Congestive heart failure
Congestive heart failure is by caused by amongst other reasons heart failure occurring due to either or both systolic and diastolic ventricular dysfunction. The use of the term “congestive heart failure” is used to imply that the patient in question is having some form of fluid overload. Congestive heart failure is a major cause of morbidity and mortality accounting for a significant proportion of hospitalizations. Of further note is that its incidence increases with advancing age (Tansley, 2010, p.1396). Although the presenting signs and symptoms of CHF have remained the same over time, great advances have been made in terms of understanding the pathophysiologic process of the disease as well as how they lead to the various symptoms and the management of the disease (Mudd & Kass, 2008, p.919). This paper will focus on the pathophysiologic process of CHF as well as its signs, symptoms and management. Further it will identify areas on which research is ongoing as well as those requiring future research on the same.
Body
The etiology of congestive heart failure has been linked to an array of factors which include but are not limited to myocardial infarctions, coronary artery disease, diabetes mellitus, cardiomyopathy, systemic or pulmonary hypertension, valvular heart disease and systemic conditions like iron overload, thryrotoxicosis and anemia that contribute not only to the development but also the severity of hypertension (BHF, 2009 as cited in Tansey 2010; Brunner, Smeltzer & Bare, 2009, pp. 793-794). Heart failure therefore results from a number of cardiovascular diseases that ultimately lead to similar heart abnormalities. These heart abnormalities in turn cause decreased filling during diastole, decreased contraction during systole or both.
Systolic heart failure causes a decrease in the amount of blood ejected during systole from the ventricle. The decrease in cardiac output stimulates the release of epinephrine and norepinephrine by the sympathetic nervous system which causes tachycardia. Whilst this initial response is meant to provide compensatory support to the failing myocardium, the continued release of epinephrine and norepinephrine causes the downregulation of beta1-adrenergic receptor sites and inflicts more damage to the cells of the heart muscle. Increased sympathetic stimulation and decreased renal perfusion resulting from the decrease in cardiac output secondary to heart failure prompts the release of renin by the kidneys. A number of molecular signaling pathways mediate both the sympathetic and the neurohormonal responses (Mudd & Kass, 2008, p.923).
The rennin released by the kidneys promotes the formation of angiotensin I which is converted into its active form angiotensin II in the lumen of blood vessels by angiotensin converting enzyme. Angiotensin II is a potent vasoconstrictor that also causes the release of the hormone aldosterone. Aldosterone stimulates the thirst center in addition to promoting the retention of sodium and fluid in an effort to increase preload and afterload and hence the cardiac output. However, this response inflicts more stress and damage to the myocardium exacerbating myocardial fibrosis. An increase in the retention of sodium and fluid manifests with weight gain and edema. Pulmonary edema presents as shortness of breath.
The neurohormones aldosterone, angiotensin and the others produced such as endothelin and prostacyclin lead to an increase in both the preload and afterload furthering increasing the stress on the ventricular walls and subsequently the heart workload. An increase in the workload of the heart causes a concurrent decrease in the contractility of the myofibrils. Decreased contractility on the other hand leads to an increase in the end-diastolic blood volume of the ventricles and hence increased stretching to the myofibers and ultimately ventricular dilation/hypertrophy. The increase in the size of the ventricle further adds to the stress on the ventricular wall increasing the workload of the heart. In an attempt to compensate for the increased workload, the heart undergoes ventricular hypertrophy that is; it increases the thickness of its muscles. However, this hypertrophy is not accompanied by a commensurate increase in capillary blood supply and thus results in myocardial ischemia. Myocardial ischemia in turn causes the death of the myofibrils even in those patients who do not have coronary artery disease (Mudd & Kass, 2008, p.922; Brunner, Smeltzer, & Bare, 2009, pp.792-793). A number of molecular pathways are thought to be linked to the development of hypertrophy. Basically, the binding of a ligand or a mechanical stimulus activates cell-surface receptors leading to the activation of stress response kinases like protein kinase C and D and phosphatases like calcineurin. These enzymes then activate transcription factors which in turn target certain genes resulting in a change in the size, shape, cellular structure and molecular regulation of heart cells a process termed cardiac remodeling (Mudd & Kass, 2008, p.922). Current research also indicates that the death of cardiomyocytes via apoptosis or necrosis may be due to an imbalance between the signaling pathways that foster cell survival and the multiple pathways that promote cell death such as those triggered by angiotensin II and sympathetic stimulation (Mudd & Kass, 2008, p.923).
