This chapter is long (those who are happy with their hemodynamic management can skip it). In spite of its length, it considers two simple elements (the A-line and the B-line) which were never yet taken into consideration in the question of hemodynamic assessment. If simplicity is integrated in a complex field, complex explanations must be given. This is why this chapter is the longest of the textbook (we even bet that, like the chapter on the BLUE-protocol of our 2010 edition is now a whole textbook, this chapter will make our next textbook).

The reader is invited to think different. The FALLS-protocol turns around one main idea: in a domain where “everything has been said,” but where passion still rules, shouldn’t the introduction of a fully new concept (based on logic, on the early detection of a precious data: lung fluid overload) be a help, even partial? We admire the high level and the highly respectable knowledge of most intensivists and world experts in hemodynamics. We are aware that our ambition may appear a bit provocative, and it is with the highest level of humility that we propose a new concept. For achieving this aim, one’s current knowledge should temporarily be forgotten, just the time for being able to understand the spirit of the FALLS-protocol. The usual targets (cardiac index changes, etc.) are not used here for instance. After this effort, the readers will take again their usual practice and use a bit, or more, as they feel, of the FALLS-protocol in their daily practice. We know that we ask huge efforts to some.

This chapter is the latest avatar of chapter 23 of our 2010 edition. Numerous questions, comments, criticisms heard here and there were answered, resulting in multiple changes. The spirit was unchanged, but many details were adapted for increasing the logic of the FALLS-protocol. We again took great care for making this chapter as moderate as possible and fully open to criticisms. The FALLS-protocol proposes a parameter which can be criticized like all parameters in this field, but whose peculiarity is to provide a direct assessment of the clinical volemia.

For performing the FALLS-protocol, which takes mainly simple cardiac sonography and lung ultrasound (both caval veins if needed), our simple unit with its 5 MHz microconvex probe is usually perfect.

The bedside work of the intensivist is to provide adequate oxygen output to the tissues. Our obsessive work is to answer this question: “How to better feed these mitochondria?” All in critical care turns around this.

Before ICUs were created (in the mid-1950s), the patients in circulatory failure died. Then, the physicians in charge of these new units did their best, using the central venous pressure (CVP), until the Swan-Ganz catheter, developed, in the early 1970s, provided more precise data, which gave them the feeling to go in a direction assumed to be the good one [1].

The Swan-Ganz catheter measures the pulmonary artery occlusion pressure (PAOP) [1, 2]. The PAOP informs on left ventricular (LV) end-diastolic pressure [2–5]. This PAOP classically guides fluid therapy [6] and defines risk for hydrostatic pulmonary edema [3, 7].

After decades of use, the Swan-Ganz catheter experiences difficult times. Some considered possible side effects [8], a questionable usefulness [7–23], and others a suboptimal use of a potentially interesting method [24–26]. Alternative techniques were considered such as echocardiography – long accessible by trans-thoracic approach, and by trans-esophageal approach, a 1976 concept [27], which became so current that we now benefit from disposable TEE probes [28]. These techniques made the Swan-Ganz catheter definitely obsolete [29–39]. Since TEE was not easily accessible (cost, training), other tools were developed, mainly continuous cardiac output devices for assessing lung water (PICCO), esophageal Doppler, pulse pressure variation, pulse contour analysis, pulse analysis of the arterial pressure, sophisticated oxygen transport assessment, or again microcirculation assessment and derived, such as gastric tonometry, sublingual capnometry, laser Doppler flowmetry, near-infrared spectroscopy, gravimetry, and so on [40–51]. Each year, a new tool merges, advocating to definitely solve the problem.

All methods, up to the most recent, are compared to previous ones. The initial reference was the LV catheterization, to which the Swan-Ganz catheter was compared (with accuracy <100 %), and subsequent tools were compared to the Swan-Ganz catheter (with accuracy <100 %). From study to study, the distortion may be substantial with the historical LV catheterization. Even this “floor” is not a direct tool for measuring clinical volemia. Therefore, how about the real value of the most recent tools?

And they provide so many data. If we take a minimal distance, we just may feel disconcerted by the left column of Table 30.1. This impressive list of data extracted from these multiple tools is probably the best proof, ab absurdo, that no gold standard really exists. We know that no isolated, static parameter of preload status is valuable for predicting fluid responsiveness [52, 53]. This assumption indicates that we do not have the direct parameter. The struggle that opposes PAC, TEE, PICCO, etc., gets routine – a godsend for the manufacturers, but some intensivists may feel a little blind in their daily work.

For lack of any perfect gold standard, the point is now to know which patients will increase their cardiac output of more than 15 %. Those who don’t would have only the risk of pulmonary edema, for no benefit. This originated elegant concepts. Fluid responsiveness is a concept based on pathophysiology of fluid dynamics [36, 40, 47, 54–56]. It is a current standard, widely used nowadays. Looking at the cardiac Doppler values for knowing the volemic status is an elegant approach, and we take major interest to data extracted from this field: restrictive flows, E/E′ ratio, etc. We just wonder how long is needed for a current investigation, how precise it is (how wide is the gray zone in current practice), how high is the expertise required for a 24/7/365 use in any hospital, and mostly how far these data are direct ways to show the lung damage in case of fluid overload, as elegant can these methods be.

