Healthcare Consideration: Research shows the powerful healing effects of the parasympathetic nervous system. In their book Compassionomics: The Revolutionary Scientific Evidence That Caring Makes a Difference , Dr. Stephen Trzeciak and Dr. Anthony Mazzarelli report that heart attack victims who had no emotional support were three times as likely to die within six months compared to those patients with emotional support (p. 50). In numerous studies of actual patients and analogue patients, as little as 40 seconds of expressed compassion lowered stress levels and produced superior clinical outcomes. A few simple phrases from clinicians such as “We’ll be with you all the way” and “You’re not alone” can manifest powerful changes in the management of and recovery from serious disease (Trzeciak & Mazzarelli, 2019, p. 251). Congestive heart failure (CHF)
unclear, but blood troponin levels are a reliable indicator of organ damage due to CHF (Schwinger, 2021). Causes of CHF include congenital defects, coronary artery disease, high blood pressure, myocardial infarction, and valve disorders. CHF is among the leading causes of death in the U.S. and worldwide. Treatment often begins with diuretics, although their effects on disease progression are not entirely known. Digoxin may be prescribed to increase ventricular action. Calcium channel blockers are contraindicated, since they inhibit the heart’s ability to forcefully contract (Xiao et al., 2023). septal defects allow deoxygenated blood to seep into the left ventricle and be sent throughout the body (Barnes & Thompson, 2023). Coarctation of the aorta (COA) is a genetic condition characterized by the narrowing of a segment of the aorta, which reduces blood flow and subsequent oxygen delivery to the cells. COA is typically repaired surgically. Surgeons may also place a stent through the reconstructed segment to help ensure adequate blood flow. As with other interventions, long-term care often involves drugs to prevent recurring blood clots (Doshi & Chikkabyrappa, 2018). Patent ductus arteriosus is when blood flows from the aorta to the pulmonary artery, mixing oxygenated and deoxygenated blood. With hypoplastic heart syndrome, the left side of the heart does not fully develop. Tetralogy of Fallot is a combination of four different defects, including right ventricular hypertrophy, ventricular septal defect, abnormal location of the aorta, and pulmonary valve stenosis (Centers for Disease Control and Prevention [CDC], 2023). ● Infectious endocarditis : Fungal, bacterial, or viral infections that damage valve tissue. Ineffective AV valves allow unlimited flow into the ventricles, causing overload and distention of the chamber as well as decreased stroke volume due to loss of muscle elasticity. Severe prolapse, specifically of the mitral valve, is common in the U.S. and carries a high mortality rate. Only surgery can repair severely damaged valves. Recent advances in catheter-based repair may offer hope for patients who are poor candidates for the rigors of more invasive surgery. Until the valve is repaired, symptoms may limit physical activity. The patient should avoid strenuous activities in which the demand for oxygen may exceed the maximum cardiac output (Aluru et al., 2022). Varicosity Accumulation of fluid in the feet or ankles may be a sign of weak heart action. A damaged or dysfunctional valve can allow a large pool of blood to push down into the veins, causing them to expand. Light walking or repeated ankle movement can help with these fluid imbalances.
Congestive heart failure is a general term referring to the heart’s limited ability to pump blood out of the left ventricle. This can result in cardiac muscle changes. Congestive heart failure inhibits the heart’s ability to expand and fill with blood, resulting in lower stroke volume and cardiac output. During physical activity, CHF patients experience higher lactate levels at lower intensities than healthy exercisers do. CHF patients’ kidneys may retain fluid. Serum troponin has also been traced to congestive heart failure. The exact mechanism of release in chronic heart failure patients is Congenital defects Congenital defects are genetically determined incomplete or dysfunctional development of one or multiple parts of the heart. These can include (Yasuhara & Garg, 2021): ● Septal defects. ● Coarctation of the aorta. Mild cases of congenital defects may be monitored if no intervention is deemed necessary. In more severe cases, surgery may be required to attempt to repair defective tissue. Congenital defects often present with cardiac arrythmias and thromboses. Treatment paradigms have evolved to include surgical options, ablation, and pacemaker insertions as well as medications to control coagulation. With the number of adults with congenital defects increasing, we can see the compounding effects of comorbidities (Yasuhara & Garg, 2021). Septal defects can be broken down into two different categories. With atrial septal defects, there is an opening in the septum that allows the blood to flow between the atria, mixing oxygenated and deoxygenated blood. Ventricular Valve disease The heart valves may become damaged or may not function properly, allowing blood to flow back up from the ventricles to the atria. This process is called regurgitation . With regurgitation of blood, less blood is pumped out to the body with each heartbeat, equating to lower stroke volume. A lower stroke volume causes the heart to pump more often ● Patent ductus arteriosus (PDA). ● Hypoplastic heart syndrome. ● Tetralogy of Fallot. and work harder in order to deliver an adequate blood supply. This can lead to conditions such as left ventricular hypertrophy (LVH), high blood pressure, and pulmonary hypertension. The condition of allowing backflow of blood is called prolapse . Valve degeneration may be caused by several factors (Aluru et al., 2022): ● Rheumatic heart disease : The immune system attacks the valve tissue. ● Marfan’s syndrome : A disease often associated with weak connective tissue. ● Torn papillary muscle : Tear of the muscle that draws flaps closed. ● Dilation of ventricle and/or tricuspid annulus. ● Ehlers-Danlos syndrome : Genetic connective tissue disorder.
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Book Code: MLA1225
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