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 Prevention of myocardial ..contd..
2. Angiotensin receptor blockers :
given to patients who are intolerant to ACEI s
losartan : 25 – 50 mg once or twice daily

3.Aldosterone antagonists :
spironolactone as discussed earlier

4.Beta adrenergic receptor blockers :

-metoprolol initial dose 6.25 mg po bid to 75 mg po bid
has shown to decrease mortality from CHF
contraindicated in: unstable heart failure ,hypotension , bradycardia
, AV block and asthma

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 D. Treatment of the underlying cause
Surgery for valvular heart disease

Implantation of cardiac prosthesis

Cardiac transplantation

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 Thank you !!

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