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330 oracic ultrasound
terms it is possible to estimate this pressure through the parameters that have been described
in the previous paragraph. Pulsed Doppler E wave and Tissue Doppler E’ wave amplitudes,
respectively related to the transmitral flow mitral (E wave) and mitral annulus motion (E’
wave), are detected. An E/E’ ratio greater than 15 indicates a left ventricular end-diastolic
pressure greater than 15 mmHg, an E/E’ ratio of less than 8 indicates a LVFP less than
15 mmHg (Fig. 33).
Figure 34 – Classification of diastolic function. A: normal subject. E waves are taller than A waves
and E’ waves are taller than A’ waves, E/E’ ratio is low, E’ velocity is more than 8 cm/sec (above: mitral
inflow pulsed Doppler interrogation; below: tissue Doppler interrogation of the septal mitral annulus
velocities). B: impaired relaxation. E wave are smaller than A wave and their deceleration time is longer
than 220 msec. E’/A’ ratio is less than 1. C: pseudonormal pattern. E/A ratio is apparently normal and E
is taller than A wave. However, tissue Doppler interrogation of the mitral annulus shows a ratio between
E’ and A’ less than 1. E’ wave velocity is low (below). D: restrictive pattern. Above: high E waves with
reduced deceleration time (<150 msec) are represented. Below: low E’ waves velocity is evident. The
E/E’ ratio is high (see text for further information).
e intermediate values are more difficult to interpret without adjunctive data. A wet lung is
suggestive of high LVFP, whereas E’ velocity less than 5 cm/sec indicates a low left ventricular
compliance
16,17
.
Echocardiography 331
In the past, several methods for estimating left ventricular filling pressure have been proposed.
Although all of the techniques showed promise in initial reports, contradictory data emerge in
duplication studies. erefore, an integrated approach to high LVFP is recommended (E/E’
ratio, E amplitude, E’ velocity, restrictive pattern of the mitral inflow, left atrial enlargement,
cardiogenic wet lung).
Conversely, a correct estimation of left ventricular end-diastolic pressure is useful if a pulmonary interstitial pattern is identified, and it is not clearly interpretable as cardiogenic or
pneumogenic (e.g. fibrosis).
Right ventricle: is it small? is it big? does it move?
In emergency medicine, pulmonary embolism (PE) is without a doubt the clinical condition
that most frequently involves the right cavities of the heart. Clinical diagnosis of PE is difficult and this gives reason for a significant discrepancy between the number of pulmonary
embolisms diagnosed in life and on the autopsy table18. e Task Force of the European
Society of Cardiology in 200019 distinguished pulmonary embolism in three groups from
the echocardiographic standpoint: massive, non-massive and with normal echocardiogram.
Massive embolism occurred with shock or hypotension (systolic blood pressure <90 mmHg
or reduction in systolic BP ≥ 40 mmHg for more than 15 minutes, if not caused by rhythm
disturbances, hypovolemia or sepsis) and dilatation of the right cavities. Massive pulmonary
embolism therefore always occurs with echocardiographic alterations. Non-massive pulmonary
embolism does not have hemodynamic instability but shows dilatation of the right cavities
on echocardiography.
In 2008, the European Society of Cardiology published new guidelines20, that have greatly
limited the diagnostic role of echocardiography in PE. Two clinical scenarios are identified:
1. suspected “low risk” pulmonary embolism;
2. suspected “high risk” pulmonary embolism.
Low risk PE is not associated with hypotension or shock, while high risk PE occurs with
shock and hypotension.
Suspected “low risk” pulmonary embolism is differentiated on the basis of clinical probability:
low, intermediate and high. If the clinical probability is intermediate or low, the patient is
layered with the D-dimer dosage and if this is not increased, the possibility of pulmonary
embolism can be excluded. In patients with positive D-dimer, CT angiography with multiple
detectors that will confirm or exclude PE should be performed. In patients with a high clinical probability, the D-dimer is not provided and the immediate execution of angio-CT with
multiple detectors is recommended; if positive, it will enable the treatment and, if negative,
further investigations will eventually be considered.
In suspected “high risk” PE (with shock or hypotension), the immediate execution of angio-CT,
if readily available, is proposed. e echocardiogram is considered if CT angiography is not
available or if the patient has a severe hemodynamic instability that would make it too risky to
transport him/her to Radiology. In such a context, clinical evidence of right ventricular dilatation justifies the fibrinolytic treatment without further diagnostic examination (Figs. 35-36).
Echocardiography in all cases has a crucial role in the risk stratification of patients with pulmonary embolism22. e ultrasonographic evidence of right ventricular dysfunction associated
with positive troponins, for example, identifies high-risk individuals for whom fibrinolysis,
if there is low risk of bleeding, can be considered23.
