acute dyspnea and decompensated heart failure€¦ · with ahf in the united states.7–9 patients...

Acute Dyspnea andDecompensated Heart
Failure Peter S. Pang, MD, MSa,*, Sean P. Collins, MD, MScb,Mihai Gheorghiade, MDc, Javed Butler, MDd
KEYWORDS

� Acute heart failure � Emergency department � Risk-stratification � Observation units

KEY POINTS

� Use of lung ultrasound significantly improves diagnostic accuracy.

� Robust evidence to treat acute heart failure (AHF) in the emergency department setting remainspoor. However, existing therapies improve symptoms and hemodynamics, although whetherthey improve outcomes is less well known.

� We propose a framework to ensure optimal management of the AHF patient, based on existing ev-idence. This is known as the 6-axis model.

INTRODUCTION

Few other acute presentations result in such para-doxic outcomes as acute heart failure (AHF).Patients feel substantially better with current treat-ment, yet outcomes are dismal: up to one-third ofhospitalized patients experience death or rehospi-talization within the next 3 months,1 suggestinginitial symptom improvement fails to substantiallyalter underlying pathology, akin to treating thefever yet ignoring the abscess. Improvements inhemodynamics alone has not led to improved out-comes, nor has any other targeted intervention.2,3

The one possible exception being noninvasiveventilation.4 Substantial efforts to improve out-comes have yielded poor returns on investmentto date. Because most patients feel better, howev-er, perhaps some consolation can be found.5 Withmore than 1 million hospitalizations annually in theUnited States,6 improving outcomes remains thegreatest unmet need in AHF.

Disclosure: See last page of article.a Department of Emergency Medicine, Indiana Universityolis, IN 46202, USA; b Department of Emergency MedicinHall, Nashville, TN 37232, USA; c Department of Medicinicine, 420 East Superior Street, Chicago, IL 606011, USA;101 Nicolls Road, Stony Brook, NY 11794, USA* Corresponding author. Department of Emergency Med46202.E-mail address: [email protected]

Cardiol Clin 36 (2018) 63–72https://doi.org/10.1016/j.ccl.2017.09.0030733-8651/18/� 2017 Elsevier Inc. All rights reserved.

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Background

The emergency department (ED) initiates hospital-based management for more than 80% of patientswith AHF in the United States.7–9 Patients mostcommonly present with shortness of breath or dys-pnea.10–12 Correct diagnosis is paramount yet canbe challenging, given the broad differential for sucha chief complaint, especially for patients with multi-ple comorbidities. Because there is no gold stan-dard, heart failure remains a clinical diagnosis,diagnostic accuracy in the ED ranges from 71% to86%.13 At times, the patient’s condition mandatestreatment before a definitive diagnosis. Unfortu-nately, the evidence base for the pharmacologicmanagement ofAHF in theED ispoor,with noguide-line recommendations meeting the highest Level 1,Class A grade.14–16 Although modern day manage-ment has evolved away from rotating tourniquetsand blood-letting, the remaining pharmacologicarmamentarium for AHF management is largely the

School of Medicine, 720 Eskenazi Avenue, Indianap-e, Vanderbilt University School of Medicine, 215 Lighte, Northwestern University Feinberg School of Med-d Department of Medicine, Stony Brook University,

icine, 5/3rd Office Building, 3rd Floor, Indianapolis, IN

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Pang et al64

same as 50 years ago.17 Lack of evidence does notequal ineffective, only that we do not know whethercurrentAHFpharmacologic treatment reduces reho-spitalization or mortality. Nevertheless, patientsrequire treatment. In this article, we present a frame-work for initial management.

Diagnosis

As mentioned, patients presenting in extremisrequiring simultaneous treatment as the diagnosisis confirmed. However, for most patients, suffi-cient time exists to form an initial diagnostic andtreatment plan.It is worth reiterating; AHF is a clinical diagnosis.

