- Email: [email protected]
Residual congestion and clinical intuition in decompensated heart failure
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ARTICLE IN PRESS
Rev Clin Esp. 2019;xxx(xx):xxx---xxx
Revista Clínica Española www.elsevier.es/rce
SPECIAL ARTICLE
Residual congestion and clinical intuition in decompensated heart failure夽 J.I. Pérez Calvo a,b,c,∗ , J. Rubio Gracia a,c , C. Josa Laorden a,c , J.L. Morales Rull d,e a
Servicio de Medicina Interna, Hospital Clínico Universitario Lozano Blesa, Zaragoza, Spain Facultad de Medicina, Universidad de Zaragoza, Zaragoza, Spain c Instituto de Investigación Sanitaria de Aragón, Zaragoza, Spain d Servicio de Medicina Interna, Hospital Universitario Arnau de Vilanova, Lleida, Spain e Instituto de Investigación Biomédica Dr. Pifarré, Lleida, Spain b
Received 3 January 2019; accepted 19 February 2019
KEYWORDS Heart failure; Congestion; Residual congestion; Diuretic therapy
PALABRAS CLAVE Insuficiencia cardiaca; Congestión; Congestión residual; Terapia diurética
Abstract Congestive symptoms are the key to recognizing decompensated heart failure, whose treatment is based on reducing the congestion until a clinical situation has been reached that allows the patient to be discharged to continue outpatient treatment. The important aspect is not the degree of congestion at admission but rather the congestion that persists after energetic diuretic therapy. The persistence of congestive signs following an apparently correct and effective therapy has been called residual congestion and is associated with a poor prognosis. The tools for determining this condition are still rudimentary. Methods therefore need to be developed that enable a more accurate assessment. © 2019 Elsevier Espa˜ na, S.L.U. and Sociedad Espa˜ nola de Medicina Interna (SEMI). All rights reserved.
La congestión residual y la intuición clínica en la insuficiencia cardiaca descompensada Resumen Los síntomas congestivos son la clave para reconocer las descompensaciones de la insuficiencia cardiaca. Su tratamiento se basa en la reducción de la congestión hasta alcanzar una situación clínica que permita el alta del paciente para continuar el tratamiento ambulatoriamente. Lo importante, no obstante, no es el grado de congestión al ingreso, sino la que persiste
夽
Please cite this article as: Pérez Calvo JI, Rubio Gracia J, Josa Laorden C, Morales Rull JL. La congestión residual y la intuición clínica en la insuficiencia cardiaca descompensada. Rev Clin Esp. 2019. https://doi.org/10.1016/j.rce.2019.02.004 ∗ Corresponding author. E-mail address: [email protected] (J.I. Pérez Calvo). 2254-8874/© 2019 Elsevier Espa˜ na, S.L.U. and Sociedad Espa˜ nola de Medicina Interna (SEMI). All rights reserved.
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J.I. Pérez Calvo et al. después de un tratamiento diurético enérgico. A la persistencia de signos congestivos después de un tratamiento aparentemente correcto y eficaz, se le ha denominado «congestión residual» y se asocia con mal pronóstico. Las herramientas para su estimación son todavía rudimentarias, por lo que deben desarrollarse métodos que permitan una valoración más precisa. © 2019 Elsevier Espa˜ na, S.L.U. y Sociedad Espa˜ nola de Medicina Interna (SEMI). Todos los derechos reservados.
