Pathophysiology of Congestive Heart Failure

Use current resources not older than five years.
*Identify alterations associated with congestive heart failure. Consider the pathophysiology
of the alterations. Think about how these alterations produce pathophysiological changes
in at least two body systems.
*Describe congestive heart failure, as well as associated alterations. Explain the
pathophysiology of the alterations, including changes that occur in at least two body
systems.
*Reflect on how patient factors such as genetics, gender, ethnicity, age, and behavior might
impact the pathophysiology of the alterations you identified, as well as the diagnosis and
treatment of congestive heart failure.
*Explain how genetics, gender, ethnicity, age, and behavior might impact the
pathophysiology of the alterations you identified, as well as diagnosis and treatment of
congestive heart failure.
*Construct a mind map on congestive heart failure. Include the epidemiology,
pathophysiology of alterations, risk factors, and clinical presentation, as well as the
diagnosis and treatment of the disorder.

Pathophysiology of Congestive Heart Failure

Congestive heart failure (CHF) is also referred to as congestive cardiac failure or heart
failure. A person experiences CHF in cases where the heart cannot provide adequate pump action
for maintaining a blood that can sustain the body’s needs. It is caused by hypertension (systolic
and diastolic dysfunction), ischemic heart disease, valvular heart disease, or myocardial
infarction or systolic dysfunction and is associated with numerous lifestyle factors. Some of the
alterations associated with CHF include connexin expression, blood volume, and contractile
function (Francis, 2010).

Pathophysiology

CHF is as a result of abnormalities in cardiac rhythm, function, structure, and conduction.
In addition to the fact that CHF indicates that the heart is unable to maintain sufficient oxygen
delivery, it also implies a systemic response in an attempt to compensate for this insufficiency.

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Cardiac output is determined by stroke volume and heart rate. Furthermore, afterload, preload,
and contractility determine stroke volume (Parmley, 2012). These variables are important in that
they help in comprehending the disease’s pathophysiologic consequences as well as potent
treatments. It is also worth noting that cardiopulmonary interactions are crucial in understanding
the disease. The heart is a dynamic pump that not only depends on the inherent properties but on
what gets pumped in and what it is supposed to pump against as well. The preload refers to the
volume given to the pump to send forward, the contractility is the pump, while the afterload
denotes what the heart is supposed to work against (Francis, 2010).
Usually, the preload is expressed as the left ventricle’s volume or end-diastolic pressure.
Clinically, it is assessed through measuring the pressure on the right atrial. Preload is dependent
on any ventricular filling’s restriction and intravascular volume. Considering that the heart is
located in the thoracic cavity, an elevated positive pleural pressure reduces right-atrial’s pressure,
which minimizes ventricular filling. Considering that the cardiac pump is a muscle, it responds to
volume with a determined output. If there is increased volume, more volume is also pumped out
during a usual physiologic state to determined plateau, which is the relationship elaborated by
Frank-Starling law (Parmley, 2012).
The heart’s diastolic function is determined by the left ventricle’s distensibility or
elasticity and myocardial relaxation. Myocardium’s relaxation takes place during early diastole.
The left ventricle’s ‘untwisting’ is an active procedure whose output is a suction effect, which
augments the filling on the left ventricle (Parmley, 2009). If the usual left-ventricular’s
relaxation or distensibility is lost through functional alterations (ischemia) or structural
alterations (left-ventricular hypertrophy), ventricular filling or preload is impaired. Cases of
diastolic dysfunction are associated with exercise intolerance and are as a result of ventricular

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filling’s impairment, that increases pulmonary venous pressure and left-atrial pressure, and leads
to pulmonary congestion. On the same note, insufficient cardiac output in exercise cases leads to
poor skeletal muscles’ perfusion, particularly the respiratory accessory muscles and leg muscles
(Francis, 2010).
Cardiac contractility is the 2 nd stroke volume’s variable and it denotes the heart’s
muscular pumping. Commonly, it is expressed as ejection fraction. Depending on the autonomic
input, the heart responds to the similar preload using various stroke volumes, based on the
heart’s inherent characteristics (Parmley, 2009).

Age, diagnosis, and treatment

CHF is more common in elderly people since they have a higher probability for multiple
comorbid conditions including chronic lung disease, diabetes, hypertension, and angina. The
chances for the disease escalate with advancing age. It is the most frequent reason for
hospitalizations in individuals aged 65 years and more. The aging process contributes greatly to
the changes present in elderly people’s cardiovascular system. The arterial tree’s stiffening
interferes with left ventricular geometry and afterload. Irrespective of the fact that the resting
systolic function of the left ventricular is maintained, its diastolic function transforms
substantially (Parmley, 2012).
Preliminary diagnosis of the disease can be made through a keen physical examination
and medical history. a medical history identifies risks such as obesity, lifestyle factors (drug use,
alcohol use, and smoking), thyroid problems, heart disease, diabetes, abnormal cholesterol
levels, and high blood pressure. Along with the medical history, some physical signs such as
tenderness or swelling of the liver, abnormal lung sounds, abnormal heart sounds, and enlarged
liver strongly indicate the presence of the disease (Francis, 2010). There can also be laboratory

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tests on the blood and urine as well as electrocardiogram, angiography, echocardiography, and
exercise stress test.
It is important to treat the conditions related to heart disease early enough so as to prevent
its occurrence. Management and treatment of the disease aims at prolonging life, improving
quality of life, making physical activity comfortable, and treating underlying conditions.
Treatment can be based on drugs such as digoxin, beta-blockers, and ACE inhibitors,
biventricular pacing, surgery, ventricular assist devices, or heart transplant (Parmley, 2009).

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References

Francis, A. K. G. S. (2010). Pathophysiology of congestive heart failure. The Cleveland Clinic
Cardiology Board Review, 317.
Parmley, W. W. (2012). Pathophysiology of congestive heart failure. The American journal of
cardiology, 55(2), A9-A14.
Parmley, W. W. (2009). Pathophysiology of congestive heart failure. Clinical cardiology, 15,