DOI: 10.1111/echo.

13657

REVIEW

The lung water cascade in heart failure

Eugenio Picano MD, PhD1  | Maria C. Scali MD, PhD2

1
CNR Institute of Clinical Physiology, Pisa,
Italy In heart failure patients, we hypothesize the occurrence of the “lung water cascade,”
2
Nottola Hospital, Siena, and Cardiothoracic with the various markers hierarchically ranked in a well-­defined time sequence: (1)
Department, Pisa University Hospital, Pisa, early, proximal hemodynamic event with increase in pulmonary capillary wedge pres-
Italy
sure; (2) intermediate, direct imaging sign of pulmonary edema (easily detectable at
Correspondence bedside by lung ultrasound as B-­lines); (3) late, distal clinical symptoms and signs such
Eugenio Picano, Italian National Research
Council, Institute of Clinical Physiology, Pisa, as dyspnea and pulmonary crackles. Completion of the cascade (from hemodynamic to
Italy. pulmonary to clinical congestion) can require minutes (as with exercise), hours or even
Email: picano@ifc.cnr.it
weeks (as with impending acute heart failure). Backward rewind of the downhill cas-
cade can be achieved with timely pulmonary decongestion therapy, such as diuretics
or dialysis, restoring a relatively dry lung. Any therapeutic intervention is more likely to
succeed in the early steps of the cascade, at the imaging stage of asymptomatic pul-
monary congestion, rather than downstream near to the end of the cascade, when
clinical instability occurred.

KEYWORDS
B-lines, edema, lung, ultrasound

1 |  CASCADES IN CARDIOLOGY
In biology, a cascade is a series of events in which one event triggers
the next, in a linear fashion. The example most familiar to cardiologists
is the “ischemic cascade.” The initial event is a transient regional im-
balance between oxygen supply and demand, which usually results in
1
myocardial ischemia. The ischemic cascade has long been recognized
in the experimental laboratory, but it was only in the stress imaging
era that it could be fully understood and exploited by cardiologists.
Regional perfusion heterogeneity is the forerunner of ischemia, fol-
lowed by regional wall-­motion abnormalities, and only at a later stage
by classic markers of electrocardiographic changes and chest pain.
The pathophysiological framework of the ischemic cascade was help-
ful for the clinical cardiologist to understand the observed gradient
in diagnostic sensitivity for the identification of coronary artery dis-
ease during stress testing, with chest pain being the least specific
Abbreviations: ACB, alveolar-capillary barrier; EVLW, extra-vascular lung water; LUS, lung
ultrasound.
and cardiac functional imaging providing better diagnostic accuracy
through regional perfusion3 and wall-­motion4 changes.5,6
The sequence of events leading to pulmonary edema during heart
failure can also be conceptualized as a cascade, whose sequence was
unveiled with the advent of lung ultrasound (LUS) for bedside imaging
of extra-­vascular lung water (EVLW).7–9 This allowed clinical cardiolo-
gists to see what experimental physiologists had always known10,11:
Clinical pulmonary congestion is a late pathophysiological event,
2 which follows by days or weeks the increase in left ventricular end-­
diastolic pressure and pulmonary capillary wedge pressure (hemody-
namic congestion).12,13 The initiating event (the source) of the cascade
is the imbalance of Starling’s equilibrium in the alveolar-­capillary bar-
rier (Figure 1), resulting in an increased accumulation of EVLW, from
the normal values of <500 mL (or <10 mL/kg of body weight) to mild
(500–1000), moderate (1000–2000) or severely abnormal (>2000 mL)
increase in EVLW.10–12 In between hemodynamic and clinical pulmo-
nary congestion, the intermediate event is the imaging sign, detectable
by LUS as B-­lines, which act as a proximal biomarker and an intermedi-
ate endpoint of pulmonary edema, linked biophysically to an increase
in water-­to-­air ratio per unit of lung volume tissue.14–16 The late clinical

Echocardiography. 2017;34:1503–1507. © 2017, Wiley Periodicals, Inc. |  1503

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1504       PICANO and SCALI

THE LUNG WATER CASCADE

Events
F I G U R E   1   The lung water cascade.
PATHOPHYSIOLOGY
Starling equation unbalance In cardiogenic pulmonary edema, the
triggering event of increased pulmonary
capillary wedge pressure (hemodynamic
B-lines IMAGING
congestion) leads to the imbalance
of Starling forces with transition to
accumulation of interstitial lung water
Crackles/Dyspnea/Weight gain SYMPTOMS/SIGNS (pulmonary congestion), followed (after
minutes or hours or days, depending on
the acute or chronic condition) only at a
more advanced stage by symptoms and
signs of clinical congestion (with dyspnea,
Time pulmonary crackles, and weight gain)

