Intensive Care Med (2022) 48:482–485
https://doi.org/10.1007/s00134-022-06639-8
WHAT’S NEW IN INTENSIVE CARE
Ten questions ICU specialists should address
when managing cardiogenic acute pulmonary
oedema
Nadia Aissaoui1* , Olfa Hamzaoui2 and Susanna Price3
© 2022 Springer-Verlag GmbH Germany, part of Springer Nature
Acute pulmonary oedema (APE) is one of the most com- potential overlap between ARDS and APE since ARDS
mon causes of unscheduled hospital admissions among definition includes “Respiratory failure not completely
patients 65 years old or older [1, 2], with up to half being explained by excessive volume loading or cardiac failure”
critically ill [2]. APE is associated with a high mortality [3].
and rate of re-hospitalisation. Whilst in-hospital mortal-
ity ranges from 4 to 10%, the readmission rate for APE How about pathophysiology?
increases with time after discharge, ranging from 15% The pathobiology of APE is more complex than the
at 1 month to 45–50% at 6 months. One in three APE hydrostatic vs. the permeability dichotomy previously
patients dies within 1 year [1, 2]. In this document we used [4, 5]. Alveolar oedema is generated by a rapid
outline 10 key questions ICU specialists should address increase in the hydrostatic pressure in the pulmonary
when managing APE. capillaries and has a low protein concentration compared
to plasma (Fig. 1) [4]. Resolution of this APE is usually
What are we talking about? rapid, mainly because the alveolar-epithelial barrier is not
APE is usually defined by the sudden increase in pulmo- damaged [4, 5]. Sustained pulmonary injury might hap-
nary capillary wedge pressure as a result of acute and pen in relation with disruption in alveolar capillary units
fulminant left ventricle (LV) (systolic and/or diastolic) leading to acute inflammation. In a prospective study
failure or acute severe mitral regurgitation [1]. Among conducted in 65 mechanically ventilated patients with
the various clinical phenotypes of acute heart failure severe hydrostatic pulmonary edema, Verghese and his
(AHF), four major clinical presentations can be described colleagues reported an impairment alveolar-epithelial
with possible overlaps between them and APE represents barrier in 25% of patients. Such patients respond less well
30–80% of AHF clinical phenotypes (Electronical sup- to diuretics and often require mechanical ventilation [5].
plement material, ESM 1) [1, 2]. Clinical criteria related
to lung congestion include dyspnea with orthopnea, Organ cross talk: which actors?
increased respiratory rate, increased work of breathing APE leads to a cascade sequence of inter-organ cross-
and respiratory failure (Fig. 1) [1]. Hypoxia is a manda- talk, including lungs and kidneys, but also liver, intestine,
tory feature of APE. In some cases, APE and acute res- brain, neuro-endocrine and vascular system [6]. Conges-
piratory distress syndrome (ARDS) can be difficult to tion is an essential pathophysiological mechanism leading
differentiate or may even co-exist. Indeed, there is a to organ dysfunction. Hypoperfusion can also contribute
in cases of cardiogenic shock (ESM 1). The neurohormo-
*Correspondence: nal and inflammatory response to systemic congestion
1
Assistance publique des hôpitaux de Paris (APHP), Cochin Hospital, and/or peripheral hypoperfusion, may further contrib-
Intensive Care Medicine, médecine interne reanimation, Université de ute to organ injury. However, all the pathophysiological
Paris and Paris Cardiovascular Research Center, INSERM U970, 25 rue
Leblanc, 75015 Paris, France mechanisms remain incompletely understood. The injury
Full author information is available at the end of the article
https://doi.org/10.1007/s00134-022-06639-8
WHAT’S NEW IN INTENSIVE CARE
Ten questions ICU specialists should address
when managing cardiogenic acute pulmonary
oedema
Nadia Aissaoui1* , Olfa Hamzaoui2 and Susanna Price3
© 2022 Springer-Verlag GmbH Germany, part of Springer Nature
Acute pulmonary oedema (APE) is one of the most com- potential overlap between ARDS and APE since ARDS
mon causes of unscheduled hospital admissions among definition includes “Respiratory failure not completely
patients 65 years old or older [1, 2], with up to half being explained by excessive volume loading or cardiac failure”
critically ill [2]. APE is associated with a high mortality [3].
and rate of re-hospitalisation. Whilst in-hospital mortal-
ity ranges from 4 to 10%, the readmission rate for APE How about pathophysiology?
increases with time after discharge, ranging from 15% The pathobiology of APE is more complex than the
at 1 month to 45–50% at 6 months. One in three APE hydrostatic vs. the permeability dichotomy previously
patients dies within 1 year [1, 2]. In this document we used [4, 5]. Alveolar oedema is generated by a rapid
outline 10 key questions ICU specialists should address increase in the hydrostatic pressure in the pulmonary
when managing APE. capillaries and has a low protein concentration compared
to plasma (Fig. 1) [4]. Resolution of this APE is usually
What are we talking about? rapid, mainly because the alveolar-epithelial barrier is not
APE is usually defined by the sudden increase in pulmo- damaged [4, 5]. Sustained pulmonary injury might hap-
nary capillary wedge pressure as a result of acute and pen in relation with disruption in alveolar capillary units
fulminant left ventricle (LV) (systolic and/or diastolic) leading to acute inflammation. In a prospective study
failure or acute severe mitral regurgitation [1]. Among conducted in 65 mechanically ventilated patients with
the various clinical phenotypes of acute heart failure severe hydrostatic pulmonary edema, Verghese and his
(AHF), four major clinical presentations can be described colleagues reported an impairment alveolar-epithelial
with possible overlaps between them and APE represents barrier in 25% of patients. Such patients respond less well
30–80% of AHF clinical phenotypes (Electronical sup- to diuretics and often require mechanical ventilation [5].
plement material, ESM 1) [1, 2]. Clinical criteria related
to lung congestion include dyspnea with orthopnea, Organ cross talk: which actors?
increased respiratory rate, increased work of breathing APE leads to a cascade sequence of inter-organ cross-
and respiratory failure (Fig. 1) [1]. Hypoxia is a manda- talk, including lungs and kidneys, but also liver, intestine,
tory feature of APE. In some cases, APE and acute res- brain, neuro-endocrine and vascular system [6]. Conges-
piratory distress syndrome (ARDS) can be difficult to tion is an essential pathophysiological mechanism leading
differentiate or may even co-exist. Indeed, there is a to organ dysfunction. Hypoperfusion can also contribute
in cases of cardiogenic shock (ESM 1). The neurohormo-
*Correspondence: nal and inflammatory response to systemic congestion
1
Assistance publique des hôpitaux de Paris (APHP), Cochin Hospital, and/or peripheral hypoperfusion, may further contrib-
Intensive Care Medicine, médecine interne reanimation, Université de ute to organ injury. However, all the pathophysiological
Paris and Paris Cardiovascular Research Center, INSERM U970, 25 rue
Leblanc, 75015 Paris, France mechanisms remain incompletely understood. The injury
Full author information is available at the end of the article
