Barbara Bush heart failure

Barbara Bush heart failure

Introduction

Barbara Bush served as the First Lady of the United States (US) between 1989 and 1993. She was the wife of George Bush, the 41st President of the US. Before her role as the first lady, she was the Second Lady between 1981 and 1989. Moreover, among her children are Jeb and George Bush, who served as governor of Florida and the 43rd President respectively. Regarding her medical history, in 1988, Barbara was diagnosed with Graves’ disease. The disease, also referred to as toxic diffuse goiter, is an autoimmune condition that affects the thyroid and is the leading cause of hyperthyroidism.

Years later, she was diagnosed with chronic obstructive pulmonary disease and congestive heart failure. Her caregivers expressed that her 25 years as a smoker may have played a key role as the cause of the two conditions. She quit the habit in 1968. Also, in 2008, she was hospitalized due to abdominal pain, and as a consequence, she underwent surgery on the small intestine. In 2009, she underwent surgery for aortic valve replacement, and she was treated for pneumonia in 2013. On April 15th of this year, their family spokesman released a statement on Barbara’s failing health and that she had chosen to stay at home for palliative care. She died on 17th April 2018 at the age of 92.

Heart failure refers to a pathophysiologic condition whereby the heart is unable to pump blood at a rate that meets the metabolic needs of tissues. The heart can only pump blood adequately to tissues by elevating the diastolic filling pressure. The condition results from an abnormality in cardiac function, which may or may not be detectable. Also noteworthy is the fact that heart failure can also occur when the cardiac function is near-normal but under conditions of increased demand (Morton et al., 2017). To preserve the heart’s pumping function, various compensatory mechanisms are initiated in the cardiovascular system. These mechanisms include increased cardiac filling pressure, blood volume, cardiac muscle mass and the heart rate. However, these mechanisms only serve to increase metabolic demands of the myocardium, which, over time leads to worsening of the condition (Jurgens et al., 2015). Most importantly, over time,there is remodeling of the myocytes and the myocardium which leads to their increase in mass and volume. The remodeling leads to increased oxygen demand, ischemia, and impaired contractility.

The clinical manifestations of heart failure include exertional dyspnea which refers to breathlessness after mild activity. In the early stages of heart failure, the breathlessness may appear to be normal since it occurs during strenuous activity. However, as the condition progresses, dyspnea manifests even with ordinary activity (Morton et al., 2017). Moreover, another manifestation is orthopnea, which is shortness of breath that happens when one lies flat and is only relieved when the head is propped up using pillows or when the individual changes posture to a sitting position. The patient may also present with jugular venous distension, pulmonary edema, and palpitations. The patient may also be frail with a feeling of heaviness in the limbs which is attributed to poor perfusion of the individual’s skeletal muscles. Other clinical manifestations include peripheral cyanosis, ascites, and peripheral edema as well as cerebral symptoms like confusion, nightmares, memory impairment and headaches.

History

Historically, Thomas Lewissimply described heart failure as a state where the heart fails to release its contents. He was also the first person to attribute smoking to myocardial infarction and heart failure after he suffered both due to his 70 cigarettes-a-day smoking habit. It was in 1950 that Paul Wood modified the definition to include failure of the heart to maintain sufficient circulation for the body’s needs. Later on, it was discovered that the manifestations were a bit different for various patients. Research revealed that heart failure might be predominantly right-sided or left-sided. The predominant signs of right-sided failure include congestive hepatomegaly, ascites, and anasarca (Jurgens et al., 2015). These were due to increased pressure on the rightside of the heart that is transmitted back into the portal venous circulation. This manifests as an increase in abdominal girth as well as pain in the right upper and epigastric quadrants due to fluid accumulation. In essence, distinguishing hepatic failure from right-sided heart failure is often difficult. On the other hand, left-sided heart failure is mainly characterized by dyspnea due to cardiogenic pulmonary edema.

Some of the physiological stressors that may aggravate heart failure include underlying conditions like structural abnormalities of the heart and some medications (Morton et al., 2017). Moreover, infections and anemia can also worsen the symptoms. In chronic heart failure, the reduction in cardiac output results in some physiological compensation mechanisms to maintain blood supply to the tissues.

The first mechanism is a reduction in arterial pressure. This is as a result of an increase in sympathetic activity due to the release of catecholamines in the blood. The result is vasoconstriction, which serves to restore the blood pressure. However, there is a concomitant increase in peripheral resistance, which increases the workload on the heart. The heart has to increase contractility leading to more metabolic demand from the myocardium. The increased sympathetic activity also stimulates the release of vasopressin that promotes fluid retention at the kidneys to increase the blood volume and, in turn, pressure. The second mechanism involves the release of renin, angiotensin, and aldosterone due to under-perfusion of the kidneys. As a result, there is salt and water retention leading to edema in the extremities. Under-perfusion of skeletal muscles leads to muscle atrophy, weakness and exercise intolerance. The third mechanism involves myocardial remodeling in the long term due to a chronic elevation in levels of circulating catecholamines, aldosterone, renin and angiotensin. There is hypertrophy in the myocardium to enable the heart to overcome the increased preload and pump blood to tissues (Jurgens et al., 2015). However, in the long run, the compensatory mechanisms worsen heart failure as the demands of the heart also increase as the compensatory mechanisms take effect.

