Acute hemodynamic pulmonary edema, referred to as AHPE, is usually a disease of the left heart (here called acute cardiogenic pulmonary edema) and sometimes the consequence of a fluid overload, hence the general term AHPE.

The dyspnea usually begins with a feeling of tightness of the thorax, which seems heavy. The dyspnea is relieved by sitting. A history of cardiac disease is often present. Auscultation shows the main sign, rales. Bedside radiograph typically shows bilateral, symmetric signs of congestion. Blood gases show hypoxia and hypocapnia. BNP is elevated in cardiac causes.

The signs of the underlying cause are numerous (clinical, ECG, biological, etc.).

Each of these signs can be absent and difficult to assess (e.g., rales in bariatric patients). Radiography provides its dose of radiation, is not always present through the world, and can be difficult to read in challenging or any patients, up to a normal initial pattern. Arterial blood gases are painful procedures and provide rather limited information.

Imaging tests would not be so useful if the clinical examination answered perfectly the question. Rales can be absent at an early stage [1] or replaced by wheezing, yielding the cardiac asthma. Fine auscultation is illusory in ventilated patients or in point-of-care medicine, airplane, crowded ER, etc.

As regards imaging, we simplify our last edition, gathering in the same paragraph all situations where the radiographic diagnosis is tricky (subnormal radiograph, because it is made too early, but also in genuine severe cases of pulmonary edema [2, 3]), difficult (ill-defined), not immediately available (extreme emergency), or not available at all (extra-hospital settings mainly, poor countries). We assume that the radiologic signs speak only in advanced stages. A radiograph taken in optimal conditions can be difficult to interpret [4]. Taken in an emergency, at the bedside it cannot be but worse. Signs like vascular redistribution do not work in supine patients. X-ray sensitivity in detecting interstitial edema can range between 45 and 18 % [5, 6]. Kerley B-lines can be observed in exacerbation of COPD [7].

AHPE provides the B-profile, which theoretically concludes the BLUE-protocol, with a 97 % sensitivity and a 95 % specificity.

PLAPS are seen in 88 % of cases. Echocardiography can show simple signs (global left ventricle hypocontractility) or more subtle signs, requiring Doppler. Please consult reference textbooks for this, since the aim of the BLUE-protocol is to provide a diagnosis, which is pulmonary edema. Where does it come from is another (basic) question. The inferior caval vein is not seen in all cases, far from this. When it is seen, a dilatation is far from the rule (we currently see again all our cases).

Lung ultrasound for diagnosing interstitial syndrome is increasingly used, we quote only a very few from the first works [8–11].

The B-profile rules out pneumothorax, simple COPD (even severe), and simple asthma (even severe).

The B-profile makes the diagnosis of pulmonary embolism unlikely. Apart from ICU-acquired embolism, the B-profile was not seen in patients with embolism in the BLUE-protocol and makes 2 % of patients in a larger series (under submission). These cases of pulmonary embolism with diffuse interstitial syndrome may be explained by severe right ventricle dilatation and paradoxical septum (generating elevated left pressures), which means that a simple emergency cardiac sonography would immediately (in patients with a cardiac window) correct the diagnosis (an enlarged right ventricle with a small left ventricle and a septal shift). This cardiac sonography, part of the Extended BLUE-protocol, is done always, after the BLUE-protocol. Note that we are surprised not to see more B-profiles in our series of severe pulmonary embolism, which may mean that our explanation (septal interference generating elevation of PAOP) is not the best one.

Pneumonia is a main differential diagnosis, since some show the B-profile. The physician is warned by some clinical elements (fever, mainly). We devoted the answer in Chap. 22 for a small part and the larger part in Chap. 35. Here, the physician is invited to extend the BLUE-protocol to part or whole of these targets: shifting the B-profile to a C-profile, searching for non-decreased left heart function, measuring volume of PLAPS, puncturing a pleural effusion (read the section on thoracentesis in Chap. 35), etc.

Patients without the B-profile and considered as severe pulmonary edema (3 % in our series) should also raise the question of a possible error from the managing team.

Diseases outside the BLUE-protocol: chronic interstitial diseases make the main group. They are part of the 3 % of patients excluded for rarity and account for one-third of them, i.e., 1 % of the patients, seen in the conditions of the BLUE-protocol 24 times less often than hemodynamic pulmonary edema (read Chap. 35).