Pulsus Paradoxus

Sindromi costrittive
pericardiche
Pericardite costrittiva
Cardiomiopatia restrittiva
Tamponamento cardiaco
TAMPONAMENTO
CARDIACO
TAMPONAMENTO CARDIACO
situazione acuta e grave
Acute Tamponade

Occurs due to rupture of the heart or aorta, trauma, or
as a complication of catheter or pacemaker procedures

Acute cardiac tamponade is generally sudden in onset,
may be associated with chest pain and dyspnea, and is
life-threatening if not promptly treated. The central
venous pressure is typically markedly elevated, while
hypotension is common due to the decline in cardiac
output. The heart sounds are often muted.
Subacute Tamponade

Occurs due to neoplasm, uremia, or idiopathic pericarditis

Patients may be asymptomatic or may complain of
dyspnea, chest discomfort or fullness, peripheral edema,
fatiguability, or other symptoms referable to increased
filling pressures and limited cardiac output.

The physical examination may reveal hypotension with a
narrow pulse pressure, reflecting the limited stroke volume.
However, patients with preexisting hypertension may
remain hypertensive.
Eziologia
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Neoplasia
Pericardite idiopatica
Uremia
IMA
Batteri
TBC
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Radiazioni
Mixedema
Dissezione di AA
Sindrome post
pericardiotomica
LES
Cardiomiopatia
FISIOPATOLOGIA
DEL TAMPONAMENTO CARDIACO
Tamponamento cardiaco
Cardiac Tamponade

Early stage


mild to moderate elevation of central venous
pressure
Advanced stage
 intrapericardial pressure
 ventricular filling,  volume
 hypotension
 impaired organ perfusion

Cardiac Tamponade
pathophysiology

fluid accumulation within the pericardial space resulting in
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left to right heart interdependence
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increased intracardiac pressure
progressive limitation of ventricular diastolic filling
reduction of stroke volume and cardiac output
Competition for room in the abnormally fixed pericardial space
(chamber interaction) is by far the principal mechanism
blood pooling in the lungs during inspiration
Sintomi
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Dispnea
Dolore toracico
Tosse
Disfagia
Dolore addominale
Singhiozzo
Sazietà preoce
Nausea
Sintomi
Critical tamponade is a form of cardiogenic shock,
and the differential diagnosis may initially be elusive.
Since most symptoms are nonspecific, tamponade
must be suspected in many contexts — for
example, in patients who have wounds of the chest
or upper abdomen and hypotension or in those who
have hypotension preceded by symptoms of an inciting
pericardial disease, such as chest discomfort
and pleuritic pain.
Triade di Beck


Descritta nel 1935 da Claude S. Beck
Caratteristiche del tamponamento
Ipotensione arteriosa sistemica
 Aumento della pressione venosa sistemica
 Toni ovattati

Segni clinici

Generali
 Ansietà
 Sudorazione
algida
 Tachipnea
Tachicardia
 Distensione venosa
giugulare
 Cianosi periferica

Segni clinici
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Ovattamento dei toni cardiaci
Sfregamenti

Polso paradosso

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First described by Kussmaul in 1873 as a
palpable decrease or absence of the radial pulse
during inspiration.
Central Venous Pressure

Kussmaul’s Sign

venous return increases with inspiration and a
high right atrial pressure resists filling resulting
in an increased JVP
SEGNO DI KUSSMAUL
TAMPONAMENTO:POLSO PARADOSSO

Place the patient in a position of comfort and conduct manometric studies
during baseline respiration.

Raise sphygmomanometer pressure until Korotkoff sounds disappear.

Lower pressure slowly until first Korotkoff sounds are heard during early
expiration with their disappearance during inspiration.

Record this pressure.
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Very slowly lower pressure until Korotkoff sounds are heard throughout the
respiratory cycle with even intensity.

Record this pressure.

The difference between the two recorded pressures is the Pulsus Pardoxus.

Significant pulsus paradox is greater than or equal to 10% of the pressure at
which all Korotkoff sounds are heard with even intensity.
PALPATING PULSUS PARADOXUS

Severe pulsus paradoxus can easily be
palpated in the radial, brachial, or femoral
pulses as a weakening or disappearance of
the pulse during inspiration (which is best
observed by watching or palpating the rise
and fall of the chest)
MEASURING PULSUS PARADOXUS

