Congestive Heart Failure
Student’s Name:
Institutional Affiliation:
Congestive Heart Failure
Congestive heart failure is a disease where the heart cannot pump enough cardiac output for normal tissue metabolic requirements, or it does it with abnormally elevated cardiac output (Iqbal, Kaleem, & Hanif ,2015). Heart failure is manifested by reducing blood volume pumped by the heart and stagnation of blood in the veins (Iqbal, Kaleem, Hanif ,2015). Various cardiovascular abnormalities associated with heart failure include ventricular output obstruction, ischemic heart disease resulting in failure of ventricular contraction, arrhythmias, and volume overload (Iqbal, Kaleem, Hanif ,2015). From the patient history presented, J.C is suffering from Heart Failure. Heart failure can be acute or chronic, and it shows as left sided or right sided failure.
Risk Factors
From JC’s past medical history, the risk factors for heart disease are obesity being that she is overweight, old age, positive family history of atherosclerosis and heart attack, replacement of aortic valves and bypass surgery of coronary artery, and smoking. The patient also has a history of hypertension, dyslipidemia, coronary artery disease, atrial fibrillation and Diabetes mellitus type 2. In the review of Iqbal, Kaleem, and Hanif (2015), heart failure always develops secondary to risk factors which include age, diabetes mellitus type 2, smoking, coronary artery diseases, and hypertension.
Pathophysiology of Congestive Heart Failure
The syndromes of congestive heart failure develop as a result of pathology in cardiac rhythm, structure, conduction and function (Iqbal, Kaleem, & Hanif ,2015). This results in inadequate cardiac output for standard metabolic requirements of the body or it does that at an elevated cardiac pressure. Cardiomyopathy is heart muscle abnormalities that can be hypertrophic, dilated, and restrictive or mixed pattern (Nicholson, 2014). Dilated cardiomyopathy results in cardiomegaly and is the major cause of mortalities (Nicholson, 2014). Idiopathic cardiomyopathy, alcohol cardiomyopathy, and degenerative valve diseases have been stipulated to be the major causes of heart failure in developing countries (Nicholson, 2014).
Compensatory Mechanisms
According to Nicholson (2014), in the occurrence of heart failure, there are various systemic compensation mechanisms which work to restore normal blood volume and pressure. The different compensatory mechanisms include activation of neurohumoralm systems, which works to expand blood volume by retention of salt, water, and tachycardia (Nicholson, 2014). Neurohumoral response involves renin-angiotensin activation pathway, sympathetic nervous system and ANP secretion (Nicholson, 2014).
Ventricular dilatation is another compensatory mechanism, which improves myocardial contraction by myofibril stretching. Frank Sterling’s mechanism explains that cardiac output is a measure of preload, afterload and ventricular contraction (Nicholson, 2014). Increased preload causes an increased myocardial contraction up to a certain limit in which further compensation results in damage to the heart muscles. Compensatory mechanisms occur at a cost since increased heart rate leads to a higher contraction, which increases metabolic requirements for the heart (Nicholson, 2014).
Left and Right Side Heart Failure
Heart failure of the left side Heart develops with a diminished left blood pumped by the left ventricle and an elevation in pressure of pulmonary venous system or of the left atria. Left heart failure manifests as edema, pulmonary congestion, and reduced renal perfusion, which causes retention of salts and water and a reduction in CNS perfusion, which causes hypoxic encephalopathy (Kransdorf et al.,2016). Systolic and diastolic heart failure are morphologies of left sided heart failure. Systolic failure entirely manifests in the left ventricle with cardiomegaly, while diastolic heart failure is associated with pulmonary congestion with normal to slightly elevated ventricles (Kransdorf et al.,2016). Right sided heart failure is caused by a reduction of right ventricular output. The manifestation is due to venous and systemic congestions, which affect major organs resulting in hepatomegaly, splenomegaly, pericardial and pleural effusions, and hypoxic injury (Kransdorf et al.,2016).