Patient care technologies have made it easier to assess, diagnose and manage the condition in the early stages thus leading to a reduction in morbidity and mortality (Morton et al., 2017). In monitoring and management of heart failure, simple tools such as catheters as well as complex equipment such as the electrocardiogram, X-ray machine, angiography imaging equipment and pulse oximeters are used. Also, monitoring of metrics such as B-type natriuretic peptide levels has historically been an essential part of care.

Planning

The short-term goals of heart failure management involve relieving symptoms like shortness of breath, peripheral edema and decreased exercise tolerance. Moreover, another short-term goal is to improve functional capacity which is essential in improving the quality of life for the patient (Jurgens et al., 2015). On the other hand, long-term goals include reducing mortality as well as slowing or retarding the structural abnormalities attributable to heart failure.

Nursing concerns in heart failure span a wide range of roles from initial patient assessment to monitoring and management. In the initial patient triage, the nurse practitioner is charged with eliciting the patient history, assessing the severity of the patient’s health status (Benhase et al., 2018). The nurse practitioner is normally trained to perform clinical assessment which helps them identify clinical manifestations of heart failure such as signs of congestion. The patient can then be referred for chest X-ray. Also, identifying the clinical stability of the patient during triage enables the nurse practitioner to promptly determine and transfer the patient to the appropriate level of care. This ensures the patient’s safety as well as effective therapy. The assessment may include objective determination of the severity of dyspnea by checking the respiratory rate, tolerance when lying down, oxygen saturation and use of the dyspnea severity scale. Additionally, the hemodynamic status, heart rhythm and cardiac output of the patient are essential. Also, s/he can check for jugular venous pressure, peripheral edema and pulmonary rales (Benhase et al., 2018). Laboratory blood tests, as well as the determination of anxiety levels using an objective assessment tool, is also part of the initial triage. Patient care technologies may include the electrocardiogram to assess heart function, ultrasound for echocardiography and angiography to determine underlying problems in blood vessels.

Interventions

Nursing interventions may involve administering and monitoring treatment, patient education and assessment of changes in clinical status. With relation to activity intolerance, the nurse must check for vital signs prior and after activity. An electrocardiogram is invaluable in monitoring. The rationale is that during activity, orthostatic hypotension may occur due to compromised cardiac function. The nurse must also document the patient’s response to exercise and look out for symptoms such as tachycardia, dysrhythmias, and pallor (Benhase et al., 2018). The nurse should assist with self-care activities and range of motion exercises. As for edema, the nurse should monitor patient’s urine output and check for frequency and color of urine. Low output of concentrated urine may be a result of low renal perfusion. Devices such as catheters are useful in monitoring, but proper care is necessary to prevent urinary tract infections. S/he should also monitor fluid intake and establish schedules so that the patient can adhere to restrictions. The nurse could also auscultate for breath sounds and look out for adventitious sounds. The nurse will also administer medications as necessary. The mainstay for edema management is diuretic therapy with agents such as furosemide and spironolactone (Mebazaa et al., 2015). Potassium supplements may be added to the regimen in case there are significant potassium losses.

In case of decreased cardiac output, the nurse should monitor apical pulse, note heart sounds, palpate for peripheral pulses as well as monitor blood pressure. Medications may include vasodilators like nitrates, hydralazine, and prazosin. Vasodilators are essential components in heart failure treatment as they reduce ventricular workload through a reduction in circulating volume as well as systemic ventricular resistance. Also, angiotensin-converting enzyme inhibitors like enalapril and lisinopril; as well as angiotensin II receptor antagonists like irbesartan and valsartan aid in increasing cardiac output andreducing the blood and ventricular filling pressures (Mebazaa et al., 2015). Moreover, digoxin and inotropic agents like milrinone are effective in short-term cases unresponsive to other classes of drugs. Inotropic agents promote vasodilation and enhance myocardial contractility. Anticoagulants can be employed prophylactically to prevent blood clots. The nurse can also improve gas exchange by suction of secretions when necessary, elevating the position of the head and monitoring for cyanosis (Jurgens et al., 2015). Pulse oximetry may be used to identify reduced oxygenation.

Patient education is also important. Education on matters such as weight loss, monitoring of sodium intake to less than 2 grams per day and fluid restrictions to less than 2 liters daily may assist in the management of heart failure (Mebazaa et al., 2015). Also, modifying habits by ceasing smoking and alcohol consumption as well as exercising according to one’s capabilities are important.

Evaluation

Evaluation of the progress of improvement of symptoms and quality of life can be done through various ways. The nurse should consistently monitor the patient for any changes in signs and symptoms and inform the other members of the healthcare team on the progress. Additionally, s/he should identify any problems arising and offer recommendations based on the findings. The most important parameters for monitoring effectiveness of treatment include improvement of dyspnea, heart rhythm, cardiac output and the systolic and diastolic pressures (Benhase et al., 2018). It is important that the measurements for the parameters mentioned above are in line with the desired objectives that were determined after assessment of the patient. The blood pressure, heart rhythm and cardiac output are the parameters that bear the most weight when assessing the effectiveness of treatment.

The nurse can evaluate improvements in dyspnea by assessing the patient’s tolerance to different levels of activity. Moreover, to evaluate for fluid volume status of the patient, the nurse reviews the fluid intake and urine output and adjusts the consumption or medication to relieve edema accordingly. Additionally, the patient’s weight may be an indicator of the progress of treatment for ascites. Regarding long-term monitoring, monitoring of B-type natriuretic peptide level is essential. The nurse can also do home visits or admit the patient into a nursing care home (Mebazaa et al., 2015).

 

 

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