Anaesth Crit Care Pain Med 44 (2025) 1–12

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Anaesthesia Critical Care & Pain Medicine

journal homepage: www.elsevier.com

Review article

Therapeutic novelties in acute heart failure and practical perspectives

Benjamin Deniau a,b,c,d,e,*, Ayu Asakage f, Koji Takagi g, Etienne Gayat a,b,c,d,
Alexandre Mebazaa a,b,c,d,e, Amina Rakisheva h
a
Department of Anesthesia, Burn and Critical Care, University Hospitals Saint-Louis - Lariboisière, AP-HP, Paris, France
b
UMR-S 942, INSERM, MASCOT, Paris University, Paris, France
c
Paris Cité University, Paris, France
d
FHU PROMICE, Paris, France
e
INI CRCT Network, Nancy, France
f
Department of Emergency Medicine and Critical Care, Center Hospital of the National Center for Global Health and Medicine, Tokyo, Japan
g
Momentum Research Inc, Durham, NC, United States
h
City Cardiological Center, Almaty, Kazakhstan

A R T I C L E I N F O A B S T R A C T

Article history: Acute Heart Failure (AHF) is a leading cause of death and represents the most frequent cause of
Available online 21 January 2025 unplanned hospital admission in patients older than 65 years. Since the past decade, several randomized
clinical trials have highlighted the importance and pivotal role of certain therapeutics, including
Keywords: decongestion by the combination of loop diuretics, the need for rapid goal-directed medical therapies
Acute heart failure implementation before discharge, risk stratification, and early follow-up after discharge therapies.
Decongestion therapy Cardiogenic shock, defined as sustained hypotension with tissue hypoperfusion due to low cardiac
Goal directed medical therapy
output and congestion, is the most severe form of AHF and mainly occurs after acute myocardial
ESC guidelines
AHA/ACC/HFSA guidelines
infarction, which can progress to multiple organ failure. Although its prevalence is relatively low,
cardiogenic shock complicates 12% of acute myocardial infarction. After a brief summary of the
epidemiology of AHF and cardiogenic shock, followed by key pathophysiological points, we detailed
current treatments in AHF and cardiogenic shock what every anaesthesiologist and intensivist needs to
know, based on the latest guidelines and randomized clinical trials published in recent years.
C 2025 The Author(s). Published by Elsevier Masson SAS on behalf of Société Française d’Anesthésie et de

Réanimation (SFAR). This is an open access article under the CC BY license (http://creativecommons.org/
licenses/by/4.0/).

Introduction angiotensin system inhibitors (RASi) and mineralocorticoids

receptor antagonists (MRAs)), risk stratification and early fol-
Acute Heart Failure (AHF) is a leading cause of death and low-up after discharge therapies. To date, the major role of
represents the most frequent cause of unplanned hospital sodium-glucose co-transporter 2 inhibitors (SGLT2i) is no longer
admission in patients older than 65 years [1–3]. As congestion debatable and must be a part of the therapeutic arsenal of AHF
represents the pathophysiological cornerstone of AHF, deconges- patients. Cardiogenic shock (CS), the most severe form of AHF,
tive therapies initiated before or on admission play a central role in frequently complicates AHF. Cardiogenic shock is defined as a low-
the initial management of AHF patients which should be followed, cardiac output state due to cardiac dysfunction with low end-
before discharge, by rapid implementation of guideline-directed organ perfusion. Although aetiologies of CS are various, patho-
oral medical therapies (GDMT) for HF [4]. Since the past decade, physiology comprises overlapping components, notably decreased
several randomised clinical trials have highlighted the importance cardiac output, central haemodynamic alteration, microcirculatory
and pivotal role of certain therapeutics, including decongestion by dysfunction and systemic inflammatory response syndrome. The
the combination of loop diuretics, the need for rapid GDMT prognosis of CS was greatly improved by the routine use of early
implementation before discharge (i.e., beta-blockers (BBs), renin- revascularisation and the improvement of mechanical devices.
After a brief epidemiological summary of AHF, we will detail
congestion assessment and current treatments, from the first
* Corresponding author.
hours to the days before discharge, based on the latest guidelines
E-mail address: benjamin.deniau@aphp.fr (B. Deniau).

https://doi.org/10.1016/j.accpm.2025.101481
2352-5568/ C 2025 The Author(s). Published by Elsevier Masson SAS on behalf of Société Française d’Anesthésie et de Réanimation (SFAR). This is an open access article under
the CC BY license (http://creativecommons.org/licenses/by/4.0/).
B. Deniau, A. Asakage, K. Takagi et al. Anaesth Crit Care Pain Med 44 (2025) 1–12

