Congestive heart failure (CHF) has become a serious health issue throughout the world. By 1999, five to seven million people in North America were living with this disease. In addition, there were twenty million others in the rest of the world (Jobin, Maltais, & LeBlanc, 2000). According to statistics from different studies, the hospitalization cost for heart failure patients, is more than double of all forms of cancers.
Congestive heart failure (CHF) refers to the heart’s inability to meet oxygen requirements of the body tissue when operating normally or at elevated filling pressure (Wolfsthal, 2007). Congestive heart failure (CHF) is a syndrome arising from the combination of many diseases that affect the working of the heart. CHF can result either due to systolic dysfunction or diastolic dysfunction. Normally, the heart works by contraction and relaxation thereby pumping the blood throughout the body. Systolic dysfunction results from problems with contraction of the heart. Diastolic dysfunction results from problems in relaxation (Wolfsthal, 2007). In CHF, circulatory congestion can result, either as systemic venous circulation resulting to peripheral edema or can result to pulmonary circulation congestion leading to pulmonary edema. Pulmonary edema is a life threatening condition (Tuttle-Yoder & Fraser-Nobbe, 1995). It should, however, be noted that, acute CHF in most cases results from myocardial infarction.
The signs and symptoms of the congestive heart failure (CHF) differ depending on the side of the heart affected. When the congestion is on the left side, pulmonary circulation congestion occurs which in turn leads to dyspnea (shortage of breath). On the other hand, if it occurs on the right hand side, systemic venous circulation results. Systemic venous circulation manifests itself by distended neck veins, hepatomegaly and edema (Tuttle-Yoder & Fraser-Nobbe, 1995). In systolic dysfunction, the contraction of the heart in terms of degree of contractility reduces. In the contractility, the heart is unable to withstand the afterload (force against contraction) and preload (the sarcomere stretch before contraction). Decreased contractility can be caused by myocardial infarction (MI), valvular heart disease, hypertension, and cardiomyopathies (Wolfsthal, 2007). In myocardial infarction, a part of the myocardium undergoes necrosis and, therefore, cannot generate the force required to pump the blood effectively. MI normally results to weakening of the ventricle. If large areas are affected, myocardium results to CHF. Valvular heart disease results due to stenosis (regurgitation of the cardiac valves) thereby placing a lot of load on the heart. In most cases, cardiomyopathies results due to the injury on the myocardium. This injury can be due to toxic chemicals or the diseases. Increased afterload makes it harder for the heart muscles to shorten, thus resulting to reduced cardiac output (Wolfsthal, 2007).
In diastolic dysfunction, alteration of active and passive factors that affect the diastole results. Active relaxation result due to pumping out of calcium from the myocardium. Active relaxation occurs before the passive filling of ventricles with the blood previously stored in the atria. Diastolic dysfunction can result due to abnormalities in the active relaxation, abnormality in the passive filling also due to the neurohumoral hypothesis of heart failure. In abnormalities, in the active relaxation, this dysfunction can result due to impairment of the calcium reuptake at the beginning of the diastole. The abnormalities in the passive filling can be due to the myocardium being stiffer than normal. The stiffness can be caused but the increase in the thickness of the chamber walls than normal. Lastly in the neurohumoral hypothesis, the heart failure leads to the activation of related neurohumoral systems and hormones. When persistently over activated, they turn into cardio toxic agents. They, therefore, lead to the decline in the cardiac function. According to this hypothesis, the blockage of these systems should be beneficial to the treatment of congestive heart failure (CHF).
Some of the physical signs are tachycardia, pulmonary rales, cardiac enlargement, fourth (S4) and third (S3) heart sounds. Other physical factors include the neck vein distention, hepatic enlargement, edema and ascites. In tachycardia, elevated heart rate results due to increased release of the catecholamine. They occur as a compensating mechanism, in the attempt, to maintain the normal cardiac output even in the decreased stroke volume. In pulmonary rales, increased hydrostatic pressure results to the transudation of the fluid into alveoli. Then as the air circulates, cracking sounds results when taking the heart sounds. Not all of these cracking sounds are symptoms of CHF and, therefore, care should be taken. The fourth heart sounds (S4) results from patients in sinus rhythm and heart failure due to the noncompliance of the left ventricle. Therefore, they are also excellent indicators of the CHF. This S4 probably arises due to the reverberation of the blood during ejection of blood into the left ventricle. Aging can also lead to the production of S4. Therefore, more tests should be done to ascertain the presence of CHF. Third heart sounds also known as ventricular gallop occurs mainly in early diastole and is the most reliable sign of the left heart failure. It also occurs due to the rapid filling of the left ventricle. Although it is a reliable sign of heart failure, S3 is common in individuals older than forty years and young athletes. Increased systemic venous pressure results to transudation of fluids into peritoneal space. This consequently leads to elevated neck veins and ascites which can indicate the presence of CHF. Other signs of left-side heart failure include cough, fatigue, crackles, weakness and fatigue (Singh, 2011).
The clinical symptoms and features that assist the physical ones in the identification of the CHF are paroxysmal nocturnal dyspnea and orthopnea. In addition, Nocturia and edema can also be used. In dyspnea, the individual experiences the feeling of breathlessness and reduced cardiac output to the periphery (Wolfsthal, 2007). Orthopnea refers to dyspnea that occurs due to lying in a recumbent position. It can be relieved by the raising of the head. Paroxysmal nocturnal dyspnea refers to dyspnea that awakens the patient from the sleep. It may also occur due to lying in the recumbent position thereby resulting to the pooling of blood in the vasculature and increase, in left ventricular filling pressure, (Wolfsthal, 2007). For paroxysmal nocturnal dyspnea, the symptoms disappear after the patient has been standing for five to twenty (5-20) minutes. Nocturia, on the other hand, results due to increased renal blood flow when the patient is in the recumbent position or asleep. Lastly, edema and particularly cardiac edema occur when systemic hydrostatic venous pressure is higher than systemic oncotic venous pressure.