332 oracic ultrasound
Suspected non-high-risk PE
i.e.withoutshockorhypotension
Assess clinical probability of PE
implicitorpredictionrule
Low/intmediateclinicalprobability
or“PEunlikely”
Highclinicalprobability
or“PElikely”
D-dimer
negative
No treatment*
NoPE±
No treatment*
positive
Multidetector CT
Treatment*
PE+
Multidetector CT
NoPE
No treatment* or
PE
Treatment*
investigate further
Figure 35 – Flow-chart in suspected “low risk” pulmonary embolism. From: Task Force for the
Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC).
Guidelines on the diagnosis and management of acute pulmonary embolism. Eur Heart J 2008; 29(18):
2276-2315.In these guidelines, compression ultrasonography of the lower limbs (CUS) is suggested only
in the case of negative single detector CT angiography. It should also be remembered that the CUS is
positive in approximately 10% of patients with suspected pulmonary embolism and that when positive,
in a hemodynamically stable patient, angio-CT can be avoided21.
Suspected high-risk PE
i.e.withshockorhypotension
CT immediately available*
no
yes
Echocardiography
RVoverload
no
Search for other causes
Thrombolysis/embolectomy
notjustied
yes
Noothertestsavailable
orpatientinstable
CTavailableand
patientstabilized
positive
PE-specific treatment
justified
Considerthrombolysisor
embolectomy
CT
negative
Search for other causes
Thrombolysis/embolectomy
notjustied
Figure 36 – Flow-chart in suspected “high risk” pulmonary embolism. From: Task Force for the
Diagnosis and Management of Acute Pulmonary Embolism of the European Society of Cardiology (ESC).
Guidelines on the diagnosis and management of acute pulmonary embolism. Eur Heart J 2008; 29(18):
2276-2315.
Echocardiography 333
e echocardiographic elements typically found during hemodynamically significant pulmonary embolism are:
• Dilation (diameter > 42 mm at the base) and hypokinesia of the right ventricle.
• Increased ratio right ventricle/left ventricle caused by the bulging of the interventricular
septum toward the left ventricle (on the short axis the systodiastolic flattening of the interventricular septum typically produces a D-morphology of the left ventricle).
• Dilatation of right ventricular outflow tract (diameter > 27 mm at end diastole), proximal
pulmonary arteries and pulmonary hypertension assessed through the tricuspid regurgitant
jet velocity (speed which generally lies between 3 and 3.5 m/sec) (Fig. 37) (Clips 24-29).
Figure 37 – Evaluation with continuous-wave Doppler of the tricuspid regurgitant jet in patient with
pulmonary embolism and shock. A: jet velocity is 3.70 m/sec, gradient between ventricle and atrium
of 54.6 mmHg; the right atrial pressure is around 15 mmHg, systolic blood pressure in the pulmonary
artery is 69.6 mmHg. B: after fibrinolytic therapy the speed of the jet is reduced to 2.46 m/sec with a
gradient of 24.3 mmHg; the pressure in the right atrium is around 8 mm Hg, systolic blood pressure in
the pulmonary artery is around 32.3 mmHg.
Clip 24 – Apical 4 chambers scan. Patient with acute respiratory distress,
hypotension and hypoxemia in the course of pulmonary embolism. Presence
of dilated right cavities with systolic bulging toward the left cavities of the
interatrial and interventricular septa.
Clip 25 – Apical 4 chambers scan in patient with submassive PE.
Clip 26 – Subcostal 4 chambers scan in patient with massive PE. Marked
dilatation and reduced kinetics of the right ventricle.
Clip 27 – Parasternal short-papillary axis scan, in patient with massive
PE. Marked dilatation of the right ventricle and interventricular septal
systodiastolic flattening, which gives a D-morphology to the left ventricle.
334 oracic ultrasound
Clip 28 – Apical 4 chambers scan in patient with massive PE. Marked
dilatation of the right cavities and septal shift to the left, because of the
increase in pressure in the right cavities.
Clip 29 – Subcostal short-mitral axis scan in patient with massive PE.
Dilatation of the right ventricle and left ventricular D-morphology for the
systodiastolic flattening of the interventricular septum.
e inferior vena cava (IVC) is also dilated and does not collapse in the inspiratory phase
(Clip 30). IVC diameter >21 mm that collapses <50% with a sniff suggests high right atrium
pressure (10-20 mm/Hg).
Clip 30 – Inferior vena cava in a patient with massive PE, it is dilated and
without any change in respiratory activity.
In pulmonary embolism McConnell described a typical regional hypokinesia sparing the apical
portion of the right ventricle
24,25
. Its reason is not entirely clear, but this sign is not generally
found in other situations of systolic overload of the right ventricle. McConnel sign has a
sensitivity of 77% and a specificity of 94% for the diagnosis of acute pulmonary embolism,
and it tends to disappear if the treatment is effective (Clip 31).