Several matters relating to heart failure (HF) were discussed at the last congress held by the Spanish Society of Internal Medicine (SEMI, Sociedad Espa˜ nola de Medicina Interna). Remarkably, congestion has returned to the headlines and is raising clinical and scientific interest. The congestive signs that characterize HF syndrome were already recognized and described by Hippocrates in Ancient Greece in the 5th century B.C.1 There is no doubt that the pathophysiology on which Hippocratic medicine was based was not the current one, given that, at that time, the syndrome was explained by an imbalance between the different humors. Objectively speaking, however, was this pathophysiological concept mistaken? To be more precise, was this concept more mistaken than the one that we currently use? The return of congestion to the forefront of interest among the medical community is likely to reflect a lack of understanding of its pathophysiological mechanisms and consequences.2,3 Etymologically, the term ‘‘congestion’’ derives from the Latin word ‘‘con-gestus-tio’’, which refers to an excessive accumulation of fluid in certain parts of the body. Patients admitted to clinics due to a decompensated HF primarily exhibit symptoms and signs of congestion4 (dyspnea, orthopnea, edema, hepatomegaly, jugular vein engorgement, etc.). The symptoms of congestion in cases of HF are a result of extracellular fluid retention secondary to increased ventricular filling pressure. The congestive manifestations, together with those derived from the associated hypoperfusion, define the decompensated HF syndrome and enable its quick classification into groups requiring varied therapeutic measures.5 The fact that this ancient classification based on clinical aspects is included in the latest guidelines of the European Society of Cardiology6 indicates its importance.6 The detection of congestive symptoms and signs has limitations. On the one hand, its propedeutics requires training7 and the acquisition of possibly numerous techniques,8 thus implying a certain degree of variability in the actual data acquisition process. As is the case for many other diagnostic methods, clinical symptomatology is fairly unspecific, with a high negative predictive value but a low positive predictive value.4,9,10 In addition to clinical methods, the degree of congestion can be determined by ultrasonography (Table 1).4 Although this is still just speculation, it is likely that systemic congestion11,12 or that of the splanchnic territory,13 triggers inflammatory mechanisms14,15 that play a crucial role in the pathophysiology of decompensated heart failures.
Table 1 Performance of the various techniques for determining the degree of congestion. Parameter a
Clinical methods Inspiratory collapse of the inferior vena cava (<50%) E-wave velocity >50 cm/s E/e ratio > 12 Diffuse B-lines in the pulmonary ultrasound
Sensitivity
Specificity
13---94% 12%
10---90% 27%
92% 66% 86%
28% 55% 40%
Source: Mullens et al.4 a Assessment of the presence and degree of jugular distension, hepatomegaly, edema, dyspnea and crackles.
There is no doubt that congestive signs and symptoms are the herald of decompensated heart failures4 ; in fact, the fight against this congestion focuses the treatment on the patients’ hospital admission.4,16 Given that the persistence of congestive signs at discharge is associated with an increased risk of rehospitalization and mortality due to HF,17---20 complete decongestion could be the primary therapeutic aim in cases of decompensated HF. In light of the findings of recent studies,18,19 reaching a degree of decongestion that achieves symptomatic relief and allows patient discharge might still not be enough, given that there are substantial differences between decongestion that relieves symptoms and decongestion that improves the prognosis. The subtle degree of congestion that persists after the initial treatment, which is barely relevant from a symptomatologic point of view but has a negative effect on mortality, can be called ‘‘residual congestion’’. Using a simple score system based on the presence of dyspnea, orthopnea, asthenia, crackles, edema, and jugular venous distention (Table 2) applied to a cohort of 2061 patients with HF and a reduced left ventricular ejection fraction, Ambrosy18 proved that the higher the score, the higher the mortality and the number of readmissions due to HF during the follow-up. In a subsequent study, Rubio et al.19 proved that clinically inapparent residual congestion is very common at discharge and confirmed its poor prognosis using a simplified score (Table 2) that solely included the degree of orthopnea, jugular venous distention and edema measured in a cohort of 1572 patients with HF and a reduced left ventricular ejection fraction. In this study,19 only 23% of the
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Residual congestion and clinical intuition in decompensated heart failure Table 2
3
Congestion assessment using clinical scores. Ambrosy score18
Signs/symptoms
0
1
2
3
Dyspnea Orthopnea Asthenia Jugular venous distention (cm H2 O) Pulmonary crackles Leg edema
Absent Absent Absent <6 Absent Absent
Minimal Minimal Minimal 6---9 In base Mild
Frequent Frequent Frequent 10---15 <50% Moderate
Continuous Continuous Continuous >15 >50% Pronounced
0
1
2
3
Absent Absent <6
1-Pillow Mild 6---10
2-Pillow Moderate >10
>30 Pronounced ---
Rubio score19
Orthopnea Edema Jugular venous distention (cm H2 O)
