Nearly one third of acute heart failure (AHF) patients die or are rehospitalized within 90 days after discharge in the United States, with similar numbers in Europe. Despite a decade of intensive research efforts, substantially improving outcomes remains an elusive goal. Reducing morbidity and mortality remains the greatest current challenge of AHF management.
Background and Epidemiology
More than 6.5 million Americans have heart failure (HF), with more than 1 million new diagnoses each year. By 2030, the prevalence of HF is projected to increase 46%, with HF related costs exceeding 70 billion US dollars (see also Chapter 18 ). Despite the increasing prevalence, AHF admissions have stayed relatively flat or even decreased, at least by primary discharge diagnosis. Approximately 1 million hospitalizations with a primary discharge diagnosis of AHF occur every year. Although the trajectory of primary discharge diagnoses has stayed flat, when all diagnoses are considered, AHF hospitalizations are rising ( Fig. 36.1 ). Already, AHF is the most common and costliest cause of hospitalization and rehospitalization for older Americans.
While rehospitalization rates have marginally improved, both rehospitalization and mortality rates remain high. In 2008, for Medicare beneficiaries, 30-day readmissions were 23.5% with a 7.9% postdischarge mortality. By 2014, 30-day readmissions had decreased to 22.7%, with an 8.6% postdischarge mortality. Within 5 years, 75% of patients hospitalized with HF will be dead, irrespective of a reduced or preserved ejection fraction (EF) ( Fig. 36.2 ).
Amid such poor outcomes and high health care costs are health inequities; disparities evident by race, gender, and socioeconomic status. For first episodes of AHF, black males and females have the highest incidence ( Fig. 36.3 ). For socioeconomically disadvantaged patients, initial admissions and readmissions are markedly higher.
In 2003, Dr. Braunwald described HF as the “last great battleground in cardiology.” Ironically, as more and more patients live longer with cardiovascular disease—a testament to the tremendous advances in reducing the burden of ischemic heart disease and sudden cardiac death—such patients are at risk for developing HF ( Fig. 36.4 ). As the population ages, unless outcomes improve, the burden of AHF will increase. Disparities may also worsen.
Definition: what is acute heart failure? Why does the definition matter?
AHF is a clinical diagnosis. No single test or physical exam feature definitively “rules in” or “rules out” AHF. Thus there is no diagnostic “gold standard.” Perhaps unsurprisingly, there is neither a universal, well-accepted definition of AHF, nor a nomenclature to describe the various AHF syndromes. Various names have been used, including acute decompensated heart failure (ADHF), hospitalization for heart failure (HHF), and acute heart failure syndromes (AHFS). Currently, AHF is the most widely used and is the current terminology in several consensus guidelines.
Agreement upon a definition is not an academic exercise; it has significant clinical implications. Describing AHF in an 85-year-old female with no past history of HF and a systolic blood pressure at presentation of 210/120 mm Hg does not appropriately describe the 65-year-old male with known ischemic heart disease, EF of 10%, on maximal guideline recommended HF therapies awaiting transplantation. Such heterogeneity of the AHF presentation broadens when comorbid conditions and precipitants of AHF are considered. Lack of consensus on a definition hinders both policy and research; the slow rate of progress to reduce morbidity and mortality may be directly related to the inability to define exactly what problem we are addressing.
Unfortunately, no universal definition is proposed. For the purposes of this chapter, AHF is defined as “signs of symptoms of heart failure requiring urgent or emergent therapy.”
Pathophysiology of Acute Heart Failure
Unlike chronic HF with reduced ejection fraction (HFrEF), the pathophysiology of AHF is less well understood. In chronic HF, neurohormonal activation (renin-angiotensin-aldosterone—sympathetic nervous system), adverse hemodynamic conditions, energetics, and inflammation, are all well-established, overlapping pathophysiologic constructs. While these mechanisms are undoubtedly also present in AHF, their relative contribution to the AHF presentation is less well known.
A conceptual model for understanding the complexity of the pathophysiology of AHF is shown in Fig. 36.5 . An AHF episode most likely occurs on top of a structural/functional cardiac abnormality (Stage B HF). A precipitant triggers or incites the initial AHF event. This precipitant, combined with the underlying structural/functional abnormality—complicated by other comorbid conditions—ultimately leads to AHF. Once AHF has begun, a cascade of other abnormalities occurs, affecting the heart itself, vasculature, neurohormonal system, kidneys, and liver, as well as inciting inflammatory pathways. These mechanisms act as potential amplifiers, exacerbating the current AHF episode.