Thus, no single blood test, image, historical feature,or examination finding absolutely confirms thepresence of heart failure (HF). In fact, the sensitivityof classic HF examination findings is quite poor.Although an S3 and jugular venous distention arequite specific, their sensitivity and interrater reli-ability are poor.18 Natriuretic peptides improvediagnostic accuracy considerably.19 However, arecent systematic reviewexamining the clinical util-ity of natriuretic peptides using interval likelihoodratios, to better account for Natriuretic Peptides(NP) as a continuous variable, suggests the diag-nostic “power” of NP lies more in ruling outAHF.13 To “rule-in” AHF, lung ultrasound is one ofthe most useful, easy, and rapid tests to performat the bedside13,20 (Fig. 1). Although multiplescoring systems exist to quantify the number ofB-lines,21,22 the presence of multiple B-lines in atleast 2 areas of each hemithorax facilitates confir-mation of the diagnosis in the correct clinicalsetting.

Initial Classification in the EmergencyDepartment

Perhaps more than any other term, heterogeneitybest describes the AHF population. In addition to

Fig. 1. Lung ultrasound. Arrows point to B-lines.

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differences in cardiac structure and function, un-derlying etiology of HF, and precipitant of AHF,marked differences in patient characteristics, co-morbid conditions, and background therapies,highlights the challenges of a singular, uniformconstruct to manage all AHF. As discussed inmore detail as follows, we recommend the impor-tance of thorough knowledge of underlyingcardiac substrate, precipitants, and amplifyingmechanisms of decompensation to best managepatients. This strategy accounts for patient differ-ences. Nevertheless, some baseline characteris-tics are worth highlighting. Patients with AHF onaverage are older (73 years), with womencomprising approximately half of AHF presenta-tions.23 Nearly half of patients with AHF have arelatively preserved (>40%) ejection fraction. LikeAHF, no pharmacologic therapy definitivelyimproves outcomes for patients with HF and a pre-served ejection fraction (HFpEF).14,16 This is afundamental difference compared to HF withreduced EF (HFrEF), though mineralocorticoidreceptor antagonists are a potential notableexception.24 Irrespective of a reduced versus pre-served EF, the comorbid burden for AHF is high,particularly for ischemic heart disease, diabetes,atrial fibrillation, and hypertension, as well aschronic obstructive pulmonary disease (COPD).Given the heterogeneity of the patient popula-

tion and presentation, combined with the lack ofrobust evidence, we propose a framework to aidthe acute care provider in initial management.This is taken from the Gheorghiade and Braun-wald25 6-axis model. Before in-depth discussionof the model, it is important to highlight what weconsider less important in the ED setting regardingacute management.

Preserved Versus Reduced Ejection Fraction

ED management rarely differs based on ejectionfraction (HFpEF vs HFrEF). Although these arethe most commonly used terms currently, pastterms such as diastolic dysfunction and systolicdysfunction have also been used to broadlydescribe patients based on EF. Such a lack ofdistinction in acute management is a striking dif-ference compared with chronic HF.Although knowledge of EF does not commonly

changeacutemanagement,bedsideor formalecho-cardiography (ECHO) may aid in diagnosing theextent and severity of right sided failure, presenceof pericardial fusion, and valvular disease. Suchknowledgemay also aid in immediatemanagement.At the present time, emergent ECHO is rarely per-formed in the ED setting outside of point-of-care ul-trasound performed by emergency physicians.

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Acute Dyspnea and Acute Heart Failure 65

A Framework for Initial Management: The 6-Axis Approach

The 6-axis model is intended as a guide (Fig. 2),establishing a multifaceted framework to ensurethe clinician considers various key aspects of initialAHF management. Certain aspects may be ofgreater or lesser importance depending on the pa-tient. Importantly, the 6-axis model is intended tobe dynamic: reevaluation is essential. At eachpoint of evaluation and reevaluation, except forde novo versus chronic HF, each spoke of the

Fig. 2. The 6-axis model. (A) Represents initial ED presentatponents of the 6-axis model may increase or decrease in imthe dynamic nature of AHF. By discharge, ensuring comorpatient had de novo vs chronic HF might significantly impM, Braunwald E. A proposed model for initial assessmenJAMA 2011;305(16):1703; with permission.)


model should be considered. For example, initialpresentation may differ from predischargeregarding the importance of each axis. Responseto management or failure to respond, as well as re-sults of testing, may yield new insights regardingthe reasons why patients have decompensated,allowing further tailored management.