patients showed no signs of congestion at discharge, while 48% and 29% had mild to severe symptoms of congestion that were associated with an increased rate of re-hospitalizations and mortality, respectively. It is clear that the challenge in the immediate future will be to detect and combat residual congestion that resists the action of intensive diuretic therapy immediately on admission. To meet this challenge effectively and safely, we must first recognize it. These clinical scores can most likely be supplemented with the patients’ diuretic response20 ; biochemical parameters, such as their hematocrit21 ; and variations in natriuretic peptide (NP)22,23 concentration or carbohydrate antigen 125 (CA-125).24 The usefulness and performance of ultrasonography25,26 procedures and of other noninvasive methods, such as bioelectrical impedance analysis, must also be analyzed.27,28 There is little evidence about the role of congestion in the decision-making process at discharge and the perception of residual congestion, which is an emerging situation in daily clinical practice. To further delve into these two aspects, we prepared an anonymous 13-item survey that was distributed by e-mail to the members of the Heart Failure Group (Grupo de Insuficiencia Cardíaca, GIC) of SEMI, which was accessible from the 22nd of August to the 23rd of September 2018. The survey focused on determining how congestion was assessed and the importance that the respondents gave to the method used at two key points of the condition’s progress: (1) on completion of an intensive diuretic treatment; i.e., when the congestive symptoms that motivated the admission are considered to be resolved and (2) when the decision to proceed with the discharge is made; i.e., when the congestion is considered to no longer exist or to be safely treatable on an outpatient basis (supplementary material). A total of 253 specialists, most of whom worked in internal medicine departments (247), completed the survey; their answers can be consulted in the GIC blog (http://cardioclinico.com) and the supplementary material. The respondents based their identification of cases of congestion and the determination of its degree on its characteristic symptoms and signs (dyspnea, orthopnea, jugular venous distention and edema; over 50% for each), the NP
concentration (43%), the ultrasound findings of the inferior vena cava (45%), the ultrasound findings of the lungs (43%) and the CA-125 levels (16%). A total of 247 respondents selected the answer concerning the early response of the congestion that allows for de-escalating the diuretic treatment and replacing the intravenous route with an oral one. Most of the respondents resorted once again to the assessment of the patients’ clinical symptoms (improved dyspnea [80%], reduced edema [78%] or weight [63%]) and a stable dose of oral diuretics (62%). Eighty-six percent of the participants reported that they based their assessment on diuretic efficacy, although this parameter was measured in several ways and was related to a reduction of the signs and symptoms of congestion in 86% of cases, followed by the NP concentration (24%), the serial lung ultrasound findings (8%) and those of an ultrasound of the inferior vena cava (5%). The respondents were openly asked whether ‘‘residual congestion’’ suggested anything to them and, if so, how they interpreted the term. Of the 247 respondents, 185 (75%) reported being aware this clinical situation, and their perception, although variable, was reasonably in line with what could be expected from a clinical point of view (individualized responses can be consulted in the blog). Discharge was primarily prompted by a reduction of the edema (72%), a functional class improvement (63%) and a stable dose of oral diuretics (62%), once again, based on eminently clinical criteria. Remarkably, most decisions made in relation to the assessment, monitoring and treatment of congestion in cases of decompensated heart failures are based on clinical perception, i.e. on symptomatologic aspects. Nevertheless, this is also logical if we consider that there are no quantitative tools available for its correct measurement and that awareness of the importance of congestion persisting in a latent state despite treatment is very recent. We should also note the use of complementary methods, such as assessing the NP concentration and the use of lung ultrasonography to evaluate the clinical progress of congestion. Although both methods have clearly been shown to be useful in diagnosing HF, especially in cases
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4 of decompensated heart failure,29,30 there is insufficient evidence of their reliability for serial use (e.g., in daily clinical practice) to determine the degree of congestion31,32 ; therefore, their results should be interpreted with caution for decision making. This manuscript has methodological limitations. First, this study was based on an ad hoc survey. Second, despite being significant, the number of responses accounted for slightly less than half of the survey recipients. However, the purpose of the study was to analyze the subjective perception of internists accustomed to treating patients with decompensated heart failure, particularly regarding residual congestion, which has been understudied to date and therefore lacks strong evidence. The results of this survey prove that clinical intuition, an aspect that would barely reach a C recommendation score in the context of evidencebased medicine, is a powerful tool in daily clinical practice. This intuition involves the ability to detect a real problem for which there are still no answers and to reasonably face it following a consensual approach. The task before us is to determine the exact threshold of residual congestion that can provide relevant prognostic information in clinical practice, a threshold to be set between its detection using accessible but not very sensitive clinical methods and a sensitive but invasive heart catheterization. We must tackle this task cooperatively without delay, given that the use of intuition and possibilities are not alien to the HF group.
J.I. Pérez Calvo et al.
5. 6.
7. 8. 9.
10.
11.
12. 13.