and randomised clinical trials published in recent years. Finally, we pressures ( = pulmonary fluid accumulation), leads to impaired
will develop a definition, pathophysiology and current treatments organ perfusion, notably kidneys, liver, lungs and gut [15]. More-
of CS that every anaesthesiologist and intensivist needs to know on over, right ventricle dysfunction worsens the decrease of venous
the subject. return and leads to aggravating systemic congestion. The occur-
rence of organ dysfunction during AHF is associated with poor
Definition, epidemiology and prevalence of acute heart failure outcomes [16]. Thus, decongestive therapy in AHF patients aims to
relieve congestion and achieve a state of euvolemia, supporting the
Defined as the new onset or recurrence of signs of heart failure central role of diuretics in the therapeutic management of AHF
(HF), diagnosis of acute heart failure (AHF) is based on the presence patients. Assessment of congestion is central to correctly to
of dyspnoea, fatigue, pulmonary rales and distended jugular veins determine optimal diuretic strategy.
at physical examination. The presentation of AHF can differ
according to the patient’s medical history. The first situation, the Assessment of congestion
more frequent, is the acutely decompensated HF (with symptoms
of congestion) in patients with a known HF history. The second A universally accepted diagnostic algorithm for quantification
situation, the de novo AHF, corresponds to the occurrence of of congestion and identification of precise therapeutic targets is
symptoms of congestion in patients without a history of AHF lacking. Unresolved congestion, occurring in 40% of admitted AHF
[3,5]. Acute HF is a major and global public health problem, patients at hospital discharge, is an independent predictor of poor
associated with high morbidity and mortality [1,2,6]. One million outcomes [17]. However, congestion may be difficult to detect and
patients in Europe and the United States of America are admitted assess notably when signs are mild [15]. Several tools are available
with the diagnosis of AHF each year [7,8]. In a recent prospective to assess congestion in AHF patients in the acute phase.
analysis involving 18 553 AHF patients, Tromp et al. found that the
median age of AHF patients was 67 [IQR 57–77] years, with a  Signs and symptoms of congestion
minority of women (39%) [1]. In-hospital mortality of AHF is
estimated to be 2.5%, reaches 10% within 60 to 90 days after Although physical signs and symptoms are frequent in AHF
hospital discharge and increases to 25–30% in the year following patients, only moderate to high levels of congestion can be
discharge [9–13]. To note, the in-hospital mortality rate was higher detected by physical assessment. Clinical findings include dys-
in AHF patients admitted for respiratory infection as a precipitant pnoea, orthopnoea, systemic oedema, jugular veins distension and
factor (over 4%) [1]. We observed a steady decrease in mortality third heart sound [15]. Unfortunately, signs and symptoms of
related to AHF over the last three decades while readmissions congestion are late manifestations of increased cardiac filling
remain unacceptably high (10–30% at 90 days and 46% at one year) pressures [18].
[14].
 Clinical congestion score
Congestion: the pathophysiological cornerstone of AHF
Grading congestion scores could be an interesting tool for daily
congestion assessment (including clinic, biological and dynamic
The pathophysiology of AHF is complex and not completely
manoeuvres items) but needs to be validated before its recom-
resolved, but could be summarized as a vicious circle leading to
mendation [19]. To date, no scores are daily used or clinical
pulmonary and systemic venous congestion. Thus, left ventricular
assessment of congestion in AHF patients. These scores are often
dysfunction leads to decreased blood pressure with impaired
used as prognostic rather than diagnostic tools and their clinical
tissue oxygen delivery and neurohormonal activation resulting in
utility needs to be determined.
systemic venous congestion (Fig. 1). Systemic venous congestion,
by decreasing venous return to right cavities ( = systemic
 Congestion biomarkers
interstitial fluid accumulation) and by increasing left filling

Fig. 1. Pathophysiology of acute heart failure. BP: blood pressure, LV: left ventricle, RV: right ventricle.

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B. Deniau, A. Asakage, K. Takagi et al. Anaesth Crit Care Pain Med 44 (2025) 1–12