Clinical Severity

Initial clinical impression guides urgency of man-agement. Vital signs are essential to rapidly gauge

ion and management. (B) Highlights how certain com-portance during hospitalization. (C) Further highlightsbidities were addressed is critical. Whether or not theact further disease management. (From Gheorghiadet and management of acute heart failure syndromes.


Pang et al66

severity. Patients who present in extremis requireimmediate stabilization and resuscitation. Exam-ples include flash pulmonary edema and cardio-genic shock. After stabilization, symptomaticmanagement is important but secondary to identifi-cation and treatment of the underlying precipitant.

Blood Pressure

Systolic blood pressure (SBP) is a known prog-nostic marker in AHF; patients with higher SBPhave better outcomes.1 We recommend furthersubclassification based on SBP to guide initialtherapeutic choices, such as more diuretic heavyversus more vasodilator.26 Although there isconsiderable overlap, we use cutpoints to aidthe clinician: (hypotensive 5 <100 mm Hg,normotensive as 100–140, and hypertensiveas >140 mm Hg) (Table 1). Most patients withAHF present “warm and wet.”27 Although SBPis an excellent guide, it is based on this assump-tion of “warm and wet,” or a well-perfused pa-tient with clinical evidence of congestion.Patients who are “cold and wet” (have systemicvasoconstriction but a low cardiac output) mayhave poor end-organ perfusion despite a rela-tively normal SBP.The hypotensive subgroup is much less com-

mon but a particularly challenging patient tomanage. Patients with a history of severelyreduced ejection fraction may have a low SBP atbaseline. Thus, reflexive diagnosis of shock andinitiation of inotropes is unwarranted. Althoughchallenging, first establishing whether the acutepresentation differs from baseline is needed.Then, although rarely done by the emergencyphysician, decongestive strategies (ie, vasodila-tors and intravenous loop diuretics) may be usedto optimize loading conditions for such patients.Although uncommon for urgent consultation forAHF, consideration for the hypotensive group isrecommended. Ideally, communication with thephysician who knows the patient well would facil-itate establishing a baseline.

Table 1Initial management based on systolic blood pressure

Hypotensive(SBP <100 mm Hg)

IV loop diuretics .

Vasodilators .

Inotropesa 1111

Abbreviations: 1, strength of the recommendation; IV, intravea Assumes patient is truly in shock, vs a low blood pressure


Heart Rate and Rhythm

For patients with severe systolic dysfunction, heartrate (HR) contributes substantially to cardiac output,given the minimal ability to augment stroke volume.Thus, bradycardias, or relative bradycardia, even ifminor, may impair cardiac output. On the otherhand, in the setting of a stiff left ventricle (or diastolicdysfunction) a very rapidHRmaybedeleterious. Forthese patients, reduced filling time in the setting ofdecreased left ventricle compliance may initiate orpropagate AHF symptoms.The most common dysrhythmia to present in the

context of AHF is atrial fibrillation (AF). A history ofAF is a risk factor for developing HF and vice-versa. For some patients, their first presentation ofAHF may be due to AF with rapid ventricularresponse. For unstable patients, guidelines recom-mend cardioversion. For most patients, however,treatment of AF follows a well-established para-digmof asking the following questions: (1) Is rhythmcontrol immediately necessary? (2) How muchshould I control the rate and how? (3) All patientsshould be risk stratified for stroke.For patients with a known history of AF, man-