14.
Conflicts of interest The authors declare that they have no conflicts of interest with this article.
15.
Acknowledgments
16.
The authors would like to extend their gratitude to the members of the Working Group on Heart Failure and Atrial Fibrillation (Grupo de Trabajo de Insuficiencia Cardiaca y Fibrilación Auricular) of SEMI, particularly to those who selflessly completed the survey.
17.
Appendix A. Supplementary data Supplementary data associated with this article can be found, in the online version, at doi:10.1016/ j.rceng.2019.02.013.
18.
19.
References 1. Katz AM. The ‘‘modern’’ view of heart failure. How did we get there? Circ Heart Fail. 2008;1:63---71. 2. Casado Cerrada J, Pérez Calvo JI. Da˜ no orgánico y síndrome cardiorrenal en la insuficiencia cardiaca aguda. Med Clin (Barc). 2014;142 Suppl. 1:26---31. 3. Rubio Gracia J, Sánchez Marteles M, Pérez Calvo JI. Implicación de la congestión venosa sistémica en la insuficiencia cardiaca. Rev Clin Esp. 2017;217:161---9. 4. Mullens W, Damman K, Harjola VP, Mebazaa A, Brunner-La Rocca HP, Martens P, et al. The use of diuretics in heart failure with
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congestion --- a position statement from the Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail. 2019;21:137---55, doi:10.1002/ejhf.1369. Stevenson LW. Tailored therapy to hemodynamic goals for advanced heart failure. Eur J Heart Fail. 1999;1:251---7. Ponikowski P, Voors AA, Anker SD, Bueno H, Cleland JGF, Coats AJS, et al. 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). Developed with the special contribution of the Heart Failure Association (HFA) of the ESC. Eur J Heart Fail. 2016;18:891---975. McGee S. The heart. In: McGee S, editor. Evidence-based physical diagnosis. 4th ed. Elsevier: Philadelphia; 2018. p. 301---14. Leier CV. Examining the jugular vein is never vain. Circ Heart Fail. 2010;3:175---7. McKee PA, Castelli WP, McNamara PM, Kannel WB. The natural history of congestive heart failure: the Framingham study. N Engl J Med. 1971;285:1441---6. Jimeno Sainz A, Gil V, Merino J, García M, Jordán A, Guerrero L. Validez de los criterios clínicos de Framingham para el diagnóstico de insuficiencia cardíaca sistólica. Rev Clin Esp. 2006;206:471---539. Fallick C, Sobotka PA, Dunlap ME. Sympathetically mediated changes in capacitance: redistribution of the venous reservoir as a cause of decompensation. Circ Heart Fail. 2011;4:669---75. Guglin M. Key role of congestion in natural history of heart failure. Int J Gen Med. 2011;4:585---91. Verbrugge FH, Dupont M, Steels P, Grieten L, Malbrain M, Tang WH, et al. Abdominal contributions to cardiorenal dysfunction in congestive heart failure. J Am Coll Cardiol. 2013;62:485---95. Colombo PC, Onat D, Harxhi A, Demmer RT, Hayashi Y, Jelic S, et al. Peripheral venous congestion causes inflammation, neurohormonal, and endothelial cell activation. Eur Heart J. 2014;35:448---54. Paulus WJ, Tschöpe C. A novel paradigm for heart failure with preserved ejection fraction: comorbidities drive myocardial dysfunction and remodeling through coronary microvascular endotelial inflammation. J Am Coll Cardiol. 2013;62:263---71. Gheorghiade M, Filippatos G, de Luca L, Burnett J. Congestion in acute heart failure syndromes: an essential target of evaluation and treatment. Am J Med. 2006;119 Suppl. 