Heart failure occurs when the pumping capacity of the heart is compromised
Heart failure occurs when the pumping capacity of the heart is compromised. It is a condition which the heart has trouble pumping blood because it has become weak or stiff; thereby decreasing its ability to meet the demand of the body’s need for oxygen and nutrients. It is significant to understand that the symptoms of heart failure may be due to systolic dysfunction emanating from the right or left side of the heart, or may occur with preserved systolic function with symptoms due to the abnormal diastolic function of the heart. Systolic failure happens when the heart is not contracting well, meaning the blood can’t get out of the heart so the blood can’t get in because there is still blood in the heart. In diastolic failure, the blood can’t come into the heart because the ventricle is too thick and as a result of that, if the blood can’t come into the heart there is no blood to pump out causing HF. Heart failure can demonstrate in many ways, depending on how extent ventricular remodeling and dysfunction have advanced. Heart failure may be discovered because of a known clinical condition such as MI or because decreased exercise tolerance, fluid retention, or admission to the critical care unit for an unrelated condition (https://www.clinicalkey.com/nursing/).
American Heart Association (AHA) estimated that there were 5.1 million of people with HF in the
United States in 2006 and 23 million people with HF worldwide (AHA,2013). Heart failure and
LV dysfunction has a correlation with age. The prevalence among men is 8 per 1,000 at age 50-
59 years, increasing to 66 per 1,000 at ages 80-89 years. Similar values (8 and 79 per 1000)
were noted in women. The prevalence in African-Americans is reported to be 25%higher than
in whites (Vasan ; Wilson, 2018). It is estimated that by 2030, an additional 3 million people
will be diagnosed with heart failure (http://www.clinicalkey.com/nursing/).
Acute vs chronic
Acute and chronic heart failure can be determined depending on the rapid progression of the
syndrome. The presence and the activation of compensatory mechanisms, and the presence
or absence of fluid accumulation in the interstitial space. Acute heart failure has a sudden
onset, with no compensatory mechanisms. The patient may experience acute pulmonary
edema, low cardiac output, or cardiogenic shock. The deterioration into acute heart failure can
be precipitated by the onset of dysrhythmias, acute ischemia, sudden illness, or cessation of
medications. This may necessitate admission to critical care unit, on the other hand, patients
with chronic heart failure is an ongoing process, with symptoms that may be made tolerable by
medication, diet, and a reduced activity level. Patients with chronic heart failure are
hypervolemic, have sodium and water retention, and have structural heart chamber changes
such as dilatation or hypertrophy. Hypertension is the primary precursor of heart failure in
women, whereas CHD, specifically MI, is the primary cause of heart failure in men.
In right-sided heart failure, the right ventricle fails to pump blood effectively, and blood may back up into other areas of the body (Kumar, Abba, ; Aster, 2013). The right side of the heart has an
ineffective right ventricular contractile function. Patients with right heart failure leak fluid into the
tissue and organs that deliver blood to the right heart through the vena cava. Usually, right
ventricular failure is commonly caused by failure of the left side of the heart. The common
manifestations of right ventricular failure are jugular venous distention, elevated central venous
pressure, weakness, peripheral or sacral edema, hepatomegaly (enlarged liver), jaundice, and
liver tenderness. Gastrointestinal symptoms also include poor appetite, anorexia, nausea, and
an uncomfortable feeling of fullness. Right-sided failure also can occur in patients with primary
pulmonic or tricuspid valve disease, or congenital heart disease causing chronic volume and
pressure overloads (Voelkel, 2006).
Failure of the left ventricle to contract results in a low cardiac output state, leading to
vasoconstriction of the arterial bed that increases systemic vascular resistance and creates
congestion and edema in the pulmonary circulation and alveoli. When the left ventricle cannot
pump blood to the body and fluid backs up and leaks into the lungs causing shortness of
breath. Clinical manifestations of left ventricular failure include decreased peripheral perfusion
with weak or diminished pulses, cool, pale extremities, and in later stages, peripheral cyanosis.
Over time, with the progression of the disease state, the fluid accumulation behind the dysfunctional
left ventricle elevates pulmonary pressures, that contributes to pulmonary edema and
congestion, and produces dysfunction of the right ventricle resulting in failure of the right side of
the heart (Hughes, 2009).