67 years Old Working Women Case Study
This is the case of a 67 years old lady who still works full time. She is unmarried but lives with her pet dog. Upon admission to the hospital ward, she has been diagnosed with heart failure and atrial fibrillation. Being presented with a BMI of 39, it is clear that she is overweight as the normal range for BMI is between 18-25. Moreover, the patient has also a past history of type 2 diabetes mellitus and hypertension for many years. Now some light will be put on the diagnosed diseases of the patient in the coming paragraphs about the detailed pathophysiology, risk factors, complications, treatment and management.
A fast an irregular heart rate is often termed as the atrial fibrillation. The downstream diseases cause by this include most commonly a higher risk for heart failure and strokes apart from other cardiac complications being associated with it. The reasons for the irregularity and fast speed of heart beat lies in the irregular beating of the heart’s upper two chambers known as atria. Also, the coordination of the atria with the lower chambers of heart – the ventricles – is also lost. Most common symptoms of atrial fibrillation include weakness, breath shortness and heart palpitations (Mayo Clinic).
The pathophysiology of atrial fibrillation and the resulting heart failure due to it, is complex a complex process. Also, it is not fully understood yet due to its multifaceted nature combined with the interconnectivity of different diseases as causative agents for one another. It has also been suggested by various studies that atrial fibrillation not only facilitates but also is involved in the progression of the heart failure through studies where they monitored the incidence and prevalence of the atrial fibrillation patients over the years. The outcome demonstrated a maximum of 4.4 percent more heart failure in such individuals (Maisel & Stevenson, 2003; Wang et al., 2003).
The reduction in cardiac output as a result of atrial fibrillation can be attributed to various mechanisms. One of these is the elevated rates of resting heart beats per minute. This exaggerated heart rate, especially after exercise, results in the reduction of the diastolic filling time too. These, combined, cause a decreases cardiac output resultantly. The main reason for this impairment in diastolic filling is mainly due to this loos of synchrony in the atrioventricular pumping. As an outcome, this also results in the lessening of the volume of stroke thus consequently increasing the mean value of the diastolic atrial pressure. Overall, this results in a decrease of about 20 percent in a proper cardiac output. Moreover, the irregularities in the responses of ventricles also affect the ventricular function along with their hemodynamic statuses. This is also an independent process resulting in diminished cardiac output (Dries et al., 1998; Naito, David, Michelson, Schaffenburg, & Dreifus, 1983).
In the development of the cardiomyopathy induced by tachycardia, then the most evident relationship is seen between the heart failure and atrial fibrillation. This is especially true for patients in which the ventricular rate is poorly controlled during the process of the development of the atrial fibrillation. Atrial fibrillation also constitutes the most common cause of cardiomyopathy induced by tachycardia conditions, the exact mechanism of which remains unknown still. Also, an improvement in the ejection fraction has also been observed in the patients in which radio waves have been used to treat atrial flutter or fibrillations. These patients show the prevalence of 20-50% of tachycardia induced cardiomyopathy. Though not fully understood and need to have extensive research done on its mechanism, the studies on animal models have suggested myocardial ischemia, energy depletion and abnormal regulation of calcium as the mechanisms for tachycardiac cardiomyopathies. Other studies has also revealed that treatments which eliminate the arrhythmias of the heart also have been proven efficient in the management of the heart’s hemodynamic states and the clinical manifestation of the heart failure disease (Gentlesk et al., 2007; Luchsinger & Steinberg, 1998; Shinbane et al., 1997; Van Gelder et al., 1993).
There are some instances where a preceding heart failure produced such changes in the atrium which ultimately leads to the atrial fibrillation. The known mechanisms for these range from elevated pressures of cardiac filling, irregularities in the concentrations of intracellular calcium to dysregulations of neuroendocrine and autonomic systems functions. As a result of the aforementioned changes, the initiation for the process of the atrial fibrillation takes place via diminished refractory period of atria, slowed conduction of the atrium, and a decreased synchronization of the atrial repolarization. When the atrial pressure and volume are increased there is an atrial stretch induced in the tissue. This stretch then activates the ionic currents dependent upon this stretch activation ultimately resulting in the alterations in the conduction properties of the heart. Various studies have found a reduced susceptibility in via gadolinium treatments which mainly functions to inhibit the currents produced by stretch activation and overloading of atrial pressures (Bode, Katchman, Woosley, & Franz, 2000; Maisel & Stevenson, 2003; Solti, Vecsey, Kékesi, & Juhász-Nagy, 1989).