1:S3---10. Lala A, McNulty SE, Mentz RJ, Dunlay SM, Vader JM, AbouEzzeddine OF, et al. Relief and recurrence of congestion during and after hospitalization for acute heart failure: insights from Diuretic Optimization Strategy Evaluation in Acute Decompensated Heart Failure (DOSE-AHF) and Cardiorenal Rescue Study in Acute Decompensated Heart Failure (CARESS-HF). Circ Heart Fail. 2015;8:741---8. Ambrosy AP, Pang PS, Khan S, Konstam MA, Fonarow GC, Traver B, et al. Clinical course and predictive value of congestion during hospitalization in patients admitted for worsening signs and symptoms of heart failure with reduced ejection fraction: findings from the EVEREST trial. Eur Heart J. 2013;34:835---43. Rubio-Gracia J, Demissei BG, ter Maaten JM, Cleland JG, O’Connor CM, Metra M, et al. Prevalence, predictors and clinical outcome of residual congestion in acute decompensated heart failure. Int J Cardiol. 2018;258:185---91. Ter Maaten JM, Valente MA, Damman K, Hillege HL, Navis G, Voors AA. Diuretic response in acute heart failure pathophysiology, evaluation, and therapy. Nat Rev Cardiol. 2015;12:184---92. Grau Amorós J, Formiga F, Aramburu Bodas O, Armengou Arxe A, Conde Martel A, Quesada Simón MA, et al. Hemoconcentration as a prognostic factor after hospital discharge in acute heart failure in the RICA registry. Rev Clin Esp. 2019;219:1---9, doi:10.1016/j.rce.2018.07.003. Bettencourt P, Friões F, Azevedo A, Dias P, Pimenta J, RochaGonc ¸alves F, et al. Prognostic information provided by serial
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measurements of brain natriuretic peptide in heart failure. Int J Cardiol. 2004;1:45---8. Metra M, Nodari S, Parrinello G, Specchia C, Brentana L, Rocca P, et al. Serial changes and independent prognostic value of NTproBNP and cardia troponin-T. Eur J Heart Fail. 2007;9:776---86. Nú˜ nez J, Llàcer P, Nú˜ nez E, Ventura S, Bonanad C, Bodí V, et al. Antigen carbohydrate 125 and creatinine on admission for prediction of renal function response following loop diuretic administration in acute heart failure. Int J Cardiol. 2014;174:516---23. De Vecchis R, Baldi C. Inferior vena cava and hemodynamic congestion. Res Cardiovasc Med. 2015;4:3, doi:10.5812/cardiovascmed.28913v2. Josa-Laorden C, Giménez-López I, Rubio-Gracia J, RuizLaiglesia F, Garcés-Horna V, Pérez-Calvo JI. Valor pronóstico de la medición del diámetro y colapso inspiratorio de la vena cava inferior en la insuficiencia cardiaca aguda. Rev Clin Esp. 2016;216:183---90, doi:10.1016/j.rce.2015.11.012. Buchholz AC, Bartok C, Schoeller DA. The validity of bioelectrical impedance models in clinical populations. Nutr Clin Pract. 2004;19:433---46. Santarelli S, Russo V, Lalle I, de Berardinis B, Vetrone F, Magrini L, et al. Prognostic value of decreased peripheral congestion
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detected by Bioelectrical Impedance Vector Analysis (BIVA) in patients hospitalized for acute heart failure: BIVA prognostic value in acute heart failure. Eur Heart J Acute Cardiovasc Care. 2017;6:339---47. Januzzi JL Jr, Chen-Tournoux AA, Christenson RH, Doros G, Hollander JE, Levy PD, et al. N terminal pro-B-type natriuretic peptide in the emergency department: the ICON-RELOADED study. J Am Coll Cardiol. 2018;71:1191---200. Liteplo AS, Marill KA, Villen T, Miller RM, Murray AF, Croft PE, et al. Emergency thoracic ultrasound in the differentiation of the etiology of shortness of breath (ETUDES): sonographic B-lines and N-terminal pro-brain-type natriuretic peptide in diagnosing congestive heart failure. Acad Emerg Med. 2009;16:201---10. O’Hanlon R, O’Shea P, Ledwidge M, O’Loughlin C, Lange S, Conlon C, et al. The biologic variability of B-type natriuretic peptide and N-terminal pro-B-type natriuretic peptide in stable heart failure patients. J Card Fail. 2007;13:50---5. Erratum in: J Card Fail. 2007 Mar;13:163. Platz E, Merz AA, Jhund PS, Vazir A, Campbell R, McMurray JJ. Dynamic changes and prognostic value of pulmonary congestion by lung ultrasound in acute and chronic heart failure: a systematic review. Eur J Heart Fail. 2017;19:1154---63.
