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Definition
Heart failure could be divided into:
1* Low-output heart failure
2* High-output heart failure, which is a rare condition
We routinely use the term "heart failure" to describe low-output heart failure.
Heart failure is defined as: failure of the left ventricular muscle to eject
enough blood into the circulation and deliver enough O2 and nutrients to the
body tissues. So it is a mechanical problem. The doctor added a new component
to the definition which is: "Failure of the diastolic filling of the left ventricle."
and the reason for this addition is that, there is a variant that is called
Diastolic heart failure.
Diastolic heart failure (impaired ventricular filling) is caused mainly by:
1- Left ventricular hypertrophy. (LVH)
2- Constrictive pericarditis.
In this condition (diastolic heart failure), there is NO problem in the ejection,
i.e. normal ejection fraction. So that:
HF (heart failure) is: mechanical pumping failure of the left ventricle to
deliver enough oxygen and nutrients into the circulation, with/without
inability to retain blood in the diastolic phase of cardiac cycle.
Concerning the high-output heart failure, there are certain causes of this rare
condition including:
* Thyrotoxicosis.
* Arteriovenous fistula.
* Paget's disease of the bone.
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veins till it reaches the alveolar capillaries, when the pressure there is
elevated above 25 mmHg, transudation of fluids takes place in the alveoli,
and then into the pulmonary interstitial spaces, then the complaints of
left heart failure which are dyspnea (as a symptom) and basal lung
crepitations (as a sign), will start.
Backward heart failure:
Following the previous scenario (the forward heart failure, or the left
ventricular heart failure), when the pressure is elevated in the alveolar
capillaries, this will lead to elevated pressure in the pulmonary venules i.e.
secondary pulmonary hypertension (It is secondary to left heart failure).
The pulmonary hypertension will lead to dilatation of the right ventricle,
at this moment the previous signs and symptoms of left heart failure
(Dyspnea and basal lung crepitaions) will be replaced by the signs and
symptoms of right heart failure (Elevated jugular venous pressure, liver
congestion, ascites, lower limbs edema).
So:
* Forward heart failure = Left ventricular failure.
* Backward heart failure = Right ventricular failure.
So forget about these two terms (forward and backward HF).
Second, by the onset:
* Acute heart failure.
* Chronic heart failure.
Again, when we use the term "Heart failure", we mean by that chronic
heart failure. Acute heart failure occurs just in certain conditions. The
patient is healthy, with a normal heart, so, what is the etiology of acute
heart failure?
Acute heart failure occurs in the following 4 conditions:
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1- Cardiac dyspnea: The single most important symptom of left heart failure is
cardiac dyspnea in its different components, exertional, PND and orthopnea.
2- Fatigue: rarely left heart failure causes fatigue; fatigue is mostly caused by
right heart failure.
3- Isolated nocturia: It means impaired diurnal variation. Normal adults
urinate two to three times per 24 hours; two times during the daytime, and one
time during the night, OR only during the daytime. If the condition is reversed,
like, if he/she urinates two or three times during the night, and one time during
the daytime (i.e. night > daytime) this is isolated nocturia and is related to
several conditions:
1- Early stages of left heart failure.
2- Early stages of renal failure.
3- In children with nocturnal enuresis.
You have to differentiate between: isolated nocturia, Polyuria and frequency.
* Isolated nocturia: mentioned previously.
* Polyuria: is a condition usually defined as excessive or abnormally large
production or passage of urine. It occurs in conditions like:
Diuretics use, DM, DI, Addison's disease, chronic renal failure
* Increased frequency in conditions like: Irritation of the trigone of the
bladder by cystitis, tumors, stones.
Again, the most important symptom of left heart failure is cardiac dyspnea.
The elements of cardiac dyspnea (exertional, PND and orthopnea) come in
order. So it is unlikely to have orthopnea without experiencing the stage of
exertional dyspnea. If the exertional dyspnea is not treated, it will proceed
into PND and orthopnea.
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4- Pleural effusions.
5- Tricuspid regurgitation murmurs.
6- Specific signs for the underlying cause.
Further investigations
1- Chest X-ray.
2- ECG, which may detect arrhythmia, conduction defects, previous MIs.
3- Echocardiography.
4- CBC, Renal profile, Fasting blood sugar (FBS), Lipids, ABGs.
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1- Bed rest, should not be needed for more than two to three days, because the
patient should be mobilized as early as possible.
2- Oxygen: The patient should not be put on O2 for more than 2 to 3 days as
well, when the O2 saturation is less than 84%. Once the congestion and the
capillary pressure in the alveoli are reduced, his need for O2 should stop.
But, what if a patient has a continued need for O2, for example: an HF patient
was put on oxygen and diuretics for more than 7 days, whenever the O2 is
removed, the O2 saturation drops down below normal?!
A: This should pay the attention into another condition in addition to the HF,
for example: COPD, Pulmonary embolism...
3- Low salt diet.
4- Treatment of the precipitating cause.
5- Treatment of the underlying cause.
6- Drug therapy, which includes:
a) Spironolactone, which is associated with increased survival in patients with
HF.
b) ACE inhibitors: They are vasodilators and preload acting drugs, and they are
associated with increased survival in patients with HF.
c) Diuretics.
d) Beta-blockers: Remember that not all beta-blockers can be used in the
treatment of HF patients, for example, if a patient is presented to the hospital
with heart failure, and he/she is already on beta blockers, we have to STOP
beta-blockers.SO:
Q: How can beta-blockers be used in the treatment of HF?
A: There are four points:
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*) Not all beta-blockers could be part of the treatment of HF; there are
certain beta-blockers which have mostly alpha/beta antagonistic activity which
includes 4 agents:
1- Carvedilol 2- Metoprolol (I think it has selective B1 antagonistic activity!),
3-Bisoprolol 4- Nebivolol (has nitric oxide-potentiating vasodilatory effect).
*) Beta-blockers are not used in all conditions of HF; they are used mostly as
part of the treatment of HF due to CardioMyopathies. So they are not used for
diastolic-dysfunction heart failure.
*) These agents are introduced during compensation, not during
decompensation.
Note: Compensated Vs. Decompensated HF (from Lippincot).
The falling heart evokes three major compensatory mechanisms to enhance cardiac
output. Although initially beneficial, these alterations ultimately result in further
deteriorations of cardiac function. These mechanisms include:
- Increased Sympathetic activity.
- Activation of the renin-angiotensin system.
- Myocardial hypertrophy.
If these mechanisms adequately restore cardiac output, the HF is said to be
compensated. However, these compensations increase the work of the heart and
contribute to further decline in cardiac performance. If the adaptive mechanisms
fail to maintain cardiac output, the HF is termed as decompensated.
Note: Concentric LVH means: the chamber radius may not change; however,
the wall thickness greatly increases. (Compare with eccentric hypertrophy.)
The END
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Attack
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