One of the common mechanisms for the pathophysiological development of both the atrial fibrillation and heart failure is the intracellular calcium dysregulation. Researchers have found a downregulation of two key proteins in the progression of atrial fibrillation. These are ryanodine receptor protein and a calcium ATPase pump present in the sarcoplasmic reticulum of the cardiomyocytes. Moreover, some experimental models have also found increased currents which are brought about by the sodium-calcium exchanger ultimately leading to delayed depolarization and activity triggering afterwards. Some other reasons for heart failure include increased interstitial fibrosis of heart muscles especially of atria causing abnormal conductance and serving as substrates for atrial fibrillation to begin with as well as alterations in neuronal hormones occurring in heart failure thus promoting remodeling of heart structure and atrial fibrosis (Beuckelmann, Näbauer, & Erdmann, 1992; Cha et al., 2003; Li, Fareh, Leung, & Nattel, 1999; Ohkusa et al., 1999).
When heart failure was studied using animal models, then the dysregularities of the calcium concentrations inside the protoplasm along with calcium overload by sarcoplasmic reticulum was clearly demonstrated. Also, the mediation of the increased calcium load combined with reduced inhibition of the sarcoplasmic ATPase pump, both were shown to be mediated by the prolonged action potential. Moreover, a decrease in transverse T-tubules network’s density has also been found to be a causative factor in the atrial arrhythmias during heart failure (Patel, Vaduganathan, Shah, & Butler, 2017).
There are three main type of clinical manifestations associated with heart failure i.e., affecting left side, right side or both of them. However, the most common of these are the left side heart failure. Based on the signs and symptoms of the patient, it can be assessed which side of the ventricles is likely to have gotten affected as the failure of each side presents itself with different indices. For example, the left ventricle heart failure is diagnosed by one or more of the following symptoms: exertion or dyspnea; chest congestion; dry cough initially that is also nonproductive; frothy sputum that can be blood tinged sometimes; inadequate perfusion of tissues; weak pulse; tachycardia; fatigue; and sometimes nocturia. On the other hand, the symptoms of the right sided ventricular dysfunction include: congestion of the peripheral tissues as well as visceral organs; lower body edema especially of lower limbs; liver enlargement; ascites; nausea; weight gain and weakness. By overviewing these symptoms, it becomes quite evident that the patient presented in the ward has been suffering from the right-sided heart failure. Due to the presence of vascular congestion, heart failure is also commonly known as the congestive heart failure, though this term is now mostly considered outdated by the cardiac specialists (Ali Ahmed, Jones, & Hays, 2008; Riley, 2015).
Since the current case is of a geriatric heart failure type, it is necessary to develop an understanding about how to assess and manage so as to lay the sloid basis not only for the appropriate care but also aid in the facilitation of the patients in the long term care locales. For this purpose, the ‘DEFEAT’ mnemonic was followed. Briefly, it stands for: D – diagnosis; E – etiology, F – fluid volume; E – ejection fraction; and T – treatment (Ali Ahmed et al., 2008).
The first step, the diagnosis, is important to conduct, in particular before the order of any usual tests – the echocardiogram. However, in cases like this one, where a clinical diagnosis had already been done, checking how the diagnosis was made was necessary and was done. The etiology of the patient was next to be studied. Among this, the most common are having a look at the hypertension and myocardial infarction histories of the patient. As is clear from the report, hypertension was already there. However, it is also good to keep in view multiple factors in elderly heart failure patients to manage their long term care. Another factor of importance and probably a risk factor too was the history of diabetes type II in the patient. These assessments are especially important for care planning to prevent progression of the disease (A. Ahmed, 2007; Ali Ahmed et al., 2008).
The third important assessment technique is the examination of the fluid volume of the patient. The best way of doing this via estimation of the jugular vein pressure on the neck. The examination of external jugular veins is particularly important when limitations are considered properly. Since they are superficially present, they are facing both external pressures as well as internal pressures due to obstructions. Next comes the ejection fraction test which is done when the diagnosis of heart failure has been made. Therefore, it is also suitably applicable to the current scenario. Not only it serves as a marker for prognosis but also helps in guiding the therapeutic actions for the patient (A. Ahmed, 2007).
The perfect positions of the nursing care and the ultimate goal is to achieve improved outcomes of the patients. For the improvement of the heart failure prognosis for the patient presented in this case, the main care tasks and nursing interventions were: development of the educational materials on the basis of practice guidelines so as to help patients lessen the outcomes; proper assessment for improved aftermaths; designing instructions for patients; implementation of patient monitoring programs with special emphasis on tele-monitoring; and structuring programs for quality improvements (Pi & Hu, 2016).
