Linking To And Excerpting From “2019 ACC Expert Consensus Decision Pathway on Risk Assessment, Management, and Clinical Trajectory of Patients Hospitalized With Heart Failure”

Today, I review, link to, and excerpt from the “2019 ACC expert consensus decision pathway on risk assessment, management, and clinical trajectory of patients hospitalized with heart failure: a report of the American College of Cardiology Solution Set Oversight Committee”. J Am Coll Cardiol. 2019;74:1966-2011. [No Abstract] [Full-Text HTML] [Full-Text PDF]. Please note:

The committee decided not to distinguish HF on the basis of ejection fraction (EF) except where specifically noted. Although the evidence base for therapeutic interventions differs, the goals of decongestion and the importance of consideration of comorbidities and factors that influence adherence are common to patients admitted with reduced ejection fraction (HFrEF) or preserved ejection fraction (HFpEF). Management of patients with midrange ejection fraction (HFmrEF) shares similarities with management of both HFrEF and HFpEF 22, 23, 24.

All that follows is from the above resource.

1. Table of Contents
2. Preface
3. 1. Introduction
4. 2. Methods
5. 3. Assumptions and Definitions
6. 4. Pathway Summary Graphic
7. 5. Description and Rationale
8. 6. Node: Admission
9. 7. Node: Daily Trajectory Check
10. 8. Node: Transition Point
11. 9. Node: Discharge Day
12. 10. Focused Discharge Handoff
13. 11. Node: Early Post-Discharge Follow-Up
14. 12. Palliative Care
15. 13. Discussion and Implication of Pathway
16. Acknowledgments
17. President and Staff
18. Appendix 1. Author Relationships With Industry and Other Entities (Relevant)—2019 ACC Expert Consensus Decision Pathway on Risk Assessment, Management, and Clinical Trajectory of Patients Hospitalized with Heart Failure
19. Appendix 2. Peer Reviewer Relationships With Industry and Other Entities —2019 ACC Expert Consensus Decision Pathway on Risk Assessment, Management, and Clinical Trajectory of Patients Hospitalized with Heart Failure
20. Appendix 3. Abbreviations
21. Appendix 4. Advance Care Planning
22. Appendix 5. Alternative format for the Focused Discharge Handoff
23. References

3.1. Definitions

GDMT: Guideline-directed medical therapy

Optimal therapy: Treatment provided at either the target or the highest tolerated dose for a given patient.

EF: Ejection fraction

HFrEF: Heart failure with reduced left ventricular ejection fraction (EF ≤0.40)

HFpEF: Heart failure with preserved left ventricular ejection fraction (EF ≥0.50)

HFmrEF: Heart failure with midrange ejection fraction (EF <0.50 but >0.40)

4. Pathway Summary Graphic

Figure 1. Clinical Course of Heart Failure

Graphic depiction of course of heart failure admission, showing the degree of focus on clinical decompensation (red), discharge coordination (blue), ongoing coordination of outpatient care (light blue), and optimization of guideline-directed medical therapy (green), with ongoing assessment of the clinical course (circle with arrows), and key time points for review and revision of the long-term disease trajectory for the HF journey (compass signs).