patients, with the provision of standardized transitional care, Lee

Natriuretic peptides, such as B-type natriuretic peptide (BNP), et al. observed a reduction of 12% in the risk of death from any
N-terminal fragment pro-B-type natriuretic peptide (NT-proBNP) cause or hospitalization for cardiovascular causes within 30 days
and atrial natriuretic peptide, are interesting candidates to assess after AHF episode [34]. This risk remained lower at 20 months after
volume status and guide decongestive therapies but fluid overload the AHF episode. Implementation of these tools may provide a
may not the sole cause of increased levels of these biomarkers pathway for early and safe discharge from the hospital or ED.
[20,21]. Interestingly, a decrease greater than 30% at day 5 of However, these results need to be confirmed by large international
natriuretic peptides in AHF patients after fluid removal with a cohorts before recommendations in guidelines.
discharge value < 1500 pg/mL are good prognostic markers
[22]. Due to the large use of sacubitril/valsartan in HF and its  Decongestive therapy and diuretics
interpretation, NT-proBNP is likely to become the standard
natriuretic peptide to use in AHF patients. Finally, apart from As congestion is the pathophysiological cornerstone of AHF,
natriuretic peptides, renal (in case of worsening renal function) decongestive therapies are recommended to treat fluid overload
and liver function markers (cholestatic liver injury due to and quickly achieve optimal fluid status [6,35]. The latest
congestion) are interesting markers of congestion and can drive guidelines recommend that AHF patients with evidence of
an optimal decongestive therapy. significant fluid overload should be treated with intravenous loop
diuretics to improve symptoms and reduce morbidity [35]. More-
 Imaging tools over, therapy with diuretics should be titrated to resolve clinical
evidence of congestion to reduce symptoms and rehospitalizations
In AHF patients, chest X-ray signs of AHF include peri-bronchial [35].
cuffing, cardiomegaly, pulmonary venous congestion and pleural
effusion [15]. Transthoracic echocardiography is considered the o Loops diuretics and diuretics combination
gold standard for the evaluation of volume status and left
ventricular filling pressures [23], set on the transmitral flow and Two major and recent clinical trials on decongestive therapies
diastolic tissue wave (E/e’). Lung ultrasound by using the analysis recently published provide important insights on decongestive
of B-line artefacts [24–26], can be considered for the diagnosis of therapy in AHF patients. Firstly, a recent, multicentre, randomized,
pulmonary oedema in AHF patients with a good sensitivity (94%) double-blind, clinical trial assessing the diuretic effects of
and specificity (92%) [27]. Recent studies found that change in lung acetazolamide in decompensated HF showed that the association
ultrasound congestion scoring in AHF congestive patients was of intravenous acetazolamide was associated with a greater
associated with readmission-free survival [28]. Some authors incidence of successful decongestion within 3 days after initiation
proposed inferior vena cava diameter and per cent change to guide of decongestive therapy [36,37]. However, the authors did not find
decongestion in AHF patients. Data are inconsistent and need to be a reduction in death from any cause in the group of AHF patients
confirmed [29]. treated by the combination of diuretics [36]. Secondly, a
multicentre placebo-controlled randomized trial showed the
beneficial effect of addition of hydrochlorothiazide to loop
Therapeutic management and treatments of AHF in the first diuretics in AHF patients on weight loss, with no changes in
hours patient-reported dyspnoea 72 hours after initiation of deconges-
tive therapy [38]. However, the authors did not find any difference
in mortality and rehospitalization rates between groups [38]. Due
to the lack of impact on clinical outcomes, this combination was
 Identification of etiology and precipitant factor not recommended in the latest guidelines update [30]. Thus,
further data are needed.
Rapid diagnosis and identification of precipitant(s) factor(s) are Guidelines recommend the use of intravenous loop diuretics in
central in the first hours of AHF. Aetiologies of AHF are various and AHF patients [6]. Concerning the time-to-intravenous loop
determine the patient’s management [30]: acute coronary diuretics, data suggest that delaying the administration of
syndrome, hypertensive emergency, rapid arrhythmias or severe intravenous furosemide could increase mortality with inconclu-
bradycardia/conduction disturbance, acute mechanical causes (e.g. sive results. Ouwerkek et al. found no association between longer
pulmonary embolism), infection (e.g. myocarditis, endocarditis) time-to-diuretics and in-hospital mortality but found an associa-
and tamponade. All the aetiologies are regrouped under the tion with 30-day mortality [39]. Further studies are needed to
CHAMPIT acronym [6]. Thus, specific etiological therapies should confirm these results. Concerning the mode of injection of loop
be implemented as early as possible. Recent clinical trials and diuretics, a recent clinical trial showed the absence of difference in
meta-analyses, from the acute to the post-discharge phase, have improved global assessment of dyspnoea between continuous
redefined the objectives and the management of AHF patients [30]. infusion versus bolus injection in AHF patients [40]. To note, in the
case of bolus injections, a 6-h interval is needed between two doses
 Risk stratification and patient placement to maximize the time the diuretic tubular concentration is
adequate to trigger a natriuretic response [23].
Before admission in a specialized department (critical care or
cardiology), AHF patients are often cared for in the emergency o Evaluation of diuretic response and management of diuretic
department (ED), where the decision to admit the patient or resistance
discharge at home is often based on clinical judgment. Unfortu-
nately, the risk of discharge at home of a high-risk AHF patient is Weight loss is a surrogate measure of diuretic response, but
important, with the possibility of serious adverse events or death remains insensitive and accurate [41,42]. According to the mode of
[31]. To improve clinical decisions, risk stratification is a tool that action of certain diuretics, natriuresis measurements could be an
could help ED physicians [31]. Recently, by combining a validated interesting marker to assess the response of decongestion therapy
point-of-care tool for risk stratification [31–33] in the ED to but also a potential treatment to target. Studies found an
support clinicians’ decisions about admissions or discharge of AHF association between insufficient natriuresis and increased risk of