An important clinical skill for following
patient is the ability to estimate the severity
of pulsus paradoxus:
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Using a sphygmomanometer in the standard
fashion but deflate the cuff more slowly than usual
During deflation, the first Korotkoff sounds are
audible only during expiration, but with further
deflation, Korotkoff sounds are heard throughout
the respiratory cycle.
The difference between the systolic pressures
quantifies pulsus paradoxus
Do not instruct the patient to breathe deeply
during this evaluation. This can influences the
severity of the pulsus
SIGNIFICANCE OF PULSUS
PARADOXUS IN TAMPONADE
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Pulsus paradoxus precedes severe
hemodynamic deterioration
When pulsus paradoxus is detectable in
cardiac tamponade, the tamponade is at
least moderate in severity
Almost all patients with pulsus paradoxus
from tamponade need to have pericardial
fluid removed
Pulsus Paradoxus
tamponamento senza polso
 Difetto del setto
interatriale
 Severa stenosi aortica
 Insufficienza aortica
 Disfunzione
ventricolare sinistra
polso senza tamponamento
 COPD
 Embolia polmonare
 Infarto del ventricolo
destro
 Pericardite effusivocostrittiva
 Cardiomiopatia
restrittiva
 Obesità severa
 Ascite tesa
Diagnosi elettrocardiografica di
tamponamento cardiaco
ECG Finding
Sensitivity
Specificity
Electrical Alternans
76 - 93 %
8 - 33 %
Low Voltage
P-R depression
99%
25%
86%
187 patients with echocardiographically diagnosed pericardial effusion.
Eisenberg, M.J. et. al. Chest. 1996: 110, 318-24.
42%
ECOCARDIOGRAFIA
Segni ecocardiografici
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Versamento pericardico
Collasso dell’atrio destro
Collasso diastolico del ventricolo destro
Swinging heart
Variazioni respiratorie delle velocità di flusso
valvolari mitralico e tricuspidalica
Swinging of the Heart
Two dimensional echocardiographic
features of cardiac tamponade

Moderate or large effusion

RA / RV expiratory compression collapse

IVC distention with diminished respiratory response

Left atrial compression
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Reduced chamber size (especially the right ventricle)

Reciprocal size changes with respiration between right and left
ventricles
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Exaggerated and reciprocal respiratory variation of the mitral and
tricuspid valve flow velocities
** Many of the right ventricular findings may be absent in the patient with
elevated RV pressure (RVH, PA hypertension, volume expansion)
RA and RV diastolic collapse

RA / RV walls are thin and easily compressible when
pericardial pressure is elevated .
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RA collapse
RV collapse
IVC dilatation
Sens
55%
48%
97%
Spec
88%
95%
66%
PPV
10%
38%
7%
NPV
99%
99%
99%
absence of right atrial or ventricular collapse virtually
excludes tamponade while their presence serves to suggest
its potential presence or eventual development.
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Evaluation of the inferior vena cava

The central blood volume and the filling pressure of the RV
can be estimated by measuring the size of the IVC and its
response to respiration

Normally, the vena caval diameter will be < 17 mm, and
will decrease by > 5 mm during inspiration. The negative
pressure exerted by thoracic inspiratory expansion is of a
magnitude similar to the mean RA and RV diastolic
pressure
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With  central blood volume and right heart filling
pressure, the IVC becomes dilated > 20 mm, and the ability
of an inspiratory effort to collapse the vessel is lost
Evaluation of the inferior vena cava

The IVC is the single most reliable structure in terms of
avoiding major diagnostic errors
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Majority of the time, tamponade will have evidence of IVC
plethora
Sens
Spec
PPV
NPV
IVC dilatation
97%
66%
7%
99%
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False positives include
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mechanically ventilated with positive end-expiratory pressure
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right heart failure
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pericardial constriction
When to treat pericardial effusion ?
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cardiac tamponade is not an all-or-nonphenomena
spectrum of abnormal hemodynamics
limited data exist with respect to the
optimal timing of intervention for
pericardial effusion
decision to Intervene requires careful
consideration of the balance of risks and
benefits to the patient
Treatment Options
Nonsurgical
 pericardiocentesis
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blind
ECG guided
Echo guided
CT guided
balloon pericardiotomy
Surgical
 subxiphoid
 video-assisted
thoracoscopy
 pericardial-peritoneal
 pericardial window
 pericardiectomy
Pericardiocentesis
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Diagnostic tap
usually not indicated
 rarely have positive cytology or infection that
can be diagnosed
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Therapeutic drainage
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indicated for significant elevation of the central
venous pressure
Echo-guided Pericardiocentesis
SAFE and EFFECTIVE
 locating the optimal site of puncture
 determining the depth of the pericardial
effusion and the distance form the puncture
site to the effusion
 monitoring the results of the
pericardiocentesis
Pericardial Window (surgical)
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Balloon dilatation of a needle
pericardiostomy
subxyphoid surgical pericardiostomy
video-assisted thoracoscopy with localized
pericardial resection
anterolateral thoracotomy with parietal
pericardial resection
Pericardiocentesi
PERICARDIOCENTESI
Pericardite costrittiva
Pericardite costrittiva
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An uncommon post inflammatory disorder
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Incarceramento del cuore in un pericardio rigido
Caratterizzata da pericardio ispessito, fibrotico e
frequentemente ispessito
Raramente si sviluppa dopo un episodio di
pericardite acuta
more likely to develop after subacute pericarditis
with effusion that evolve over several weeks
Eziologia
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idiopathic
infectious
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tuberculosis
virus
bacteria
histoplasmosis
drugs
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hydralazine
cromolyn sodium
procainamide
penicillins
isoniazid
minoxidil
phenylbutazone
methysergide
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radiation
chest trauma or surgery
epicardial defibrillator patches
connective tissue disease
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SLE, RA, dermatomyositis
renal failure (on dialysis)
myocardial infarction
neoplasm
sarcoidosis
porphyria cutanea tarda
asbestosis
Whipple disease
Cardiopatia indotta da radiazioni
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Many patients sustain both pericardial and
myocardial injury (incidence 6% to 96%)
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Early pericarditis (first 6 months to several years):
acute pericarditis with or without effusion
incidence of effusive pericarditis is approx 20% -30%
Chronic pericardiopathy
is a common sequel, not necessarily preceded by acute
pericarditis, comes in the form of
effusive constrictive
constrictive
occult constrictive
Diagnosi differenziale
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restrictive cardiomyopathy
cardiac tamponade
right ventricular failure
mitral and tricuspid valve disease
Segni clinici
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Jugular venous elevation
  JVP with inspiration (Kussmaul’s sign)
Heart
 diastolic pericardial knock
 absent or decreased apical impulse
Abdomen:
 ascites
 pulsatile hepatomegaly
Extremities: peripheral edema
Pulsus paradoxus