The laboratory assessment of congestive heart failure in patients, involve the use of chemicals, waves and measuring of the blood pressures in many parts of the body. In the determination of the extent of myocardial infarction (MI), an electrocardiogram (ECG) can be used. When using the electrocardiogram the presence of Q waves helps in the confirmation that the MI has been the cause of the CHF (Wolfsthal, 2007). A chest radiograph can also be used. Chest radiograph can monitor cardiac chamber enlargement and congestion. An echocardiogram can also be used to identify the chamber enlargement as well as quantifying the ventricular and valve function (Wolfsthal, 2007). Use of radionuclide ventriculography can be used in measuring range of the right and left ventricular ejection fractions. In addition, the use of Doppler interrogation techniques can be applied in determining the direction and rate of blood flow. Doppler interrogation can detect quantify valvular stenosis. Any variation from the individuals normal may indicate the possibility of valvular regurgitation and intra-cardiac shunts. Lastly during the cardiac catheterization, many cardiac characteristics can be evaluated. These include the chamber size, valvular stenosis, intra-cardiac pressures and other coronary anatomy.
The extent of stretching in the heart muscle cells can also be monitored by the use of the Brain Natriuretic Peptide (BNP). This is a polypeptide secreted by the muscles of the heart ventricles in response to overstretching. Increased filling pressures in the heart leads to dyspnea, production of the atrial natriuretic peptides (ANP) and Brain natriuretic peptides (BNP) (Siegenthaler, 2007). By monitoring the levels of ANP and BNP, we can rule on the possibility of heart failure, pulmonary hypertension, pulmonary embolism, acute coronary syndrome and renal failure. High levels of BNP (BNP > 400pg/mL) are strongly suggestive of cardiac dyspnea. Normal levels (BNP < 100pg/mL) highly excludes any cardiac cause. In addition, high levels of BNP may suggest general volume overload or liver failure that may occur in response to hepatic cirrhosis. The level of the BNP also correlates to the severity of the heart failure, if detected (Siegenthaler, 2007). The best diagnosis tool for the CHF is the echocardiography. It can be used in the determination of congenital defects or cardiomyopathy presence. Echocardiography can also be used in the assessment of heart size, cardiac function, hypertrophy and dilation (Potts & Mandleco, 2011).
All therapies aim at reducing of the volume overload, improvement of the contractility, reducing afterload and in the decreasing of cardiac work. These therapies are in the form of drug therapy and nursing care (Potts & Mandleco, 2011). The patients of CHF are in most cases edematous and compromised respiratory functions arising from the fluid overload. They, therefore, need fluid restriction drugs for the lungs. Therefore to lower the amount of the fluid that has accumulated, diuretics can be administered. In addition to decrease the hearts overload, Angiotensin-Converting Enzyme (ACE) inhibitors can be used (Singh, 2011). “ACE inhibitors can restore the cardiac and hormonal response to volume overloads, and thus, reduce natriuretic in mild heart failure” (Jobin, Maltais, & LeBlanc, 2000). Administration of morphine reduces pain also lowers the peripheral resistance. In severe cases, oxygen (O2) should also be given, in order to reduce anxiety and facilitate breathing. In cases where there are chest pains, nitroglycerin (nitro) can be used. Nitroglycerine also acts as a vasodilator (Singh, 2011). Normally these patients require rest to conserve energy. Other therapies include administration of Angiotensin II Receptor blockers to reduce the effects of angiotensin II. To patients who are intolerant to ACE inhibitors the Angiotensin II Receptor blockers can be administered. Other medical related therapies are diuretics (for improvement of congestive symptoms), digitalis (to increase the ejection fraction of the left ventricle) as well as administration of β-Blockers. The β-Blockers can be administered for inhibition of sympathetic nervous system thereby limiting progression of heart failure (Jobin, Maltais, & LeBlanc, 2000). In infants whose the heart failure is secondary to congenital defects then, the primary treatment is the surgical correction (Potts & Mandleco, 2011).
Although no long-term randomized study on the effects of ACE inhibitors exists, the adverse effects of ACE inhibitors and Angiotensin II Receptor blockers can be related to angiotensin suppression and potentiation. Angiotensin refers to hypotension, potassium retention and worsening renal function. On the other hand, potentiation refers to coughing and angioedema (Jobin, Maltais, & LeBlanc, 2000). The use of beta blocker medication has led to the increased cases impotence among the older men (Wallace, 2007). These drug-disease interactions encourage the discontinuation of the medication, and the search of the alternatives that do not impact on related disease processes.
When diagnosed with CHF, Patients need to be prepared psychologically on how to live positively with the illness. Another part of the patient that should be considered is the family relations. These members should also be prepared psychologically on how to assist their patients at home psychologically and physically. Regardless of age, patient teaching is a vital component in disease management (Wallace, 2007). Unhealthy behaviors like drinking, smoking, or poor nutrition should be broken as they deteriorate the disease. The patients of CHF should eat less salt and limit fluid intake. Patients diagnosed with CHF should monitor their weight regularly. This should be done every morning at the same time. During measuring of the weight, same clothes and scale should be used. The patient should call the doctor if he notices sudden change in weight, increased swelling of the legs or ankles as well as having trouble in breathing when resting or sleeping at night. While dealing with the older adult population, ultimate care should be given to the management of pathological diseases of aging. Lastly, exercises and better night sleep should be encouraged for continued improved health (Wallace, 2007).