Related to this pathophysiological construct is the concept of organ injury. It is common to see myocardial injury in the form of troponin release or acute kidney injury in the setting of AHF. Whether such organ injury contributes to the AHF episode, results from it, or both has not been definitively established. What is clear is the association of organ injury with worse outcomes. Fig. 36.6 graphically demonstrates this concept, as well as the idea that prevention of such injury may alter the patient’s outcome. This concept gained momentum in the RELAX-AHF-1 (Serelaxin, recombinant human relaxin-2, for treatment of acute heart failure) trial, where marked and congruent differences in biomarkers were observed, suggesting such prevention of injury may have resulted in improved 180-day mortality. Unfortunately, the mortality benefits were not replicated in a confirmatory trial.
Ultimately, to what extent and severity each of these overlapping pathways contributes to AHF, remains to be defined. We do not yet know what exactly to target in each patient that will result in improved outcomes. We do know that certain pathologic conditions—such as elevated left ventricular end diastolic filling pressures—are a hallmark of AHF and associated with worse outcomes. However, acutely improving hemodynamics has yet to result in less morbidity or mortality. At present, identifying markers associated with worse outcomes has yet to translate into targets for therapy.
Comorbid Conditions
The presence of comorbid conditions adds another layer of complexity to the AHF presentation. The “pure” AHF phenotype, however defined, is rare. Rather, the patient with other underlying medical comorbid conditions (i.e., hypertension, chronic obstructive pulmonary disease, diabetes, ischemic heart disease; see also Chapter 48 ) and social determinants of health (i.e., insurance status, caregiver support, adequate nutrition, lack of housing) is by far the norm. Whether these conditions contribute to AHF or are worsened by AHF is not always clear. During both initial and inpatient management, each potential comorbid condition must be accounted for, as described later.
It is doubtful a single, universal construct exists to encompass the entire pathophysiology of AHF. Although patients present with similar signs and symptoms, their underlying biology is unique. Perhaps this desire to lump all of AHF phenotypes together, rather than divide, has contributed to our limited ability to improve outcomes.
Initial Management
Despite the heterogeneity of the AHF patient, general principles of initial management may be applied and are outlined as follows. Prompt diagnosis, initial decongestive management, as well as management of comorbid conditions, and robust transitional care—followed by guideline adherent disease management—form the foundation of AHF care.
Previously proposed classifications of AHF patients to facilitate initial management categorize patients once; we recommend reassessment and reclassification during the entire course of a patients’ hospital stay. Such reassessments recognize the dynamic nature of AHF.
Emergency Department Management
The majority of hospitalized AHF patients initially present to the emergency department (ED). The traditional axiom of airway, breathing, circulation (ABCs) applies; however, most patients do not present in extremis. The two polar archetypes are the flash pulmonary edema patient, typically due to hypertension, and the cardiogenic shock patient. After ensuring the ABCs, elucidating and managing the precipitant is paramount—for example, AHF secondary to a massive myocardial infarction (MI) or valve rupture. Although such presentations are not common, this principle of management applies to even less urgent cases. Table 36.1 approaches the AHF patient in the ED as a series of clinical questions. Fig. 36.7 shows an algorithmic approach toward the AHF patient in the ED or clinic setting.
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Diagnosis
Delays in diagnosis and subsequent treatment are associated with worse outcomes. Patients rarely present with a diagnosis, however; rather, they present with a “chief complaint.” Thus determining whether the patient’s reported “shortness of breath” is due to AHF or an alternative diagnosis relies on history and physical examination, combined with ancillary studies ( see also Chapter 31 ). Unfortunately, the history and physical exam lack sensitivity. Paroxysmal nocturnal dyspnea and orthopnea should be assessed, but they lack specificity. An S3 gallop (remarkably challenging to hear in a busy ED) and jugular venous distention are the most specific, but insensitive and clinician dependent. Despite congestion being the sine qua non of AHF, measuring congestion reliably, with robust intra- and interobserver agreement, is challenging. Nevertheless, a thorough history (especially a past history of HF) and physical exam, combined with traditional ancillary studies of chest x-ray, EKG, basic metabolic profile, and complete blood count, are recommended.
