Heart failure (HF) is a clinical syndrome caused by failure of the heart to meet the demands of the body, with symptoms due to elevated intracardiac filling pressures and/or decreased effective cardiac output. The most common classification of HF is based on the left ventricular ejection fraction (LVEF), as determined by some form of cardiac imaging (most commonly an echocardiogram). The LVEF cutoff for HF with reduced ejection fraction (HFrEF, also known as systolic heart failure) is <50%, or more strictly <40%. Patients with LVEF >50% are considered to have HF with preserved ejection fraction (HFpEF, previously known as diastolic heart failure). While these two entities are indistinguishable based on clinical signs and symptoms alone, they differ in all other aspects: gross anatomy, histology, radiographic and hemodynamic findings, and, not surprisingly, treatment effects. The etiology of HF is due to some form of myocardial insult (Table 16.1), with HFrEF better understood than HFpEF.

The pressure–volume loops best illustrate the hemodynamic differences between HFrEF and HFpEF (Figure 16.1). Since patients with HFrEF have reduced myocardial contractility, the left ventricle dilates to accommodate a higher preload necessary to maintain an effective cardiac output. In hemodynamic terms, a patient with HFrEF has higher left ventricular end‐diastolic volume (LVEDV) and pressure (LVEDP), as well as lower stroke volume, pulse pressure, and effective cardiac output, which then translate to higher left ventricular end‐systolic volume (LVESV) and pressure (LVESP). As the degree of systolic dysfunction worsens, the pressure–volume loop further shifts toward the right. Likewise, in the presence of significant mitral regurgitation, the stroke volume and effective cardiac output are further reduced due to the absence of isovolumetric contraction.

The exact mechanism causing HFpEF is still unknown. An autopsy series of patients with HFpEF showed more cardiac hypertrophy, epicardial coronary artery disease, coronary microvascular rarefaction, and myocardial fibrosis compared to age‐matched control subjects [1]. In contrast to HFrEF, the resulting “stiffer” left ventricle develops higher filling pressures given the same incremental changes in volume (Figure 16.1). Thus, a much lower LVEDV is needed to overcome the aortic pressure, resulting in reduced stroke volume, effective cardiac output, and LVESV. LVEF, defined as the ratio of stroke volume to LVEDV, is preserved because both the numerator and denominator are reduced.

History, physical examination, cardiac biomarkers, chest X‐ray, and occasionally cardiac imaging are central in the medical management of acute on chronic heart failure. In some cases it may be difficult to estimate accurately the true hemodynamic status of the chronic HF patient using these tools alone. Physical examination findings of HF can be absent in as many as 40% of patients with elevated pulmonary capillary wedge pressures (PCWP) [2, 3]. Additionally, the chest X‐ray often does not show evidence of pulmonary congestion in advanced HF patients due to increased pulmonary lymphatic drainage [4]. In this light, judicious utilization of right heart catheterization can be very helpful in some clinical scenarios.

It is noteworthy that routine pulmonary artery catheter (PAC) use has never been shown to improve mortality or long‐term clinical outcomes in patients with HF [5–12]. In the randomized, multicenter Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness (ESCAPE) trial, the addition of routine PAC to clinical assessment, compared to clinical assessment alone, did not improve clinical outcomes in patients with severe symptomatic and recurrent systolic heart failure [12]. Clinical status significantly and continuously improved in both groups, but there was a consistent trend suggesting greater clinical improvement in the PAC group (especially at the 1‐month but not at the 6‐month follow‐up). Not surprisingly, inpatient mortality and survival at 6 months were similar in both groups and adverse in‐hospital events (driven by PAC infection) were higher in the PAC group. As is true for most advanced HF patients, improvements in functionality and quality of life are more meaningful than prolongation of life. Thus, PAC can be useful for optimizing hemodynamic management of the decompensated HF patient when clinically indicated. Table 16.2 lists some of the indications for right heart catheterization.

The hemodynamic findings of HFrEF and HFpEF are often similar in terms of elevated intracardiac filling pressures, but decreased effective cardiac output is usually seen only in advanced HFpEF, whereas it is seen earlier in HFrEF. Patients with chronic HF usually have higher baseline intracardiac pressures than those with acute HF, because chronic HF patients typically require higher filling pressures to maintain optimal cardiac output (as illustrated by the Frank–Starling relationship, Figure 16.2). Thus the “normal” parameters are slightly higher for chronic HFrEF patients than the “ideal” normal range for patients with normal cardiac function. Specific conditions such as restrictive cardiomyopathy, constrictive pericarditis, and hypertrophic cardiomyopathy will be discussed elsewhere in this book.