agement of AHF itself often lowers HR by reducingadrenergic drive. As mentioned earlier, in patientswith a preserved EF, HR control is particularlyimportant, given the “stiffness” or lack of compli-ance of the left ventricle. By definition, a fasterHR results in relatively less filling time. Thus ratecontrol, either through AHF management, directrate control, or both is strongly recommended.Common rate control agents, such as

non-dihydropyridines and beta blockers, arecommonly used to treat AF in the setting of AHF.Although less commonly used, digoxin also shouldbe considered.28 For patients with a preserved EF,choice of agent will matter less versus achievingrate control. For patients with reduced EF, cautionis warranted before reflex use of non-dihydropyridines or beta blockers. Permissivetachycardia, especially in those with severelyreduced EF, may be needed to ensure sufficient

Normotensive(SBP 100–140 mm Hg)

HypertensiveSBP >140 mm Hg

1111 11

11 1111

. .

nous; SBP, systolic blood pressure.that is baseline for patient due to severely reduced EF.



cardiac output. Oftentimes, emergency physiciansmay not consider the downstream effects of over-zealous rate control, as the immediate effects areseldom seen in the ED.

Precipitants

Identification and treatment of the precipitant ofAHF is fundamental to good management. Con-trary to traditional teaching, medication noncom-pliance and dietary indiscretion are not the mostcommon causes of decompensation.29 Rather,infection and ischemia are more common. Failureto identify the underlying cause is not just an EDphenomenon; a remarkable proportion of patientswith new-onset heart failure never have an evalua-tion for underlying ischemic heart disease eitherduring hospitalization or in the following monthsafter presentation.30 Thus, careful considerationof what prompted the patients presented is essen-tial to avoid deterioration during hospitalization.

Comorbidities

Among the many challenges of managing AHF isconsideration of the patients’ cardiovascular (CV)and non-CV comorbid conditions. Occasionally,a comorbidity may trigger decompensation, suchas a COPD exacerbation. Acutely worsening renalinsufficiency is another example, as is acute coro-nary syndrome. In general, however, comorbiditiesrarely require immediate ED management. Rather,once the patient is stabilized and during the pre-discharge phase, due consideration of how HFwill be managed within the context of other chronicdiseases is warranted.

De Novo Versus Decompensated ChronicHeart Failure

As a general rule, patients with de novo or new-onset HF should be hospitalized. In addition tofurther management, establishing underlying car-diac structure and function, presence or absenceof coronary artery disease, as well as educationregarding a new chronic disease may be chal-lenging to perform expeditiously in the outpatientsetting. A 3-prong pathophysiologic approach isrecommended: (1) cardiac substrate, (2) triggersor precipitants of AHF, and (3) amplifying mecha-nisms (ie, neurohormonal activation or ongoingischemia).31 After stabilization, each should beconsidered and managed appropriately. For allpatients, adherence to guideline recommendedtherapies are essential. Perhaps surprisingly, stra-tegies to reduce rehospitalization lack robust evi-dence.32 Clearly, such strategies work for someinstitutions, but rarely are they universal.33,34 Forpatients with chronic HF, thorough evaluation


has ideally, already occurred; hospitalization pre-sents an opportunity for further education andoptimization of guideline directed medical therapy.

RISK-STRATIFICATION AND DISPOSITION

Although more than 80% of patients with AHF areadmitted from the ED, not all require hospitaliza-tion.7,35,36 More than a decade ago, 1 report sug-gested nearly 50% of patients with AHF could bedischarged home.37 Unfortunately, for the smallproportion of patients discharged, little is knownregarding their outcomes. The best evidencecomes from Canadian datasets. Based on thesedata, emergency physicians risk stratify poorly,as discharged patients are at higher risk for badoutcomes.38

Biomarkers, such as natriuretic peptides andtroponin, are guideline recommended for prog-nosis.16 Lower levels of such markers indicatelower risk; however, absence of high risk doesnot equal low risk. In other words, low levels ofsuch biomarkers has never been shown to equalsafe ED discharge. Other existing risk instrumentseither fail to perform well enough or have yet to bewell-validated.38,39 Thus, evidence-based, univer-sal recommendations regarding who is safe todischarge do not yet exist.

