Books By Heart
Fairy Dawdy
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I have been self-publishing my books since 2010, and in that time, I've sold well over half a million copies of my books. I'm not a superstar or a huge bestseller, but I have built an amazing career that brings me great joy. Here at Heart Breathings, I hope to help you find that same level of success. Let's do this.
Congestive heart failure (CHF) is a complex clinical syndrome characterized by inefficient myocardial performance, resulting in compromised blood supply to the body. CHF results from any disorder that impairs ventricular filling or ejection of blood to the systemic circulation. Patients usually present with fatigue and dyspnea, reduced exercise tolerance, and systemic or pulmonary congestion. The etiology of HF is variable and extensive. A comprehensive assessment is required when evaluating a patient with HF. The general management aims at relieving systemic and pulmonary congestion and stabilization of hemodynamic status, regardless of the cause. This activity reviews the evaluation and management of congestive heart failure and highlights the role of the healthcare team in improving care for patients with this condition.
Objectives:
- Apply the staging and classification systems of heart failure.Assess and monitor patients with heart failure for signs of decompensation, fluid retention, and response to treatment.Select appropriate diagnostic tests, like echocardiography and biomarker assays, to aid in heart failure diagnosis and monitoring.Collaborate with multidisciplinary healthcare teams, including cardiologists, nurses, and pharmacists, to ensure coordinated and comprehensive care for heart failure patients.
The etiology of heart failure (HF) is variable and extensive. The general management aims at relieving systemic and pulmonary congestion and stabilization of hemodynamic status, regardless of the cause. The treatment of HF requires a multifaceted approach involving patient education, optimal medication administration, and decreasing acute exacerbations.
The New York Heart Association Functional Classification is used for patients with symptoms of HF. This system is subjectively determined by clinicians and is widely used in clinical practice to direct therapy.
There are many etiologies of CHF, and coronary artery disease (CAD) causing ischemic heart disease is the most common cause. Every attempt should be made to identify causative factors to help guide treatment strategies. The etiologies can be broadly classified as intrinsic heart disease and pathologies that are infiltrative, congenital, valvular, myocarditis-related, high-output failure, and secondary to systemic disease.[2][4] These classifications have significant overlap. The 4 most common etiologies responsible for about two-thirds of CHF cases are ischemic heart disease, chronic obstructive pulmonary disease (COPD), hypertensive heart disease, and rheumatic heart disease. Higher-income countries have higher rates of ischemic heart disease and COPD; lower-income countries have higher rates of hypertensive heart disease, cardiomyopathy, rheumatic heart disease, and myocarditis.
Ischemic heart disease is by far the most common cause of CHF worldwide. Ischemia leads to a lack of blood flow to heart muscles, reducing the EF. Incidence is increasing in developing countries as they adopt a more Western diet and lifestyle, and improved medical care decreases the infectious burden in these countries (myocarditis is often infection-related.)
Valvular heart disease is another common intrinsic heart condition that can cause CHF. Rheumatic heart disease is the most common cause of valvular heart disease in children and young adults worldwide. It is caused by an immune response to group A Streptococcus and primarily causes mitral and aortic stenosis.[5] The most common overall cause of valvular disease is age-related degeneration, and the aortic valve is the most commonly affected valve. Women are more likely to experience mitral valve rheumatic heart disease or mitral valve prolapse, while men are more likely to suffer from aortic valve diseases such as regurgitation or stenosis. Endocarditis is also more common in men.