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mortality and rehospitalization [43,44]. The diuretic response Non-invasive ventilation (NIV) is considered a major point of
should be quickly assessed after the start of decongestive therapy, the therapeutic management of AHF patients, commonly used
by performing a spot urine sodium content measurement after 2– since the 1980s. By applying positive pressure by three modalities
6 h and/or by measuring the hourly urine output. An objective of (continuous positive airway pressure (CPAP), pressure support
urine sodium content >50–70 mEq/L at 2 h and/or by a urine ventilation (NIPSV) or high-flow nasal cannula (HFNC)) in
output >100–150 mL/h during the first 6 hours is considered a conscious AHF patients, NIV reduces the need for endotracheal
satisfactory diuretic response [6,41]. In case of insufficient diuretic intubation and decreases the risk of ventilator-associated pneu-
response, dose of loop diuretics should be doubled. If the diuretic monia [56]. The latest ESC guidelines recommended NIV as a Class
response remains inadequate despite optimal doses, association IIa recommendation with a level of evidence B in AHF patients with
with alternative tubular sites of action may be considered (e.g. respiratory distress (defined as respiratory rate > 25/min and/or
acetazolamide or thiazides) [36]. SpO2 < 90%) [6]. Although randomized clinical trials and meta-
analyses highlighted the benefits of NIV in AHF patients when
 Sodium-glucose co-transporter 2 inhibitors (SGLT2i) compared to conventional oxygen therapy, data on mortality and
long-term outcomes are inconclusive. Large randomized clinical
Initially used for type 2 diabetes mellitus, studies highlighted the trials are needed to confirm these results. In addition, the delay of
pivotal of SGLT2i in chronic HF patients’ prognosis improvement the beginning of the NIV remains an important question, because
[30,35,45–47]. Sodium-glucose co-transporter 2 inhibitors act by some studies found that an early application of NIV in AHF patients
inhibiting the SGLT-2 proteins expressed in the renal proximal was associated with a reduced requirement for mechanical
tubules to reduce the reabsorption of filtered glucose and promote ventilation [57–59]. Finally, NIV was historically contraindicated
urinary glucose excretion. However, exact mechanisms remain in acute pulmonary oedema in the setting of acute myocardial
elusive notably in HF. In 2022, Voors et al. authors found that the infarction after the results of two studies suggested that NIPSV
treatment of clinically stable AHF patients by empagliflozin 10 mg could precipitate acute myocardial infarction [60,61]. These results
by day until day 90 was associated with a better clinical benefit at have never been confirmed by other studies. Thus, because of the
90 days when compared to placebo [48]. The efficacy of the absence of a relationship between NIV and the risk of acute
treatment was independent of left ventricular ejection fraction and myocardial infarction, NIV is a safe technique to consider in this
diabetes status, with a rate of events similar between the two arms type of patient. However, further studies are needed in this
[48]. Moreover, Biegus et al. found that treatment by empagliflozin indication of NIV. A close clinical and biological monitoring of AHF
in AHF patients resulted in an early, effective and sustained patients when NIV is used is needed to ensure the success of the
decongestion associated with clinical benefit at day 90 [49]. Al- technique. Respiratory rate, oxygen saturation, pH and PaCO2 are
though these treatments are promising in AHF, the efficacy of the most common and easy parameters to monitor in patients
SGLT2i needs to be confirmed by large randomized clinical trials. under NIV. One of the keys to the success of NIV is the optimal
synchronisation between the patient’s breathing and the ventilator
 Vasodilators [62–64]. The most common cause of asynchrony is air leakage,
which can be prevented by an optimal adjustment of the facial
Results on the benefits of intravenous infusion of vasodilators on mask, a shortening inspiration time, a change in pressure support
long-term outcomes are inconclusive despite the clinical evidence and modification of inspiratory and expiratory triggers.
of hemodynamic and clinical improvement. In a recent clinical trial In AHF patients, NIV must be continued until a satisfactory
including older patients admitted to the emergency department recovery has been achieved and needs to be stopped in case of the
(ED) for AHF, Freund et al. the use of intravenous nitrate boluses and presence of criteria of mechanical ventilation (e.g., cardiac or
management of precipitating factors did not result in a reduced respiratory arrest, worsening of altered mental status, progressive
number of days alive at 30 days compared to the usual care [50]. By worsening of pH, PaCO2, PaO2, signs of fatigue, need to protect the
treating AHF patients with intensive vasodilation compared to airway, persistent haemodynamic instability, agitation and/or
usual care, recent findings suggest no benefit in all-cause mortality intolerance to NIV) or in case of contraindications [65]. Weaning of
and AHF rehospitalization at 180 days of this strategy [51]. Recent NIV in AHF patients is ensured by a decrease of FiO2, positive end-
ESC guidelines recommend the use of intravenous vasodilators (e.g. expiratory pressure and ventilation setting. The use of high flow
nitroglycerine 1–2 mg boluses) in case of high systolic blood nasal cannula must be considered in case of predicted difficulty of
pressure (systolic blood pressure > 110 mmHg), started at low NIV weaning [66,67]. However, data are needed to confirm the
doses and up-titrated to achieve clinical improvement and blood benefits of HFNC in NIV weaning in AHF patients.
pressure control (Class IIb, Level B) [6].
o Morphine and anxiolytic treatments
 Iron supplementation therapies
Sedative treatments such as morphine and short half-life
Iron deficiency affects more than 50% of AHF patients and is benzodiazepines (e.g. midazolam) could have potential indications
associated with poor outcomes conferring an increased risk of in AHF to reduce anxiety and dyspnoea. However, clinical trials
rehospitalizations and death [52,53]. Therefore, diagnosis and failed to show the benefits of sedative treatments on the mortality
treatment of iron deficiency with ferric carboxymaltose or ferric of patients admitted for AHF in the ED [68]. Moreover, serious
derisomaltose after an AHF episode are highly recommended by adverse events were more common in the morphine group,
the latest guidelines [6,30]. Two major randomized clinical trials confirming the results of previous studies [69–71]. Further studies
were recently published on the subject and recommend the use of are needed but routine use of opiates in AHF patients is currently
intravenous iron treatment to reduce the risk of hospital admission not recommended [6].
for HF after an episode of AHF [54,55].
Oral long-lasting therapies to implement before discharge
 Other measures
o Non-invasive ventilation

