What Interventions Are Effective for Managing Dyspnea in Heart Failure?

Introduction and Scope of the Problem

Heart failure (HF) is a chronic and progressive illness that currently affects more than 6 million American adults and is projected to increase to more than 8 million individuals by 2030. Patients with advanced HF (American College of Cardiology/American Heart Association Stage D) have a multitude of symptoms, including pain, dyspnea, fatigue, depression, cachexia, and anorexia, which persist despite optimal medical therapy. Of these symptoms, dyspnea is consistently reported in at least half of patients with HF, peaking in the last six months of life. Dyspnea intensity serves as an indicator of risk for hospitalization and mortality and has been identified as the most frequently reported symptom prompting patients to present to the emergency department. Accordingly, effective management of dyspnea directly impacts a patient’s quality of life.

The American Thoracic Society defines dyspnea as a subjective experience of discomfort related to breathing which can vary in both quality and intensity. Dyspnea results from the interplay of physiological, psychological, social, and environmental factors. For patients with advanced HF, effective approaches to dyspnea management are based on an understanding of the pathophysiology underlying compromised cardiac function.

Relevant Pathophysiology

Dyspnea in patients with HF has been attributed to multiple factors. In general, causes of breathlessness may be divided into three broad categories: (1) abnormalities of central hemodynamic function, (2) abnormalities of pulmonary function, and (3) abnormalities of skeletal muscles resulting in fatiguability (including diaphragmatic weakness). Further, pathologies which frequently coexist in patients with advanced HF, such as atrial fibrillation, asthma, chronic obstructive pulmonary disease (COPD), and anemia, may contribute to dyspnea symptoms. Traditional explanations of dyspnea have focused primarily on central hemodynamic dysfunction. In systolic HF (or heart failure with reduced ejection fraction, HFrEF), the inability of the heart to pump blood forward results in increased left ventricular end diastolic volume (or preload) in accordance with the Frank-Starling mechanism. Fluid then accumulates in the pulmonary circulation and results in pulmonary interstitial edema. In diastolic HF (or heart failure with preserved ejection fraction, HFpEF), impaired ventricular relaxation and increased myocardial stiffness result in a poor ability to respond to changes in cardiac load. Increased preload may cause rapid-onset pulmonary edema, in which decreased preload may cause hypotension. Pulmonary sources of dyspnea may include bronchoconstriction (which is also present in acute pulmonary edema), ventilation-perfusion mismatch, and decreased diffusion capacity. Chronic HF is also associated with muscle wasting, decreased strength, and decreased endurance. Therefore inspiratory muscle weakness and a related increase in the proportion of muscles needed to maintain the work of breathing has also been implicated in HF-related dyspnea.

From a neurological perspective, the sensation of dyspnea may be due to increased ventilatory drive caused by afferent signals in the central nervous system (e.g., chemoreceptors, pulmonary vagal afferent nerves, peripheral mechanoreceptors), the brainstem, and the cerebral cortex. The interaction of these afferent systems results in signals to respiratory muscles to increase breathing. This may explain why studies have failed to link a patient’s subjective symptom of breathlessness to objective data, including left ventricular ejection fraction, cardiac output, pulmonary-capillary wedge pressure, oxygen saturation, or spirometry. This proposed mind–body connection may also help explain why social and demographic factors such as gender, age, comorbid disease, sleep disturbance, depression, and anxiety may also impact the variable presentation of symptoms.

Dyspnea is a subjective symptom and, as such, it is the patient’s experience which is most important. An initial approach may be to simply ask the patient about their breathing; however, patients may use many terms to describe dyspnea which differ from common medical terminology. This may include terms such as suffocating or air hunger , or stating that their breathing “requires effort.” Full evaluation should include the severity of distress from dyspnea, frequency of symptom burden, exacerbating or alleviating conditions (i.e., posture, activity, rest), and symptom duration. For patients with chronic dyspnea, it may be necessary to inquire how their lifestyle has been affected by their shortness of breath, including reduced activities or abandonment of hobbies.

Multiple scales have been developed in an attempt to standardize symptom measurement, and they are summarized in Table 17.1 . For example, scales such as the Modified Medical Research Council (mMRC) Dyspnea Scale, Baseline/Transition Dyspnea Index (BDI/TBI), and Modified Borg Scale are validated tools for objectively measuring chronic dyspnea. Unfortunately, these scales, which are used widely in respiratory disease, are often not sensitive enough to assess acute changes in dyspnea such as that occurring with an HF exacerbation. Therefore clinical trials in patients with HF have utilized Likert scales and visual analogue scales (VAS). Likert scales typically ask patients to rate their response to therapy on a 3-, 5-, or 7- point scale, while VAS asks patients to rate their breathing on a scale of 0 to 100 (with 100 being the best imaginable ability to breathe). Dyspnea may also be evaluated as a component of a patient’s total disease burden. The New York Heart Association (NYHA) functional classification system groups patients by severity of symptoms (including dyspnea) with graded activity and is used widely as a means to prognosticate and monitor response to HF therapy. Within palliative care, the revised Edmonton Symptom Assessment System (ESAS-r) provides a means for patients to self-report symptom intensity among nine common domains (including shortness of breath). Regardless of tool utilized, it is ultimately the patient’s subjective experience which should dictate how shortness of breath is managed.

Summary of Evidence Regarding Treatment Recommendations

The first goal of treatment for dyspnea in HF is to identify and correct the underlying pathophysiology of cardiac dysfunction when possible. Generally, improving dyspnea by addressing fluid overload involves diuretics (preload management); vasodilators (afterload management); and improving cardiac output (via rate control or positive inotropic agents). In these cases, there is a synergy between traditional HF management and palliative management of symptoms. A complete review of the treatment for HF is beyond the scope of this chapter. Numerous routinely used medications, including guideline-directed medical therapy, have demonstrated the ability to reduce symptoms of heart failure in patients with HFrEF. Beta-blockers, angiotensin converting enzyme (ACE) inhibitors, angiotensin-II receptor blockers (ARBs), and angiotensin receptor-neprilysin inhibitors (ARNIs) have all demonstrated a reduction in symptoms (including breathlessness) in clinical trials. Nitrates have not shown a similar benefit in treating breathlessness, although the addition of nitrates and hydralazine to standard therapy in treating HFrEF has been shown to decrease morbidity and mortality.