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Heart Failure

DEFINITION

A cardiac output insufficient in meeting the metabolic demands of the body, as a result of any
structural or functional cardiac disorder.

Clincal syndromes of heart failure:
High output HF
In the case of high output HF, the metabolic demands of the body outweigh even an
increase in cardiac output.
Low output HF
Failure of the heart as a pump.

Left ventricular failure
Impaired function of the LV, resulting in congestion of blood in the pulmonary veins,
leading to RV failure.
Right ventricular failure
Impairment of the RV, resulting in a backlog of blood into the systemic circulation.

N.B It is rare to see pure failure on a single side as the complex syndrome rarely affects one
side only. A notable exception is RV failure due to pulmonary hypertension.


AETIOLOGY

Low Output HF High Output HF
Ischaemic heart disease (35-40%)
- myocardial infarction leading to decreased
myocardial contractility
Anaemia
Cardiomyopathy (dilated) (30-34%) Thyrotoxicosis
Hypertension (15-20%)
- due to increased resistance or due to
increased blood volume via renal failure or
overtransfusion
Pregnancy
Cardiomyopathy (undilated)
- hypertrophic/obstructive, restrictive
L to R shunt (AV shunt)
Valvular heart disease Beri-beri
Congenital heart disease (ASD,VSD) Septicaemia
Alcohol and drugs (e.g chemo) Haemochromatosis
Right heart failure
- RV infarct, pulmonary hypertension, PE,
COPD
Pagets disease
Arrythmias
- AF, bradycardia , tachycardia

Compromised cardiac filling
- constrictive pericarditis, pericardial effusion




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PATHOPHYSIOLOGY



In patients with heart failure the stroke volume falls considerably. This causes cardiac output to
fall leading to:
Blood pressure to fall (BP = CO x resistance) and this is sensed by baroreceptors and
through a fall in renal blood flow.
Signals from baroreceptors result in the stimulation of the sympathetic nervous system.
This restores blood pressure to normal levels by increasing heart rate (via B1-receptors)
and blood volume (B-adrenoceptors in the kidney) and increasing vascular resistance
(a1-receptors in arterioles).
The CO is therefore compensated for at the expense of increased HR, peripheral
vascular resistance (afterload) and blood volume (preload).

The vicious cycle:
The increased rate of the heart, coupled with
the increased resistance (increase in
afterload) leads to thickening of the ventricular
walls.
This thickening causes a reduction in the
volume of the ventricle chamber, further
reducing stroke volume. Physiologically the
thickening is caused by myocyte hypertrophy
with increased collagen synthesis and altered
myosin gene expression.
The reduction in renal perfusion activates
RAAS. This leads to salt and water retention
in the tissue and pooling of blood in the
central veins
The increase in CVP leads to an increase in
preload.
Preload obeys Starlings Law: As end
diastolic volume increases, stroke volume,
and thereby cardiac output, increases until
the physiological limit is reached. As the CO
compensation has already occurred in previous cycles, the physiological limit is therefore
reached and stroke volume can no longer increase.
This means the heart becomes overloaded with blood and becomes dilated.

Pathophysiological changes
Ventricular dilatation
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Myocyte hypertrophy with increased collagen synthesis and altered myosin gene
expression
Increased ANP secretion
Salt and water retention
Sympathetic stimulation
Peripheral vasoconstriction
Altered sarcoplasmic Ca2+ ATPase density. This means that there is a prolongation of
contraction and relaxation.
















SIGNS & SYMPTOMS

N.B RVF leads to a backlog into the systemic
circulation leading to systemic symptoms whilst
LVF leads to a backlog in the pulmonary
circulation leading to respiratory symptoms. CHF
(both RVF and LVF occurring at the same time)
incorporates all symptoms.

Symptoms
Increased venous pressure leads to alveolar
oedema, impairing gas exchange and reducing
the compliance of the lungs. Manifests as:
Dyspnoea
Orthopnoea (lying flat increases venous
return, making breathlessness worse)
Paroxysmal nocturnal dyspnoea
Fatigue
Dizziness (hypotension leading to
decreased cerebral perfusion)

Signs
Cardiomegaly (leading to displacement
of the apex beat)
Raised JVP
Tachycardia (compensatory mechanism in an attempt to increase CO)
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Hypotension
Bi-basal crepitations (LVF)
Pleural effusion (LVF)
Ankle and sacral oedema (RVF)
Ascites (RVF)
Tender hepatomegaly(RVF)

INVESTIGATIONS & DIAGNOSIS

Investigations
Blood tests
FBC, LFTs, U&Es, B-type
natriuretic peptide (BNP), cardiac
enzymes and TFTs are all useful.
Chest X-ray
Looking for cardiomegaly,
pulmonary congestion with upper
lobe division, fluid in fissures,
Kerley B lines and pulmonary
oedema.
ECG
Previous MI or an arrythmia.
Echocardiography
Essential investigation checking for dimensions and funtion of the heart (especially LV)
and valves.
Nuclear cardiology
Can quantify ejection fraction.
Cardiac catheterisation
Can diagnose HF caused by ischaemia.

N.B If ECG and BNP are normal, HF is unlikely; if either are abnormal, then echocardiography
is required.

Diagnosis












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MANAGEMENT



General life-style advice
Diet
- Lose weight and obtain healthy BMI
- Large meals avoided
- Reduce salt intake
- Reduce alcohol intake
- Fluid restriction (severe HF)
Stop smoking
Bed rest during exacerbations but low-level endurance activity otherwise
Vaccinations (pneumococcal and influenza)

Medical management
Diuretics
- Act by promoting the renal excretion of salt and water by blocking tubular reabsorption
of sodium and chloride.
- Loop diuretics (e.g furosemide) should be given in patients with fluid overload.
- In severe HF combination of loop and thiazide diuretics (e.g bendroflumethazide) may
be required.
- Serum electrolytes and renal function must be monitored regularly, due to risk of
hypokalaemia and hypomagnesaemia.
ACE inhibitors
- Acts by blocking the conversion of Ang I to Ang II, thereby acting as a vasodilator (Ang
II is a potent vasoconstrictor).
- Also has mild diuretic effect as reduces aldosterone secretion.
- S/E include cough, hypotension, hyperkalaemia and renal dysfunction.
- C/I: pregnancy
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Angiotensin II receptor antagonists (ARA)
- Block Ang II receptor
B-Blockers
- Inhibit sympathetic activity on the heart, reducing HR and CO.
Cardiac glycosides Digoxin
- Positive inotropic effect in sinus rhythm.
Vasodilators
- Reduces pre-load and after-load.
- Indicated in patients who cannot tolerate ACE-I or ARAs.



Surgical management
Biventricular pacemaker
In advanced heart failure discoordinated ventricular contraction occurs, meaning that
different parts of the ventricle contracts at different times. This leads to loss of cardiac
output, as blood moves around the ventricle. Complications include: thromboembolism
(risk reduced with warfarin), AF (give digoxin) and pump failure.
Cardiac transplantation

PROGNOSIS

Heart failure is associated with significantly reduced physical and mental health, resulting in a
markedly decreased quality of life. With the exception of heart failure caused by reversible
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conditions, the condition usually worsens with time. Although some people survive many years,
progressive disease is associated with an overall annual mortality rate of 10%.


Acute Heart Failure
P. 787 OHCM Severe pulmonary oedema