RESEARCH PAPER DISEASE PHYSIOLOGY/PATHOLOGY: FINAL
Heart failure occurs when the heart muscle doesn't pump blood as well as it should.
When this happens, blood often backs up and fluid can build up in the lungs, causing shortness
of breath.Certain heart conditions gradually leave the heart too weak or stiff to fill and pump
blood properly. These conditions include narrowed arteries in the heart and high blood
pressure.Proper treatment may improve the symptoms of heart failure and may help some people
live longer. Lifestyle changes can improve quality of life. Try to lose weight, exercise, use less
salt and manage stress. But heart failure can be life-threatening. People with heart failure may
have severe symptoms. Some may need a heart transplant or a device to help the heart pump
blood.Heart failure is sometimes called congestive heart failure. Heart failure develops when
there are changes to the structure of the heart muscle and it can't pump blood as efficiently as it
should. When this happens blood can back up and fluid may build up in the lungs or arms and
legs, indicating congestive heart failure. Congestive heart failure is a syndrome that can be
caused by a variety of abnormalities, including pressure and volume overload, loss of muscle,
primary muscle disease or excessive peripheral demands such as high output failure. In the usual
form of heart failure, the heart muscle has reduced contractility. This produces a reduction in
cardiac output, which then becomes inadequate to meet the peripheral demands of the body. The
4 primary determinants of left ventricular (LV) performance are generally altered as follows: (1)
There is an intrinsic decrease in muscle contractility. (2) Preload or left atrial filling pressure is
increased, resulting in pulmonary congestion and dyspnea. (3) Although systemic blood pressure
is often reduced, there is an increase in systemic vascular resistance (afterload), which can
further reduce cardiac output. (4) Heart rate is generally increased as part of a compensatory
mechanism associated with an increase in sympathetic tone and circulating catecholamines
Coronary disease often causes an imbalance between myocardial oxygen supply and
demand. An increase in heart size may be particularly deleterious by increasing wall tension
because of the Laplace relation and increasing myocardial oxygen consumption.Intrinsic
compensatory mechanisms include an increase in catecholamines, which increase contractility
and heart rate in an attempt to maintain cardiac output; cardiac muscle hypertrophy, which helps
maintain cardiac function; a rise in LV filling pressure, which can optimize performance
according to the Frank-Starling mechanism; and an increase in peripheral arterial-venous oxygen
extraction so as to maximize the oxygen delivered for a given cardiac output. Although these
compensatory mechanisms are initially helpful, many of them may actually be excessive, such as
an increase in catecholamines and systemic vascular resistance.
RESEARCH PAPER DISEASE PHYSIOLOGY/PATHOLOGY: FINAL
Fig. 2. The Frank-Starling law of the heart states that as the ventricular volume increases and
stretches the myocardial muscle fibers, the stroke volume increases, up to its maximum capacity.
Additionally, inadequate cardiac output during exercise results in poor perfusion of
skeletal muscles, especially the leg muscles and the accessory muscles of respiration.8 The
second variable of stroke volume is cardiac contractility, which represents the muscular pumping
of the heart and is commonly expressed as the ejection fraction. Based on autonomic input, the
heart will respond to the same preload with different stroke volumes, depending on inherent
characteristics of the heart. A heart with normal systolic function will maintain an ejection
fraction of over 50–55%. A previous myocardial infarction may result in nonfunctioning
myocardium that will impair contractility. A recent concept is that ischemic myocardial tissue
can be nonfunctioning (hibernating) but revitalized by surgical or medical therapy directed at
ischemic heart disease.9 Other depressants of myocardial systolic function include
pharmacologic agents (calcium-channel blockers), hypoxemia, and severe acidosis. The final
determinant of stroke volume is afterload. In basic terms, afterload is the load that the pump has
to work against, which is usually clinically estimated by the mean arterial pressure. The normal
cardiac output is relatively insensitive to afterload up to 140 mm Hg. However, the afterload
represents not only the vascular resistance but also the wall tension and intrathoracic pressure
that the myocardium must work against. Together, these 3 variables are impaired in the patient
with CHF.
Chronic heart failure is a complex cardiac condition that encompasses several etiologies
and comorbidities. It arises in the differential diagnosis in all adult patients who present with
dyspnea and/or respiratory failure. Definitive diagnosis is established by a careful history and
physical examination and supportive laboratory data. A chest radiograph is useful in excluding a
RESEARCH PAPER DISEASE PHYSIOLOGY/PATHOLOGY: FINAL
pulmonary etiology (eg, pneumonia); however, a spiral computed-tomography angiogram may
be required if the diagnosis of pulmonary emboli is entertained. The availability of measuring
serum brain natriuretic peptide and bedside echocardiography has aided in our diagnostic
precision. Therapy is primarily directed toward normalizing the underlying physiologic changes
with ACE inhibitors and slow titration of blockers. Diuretics are useful in reducing pulmonary
vascular congestion, which may reduce or resolve dyspnea. Excessive therapy often reduces
cardiac output or causes symptomatic hypotension, which occurs most commonly in patients
with diastolic dysfunction.
Citations:
Swan HJC, Parmley WW. Congestive heart failure. in: Sodeman WA Pathologic Physiology.
Fifth Edition. W.B. Saunders, Philadelphia1973: 273- 294
Parmley WW. Circulatory function and control in: Cecil Textbook of Medicine. W.B. Saunders,
Philadelphia 1979: 1063-1072.
Parmley WW.Cardiac failure in: Rosen M Hoffman B Cardiac Therapy. Martinus Nijhoff, The
Hague1981: 21-44.
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