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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5769_Библиотеки_им_академика_М_И_Перельмана
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150 oracic ultrasound
In patients with pulmonary edema, ultrasound shows numerous artifacts spread over the lung
16-18
fields
. ese are echogenic B Lines, which start from the pleural surface and are visible
on the entire screen (Fig. 1) (Clips 1-4).
B LINES
B LINES
Figure 1 – B Lines in patients with acute cardiogenic pulmonary edema.
Clips 1, 2, 3, 4 – Acute cardiogenic pulmonary edema. Numerous B Lines.
In Clip 4: evidence of pleural effusion.
B LINES
In full-blown cases of edema, the ultrasound pattern of the lung, which is typically made of
thin transverse echoes (reverberations) screened in depth (A Lines), is replaced by a pattern
of vertical echogenicity consisting of B Lines (Fig. 2).
Parenchymal lung patology 151
NORMAL
Figure 2 – A: normal lung; B: lung in pulmonary edema.
PULMONARY EDEMA
e presence of the ultrasound interstitial syndrome identifies edema with a sensitivity of
100%. e presence of an ultrasound pattern of normality excludes the possibility of an acute
cardiogenic pulmonary edema.
e concentration of comet tail artifacts on the pleural surface and their diffusion on lung
fields is variable. is appears in relation to the seriousness of the edema and with radiographic
score of pulmonary edema11 (Fig. 3). e direct correlations observed between BNP and pro
BNP and the presence of B Lines18 reveal the bond that exists between hydrostatic edema and
functional overload of the myocardium. It was also demonstrated that the amount of B lines
in cardiogenic edema correlates with NYHA decompensation class, with decreased ejection
fraction, and with the degree of diastolic dysfunction
B LINES
19-20
.
B LINES
Figure 3 – Early pulmonary edema. The concentration of B Lines is relatively modest.
e clinical and radiological existence of cardiogenic pulmonary edema, in fact, coincides
with the formation of artifacts that are first thinned and more numerous at the lung bases,
then extended over the entire surface of the lungs and confluent. Being a hydrostatic edema,
B Lines appear first at the bases and then in the middle and upper lung fields (cardiogenic wet
152 oracic ultrasound
lung). For the same reason in cardiogenic edema “spared areas” are not observed in subjects
without large emphysematous bubbles. ey are typical of non-cardiogenic pulmonary edema.
Even in normal subjects artifacts at the basal level may appear, they are usually visible through
the last intercostal space and posteriorly. eir meaning is of uncertain and not necessarily
related to pathology. Generally these do not exceed the number 8 in both lung fields (Fig. 4).
B LINES
LIVER
B LINES
Figure 4 – Presence of isolated B Lines at the right lung base in normal subject.
What produces B Lines in the edematous lung is not sufficiently clear. Lichtenstein’s3 hypothesis according to which B-Lines are generated by the large difference in acoustic impedance
between alveolar air and interlobular septa thickened by edema, is simplistic. It is possibly valid
in the “septal syndrome”, expressed by thinned B Lines (1-3 cm away from each other). We
also believe that resonance phenomena, as proposed by Avruch21 when he described the ringdown artifact, could be an acoustic interactions related to bullous systems in vitro, but not the
principal event in the production of B Lines in vivo, and especially in the pathological lung.
In general, it is more likely that the expansion of the interstitium, projected on the pleura,
produces discontinuity of the reflector. It is able to produce acoustic microholes along the
pleural surface. ese discontinuities induce focal reverberations (or internal reverberations)
and complex random interaction phenomena (constructive/destructive interferences, or other
effects of acoustic summation such as the “beats”
4,6
).
In qualitative terms, the acoustic interactions described above, would produce B Lines
(in figurative and elemental way, a kind of “glare” of the machine) and the pleural microdiscontinuities would be the basis of the punctiform origin of the B Lines.
In this perspective, even the simple venous perilobular distension in heart failure, critically alters
the relationship between air and fluid in the subpleural interlobular septa. is enlargement
may generate images through the described mechanisms in a very precocious phase of the
heart decompensation. is hypothesis is particularly attractive in light of the rapid change
in the cardiogenic interstitial syndrome after treatment with vasodilators and diuretics22.
e rapid appearance of interstitial syndrome, well before dyspnea occurs, in patients with
borderline heart failure undergoing exercise testing or stress echocardiography should not
be underestimated. is kind of “echostress” may have important diagnostic and prognostic
potentials.