The education of the patient included many topics so as to make patient education effective. First of all, she was advised to comply strictly with the diet plan which has been devised specially for by a dietician in accordance to maintain a healthy heart condition. Special emphasis was made on controlling sodium in the diet as she had a history of hypertension and high sodium diet can lead to increased risks of stroke and heart diseases (Kong, Baqar, Jerums, & Ekinci, 2016).
Another primary role of nursing care for this patient included continuing assessment of the patient based on her needs. For example, she was taught to have foods with fluid restrictions with continued monitoring of her fluid status. This was important since the patient was overweight. The usual assessment of the patient fluid included several indicators such as weight gain, orthopnea and peripheral edema and hence an increase or decrease of the baseline dose of diuretics depended and adjusted according to these. Apart from these, other ongoing assessment included monitoring the change of dietary behavior, amount of activity declines, worsening effect on thirst, elevations of fluid intake, and proper adherence to the prescribed medications (Kong et al., 2016).
Although nursing care plays an important role in management and improvement of a patient’s health outcomes, but self-care plays a long term effect in health maintenance after discharge of the patients. Therefore, proper discharge plan was made for the patient to follow the prescribed medications, exercises and diet. It has been found by the studies that the promotion and education of self-care proves beneficial in reducing the risk of readmission in hospitals. The crucial points to educate the patient in this scenario included knowledge transfer to patient about her specific symptoms in layman language with special focus of the age related and medical history related risk factors and symptoms, teaching about social issues and how to manage them, and cognition related factors. More notably, the tele monitoring theme was also included in the post discharge plan of the patient for regular, easy and efficient monitoring of the patient. These interventions were included particularly due to their increasing benefits being observed especially in the old age patients (Dickson et al., 2014; Zavertnik, 2014).
Lastly, various studies have found the positive effects of the aerobic exercises and trainings not only for increasing cardiac systolic functions but also for improving exercise capacity in heart failure patient. Therefore, exercise was recommended to the patient in the form of taking her dog to a walk so that she might not feel alone during that time and feel it more enjoyable rather than a burden on herself. However, she was also advised to start from the beginner level and not to do too much exertion as it could prove dangerous to her. Only after developing some capacity, she was advised to go for moderate level exercise as it has been found to be the best choice for heart failure patients (Brum et al., 2011).
Rivaroxaban (trade name Xarelto®) was prescribed to the patient at 20 mg single dose in the morning. It is a novel anticoagulant drug taken through oral route and has been approved in a range of countries for risk reduction of stroke and systemic embolism in heart patients. It is particularly prescribed to patients having nonvalvular atrial fibrillation apart from managing other risk factor too. Other uses of Xarelto include the prevention and treatment of venous thromboembolism after bone replacement surgeries as well as its recurrence, pulmonary embolism and deep vein thrombosis. Also, another of its rather recent use includes the preventive therapeutic use for atherothrombotic events, often in combination with other drugs such as acetylsalicylic acid, particularly in patients with elevated cardiac disease biomarkers (Agency, 2017; Haas, Bode, Norrving, & Turpie, 2014). The molecular mechanism of Rivaroxaban involves the inhibition of a coagulation factor in the coagulation pathway known as Factor Xa or thrombin. It can also be described as a direct inhibitor of the factor Xa binding directly and reversibly with the protein via its S1 and S4 pockets. Chemically, Rivaroxaban is a small molecule derivative of oxazolidinone and works via competitive inhibition of its target protein (Samama, 2011). The nursing care about the administration of this drug to the patient included a prior consideration of the factor under which it should not be given. These include kidney disease, being child or infant, liver failure, pregnancy or breast feeding conditions, prosthetic heart valves, presence or absence of epidural catheters as well as recent surgeries. Since none of these conditions were present in the patient, the drug was safe to use but with future monitoring of the just mentioned conditions.
