Heart failure is the inability of the heart to pump adequate blood to the body tissues and maintain its continuous flow. The body cells become hypoperfused and produce little energy due to lack of enough supply of nutrients and oxygen. At the same, time the toxic products accumulate in the body as their movement is stagnated in the tissues. It may be on the left side, right side or both side of the heart to involve a single or both ventricles.
Heart failure occurs from any condition that reduces the efficiency of the heart muscles thus weakening the force of contraction. It leads to accumulation of blood in the ventricles during their filling in diastole (Poole-Wilson et al., 2003). Normally, when the heart has large volume of blood, contractile force and the cardiac output are increased. However, this adaptive mechanism fails to occur in heart failure leading to stagnation of blood in the ventricles. At the same time, more blood is retained in the venous system since there is no space in the right ventricle. The heart muscles become overstretched. Cross linking the actin and myosin filament reduces and the overall contractility of the heart reduces.
The heart rate increases as a compensatory mechanism to the lowering cardiac output. The baroreceptors in the brain cause stimulation of sympathetic activity. It leads to release of more catecholamines. By binding to the beta receptors, the catecholamines cause vasoconstriction of the blood vessels. In aIDition, they cause an increase in the peripheral resistance. The compensatory mechanism aims at increasing the blood pressure back to normal. However, makes the condition worse in that, the heart muscles require more nutrients for contraction. They also require more force of contraction to counter the peripheral resistance (Fox et al., 2007). As systolic and diastolic contraction start to fail, there is a reduction in the stroke volume. The end systolic volume increases due to the reduced contractility of the heart and the less blood ejected from each ventricle. Less blood at the end of diastole means there is poor ventricular filling which occurs when the compliance of the ventricular walls fails.
The heart tends to hypertrophy (increase in physical size) in an attempt to make the contractility efficient. As a result, there is increase in stiffness of the heart muscles. The increase in the ventricular volume reduces the stroke volume due to inefficiency in contractility (Shigeyama et al., 2005). A fall in the arterial blood pressure and reduced kidney perfusion is observed. Stagnation of the blood in the left ventricle causes pulmonary hypertension due to the more blood retained in the lungs.
Reduction in the tissue perfusion and low blood volume activates the Renin- Angiotensin Aldosterone system (RAAS). This system is sensitive to low cardiac output (CO) and it aims at increasing the fluid volume in the body (Andrew, 2002). Reduction in the fluid that passes the macular densa causes the juxtaglomelular cells to release Renin enzyme. It causes activation of angiotensinogen to angiotensin I. Angiotensin converting enzyme is a key player in this system because it activates angiotensin I to angiotensin II. RAAS system causes reabsorption of sodium ion from the kidney nephron. Consequently, the water follows the electrolyte by osmosis thus increasing the fluid volume in the body. It is this system that the angiotensin converting enzyme inhibitors and angiotensin II blockers drugs target in an attempt to reduce hypertension that develops in heart failure. They prevent reabsorption of more fluid from the kidney nephron.
Fluid retention by RAAS system causes an increase in the ventricular preload and the cardiac output until the cardiac output again meets the RAAS activation threshold. When ventricular dysfunction continues, the cardiac output cannot longer reach the activation threshold of RAAS system. Thus, unable to reach a new higher set point, RAAS system becomes continuously activated in proportion to the low cardiac output in the futile attempt to raise the CO. Continuous activation of RAAS system becomes ineffective and causes the edema due to the retained fluids (Andrew, 2002).
Overall reduction in the cardiac reserve may follow. The heart has a requirement to cope up within normal metabolic demands as well as during subsequent elevation in exertion. In the case of heart failure, this reserve get very low and becomes depleted (Andrew, 2002).The reserve only serve for a limited time afgter which the heart has to get other compensatory mechanism to get nutrients.
Altered metabolism of glucose to yield energy in the cells of the myocardium is a significant component in the pathophysiology of heart failure. According to Doehner et al (2010), there is a shift in the glucose and free fatty acid balance observed in heart failure. This leads to reduced energy production and thus energetic effectiveness. In aIDition, metabolism of the fatty acids leads to formation of ketone bodies. These can increase the PH of the blood, a condition referred to as metabolic acidosis.
Insulin, a hormone produced from the pancrease, is solely responsible for the balancing of the energy giving substrate. It specifically regulates the entry of Glucose into the cells. Insulin resistance as observed in patients with type II diabetes mellitus, has been observed in patients secondary to heart failure. Although there is a lot of glucose in the blood, the cells are unable to absorb it for metabolism to release energy. The cells become less sensitive to insulin. The cells turn to the free fatty acid as the substrate for metabolism to yield energy
Insulin responsive glucose transporter protein GLUT4 is the predominant transporter for glucose uptake in the cells. Reduction in GLUT4 is common in patients with type II diabetes. A similar observation is present in patients with heart failure. In his studies, Paternostro (1999) found a reduced GLUT4 transporter in patients with chronic heart failure. He further observed and increase in the concentration of free fatty acid in the same patient. This suggests a disturbance in the metabolism process in the myocardium that leads to poor energy production and thus poor contractility.
