heart failure pdf - حسنين محمد سعيد

Heart failure

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Heart failure  describes  the  clinical  syndrome  that develops  when the  heart
cannot  maintain  adequate  output,  or can  do  so  only at  the expense  of
elevated  ventricular  filling pressure.

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In mild  to moderate forms  of  heart  failure,  symptoms  occur  only  when
the metabolic  demand  increases  during  exercise or  some  other form of
stress.  In severe heart  failure,  symptoms  may be  present  at rest.

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In clinical  practice,  heart failure  may be diagnosed  when a patient  with
significant  heart disease  develops  the  signs  or symptoms  of  a low  cardiac
output,  pulmonary  congestion  or systemic  venous  congestion  at  rest  or on
exercise

Left heart failure

This is characterised by a reduction in left ventricular output and an

increase in left atrial and pulmonary venous pressure.

If left heart failure occurs suddenly – for example, as the result of an

acute MI – the rapid increase in left atrial pressure causes pulmonary

oedema.

If  the  rise in atrial  pressure  is more gradual,  as  occurs with mitral

stenosis, there is reflex pulmonary vasoconstriction, which protects the

patient from pulmonary oedema.

However, the resulting increase in pulmonary vascular resistance causes

pulmonary hypertension, which in turn impairs right ventricular function.

Right heart failure

This  is  characterised  by a reduction  in  right  ventricular  output  and an
increase  in  right  atrial  and  systemic  venous  pressure.
The most common  causes  are chronic  lung  disease,  pulmonary  embolism
and  pulmonary  valvular  stenosis.

The term ‘cor  pulmonale’  is used  to describe  right  heart  failure  that is
secondary  to chronic lung  disease.

Biventricular heart failure

In biventricular  failure,  both  sides  of the heart  are  affected. This
may occur  because  the  disease  process,  such  as dilated
cardiomyopathy  or  ischaemic  heart  disease,  affects both  ventricles
or because  disease  of the left heart  leads  to chronic  elevation of
the  left atrial  pressure,  pulmonary  hypertension  and right heart
failure.

Prognosis

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Although  the  outlook  depends,  to some  extent,  on the
underlying  cause of  the problem,  untreated  heart failure generally
carries  a poor  prognosis;  approximately

50%

of patients with

severe heart failure due to left ventricular dysfunction will die
within

2 years

because of either pump

failure or malignant

ventricular arrhythmias.

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The most  common  causes  are  coronary artery  disease  and
myocardial  infarction  but  almost  all forms  of heart  disease  can
lead to heart  failure

Pathogenesis

Heart failure occurs when cardiac output fails to meet the
demands of the circulation. Cardiac output is determined by

preload

(the volume and pressure of blood in the ventricles at the

end of diastole),

afterload

(the volume and pressure of blood in

the ventricles during systole) and

myocardial contractility

, forming

the basis of Starling’s Law.

Ventricular dysfunction
 Ventricular dysfunction is the most common cause of heart failure. This

can occur because of impaired systolic contraction due to myocardial

disease, or diastolic dysfunction where there is abnormal ventricular

relaxation due to a stiff, non-compliant ventricle. This is most commonly

found in patients with left ventricular hypertrophy. Systolic dysfunction

and diastolic dysfunction often coexist, particularly in patients with

coronary artery disease.

 Ventricular dysfunction reduces cardiac output, which, in turn, activates

the sympathetic nervous system (SNS) and renin angiotensin aldosterone

system (RAAS). Under normal circumstances, activation of the SNS and

RAAS supports cardiac function but, in the setting of impaired

ventricular function, the consequences are negative and lead to an

increase in both afterload and preload.

Activation of the RAAS causes vasoconstriction and sodium and water

retention. This is primarily mediated by angiotensin II, a potent constrictor of

arterioles, in both the kidney and the systemic circulation.

 Activation of the SNS also occurs and can initially sustain cardiac output

through increased myocardial contractility and heart rate. Prolonged

sympathetic stimulation has negative effects, however, causing cardiac myocyte

apoptosis, cardiac hypertrophy and focal myocardial necrosis.

 Sympathetic stimulation also contributes to vasoconstriction and predisposes

to arrhythmias. Sodium and water retention is further enhanced by the release

of aldosterone,

endothelin-1

(a potent vasoconstrictor peptide with marked

effects on the renal vasculature) and in severe heart failure,

vasopressin

(antidiuretic hormone, ADH).

Natriuretic peptides are released from the atria in response to atrial dilatation

and compensate to an extent for the sodium-conserving effect of aldosterone,
but this mechanism is overwhelmed in heart failure.

