Dr.

Lewa

CONGESTIVE CARDIAC FAILURE

Def: Congestive cardiac failure is a clinical syndrome resulting from a structural or fxnal cardiac
disorder with impaired ability of the ventricles to fill or eject blood at a rate commensurate to the
body’s metabolic demands.

Epidemiology
Heart failure is frequently due to coronary artery disease. The prevalence rises from about 1% at
50-59yrs to between 5-10% at 80-89yrs.
In the UK, most of the patients with heart failure are > 65yrs. Congestive cardiac failure carries a
poor prognosis with about 50% of patients with LV dysfxn dying within 2 yrs of diagnosis.
Many of the patients with CCF die from:-
 Sudden cardiac dysarrhythmias
 Myocardial dysfxn

Aetiology of CCF
- Pump Failure
 Muscle dysfxn; IHD, Cardiomyopathy, poisons.
 Restricted filling; mitral stenosis, pericarditis, cardiac tamponade.
 Heart rate abnormality
- Excess preload
 Regurgitant valves
 High output states; anaemia, thyrotoxicosis, thiamine deficiency.
- Chronic Excess after Load
 Long standing HTN
- Others
 infections
 electrolyte imbalance

Precipitants of heart failure

1. Anaemia
2. Infections including pneumonia and infective endocarditis
3. Uncontrolled HTN
4. Uncontrolled hyperglyceamia
5. Thyrotoxicosis –patients with heart failure must have the thyroid gland examined
6. Excessive exercise
7. Drugs – NSAIDS, steroids, Ca CBs
8. Pulmonary embolism
9. Patients already on medication (for CCF) and are non- compliant
10. Substance abuse
11. A new MI
12. Pregnancy
13. Arrhythmias
14. Electrolyte imbalance of whatever cause

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Pathophysiology
The pathophysiologic changes are usually due to overwhelmed compensatory mechanisms for
the heart to meet the body’s metabolic demands. The pathology results from:-
i) Haemodynamic changes
- Decreased output due to systolic dysfxn and decreased filling due to diastolic dysfxn
- The ejection fraction; a measure of EDV is decreased in systolic dysfxn as occurs in
decreased ventricular contractility like MI, myocarditis, dilated cardiomyopathy.
- Systolic dysfxn also occurs in ventricular outflow obstruction (pressure overload) as in
HTN,AS, PS, or it can occur in ventricular inflow obstruction as in MS, TS or in
ventricular volume overload like in MR, AR, VSD & ASD.
- Diastolic dysfxn results from impaired relaxation. In normal physiology, the heart’s
filling is passive, mostly from the normal atria. A second filling; atrial kick also brings
residual blood into the heart.
- The early/atrial kick ratio is normally greater than one (1) or 2 but in diastolic dysfxn, the
E.A ratio (measured using echo) is <1. In diastolic dysfxn, the ejection fraction is normal
and CO may be initially normal but with time, LV end diastolic pressure is shifted to the
left leading to CCF.
- Diastolic dysfxn can occur in:-
 Constrictive pericarditis
 Restrictive cardiomyopathy
 LVH
 Cardiac tamponade
ii) Neurohormonal changes
A fall in cardiac output usually activates counter regulatory neurohormonal mechanisms that
in normal physiological circumstances would support cardiac fxn.
Stimulation of the RAAS leads to vasoconstriction, salt and water retention, and sympathetic
activation mediated by angiotensin II, which is a potent constrictor of arterioles both in the
kidney and systemic circulation. This may initially maintain cardiac output through increased
myocardial contractility, HR and peripheral vasoconstriction. But prolonged sympathetic
stimulation leads to cardiac myocyte apoptosis, hypertrophy and focal myocardial necrosis.
Salt and water retention is promoted by the release of aldosterone, endothelin, severe heart
failure and ADH. Natriuretic peptides act as physiological antagonists to the fluid conserving
effect of aldosterone.
iii) Cellular changes and remodelling
After myocardial infarction, cardiac contractility is impaired and neurohormonal activation may
lead to hypertrophy of non –infarcted segments, with thinning, dilatation and expansion of the
infarcted segment (remodelling). This may lead to further deterioration in ventricular fxn and
worsening heart failure.
Remodelling leads to changes in calcium handling, adrenergic receptors, contractile apparatus
and myocyte structure.
NB: Mediators of cardiac remodelling
i) Norepinephrine and epinephrine (toxic to the heart muscles)
ii) Aldosterone
iii) ADH