96%
30-70%
57%
70%
almost always < 10 mm Hg; otherwise, considered tamponade
Diagnosi
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insidious onset , often not recognized in its
early phases by exam, x-ray, ECG, echo
average duration of symptoms before diagnosis
was 23.4 months ( range 1 to 264 months)
tendency to overlook elevated JVP
subacute
chronic
diastolic knock
Kussmaul’s
pulsus paradoxus
+
+
< 10 mm Hg +
++
++
+
Test diagnostici
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Electrocardiogram
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Chest radiograph
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sinus tachycardia, atrial fibrillation, ST flattening, Twave inversion, low QRS voltage, right axis deviation /
RVH
pericardial calcification (44% to 70% in the past), must
be distinguished from left ventricular aneurysm
calcification
MRI and computed tomography

pericardial thickening over the right ventricle (sensitivity
88%, specificity 100%, diagnostic accuracy 93%)
Segni ecocardiografici

Pericardial thickening and adhesion: lack of
"sliding"; heart motion transmitted to other
organs ("tugging")
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Septal bounce: abrupt transient rightward
movement
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IVC plethoric and unresponsive to
respiration; hepatic veins dilated
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Left and right ventricular size decreased;
heart tubular in shape
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Mild biatrial enlargement
Segni ecocardiografici
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"halo sign” - separation of the entire
pericardium by a small fixed space
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If the myocardium appears to pull the pericardium without
altering the small echo-free separation of these layers,
adhesion is suspected in the area examined
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best places to look for abnormal motion of the myocardium
relative to the pericardium is anterior to the right
ventricular outflow tract or at the lateral apex in the four
chamber view
Pericardiectomia
decorticazione
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In hospital mortality vary between 0% and 10%
predictors of poor outcome:
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underlying malignancy
radiation-induced
previous paracardial surgery
NYHA class IV symptoms
myocardial atrophy
myocardial inflammation and scarring
Effusive Constrictive Pericarditis
 coexistence
of constrictive pericarditis
and tamponading fluid
MANIFESTAZIONI CLINICHE
DELLA PERICARDITE COSTRITTIVA
Cardiomiopatia restrittiva
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Risulta dall’infiltrazione patologica del miocardio
da vari processi
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Amiloidosi/sarcoidosi
Malattie da accumulo di glicogeno, emocromatosi,
sindrome ipereosinofila
Risulta in un anomalo riempimento ventricolare
diastolico e disfunzione sistolica di vario grado
Cardiomiopatia restrittiva
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Differentiation from constrictive pericarditis
may be difficult because of similar clinical and
hemodynamic presentations
Clues from history, physical exam, ECG,
echo, CT and MR scan
Cardiomiopatia restrittiva
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amyloidosis is most likely to simulate
constrictive pericarditis
Digoxin should be avoided in patients
with cardiac amyloidosis because of
enhanced susceptibility to digoxin
toxicity
No therapy is known to be effective in
reversing the progression of cardiac
amyloidosis
Cardiomiopatia restrittiva
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Echocardiography may reveal thickening of the
myocardium and varying degrees of systolic
ventricular dysfunction.
Doppler echocardiographic analysis may
demonstrate evidence of abnormal diastolic filling
patterns and elevated venous pressure
The ECG may show conduction system disease or
low voltage, in contrast to the increased voltage
seen with ventricular hypertrophy
Segni ecocardiografici

Absence of pericardial adhesion and
thickening

Left ventricular mass that is normal or
increased; myocardial reflectance increased

Moderate to severe biatrial enlargement
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Frequent AV valve regurgitation

Signs of pulmonary hypertension

AV valve excursion on M-mode unaffected
by respiration
Ruolo della biopsia endomiocardica

RV endomyocardial biopsy may be
diagnostic and should be considered in
patients in whom a diagnosis is not
established

However, need for biopsy has been reduced
with progress in noninvasive modalities:
echocardiography, Doppler, MRI