Heart failure (HF) is a progressive disease which affects more than five million Americans (Yancy et al. , 2013). HF negatively impacts quality of life and it is associated with frequent hospitalizations and high mortality. Evidence-based practice guidelines aid health care professionals with treatment management and provide pathways to optimize individual patient care. The main goal of treatment is to slow the progression of the disease and control its symptoms. These pathways address all stages of the disease beginning with the early recognition of patients at risk and ending with the need for end-of-life care. Pathophysiology
Heart failure (HF) is a condition in which the heart is not able to sustain sufficient cardiac output to perfuse the body and it develops secondary to other diseases that affect the structure or function of the cardiac muscle. Diseases such as hypertension (HTN), ischemic heart disease, diabetes, metabolic syndrome, valvular disorder and arteriosclerosis are associated with HF. Cardiomyopathy is a structural abnormality of the heart and can be the result of hormonal problems (diabetes, hyperthyroidism, and growth hormone alterations), exposure to toxins (cocaine, some medications, alcohol), myocarditis, and inflammatory changes (Yancy et al. 2013).
Despite the underlying cause, the structural changes of the heart restrict efficient filling/ relaxation (diastolic dysfunction) and contractions (systolic dysfunction) of the cardiac muscle, resulting in decreased cardiac output. In response to a decreased cardiac output, the body attempts to compensate. According to Porth, 2011, the sympathetic nervous system releases catecholamines to improve the contractility and increase heart rate; it causes vasoconstriction which results in an increased vascular resistance (afterload).
Decreased blood flow to the kidneys results in activation of renin-angiotensin-aldosterone system (RAAS). Renin produced by kidneys stimulates production of angiotensin, a vasoconstrictor, which causes sodium reabsorption, release of norepinephrine and activates secretion of aldosterone by the adrenal glands. Aldosterone increases sodium reabsorption and water retention. Decreased cardiac output also stimulates the release of antidiuretic hormone from the posterior pituitary which additionally increases water retention and thirst.
An increase in vascular volume results in an increase in the amount of blood returning to the heart (increase in preload). In order to produce a stronger contraction, the cardiac muscle stretches (Frank-Starling mechanism) and if overstretching is prolonged, the cardiac muscle becomes less flexible. In addition, the heart works harder to pump the blood and cardiac muscles’ demand for oxygen increases. Some of the fibers become ischemic which results in a decrease in the size of the ventricles’ chambers and contributes to its stiffness (hypertrophy).
The stretched muscle loses elasticity and the ability to efficiently contract. This is a permanent change and this process is called ventricular remodeling (Huether & McCance, 2011). The compensatory pathways compensate the decreased cardiac output for some time, but when used for a long time, further damage occurs and progression of HF is inevitable. Heart failure can be described as a systolic (ventricles’ ability to contract) and diastolic (ventricles’ ability to relax and passively fill with blood) dysfunction.
The systolic dysfunction is associated with a decreased ejection fraction (EF), which is the percentage of blood ejected with each beat. The EF of a healthy heart is between 60 and 75% while patients with systolic HF would have EF below 40% (Yancy et al. , 2013). Therefore, systolic dysfunction is called HF with reduced EF. Contrary, during diastolic HF (called HF with preserved EF), the EF is usually about 50% (Yancy et al. , 2013). Presentation of symptoms depends on which side of the heart is involved; the disease often begins with left sided failure but later both ventricles are involved.
Left sided HF is associated with an impaired ability of the heart to push blood into systemic circulation, therefore symptoms of pulmonary congestion (leading to pulmonary edema) and decreased tissue perfusion due to lower cardiac output, as well as activity intolerance are common. On the other hand, the failing right ventricle is less efficient with moving blood from systemic veins to pulmonary circulation. This results in congestion of peripheral tissues characterized by dependent edema, ascites, and liver congestion leading to symptoms of impaired liver function.
The New York Heart Association (NYHA) provides classification of the HF and divides it into four classes based on severity of the symptoms (Yancy et al. , 2013). Literature Review The literature review included exploring evidence based guidelines regarding management of HF. Congruency existed regarding the importance of proper management of patients who are at risk of developing HF such as patients with HTN, diabetes, dyslipidemia, arrhythmias, valvular disorders, renal disease, and patients with previous myocardial infractions (MI) (Yancy et al. 2013).
Early recognition and proper management of underlying diseases can prevent or delay remodeling of the cardiac muscle and progression of HF. A diagnosis is made based on a patients’ symptoms and testing. Laboratory studies should include a complete blood count, chemistry, troponin, thyroid function, lipid profile, and B-type natriuretic peptide (BNP) (or N-terminal pro B-type natriuretic peptide) (Kransdorf & Kittleson, 2012).
Other tests include a chest x-ray (to determine the size of the heart and pulmonary congestion), 12-lead electrocardiogram (to assess conductivity and arrhythmias), and a 2-dementional echocardiogram (to obtain information about the heart’s structure and function, including EF). Yancy et al. (2013) stated that in some cases, magnetic resonance imaging can provide a more precise determination of the EF; invasive evaluation such as monitoring with pulmonary artery catheter and endomyocardial biopsy should not be routinely done.