 Goal directed medical therapies

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B. Deniau, A. Asakage, K. Takagi et al. Anaesth Crit Care Pain Med 44 (2025) 1–12

Acute heart failure and anesthetic management

The latest North American and European guidelines for chronic
HF recommended that GDMT for HF includes BBs, angiotensin- Every year, up to 5% of the worldwide population requires
converting enzyme inhibitors (ACEi) and MRAs for HFrEF and major surgery [78], and up to half of adults > 45 years requiring
SGLT2i for all HF patients regardless of LVEF [72]. Research after non-cardiac (NC) major surgery present at least 2 or more
discharge of AHF patients has recently progressed during recent cardiovascular risk factors, testifying of the growing prevalence
years. Acute HF is characterised by a significant neurohormonal of cardiac peri-operative morbidity. Decompensated or untreated
inflammatory activation strongly associated with increased HF is associated with a high peri-operative risk, including peri-
adverse outcomes, whose extension and persistence is called the operative myocardial infarction/injury, stent thrombosis, AHF,
‘‘vulnerable’’ period, persisting 3 to 6 months after AHF episode relevant arrhythmias, stroke and death [79]. The surgical
[73,74]. This period is a high risk of serious adverse events, procedure leads to increased catecholamines release as stress
rehospitalisation and death [74]. Interestingly, recent studies response, neuro-endocrine and sympathovagal imbalance. More-
found that post-discharge intervention implemented before over, vascular resistances could be modified during surgery due to
discharge (i.e., SGLT2i, angiotensin receptor-neprilysin inhibitors variations in body core temperature, blood loss and fluid shifts
(ARNi), ACEi, angiotensin receptors blockers (ARBs), BBs and decompensating an already precarious state. Anaesthetic manage-
MRAs) and prolonged during the vulnerable phase, are corners- ment of HF patients depends on 1/ the degree of HF, 2/ the cause of
tones to improving AHF patients’ outcomes. Recently, major cardiomyopathy and 3/ the surgical procedure. Of course, in the
randomised clinical trials focused on GDMT before and after case of AHF, and as far as possible, surgical procedures should be
discharge AHF patients were published [4,48,75–77]. postponed for the purpose of medical therapy, modification of risk
To date, based on the latest European guidelines for the factors and cardiac investigations if needed [80]. A multidisciplin-
diagnosis and treatment of AHF, an intensive strategy of initiation ary approach, including anaesthesiologists/intensivists, surgeons
and rapid up-titration of GDMT before discharge and during and cardiologists is always requested.
frequent and careful follow-up visits in the first 6 weeks following
HF hospitalization is recommended (Class I, Level B) to reduce the Clinical risk assessment
risk of HF rehospitalization or death [30]. Latest guidelines
recommend intravenous iron supplementation in symptomatic Perioperative cardiovascular morbidity and mortality are
patients with HF and iron deficiency (Class I, Level A) and determined by patient (age, cardiovascular risk factors and
intravenous ferric carboxymaltose or ferric carbomaltose should comorbidities) and surgical procedure risk factors. Initial patient
be considered in symptomatic HF patients with iron deficiency to cardiovascular assessment should evaluate accurate history,
reduce the risk of HF hospitalization (Class IIa, Level A). physical examination and standard laboratory tests (e.g. haemo-
Fig. 2 summarizes therapeutics measures for AHF based on the globin and renal function). An electrocardiogram and measure of
latest randomized clinical trials and guidelines. cardiovascular biomarkers (e.g. cardiac troponin and/or NT-

Fig. 2. Therapeutics measures and treatments in acute heart failure based on the latest major clinical trials and recent ESC AHA/ACC/HFSA guidelines. AHF: acute heart failure,
ACEi: angiotensin-converting enzyme inhibitors, ARB: antagonist receptor blocker, ARNi: angiotensin receptor neprilysin inhibitors, BB: beta-blocker, CPAP: continuous
positive airway pressure, eGFR: estimated glomerular filtration rate, EI: endotracheal intubation, GDMT: goal-directed medical therapies, IV: intravenous, K+: kaliemia, MRA:
mineralocorticoid receptor antagonist, MV: mechanical ventilation, NIPSV: non-invasive pressure support ventilation, NT-proBNP: N terminal pro brain natriuretic peptide,
SGLT2i: sodium-glucose co-transporter 2 inhibitor.

