» Articles » Congestion And Diuretic Resistance In Acute Or Worsening Heart Failure Congestion And Diuretic Resistance In Acute Or Worsening Heart Failure Ingibjörg Kristjánsdóttir Tonje Thorvaldsen Lars H Lund Login or register to view PDF. Order reprints Abstract Hospitalisation for acute heart failure (AHF) is associated with high mortality and high rehospitalisation rates. In the absence of evidence-based therapy, treatment is aimed at stabilisation and symptom relief. The majority of AHF patients have signs and symptoms of fluid overload, and, therefore, decongestion is the number one treatment goal. Diuretics are the cornerstone of therapy in AHF, but the treatment effect is challenged by diuretic resistance and poor diuretic response throughout the spectrum of chronic to worsening to acute to post-worsening HF. Adequate dosing and monitoring and evaluation of diuretic effect are important for treatment success. Residual congestion at discharge is a strong predictor of worse outcomes. Therefore, achieving euvolaemia is crucial despite transient worsening renal function. Keywords Diuretic resistance, acute heart failure, worsening heart failure, congestion, worsening renal failure, prognosis Disclosure TT has received speaker’s fees from Orionpharma, Bayer, and Novartis. LHL has received research grants to author’s institution, speaker’s and/or consulting fees from AstraZeneca, Novartis, Bayer, Vifor Pharma, Relypsa, Abbott, Sanofi, Merck, and Pharmacosmos. IK has no conflicts of interest to declare. Correspondence Tonje Thorvaldsen, Heart and Vascular Theme, Section for Heart Failure, Karolinska University Hospital, Heart Failure Research Group, Karolinska Institutet, 17176 Stockholm, Sweden. E: [email protected] Received date 06 December 2020 Accepted date 07 May 2020 Citation Cardiac Failure Review 2020;6:e25. DOI http://sci-hub.tw/10.15420/cfr.2019.18 Open access This work is open access under the CC-BY-NC 4.0 License which allows users to copy, redistribute and make derivative works for non-commercial purposes, provided the original work is cited correctly. From Acute Heart Failure Towards Worsening or De Novo Heart Failure The natural history of heart failure (HF) is characterised by disease progression and episodes of worsening HF and acute decompensation requiring outpatient treatment intensification, emergency department or in-hospital care. Acute HF (AHF), also known as acute decompensated HF, is defined as a progressive and sometimes rapid onset or worsening of symptoms and/or signs of HF.1 AHF may present as new onset HF (de novo HF) or worsening chronic HF (WHF), where WHF may be defined as worsening signs and symptoms requiring additional therapy. WHF represent 80–90% of HF hospitalisations.2 Compared with WHF, de novo HF patients have a different clinical profile. Generally, the patients are younger, with less previous MI and less global comorbidity burden.3 Accordingly, mortality rates are lower and the potential for improvement and possibly recovery is greater in de novo than in chronic HF (CHF).4,5 However, hospitalisation for de novo HF is still considered a critical event in the trajectory of the disease, given that mortality rates are tripled compared with patients who are never hospitalised.6 AHF is increasingly recognised as an event rather than a distinct syndrome, and this event is heterogeneous with variable onset and presentation, may increasingly be managed in outpatient day clinics or emergency departments, and may be more appropriately termed WHF. In patients with WHF, the profile of haemodynamic congestion is similar regardless of reduced (HFrEF) or preserved ejection fraction (HFpEF), but patients with HFpEF as compared with HFrEF appear to have more interstitial than intravascular fluid overload, possibly due to reduced venous capacitance and lower arterial compliance.7–9 Patients hospitalised for HF are at high risk for adverse outcomes in hospital, but also after discharge.10 In the European Heart Failure Long-term Registry (ESC-HF-LT) 1-year mortality in AHF and in chronic stable HF was 23.6% and 6.4%, respectively. Rates of death or hospitalisation for HF were 36% in AHF patients and 14.5% in CHF patients.11 Despite intensive research, no treatment has yet been shown to reduce mortality or risk of rehospitalisation in AHF.12 However, with optimal therapy it has been suggested that early rehospitalisation may be preventable in up to 70% of cases.13 Congestion Regardless of HF aetiology, HF patients can be divided into four different profiles depending on clinical status. Patients may be described as either wet or dry, depending on their congestion status, and as warm or cold, depending on their perfusion status, with the combination of wet and cold (congested and hypoperfused) having the worst prognosis.14 Clinical signs of hypoperfusion include cold, sweaty extremities, narrow pulse pressure, dizziness, oliguria and mental confusion. Typical clinical signs of congestion include increased jugularis venous pressure, orthopnoea, pulmonary rales, peripheral oedema, third heart sound and hepatomegaly. The terms congestion and fluid overload are often used interchangeably, however haemodynamic congestion reflects increased cardiac filling pressures, but does not necessarily equal volume overload in the extracellular compartments, particularly in the acute setting. Over time, if haemodynamic congestion continues to progress, clinical signs of congestion may evolve. In contrast, in acute pulmonary oedema, pulmonary congestion is predominantly due to an acute increase in afterload with a relative volume redistribution rather than an absolute fluid accumulation.15 Overall, congestion and fluid overload (the wet haemodynamic profile) is the most common profile in patients presenting with AHF. Less than 10% of patients present with signs of hypoperfusion and low blood pressure (the cold haemodynamic profile).16,17 Even if patients have some degree of pulmonary congestion, relatively few present with fulminant pulmonary oedema18,19 and the majority of patients instead have gradual onset of backward failure, fluid retention, congestion and often (but not always) weight gain.2