Parenchymal lung patology 153
In a study of Agricola and his coworkers23, in patients undergoing exercise testing, the B
Lines increased numerically during PostExertional phase and this variation correlated with
the change in capillary wedge pressure relative to that effort.
Moreover, the same author demonstrated that on a small number of subjects a quantitative
score for B Lines correlated with pulmonary capillary wedge pressure and with extravascular
lung water determined by the PiCCO method24.
A more recent study has shown that the absence of B Lines (A Lines pattern) had a sensitivity of 67% and a specificity of 90% for a capillary wedge pressure less than 13 mm/Hg. e
specificity increased to 93% for wedge values lower than 18 mm/Hg25.
Many studies of recent years demonstrate that B Lines allow the diagnosis of an edematous
lung or the increase in extravascular water, whatever its etiology.
Omitting the inflammatory and contusive edema (localized in the majority of cases), discussed
elsewhere, other situations deserve particular attention. e high-altitude edema causes an
increase in extravascular lung water from asymptomatic levels to respiratory failure. Its etiology may be in part hydrostatic and in part due to alveolar capillary membrane permeabilization. Ultrasound of healthy subjects who go to high altitudes (higher than 5000 m above sea
level) shows interstitial syndrome in a high percentage (83%), that regresses after returning
to lower levels26.
B Lines also appear in 45% of subjects after free diving, with or without non-specific symptoms or dyspnea/hemoptysis27.
Non-cardiogenic edema (ARDS), especially if explored only with sector or convex probes,
shows some similarities with cardiogenic edema. e two types of edema can be differentiated according to the clinical context in which respiratory failure occurs and to some other
peculiarities that will be described later13 (Clip 5).
Clip 5 – Early ARDS. There is no finding to differentiate this situation from
that of acute cardiogenic pulmonary edema.
Fibrotic interstitial diseases, especially during their active phase, may produce artifacts that
resemble those of typical pulmonary edema. ere are not many descriptions of this phenomenon. Reissig’s clinical records28 are definitely comprehensive with regard to diagnostic
terms. Recently Lo Giudice and colleagues29 have also observed this phenomenon.
In these cases, an expanded interstitium not due to a simple increase in extravascular water
is evidently capable of generating vertical artifacts or B Lines.
It is obvious that the differentiation of these rarer forms is important because they provide
specific therapeutic approaches.
e interstitial fibrosis generates less pronounced and shorter artifacts, often over imposed on
a homogeneously echogenic (white) background. e pleura, investigated with high frequency
probes, shows surface irregularities and a greater apparent “thickness”. Sometimes superficial
fibrous micronodules generate images similar to B Lines, but non-punctiform in their origin.
False diagnosis of pulmonary edema due to a non-edematous widening of the interstitium
may be reduced if the sonographer pay attention to the images and to the clinical picture.
Considering the specific cardio-thoracic context in which ARDS appears, it is clear that the
154 oracic ultrasound
presence of an alveolar-interstitial syndrome (“wet lung”) identifies primarily patients with cardiogenic pulmonary edema. Further experimental and clinical confirmations are however useful.
Heart in cardiogenic pulmonary edema.
Integration between echocardiography and lung ultrasound
As outlined in the previous section, a wet cardiogenic lung requires a careful examination
of the heart, focused on the assessment of valvular and systo-diastolic function. For details,
please refer to the chapter on echocardiography. is section is about the role of the integration between lung ultrasound and echocardiography in patients with acute dyspnea, where
cardiogenic etiology is suspected.
e starting point are the guidelines on the diagnosis of acute heart failure published in 2008
and 2012 by the European Society of Cardiology30.
Figure 5 shows the flow chart (2012) recommended in cases of suspected acute heart failure.
Points included in this diagnostic algorithm will be critically analyzed.