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proBNP) depends on the patient-related and surgery-related risk is postponed, the question of continuation and discontinuation of
(Class I, Level B). In non-emergency situation, and in case of poor HF medications should be answered. Table 1 summarises the latest
functional capacity and/or high NT-proBNP/BNP levels detected recommendations for pharmacological cardiovascular treatments
before high-risk NC surgery, the latest ESC guidelines recommend in AHF patients before NC surgery. Antiplatelets and oral
the realisation of transthoracic echocardiography (Class I, Level B) anticoagulants are not included as they are subject to specific
[79]. recommendations.
The surgical-related risk is determined by the urgency, and the
type (ESC guidelines classified surgery into three groups: low Perioperative management and anaesthesia
surgical risk (<1%), intermediate surgical risk (1–5%) and high
surgical risk (>5%)) and the duration of the procedure. Acute Routine use of intra-operative monitoring improves the safety
procedures are associated with higher cardiovascular peri-opera- of surgical outcomes without data available on prognosis
tive risk, reason why the optimal timing of NC surgery should be as relevance. Indeed, no strong evidence on invasive arterial and
multidisciplinary and discussed as possible. Concerning the type of central venous monitoring and outcomes in AHF patients is
surgical approach, new techniques (laparoscopy, vascular and available. However, invasive monitoring helps anesthesiologists to
endovascular procedures and video-assisted NC surgery) have anticipate or limit hemodynamic changes. Minimal cardiovascular
been introduced to replace open surgery and to reduce overall risk. monitoring should include blood pressure (non-invasive or
These techniques cause less tissue trauma and intestinal paralysis invasive), electrocardiogram and pulse oximetry [79]. Transtho-
and are associated with reduced pain, better postoperative racic echocardiography is used in case of decompensated or AHF in
pulmonary function and diminished fluid shifts [79]. However, major surgery to monitor cardiac output or during cardiac surgery.
precautions with these procedures should be taken in decompen- The decision to implement cardiovascular monitoring depends on
sated or acute HF patients. Indeed, pneumoperitoneum induced by individual patient-directed assessment. Cardiac monitoring by
laparoscopy increases intra-abdominal abdominal pressure with arterial pulmonary catheter is not routinely recommended.
direct consequences such as the reduction of venous return, and Anaesthetic technique (general vs. locoregional technique)
the risk of reducing cardiac output already decreased during AHF. should be discussed with surgeons. In the case of general
Thus, the latest ESC guidelines recommend endovascular or video- anaesthesia, the choice of anaesthetic agents is of major
assisted procedures for patients with high cardiovascular risk for importance, notably by limiting the risk of hypotension and
patients undergoing vascular or pulmonary surgery (Class IIa, Level end-organ perfusion, already impaired in decompensated and AHF.
B) [79]. Findings suggest no association between volatile or intravenous
Before surgery, smoking cessation and control of CV risk factors anaesthetic agents and post-operative cardiac events in NC surgery
are always recommended in AHF patients, as it is associated with [79]. Finally, locoregional could be an alternative to general
reduced postoperative complications and mortality. When surgery anaesthesia in certain cases. However, neuraxial blockade induced

Table 1
Management of pharmacological cardiovascular treatments in AHF patients before non-cardiac surgery.

Pharmacological treatment Indications/benefits Recommendations

Beta-blockers  Reducing myocardial oxygen consumption by reducing Pre-operative initiation before high-risk NC surgery must
contractile force and heart rate (cardioprotection) be considered in patients with 2 risk factors (Class IIb,
 Reducing acute inflammatory responses (metoprolol) Level A)

Peri-operative continuation if chronic treatment (Class I,

Level B)

Amiodarone  Prevention of post-operative atrial fibrillation No recommendation

Statins  Reducing cholesterol biosynthesis Peri-operative continuation

 Anti-atherosclerotic effects (Class I, Level B)

Renin-angiotensin-aldosterone  Reducing systemic inflammation Data inconclusive

system inhibitors  Nephroprotection
 Reducing of all-cause mortality in HF patients Peri-operative continuation in stable HF patients should be
considered
(Class IIb, Level C)
Calcium channel blockers  Improving balance between myocardial oxygen supply Data inconclusive
and demand
Peri-operative continuation but withholding the dose on
the day of surgery
Alpha-2 receptors agonists  Reducing post-operative ganglionic noradrenaline out- No recommendation
put
 Reducing catecholamines surge during surgery

Diuretics  Reducing systemic congestion For patients on chronic diuretics to treat hypertension,
discontinuation of diuretics on the day of surgery should be
considered
(Class IIa, Level B)
Ivabradine  Alternative to beta-blockers No recommendation
 Reducing heart rate without hypotensive effect

Sodium-glucose co-  Inhibiting the SGLT-2 proteins expressed in the renal Interruption for at least 3 days before surgery
transporter-2 inhibitors proximal tubules to reduce reabsorption of filtered (Class IIa, Level B)
glucose
 Promoting urinary glucose excretion

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sympatholysis with a high risk of severe hypotension [80]. Analge- increase in short and long-term survival by improving impaired
sic effects accelerated recovery, and decreased postoperative cardiac output and end-organ perfusion [86]. Data on the
complications are interesting benefits of locoregional anaesthesia superiority of one inotrope over another in this indication are
in AHF patients but need to be confirmed. Moreover, no data are lacking, but norepinephrine is the most studied molecule in this
available on the benefit of locoregional vs. general anaesthesia on indication [87]. Finally, oxygen therapy should be considered in
HF patient’s prognosis. patients with SpO2 < 90% by implementing NIV in patients with
acute pulmonary oedema [65]. In case of persistent hypoxemia or
Management of AHF in the intensive care unit hypercapnia, intubation should be quickly considered.