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iv) Cytokines – These are secreted by macrophages, lymphocytes, monocytes which

release IL and TNF that are important in the cycle of myocyte hypertrophy and cell
death.
IL – 1 may accelerate myocyte hypertrophy, endothelin is a potent vasconstrictor and
excessive endothelin release may be responsible for pulmonary arterial HTN and
LVF. It’s also associated with myocyte growth and deposition of matrix.

Clinical syndromes of heart failure

1. Left ventricular failure
2. Right ventricular failure
3. Systolic heart failure – inadequate cardiac or forward failure.
4. Diastolic heart failure ( backward failure)
5. High output failure – associated with high cardiac output ( A-V shunt, beriberi, severe
anaemia or thyrotoxicosis) and elevation in pulmonary venous pressure.
6. Biventricular heart failure (Lt + Rt ventricular failure)
7. Acute and chronic heart failure

Presentation
S + S are not sensitive and specific and include:
- Dyspnoea, fatigue due to fluid retention.
- Pulmonary or peripheral oedema due to fluid retention. Patient could even have anarsaca.
- Orthopnoea, paroxysmal nocturnal dyspnoea or nocturnal cough with sputum production.
- Wheeze (cardiac asthma)
- Weight loss and muscle wasting ( cardiac cachexia)
- In RVF – patient has peripheral oedema or anarsaca, abdominal distension due to ascites,
breathlessness, nausea, anorexia, facial engorgement, pulsation in the neck.

Framingham clinical criteria for the diagnosis of heart failure:

Major criteria
1. Paroxysmal nocturnal dyspnoea (PND) –Depression of resp. centre makes patient wake
up at night once PaO2 levels fall. PND is also called cardiac asthma.
2. Orthopnoea – redistribution of retained fluid leads to increase in venous return to the
heart.
NB: The above 2 features occur with fluid retention.
3. Elevated JVP
4. Rales or crackles
5. Cardiomegally on CXR
6. S3 gallop
7. Plain pulmonary oedema on CXR
8. Weight loss of > 4.5kg in 5 days in response to treatment for heart failure.

Minor criteria
1. Bilateral leg oedema
2. Nocturnal cough

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3. Dyspnoea on ordinary exertion

4. Hepatomegally
5. Pleural effusion
6. Tachycardia >120/min
7. Weight loss > 4.5kg in 5 days in response to treatment.

Diagnosis of heart failure

2Major criteria or
1Major and 2 minor
Diagnosis of heart failure is usually made from:-
1. History
i) Precipitants must be looked for in the history
ii) Look for the underlying cause
- Identify the cause and if reversible correct it and the patient will be fine.
- Congenital valvular lesions
 Symptoms of heart failure from childhood.
 Recurrent admissions from childhood
 Failure to thrive
 Slow in educational progression
- Rheumatic fever – may be history of tonsillitis
- History of DM and other risk factors for coronary heart disease; smoking, obesity,
alcohol.
- Recent delivery – think of cardiomyopathy
- Drugs – ARVs and their SE
- Chemotherapy –doxorubicin
- Hiv infxn
iii) New York heart association
Enquire on activity and symptoms for
classification of heart failure
2. Physical examination
Patient may be ill –looking depending on severity, dyspnoic, tachypnoic, cyanosed, pale,
jaundice, leg oedema.
Vital signs –Temp, PR, RR, BP
Hands – pallor, cyanosis, splitter h’ges, finger clubbing, Osler’s nodes, nicotine staining.
Pulse – Rate, rhythm, volume, character compare both Rt and Lt radial pulse and take all
other pulses (all of them).
BP – Low systolic Bp or high systolic Bp
- Wide or narrow pulse pressure
Neck – distended neck veins JVP
Examine for thyroid gland enlargement
Chest – Abnormal chest (shape), scars, distended veins
- Hyperactive precordium
- May be displaced apex beat; heaving apex, tapping apex (ms)