Suspected acute onset heart
failure
Echocardiography BNP/NT-pro BNP
If heart failure
confirmed, determine
etiology and start
appropriate treatment
Figure 5 – Flow-chart proposed by the European Society of Cardiology for the diagnosis of acute heart
failure (McMurray JJV, Adamopoulos S, Anker SD
of acute and chronic heart failure 2012. Eur Heart J 2012;33:1787-1847.
NT-pro BNP < 300 pg/ml or
BNP < 100 pg/ml
Heart failure unlikely
ECG
Chest X-ray
ECG normal
and
et al.
ECG abnormal
or
NT-pro BNP ≥ 300 pg/ml or
BNP ≥ 100 pg/ml
Echocardiography
ESC Guidelines for the diagnosis and treatment
Evaluation of signs and symptoms is the first step. e sensitivity and specificity of the clinical
examination in detecting increases in filling pressures of the left ventricle or reduced ejection
fraction are rather low. In particular, the literature reports values of sensitivity and specificity
respectively around 54% and 69%31.
ECG is seldom normal in patients with acute heart failure (<10%) but is frequently abnormal
in patients with non-cardiogenic dyspnea. ECG has good sensitivity but poor specificity.
Parenchymal lung patology 155
Arterial blood gas analysis should be performed in all patients with acute respiratory failure,
but it certainly does not have high diagnostic value with regard to the diagnosis of acute
pulmonary edema.
Chest X-ray can provide information about the extent of pulmonary congestion, the size of
the cardiac shadow, the presence of pleural effusions or the presence of lung diseases that
cause or aggravate dyspnea.
ere are two limits of not negligible importance. e first relates to the inability of X-ray to
detect increases in extravascular lung water less than 30%. In these situations, the chest x-ray
may be completely normal
32,33
. e second limit relates to the fact that most of the time, in
critically ill patients, chest X-ray is performed in the supine or half-seated position, getting
one single antero-posterior view.
In these conditions portable equipments are used, so that the accuracy is often not optimal.
With regard to the natriuretic peptides, their diagnostic utility in acute failure has limitations.
eir negativity has a reasonable negative predictive value to exclude acute failure, but the
evidence is not as strong as with regard to the diagnosis of chronic heart failure. Moreover, at
present, there is still no agreement on the reference values of the natriuretic peptides in acute
failure. Finally, in cases of “flash” pulmonary edema or edema due to acute mitral regurgitation, the values of natriuretic peptides may be normal at onset30.
Positive clinical history of cardiac disease due to chronic heart failure is without a doubt very
important but it is not uncommon for these patients to have acute dyspnea secondary to
other diseases (e.g. pneumonia, pulmonary embolism, ARDS).
Only a complete negative cardiac anamnesis and clinical objectivity excludes the possibility
of acute heart failure and must orient towards a pneumogenic etiology of dyspnea.
e first evaluation should estimate the ejection fraction (EF), which allows distinguishing
patients with EF preserved if more than 45-50%, and patients with reduced EF (< 40%). In
the case of preserved EF, three possibilities should be considered: diagnostic error, transient
systolic dysfunction or diastolic dysfunction. In the case of EF, less than 40% the diagnosis
could be of left ventricular systolic dysfunction.
We believe some considerations should be made on these issues.
ere are not many chances to perform a real-time echocardiography. At present emergency
physicians do not have particular echocardiographic skills and in many situations the availability of an experienced cardiologist, 365 days a year and 24 hours a day is not possible.
Considering normal an ejection fraction if it is more than 45-50% is somewhat arbitrary. In
addition, EF is not only contractility, being strongly influenced by blood volume, preload
and afterload, heart rate and by the integrity of the valvular apparatus.
Another criticism is related to the evaluation of diastolic function in emergency. Doppler
study of transmitral flows and/or of the pulmonary veins in a patient with respiratory distress
is extremely problematic and complicated.
In conclusion, we believe that ECG associated with the Doppler study, once the diagnosis of
acute heart failure is correct, remains an essential tool to establish the exact cause (assessment
of biventricular function, valvular apparatus, pericardial diseases, mechanical complications
of acute myocardial infarction).
156 oracic ultrasound
Two clinical cases of patients with dyspnea are described below. ey show that the ultrasound
study of the lung helps in formulating the correct diagnosis, even when the physician is not
particularly well versed in echocardiography.
