Pericardite costrittiva cardiomiopatia restrittiva tamponamento cardiaco
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Pericardite costrittiva Cardiomiopatia restrittiva Tamponamento cardiaco. Sindromi costrittive pericardiche. TAMPONAMENTO CARDIACO. TAMPONAMENTO CARDIACO situazione acuta e grave. Acute Tamponade.

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Pericardite costrittiva cardiomiopatia restrittiva tamponamento cardiaco

Pericardite costrittiva

Cardiomiopatia restrittivaTamponamento cardiaco

Sindromi costrittive pericardiche


Tamponamento cardiaco

TAMPONAMENTO CARDIACO


Sindromi costrittive pericardiche

TAMPONAMENTO CARDIACO

situazione acuta e grave


Acute tamponade

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

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

Eziologia

Neoplasia

Pericardite idiopatica

Uremia

IMA

Batteri

TBC

Radiazioni

Mixedema

Dissezione di AA

Sindrome post pericardiotomica

LES

Cardiomiopatia


Sindromi costrittive pericardiche

FISIOPATOLOGIA

DEL TAMPONAMENTO CARDIACO


Tamponamento cardiaco1

Tamponamento cardiaco


Cardiac tamponade

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

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

Sintomi

Dispnea

Dolore toracico

Tosse

Disfagia

Dolore addominale

Singhiozzo

Sazietà preoce

Nausea


Sintomi1

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

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

Segni clinici

Generali

Ansietà

Sudorazione algida

Tachipnea

Tachicardia

Distensione venosa giugulare

Cianosi periferica


Segni clinici1

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

Central Venous Pressure

Kussmaul’s Sign

venous return increases with inspiration and a high right atrial pressure resists filling resulting in an increased JVP


Sindromi costrittive pericardiche

SEGNO DI KUSSMAUL


Sindromi costrittive pericardiche

TAMPONAMENTO:POLSO PARADOSSO


Sindromi costrittive pericardiche

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

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

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

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 paradoxus

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 effusivo-costrittiva

Cardiomiopatia restrittiva

Obesità severa

Ascite tesa


Sindromi costrittive pericardiche

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.


Sindromi costrittive pericardiche

ECOCARDIOGRAFIA


Segni ecocardiografici

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

Swinging of the Heart


Two dimensional echocardiographic features of cardiac tamponade

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)‏


Ra and rv diastolic collapse

medslides.com

RA and RV diastolic collapse

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.


Evaluation of the inferior vena cava

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 cava1

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 plethoraSens SpecPPV NPV IVC dilatation97% 66% 7% 99%

False positives include

mechanically ventilated with positive end-expiratory pressure

right heart failure

pericardial constriction


When to treat pericardial effusion

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 options

Treatment Options

Nonsurgical

pericardiocentesis

blind

ECG guided

Echo guided

CT guided

balloon pericardiotomy

Surgical

subxiphoid

video-assisted thoracoscopy

pericardial-peritoneal

pericardial window

pericardiectomy


Pericardiocentesis

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

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

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


Sindromi costrittive pericardiche

PERICARDIOCENTESI


Pericardite costrittiva

Pericardite costrittiva


Pericardite costrittiva1

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


Eziologia1

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

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

Diagnosi differenziale

restrictive cardiomyopathy

cardiac tamponade

right ventricular failure

mitral and tricuspid valve disease


Segni clinici2

Segni clinici

Jugular venous elevation96%

 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

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 JVP

subacute chronic

diastolic knock + ++

Kussmaul’s + ++

pulsus paradoxus < 10 mm Hg + +


Test diagnostici

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 ecocardiografici1

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 ecocardiografici2

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

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

Effusive Constrictive Pericarditis

coexistence of constrictive pericarditis and tamponading fluid


Sindromi costrittive pericardiche

MANIFESTAZIONI CLINICHE

DELLA PERICARDITE COSTRITTIVA


Cardiomiopatia restrittiva

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 restrittiva1

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 restrittiva2

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 restrittiva3

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 ecocardiografici3

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

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


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