5. Description and Rationale

5.1. Key points

• 1.
  The pathway to improve outcomes after HF hospitalization begins with admission, continues through the process of decongestion and transition to oral therapies before the day of discharge, and connects through the first post-discharge follow-up.
• 2.
  Clinical trajectory of HF should be assessed continuously during admission. Three main in-hospital trajectories have been defined: improving towards target, stalled after initial response, or not improved/worsening. These translate into different management strategies throughout hospitalization and post-discharge.
• 3.
  Evaluation of the long-term course of HF should be part of the initial comprehensive assessment, reviewed on the day of transition to oral therapy, and re-assessed at the first follow-up visit for persistent or new indications of high risk leading to consideration of advanced therapies or revision of goals of care.
• 4.
  Key risk factors modifiable during hospitalization include the degree of congestion as assessed by clinical signs and natriuretic peptides and the lack of appropriate guideline-directed medical therapies. Improvement in these factors is associated with improved prognosis, but failure to improve, including failure to tolerate guideline-directed medical therapy (GDMT) for HF, is associated with a much worse prognosis.
• 5. Common comorbidities, including diabetes; anemia; and kidney, lung, and liver disease, should be assessed during initial evaluation and addressed throughout hospitalization and discharge planning.
• 6. The day of transition from intravenous to oral diuretic therapy should trigger multiple considerations related to the overall regimen for discharge, verification of completion of patient education components, caregiver education, and plans for discharge.
• 7. The discharge day should be a time to review and communicate with identified providers rather than to initiate new therapies.
• 8. The elements of the hospitalization events and plans that are most crucial for continuity of care after discharge should be documented in a format that is available to all members of the outpatient team and easily accessible when a patient calls or returns with worsening symptoms.
• 9. Principles of palliative care applied by the in-hospital care team or by palliative care specialists may be particularly relevant when an unfavorable trajectory warrants communication about prognosis, options, and decision-making with patients and families.
• 10. The first follow-up visit should address specific aspects, including volume status, hemodynamic stability, kidney function and electrolytes, the regimen of recommended therapies, patient understanding, adherence challenges (including insurance/coverage issues), and goals of care.

6. Node: Admission

6.1. Evaluation in the ED

ED data show that 80% of all HF hospitalizations are admitted from the ED 27, 28. Although many advances have improved chronic HF management, there is sparse evidence regarding strategies for triage and management in the ED 13, 15, 16, 17, 18, 19, 25, 26, 29, 30. Most patients with acute decompensated heart failure (ADHF) are admitted for symptomatic treatment of congestion with intravenous diuretics and to a much lesser degree for respiratory failure, cardiogenic shock, incessant ventricular tachycardia, or the need for urgent diagnostic or therapeutic procedures 6, 20, 21, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40. Although fewer than 10% of ED visits with ADHF have acute life-threatening illness, and the majority of patients presenting are clinically stable 11, 38, 39, 41, the post-discharge event rate is high even though over 80% to 90% of patients are admitted 28, 42, 43.

A framework for risk stratification in the ED is shown in Figure 2, intended as a guide to thought processes during initial evaluations rather than a formal description of admission criteria and administrative processes surrounding admission. Patients who are critically ill at presentation or those with new-onset HF are admitted.

Figure 2. Risk Stratification Algorithm for Emergency Department Patients With Acute Heart Failure

*Marked leg edema, ascites, or scrotal or perineal edema may be clinical signs of marked congestion. The degree of radiographic and biochemical abnormalities may also indicate the degree of congestion. ED = emergency department; HF = heart failure.

Patients with known HF and a marked degree of congestion and those not at low risk (Table 1) are also usually admitted.

Early therapy for acute HF is crucial even if patients are ultimately admitted. Medical therapy is discussed in Sections 7.2, 7.4, 7.5, and 7.6. Diuretic dosing for decongestion is considered in detail in Section 7.2.

6.2. Comprehensive Initial Assessment—Setting the Inpatient Goals

The two central themes of care for patients hospitalized for decompensated HF are decongestion and optimization of the therapies recommended for HF, but multiple other goals also need to be met. The coordinated care plan includes evaluation as necessary of the primary etiology of the heart disease and potential aggravating factors that would require specific intervention, both cardiac and noncardiac (34) (see Table 2).

6.2.1. Assessing Hemodynamic Profiles

Most patients present with at least 1 symptom and 1 sign of congestion that can be tracked as targets during decongestion and may serve as sentinel symptoms for recurrent congestion after discharge 70, 74, 77, 78 (Table 3). The jugular venous pressure (JVP) reflects elevated right-sided filling pressures and is also a sensitive indicator of elevated left-sided filling pressures in patients with HF 75, 79. Rales, when present, usually indicate higher filling pressures than baseline, but are often absent in chronic HF due to pulmonary lymphatic compensation. Extensive pitting edema, ascites, or large pleural effusions reflect large extravascular reservoirs that may take many days to mobilize.