Lack of evidence has not hindered efforts todecrease hospital readmissions, however.32 Somemethods clearly work, although it is challenging touniversally recommend a strategy that would workat every hospital.33,34 Similarly, expert consensus,informed by existing evidence, should inform indi-vidual hospital or health care system strategies toreduce hospital admissions from the ED.

Overall, emergency physicians have a low toler-ance for risk.40 Suggesting EDs move from morethan 80% admission to 50% or 60% would bedifficult, especially absent better evidence. Obser-vation units or short-stay units are a viable alterna-tive to direct discharge.

Observation Units for Heart Failure

Observation for patients with AHF has beenongoing for well over a decade.41,42 Both retro-spective analyses and small studies support thesafety, effectiveness and potential cost-savingsof AHF observation unit (OU) management.9,43–49

In a retrospective study of 358 patients using Soci-ety of Cardiovascular Patient Care guidelines, lesshospital bed day utilization and similar 30-dayreadmission rates (12.5% vs 10.0%) wereobserved, respectively after adjustment for age,race, sex, BNP (B-type natriuretic peptide), renalfunction, and EF.48 Patients who were not ready


Pang et al68

for discharge after OU management wereadmitted to the hospital for further treatment.Compared with patients with low-risk chest pain

sent to the OU for “rule-out” ACS (acute coronarysyndrome), patients with AHF are older with signif-icantly more comorbidities. Thus, carefuldischarge planning, including close follow-up isessential. Without an excellent working relation-ship with cardiologists, an OU strategy will likelyfail. Fig. 3 is a suggested algorithm for EDdisposition.Finally, observation also affords a luxury gener-

ally absent in the ED setting: time. Thus, responseto therapy, assessment of functional status,addressing comorbidities, as well as education,follow-up, and contact with the primary cardiolo-gist or primary care physicians can occur. Further-more, time for social work and case managementconsultation is also possible. The 6-axis modelshould also be revisited before OU discharge toensure no acute issues have been missed. Similar

Fig. 3. ED disposition of patients with AHF. (From Miro Odepartment patients diagnosed with acute heart failure:J Emerg Med 2017;24(1):2–12; with permission.)


to inpatient management, Get With the GuidelinesHF is recommended during predischarge planning.

Other Considerations

Observation (or hospitalization) is an opportunityto optimize (or plan to optimize) care. Focusingsolely on volume management may miss an op-portunity. Fig. 4 outlines different facets of AHFto consider before discharge. Not all have to beperformed during hospitalization; however, eachshould be considered.

Future Directions

Prognosis after hospitalization for AHF remainspoor. More than a third of patients die or arerehospitalized within 90 days after discharge.1 At-tempts to improve outcomes with novel therapieshave largely failed. Such failures suggestimproving mortality with a short-term infusion dur-ing hospitalization is a daunting hurdle.50 Although

, Levy PD, Mockel M, et al. Disposition of emergencyan international emergency medicine perspective. Eur


a

a

a

a a

a

a

a

a

a

b

a

Fig. 4. Comprehensive assessment and targeted implementation of evidence-based therapies. ACE-I, angiotensinconverting enzyme inhibitor; ARB, angiotensin receptor blocker; CRT, chronic resynchronization therapy; Hydral,hydralazine; ICD, implantable cardiac defibrillator; ISDN, isosorbide dinitrate; JVP, jugular venous pulse; LV, leftventricle. a Select patients. b Viable but dysfunctional myocardium. (Adapted from Pang PS, Komajda M, Gheor-ghiade M. The current and future management of acute heart failure syndromes. Eur Heart J 2010;31(7):784–93;with permission.)

Fig. 5. Potential to Expand the 6-axis Model. (Data fromGheorghiadeM, Braunwald E. A proposed model for initialassessment and management of acute heart failure syndromes. JAMA: the journal of the AmericanMedical Associa-tion 2011;305(16):1702–3.)