event is represented by dyspnea, pulmonary crackles and weight gain,
overall unspecific and late signs of pulmonary congestion.8,17,18
The conceptualization of the hypothesized “lung water cascade”
has some potential merits: (1) It incorporates in the very same definition
the concept of cascade, that is, a series of events in which one event
triggers the next; (2) It intuitively illustrates the concept that the clinical
signs of congestion, although routinely used for decision making, are a
distal sign of lung water accumulation, which is the key pathophysiolog-
ical event triggering acute heart failure and an elusive diagnostic target
in the pre-­LUS era;19 (3) It makes clear that any therapeutic interven-
tion is more likely to succeed in the early steps of the cascade, rather
than downstream close to the end of the cascade. In addition, from a
purely semantic viewpoint, the term “cascade” fits nicely with the de-
scription of water falling, along a gradient of pressure, from the intra-
vascular (from 5 to 50 mm Hg, from normal to very abnormal values) to
the extra-­vascular pulmonary space (with a slightly negative pressure in
the interstitium). The similarities and differences between the cardiac
ischemic cascade and lung water cascade are summarized in Table 1.
T A B L E   1   The lung water and ischemic cascades in cardiology
Cardiac ischemia Lung water
cascade cascade
Underlying disease CAD Heart failure
2 | B-­L INES FOR STAGING HEART FAILURE
The emerging biomarker for the noninvasive, real time evaluation of
pulmonary edema is B-­lines detected by LUS, which can be meas-
ured anytime, anywhere, by anybody, even with pocket-­size or port-
able instruments. B-­lines are easily identified on anterolateral chest
as comet-­like signals arising from hyperechoic pleural line with a to-­
and-­fro movement synchronized with respiration. The recommended
protocol for evaluating B-­lines is performed by scanning 28-­region
protocol on the anterior chest. The number of B-­lines in each space
may range from 0 (normal pattern, black lung) to 10 (white lung, alveo-
lar edema) with all values in between indicating increasing severity of
interstitial edema with a black-­and-­white pattern, ranging from mild
(1–3 B-­lines), moderate (4–6 B-­lines), or severe edema (7–10 B-­lines).
The number of B-­lines in each space is usually summed up to generate
a quantitative B-­lines score.9
However, the original, comprehensive 28-­site scan requires about
3 minutes and can be too complicated and time-­consuming for a rou-
tine use in real world echocardiography and—even more—in stress
echo laboratories. A similar information can be obtained with much
less time with a 4-­region scan, dismissing relatively dry regions and
including only the wet spots which have the highest density of B-­lines
at rest and during stress. The wet spots are horizontally aligned on the

Target organ Myocardium Lung third intercostal space, and vertically with anterior-­axillary and mid-­
axillary line, symmetrically on the right and left anterior-­lateral chest.
Vital function LV contractility Gas exchange
These spaces are for lung water what V5 or V6 leads are for electrocar-
Pathophysiology Supply-­demand Starling equation
mismatch unbalance diographic detection of myocardial ischemia: the preferential site of

Early hemodynamic Regional flow Increased capillary significant, acute modifications.20

event reduction pressure Although some soft computing algorithms have already been de-
Intermediate imaging Perfusion, B-­lines veloped and validated to make this diagnosis completely operator-­
event wall-­motion defect independent,21 the current conventional eyeballing analysis is easy
Late clinical event ECG changes, Chest Pulmonary and highly reproducible when reading criteria are agreed in advance,
pain crackles, dyspnea with short training of a few hours, acquisition time of a few minutes,
Catastrophic distal Myocardial Overt pulmonary analysis time of few seconds, and low variability even between in-
event infarction edema experienced observers.22 B-­line changes are present in the absence
CAD = coronary artery disease. of symptoms, giving this sign an advantage by hours or days over

