1. Outline the causes, incidence and risk factors of the identified condition and how it can impact on the patient and family.
2. List five (5) common signs and symptoms of the identified condition; for each provide a link to the underlying pathophysiology
a. This can be done in the form of a table – each point needs to be appropriately referenced
3. Describe two (2) common classes of drugs used for patients with the identified condition including physiological effect of each class on the body
a. This does not mean specific drugs but rather the class that these drugs belong to.
4. Identify and explain, in order of priority the nursing care strategies you, as the registered nurse, should use within the first 24 hours post admission for this patient?
To intervene the reason behind Mrs. Sharon’s breathing shortness it was found that the causes of congestive heart failure may include hypertention, coronary artery disease, long-term alcohol consumption, heart valve disorder and few unknown causes, such as: post myocarditis (Butler, 2011). In case of elevated blood pressure (more than 120/80 mm Hg), the condition can cause congestive heart failure. Mrs. Sharon’s coronary artery got badly damaged and it is a diseased condition that damages the coronary arteries of heart by limiting the flow of the blood. Coronary arteries are the small arteries that deliver blood to the heart (Thorsgard & Bart, 2009). Fatty substances and cholesterol can block these arteries and cause narrowing of these arteries, which subsequently lead to the condition of congestive cardiac failure. Heart valves controls the movement of blood flow by closing and opening, allow the blood flow to get in and out of the heart chambers. In case of diseased valves, they fail to properly close and open and may compel the ventricles to function harder during the pumping of blood. Mrs. Sharon has presented to the emergency department due to her increased breathing shortness, dizziness and nausea, which perhaps associated with the condition of CCF. Its presence along with acute exacerbation is supported by her ECG and chest X-ray report. It is estimated that 300,000Australians are currently suffering from CHF and almost 30,000cases are identified every year. According to AIHW, prevalence of hypertension, alcohol consumption, coronary disease, diabetes and obesity are the risk factors, which can lead to congestive heart failure (Aihw.gov.au, 2015). According to Bahrami et al. (2008), there is an association between congestive heart failure and differences in ethnicity. They mentioned that higher chances of CHF incident among the African Americans are associated with variations in the occurrence of diabetes mellitus and hypertension and also socio-economic status (Bahrami et al., 2008). The CHF mechanisms differed by cultural background; as in case of the African Americans, myocardial infarction has least influence among this population. CHF is a consequence of atherosclerosis and hence risk factors related with CHF are the same. These are: hypertension, diabetes, and myocardial infarction, high level of cholesterol, heart enlargement, family history, heart valve complications and smoking (Jonas, 2001). In Mrs. Sharon’s case, her blood pressure was 105/55 mm Hg, which is lower than the standard blood pressure measurement, hence risk factors associated with hypertension can be ruled out. Her ECG report showed that she has sinus bradycardia, which can be considered as the associated risk factor (Sun, Reiser & Chou, 2006). Her x-ray report showed cardiomegaly, which can be considered as the associated risk factor. The rationales behind cardiomegaly may include elevated blood pressure which is improperly treated for longtime, coronary artery disease, alcohol abuse, viral carditis and postpartum cardiomyopathy. In Mrs. Sharon’s case, blood pressure problem can be assumed as contributing factor for cardiomegaly. Mrs. Sharon’s condition of congestive heart failure can affect her and her family members. CHF can diminish her daily living activities and can increase anxiety and stress, which in turn can affect his/her emotional expression and behaviors with family members and others (Moore, 2010). Therefore, family members should have the understanding of how to deal with the patients during this phase. Mrs. Sharon’s acute exacerbation and sinus bradicardiya are expected to be associated with the digoxin toxicity. If the kidneys are working inadequately, digoxin can store inside the system and cannot be removed via urination. Any complication which affects the functionality of the kidneys, such as: dehydration makes digoxin toxicity more likely.