Case 1
57 year-old woman, known for dilated cardiomyopathy with implantable defibrillator. She
goes to Emergency Room for worsening dyspnea and exercise tolerance.
Echocardiography confirms the well-known marked dilatation of the left ventricle with severe
systolic dysfunction (Clip 6). In this context, it seems reasonable to treat the patient with
diuretics. Lung ultrasound, however, shows a “dry” lung with only a few B Lines at lung bases
(Clip 7). is element excludes de facto the cardiogenic etiology of dyspnea. e ultrasound
shows that the inferior vena cava is very small and completely collapsed (Clip 8). e chest
radiograph confirms the absence of venous congestion (Fig. 6). e patient’s symptoms are
due to hypovolemia induced by the massive diuretic therapy. e infusion of 1500 cc of saline
solution solves the clinical situation.
Figure 6 – Chest X-ray shows no sign of venous congestion.
Clip 6 – Scan shows a markedly dilated and dysfunctional left ventricle.
Clip 7 – Transverse scan at the lung base showing “dry” lung (linear probe).
Clip 8 – Longitudinal scan: the inferior vena cava is small and completely
collapsed in inspiratory phase (sector probe).
Parenchymal lung patology 157
Case 2
65-year-old male with no previous noteworthy medical history. He comes to the emergency
department with severe dyspnea since a few hours. ECG is normal. On auscultation of the
chest rhonchi, rales and crackles are evident at the right base. Chest X-ray (Fig. 7) raises the
suspicion of a right basal infiltrate and shows a normal-sized cardiac shadow.
Figure 7 – Chest X-ray performed in ER does not show pulmonary edema.
Echocardiography performed by emergency department physicians, is normal and, in particular, no dilatation of the heart chambers and/or gross abnormalities of the systolic function
are detected (Clip 9). e lung ultrasound shows a “cardiogenic wet lung” (bilateral B Lines,
gradient from the bases to the top fields in the absence of spared areas, normal pleural line,)
(Clip 10). e lung ultrasound strongly suggests cardiogenic pulmonary edema and it requires
a more careful evaluation of echocardiogram. e color Doppler examination reveals a severe
aortic insufficiency (reasonably acute because of the normal size of the left ventricle) (Clip 11).
Transesophageal echocardiography will document the rupture of an aortic cusp (Clip 12).
Clip 9 – Apical 4-chambers scan shows normal dimensions and kinetics of
the cardiac chambers.
Clip 10 – Longitudinal scan that highlights several B Lines and normal
pleural line (convex probe).
Clip 11 – Apical 5-chambers scan. Color Doppler shows severe aortic
insufficiency.
Clip 12 – Transesophageal echocardiography shows the rupture of the right
aortic cusp.
158 oracic ultrasound
ese two cases show that lung ultrasound may provide decisive elements for the diagnosis.
e first case highlights the usefulness of integrating heart ultrasound with lung ultrasound.
e second case shows that an ultrasound of cardiogenic pulmonary edema requires careful
assessment of the heart that often requires adequate expertise.
Figure 8 summarizes a simple and rational approach for the patient with acute dyspnea.
ACUTE
DYSPNEA
LUNG
ULTRASOUND
“DRY” LUNG
“CARDIOGENIC
WET” LUNG
• COPD
• Pneumothorax
• Pulmonary embolism
• Asthma
• Pneumonia
• Atelectasis
• Other
Figure 8 – Diagnostic flow-chart in patient with acute dyspnea. Ultrasound evaluation starts from the
study of the lung. In the case of dry lung the cardiogenic nature can be excluded. In the case of “wet
cardiogenic lung”, a careful and comprehensive echocardiographic assessment is necessary.
Echocardiography
• Assessement of
systo-diastolic function
• Assessement of valvular
apparatus
• Other
The dyspnoeic patient
Dyspnea is a common symptom. Sometimes it represents a simple pathology, some other
times it can be a manifestation of a life-threatening situation.
