Sindromi costrittive

pericardichePericardite costrittiva

Cardiomiopatia restrittiva

Tamponamento cardiaco

TAMPONAMENTO CARDIACO

TAMPONAMENTO CARDIACOsituazione 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 Neoplasia Pericardite idiopatica Uremia IMA Batteri TBC

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 Tamponadepathophysiology

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

Sintomi 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,

tamponademust be suspected in many contexts — forexample, in patients who have wounds of

the chestor upper abdomen and hypotension or in

those whohave hypotension preceded by symptoms of

an incitingpericardial disease, such as chest

discomfortand 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 Ovattamento dei toni cardiaci Sfregamenti Polso paradosso

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. 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: 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

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 Paradoxustamponamento 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

effusivo-costrittiva

Cardiomiopatia restrittiva

Obesità severa Ascite tesa

ECG Finding Sensitivity Specificity

Electrical Alternans 76 - 93 % 8 - 33 %

Low Voltage 99% 25%

P-R depression 86% 42%

Diagnosi elettrocardiografica di tamponamento cardiaco

187 patients with echocardiographically diagnosed pericardial effusion.

Eisenberg, M.J. et. al. Chest. 1996: 110, 318-24.

ECOCARDIOGRAFIA

Segni ecocardiografici

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 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)

38medslides.com12/02

RA and RV diastolic collapse

RA / RV walls are thin and easily compressible when pericardial pressure is elevated .

Sens Spec PPV NPV RA collapse 55% 88% 10% 99% RV collapse 48% 95% 38% 99%IVC dilatation 97% 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.

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

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

Majority of the time, tamponade will have evidence of IVC plethora

Sens Spec PPV NPV IVC dilatation 97% 66% 7% 99%

False positives include mechanically ventilated with positive end-

expiratory pressure right heart failure pericardial constriction

When to treat pericardial effusion ?

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

Treatment OptionsNonsurgical pericardiocentesis

blind ECG guided Echo guided CT guided

balloon pericardiotomy

Surgical subxiphoid video-assisted

thoracoscopy pericardial-

peritoneal pericardial window pericardiectomy

Pericardiocentesis Diagnostic tap

usually not indicated rarely have positive cytology or

infection that can be diagnosed Therapeutic drainage

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)

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

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

Eziologia idiopathic infectious

tuberculosis virus bacteria histoplasmosis

drugs hydralazine cromolyn sodium procainamide penicillins isoniazid minoxidil phenylbutazone methysergide

radiation chest trauma or

surgery epicardial defibrillator

patches connective tissue

disease SLE, RA,

dermatomyositis renal failure (on

dialysis) myocardial infarction neoplasm sarcoidosis porphyria cutanea

tarda asbestosis Whipple disease

Cardiopatia indotta da radiazioni

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

Diagnosi differenziale

restrictive cardiomyopathy cardiac tamponade right ventricular failure mitral and tricuspid valve disease

Segni clinici Jugular venous elevation 96%

JVP with inspiration (Kussmaul’s sign) Heart

diastolic pericardial knock30-70%

absent or decreased apical impulse Abdomen:

ascites57%

pulsatile hepatomegaly70%

Extremities: peripheral edema Pulsus paradoxus

almost always < 10 mm Hg; otherwise, considered tamponade

Diagnosi 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 JVPsubacute

chronicdiastolic knock +

++Kussmaul’s + ++pulsus paradoxus < 10 mm Hg +

+

Test diagnostici Electrocardiogram

sinus tachycardia, atrial fibrillation, ST flattening, T-wave inversion, low QRS voltage, right axis deviation / RVH

Chest radiograph 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")

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

Segni ecocardiografici "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

Pericardiectomia decorticazione

In hospital mortality vary between 0% and 10%

predictors of poor outcome: 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

Risulta dall’infiltrazione patologica del miocardio da vari processi 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

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

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

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 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