Lung ultrasound
Lung ultrasound is based primarily on the detection of lung sliding and the interpretation of artifacts generated by ultrasonographic waves.
The presence of lung sliding excludes a pneumothorax under the probe with certainty and requires a minimal training to recognize [
12‐
15]. While not specific (Table
2), its absence in the appropriate context can be highly suggestive of a pneumothorax. The “lung point”, which is pathognomonic for a pneumothorax, is observed when lung sliding is intermittently absent from the ultrasound field at expiration [
16]. A lung point might not be observed in the case of tension pneumothorax because the lung is expected to be completely collapsed.
Table 2
Potential causes of abolished lung sliding other than pneumothorax
Pneumonia |
Acute respiratory distress syndrome (ARDS) |
Pleurodesis, pleural scarring |
Severe emphysema |
Bronchial obstruction |
Mainstem intubation |
Apnea |
It is also possible to detect an interstitial syndrome by observing the characteristic and reproducible artifacts called B-lines [
17‐
19]. They represent abnormal extravascular lung water. An interstitial syndrome is defined by the presence of at least three B-lines in the width of an intercostal space (the “B-profile”). A B-profile can represent cardiogenic pulmonary edema [
20‐
22] but is not specific for this pathology. It can also be found with other interstitial diseases, such as pulmonary fibrosis, ARDS and pulmonary contusions. The presence of a B-line also excludes a pneumothorax as it originates from the pleura [
23]. Pure cardiogenic shock is unlikely to be the primary cause of hemodynamic instability in the presence of a normal lung pattern on ultrasound [
20], suggesting that fluid administration is probably safe.
Focused echocardiography and fluid responsiveness
A focused bedside cardiac ultrasound comprising four views (subcostal view, parasternal long and short axis views, and apical four-chamber view) has been previously described [
10,
24,
25]. It provides critical information for patient care, namely information about left/right ventricular size and function, volume status and pericardium assessment. Physicians with limited ultrasound training can correctly estimate the qualitative left ventricular function [
26‐
28]. These qualitative assessments correlate well with quantitative assessments [
29,
30].
The cardiac subcostal view is sensitive view for the detection of a pericardial effusion and it often is the only available window in critically ill patients or in the context of cardio-pulmonary resuscitation. For those reasons, it is the initial cardiac view performed in our algorithm.
Tamponade is a diagnosis that must be considered as a reversible cause of shock in the unstable patient [
2]. Bedside ultrasound has greatly facilitated its detection as pericardial effusion can easily be demonstrated. Tamponade physiology is suggested by a pericardial effusion causing right atrial or ventricular collapse in diastole [
31,
32]. It is possible to observe a pendulum movement of the heart in the presence of a massive effusion (a “swinging heart”). Tamponade should be associated with an elevated central venous pressure that can be demonstrated in the subcostal window by a plethoric (>20 mm) inferior vena cava (IVC) without respiratory variation.
Assessing the diameter of the IVC and its respiratory variation will also allow for the estimation of fluid responsiveness. An inferior vena cava diameter of less than 20 mm (measured proximal to the hepatic vein) and respiratory variation of more than 50% are associated with a normal to low central venous pressure (CVP) [
33], which is a good predictor of fluid responsiveness. A small (diameter less than 10 mm) IVC has been shown to correlate with hypovolemia in the trauma patients [
34]. Thus, significant respiratory variation or collapse of the IVC of patients presenting in shock should always be taken into consideration [
35], especially if it is associated with a hyperdynamic left ventricle (LV) because this also suggests hypovolemia. As previously noted, dilation (more than 20 mm) and the loss of respiratory variability in the inferior vena cava suggest an elevated central venous pressure. Respiratory variation of the inferior vena cava is often altered in mechanically ventilated patients, in cirrhosis [
36] and in chronic pulmonary diseases, and should be interpreted accordingly. While respiratory variation of the IVC can be a good predictor of fluid responsiveness in hypotensive patients who are mechanically ventilated [
37,
38], a plethoric IVC without respiratory variation is not in and of itself a contraindication to fluid administration in this population. The lack of respiratory variation should be closely interpreted within the clinical context because, like high values of CVP, it does not necessarily imply a lack of fluid responsiveness.
The qualitative evaluation of LV function allows for further refinement in the initial evaluation of shock. The expected myocardial response in the presence of hypovolemic, distributive or obstructive shock is left ventricular hyperdynamism because these conditions are associated with poor LV filling. This may be suspected when wall “kissing” occurs in systole. A small inferior vena cava and normal lung pattern are also expected if hypovolemia is the cause of hypotension. Sepsis should be one of the first conditions considered when a hyperdynamic left ventricle is encountered in nontraumatic undifferentiated shock [
39]. Another condition that can present with shock and a hyperdynamic left ventricle is severe acute mitral regurgitation as will be seen when a chordae tendinae ruptures. This could potentially be erroneously interpreted as hypovolemia by the non-expert sonologist with limited experience in Doppler technique. However, in contrast to hypovolemia, severe acute mitral regurgitation would likely be associated with a B-profile and less compliant inferior vena cava (as it is associated with higher filling pressures). This constitutes an example where, as stated before, lung ultrasound findings can influence the echocardiographic interpretation.
Focused echocardiography showing left ventricular hypokinesia may be an indicative of cardiogenic shock. If poor cardiac function is the cause of shock, the clinician should usually be able to demonstrate a B-profile on lung ultrasound (along with a plethoric IVC). Indeed, LV dysfunction severe enough to cause cardiogenic shock is expected to be associated with high filling pressures. The foreknowledge of lung pattern may thus help in interpreting the subsequent echocardiography findings because a hypokinetic left ventricle associated with a normal lung pattern suggests cardiac co-morbidity (i.e., chronically depressed LV function) rather than pure cardiogenic shock, more so in the presence of a small IVC. One should also consider other pathologies in this situation and provide adequate fluid resuscitation, with the caveat that resuscitation may be complicated given the limited cardiac reserve. In addition to myocardial ischemia, other potentially reversible conditions causing myocardial dysfunction can be considered and are listed in Table
1.
Pulmonary embolism (PE) is also a cause of undifferentiated shock. Hemodynamically significant PE is consistently associated with acute right ventricular strain [
40]. Signs suggesting the right ventricular strain can often be found in the apical four-chamber and parasternal short-axis views. Increased pressure may lead to paradoxical movement of the septum wall [
41] and give rise to a “D-shape” left ventricle in the short-axis view. The obstructive shock caused by pulmonary embolism is expected to be associated with a plethoric inferior vena cava without respiratory variation. The sonologist should be aware that smaller PEs not large enough to cause hemodynamic compromise do not consistently cause identifiable cardiac sonographic findings [
42].