Chest X-Ray and Lung Ultrasound
One of the greatest clinical benefits of the chest x-ray (CXR) is identifying alternative diagnoses; the sensitivity and specificity are less than 80% for the diagnosis of AHF. The imaging modality recommended at the bedside is lung ultrasound ( Fig. 36.8 ). More than any other test, including natriuretic peptides (NPs), lung ultrasound (LUS) has the most robust likelihood ratio (LR) + 7.4 (95% CI 4.2–12.8) and LR − 0.16 [95% CI 0.05–0.51]), to aid in diagnosis. Sonographic detection of pulmonary edema is represented by B-lines, discrete artifacts resulting from the reverberation of sound waves off of fluid-filled pulmonary interstitium. In the proper clinical setting, B-lines represent pulmonary edema. The most recent European Society of Cardiology (ESC) guidelines now include LUS as an adjunct to diagnosis.
Focused Ultrasound
Formal echocardiography is rarely done in the United States in the ED setting. This does not obviate its value. For patients with worsening HF, reassessment of myocardial structure and function is recommended, especially if a clear etiology or precipitant is not identified. While point-of-care ultrasound does not replace formal echocardiography, point-of-care ultrasound or FoCUS (focused ultrasound) is often performed by noncardiologists at the bedside. This rapid approach is recommended by cardiology and noncardiology societies. For example, qualitative assessments of right and left ventricular function, identification of tamponade, and hypovolemia may be critical to aid in the management of the shock patient. The European Association of Cardiovascular Imaging outlines three broad frameworks for emergency FoCUS echocardiography: (1) diagnostic, (2) symptom or sign based, and (3) resuscitative. However, FoCUS does not replace formal echocardiography.
Natriuretic Peptides and Troponin (see also Chapter 33 )
NPs facilitate diagnosis. In addition, NPs are excellent discriminators of risk (i.e., prognosis). Despite their value and guideline recommendation, recent meta-analysis suggests their greatest value is in excluding AHF. While very high values help rule in AHF, intermediate values have less diagnostic discrimination. Using thresholds of 100 pg/mL for BNP and 300 pg/mL NTproBNP, a low value significantly reduces the posttest probability of AHF (LR = 0.1).
Guidelines also recommend troponin testing in AHF. Not only does this aid in identification of occult MI, troponin discriminates higher risk patients. With the advent of higher sensitivity assays, the proportion of AHF patients with evidence of myocardial injury outside of ACS exceeds 90%.
Initial Classification
Once the diagnosis of AHF has been made, the algorithm ( Fig. 36.9 ) outlined by the European Society of Cardiology outlines a pragmatic approach to initial classification and management of the AHF patient. The vast majority of patients present as “Wet and Warm,” based on the hemodynamic profiles established by Nohria and Stevenson ( Fig. 36.10 ). Thus most AHF management algorithms predominantly focus on this category. While the “Wet and Cold” patient is only a small fraction of AHF presentations, these are the most challenging to manage. In the classification scheme presented as follows, specific doses and types of medications are not discussed, as they will be reviewed in greater detail later in this chapter.
Warm and Wet—Vascular Type
As highlighted in Fig. 36.9 , elevated systolic blood pressure is common. Contemporary registries, such as Get With The Guidelines HF and EurObservational, note mean systolic blood pressure (SBP) of 140 and 133 mm Hg, respectively. These patients benefit from both vasodilators and IV loop diuretic therapy. The flash pulmonary edema patient represents the prototypical AHF patient with elevated blood pressure. Such patients present in extremis, sitting bolt upright (tripod position), gasping, with systolic blood pressures commonly above 180 mm Hg. Jugular venous distention, diffuse crackles, and minimal to no lower extremity edema are common findings. Rapid noninvasive ventilation (assuming an appropriate mental status), sublingual nitrates followed by IV vasodilators, and a small dose of IV loop diuretics often results in dramatic improvement.