Five common indications of the congestive heart failure for Mrs. Sharon includes shortness in breathing, crackles sound in the lungs, ascites or fluid accumulation, dizziness and apex beat. Pathophysiology associated with her shortness in breathing is due to congestive heart failure. It presents nocturnal dyspnea and orthopnea, may be because of the feeling of inadequate oxygen, chest tightness and daily living activity. Congestive heart failure takes place when a heart fails to properly circulate the blood successfully and fails to maintain the flow of blood to meet the system’s requirements (Saksena, 2005). In such cases if body is not receiving adequate amount of oxygen it is quite obvious that this particular individual will feel suffocated or will be having breathing shortness. In the absence of adequate amount of oxygen and also inefficient heart pumping, the less oxygenated blood will fail to meet the needs of each and every cells of the system. Her condition of crackles or rales can take place by accumulation of fluid within the atelectasis or small airways. These are generally mentioned as discontinued sounds. This type of sound is heard when air is forcefully pass respiratory passage, which are narrowed down by pus, mucus or fluid. Rales that do not get clear after coughing may represent the presence of heart failure. The reason behind ascites or fluid accumulation is that her condition of heart failure worsens few areas in the leg, like ankle and eventually abdominal area collects fluids, and this condition is referred to as ascites. This might happen because the system retains too much sodium chloride or salt. The excess amount of sodium chloride causes the system to save water. After that this water leaks out into interstitial tissue linings and appears as ascites. Mrs. Sharon also feels dizziness. As it is already mentioned that shortness of breathing in heart failure is due to inadequate amount of oxygen that system receives and the less oxygenated blood fails to meet the needs of each and every cells of the system. Dizziness happens when brain receives lack of oxygenated blood (Pang & Levy, 2010). In the condition of heart failure two factors contribute to the condition of dizziness: one, insufficient amount of blood flow to the brain, as heart fails to properly pump the blood and the next one is lack of oxygenated blood. Her apex beat is due to congestive heart failure. It is seen that congestive cardiac failure includes laterally dislocated apex beat and this happens if heart is increased, which is applicable for Mrs. Sharon’s case, as her x-ray report showed cardiomegaly. Mrs. Sharon’s ECG and X-ray report suggest congestive cardiac failure with or without digoxin toxicity. The probable indications associated with digoxin toxicity are confusion, irregular pulse, appetite loss, vomiting, nausea, palpitation and so on. Mrs. Sharon’s acute exacerbation and sinus bradicardiya are expected to be associated with the digoxin toxicity.
Mrs. Sharon is administered with digoxin, which is cardiac glycosides. Digoxin is derived from foxglove or digitalis and used to control cardiac parameters. It especially treats congestive heart failure. Digoxin is an approved drug by Food and Drug Administration (FDA in USA) for use to treat heart failure. Common clinical experience with Digoxin is obtained from older population (Drugbank.ca, 2015). However, digoxin is excreted by the kidneys. The risk associated with toxic reactions to digoxin may be bigger among the patients with impaired renal function. Digoxin comprises aglycone digoxigenin and three sugars. It has positive inotropic and negative chronotropic activity. Digoxin controls ventricular rate in arterial fibrillation. Digoxin obstructs sodium potassium ATPase. Sodium potassium ATPase is a membrane pump and it increases the intracellular sodium amplification (Drugbank.ca, 2015). Calcium sodium exchanger sequentially aims to extrude sodium molecules and by doing so, uptake more calcium. Increased concentration of intracellular calcium may support contractile protein activation, for example: actin and myosin. Digoxin acts on the cardiac electrical activity and accordingly amplifying the gradient of phase four depolarization. This mechanism shortens the action potential duration and reducing maximum diastolic potential. One common side effect of this drug may include exhaustion. Mrs. Sharon is administered with Frusimide, which is a strong loop diuretic, which is used to treat fluid accumulation within the system or also referred to as edema treatment that assists to eliminate excess fluid from the body (Nlm.nih.gov, 2015). The edema can be the result of heart failure, kidney disorder, cirrhosis and nephritic syndrome. It removes excess fluid from the system by increasing the urine production. It functions relatively faster. In case of Mrs. Sharon suggesting her with Frusemide administration is justified as it can be assumed that because of the congestive heart failure, she might have developed the problem of fluid accumulation. Fruimide can decrease potassium level in the blood and the mechanism is known as hypokalemia and can typically affect the individuals administering with digoxin. It is justified to mention that administering Mrs. Sharon with cardiac glycosides and loop diuretic are very significant in order to treat her condition of congestive heart failure and ascites.
Priority wise the complications, which should be taken under nursing consideration include shortness of breath, dizziness, nausea, swollen ankles. So, initial 24hours nursing plan is very essential. Mrs. Sharon’s assessment represents: irregular pulse rhythm, bradycardia, generalized weakness, paleness, Decreased heart output. Her diagnosis includes increased heart output (altered rhythm and heart rate); bradycardia. Her treatment planning should include
Short term: 3-4hours later after nursing interventions, Mrs. Sharon will take part in functions, which diminish the heart workload.