We have the same questions regarding other arising concepts, such as this elegant one of abdominal compartment syndrome [57, 58]. Even if all these techniques would work perfectly, they would just tell that the patient increases (or not) the cardiac output. Do these techniques tell the patient needed such an increase is a quandary which we point as central in the spirit of the FALLS-protocol (which as we will see uses a different approach for answering). In late disorders of septic shock comes the far more subtle situation where microcirculation alterations, capillary leak, interstitial and endothelial cell edema, hyperchloremic acidosis, coagulopathy, etc., are mingling, time for multiple organ failure [59, 60]. At this step, it is even not clear whether the tissues really require supplementations in oxygen. The question is probably no longer about the quantity of fluid to administer, whatever the tool used – the usual strategies for hemodynamic optimization become of limited efficiency [61, 62]. Knowing at any price that the cardiac output of a shocked patient increases under fluid therapy is questionable if it is of no benefit to this patient.

Consequently, in the ICU corridors and congresses – a constant phenomenon since the day we began in intensive care (1985) – multiple voices sing dissonant songs. This may confuse those worried by the feeling they may work blindly, whereas the others feel fully reassured using one given approach (PICCO here, ECHO there, etc.). The latter ones argue to the former ones that they did not understand the tool or did not read the user guide, etc. Habits, more than evidence-based medicine, seem to rule. If we are not fully wrong, medicine is not an exact science, and this makes the bed for authoritative behaviors.

In this peak of complexity, where some advocate a return to more simplicity [63], simple maneuvers [32, 64], every point can be debated, even the place of familiar parameters such as cardiac output: not everyone admits its targeting may affect patient’s outcome [65], and expert opinions do not recommend its routine measurement [66]. Each current tool has advantages and drawbacks [67]. Table 30.2 shows some of them.

Probably, the modern medicine has progressed with respect to the era of the CVP. Probably, the issues of hemodynamic therapy are partly solved using modern tools. However, we still hear discordant comments in the corridors of the many ICUs we have the privilege to visit trough the world: read Anecdotal Note 1. These comments probably reflect the real life of usual ICUs.

To the classical question: Which technique(s) should I introduce in my ICU? Which ones are the good ones? Between progresses and trends, admitting the hypothesis that what is modern is good, may we oppose the notion of the sinusoidal profile? A revolutionary novelty of 1 day is forgotten when the next tool is available. Initial enthusiasm for a novelty, full discredit some years later (usually one decade), and more balanced conclusions after prolonged use, this is a familiar tune. Like a single voice, the whole community goes left. Several years after, it makes the opposite turn, and so on. This profile, seen in 100 instances, makes winners and losers of one day. For example, the supranormal value in oxygen delivery in the septic shock was an honorable target [68], before being discredited [69]. Corticoids in sepsis, new immunotherapies in sepsis, etc., up to fluid therapy, typically obey to this sinusoid. During decades, in the hot minutes of shock management, doctors gave fluids cautiously with the fear of the major issue, pulmonary edema [3]. Then they faced this issue of insufficient fluid therapy, keeping the patient in occult hypovolemia (with hemodynamic risk if vasoactive drugs were administered together). Then they were taught to give (early and) massive fluid therapy in septic shock [70]. This has ruled during more than one decade as an evidence. And now, this protocol is thoroughly and completely discredited [61, 71, 72]. This sinusoid music rhythms our life of intensivists. It makes it, it is true, somehow exciting, a “hot” profession definitely, where we can hear prestigious and passionate tenors sharing their point of view on a question which fills the congresses, with complex, thrilling pro/con debates between experts.

So currently, a strong ruling idea, the reality (of today) is a limitation in fluid therapy. Recommendations of yesterday (“early and massive fluid therapy in sepsis”) are now erased by modern spectacular teasers: “Dry, the patient survives. Wet, the patient dies.” The must is the “dry attitude.” Without nuance, “fluids kill,” etc. These old and new trends arose and arise from prestigious journals (the EGDT as well as its executors). Now, the patient will benefit from the modern trend, built by the Surviving Sepsis Campaign Guidelines, ProCESS, ARISE, and “other” FEAST, FIRST, CRYSTAL, and 6S trial. All in all, the consensus seems to express that the early steps (minutes, hours) should make liberal fluid therapy, whereas the later steps (days, weeks) should be conservative. From all these orders and counterorders which spread from congresses and corridors, we have the confused feeling (possibly completely wrong) that currently the trend is to definitely keep the patient dry to the point that standard physicians feel nearly guilty when they prescribe fluids. There should be no place for emotion, only for facts, yet medicine is still medicine: again, how do we locate our patient within the middle part of this familiar curve indicating the area of optimal volume load [73]?