Intensive care unit admission of AHF patients varies from 5% to Cardiogenic shock
45.4% of overall AHF, according to registries, and is associated with
a high risk of death [14,81]. Indications of ICU admission are broad Definition
and notably rely on the existence of organ failure [82]. As described
for AHF, management of AHF in ICU is mainly based on Cardiogenic shock (CS) is a low-cardiac output state and life-
decongestive therapy, associated with the preservation of end- threatening syndrome due to cardiac dysfunction and is defined as
organ perfusion for adequate systemic perfusion. To reach this a shock state with sustained reduced systolic blood pressure
goal, intensivists should consider pharmacological and non- (<90 mmHg or need of pharmacological or mechanical support to
pharmacological interventions. In case of evolution to cardiogenic maintain systolic blood pressure > 90 mmHg) with low end-organ
shock, early treatment by mechanical circulatory (MCS) support perfusion [88,89]. Cardiogenic shock remains the most severe form
should be considered. of AHF, with a high in-hospital (30–50%) and one-year mortality
Management of decongestive therapy in AHF admitted in ICU (50–60%) [88–90]. Although its prognosis is terrific, outcomes of CS
does not differ from standard decongestive therapy for AHF, but patients (complicating 4–12% of the acute coronary syndrome) was
the maintenance of normovolemia to prevent reduced end-organ improved thanks to the routine use of early revascularisation and
perfusion following hypovolemia is challenging and often requires improvement of hemodynamic mechanical devices [88,91]. Al-
cardiovascular monitoring and progressive escalation therapy. though CS is more common during ST-elevation myocardial
Loops diuretics are the molecule of choice in this indication. In case infarction than non-ST-elevation myocardial infarction, CS could
of acute kidney injury, (particularly when accompanied by be observed in non-ischaemic aetiology (e.g., myocarditis, Tako-
hyperkaliemia or metabolic acidosis) or insufficient response to Tsubo syndrome, cardiomyopathies, peripartum cardiomyopathy,
loop diuretics despite optimal doses (as described above), renal valves lesion, post-cardiac surgery, intoxication).
replacement therapy for decongestion should be quickly consid-
ered. Other than this indication, the benefits of renal replacement Pathophysiology of CS (Fig. 3)
therapy vs. diuretics for decongestion are unclear [83–85]. To
reduce left and right-sided filling pressures, vasodilators and The diagnosis of CS is based on the association of low systolic
inotropes should be considered. As described above, although blood pressure < 90 mmHg, combined with end-organ hypoper-
intravenous vasodilators reduce preload, decrease afterload and fusion (cold extremities, confusion, oliguria), increased lactate
increase cardiac output, their clinical benefits have never been level > 2 mmol/L and reduced cardiac index < 2.2 L/min/
demonstrated in AHF patients with normal blood pressure. m2. Although aetiologies are various, the pathophysiology of CS
However, they allowed a rapid control of high blood pressure if shares overlapping components, including reduced cardiac output
necessary. Concerning the use of inotropes (e.g., beta-adrenergic due to depressional contractility, haemodynamic alterations with
receptor agonists, phosphodiesterase III inhibitors and calcium low blood pressure, increased left and right ventricles pressures,
sensitisers) in AHF patients admitted to ICU, findings suggest an microcirculatory dysfunction, systemic inflammatory response

Fig. 3. Pathophysiology of cardiogenic shock. eNOS: endothelial nitric oxide synthase, iNOS: inducible nitric oxide synthase, LV: left ventricle, SBP: systolic blood pressure,
SVR: systemic vascular resistances.

7
B. Deniau, A. Asakage, K. Takagi et al. Anaesth Crit Care Pain Med 44 (2025) 1–12

and organ dysfunction (Fig. 3) [89,90]. Compensatory mechanisms

Centrifugal flow continuous pump from

the right atrium to the aorta, including

 Irreversible non cardiac organ failure

membrane oxygenation (VA-ECMO)
to reduce cardiac output include systemic vasoconstriction,
improving coronary and peripheral perfusion, but increase cardiac
afterload leading to organ failure [89]. At the same time, systemic

Veno-arterial extracorporeal
inflammation induced by cardiac injury leads to pathological

Right and left ventricles

vasodilation (high levels of nitric oxide due to endothelial and

Biventricular support

 Aortic dissection
inducible nitric oxide synthase), negative inotropic effect and the
release of vasodilating inflammatory mediators like interleukins

Femoral artery
Femoral vein
and tumour necrosis factors [89]. Finally, macro and micro-

oxygenator
haemodynamic alterations lead to multi-organ dysfunction
(Fig. 3).

Classification and phenotyping of CS

artery bypass system with

Etiologies of CS are various, making its classification difficult.

