Use current resources not older than five years.

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).


            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. 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 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 2nd 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 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).


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, I5.