Some teasers, as far as we understood, seem more balanced than the trend (from Michael Pinsky without mistake): “Dry lungs, happy lungs. Dry liver, dead liver.” Would this mean that not all the current voices run in the same direction like one man? Is the problem not completely solved? Other sounds, from respectable key-opinion leaders, seem to point out that the great recent studies which invalidated the EGDT are possibly more of an opportunity to publish than a real advance. They insist on the point that time is of essence. As students, we had the slight idea that in a critically ill patient, it was better to be fast than slow. So none of these guidelines really changed our practice to consider a shock as an emergency.

Fluids kill. Let us admit. Our candid question is: for how long? Should we keep nothing from our previous concepts, without nuance? Physicians now know (or think they know) that too liberal fluid therapy is not good, but do they have the tool which indicates the endpoint with certitude?

We understand that simple ultrasound is introduced in a delicate setting, still open for some [74], less for others who apparently possess the right tool [75].

Can a different approach be considered for the longstanding problem of hemodynamic assessment?

Can our beloved principle of simplicity be used in such a complex field?

An anxious intensivist, willing to give maximal security to this critically ill patient, would insert a Swan-Ganz catheter, plus a PICCO device, make liberal echocardiography, and use all other possible tools. This intensivist would benefit from an impressive list (Table 30.1). Look at a remarkable point: on the left, this huge amount of data (Table 30.1, left column) and on the right, such a limited list of practical options (Table 30.1, right column). Apart from disobstruction of an obstacle (clot, gas, pericardial fluid), apart from specific therapies of given causes of shock (e.g., hemodiafiltration in septic shock, etc.), there are just three options for trying to stabilize a shocked patient: inotropics, vasopressors, and fluids. Just these three limited options – for saving a life – whatever the quality and sophistication of very fine articles [1–76].

Let us study Table 30.1. Shall we say to our nurse that the value of the indexed LV end diastolic volume is 1.23 ml or 109.15 l? What would the nurse understand? She, or he, waits rather precise instructions, to give, or not to give fluids. When we have to give precise instructions, things get suddenly extremely simple in terms of choice (again): inotropics or not, vasopressors or not, fluids or not.

The contrast between the left and right columns of Table 30.1 (i.e., the major complexity of usual tests and the so simple alternative “fluids or no fluids”) was the starting point of the FALLS-protocol.

How to recognize those lungs which are still dry from those already wet? Can lung ultrasound be of any help? While carefully respecting all positions, we felt free to add one more data to the impressive left column of Table 30.1: lung ultrasound – A-lines and B-lines precisely. Interstitial edema was one application of ultrasound [77] with clinical uses [78, 79]. Thinking that any new idea in this symphony should be considered – if it can provide any help, even minor, even debatable – our idea is to take, again, our 29-cm wide gray-scale ultrasound unit with its simple microconvex probe, the one which we used already for carrying on 100 life-saving applications.

Would lung rockets help in assessing the lung tolerance to fluid therapy, i.e., fluid administration limited by lung sonography (i.e., FALLS-protocol)? In our 2010 edition, the FALLS-protocol was part of the slightly pompous “limited investigation considering hemodynamic therapy.” Now for making short, the FALLS-protocol is this multi-organ approach, including heart and lungs (and veins if needed).

May the FALLS-protocol answer to these two basic questions, purposely recalled:

Lung ultrasound was not supposed to exist. It now advocates to provide a direct parameter of volemia. This calls for some precautions, and we will need three critically important tools:

We visit a shocked patient. The physical examination may be sufficient (typical pulsus paradoxus, etc.) or not. In this case, ultrasound is of major help. We use the Max Harry Weil’s classification of shocks [88], slightly adapted for allowing a sequential use of ultrasound (Fig. 30.3). Since the heart is a traditional site for answering this question, we have respected this vital organ by dealing with it first, in a simplified model. The FALLS-protocol suggests to place lung ultrasound immediately after. For a schematic demonstration, we assume the case of a patient victim of an acute circulatory failure with fully unknown origin.

Like any traditional shock management, the FALLS-protocol will mingle diagnostic and therapeutic actions. The therapeutic actions will not be “symptomatic” but enlightened.

We use a single probe for expediting the approach of heart, lungs, and veins (and belly): this is holistic ultrasound.

At this step, we have never used the Doppler button.

In this latest avatar of the FALLS-protocol, the case of the B-profile is increasingly considered apart.

The B-profile means usually hemodynamic pulmonary edema, and the physician can be satisfied with this diagnosis, if occurring in a suggestive setting. In acute respiratory failure, the B-profile was usually associated with hemodynamic pulmonary edema (in circulatory failure, the word would be cardiogenic shock), rarely pneumonia/ARDS (in circulatory failure, the word would be lung sepsis), exceptionally chronic interstitial lung disease, or CILD (in acute circulatory failure, this would be any coincidental cause of shock); we therefore concentrate only on the first two causes (for CILD, several items, including the simple one of thick free RV wall, usually allow diagnosis, see Chap. 35).

Therefore, when the setting is not simple, cardiogenic shock must be distinguished from lung sepsis with a B-profile. The problem of the FALLS-protocol is simple: a cardiogenic shock does not require fluids (schematically), but a septic shock, yes. The physician has just to gather arguments for lung sepsis. These arguments are numerous, their sum usually allows the diagnosis.