Clinical profiles of patients with HF are shown in Figure 3. Patients identified with congestion should be further considered for whether filling pressures are elevated in proportion for both the right heart and the left heart (right atrial pressure >10 mm Hg and pulmonary capillary wedge pressure >22 mm Hg; 75% to 80% of patients with chronic HFrEF, less defined for HFpEF) 42, 80. The wet and warm clinical profile without evidence of hypoperfusion characterizes over 80% of patients admitted with reduced EF and almost all with preserved EF except those with small left ventricular cavities of restrictive or hypertrophic cardiomyopathies 39, 42. The cold and wet profile describes congestion accompanied by clinical evidence of hypoperfusion, as suspected from narrow pulse pressure, cool extremities, oliguria, reduced alertness, and often recent intolerance to neurohormonal inhibition. Sleepiness, impaired concentration, and very low urine output may also be present. These patients may require adjunctive therapy with vasodilator or inotropic agents or decrease of medications with negative inotropic effects to improve cardiac output and facilitate diuresis. Patients who appear to have low cardiac output without clinical congestion (cold and dry profile) often have unrecognized elevation of filling pressures, which may be revealed by invasive hemodynamic measurement. Uncertainty regarding hemodynamic status is associated with worse outcomes and is an indication for invasive hemodynamic assessment 15, 81. True hypoperfusion without elevated filling pressures accounts for fewer than 5% of admitted patients (39) and usually reflects aggressive prior therapy with tight adherence. A patient hospitalized with apparent decompensation in whom both filling pressures and perfusion appear to be normal should be carefully evaluated for other causes of symptoms, such as transient ischemia or arrhythmias, or noncardiac diagnoses such as pulmonary disease.

Figure 3. Classification of Patients Presenting With Acutely Decompensated Heart Failure

6.2.2. Consideration of Comorbidities

A key component of the comprehensive initial assessment is evaluation of patient comorbidities (Table 4). These comorbidities and their therapies should be carefully considered for their role in HF decompensation and as independent targets for intervention. For example, diabetes mellitus and pulmonary disease are each present in 30% to 40% of patients hospitalized with HF and play a role in disease severity and risk for decompensation (82). Kidney dysfunction can precipitate congestion and can also limit initiation of GDMT. Frailty is another common comorbidity in HF, particularly for the elderly 83, 84, and its association with health, functional status, and late-life disability is an increasingly important focus for patients with HF and their caregivers. Approximately 50% to 70% of older patients admitted with ADHF present with some degree of frailty, although this may be reversed or attenuated with interventions 85, 86. Consideration should be given at the time of hospitalization to the need for physical therapy consultation.

6.2.3. Initial Risk Assessment

This document centers on evaluation of the clinical trajectory of HF, as an assessment of both daily clinical progress and the long-term disease course, incorporating the prior history with specific risk factors at admission, the day-by-day progress toward the goals of hospitalization, and the re-assessment before discharge. The risk factors that enter into this assessment may be fixed, as for age or number of previous hospitalizations, or potentially modifiable, as for natriuretic peptide levels. Much of the available data concerning risks in HF can be viewed through their impact on trajectory. Improvement in modifiable risk factors, such as clinical congestion, elevated natriuretic peptide levels, and inadequate recommended medical therapy, is associated with improved prognosis.

Because a key message of this document is the importance of serial assessment from admission through discharge, the risk factors listed in Table 5 are categorized according to the time when they may be known during the hospitalization. In setting goals to decrease risk and improve outcomes after hospitalization and later, it may be helpful to focus on those risk factors most likely to be modifiable.

Risk factors known at the time of hospitalization include age, duration of HF, and frequency of hospitalization. Chronic risks that may be previously or newly recognized at the time of admission include right ventricular dysfunction, persistent Class IV symptoms, and nonadherence with medications and/or salt/fluid restrictions. Multiple correlates of chronic renal dysfunction and right ventricular dysfunction predict higher risk, but it is not clear how and whether these risks are modified by the interventions during hospitalization. Of the biomarkers measured clinically, natriuretic peptide levels are the most robust predictors of readmissions and death 24, 55, 63, 68, 111, 112, and also highly modifiable with successful decongestion, after which levels continue to decrease for days after discharge. The magnitude of decrease in natriuretic peptide levels during therapy is closely associated with decreased risk, and increase or failure to decrease levels is associated with higher risk 109, 110. Absolute levels at discharge are also highly predictive of rehospitalization, need for advanced therapies such as transplant or mechanical circulatory support, and mortality. There is increasing interest in urinary sodium concentration during intravenous diuretic therapy as a biomarker of better outcomes that relates closely to renal responsiveness, whether in a 24-hour collection or as the first spot urine after intravenous diuretic 114, 126.