Pharmacological treatment for the patient at risk of developing the HF should begin by initiating treatment with medications which interrupt RAAS such as an angiotensin-converting enzyme inhibitors (ACE inhibitors) or angiotensin-receptor blockers (ARB). Deedwania and Carbajal (2012) stated that early treatment with ACE inhibitors delays deterioration of the cardiac muscle by slowing the cardiac remodeling process. Patients who experience the adverse effects of ACE inhibitors such as cough, renal dysfunction, or life threatening angioedema should be treated with ARBs.
Patients with a previous MI, valvular disorders, left ventricular hypertrophy and a decreased EF benefit from the use of beta blockers. Decreased stimulation from the sympathetic nervous system helps to reduce heart rate, control arrhythmias, and enhance myocardial perfusion (Nicholson, 2015). For symptomatic patients with pulmonary or peripheral congestion, a loop diuretic is added to the regimen; thiazides can be an alternative or adjunctive therapy to loop diuretics (Basraon & Deedwani, 2012).
In addition, the use of an aldosterone antagonist is recommended for HF patients who remain symptomatic despite treatment with ACE inhibitors (or ARBs) and beta blockers. The use of nitrates in combination with hydralazine is effective especially for the African American population; digitalis can benefit some patients and anticoagulation is suggested for patients with atrial fibrillation (Yancy et al. , 2013). As the disease progresses and the patient is symptomatic at rest, the use of inotropic agents (dopamine and dobutamine) may be needed to improve contractility of the cardiac muscle (Huether & McCance, 2011).
According to Yancy (2013), inotropic agents can be used as short-term therapy in hospitalized patients or as a palliative measure to aid in symptom control. Patients with ischemic heart disease may need cardiac catheterization and intervention such as stent placement or a coronary artery bypass graft; patients with valvular disorders may need valve repair or replacement procedures. Patients with arrhythmias and patients with an EF below 35% can be candidates for device therapy such as cardiac resynchronization therapy and/or an implantable cardioverter defibrillator (ICD).
These devices may prevent sudden cardiac death related to life threatening arrhythmias; there are guidelines regarding the eligibility for this treatments. Some patients may be candidates for cardiac transplant (Yancy, 2013). Intensive patient education is key to successful manage HF; teaching and follow-up appointments should begin immediately during and after hospitalization (Simpson, 2014). Many patients can benefit from referrals for home telemonitoring and outpatient HF clinic (Manning, Wendler, & Baur, 2010). This aids not only with management of HF, but it also provides patients with an additional support system.
Conway (2015) states that changes in behavior and proper self-care are crucial, and involvement of a patient’s family in the teaching process can result in increased adherence. Education should include information regarding the diagnosis, progression of the disease, prognosis, treatments, and monitoring symptoms such as weight, edema, and dyspnea. Teaching about life modifications such as smoking cessation, use of alcohol, proper diet (limitation in sodium intake), and possible fluid restrictions is important. Preventive measures, such as immunizations, are recommended for HF patients.
Patients with mild to moderate HF should exercise regularly and proper cardiac rehabilitation resulted in 11% decreased of mortality rate (Conway, 2015). A decrease in the quality of life associated with the progression of HF increases the risk of depression and early recognition of depression and social support is important. Summary of Interview My neighbor was diagnosed with HF about a year ago, and her journey with this disease appears to be typical to the progression of the disease described in literature. Until age 55, when she was first diagnosed with HTN, she was a healthy and active woman.
At first, she was prescribed Enalapril (ACE inhibitor), which she stopped taking without consulting her doctor, because she was feeling “lousy” and was coughing. After a few years, she was hospitalized for pneumonia, and during this hospitalization, she had several tests done; she learned that not only did she have an MI in the past (of which she was not aware of), but also she had HF. In a very short time, her life changed and she had to take multiple medications daily. She admitted that in the beginning, she was in denial and often “skipped” taking her “water pill” because it interfered with her daily activities.
However, her second admission to the hospital with dyspnea gave her a reality check and she realized that she has no other option but to treat her condition seriously. Upon discharge she was referred to a heart failure clinic and she participated in several teaching sessions organized by this clinic. She said that it allowed her to better understand HF; she made changes in her diet, takes medications and vigilantly watches for any symptoms of a HF exacerbation; currently she is on Diovan HCT (combination of valsartan and hydrochlorothizide) and Coreg.
HF changed her life and at times she has to limit her activities, but she said that she is committed to do whatever she can do to slow the progression of her disease; if she has any concerns she does not hesitate to contact her friendly nurse practitioner at the clinic. My neighbor’s story has many similarities to the progression of the disease described in literature, and her treatment is congruent with evidence-based guidelines presented by many authors. Conclusion Heart failure is a complex and progressive disease which affects the quality of life of many people.
Evidence-based guidelines developed to help manage this disease include treating the underlying condition, early identification of people at risk for developing HF, and proper pharmacological treatment. Comprehensive patient education, providing resources and support for HF patients are crucial elements of managing the progression of this disease and to ensure patients’ adherence to treatment. therefore, Proper coordination of care based on good communication between HF patients and health care providers can improve the quality of life of these patients.