Various diseases can cause the sudden or relatively rapid onset of dyspnea. ey include: airway
obstructive disease (generally exacerbations of COPD where dynamic bronchial obstruction
is relevant), pulmonary artery embolism and heart disease (increase in pulmonary capillary
wedge pressure). Other various etiologies occasionally occur (hematologic, toxic, metabolic,
neurogenic or psychic34).
Based on clinical history or objectivity, in many circumstances the differential diagnosis is
easy. However, in emergency, when medical records are absent and clinical data must be
acquired quickly, this is not true. ese difficulties may be amplified by the coexistence of
diseases involving both respiratory and cardiovascular systems. In these situations patients
with COPD or asthma, who develop left ventricular failure, show bronchoconstriction and
wheezing in association with paroxysmal nocturnal dyspnea crisis and pulmonary edema. It
was reported that diagnostic uncertainty characterizes more than 30% of patients with acute
respiratory distress in Emergency Room35.
Chest objectivity, with interstitial edema, can be surprisingly poor, even if the patient experiences a significant respiratory effort for the reduction of lung compliance36.
Parenchymal lung patology 159
erefore, the therapy cannot readily be targeted, at least until chest X-ray demonstrates an
increase of the extravascular lung water and/or pleural effusion.
e advantage to detect an ultrasound “wet lung” is the confirmation that the breathlessness
is of pulmonary origin, the greatest advantage to detect a normally specular lung is that the
patient may not have a pulmonary edema, but he or she can have a pulmonary embolism or
asthma.
ese prerogatives of ultrasound overcome many shortcomings of traditional radiography.
e radiological investigation acquires its full diagnostic potential when performed under
optimal conditions. For an accurate detection of pulmonary edema, in its various degrees and
shades, it would be necessary to perform X-ray with great accuracy. is essential condition
does not occur just in the case of the critically ill patient37.
It is known that chest radiographs in ICUs and in the emergency department, employing
mobile devices, are very different from the ideal ones, especially for detecting lung density,
lung vascularity and the cardiomediastinal shadow. Even if this diagnostic procedure still has
a role in the urgent diagnosis of dyspnea, all these factors must be taken into account because
they can complicate the achievement of an accurate diagnosis38.
e chest radiograph shows a sensitivity of 41% for detecting apical diversion of the flow;
27% for interstitial and 6% for the alveolar edema39. Up to 18% of patients with acute heart
failure shows no signs of congestion and pulmonary edema is seen in X-rays only when the
increase in extravascular lung water is at least 30%. In chronic heart failure, radiographic signs
of congestion have low diagnostic accuracy to identify individuals with high left atrial pressure. Chest radiographic signs are absent in 53% of patients with pulmonary capillary wedge
pressure from 16 to 29 mmHg and in 39% of those with wedge greater than 30 mmHg40.
Finally, among subjects with echocardiographically demonstrated cardiomegaly, 22% has a
normal cardiothoracic index41.
Chest X-ray in dyspneic patients is aimed at demonstrating a possible pleural or parenchymal pathology, able to influence the ventilatory capacity, lung compliance and alveolar gas
exchange.
However, pleural effusions may not be obvious and are underestimated by radiography performed on supine patient. In subjects with heart failure, sensitivity, specificity and diagnostic
accuracy of the chest radiograph for pleural effusion are respectively 67%, 70% and 67%42.
In the lung a pathologic involvement may be sectorial (e.g. large consolidations or areas
of atelectasis) or global (as in the case of diffuse interstitial disease or alveolar-interstitial
edematous imbibition), systematized (multilobar, lobar, segmental) or random. However, the
clinician must consider the existence of conditions causing dyspnea, which may not show
corresponding radiographic signs, first of all pulmonary embolism.
In emergency, a dichotomous distinction of patients undergoing clinical examination plays
a crucial role. Considering lung ultrasound, the primary distinction is between diffuse “wet”
and “dry”, in order to propose differential diagnostic hypotheses (in primis, edema and nonedema, respectively).
is sort of “triage”, although rough, can differentiate left ventricular failures, and cardiogenic edema, from bronchogenic or vascular dyspnea (embolism), which never show, if not
complicated, global congestive aspects in the lung.
In relation to pulmonary edema, radiology shows interstitial and alveolar aspects that are well
coded both in the case of cardiogenic and non-cardiogenic edema.
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