Atenolol is used in the treatment of hypertension and heart diseases such as acute myocardial infarction and angina pectoris. It is a second generation adrenergic antagonist of beta receptors. Its mechanism of action includes the selective binding and inhibition of the beta-1 adrenergic receptors found in a variety of tissues i.e., heart muscles and vascular smooth muscles. By binding to these receptors, this drug functions to inhibit the sympathetic system stimulation via blockage of the positive actions of both the ionotropic and chronotropic receptors. The nursing care about atenolol administration included: monitoring of allergic reactions such as rashes, fever, respiratory distress and sore throat; CNS complications – fatigue dizziness, depression, sleep disturbances, disorientation, speech abnormalities and memory loss; cardiovascular functions – arrhythmias, bradycardia, tachycardia and pulmonary edema; dermatological effects; ENT assessments; musculoskeletal complications monitoring; and respiratory function monitoring. This is because any of these can be disturbed depending on the patient, so as to take necessary actions accordingly (Dézsi & Szentes, 2017; Ong, 2007).
Metformin was prescribed to be taken twice daily with meals to the patient. Metformin, most commonly marketed under the name of Glucophage, constitutes a first line treatment option for type II diabetes. Particularly prescribed to obese patients, it is most effective with minimum side effect when taken with meal. The management of diabetic heart patients is challenging due to the complexity of both the disease. Despite the existence of initial reluctance in the management of diabetic heart patients with metformin, a broader acceptance was achieved only after the negative results from the meta-analysis studies and clinical trials have shown the negative heart effects of the insulin-sensitizing drugs and agents. The main mechanism of metformin action includes the hepatic reduction in the glucose production along with lessening the glucose absorption in the intestines. It also acts by increasing the sensitivity of insulin via enhanced glucose uptake and utilization in the peripheral cells. The nursing considerations for the metformin administration included the history taking with respect to allergies to this, any complications of diabetes with infections and fever, traumas, major surgeries, acidosis and ketosis. Other physical assessments included lesions and skin color monitoring; peripheral sensations; bowel movements and sounds; evaluation of liver and urinalysis; creatinine levels in serum; and blood glucose monitoring (Dziubak, Wójcicka, Wojtak, & Bełtowski, 2018; Ekeruo, Solhpour, & Taegtmeyer, 2013; Rena, Hardie, & Pearson, 2017).
Januvia, alias sitagliptin, was prescribed to the patient once a day in the morning time with a dosage of 100 mg through oral route. The main purpose of Januvia administration was in the management of diabetes as it has been shown to be acting as an add-on to metformin and insulin in a research study. Its molecular mechanism involves the inhibition of dipeptidyl-peptidase (DPP-4). Similar to the action of other DPP-4 inhibitors, it also acts via two pathways – causing an increase in the levels of glucagon-like peptide-1 which is an incretin hormones; and elevating the levels of gastric inhibitory peptides in the body. In addition, it has shown to be effective in HbA1c under both monotherapeutic as well as combined therapeutic regimes. It also acts to stimulate increase in insulin secretion along with decrease in glucagon secretion. The nursing care interventions for the administration of Januvia includes history taking of the patient for past allergic reactions to Januvia if any. Moreover, the patient was assessed for the presence of kidney stones, skin reactions and joint pain there reasons for which are: the requirement of dialysis of kidney problems exist; taking DPP-4 inhibitors can contribute to the development of joint pain which can be severe in some instances; and skin reactions are also common in patients taking DPP-4 medications which can range from pigmentations, skin cracking and blister. In all such situations the patient was planned to have been referred to a doctor immediately (Alba et al., 2009; Gallwitz, 2007; Kesavadev, Pillai, Shankar, Krishnan, & Jothydev, 2017).
The Sevikar was prescribed at a dosage of 25 mg every morning to the patient. Sevikar is composed of olmesartan medoxomil and constitute medicine group known commonly as antagonists of angiotensin-II receptors. Angiotensin-II is produced by the body to function in the tightening or constriction of blood vessels. By blocking the angiotensin-II receptors by Sevikar, angiotensin-II can not to bind to these receptors and hence the signaling pathways leading to the relaxation of blood vessels via these receptors is stopped. In this way it not only helps lowering blood pressure but also is used in the treatment of heart conditions related to hypertension. One of the important constituents of Sevikar is a calcium channel blocker known by the name of amlodipine besilate. By binding to these channels, it prevents them from opening and hence reduced the influx of calcium into the cardiomyocytes and blood vessels. The nursing monitoring for the patient with respect to the patient included tracking of vomiting nausea or diarrhea and immediate management should be done for this as too much water and salt loss can be fatal. Also, patient was asked for any feelings of dizziness or light headedness after the first dose of Sevikar as in the presence of these symptoms the medication might have been needed to be changed (Marques da Silva, Haag, Guest, Brazier, & Soro, 2015; Ruilope & Schaefer, 2011; Taylor & Ragbir, 2012; Werner, Tabak, Alpert, & Bergman, 2002).