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- Thrill, Lt parasternal heave

- Palpable P2
Auscultation – normal S1, S2
- S3 gallop rhythm in systolic failure
- S4 gallop rhythm in diastolic failure
- + murmurs
R/S – crackles + pleural rub
P/A – Abdo. distension
- Hepatic pulsation – tricuspid regurgitation on left heart failure
- Hepatomegally
- Ascites, thrill, shifting dullness
- Hepatojugular reflux

3. Investigation
i) FBC – Hb, WBC
ii) W/E – Electrolyte imbalance
iii) Serum creatinine
iv) LFTs – Acutely congestive – hepatic failure
- Chronically congestive – cardiac cirrhosis
v) CXR – for Framingham classification to rule out underlying pathology;
cardiomyopathy, ventricular hypertrophy, pulmonary oedema, pericardial effusion or
pleural effusion.
- Kerley ABC lines –linear opacities seen on CXR in patients with pulmonary oedema.
- Kerley A lines – longer, at least 2cm, unbranching, crossing diagonally from periphery to
hilar in the inner ½ of lungs. Are due to distension of anastomotic channels between
periphery & central channels.
- Kerley B lines – about 1-2cm long, generally horizontal and meet the pleura at right
angles to fat aspect of lungs.
- Typically seen as a ladder from below at costal angle.
- DDX – Pulmonary oedema
-CCF especially, LVF & MS
-Lymphangitis carcinomatosis
-Pulmonary fibrosis
-Parasitic infestation
-Heavy metal particles
-Haemosiderosis
- Kerley C lines –Non – specific reticular patterns. Are the least seen
4. ECG – To detect arrhythmias
5. Echo – is the best way to measure E.A ratio and for proper management.
6. MRI – Gold standard for assessing ventricular volume
7. BNP – Cardiac myocyte necrosis
-Is an expensive test
-A normal plasma level excludes heart failure

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Stages of heart failure (structural)

Stage A – A patient who has risk factors for heart failure e.g DM, smoking etc, but has no
structural heart disease or symptoms
Stage B- A patient with a structural heart dz e.g cardiomyopathy, valvular heart disease but is
asymptomatic.
Stage C – patients with prior or current symptoms of heart failure.
Stage D – refractory or end stage heart failure.

Classification of severity for heart failure

The New York heart association classification
This usually indicates the class or degree of heart failure, associated symptoms and activity
limitation.

Class / degree Symptoms and activity limitation

Class I – None No symptoms from ordinary activity
Class II – Mild HF Comfortable at rest or during mild exertion.
Dyspnoea on ordinary activity
Class III – Mod. HF Symptomatic with any activity
Class IV – Severe HF Symptoms at rest – confined to bed or chair

Management of heart failure

Aims
- To reduce symptoms
- To reduce morbidity
- To improve the quality of life
A. Quick assessment of patient
- Resuscitate patient with decompensated HF (patient with rapidly developing cardiogenic
pulmonary oedema).
- Prop up patient
- Give oxygen while checking O2 saturation
- I.V frusemide (slowly) is more effective than oral; larger doses are required in renal
failure.
- Opiates –Sedates patient, decrease anxiety and helps patient meet metabolic needs.
- Nitrates especially if systolic BP ≥ 100mmHg

B. Non pharmacological management

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1. Correct all precipitants

2. Lifestyle modification
- Comply with medications
- Salt restriction (2g/day)
- Alcohol ceasation
- Stop smoking
- Exercise training for ambulatory patients
- Limit fluid intake (input /output chart) to avoid hyponatraemia.
3. Look for underlying cause and treat or modify.
- HTN – optimize anti – HTN regime
- DM – control sugars
- Manage any coronary syndromes
- Arrhythmias – anticoagulate

