Pericardite costrittiva Cardiomiopatia restrittiva Tamponamento cardiaco. Sindromi costrittive pericardiche. TAMPONAMENTO CARDIACO. TAMPONAMENTO CARDIACO situazione acuta e grave. Acute Tamponade.
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Cardiomiopatia restrittivaTamponamento cardiaco
situazione acuta e grave
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.
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.
Dissezione di AA
Sindrome post pericardiotomica
DEL TAMPONAMENTO CARDIACO
mild to moderate elevation of central venous pressure
intrapericardial pressure ventricular filling, volume
impaired organ perfusion
fluid accumulation within the pericardial space resulting in
increased intracardiac pressure
progressive limitation of ventricular diastolic filling
reduction of stroke volume and cardiac output
left to right heart interdependence
Competition for room in the abnormally fixed pericardial space (chamber interaction) is by far the principal mechanism
blood pooling in the lungs during inspiration
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.
Descritta nel 1935 da Claude S. Beck
Caratteristiche del tamponamento
Ipotensione arteriosa sistemica
Aumento della pressione venosa sistemica
Distensione venosa giugulare
Ovattamento dei toni cardiaci
First described by Kussmaul in 1873 as a palpable decrease or absence of the radial pulse during inspiration.
venous return increases with inspiration and a high right atrial pressure resists filling resulting in an increased JVP
SEGNO DI KUSSMAUL
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.
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.
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)
An important clinical skill for following patient is the ability to estimate the severity of pulsus paradoxus:
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
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
tamponamento senza polso
Difetto del setto interatriale
Severa stenosi aortica
Disfunzione ventricolare sinistra
polso senza tamponamento
Infarto del ventricolo destro
Diagnosi elettrocardiografica di tamponamento cardiaco
ECG FindingSensitivity Specificity
Electrical Alternans 76 - 93 % 8 - 33 %
Low Voltage 99% 25%
P-R depression 86% 42%
187 patients with echocardiographically diagnosed pericardial effusion.
Eisenberg, M.J. et. al. Chest. 1996: 110, 318-24.
Collasso dell’atrio destro
Collasso diastolico del ventricolo destro
Variazioni respiratorie delle velocità di flusso valvolari mitralico e tricuspidalica
Moderate or large effusion
RA / RV expiratory compression collapse
IVC distention with diminished respiratory response
Left atrial compression
Reduced chamber size (especially the right ventricle)
Reciprocal size changes with respiration between right and left ventricles
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 / RV walls are thin and easily compressible when pericardial pressure is elevated .
Sens SpecPPV NPV RA collapse55% 88%10% 99% RV collapse 48% 95%38% 99%IVC dilatation97% 66% 7% 99%absence of right atrial or ventricular collapse virtually excludes tamponade while their presence serves to suggest its potential presence or eventual development.
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
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
The IVC is the single most reliable structure in terms of avoiding major diagnostic errors
Majority of the time, tamponade will have evidence of IVC plethoraSens SpecPPV NPV IVC dilatation97% 66% 7% 99%
False positives include
mechanically ventilated with positive end-expiratory pressure
right heart failure
cardiac tamponade is not an all-or-non-phenomena
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
usually not indicated
rarely have positive cytology or infection that can be diagnosed
indicated for significant elevation of the central venous pressure
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
Balloon dilatation of a needle pericardiostomy
subxyphoid surgical pericardiostomy
video-assisted thoracoscopy with localized pericardial resection
anterolateral thoracotomy with parietal pericardial resection
An uncommon post inflammatory disorder
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
chest trauma or surgery
epicardial defibrillator patches
connective tissue disease
SLE, RA, dermatomyositis
renal failure (on dialysis)
porphyria cutanea tarda
Many patients sustain both pericardial and myocardial injury (incidence 6% to 96%)
Early pericarditis (first 6 months to several years):acute pericarditis with or without effusionincidence of effusive pericarditis is approx 20% -30%
Chronic pericardiopathyis a common sequel, not necessarily preceded by acute pericarditis, comes in the form of effusive constrictive constrictiveoccult constrictive
right ventricular failure
mitral and tricuspid valve disease
Jugular venous elevation96%
JVP with inspiration (Kussmaul’s sign)
diastolic pericardial knock30-70%
absent or decreased apical impulse
Extremities: peripheral edema
almost always < 10 mm Hg; otherwise, considered tamponade
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
diastolic knock + ++
Kussmaul’s + ++
pulsus paradoxus < 10 mm Hg + +
sinus tachycardia, atrial fibrillation, ST flattening, T-wave 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%)
Pericardial thickening and adhesion: lack of "sliding"; heart motion transmitted to other organs ("tugging")
Septal bounce: abrupt transient rightward movement
IVC plethoric and unresponsive to respiration; hepatic veins dilated
Left and right ventricular size decreased; heart tubular in shape
Mild biatrial enlargement
"halo sign” - separation of the entire pericardium by a small fixed space
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
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
In hospital mortality vary between 0% and 10%
predictors of poor outcome:
previous paracardial surgery
NYHA class IV symptoms
myocardial inflammation and scarring
coexistence of constrictive pericarditis and tamponading fluid
DELLA PERICARDITE COSTRITTIVA
Risulta dall’infiltrazione patologica del miocardio da vari processi
Malattie da accumulo di glicogeno, emocromatosi, sindrome ipereosinofila
Risulta in un anomalo riempimento ventricolare diastolico e disfunzione sistolica di vario grado
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
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
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
Absence of pericardial adhesion and thickening
Left ventricular mass that is normal or increased; myocardial reflectance increased
Moderate to severe biatrial enlargement
Frequent AV valve regurgitation
Signs of pulmonary hypertension
AV valve excursion on M-mode unaffected by respiration
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