Clip 31 – McConnell Sign in a patient with submassive PE. The kinetics
of the right ventricle in the apical portion is retained, while the free wall is
hypokinetic.
Echocardiography is rarely able to demonstrate the presence of emboli in the pulmonary
arteries, although in our experience the short axis subcostal scan frequently allows, in the
case of massive pulmonary embolism, the visualization of thromboemboli in the pulmonary
arteries (Clips 32-34).
Clips 32, 33 – Subcostal short axis aorta scan in patient with massive PE.
Presence of hyperechoic formations floating in the right, dilated branch of the
pulmonary artery, related to thromboemboli.
Clip 34 – Subcostal short axis aorta scan in patient with massive PE.
Presence of thrombotic formation in the left branch of the pulmonary artery.
Echocardiography 335
e earliest the test is executed, the more frequent the detection of thromboemboli in the
right cavities (Clips 35-36).
Clip 35 – Parasternal short axis aorta scan in patient with massive PE and
right hemiparesis. Presence of hyperechoic formation floating in the right
atrium, apparently adherent to the atrial septum. It is a thromboembolus
straddling the oval fossa. The patient had a pulmonary embolism complicated
by paradoxical embolism.
Clip 36 – Subcostal 4 chambers scan, performed soon after the onset of
dyspnea and chest pain in a patient with recent surgery. Marked dilatation
of the right cavities and presence of voluminous thromboembolus in the right
atrium.
Finally, the role of echocardiography seems relevant in the assessment of right ventricular
kinetics in the case of right ventricular infarction, which is most often associated with diaphragmatic infarction (Clip 37).
Clip 37 – Apical 4 chambers scan. Right ventricular infarction in hypotensive
patient with electrocardiographic inferior infarction. Akinesia of the free wall
of the right ventricle.
For the differential diagnosis with pulmonary embolism, the estimation of pulmonary pressure
is useful: it will be low in the case of right ventricular infarction26 (Fig. 38).
Figure 38 – Evaluation with continuous-wave Doppler of the tricuspid regurgitant jet velocity in patients
with right ventricular infarction. The speed of the jet is 2.30 m/sec with a gradient between the right
atrium and ventricle of 21.2 mmHg; the right atrial pressure was around 12 mmHg, systolic blood
pressure in the pulmonary artery was around 33 mmHg.
336 oracic ultrasound
➣ Pericardium: is there fluid or tamponade?
e pericardial effusion is highlighted as a transonic area adjacent to the epicardium. When the
effusion is small, it is limited to the sloping portions with better visualization during diastole.
Echocardiography estimates with good approximation the amount of liquid in the pericardial sac. An effusion less than 1 cm thick is defined as mild, moderate between 1 and 2 cm,
severe when the thickness is greater than 2 cm. ese thicknesses correspond to the amount
of liquid respectively of about 300, 500 and 700 cc (Clips 38 -39).
Clip 38 – Parasternal short axis mitral scan. Mild pericardial effusion,
surrounding the left ventricle.
Clip 39 – Parasternal long axis scan. Mild pericardial effusion in front of the
right ventricle and behind the lower wall of the left ventricle.
e evaluation of the pericardial effusion includes subcostal, apical and parasternal scans. e
most important clinical problem related to the presence of pericardial effusion is to determine
whether the presence of the fluid causes or not cardiac tamponade.
e cardiac tamponade represents an obstructive event due to an increase of pericardial effusion and increased intrapericardial pressure.
e speed with which the liquid accumulates, rather than its volume, is responsible for the
occurrence of a life threatening condition. e rapid accumulation of an amount even less
than 150 ml may result in a marked increase in intrapericardial pressure, which can severely
reduce cardiac output (“surgical tamponade”)
Amounts of liquid exceeding 1000 cc gradually accumulated may not result in significant
changes in cardiac output (“medical tamponade”).
e clinical diagnosis of cardiac tamponade is not easy because the signs and symptoms are
common to other critical situations producing obstructive shock (eg, pulmonary embolism).
e peculiarity of the treatment of a critical pericardial effusion (pericardiocentesis) obviously
requires a very quick diagnosis.
Echocardiography undoubtedly has a prominent role in the diagnosis and treatment of cardiac
tamponade29. Firstly, it is able to visualize and quantify the effusion, and secondly, it detects
very accurately the signs of tamponade:
• diastolic collapse of the free wall of the right ventricle;
• collapse of the right atrium (Clips 40-42);
• collapse of the left atrium and very rarely of the left ventricle;
• dilatation of the inferior vena cava with lack of inspiratory collapse (Clip 43);
• swinging heart (Clips 44-46).
e evaluation of the collapse of the right atrium with apical 4 chambers scan is the simplest
sign of relief for the emergency physician. It should be recalled that the right atrial collapse
is a very sensitive, but not a specific sign to the presence of tamponade, as it can be observed
27,28
.