ARTICLE IN PRESS
Rev Clin Esp. 2019;xxx(xx):xxx---xxx
Revista Clínica Española www.elsevier.es/rce
SPECIAL ARTICLE
Residual congestion and clinical intuition in decompensated heart failure夽 J.I. Pérez Calvo a,b,c,∗ , J. Rubio Gracia a,c , C. Josa Laorden a,c , J.L. Morales Rull d,e a
Servicio de Medicina Interna, Hospital Clínico Universitario Lozano Blesa, Zaragoza, Spain Facultad de Medicina, Universidad de Zaragoza, Zaragoza, Spain c Instituto de Investigación Sanitaria de Aragón, Zaragoza, Spain d Servicio de Medicina Interna, Hospital Universitario Arnau de Vilanova, Lleida, Spain e Instituto de Investigación Biomédica Dr. Pifarré, Lleida, Spain b
Received 3 January 2019; accepted 19 February 2019
KEYWORDS Heart failure; Congestion; Residual congestion; Diuretic therapy
PALABRAS CLAVE Insuficiencia cardiaca; Congestión; Congestión residual; Terapia diurética
Abstract Congestive symptoms are the key to recognizing decompensated heart failure, whose treatment is based on reducing the congestion until a clinical situation has been reached that allows the patient to be discharged to continue outpatient treatment. The important aspect is not the degree of congestion at admission but rather the congestion that persists after energetic diuretic therapy. The persistence of congestive signs following an apparently correct and effective therapy has been called residual congestion and is associated with a poor prognosis. The tools for determining this condition are still rudimentary. Methods therefore need to be developed that enable a more accurate assessment. © 2019 Elsevier Espa˜ na, S.L.U. and Sociedad Espa˜ nola de Medicina Interna (SEMI). All rights reserved.
La congestión residual y la intuición clínica en la insuficiencia cardiaca descompensada Resumen Los síntomas congestivos son la clave para reconocer las descompensaciones de la insuficiencia cardiaca. Su tratamiento se basa en la reducción de la congestión hasta alcanzar una situación clínica que permita el alta del paciente para continuar el tratamiento ambulatoriamente. Lo importante, no obstante, no es el grado de congestión al ingreso, sino la que persiste
夽
Please cite this article as: Pérez Calvo JI, Rubio Gracia J, Josa Laorden C, Morales Rull JL. La congestión residual y la intuición clínica en la insuficiencia cardiaca descompensada. Rev Clin Esp. 2019. https://doi.org/10.1016/j.rce.2019.02.004 ∗ Corresponding author. E-mail address: [email protected] (J.I. Pérez Calvo). 2254-8874/© 2019 Elsevier Espa˜ na, S.L.U. and Sociedad Espa˜ nola de Medicina Interna (SEMI). All rights reserved.
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J.I. Pérez Calvo et al. después de un tratamiento diurético enérgico. A la persistencia de signos congestivos después de un tratamiento aparentemente correcto y eficaz, se le ha denominado «congestión residual» y se asocia con mal pronóstico. Las herramientas para su estimación son todavía rudimentarias, por lo que deben desarrollarse métodos que permitan una valoración más precisa. © 2019 Elsevier Espa˜ na, S.L.U. y Sociedad Espa˜ nola de Medicina Interna (SEMI). Todos los derechos reservados.
Several matters relating to heart failure (HF) were discussed at the last congress held by the Spanish Society of Internal Medicine (SEMI, Sociedad Espa˜ nola de Medicina Interna). Remarkably, congestion has returned to the headlines and is raising clinical and scientific interest. The congestive signs that characterize HF syndrome were already recognized and described by Hippocrates in Ancient Greece in the 5th century B.C.1 There is no doubt that the pathophysiology on which Hippocratic medicine was based was not the current one, given that, at that time, the syndrome was explained by an imbalance between the different humors. Objectively speaking, however, was this pathophysiological concept mistaken? To be more precise, was this concept more mistaken than the one that we currently use? The return of congestion to the forefront of interest among the medical community is likely to reflect a lack of understanding of its pathophysiological mechanisms and consequences.2,3 Etymologically, the term ‘‘congestion’’ derives from the Latin word ‘‘con-gestus-tio’’, which refers to an excessive accumulation of fluid in certain parts of the body. Patients admitted to clinics due to a decompensated HF primarily exhibit symptoms and signs of congestion4 (dyspnea, orthopnea, edema, hepatomegaly, jugular vein engorgement, etc.). The symptoms of congestion in cases of HF are a result of extracellular fluid retention secondary to increased ventricular filling pressure. The congestive manifestations, together with those derived from the associated hypoperfusion, define the decompensated HF syndrome and enable its quick classification into groups requiring varied therapeutic measures.5 The fact that this ancient classification based on clinical aspects is included in the latest guidelines of the European Society of Cardiology6 indicates its importance.6 The detection of congestive symptoms and signs has limitations. On the one hand, its propedeutics requires training7 and the acquisition of possibly numerous techniques,8 thus implying a certain degree of variability in the actual data acquisition process. As is the case for many other diagnostic methods, clinical symptomatology is fairly unspecific, with a high negative predictive value but a low positive predictive value.4,9,10 In addition to clinical methods, the degree of congestion can be determined by ultrasonography (Table 1).4 Although this is still just speculation, it is likely that systemic congestion11,12 or that of the splanchnic territory,13 triggers inflammatory mechanisms14,15 that play a crucial role in the pathophysiology of decompensated heart failures.