 Intra-arterial thrombus
 Irreversible non cardia
centrifugal blood pump
The classification of the Society for Cardiovascular Angiography

Left-atrial to femoral
TandemHeart LVAD
and Interventions (SCAI) is based on five evolutive stages of CS,

c organ failure
from A (patient at risk) to E (Extremis, refractory circulatory

Femoral artery
Left ventricle
Femoral vein
collapse) [92]. This classification is centred on acute myocardial

(LivaNova)
infarction-induced CS and has been validated in large cohorts
[93]. The hemodynamic classification of CS separates patients into
4 categories, based on peripheral circulation (warm and cold) and

retrograde across the aortic valve

volume status (wet and dry) and describes four types of CS:
classical, euvolemic, mixed and vasodilatory shock [89]. Finally,

non cardiac organ failure

Zweck et al. proposed a new classification using machine learning,

 Mechanical aortic valve

 Left ventricle thrombus
with 3 distinct clusters: ‘‘non-congested (I)’’, ‘‘cardiorenal (II)’’, and

into the left ventricle

‘‘cardiometabolic (III)’’ shock associated different risks of in-

with inflow placed

 Aortic dissection
Axial flow pump
hospital mortality [94]. Interestingly, this classification is equally

Femoral artery

 Irreversible
Left ventricle
applicable to patients with CS attributable to myocardial infarction (Abiomed)
or acute-on-chronic HF [94].
Impella

Principles of management of CS

Management of CS requires a multidisciplinary approach,

Counter pulsation device in

non cardiac organ failure

including intensivists and cardiologists. As described for AHF,
Intra-aortic balloon pump

the first step of CS management is the assessment of the severity

Left ventricle support

and diagnosis of the aetiology of CS. To reach this task, clinical

coronary perfusion)
diastole to increase

 Aortic dissection
 Aortic aneurism
the aorta (balloon

examination and non-invasive exploration are central, particularly

inflated during

Femoral artery
Axillary artery
 Irreversible
Left ventricle

trans-thoracic echocardiography, carried out as quickly as possible

Mechanical circulatory support devices available for severe and refractory cardiogenic shock.

for the diagnosis and the assessment of the severity of CS.

Monitoring should be adapted to the severity and invasively
implemented (e.g., invasive hemodynamic monitoring by arterial
blood pressure, continuous cardiac monitoring and central venous
artery bypass system with
Right-atrial to pulmonary

centrifugal blood pump

 Intra-atrial thrombus

catheter for central venous oxygen saturation) in the most severe

cardiac organ failure
Internal jugular vein
TandemHeart RVAD

cases [95]. Trans thoracic echocardiography must be daily repeated

 Irreversible non

for biventricular function assessment, cardiac output monitoring

Right ventricle

and measurement of filling pressures.

(LivaNova)

 Therapeutic management
o Specific disease management

As myocardial ischemia is the most frequent cause of

cardiogenic shock, coronary revascularisation (Class I recommen-
dation) in case of acute myocardial infarction complicated by CS is
continuous inflow from
Right ventricle support

cardiac organ failure

Axial flow pump with

the cornerstone of therapeutic management and the only therapy

Contraindications Irreversible non
pulmonary artery

associated with reduced mortality [88]. Findings of large

right atrium to

Right ventricle

randomised control trials suggest that early coronary revascula-

Femoral vein
Impella RP

risation is associated with better outcomes after discharge

(Abiomed)

[91,96,97]. In the case of CS-induced by valvular disease, cardiac

surgery in an emergency remains the gold standard of therapeutic
management but is associated with morbidity. Data on the safety
and benefits of percutaneous intervention for valvular disease in CS
Mechanism

patients are needed. In the case of arrhythmia and conduction

Insertion

disorders associated with CS, restoration of sinus rhythm is the rule

Support
Name
Table 2

in case of hemodynamic instability. In the case of atrial fibrillation,

in nearly 20% of CS patients, amiodarone remains the most efficient

8
B. Deniau, A. Asakage, K. Takagi et al. Anaesth Crit Care Pain Med 44 (2025) 1–12

and safest pharmacological agent for cardioversion in critically ill ment, notably in the case of CS-induced by acute myocardial
patients [98]. infarction. Recent classification of CS should enable better
prognosis of these patients and need to be evaluated in large
o Inotropes and vasopressors cohorts. The place of MCS in the therapeutic management of CS
patients needs to be precise.
Dobutamine and milrinone, the two main inotropic agents
Disclosure of interest
prescribed during CS, are used to manage hypoperfusion [88]. By
stimulating b-receptors to increase cardiac contractility and AM received speaker’s honoraria from Orion, Otsuka, Philips, Roche and Servier,
relaxing vascular smooth muscle to reduce afterload, dobutamine received fee as member of advisory board and/or Steering Committee and/or
research grant from 4TEEN4. EG declared competing interest with Baxter, Mindray
causes severe hypotension. Milrinone, a phosphodiesterase-3
as past consultancy and research grants from Philipps, Edwards and Deltex. Other
inhibitor, increases intracellular calcium levels, myocardial con- authors declared no competing of interest.
tractility and cardiomyocyte relaxation, this drug causes arterial
and venous vasodilation [88]. Used at the lowest doses for the Funding
shortest duration, inotropes should be used with progressive This work did not receive any grant from funding agencies in the public,
titration, and are indicated in case of persistent low cardiac output commercial, or not-for-profit sectors.
and hypotension related to left ventricle systolic dysfunction [95].
Vasopressors, including high-dose dopamine, norepinephrine Author contributions
and epinephrine, present a-receptor vasoconstricting properties All authors attest that they meet the current International Committee of
and promote myocardial contractility. A randomised clinical trial Medical Journal Editors (ICMJE) criteria for Authorship.
comparing dopamine versus norepinephrine as the first-line
vasopressor to manage CS after acute myocardial infarction did
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