Pulmonary and peripheral oedema occurs because of high left and right atrial

pressures, and is compounded by sodium and water retention, caused by
impairment of renal perfusion and by secondary hyperaldosteronism.

If the underlying cause is a myocardial infarction, cardiac contractility is

impaired and SNS and RAAS activation causes hypertrophy of non-infarcted
segments, with thinning, dilatation and expansion of the infarcted segment.
This leads to further deterioration in ventricular function and worsening heart
failure.

High-output  failure
Sometimes cardiac  failure  can occur  in  patients  without  heart
disease  due  to a  large arteriovenous  shunt,  or where there is  an
excessively  high  cardiac output  due  to beri-beri,  severe anaemia or
thyrotoxicosis.

Classification of heart failure

Left , right, congestive HF
Acute versus chronic HF
Systolic versus diastolic HF
Forward versus backward HF

Cardiac cachexia
Stages of heart failure

Complications

Several complications may occur in advanced heart failure

 Renal failure is caused by poor renal perfusion due to low cardiac output and

may be exacerbated by diuretic therapy, ACE inhibitors and angiotensin receptor

blockers (ARBs).

 Hypokalaemia may be the result of treatment with potassium-losing diuretics or

hyperaldosteronism caused by activation of the renin–angiotensin system and

impaired aldosterone metabolism due to hepatic congestion. Most of the body’s

potassium is intracellular and there may be substantial depletion of potassium

stores, even when the plasma concentration is in the reference range.

 Hyperkalaemia may be due to the effects of drugs that promote renal resorption

of potassium, in particular the combination of ACE inhibitors, ARBs and

mineralocorticoid receptor antagonists. These effects are amplified if there is renal

dysfunction due to low cardiac output or atherosclerotic renal vascular disease.



Hyponatraemia is a feature of severe heart failure and is a poor

prognostic sign. It may be caused by diuretic therapy, inappropriate

water retention due to high vasopressin secretion, or failure of the

cell membrane ion pump.



Impaired liver function is caused by hepatic venous congestion and

poor arterial perfusion, which frequently cause mild jaundice and

abnormal liver function tests; reduced synthesis of clotting factors can

make anticoagulant control difficult.



Thromboembolism. Deep vein thrombosis and pulmonary embolism

may occur due to the effects of a low cardiac output and enforced

immobility. Systemic emboli occur in patients with atrial fibrillation or

flutter, or with intracardiac thrombus complicating conditions such as

mitral stenosis, MI or left ventricular aneurysm.

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Atrial    and    ventricular    arrhythmias    are    very    common    and  may    be
related    to    electrolyte    changes    such    as  hypokalaemia    and
hypomagnesaemia,    the    underlying  cardiac    disease,    and    the    pro-
arrhythmic  effects  of sympathetic  activation.  Atrial  fibrillation  occurs  in
approximately  20%   of  patients  with   heart  failure  and causes  further
impairment  of  cardiac  function.  Ventricular ectopic  beats  and  runs  of
non-sustained  ventricular tachycardia  are  common  findings  in  patients
with  heart failure  and  are  associated  with  an  adverse  prognosis.



Sudden death occurs in up to 50% of patients with heart failure and
is most probably due to ventricular fibrillation.

Investigation

CXR
A  chest  X-ray should  be  performed  in  all cases.  This  may show
abnormal  distension  of the  upper  lobe pulmonary  veins  with  the
patient  in  the erect position.  Vascularity  of  the  lung fields becomes
more prominent  and  the right  and  left pulmonary arteries dilate.
Subsequently,  interstitial  oedema  causes  thickened interlobular
septa  and  dilated lymphatics.  These  are evident as septal or kerely B
line.

More  advanced  changes  due to alveolar  oedema cause  a hazy
opacification  spreading  from  the  hilar  regions,  and pleural  effusions

Echocardiography

Echocardiography is very useful and should be considered in all
patients with heart failure in order to:

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determine the aetiology

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detect hitherto  unsuspected  valvular heart  disease,  such as  occult
mitral  stenosis,  and  other conditions  that may be amenable  to
specific  remedies

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identify patients who will benefit from long-term drug therapy.

Serum  urea, creatinine  and electrolytes,  haemoglobin  and thyroid
function  may help  to establish  the  nature  and  severity  of the
underlying  heart disease  and  detect any complications.  BNP is
elevated  in  heart  failure  and is a  prognostic  marker, as  well as
being  useful  in  differentiating  heart failure from other causes of
breathlessness  or  peripheral  oedema.