The patient was also prescribed with 100 mg dosage of Flecainide twice a day via oral route. It serves as a first line of medication in patients diagnosed with atrial fibrillation as it comes under the group of antiarrhythmic drugs. It is also used for the treatment of patients with supraventricular tachycardia in which case it functions to restore and maintain sinus rhythms. Flecainide is also known as the anti-arrhythmic agent of class Ic. Various studies including both clinical and experimental scenarios have shown that it has both anti as well as pro-arrhythmic actions. One reason for the dual action of Flecainide is its probable interactions at various levels in the body i.e., from physiological and pharmacological to cellular levels involvement. However, more research should be done to have its exact mechanism of action at molecular level covering its duality of nature too. The nursing consideration and management about the Flecainide use in the case presented included history of allergies to Flecainide, cardiac abnormalities and cardiogenic shock, pacemaker, sinus syndrome, renal or hepatic disease and imbalance of potassium. Apart from history assessments, physical evaluations included orientation, reflexes, blood pressure, edemas, serum electrolytes, weight and renal function monitoring (Andrikopoulos, Pastromas, & Tzeis, 2015; Liu, Atkins, & Kass, 2003; Salvage et al., 2018).
Last, but not the least, Lasix was prescribed at 20 mg dosage as per requirement basis. Lasix is the tradename of furosemide which is a diuretic used often for treatment of patients with hypertension and heart problems. In the current case, the administration of Lasix was to manage edema too, that is one reason why it is prescribes on as required basis. Besides its diuretic actions, researchers have also shown furosemide to have anti-inflammatory properties via inhibiting the production and release of inflammatory cytokines form mononuclear cells in the blood. This is also beneficial in the management of local inflammation of tissues. The history assessment by nursing care was done in relation to furosemide administration to see any previous allergies to this medication, electrolyte monitoring to prevent its depletion, renal failure, lactation, pregnancy and diabetes. The physical assessments entailed: edema; liver evaluation; urinary and bowel output; serum electrolytes and calcium monitoring; blood sugar and renal function tests; urinalysis and uric acid tests; and weight monitoring (Giménez, 2006; Prandota, 2002).
A rather recent and also powerful intervention in nursing is the patient tele monitoring. This is mainly due to the readmission improvements which have been observed after this. Also, studies have suggested a major cause of heart failure readmissions to be the noncompliance with medications. Hence the prime goal of tele monitoring remains in the assessment and education of patients in special reference to their diet plans, medications and their timings as well as exercise adherence. These interactions via telephones help monitor and assess patients’’ weights, daily symptoms, dietary routines, adherence to medications, daily activities and availability of social support thereby proving beneficial in reducing complications which might arise due to heart failure (Wakefield, Scherubel, Ray, & Holman, 2013).
More recently, mobile phone technologies have also contributed a lot in increasing an understanding in the patients about heart diseases and their preventive measure. A statistical analysis shows the usage of smartphones by approximately 28% population around the world. More interventions can include the teaching of patients about the installation and then proper usage of applications related to health present in their mobile phones. It also serves to reduce barriers in overcoming the traditional barriers for receiving primary and secondary health care information such as prevention measures, information and strategies (Wakefield et al., 2013).
Although only a limited number of studies are available regarding nursing care in old patients who have suffered from heart failure, using interventions specifically focusing on the age related self-care practices in consideration with the age-related and past history related risk factors could be especially useful. Following these principles, specialized trainings and educations should be conducted for nurses along with a monitoring program for their applicability. Furthermore, the application of such programs should also be monitored in a way so as to gather data about their usefulness and the fields requiring further improvements so as to move forward in a way that is most beneficial for the patients (Rosano, Vitale, & Seferovic, 2017; Wakefield et al., 2013).
The complex nature of the heart failure and additional intricacy posed by the advanced age combined with past history makes it a prime cause of both morbidity and mortality all around the globe. While detection during the early stages of the disease have proven successful in its treatment, frequent hospitalization is often required in advanced stage cases. Moreover, due to its association with other co-morbid conditions, strict implementation of the care along with a multidisciplinary approach is inevitable to the maximum reduction of the disease’s impact, apart from the usual pharmacological management. Lastly, the patient plan was prepared by a heart failure team in accordance with and considering the intensities both the hypertensive and diabetic background and history of the patient for the best management of her condition (Kannan & Janardhanan, 2014; Rosano et al., 2017).
References
Agency, E. M. (2017). Fycompa® annex I: summary of product characteristics.