Table 1 Performance of the various techniques for determining the degree of congestion. Parameter a
Clinical methods Inspiratory collapse of the inferior vena cava (<50%) E-wave velocity >50 cm/s E/e ratio > 12 Diffuse B-lines in the pulmonary ultrasound
Sensitivity
Specificity
13---94% 12%
10---90% 27%
92% 66% 86%
28% 55% 40%
Source: Mullens et al.4 a Assessment of the presence and degree of jugular distension, hepatomegaly, edema, dyspnea and crackles.
There is no doubt that congestive signs and symptoms are the herald of decompensated heart failures4 ; in fact, the fight against this congestion focuses the treatment on the patients’ hospital admission.4,16 Given that the persistence of congestive signs at discharge is associated with an increased risk of rehospitalization and mortality due to HF,17---20 complete decongestion could be the primary therapeutic aim in cases of decompensated HF. In light of the findings of recent studies,18,19 reaching a degree of decongestion that achieves symptomatic relief and allows patient discharge might still not be enough, given that there are substantial differences between decongestion that relieves symptoms and decongestion that improves the prognosis. The subtle degree of congestion that persists after the initial treatment, which is barely relevant from a symptomatologic point of view but has a negative effect on mortality, can be called ‘‘residual congestion’’. Using a simple score system based on the presence of dyspnea, orthopnea, asthenia, crackles, edema, and jugular venous distention (Table 2) applied to a cohort of 2061 patients with HF and a reduced left ventricular ejection fraction, Ambrosy18 proved that the higher the score, the higher the mortality and the number of readmissions due to HF during the follow-up. In a subsequent study, Rubio et al.19 proved that clinically inapparent residual congestion is very common at discharge and confirmed its poor prognosis using a simplified score (Table 2) that solely included the degree of orthopnea, jugular venous distention and edema measured in a cohort of 1572 patients with HF and a reduced left ventricular ejection fraction. In this study,19 only 23% of the
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Residual congestion and clinical intuition in decompensated heart failure Table 2
3
Congestion assessment using clinical scores. Ambrosy score18
Signs/symptoms
0
1
2
3
Dyspnea Orthopnea Asthenia Jugular venous distention (cm H2 O) Pulmonary crackles Leg edema
Absent Absent Absent <6 Absent Absent
Minimal Minimal Minimal 6---9 In base Mild
Frequent Frequent Frequent 10---15 <50% Moderate
Continuous Continuous Continuous >15 >50% Pronounced
0
1
2
3
Absent Absent <6
1-Pillow Mild 6---10
2-Pillow Moderate >10
>30 Pronounced ---
Rubio score19
Orthopnea Edema Jugular venous distention (cm H2 O)
patients showed no signs of congestion at discharge, while 48% and 29% had mild to severe symptoms of congestion that were associated with an increased rate of re-hospitalizations and mortality, respectively. It is clear that the challenge in the immediate future will be to detect and combat residual congestion that resists the action of intensive diuretic therapy immediately on admission. To meet this challenge effectively and safely, we must first recognize it. These clinical scores can most likely be supplemented with the patients’ diuretic response20 ; biochemical parameters, such as their hematocrit21 ; and variations in natriuretic peptide (NP)22,23 concentration or carbohydrate antigen 125 (CA-125).24 The usefulness and performance of ultrasonography25,26 procedures and of other noninvasive methods, such as bioelectrical impedance analysis, must also be analyzed.27,28 There is little evidence about the role of congestion in the decision-making process at discharge and the perception of residual congestion, which is an emerging situation in daily clinical practice. To further delve into these two aspects, we prepared an anonymous 13-item survey that was distributed by e-mail to the members of the Heart Failure Group (Grupo de Insuficiencia Cardíaca, GIC) of SEMI, which was accessible from the 22nd of August to the 23rd of September 2018. The survey focused on determining how congestion was assessed and the importance that the respondents gave to the method used at two key points of the condition’s progress: (1) on completion of an intensive diuretic treatment; i.e., when the congestive symptoms that motivated the admission are considered to be resolved and (2) when the decision to proceed with the discharge is made; i.e., when the congestion is considered to no longer exist or to be safely treatable on an outpatient basis (supplementary material). A total of 253 specialists, most of whom worked in internal medicine departments (247), completed the survey; their answers can be consulted in the GIC blog (http://cardioclinico.com) and the supplementary material. The respondents based their identification of cases of congestion and the determination of its degree on its characteristic symptoms and signs (dyspnea, orthopnea, jugular venous distention and edema; over 50% for each), the NP