Paroxysmal Nocturnal Dyspnea
It is a respiratory disease manifesting with severe shortness of breath and continuous coughing, which usually seen at night, and it awakens people from sleep during the evening (Herdman, 2011). It is caused by depression of the respiratory centers during sleep commonly seen in patients with cardiovascular abnormalities (Herdman, 2011). JC’s PND might be due by the several pillows he is using while sleeping.
S3 Gallop
The third heart sound is also called the S3 gallop. It occurs as a result of back and forth association of blood into the ventricles (Mangione, 2012). It is significant since it is associated with heart failure caused by mitral regurgitation, ventricular septal defects, and cardiomyopathy. JC’s ABG results indicate that she has adequately compensated respiratory acidosis (Mangione, 2012). This is because the patient’s PCO2 is elevated showing acidosis, HCO3 is elevated showing metabolic compensation, and the PO2 level is normal indicating full payment.
ANP and BNP Levels
In Congestive heart failure, the levels of ANP and BNP are elevated. BNP is secreted from the ventricles while ANP is secreted from the atria though it can also be secreted from the ventricles in some cases of heart failure (Kransdorf et al.,2016). The physiological effects of BNP and ANP are vasodilation, inhibition of RAAs activation, and natriuretic (Kransdorf et al.,2016). The levels can be used to monitor treatment of heart failure.
Treatment
According to Nelveg-Kristensen et al. (2015), lisinopril is a drug whose mechanism of action is inhibition of renin-angiotensin system, thus, decreasing secretion of angiotensin 2, secretion of aldosterone, fluid retention, decreased preload and afterload, and ultimately, slowing cardiac remodeling. Simvastatin is a lipid-lowering drug under the statin class. It is an HMG-COA reductase inhibitor, thus, reducing cholesterol synthesis (Kransdorf et al.,2016). Carvedilol is a beta blocker which slows heart rate and reduces myocardial oxygen consumption. Packed red cell transfusion is essential in increased the number of red blood cells to the patients unnecessary increasing other blood elements (Kransdorf et al.,2016).
Nursing Diagnosis and Educational Needs
Nursing diagnosis for the patient would entail vital sign examination for daily assessment of the patient progress. This would be active in monitoring the patient’s conditions after therapy. The patient educational needs include advising the patient to limit physical activity, reduce water intake, manage hypertension, sodium restriction, and adhere to prescribed drugs for management of the condition (Kransdorf et al.,2016).
Conclusion
Therefore, from the aforementioned, congestive heart failure is a disease of both children and adults. The disease is multifactorial since it is due by both genetic and environmental factors. Genetic predisposition is unavoidable while environmental factors can be avoided to prevent the occurrence of the disease. In most cases, a combination of factors results in the manifestation of the disease. The disease has a good prognosis is detected in early stages as compared to late stages.
References
Herdman, T. H., (2011). Nursing diagnoses: Definitions and classification 2012-14. Hoboken: John Wiley & Sons.
Iqbal, U. J., Kaleem, M., & Hanif, M. I. (2015). Coronary artery disease; severity & its associated risk factors in causing heart failure in patients presented with stemi at gulab devi chest hospital. Professional Medical Journal, 22(5), 532.
Kransdorf, E. P., Kransdorf, L. N., Fortuin, F. D., Sweeney, J. P., & Wilansky, S. (2016). Stepwise Progression of Right-to-Left Atrial Shunting through a Combination of Patent Foramen Ovale and Tricuspid Regurgitation. Texas Heart Institute Journal, 43(2), 171-174. doi:10.14503/THIJ-14-4913
Mangione, S. (2012). Physical Diagnosis Secrets: With STUDENT CONSULT Online Access. London: Elsevier Health Sciences.
Nelveg-Kristensen, K. E., Busk Madsen, M., Torp-Pedersen, C., Køber, L., Egfjord, M., Berg Rasmussen, H., & Riis Hansen, P. (2015). Pharmacogenetic Risk Stratification in Angiotensin-Converting Enzyme Inhibitor-Treated Patients with Congestive Heart Failure: A Retrospective Cohort Study. Plos ONE, 10(12), 1. doi:10.1371/journal.pone.0144195
Nicholson, C. (2014). Chronic heart failure: pathophysiology, diagnosis, and treatment. Nursing Older People, 26(7), 29-38.