Ahmed, A. (2007). DEFEAT heart failure: clinical manifestations, diagnostic assessment, and etiology of geriatric heart failure. Heart Fail Clin, 3(4), 389-402. doi:10.1016/j.hfc.2007.07.005
Ahmed, A., Jones, L., & Hays, C. I. (2008). DEFEAT heart failure: assessment and management of heart failure in nursing homes made easy. Journal of the American Medical Directors Association, 9(6), 383-389. doi:10.1016/j.jamda.2008.03.004
Alba, M., Sheng, D., Guan, Y., Williams-Herman, D., Larson, P., Sachs, J. R., . . . Goldstein, B. J. (2009). Sitagliptin 100 mg daily effect on DPP-4 inhibition and compound-specific glycemic improvement. Curr Med Res Opin, 25(10), 2507-2514. doi:10.1185/03007990903209514
Andrikopoulos, G. K., Pastromas, S., & Tzeis, S. (2015). Flecainide: Current status and perspectives in arrhythmia management. World journal of cardiology, 7(2), 76-85. doi:10.4330/wjc.v7.i2.76
Beuckelmann, D. J., Näbauer, M., & Erdmann, E. (1992). Intracellular calcium handling in isolated ventricular myocytes from patients with terminal heart failure. Circulation, 85(3), 1046-1055. doi:10.1161/01.cir.85.3.1046
Bode, F., Katchman, A., Woosley, R. L., & Franz, M. R. (2000). Gadolinium decreases stretch-induced vulnerability to atrial fibrillation. Circulation, 101(18), 2200-2205. doi:10.1161/01.cir.101.18.2200
Brum, P. C., Bacurau, A. V., Medeiros, A., Ferreira, J. C., Vanzelli, A. S., & Negrão, C. E. (2011). Aerobic exercise training in heart failure: impact on sympathetic hyperactivity and cardiac and skeletal muscle function. Braz J Med Biol Res, 44(9), 827-835. doi:10.1590/s0100-879×2011007500075
Cha, Y. M., Dzeja, P. P., Shen, W. K., Jahangir, A., Hart, C. Y., Terzic, A., & Redfield, M. M. (2003). Failing atrial myocardium: energetic deficits accompany structural remodeling and electrical instability. Am J Physiol Heart Circ Physiol, 284(4), H1313-1320. doi:10.1152/ajpheart.00337.2002
Dézsi, C. A., & Szentes, V. (2017). The Real Role of β-Blockers in Daily Cardiovascular Therapy. American journal of cardiovascular drugs : drugs, devices, and other interventions, 17(5), 361-373. doi:10.1007/s40256-017-0221-8
Dickson, V. V., Melkus, G. D., Katz, S., Levine-Wong, A., Dillworth, J., Cleland, C. M., & Riegel, B. (2014). Building skill in heart failure self-care among community dwelling older adults: results of a pilot study. Patient Educ Couns, 96(2), 188-196. doi:10.1016/j.pec.2014.04.018
Dries, D. L., Exner, D. V., Gersh, B. J., Domanski, M. J., Waclawiw, M. A., & Stevenson, L. W. (1998). Atrial fibrillation is associated with an increased risk for mortality and heart failure progression in patients with asymptomatic and symptomatic left ventricular systolic dysfunction: a retrospective analysis of the SOLVD trials. Studies of Left Ventricular Dysfunction. Journal of the American College of Cardiology, 32(3), 695-703. doi:10.1016/s0735-1097(98)00297-6
Dziubak, A., Wójcicka, G., Wojtak, A., & Bełtowski, J. (2018). Metabolic Effects of Metformin in the Failing Heart. International journal of molecular sciences, 19(10), 2869. doi:10.3390/ijms19102869