concentration (43%), the ultrasound findings of the inferior vena cava (45%), the ultrasound findings of the lungs (43%) and the CA-125 levels (16%). A total of 247 respondents selected the answer concerning the early response of the congestion that allows for de-escalating the diuretic treatment and replacing the intravenous route with an oral one. Most of the respondents resorted once again to the assessment of the patients’ clinical symptoms (improved dyspnea [80%], reduced edema [78%] or weight [63%]) and a stable dose of oral diuretics (62%). Eighty-six percent of the participants reported that they based their assessment on diuretic efficacy, although this parameter was measured in several ways and was related to a reduction of the signs and symptoms of congestion in 86% of cases, followed by the NP concentration (24%), the serial lung ultrasound findings (8%) and those of an ultrasound of the inferior vena cava (5%). The respondents were openly asked whether ‘‘residual congestion’’ suggested anything to them and, if so, how they interpreted the term. Of the 247 respondents, 185 (75%) reported being aware this clinical situation, and their perception, although variable, was reasonably in line with what could be expected from a clinical point of view (individualized responses can be consulted in the blog). Discharge was primarily prompted by a reduction of the edema (72%), a functional class improvement (63%) and a stable dose of oral diuretics (62%), once again, based on eminently clinical criteria. Remarkably, most decisions made in relation to the assessment, monitoring and treatment of congestion in cases of decompensated heart failures are based on clinical perception, i.e. on symptomatologic aspects. Nevertheless, this is also logical if we consider that there are no quantitative tools available for its correct measurement and that awareness of the importance of congestion persisting in a latent state despite treatment is very recent. We should also note the use of complementary methods, such as assessing the NP concentration and the use of lung ultrasonography to evaluate the clinical progress of congestion. Although both methods have clearly been shown to be useful in diagnosing HF, especially in cases
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4 of decompensated heart failure,29,30 there is insufficient evidence of their reliability for serial use (e.g., in daily clinical practice) to determine the degree of congestion31,32 ; therefore, their results should be interpreted with caution for decision making. This manuscript has methodological limitations. First, this study was based on an ad hoc survey. Second, despite being significant, the number of responses accounted for slightly less than half of the survey recipients. However, the purpose of the study was to analyze the subjective perception of internists accustomed to treating patients with decompensated heart failure, particularly regarding residual congestion, which has been understudied to date and therefore lacks strong evidence. The results of this survey prove that clinical intuition, an aspect that would barely reach a C recommendation score in the context of evidencebased medicine, is a powerful tool in daily clinical practice. This intuition involves the ability to detect a real problem for which there are still no answers and to reasonably face it following a consensual approach. The task before us is to determine the exact threshold of residual congestion that can provide relevant prognostic information in clinical practice, a threshold to be set between its detection using accessible but not very sensitive clinical methods and a sensitive but invasive heart catheterization. We must tackle this task cooperatively without delay, given that the use of intuition and possibilities are not alien to the HF group.
J.I. Pérez Calvo et al.
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Conflicts of interest The authors declare that they have no conflicts of interest with this article.
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Acknowledgments
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The authors would like to extend their gratitude to the members of the Working Group on Heart Failure and Atrial Fibrillation (Grupo de Trabajo de Insuficiencia Cardiaca y Fibrilación Auricular) of SEMI, particularly to those who selflessly completed the survey.
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Appendix A. Supplementary data Supplementary data associated with this article can be found, in the online version, at doi:10.1016/ j.rceng.2019.02.013.
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