Echocardiography 337
even in case of hypovolemia (Clips 47-48). However, if the atrial collapse is present for at
least 30% of the cardiac cycle, its specificity and predictive value are close to 100%12.
Clip 40 – Subcostal 4 chambers scan. Mild pericardial effusion in patients
with thoraco-abdominal trauma and hypotension. Although the effusion is
mild, the collapse of the right atrium is evident.
Clip 41 – Apical 4 chambers scan. Mild pericardial effusion with signs of
tamponade for the collapse of the right atrium.
Clip 42 – Apical 4 chambers scan. Despite the slight pericardial effusion,
extensive collapse of the right atrium is evident. It was a young patient
admitted to the emergency department with syncope and hypotension. The
final diagnosis was of acute hemorrhagic perimiocarditis.
Clip 43 – Inferior vena cava in a patient with cardiac tamponade. Dilated
inferior vena cava without variation of the diameter during respiratory
activity.
Clip 44 – Parasternal long axis scan. Swinging heart in a case of medical
tamponade.
Clip 45 – Parasternal short axis papillary muscles view. Swinging heart in
a case of medical tamponade.
Clip 46 – 4 chambres apical scan. Swinging heart (medical tamponade).
Clips 47, 48 – Evidence of mild pericardial effusion in patients with severe
systolic dysfunction of the left ventricle. A large collapse of the right atrium
without any clinical signs of cardiac tamponade.
338 oracic ultrasound
In case of cardiac tamponade, the pulsed Doppler assessment of the transmitral and transtricuspid flows allows to detect fluctuations of speed (> 25% transmitral flow and 40% transtricuspid flow) in relation to the in- and expiratory phases. is relatively simple finding
represents the equivalent of the clinically detected paradoxical pulse (Fig. 39).
Figure 39 – Assessment with pulsed Doppler of mitral flow velocity in a patient with cardiac tamponade.
Large fluctuations of speed (> 25%) resulting from the respiratory activity.
➣ Valves: stenosis? regurgitation?
e assessment of cardiac valves by echocardiography is another field that can prove extremely
useful in urgent need, to clarify a critical clinical condition.
e measurement of transvalvular gradients or valve areas requires experience and skills. e
use of continuous and pulsed Doppler and color Doppler is essential for the comprehensive
evaluation of valvular diseases. As already stated, in this chapter the details of these methods
won’t be explored. Some clinical application of Doppler ultrasound for estimating valvular
pathology will be discussed in the next chapter. For a basic exploration, a visual assessment of
the anatomy of a valve apparatus, in a particular clinical context, may help to define a critical
pathology (acute pulmonary edema, chest pain or exertional syncope). In many cases, simple
images will provide clinical paradigmatic cases of frankly pathological anatomical situations.
Mitral valve
S: C -.
Clip 49 – Parasternal long axis scan. Patient arrives in the emergency
department with acute pulmonary edema requiring intubation. The mitral
leaflets appear thickened (fibrocalcific) and markedly hypomobile. Severe
mitral stenosis was “silent” and not known.
Echocardiography 339
Clip 50 – Apical 4 chambers scan. Thickened mitral leaflets with marked
reduction in diastolic excursion.
Clip 51 – Parasternal long axis scan. Thickened mitral leaflets with slight
reduction in diastolic excursion.
F: C -.
Clip 52 – Apical 4 chambers scan. Color Doppler highlights broad and
extensive mitral regurgitation jet.
Clip 53 – Apical 5 chambers scan. Color Doppler highlights broad and
extensive mitral regurgitation jet in the context of a severe systolic dysfunction
of the left ventricle.
Clip 54 – Apical 4 chambers scan. Patient with acute pulmonary edema
requiring intubation. The rear flap exceeds the point of coaptation with the
anterior leaflet for acute rupture of chordae tendineae (flail posterior leaflet).
Acute and severe mitral regurgitation.
Clip 55 – Apical 4 chambers scan. Patient with PE, severe left ventricular
dysfunction and flutter 2:1. Color Doppler highlights extensive mitral
regurgitation jet.
Clip 56 – Same as Clip 55. After electric cardioversion, a sharp reduction
of mitral regurgitation jet is detected, confirming the negative effects on
hemodynamics of disturbed rhythm.
Clip 57 – Apical 5 chambers scan. 78-year-old patient with recent inferior
miocardial infarction. Sudden pulmonary edema quickly followed by
shock. Auscultation detects a regurgitation murmur not previously present.
Echography shows the break at the base of the posteromedial papillary
muscle resulting in acute and massive mitral regurgitation.
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