Long term: 3-4days of nursing care, Mrs. Sharon will display hemodynamic stability.
Assessment of abnormal lung sounds and heat sounds: it permits left side heart failure detection, which may take place with persistent renal failure because of the overload of fluid as impaired kidneys are incapable to eliminate water. Monitor pulse and blood pressure is important as patients with kidney malfunction are generally hypertensive that contributes to fluid overload and initiation of rennin-angiotensin mechanism (Bakas et al., 2014). Control cardiac glycosides, as recommended and toxicity monitoring is important as digoxin has positive isotropic effect on myocardium, which strengthens contractility and thus developing cardiac output. Next important nursing intervention could be execution of strategies to take care of electrolyte imbalances and fluid, which reduces the chance for progress of cardiac output because of imbalances. Nurses should instruct patient for adequate sleep and bed rest to promote body relaxation. Result should be monitored of lab test and diagnostic evaluations are essential as test results provide hints to patient status, disease status and treatment responses. Monitoring ABGs and oxygen saturation are important as these give information about the capacity of the heart to perfuse oxygenated blood with distal tissues. Assessment of peripheral pulses and skin temperature is important as reduced perfusion, tissue oxygenation less important to anemia, inefficiency in pumping may direct to reduction in temperature, peripheral pulses, which are reduced and hard to palpate. After nursing interferences, Mrs. Sharon shall be able to take part in functions, which diminish heart workload and subsequently after 2-3days of nursing interferences, Mrs. Sharon shall achieve hemodynamic stability.
References
Aihw.gov.au,. (2015). Cardiovascular disease: Australian facts 2011 (AIHW). Retrieved 17 March 2015, from https://www.aihw.gov.au/publication-detail/?id=10737418510
Bahrami, H., Kronmal, R., Bluemke, D., Olson, J., Shea, S., & Liu, K. et al. (2008). Differences in the Incidence of Congestive Heart Failure by Ethnicity. Archives Of Internal Medicine, 168(19), 2138. doi:10.1001/archinte.168.19.2138
Bakas, T., Clark, P., Kelly-Hayes, M., King, R., Lutz, B., & Miller, E. (2014). Evidence for Stroke Family Caregiver and Dyad Interventions: A Statement for Healthcare Professionals From the American Heart Association and American Stroke Association. Stroke, 45(9), 2836-2852. doi:10.1161/str.0000000000000033
Butler, J. (2011). Congestive Heart Failure Special Issue on Advanced Heart Failure. Congestive Heart Failure, 17(4), 159-159. doi:10.1111/j.1751-7133.2011.00237.x
Drugbank.ca,. (2015). DrugBank: Digoxin (DB00390). Retrieved 17 March 2015, from https://www.drugbank.ca/drugs/DB00390
Jonas, B. (2001). Coronary heart disease, smoking and hypertension are the greatest risk factors for congestive heart failure. Evidence-Based Cardiovascular Medicine, 5(3), 73-74. doi:10.1054/ebcm.2001.0381
Moore, C. (2010). The Impact of Family Functioning on Caregiver Burden among Caregivers of Veterans with Congestive Heart Failure. Journal Of Family Social Work, 13(5), 451-462. doi:10.1080/10522158.2010.514681
Nlm.nih.gov,. (2015). Furosemide: MedlinePlus Drug Information. Retrieved 17 March 2015, from https://www.nlm.nih.gov/medlineplus/druginfo/meds/a682858.html
Pang, P., & Levy, P. (2010). Pathophysiology of Volume Overload in Acute Heart Failure Syndromes.Congestive Heart Failure, 16, S1-S6. doi:10.1111/j.1751-7133.2010.00167.x
Saksena, S. (2005). Electrophysiological disorders of the heart. Philadelphia, Pa.: Elsevier Churchill Livingstone.
Sun, W., Reiser, I., & Chou, S. (2006). Risk Factors for Acute Renal Insufficiency Induced by Diuretics in Patients With Congestive Heart Failure. American Journal Of Kidney Diseases, 47(5), 798-808. doi:10.1053/j.ajkd.2006.01.031
Thorsgard, M., & Bart, B. (2009). Ultrafiltration for Congestive Heart Failure. Congestive Heart Failure, 15(3), 136-143. doi:10.1111/j.1751-7133.2009.00054.x
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