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Pang et al70

the reasons for such lack of success is beyond thescope of this article, our limited knowledge of theunderlying pathophysiology of AHF, in all its forms,has contributed. To this day, an exact agreementon the definition of AHF remains debated!Lack of success does not mitigate the pressing

and growing unmet need. The ED continues toplay a critical role in initial diagnosis and man-agement and arguably “sets the tone” for down-stream management. Poor upfront managementmay lead to worse outcomes. A key upstreamdecision, to hospitalize or discharge, is one ofthe costliest health care decisions financially. Im-provements in ED-based risk-stratification willdecrease the number of hospitalizations.Patients still need to be treated today, however.

Although we recommend the 6-axis model as aframework for initial management, testing and vali-dation of the model is still required. In the future,additional components might be added (Fig. 5)or removed. In this example of an 8-axis model,both coronary artery disease (CAD) and biomarkerprofiles have been added. Presently, robustassessment of CAD during hospitalization is notroutine, nor should it be for every patient. Howev-er, ischemia due to CAD may be a direct contrib-utor to decompensation. Whether interventionresults in better outcomes is speculative.51,52

Existing and yet-to-be-discovered biomarkersmay also influence management and treatment.High-sensitivity troponin assays are an example.Although a large proportion of patients with AHFwith evidence of high-sensitivity troponin release,the exact reasons and how to manage suchpatients remain areas of active investigation.Such high-sensitivity assays may aid in risk-stratification.53

Finally, disparities in outcomes remains wide-spread. Such disparities disproportionately impactpatients with lower socioeconomic status, whobear a disproportionate burden of health careutilization and worse outcomes.7,54 Novel ideassuch as community paramedicine may have arole.55,56 From the ED perspective, moving froma transactional health encounter to one that is apart of the longitudinal care of patients will beessential.

SUMMARY

AHF management begins in the ED for mostpatients with AHF. Unfortunately, the evidencebase to guide ED management is poor. Thus,expert opinion, informed by existing evidenceguides the initial approach. We recommend the6-axis model as a framework for initial manage-ment. Importantly, reassessment should occur


frequently. Rather than hospitalize most patients,use of OUs may provide the necessary and suffi-cient time to ensure patients are respondingappropriately to initial management. Time inobservation also allows for more robust transi-tional care, ensuring good communication withprimary care and specialists as well as addressingother comorbid conditions, education, and socialfactors.

DISCLOSURE

P.S. Pang is or has been in the past year a consul-tant to or received honoraria from BMS, Novartis,Trevena, and Roche Diagnostics. He’s receivedresearch grants from BMS, Novartis, Roche,AHA, NHLBI, PCORI, and AHRQ.S.P. Collins Consulting: Novartis, Cardioxyl,

Trevena; research support—PCORI, NIH, Novar-tis, Bristol Myers Squibb, Cardioxyl, Cardiorentis,Trinity.M. Gheorghiade reports consulting relationships

with Abbott, Astellas, AstraZeneca, Bayer, Cardi-orentis, CorThera, Cytokinetics, CytoPherx,DebioPharm SA, Errekappa Terapeutici, GlaxoS-mithK-line, Ikaria, Intersection Medical, Johnson& Johnson, Medtronic, Merck, Novartis, OnoParmaceuticals, Otsuka Pharmaceuticals, PalatinTechnologies, Pericor Therapeutics, ProteinDesign Laboratories, Sanofiaventis, Sigma Tau,Solvay Pharmaceuticals, SticaresInterACT,Takeda, and Trevena Therapeutics.J. Butler reports receiving research support

from the National Institutes of Health, EuropeanUnion, and Patient Centered Outcomes ResearchInstitute; and serves as a consultant to Amgen,AstraZeneca, Bayer, Boehringer Ingelheim, Cardi-ocell, CVRx Medtronic, Merck, Novartis, Relypsa,and ZSPharma.

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