Ekeruo, I. A., Solhpour, A., & Taegtmeyer, H. (2013). Metformin in Diabetic Patients with Heart Failure: Safe and Effective? Current cardiovascular risk reports, 7(6), 417-422. doi:10.1007/s12170-013-0355-4
Gallwitz, B. (2007). Review of sitagliptin phosphate: a novel treatment for type 2 diabetes. Vascular health and risk management, 3(2), 203-210. doi:10.2147/vhrm.2007.3.2.203
Gentlesk, P. J., Sauer, W. H., Gerstenfeld, E. P., Lin, D., Dixit, S., Zado, E., . . . Marchlinski, F. E. (2007). Reversal of left ventricular dysfunction following ablation of atrial fibrillation. J Cardiovasc Electrophysiol, 18(1), 9-14. doi:10.1111/j.1540-8167.2006.00653.x
Giménez, I. (2006). Molecular mechanisms and regulation of furosemide-sensitive Na-K-Cl cotransporters. Curr Opin Nephrol Hypertens, 15(5), 517-523. doi:10.1097/01.mnh.0000242178.44576.b0
Haas, S., Bode, C., Norrving, B., & Turpie, A. G. (2014). Practical guidance for using rivaroxaban in patients with atrial fibrillation: balancing benefit and risk. Vascular health and risk management, 10, 101-114. doi:10.2147/VHRM.S55246
Kannan, A., & Janardhanan, R. (2014). Hypertension as a risk factor for heart failure. Curr Hypertens Rep, 16(7), 447. doi:10.1007/s11906-014-0447-7
Kesavadev, J., Pillai, P. B. S., Shankar, A., Krishnan, G., & Jothydev, S. (2017). Sitagliptin 100 mg vs glimepiride 1-3 mg as an add-on to insulin and metformin in type 2 diabetes (SWIM). Endocrine connections, 6(8), 748-757. doi:10.1530/EC-17-0100
Kong, Y. W., Baqar, S., Jerums, G., & Ekinci, E. I. (2016). Sodium and Its Role in Cardiovascular Disease – The Debate Continues. Frontiers in endocrinology, 7, 164-164. doi:10.3389/fendo.2016.00164
Li, D., Fareh, S., Leung, T. K., & Nattel, S. (1999). Promotion of atrial fibrillation by heart failure in dogs: atrial remodeling of a different sort. Circulation, 100(1), 87-95. doi:10.1161/01.cir.100.1.87
Liu, H., Atkins, J., & Kass, R. S. (2003). Common molecular determinants of flecainide and lidocaine block of heart Na+ channels: evidence from experiments with neutral and quaternary flecainide analogues. The Journal of general physiology, 121(3), 199-214. doi:10.1085/jgp.20028723
Luchsinger, J. A., & Steinberg, J. S. (1998). Resolution of cardiomyopathy after ablation of atrial flutter. Journal of the American College of Cardiology, 32(1), 205-210. doi:10.1016/s0735-1097(98)00183-1
Maisel, W. H., & Stevenson, L. W. (2003). Atrial fibrillation in heart failure: epidemiology, pathophysiology, and rationale for therapy. Am J Cardiol, 91(6a), 2d-8d. doi:10.1016/s0002-9149(02)03373-8
Marques da Silva, P., Haag, U., Guest, J. F., Brazier, J. E., & Soro, M. (2015). Health-related quality of life impact of a triple combination of olmesartan medoxomil, amlodipine besylate and hydrochlorotiazide in subjects with hypertension. Health and quality of life outcomes, 13, 24-24. doi:10.1186/s12955-015-0216-6
Mayo Clinic. Atrial fibrillation. Retrieved from https://www.mayoclinic.org/diseases-conditions/atrial-fibrillation/symptoms-causes/syc-20350624#:~:text=faster%20than%20normal.-,Atrial%20fibrillation%20is%20an%20irregular%20and%20often%20rapid%20heart%20rate,to%20175%20beats%20a%20minute.