PICANO and SCALI
dyspnea in heart failure23 or high-­altitude pulmonary edema.24,25 Only
20%–30% of patients with heart failure and B-­lines have crackles
8,18
on pulmonary auscultation. The same sequence of events can be
observed in a fast-­forward fashion during exercise, when B-­lines can
occur in the absence of dyspnea or minutes before it.26,27
With this new, user-­
friendly biomarker of EVLW at hand, the
pathophysiological concept of lung water cascade can be translated
into a clinical tool to identify different stages of pulmonary edema,
which can trigger different thresholds of intervention on the basis of
B-­lines at rest and during stress: dry lung, stress-­wet lung, and rest
wet lung (Table 2). In all these conditions that can be associated with
a wet lung, there is an initial stable phase with little or no lung fluid
accumulation, lung fluid accumulation without clinical signs (with low
levels of lung fluid accumulation amplified by exercise), and dramatic
deterioration in patient condition and urgent hospitalization concom-
28
itant with steep increase in fluid accumulation at rest. The rationale
of detecting B-­lines at rest is to shift the detection of lung water up-
stream, at an earlier stage than those of pulmonary crackles or weight
gain. Compared to rest, stress B-­lines shift the detection of lung water
further upstream, as it can be induced by pulmonary bed volume and
pressure challenge occurring during a stress such as exercise.29 A
systematic application of LUS to heart failure patient opens a new—
earlier and more accurate—diagnostic window for the highly sensitive
and specific diagnosis of lung water accumulation. The clinically silent
interstitial pulmonary edema is an early, more easily reversible, form
of disease and should be treated in the same way as silent ischemia
in coronary artery disease. The next step is the dynamic application
of LUS during stress in these patients, as this allows sampling the
lung water cascade a step upstream in the cascade, identifying more
functionally severe and more prognostically advanced stages of heart
failure.27
3 | FROM SOUND TO ULTRASOUND IN
IMAGING LUNG WATER IN HEART FAILURE
Asymptomatic ischemia can be frequently detected with electrocar-
diographic and imaging markers at rest and during stress, has the
same unfavorable diagnostic and prognostic meaning as symptomatic
ischemia, and should prompt treatment. Thus, chest pain is an im-
portant clinical symptom, but it is also a simple diagnostic optional
30
feature. To a similar extent, dyspnea is a pivotal symptom and the
reason why the patient contacts the doctor, but it is also a late, non-
specific marker of lung congestion and decongestion.31 Crackles on
T A B L E   2   The three lung water stages in heart failure
Lung at rest Dry Dry Wet
Lung on exercise Dry Wet Very wet
Resting B-­lines Absent Absent Present
Stress B-­lines Absent Present Present
Risk ADHF Low Intermediate High
ADHF = acute decompensated heart failure.
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      1505
physical examination are also insensitive and poorly specific, as are
weight gain, jugular distention, and pedal edema.32 We now have the
opportunity to better detect pulmonary congestion shifting from au-
dible sound (history taking for dyspnea and auscultation of crackles)
to ultrasound. B-­lines are an early, sensitive and highly reproducible
biomarker, readily available at bedside with a low cost, radiation-­free,
portable technology. The postulated sequence of events is also cor-
roborated by evidences obtained in a longitudinal fashion in a heart
failure population, in whom the asymptomatic pulmonary congestion
detected by B-­lines is associated (after weeks or months) with devel-
opment of clinically overt acute decompensated heart failure or other
events including death. This has been observed stable heart failure
in-­patients23 and outpatients,33,34 in patients with heart failure and
renal hemodialysis,35 or inpatients at the predischarge evaluation after
clinical stabilization.36,37 Platz et al34 reported that 85% of heart fail-
ure outpatients with asymptomatic pulmonary congestion detected
by B-­lines had no crackles at pulmonary auscultation. In a population
of stable in-­and outpatients with chronic heart failure, Scali et al27
reported that 41% had asymptomatic B-­lines at rest, and 71% dur-
ing exercise stress echocardiography. In all these conditions, the
presence of asymptomatic B-­lines (at rest and, even more strikingly,
after stress) is associated with substantially greater chance of clinical
instabilization in the short-­to medium-­term follow-­up of weeks or
months.23,27,33–37 In acute decompensated heart failure, a sequence
of events can also be outlined after treatment. Ohman et al meas-
ured B-­lines, natriuretic peptides, and dyspnea serially after pulmo-
nary decongestion therapy with diuretics. Patients showing an early
reduction of E/eʹ also showed a more marked reduction in B-­lines,
which was the strongest prognostic predictor, again suggesting that
LUS may provide a suitable marker to study the pulmonary congestion
and also the therapy-­induced pulmonary decongestion phase.38 The
proposed model of lung water cascade needs now further evidence
support through prospective studies looking more systematically to
the sequence of events both in pulmonary congestion and pulmonary
decongestion phase.
The stage is set for outcome studies comparing standard vs
­B-­line-­driven therapy in heart failure in various populations, including
heart failure with reduced or preserved ejection fraction; patients with
rest or only exercise-­induced B-­lines; with or without chronic renal
failure, and so on. These studies will move along in the conceptual
and methodological footsteps of the LUST trial (clinicaltrials.gov NCT
02310061), which stands for Lung water UltraSound guided Treatment
to prevent death and cardiovascular complications in high-­risk end-­
stage renal disease patients with cardiomyopathy. This prospective,
international, multicenter, randomized trial on 500 patients will shed
light on whether the treatment of asymptomatic pulmonary conges-
tion improves outcome.18 In the mean time, the prospective Stress
Echo 2020 international multicenter trial will collect effectiveness
data on the prognostic value of rest and stress B-­lines in over 4000
heart failure patients.39 Today, only the clinical tip of the iceberg of
dyspnea and pulmonary crackles falls within the visual field of the car-
diologist. The hypothesized concept of “asymptomatic pulmonary con-
gestion” is ready to become an integral part of mainstream cardiology

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1506       PICANO and SCALI
knowledge and a systematic part of the modern (“quadruple imaging”)
stress echo methodology, 40
allowing presymptomatic detection of the
hidden iceberg of lung water accumulation. In heart failure patients,
B-­lines at rest41 and, probably even better, during stress27 can be a
reasonable therapeutic target and it is time to test the hypothesis
whether B
­ -­lines-­guided therapy could improve outcome.
CO NFLI CTS OF I NT E RE ST
The authors have no conflict of interests to disclose.
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failure: cardiac filling pressures, pulmonary congestion and mortality.
cascade in heart failure. Echocardiography. 2017;34:1503–
Eur Heart J Acute Cardiovasc Care. 2017; May 1 [Epub ahead of print]
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