Pharmacotherapy
- Manage symptoms and improve quality of life.
I) Asymptomatic LV systolic dysfxn
- ACE –I
- Health education
- Risk factors
- Rx precipitants
II) Symptomatic LV systolic failure
1. Start with loop diuretics
- Frusemide 40mg – 80mg preferably as OD dose, all at once rather than divided doses.
- Frusemide gives symptomatic relief of fluid retention.
- Monitor U/E, weight loss 1kg/day. Frusemide is a rapid response drug, if patient not
losing weight, change to thiazide diuretic preferably I.V.
2. ACE – I – Consider in all patients with LV systolic dysfxn
ACE –I commonly used
- Captoprill
- Lisinopril
- Enalapril
ACE –I – Improves heart failure symptoms
- Prolongs life
- Reduces mortality
Principles
- Response is immediate
- Once patient is losing fluid, no worsening of symptoms.
- Start with a low dose slowly
Enalapril 10-20mg BD
Captopril 6.25mg TID max 50mg
Lisinopril 5mg OD – max 40 mg OD
Over 1-2 wks – you can double the dose to the max dose depending on response.
Monitor –cough – usually due to increased bradykinin levels
If patient develops uncontrollable cough, change to ARB

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U/E – Hyperkalemia, azotemia. Candesartan, valsartan (ARBs) tested and found to be

good but do not give in patients with MI.
ARBs usually reserved for patients intolerant of ACE-I.
3. B – Blockers – only given when patient is generally stable and the BP is good.

CI – Asthma
- COPD
- Hypotension
- 2nd or 3rd degree heart block, bradycardia & sinus syndrome.
BB commonly used:
- Carvedilol – beta and alpha blocker, anti –oxidant
- Metoprolol (selective B1)
- Bisoprolol
- Nevibolol
BB – Improve LV ejection fraction & survival in patients with symptomatic LV dysfxn.
Always start at a low dose and titrate to target max doses e.g.
Carvedilol 3.125mg BD – 25 – 50mg BD
Bisoprolol 1.25mg OD – decreased 5-10mg OD
Metoprolol 12.5mg OD – max 25mg
NB: 1st one month, patient may get worsening of symptoms because of sympathetic effect which
is blocked.
Long term effect – down regulation alters over time.
The effects are usually long term, not short term.

4. ARB – Can be used as substitute to ACE –I or as an adl on therapy in HF.

5. Aldosterone blockers / antagonists
- Spironolactone – indicated if low ejection fraction <40%
- Dose 25 -50mg daily
- It improves endothelial dysfxn (nitric oxide bioavailability) and prevents remodelling
- Decreases mortality by 30%
- Is K+ sparing
- Eplerenone 25 -50mg OD – New York heart association class III.
6. Digoxin – for purely heart failure, start with low dose digoxin 0.125mg OD.
- It reduces rate of hospitalization
- Offers symptomatic relief benefits
- Good at controlling fibrillation
- No mortality benefits
NB: No significant improvement in survival rates.
7. Vasodilators
- Nitrates together with hydrallazine (combination);
- Indications – failure to control symptoms with all above drugs.
- Hydrallazine 25mg tid plus
- Isosorbide nitrate 40mg tid
The combination of hydrallazine & nitrate has more benefits in blacks than whites.

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- Provides an alternative in patients with ACE –I intolerance or those who may require
additional therapy for BP.
- Reduces mortality in symptomatic patients ( mortality benefit)
- Reduces rate of hospitalization
- Improves quality of life
D) Management of refractory heart failure
- Implantable cardioverter defibrillator (ICD.
Indications
- After cardiac arrest
- Ventricular tachycardia that is defibrillating
- Lt ventricular assists device indications include;
- Very slow ejection fraction < 30%
- Severe myocardial infarction
- If nothing is working then consider heart transplant.

Diastolic heart failure

Management – manage underlying cause
- Use drugs that manage fluid retention ( diuretics)