Hypertension causes CHF even in the absence of CAD or ischemic heart disease. High blood pressure causes mechanical stress by increased afterload and neurohormonal changes that increase ventricular mass.[2] HTN is also strongly associated with other comorbidities for CHF development, and aggressively treating hypertension is shown to lower the incidence of CHF.[2]
Cardiomyopathy is a heterogeneous group of diseases characterized by enlarged ventricles with impaired function not related to secondary causes such as ischemic heart disease, valvular heart disease, hypertension, or congenital heart disease. The most common types of cardiomyopathies are hypertrophic, dilated, restrictive, arrhythmogenic right ventricular, and left ventricular noncompaction.[6] In addition to CHF, cardiomyopathy can present as arrhythmia or sudden cardiac death, further compelling the identification of underlying disorders. Many of these conditions have a genetic basis, and a detailed family history of sudden cardiac death, especially in first-degree relatives older than 35 years, should be taken. There are over 50 identified genes contributing to the development of dilated cardiomyopathy alone. Genetic determinants have variable phenotypic expression, and many nongenetic factors also affect the clinical symptoms. Some of these factors include diabetes, toxic exposure, or pregnancy. Fabry disease is a rare glycogen storage disease that can cause CHF symptoms through a hypertrophic cardiomyopathy pattern.[2][6]
Inflammatory cardiomyopathy is defined by myocarditis along with ventricular remodeling and cardiac dysfunction. The most common cause is viral infection. Other etiologies are bacterial, fungal, or protozoal infections; toxic substances or drugs; and immune-mediated diseases. Chagas disease is caused by Trypanosoma cruzi, which is endemic in Latin America and commonly causes myocarditis, cardiomyopathy, and CHF. Other viral causes of myocarditis and inflammatory cardiomyopathy include adenoviruses, enteroviruses, herpes virus 6, Epstein-Barr virus, and cytomegalovirus. Viruses can also activate autoimmune myocarditis, including HIV, hepatitis C virus, influenzas A and B, and coronaviruses (including COVID-19). When associated with CHF, these conditions tend to have a poor prognosis.[7]
Infiltrative cardiomyopathies cause a restrictive cardiomyopathy pattern (simar to the genetically determined restrictive cardiomyopathy variant), which is notable for normal ventricular systolic function, but with diastolic dysfunction and restrictive filling dynamics of the LV and RV. This is often associated with a high E/A ratio showing increased early filling and delayed late filling.[6][8]
Cardiac amyloidosis results from misfolded protein deposits in the heart; this leads to cardiomyocyte separation, cellular toxicity, and tissue stiffness. Patients are preload dependent and are prone to symptomatic hypotension. Currently, tamifidis is the only medication known to prevent cardiac amyloidosis. It prevents, but does not reverse, amyloid deposition. Its high cost is also a limiting factor.[1][9][1]
Sarcoidosis is an acquired cardiomyopathy that presents with conduction defects and arrhythmias due to granuloma formation. The most common cardiac manifestation is CHF. Caution must be used when treating with beta-blockers due to the associated conduction abnormalities.
Cardiac hemochromatosis is present in 15% to 20% of patients with hereditary hemochromatosis. This condition initially presents with a restrictive pattern but develops into biventricular systolic dysfunction.[8] Patients with restrictive cardiomyopathy physiology can develop hypotension when treated with traditional CHF medications due to preload dependence, so caution should be used to avoid systemic hypoperfusion.[10]
Takotsubo or stress-induced cardiomyopathy (colloquially broken-heart syndrome) is an underrecognized cause of CHF, which causes transient left-ventricular wall abnormalities that are not localized to a specific vascular territory. It has several proposed pathophysiologic mechanisms, including coronary vasospasm, microcirculatory dysfunction, and increased activation of the sympathetic nervous system. This condition is treated with medications typical for CHF with the addition of antithrombotic medications in certain clinical situations with wall motion abnormalities. Recognized cases increased significantly during the COVID-19 epidemic.[11][12][13][12]
Peripartum cardiomyopathy is a significant cause of maternal mortality. During pregnancy, cardiac output is increased by 20% to 30% due to increased heart rate and stroke volume. It presents with CHF due to LV systolic dysfunction during late pregnancy, postpartum, or up to several months after delivery. There is likely an underlying genetic component, and it is more common in women with advanced maternal age, Black race, and multifetal pregnancies. If wall motion abnormalities are present, anticoagulation is essential due to the hypercoagulable state caused by pregnancy. Recovery is variable by global region and inversely correlates with lowered EF.[14]
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