Warm and Wet—Cardiac Type
This presentation is best represented by the patient with a history of HFrEF who slowly worsens over time. Gradual weight gain, progressive peripheral edema, and worsening dyspnea on exertion are common historical features. Such patients demonstrate more total volume overload instead of the volume redistribution seen in the vascular type presentation. For such patients, aggressive decongestion, starting with IV loop diuretics, are recommended. Such patients might also benefit from vasodilatation.
Cold and Wet
Advanced HF patients—defined as those with persistent signs and symptoms of HF despite maximal guideline directed therapy—may have a low (<90 mm Hg) systolic blood pressure at baseline with narrow pulse pressures (<25% of the systolic blood pressure). For clinicians who do not routinely care for advanced HF patients, this presentation can be quite alarming. Furthermore, assessing volume status is challenging given the chronic state of congestion; this challenge is compounded when the physician has never seen the patient before and who presents for a perceived or true emergency. Finally, treatment is not benign! Inotropes or inodilators are associated with worse longer-term outcomes. Thus “treating a number” (i.e., low SBP that is baseline and sufficient for organ perfusion) is not recommended. In this setting, we propose the following clinical question to guide next steps: Is immediate and emergent action needed or is there some time to ascertain what is baseline? In the former case, all emergent actions should be undertaken ( see also Chapter 45 ). If emergent action is not necessary, urgent evaluation is critical. This should focus on volume status and potential precipitants of decompensation, including worsening HF.
Emergency Department Risk Stratification
After initial stabilization and management, the conclusion of the ED phase of management is disposition (what happens to the patient next?). In the United States, more than 80% of AHF patients who present to the ED are hospitalized. However, retrospective data suggest up to 50% of patients might be discharged or observed for a brief period of time. Given the high financial costs of hospitalizations, the impact of hospitalization itself on patients (i.e., safety, deconditioning), identifying patients safe for discharge would be of tremendous value to both patients and the health care system.
Most risk scores are designed to identify higher risk patients, allowing clinicians and health care systems to focus limited resources to those in greatest need. However, for the ED, high-risk is not the primary concern; those patients are hospitalized. Rather, it is identifying patients safe to go home, despite the high postdischarge morbidity and mortality. Several ED-based risk instruments show promise, yet none are quite ready for universal use. One example is the use of high-sensitive troponin assays; absence of myocardial injury may identify a lower risk cohort. A biomarker approach to risk-stratification, a risk-score, or a combined approach will eventually be realized; for the time being, we recommend the absence of high-risk features as an initial approach. However, the complexity of HF patients (i.e., polypharmacy, social determinants of health, multiple comorbidities) often overwhelms the compressed time frame of ED management (on average 4–6 hours, usually less). Use of observation status or an observation unit as a “bridge” may be more realistic then direct discharge. Given the high proportion of patients currently hospitalized, expecting patients to be sent home may be impractical; using observation to first demonstrate that hospitalization is not necessary for lower risk patients may ultimately lead to more directly discharges. Fig. 36.11 is one proposed algorithm to aid in disposition decision-making.
Inpatient Management (and Re-risk Stratification)
Further Assessment: Possible Causes and Precipitating Factors
Once the diagnosis of AHF is established and the patient hospitalized, further diagnostic workup must be done to exclude specific causes that may warrant specific therapy. These include, but are not limited to, an acute coronary syndrome, a hypertensive crisis, arrhythmias, infectious etiologies, pulmonary embolism, and an acute mechanical cause ( Table 36.2 ). Identifying precipitating factors may also have a prognostic value. In an analysis of 15,828 AHF patients, AHF precipitated by acute coronary syndrome or infection was independently associated with higher risk, while AHF precipitated by atrial fibrillation was associated with a lower 90-day risk of death. Other studies have shown higher readmission rates in patients with cardiovascular precipitants, though no association with postdischarge mortality.
| Acute coronary syndrome |
Arrhythmias
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| Pulmonary embolism |
Mechanical causes
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| Lack of adherence to medical therapy |
| Excessive fluid or salt intake |
| Infections, especially pneumonia |
| Cerebrovascular insult |
| Surgery |
| Renal dysfunction |
| Asthma, exacerbation of chronic obstructive lung disease Takotsubo syndrome, increased sympathetic drive |
| Toxic substances, alcohol abuse, recreational drugs |
Drugs
Peripartum cardiomyopathy |
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