As the heart contractility reduces the coronary perfusion is also affected. Less blood reaches the heart muscles which makes the myocardial cells to have hypoxia. Consequently they turn to anaerobic respiration where the free fatty acids are metabolized. Tissue hypoxia which has also been observed to cause reduced GLUT4 transporter.
The life style that individuals live can affect the concentration of GLUT4 as well. Patients who are less active have reduced GLUT4 transporter in their body. The cardiac patients are also not very active physically and are rarely involved in physical exercise due to the compromised heart contractility. Lack of physical exercise leads to weight gain and increase in fat storage. It contributes to the reduced levels of GLUT4 in those patients (Paternostro, 1999). However, the mechanism in which all these factors cause reduced GLUT4 transporter is still under study. The body weight and the fat distribution are factors important in the regulation of glucose and insulin metabolism. Reduction in the body weight and fat consumption are essential lifestyle modification to enhance proper glucose metabolism (Doehner 2010). Increase in the physical exercise is major practices that can help the individuals to cut their weight thus prevent them from developing cardiac problems.
The New Yolk Heart Association (NYH) has a classification to show the severity of heart failure. The symptoms of cardiac failure include shortness of breath, excessive fatigue and edema of the legs. Those with cardiac disease but have not symptoms during ordinary physical activities belong to NYHA class I. NYHA class II have mild symptoms during ordinary activities. NYHA class III is only comfortable during rest. NYHA class IV patients have strict limitations because they have symptoms even at rest. These remain the most important prognostic marker for clinical use in diagnosing the severity of the cardiac problem.
Heart failure and UK
Heart failure affects about 900,000 people in United Kingdom. Most of the patients have damaged hearts, but they dont have the symptoms. This number has increased due to the good prognosis, aging population and better treatment of heart failure. The major cause of heart failure is attributed to coronary artery pathology. Most patients may have suffered from myocardial infarction (Stewart et al., 2002).
Heart failure as a poor prognosis in that 30-40% of those diagnosed with the problem die within one year. Heart failure is attributed to over one million National Health Service (NHS) beds for the inpatients. 5% of all emergency admissions have heart failures. The hospital admissions due to heart failure are expected to increase by 50% over the next 25 years in UK. The attributing factor is the increasing aging population (Stewart, 2002).Heart failure have devastating effects on the quality of life of the patients. Even though they undergo treatment, the patients a not completely relieved from the symptoms (Archana, 2002).
Currently, heart failure cost 1-2% of the entire NHS budget per annum. This cost is increased by the inpatients services that the patients undergo while admitted to the hospitals. This accounts for 60% of the total amount of expenditure of NHS towards heart failure. 9% of all expenditure goes to the medication purchasing. It is responsible for 5% of all hospital; admission and readmissions within three months of discharge.
Systematic approach towards diagnosis and treatment is an important aspect in reduction of expenditure towards heart failure. In prevention several readmissions to the hospital it reduces the cost of inpatient care the NHS caters for. The European society of cardiology has come up with an algorithm that is used to diagnose heart disease easily. This reduces errors and time needed to start of treatment thus reducing the cost of operation.
As per now, the cure for heart failure is yet to be discovered. The management of the condition aims at reducing the symptoms of high blood pressure. The reduction of the symptoms may allow the patient to do some of the things he does. It involves hospital based medication and lifestyle adjustments. Drugs like the diuretics (furosemide), angiotensin converting enzyme inhibitors, beta blockers, angiotensin II receptor blocker are available for management of heart failure. In aIDition, cardiac resynchronization therapy defibrillators and pacemakers are used in emergency cases. The doctors educate the patients on Lifestyle modification including cessation of smoking, alcohol intake and to reduce the amount of salt intake. The NHS faces challenges in meeting the treatment requirement as these require most of its expenditure. The patients require the treatment for the rest of their life and hence become a burden to the NHS (Sutherland, 2010).
Despite the expensive treatment given to the patients, it is not possible to completely relieve the patient from the symptoms. The drugs help in reducing the excess fluid retained in the body by promoting its removal. Although the life expectancy is prolonged, the patients are restricted to physical activities and movement. Moreover, most of the patients diagnosed with heart failure die within one year since diagnosis. The patients may not get enough energy to be productive in the remaining period of his life. This shows that the life gain from the treatment is poor both to the patients and to the National Health Service.
Proper alternative in the management of the heart failure should be adopted. Prevention of the disease development remains the major alternative in reducing the burden of the disease. Effective education on the preventive measures to the patients plays a major role in creating the disease awareness. It would involve lifestyle modification and diet changes. Screening should be done to the patient to enable early diagnosis and commence treatment. It would be beneficial for the National Health Service to allocate some of its funds towards research. By so doing more information will be collected and more knowledge on the pathophysiology of the disease explored. Alternative ways of managing heart failure can be achieved through research. This way there will be a better prognosis of the disease in the population.
Doehner W, et al (2010). Glucose transporter GLUT4 in skeletal muscle foretells insulin resistance in non-diabetic chronic heart failure patients. International journal of cardiology 138 (2010) 19-24.
Sutherland K., (2010).Bridging the quality gap: Heart failure. The health foundation inspiring improvement. London W2CE 9RA.
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