Troponin elevations at admission or during HF hospitalization, even in the absence of acute coronary syndromes, are associated with worse outcome but have not been integrated comprehensively into overall risk assessment (64). It is not clear whether risk is modified by changes that occur in troponin after admission.

Of central importance are the symptoms and signs of congestion, typically part of the presentation for admission. Once present, higher degrees of congestion are associated with more net volume loss and longer hospital stay before decongestion, but if decongestion can be achieved, the degree of initial congestion is not associated with higher risk 67, 70, 120. Either admission or discharge with the cold and wet profile is associated with worse outcomes (124).

In this document, we describe risk assessment of patients at admission, daily review throughout the active phase of therapy, and review at the transition from intravenous to oral diuretics prior to the day of discharge. For calibration of risk during the hospitalization, the writing team felt it was important to standardize the nodes and goals of hospitalization as much as possible. In the final risk assessment prior to discharge, the progress and events from the hospital course, including unexpected need for resuscitation or intravenous inotropic therapy, are incorporated into the overall assessment to revise the long view of disease trajectory after discharge. At any time between admission and discharge, recognition of high risk for unfavorable outcomes should trigger specific considerations (Table 6), including caution regarding the initiation of therapies that may be difficult to discontinue.

7. Node: Daily Trajectory Check

The near-term clinical trajectory during hospitalization represents responsiveness to therapy in terms of clinical HF symptoms and signs and laboratory and diagnostic tests. This trajectory helps define the next steps for management, care coordination, health outcomes risk and prognosis, and disposition.

We have also highlighted a long-term trajectory assessment as a specific evaluation of progress toward resolution of symptoms and signs of congestion, adequacy of perfusion, stability of vital signs, and trends in kidney and other organ function (compass symbols in Figure 1).

Three main in-hospital trajectories have been defined according to changes in patient symptoms, clinical signs, laboratory markers and imaging if done, presence or absence of complications, assessment and treatment of comorbidities, and treatment alignment with goals of care: 1) improving towards target; 2) stalled after initial response; or 3) not improved/worsening. These trajectories translate into different management strategies throughout the hospitalization and post-discharge (Figure 4). Patients improving toward target should be considered for initiation and/or further optimization of GDMT. In those who are not improved/worsening, therapy should be intensified, and additional diagnoses, including conditions other than HF, should be considered. If deterioration continues, hemodynamic assessment and advanced therapies merit consideration. Further deterioration should prompt discussion about prognosis and goals of care. Patients who are stalled represent those whose symptoms may have improved initially but in whom residual congestion remains and diuretic resistance and/or kidney function, or other problems, may be limiting progress. The key issue in such patients is whether escalation of therapy will suffice to bring about complete decongestion, or whether that target needs to be modified, allowing a “compromise with congestion.”

7.1. Targets for Decongestion

Inpatient trajectories are primarily defined by the pace and extent of decongestion. Evaluation of the degree of clinical congestion is depicted in Figure 5. The usual goal is for complete decongestion, with absence of signs and clinical symptoms of elevated resting filling pressures 70, 78, 117, 130. Rates of rehospitalization and death are consistently lower in patients rendered free of clinical congestion by the time of discharge 67, 78. National Heart, Lung, and Blood Institute–sponsored trials of ADHF have specified goals of resolution of edema, orthopnea, and jugular venous distention 74, 77, 78, 131, 132. JVP should generally be reduced to <8 cm, dyspnea at rest should be relieved, and there should be no residual orthopnea, bendopnea, or edema 77, 78. Peripheral reservoirs of anasarca, large pleural effusions, and ascites as detectable should gradually be depleted, after which intravascular filling pressures as indicated by JVP will more rapidly decrease. The amount of net diuresis that will be needed for complete decongestion cannot be ascertained at the time of admission, and the difference between admission weight and a previous target weight often underestimates the excess fluid. Postural hypotension is often interpreted as indication of overdiuresis, but frequently reflects overvasodilation.

