Dyspnea
Dyspnea is a defining feature of functional class for HF patients and is a hallmark of worsening functional status. The pathogenesis of dyspnea in HF is defined by overactivation of ergoreceptors, which are afferent nerves sensitive to the metabolic effects of muscular work.18 Exercise, particularly thigh muscle strengthening, improves dyspnea, presumably by altering the myopathy and ergoreflex abnormalities in persons with HF.19 In a recent study of 100 consecutive patients with New York Heart Association (NYHA) functional class II–IV HF exercise was shown to improve dyspnea, peak VO2 (28 %; p=0.001) and quality of life (p=0.003).20 For these reasons, exercise should be the initial prescription for dyspnea. Maintenance of euvolemia improves, but does not eliminate, dyspnea. It is also important to continue (when able) guideline-directed medical therapies including angiotensin converting enzyme (ACE) inhibitors, beta-blockers, and mineralocorticoid antagonists. Once traditional medical therapies and nonpharmacologic therapies have been exhausted, low-dose opioids are generally felt to be first-line adjuvant therapy to treat dyspnea. Opioids decrease chemosensitivity-related dyspnea and improve exercise tolerance and peak VO2.21 Sedation may be an untoward effect, and thus the dose should be titrated to symptom relief while attempting to avoid narcosis.
Physical Pain
Up to 75 % of patients with advanced HF will experience pain.22 Nonpharmacologic therapies for pain, such as physical therapy, massage, and ice should be attempted first.23 Of the non-opioid pain medications, acetaminophen has the most favorable safety profile for patients with HF with mild to moderate somatic pain.24 Nonsteroidal anti-inflammatory drug (NSAIDs) are contraindicated in patients with HF due to propensity for causing fluid retention and exasperating renal dysfunction. Many NSAIDs, such as cyclooxygenase (COX) inhibitors, also carry black box warnings for patients with cardiovascular disease. Oral opiates may be used for management of moderate to severe pain in patients with HF. Attention should be paid to active metabolites that may accumulate in renal dysfunction, leading to delirium, or neuroexcitation. Fentanyl and methadone have no renally excreted active metabolites likely to accumulate in HF. If providers are uncomfortable with utilization of more potent opiates, consultation with a pain or palliative care specialist may be useful. Unrecognized psychological, social, and spiritual needs will often explain a nonresponding physical pain.25
Depression and Anxiety
Depression is common in those with HF.26 As functional status worsens, the incidence of depression increases: up to 42 % of patients with NYHA class IV disease experience this symptom.27 Comorbid depression is also associated with worsening of HF symptoms.28 Depression can contribute to poor adherence that can increase symptomatology, hospitalizations, and, ultimately, mortality.29–31 Selective serotonin re-uptake inhibitors (SSRIs), such as sertraline and paroxetine, have been found to be safe and effective as first-line therapy for depression in patients with HF.32,33 These medications should be started at a low dose and increased until depression improves or until recommended dose is achieved. Because both of these drugs are metabolized in the liver and excreted by the kidneys, dose reduction may be required for both renal and hepatic dysfunction.34 SSRIs can cause hyponatremia or fluid retention, particularly in patients with renal dysfunction. In addition to medical therapies for depression, exercise can result in modest improvements in depressive symptoms.35 Collaborative care is an important component of the care patients with HF who develop symptoms of depression.36 Some data suggest that cognitive behavioral therapy can decrease depressive symptoms, as well as anxiety, and that relaxation exercises with elements of CBT may decrease symptom burden.37