Complex case study analysis

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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).

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