Most patients report early improvement in symptoms, particularly dyspnea. In admissions with HFrEF, shortness of breath was reported as the worst symptom by about one-half of patients, fatigue by about one-third, and abdominal discomfort, swelling, or edema by the remaining patients. The magnitude of patient-reported improvement was least for patients with a worst symptom of fatigue. Symptoms of congestion (Table 3) usually improve before the signs of congestion have fully resolved. If guided only by symptom relief, diuresis will often be stopped too soon. Before discharge, the clinical signs of congestion (Table 3) have usually resolved in 50% to 70% of patients 6, 77, 78, 121, 133, 134, 135, 136, 137, 138, 139. Evidence of improvement in filling pressures is closely associated with the improvement in breathing early during hospitalization (140) and is consistently associated with better outcomes 67, 109, 113, 115, 116, 118, 119, 120. Reports differ about the association between weight loss and symptom improvement 122, 137, 139. Early relief of symptoms correlated with both fluid loss and weight loss in the Heart Failure Network trials, but there was poor correlation between amount of weight loss and symptom improvement 122, 137, 139, 141, 142, and weight loss alone is not associated with better outcomes 141, 142 likely because of the disparity between urine sodium output and fluid output (126) and the variable amount of fluid accumulation prior to admission. Average weight loss in recent inpatient HF trials ranges from 4 to 8 kg 74, 77.

Substantial reduction in B-type natriuretic peptide levels is anticipated during effective diuresis, frequently decreasing by 50% or more from admission (111), and a decrease in natriuretic peptide concentrations of at least 30% before discharge is strongly associated with better outcomes. Targeting reduction in natriuretic peptide concentrations, however, did not result in better outcomes than treating congestion and optimizing other guideline-directed medical therapy empirically 111, 112. Kidney function is not a reliable biomarker for volume status or change in volume status; modest increases are not linked to worse outcomes as long as the rise in creatinine is transient 143, 144 and accompanied with successful decongestion 118, 119, 120, 123, or occurs after initiation of renin-angiotensin system (RAS) or aldosterone antagonists 145, 146, 147.

The targets for decongestion may need modification for mismatch of right and left and right-sided filling pressures (Figure 3, right side). Approximately 70% to 75% of patients with decompensated chronic HFrEF have concordance of relative right and left filling pressures around thresholds of right atrial pressure of 10 mm Hg and pulmonary capillary wedge pressure of 22 mm Hg 75, 80. Clinical assessment can be helpful to confirm or challenge concordance (42), but clinical evidence for elevated left-sided pressures may be subtle in the presence of prominent right-sided findings. Information from recent invasive studies or echocardiographic hemodynamic evaluation should be brought forward to inform the hemodynamic targets. Patients in whom elevated right atrial pressures approach or exceed left-sided filling pressures often cannot undergo diuresis to a normal JVP and may be more likely to receive inotropic support (79). Conversely, patients with elevated left-heart pressures in the presence of normal right-sided pressures may continue to have orthopnea and dyspnea on minimal exertion despite diuresis to JVP in the normal range; their optimal right-sided pressures may be in the lower range of normal.

The goal of edema resolution may need to be relaxed for patients with other known contributors to peripheral edema such as chronic venous insufficiency. However, persistent net diuresis in combination with light compression, such as with elastic sport bandages, can lead to marked improvement in peripheral edema even after years of chronic swelling was presumed refractory or attributed to lymphedema. The goal to eliminate edema must also be revised in the setting of low plasma oncotic pressure, often seen in the elderly with poor nutrition. Measurement of serum albumin should be routine during HF admission to gauge mobility of edema and also to target malnutrition.

7.2. Diuretic and Adjunctive Therapy

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