Naito, M., David, D., Michelson, E. L., Schaffenburg, M., & Dreifus, L. S. (1983). The hemodynamic consequences of cardiac arrhythmias: evaluation of the relative roles of abnormal atrioventricular sequencing, irregularity of ventricular rhythm and atrial fibrillation in a canine model. Am Heart J, 106(2), 284-291. doi:10.1016/0002-8703(83)90194-1
Ohkusa, T., Ueyama, T., Yamada, J., Yano, M., Fujumura, Y., Esato, K., & Matsuzaki, M. (1999). Alterations in cardiac sarcoplasmic reticulum Ca2+ regulatory proteins in the atrial tissue of patients with chronic atrial fibrillation. Journal of the American College of Cardiology, 34(1), 255-263. doi:10.1016/s0735-1097(99)00169-2
Ong, H. T. (2007). Beta blockers in hypertension and cardiovascular disease. BMJ (Clinical research ed.), 334(7600), 946-949. doi:10.1136/bmj.39185.440382.47
Patel, R. B., Vaduganathan, M., Shah, S. J., & Butler, J. (2017). Atrial fibrillation in heart failure with preserved ejection fraction: Insights into mechanisms and therapeutics. Pharmacol Ther, 176, 32-39. doi:10.1016/j.pharmthera.2016.10.019
Pi, H.-Y., & Hu, X. (2016). Nursing care in old patients with heart failure: current status and future perspectives. Journal of geriatric cardiology : JGC, 13(5), 387-390. doi:10.11909/j.issn.1671-5411.2016.05.019
Prandota, J. (2002). Furosemide: progress in understanding its diuretic, anti-inflammatory, and bronchodilating mechanism of action, and use in the treatment of respiratory tract diseases. Am J Ther, 9(4), 317-328. doi:10.1097/00045391-200207000-00009
Rena, G., Hardie, D. G., & Pearson, E. R. (2017). The mechanisms of action of metformin. Diabetologia, 60(9), 1577-1585. doi:10.1007/s00125-017-4342-z
Riley, J. (2015). The Key Roles for the Nurse in Acute Heart Failure Management. Cardiac failure review, 1(2), 123-127. doi:10.15420/cfr.2015.1.2.123
Rosano, G. M., Vitale, C., & Seferovic, P. (2017). Heart Failure in Patients with Diabetes Mellitus. Cardiac failure review, 3(1), 52-55. doi:10.15420/cfr.2016:20:2
Ruilope, L. M., & Schaefer, A. (2011). Efficacy of Sevikar® compared to the combination of perindopril plus amlodipine on central arterial blood pressure in patients with moderate-to-severe hypertension: Rationale and design of the SEVITENSION study. Contemp Clin Trials, 32(5), 710-716. doi:10.1016/j.cct.2011.04.011
Salvage, S. C., Chandrasekharan, K. H., Jeevaratnam, K., Dulhunty, A. F., Thompson, A. J., Jackson, A. P., & Huang, C. L. H. (2018). Multiple targets for flecainide action: implications for cardiac arrhythmogenesis. British journal of pharmacology, 175(8), 1260-1278. doi:10.1111/bph.13807
Samama, M. M. (2011). The mechanism of action of rivaroxaban–an oral, direct Factor Xa inhibitor–compared with other anticoagulants. Thromb Res, 127(6), 497-504. doi:10.1016/j.thromres.2010.09.008
Shinbane, J. S., Wood, M. A., Jensen, D. N., Ellenbogen, K. A., Fitzpatrick, A. P., & Scheinman, M. M. (1997). Tachycardia-induced cardiomyopathy: a review of animal models and clinical studies. Journal of the American College of Cardiology, 29(4), 709-715. doi:10.1016/s0735-1097(96)00592-x
Solti, F., Vecsey, T., Kékesi, V., & Juhász-Nagy, A. (1989). The effect of atrial dilatation on the genesis of atrial arrhythmias. Cardiovasc Res, 23(10), 882-886. doi:10.1093/cvr/23.10.882
Taylor, A. A., & Ragbir, S. (2012). Three in one: safety, efficacy, and patient acceptability of triple fixed-dose combination medicine in the management of hypertension. Patient preference and adherence, 6, 555-563. doi:10.2147/PPA.S14764
Van Gelder, I. C., Crijns, H. J., Blanksma, P. K., Landsman, M. L., Posma, J. L., Van Den Berg, M. P., . . . Lie, K. I. (1993). Time course of hemodynamic changes and improvement of exercise tolerance after cardioversion of chronic atrial fibrillation unassociated with cardiac valve disease. Am J Cardiol, 72(7), 560-566. doi:10.1016/0002-9149(93)90352-d
Wakefield, B. J., Scherubel, M., Ray, A., & Holman, J. E. (2013). Nursing interventions in a telemonitoring program. Telemedicine journal and e-health : the official journal of the American Telemedicine Association, 19(3), 160-165. doi:10.1089/tmj.2012.0098
Wang, T. J., Larson, M. G., Levy, D., Vasan, R. S., Leip, E. P., Wolf, P. A., . . . Benjamin, E. J. (2003). Temporal relations of atrial fibrillation and congestive heart failure and their joint influence on mortality: the Framingham Heart Study. Circulation, 107(23), 2920-2925. doi:10.1161/01.Cir.0000072767.89944.6e
Werner, P., Tabak, N., Alpert, R., & Bergman, R. (2002). Interventions used by nursing staff members with psychogeriatric patients resisting care. Int J Nurs Stud, 39(4), 461-467. doi:10.1016/s0020-7489(01)00048-7
Zavertnik, J. E. (2014). Self-care in older adults with heart failure: an integrative review. Clin Nurse Spec, 28(1), 19-32. doi:10.1097/nur.0000000000000021