Anatomy And Physiology 2 Lab Name Cas

Anatomy And Physiology 2 Labname Cas

This assignment involves a detailed case study analysis of a 76-year-old female patient presenting with symptoms indicative of cardiovascular issues. The patient, Helen Johnson, has a history of rheumatic fever and now exhibits signs of congestive heart failure, including shortness of breath, swelling of the ankles, jugular venous distension, a systolic murmur, and an extra S3 heart sound. Physical examination reveals hepatomegaly with ascites and pitting edema, suggesting fluid accumulation and compromised heart function. The case also mentions treatment with digoxin and later furosemide (Lasix). The task is to closely examine her clinical presentation, interpret diagnostic findings, investigate the role of her past rheumatic fever, and explain her medications' mechanisms, alongside other relevant physiological considerations.

Paper For Above instruction

Helen Johnson's presentation reflects a complex medical scenario rooted in her cardiovascular system's dysfunction. Her chief complaints of increasing shortness of breath (dyspnea) and ankle swelling over the past three months are hallmarks of congestive heart failure (CHF). These symptoms are exacerbated by her history of rheumatic fever, which is known to cause rheumatic heart disease leading to valvular damage, particularly involving the mitral and aortic valves. The combination of her physical findings and history suggests that her current cardiac condition is a consequence of prior rheumatic valvular lesions resulting in valvular regurgitation, which imposes abnormal stress on her heart and circulatory system.

Upon examination, Helen’s jugular venous distension indicates elevated central venous pressure, a typical feature of right-sided heart failure. The systolic murmur heard best over the left upper sternal border suggests turbulent blood flow related to valvular insufficiency, particularly mitral regurgitation, which often produces a holosystolic murmur. The presence of an extra "S3" heart sound further confirms volume overload and decreased ventricular compliance, common in CHF. The S3 sound, also called the ventricular gallop, occurs due to rapid filling of the dilated ventricle and is often associated with heart failure. The murmur and S3 reflect increased preload and impaired ventricular function.

The chest X-ray showing a normal cardiac silhouette may initially seem reassuring; however, it does not rule out functional or valvular abnormalities. A normal size can coexist with significant valvular regurgitation and heart failure symptoms, especially if eccentric hypertrophy occurs without gross cardiomegaly. Therefore, further diagnostic evaluation such as echocardiography would be necessary to assess valvular integrity and ventricular function more precisely.

Helen’s hepatomegaly and ascites indicate liver congestion due to elevated venous pressures from right-sided heart failure. These findings demonstrate how inadequate pumping efficiency causes blood to back up into systemic veins, leading to increased hydrostatic pressure in hepatic circulation, resulting in hepatocyte swelling and ascitic fluid accumulation. Persistent right-sided failure may also contribute to systemic edema, as evidenced by her pitting edema in the ankles.

The presence of pitting edema two weeks after medication initiation highlights the ongoing severity of her heart failure. Despite treatments, her condition may still involve excessive fluid retention, indicating that her body’s compensatory mechanisms—such as activation of the renin-angiotensin-aldosterone system (RAAS) —are causing sodium and water retention. The edema signifies that her heart cannot effectively manage preload, leading to persistent extracellular fluid accumulation. This underscores the importance of diuretics like furosemide, which promote fluid excretion to reduce preload and pulmonary congestion.

Support stockings are prescribed to alleviate edema in the lower extremities by applying graduated pressure, enhancing venous return and preventing blood pooling. Compression stockings assist in reducing venous pressure and fluid accumulation in the dependent tissues, thus helping manage edema and improving comfort.

In Hellen’s case, the predominant physiological stress on her heart appears to be increased preload rather than afterload. Increased preload results from volume overload due to valvular regurgitation and fluid retention, leading to stretching of the ventricular walls. While increased afterload (resistance against which the heart contracts) is also significant, her symptoms and findings—such as volume overload signs—point to increased preload as the more immediate stressor. Essentially, her heart is being stretched excessively from excess blood volume, impairing its efficiency over time.

The overarching classification of her condition is congestive heart failure (CHF). In CHF, the failing heart can’t meet the body's circulatory demands, leading to fluid accumulation in the lungs and systemic tissues. To compensate, her body activates neurohormonal pathways, notably the RAAS, which initially helps maintain perfusion through vasoconstriction and fluid retention but ultimately exacerbates fluid overload. Over time, mechanisms such as ventricular remodeling and increased sympathetic activity further impair cardiac output, perpetuating the cycle of heart failure.

Digoxin was prescribed to her to improve cardiac contractility, control ventricular response rate (especially if atrial fibrillation develops), and reduce symptoms of heart failure. Digoxin acts as an inotropic agent by inhibiting the Na+/K+ ATPase pump, leading to increased intracellular calcium in cardiac myocytes. This enhances myocardial contractility, thereby increasing stroke volume and cardiac output. Additionally, digoxin has vagomimetic effects that slow conduction through the atrioventricular node, reducing heart rate and alleviating symptoms related to tachyarrhythmias, which are common in CHF patients.

After two weeks, her physician prescribed furosemide (Lasix), a potent loop diuretic aimed at reducing fluid overload. Furosemide works by antagonizing the Na+/K+/2Cl− co-transporter in the thick ascending limb of the loop of Henle, impairing sodium, chloride, and water reabsorption. This diuretic effect decreases preload and pulmonary congestion, alleviates edema, and helps lower blood pressure. It is a critical component of heart failure management, especially in cases where fluid retention is prominent.

References

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