In a nutshell therefore, the various compensatory mechanisms only serve to aggravate the heart failure and have been termed the “vicious cycle of HF”. Left-sided ventricular failure leads to a decrease in cardiac output and hence inadequate perfusion to the various tissues which presents as fatigue, shortness of breath, and dizziness due to inadequate perfusion to the brain and oliguria due to decreased perfusion to the kidneys. Meanwhile failure of the right ventricle causes congestion of the viscera as well as the peripheral tissues because the right side is unable to accommodate all the blood from the venous circulation and to eject blood. Increased venous pressure manifests with distension of the jugular vein. Congestion of the viscera manifests as ascites, hepatomegaly, edema of the lower extremities and weight gain. Edema within the abdominal organs is responsible for the anorexia and abdominal pain that manifests in heart failure. Meanwhile weakness results from reduction in the cardiac output that causes inadequate perfusion to body tissues (Smeltzer, Brunner & Bare, 2009, p.723).
Regarding diastolic heart failure, increased workload of the heart prompts an increase in the size and number of myocardial cells eventually results in diastolic heart failure. This is because these compensatory mechanisms cause resistance to ventricular filling thereby increasing the ventricular filling pressure in the presence of normal or even reduced blood volumes. Less preload causes a decrease in cardiac output. Reduced cardiac output coupled with the high ventricular filling pressures induce a neurohormonal response similar to the one described for systolic heart failure (Smeltzer, Brunner & Bare, 2009, p.723; Tansey, 2010, p.1396).
The treatment of CHF is aimed at eliminating or mitigating the effects of any of the previously mentioned etiologic factors and reducing the stress on the heart by reducing the preload and afterload. Pharmacotherapy for HF consists of a number of medications which target the pathophysiologic process. The first group of drugs used is the angiotensin converting enzymes inhibitors (ACE-Is) which prevent the conversion of angiotensinogen I to angiotensinogen II causing a net effect of vasodilatation and diuresis and thus decreasing the preload and afterload. Patients who cannot tolerate ACE-Is are put on angiotensin receptor blockers such as losartan. The latter group of drugs acts by blocking the effects of the neurohormone angiotensin II at its receptor sites and thus has the same hemodynamic effect of lowering the systemic vascular resistance and the blood pressure as the ACE-Is. A combination of hydralizine and isosorbide dinitrate can also be used for patients who are unable to tolerate ACE-Is. Hydralizine acts by lowering the systemic vascular resistance and thus the left ventricular afterload. Meanwhile, isosorbide dinitrate causes venous dilation which has a net effect of reducing the amount of blood that returns to the heart from the venous circulation and thus the preload. Betablockers on the other hand are normally given in combination with ACE-Is. They act by reducing the cytotoxic effects that occur due to the increased stimulation of the sympathetic nervous system (Brunner, Smelzer & Bare, 2009, p.795; Tansey, 2010, p. 1395).
The other group of drugs used in the management of CHF is the diuretics which decrease the edema due to heart failure by antagonizing the renal effects of aldosterone that is, they promote the renal excretion of sodium and chloride. Another group of drugs is the digitalis an example of which is the digoxin which increase the contractility of the myofibrils and hence the force myocardial contraction and subsequently left ventricular output. They also enhance diuresis and thereby aid to relieve edema. Calcium channel blockers cause vasodilatation by reducing the systemic vascular resistance due to angiotensin II and thus help reduce the afterload. Nutritional therapy focuses on reducing the intake of sodium to an amount less than 2 to 3 g/day and avoiding excess amounts of fluids. This is aimed at reducing the volume of circulating blood and hence the workload on the heart (Brunner, Smeltzer & Bare, 2009, p.795; Tansey, 2010, p.1395).
Advanced treatment therapies targeting the pathways involved in the cardiac remodeling process are currently being researched on. For instance, endogenous inhibitors of the calcineurin pathway are being targeted because it is thought that they will provide a selective and effective approach to inhibiting cardiac remodeling (Mudd & Kass, 2008, p.922). Other signaling pathways being researched on are those involved in the neurohormonal responses and the stimulation of the sympathetic system. It has been posited that the modulation of these signaling pathways like the β-AR pathway can make it possible to increase the beneficial effects of sympathetic stimulation for instance the upregulation of the gene that encodes adenylyl cyclase and blunt the harmful effects of the same and thus benefit the failing heart (Mudd & Kass, 2008, p.920). Research into prosurvival pathways like the JAK-STAT signaling pathway that suppress cardiomyocyte apoptosis as well as others like caspaces whose activation promotes cell survival holds great promise in the management of CHF and is a potential area for investigation in future research (Mudd & Kass, 2008, p.922).
Conclusion
In conclusion therefore the pathophysiology of congestive heart failure is a vicious cycle comprising of nervous, neurohormonal and cellular responses mediated by molecular pathways that in the end aggravate the myocardial dysfunction that characterizes the disease. The pathophysiologic process is inextricably linked to the various symptoms associated with the disease. Current CHF treatment modalities target key steps of the pathophysiologic process. Recent discoveries in respect to the molecular pathways involved in mediating congestive heart failure are also proving to be very promising in terms of making the management of CHF more selective and effective.
References
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