Pericardial compressive syndromes

Cardiac Tamponed

Dr. Taniya Pereira MD,MRCPConsultant Cardiologist

14/10/2014

Cardiac tamponade Characterized by the accumulation of pericardial fluid

under pressure.

Pericardial constriction

Caracterized by scarring and loss of elasticity of the pericardial sac.

Effusive constriction Characterized by constrictive physiology with a coexisting pericardial effusion.

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• Tamponade covers a spectrum of clinical severity.

Cardiac Tamponade

• Early stage– mild to moderate elevation of central venous

pressure

• Advanced stage– ↑ intrapericardial pressure

↓ ventricular filling, ↓ stroke volume– hypotension – impaired organ perfusion

Etiologies of Cardiac Tamponade

• malignancy• idiopathic pericarditis• uremia• acute myocardial infarction• diagnostic procedures with

cardiac perforation• bacterial• tuberculosis

• radiation• myxedema• dissecting aortic aneurysm• post pericardiotomy

syndrome• systemic lupus

erythematosus• cardiomyopathy

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.

Beck’s Triad

• Described in 1935 by thoracic surgeon Claude S. Beck

• 3 features of acute tamponade – Decline in systemic arterial pressure– Elevation in systemic venous pressure (e.g.

distended neck vein)– A small, quiet heart

Cardiac Tamponadeclinical features

• Symptoms– dyspnea, fatigue, agitation and restlessness,

syncope, shock, anuria

• Physical examination – pulsus paradoxus– tachycardia– increased jugular venous pressure– hypotension

Central Venous Pressure

• X - descent– descent of the base in systole

• Y - descent– occurs as the tricuspid valve opens and ventricular filling begins from

the high-pressure right atrium– in constrictive pericarditis, filling is truncated in early to mid diastole – in tamponade, filling is restricted throughout diastole

• Kussmaul’s Sign– in constriction, venous return increases with inspiration and a high

right atrial pressure resists filling resulting in an increased JVP

Central Venous PressureCardiac Tamponade Constrictive Pericarditis

presence of a rapid Y-descent argues against cardiac tamponade

PULSUS PARADOXUS

• Defined as an abnormally large decrease in systolic blood pressure (>10 mmHg) on inspiration.

• 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– 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

an exaggerated drop in SBP with inspiration (>10mmHg)

Berliner Klinische Wochenschrift 1878; 10:461

Pulsus Paradoxus

tamponade without pulsus– atrial septal defect– severe aortic stenosis– aortic insufficiency– left ventricular dysfunction

LVH with ↑ LVEDP– decreased intravascular

volume (low-pressure tamponade)

pulsus without tamponade– COPD– RV infarct– pulmonary embolism– effusive constrictive

pericarditis– restrictive cardiomyopathy– extreme obesity– tense ascites

ELECTROCARDIOGRAPHY

• sinus tachycardia• low voltage, • if pericarditis is present, the ECG findings

typical of this. • Electrical alternans is relatively specific but

not so sensitive for tamponade; rarely, this phenomenon is seen with very large pericardial effusions alone.

CHEST X’RAY

• Enlarged cardiac silhouette with clear lung fields.

• This is not usually seen in acute tamponade since at least 200 mL of pericardial fluid must accumulate.

Development of a “flask” or “H2O-bottle” shaped 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)

Large effusion with

a swinging heart

Diastolic collapse of the

right ventricular free wall

Right atrial collapse in

early ventricular

systole

RA and RV diastolic collapse

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

• Sens Spec PPV NPV RA collapse55% 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• 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

postoperative complications related to pericardial and/or mediastinal hemorrhage

• fluid (hemorrhages localized into compressive masses) in the pericardium or surrounding mediastinum can produce severe hemodynamic instability

• Such masses sometimes elude detection, lying on the periphery of the heart, or obscured by pulmonary hyperinflation from positive pressure ventilation

• transesophageal echocardiography should be performed if transthoracic echocardiography failed to detect a clinically suspected mediastinal hemorrhage

• localized compressive processes may obscure many of the usually reliable echocardiographic signs of tamponade. (For example, a hematoma may compressing only the left atrium; right atrial and ventricular collapse may be absent.)

Cardiac catheterization

• Equilibration of average diastolic pressures (usually between 10 and 30 mmHg).

• Inspiratory increase in right-sided pressures and reduction in left-sided pressures that are responsible for pulsus paradoxus.

Low-pressure tamponade

• If hypovolemic at presentation a low-pressure tamponade in which the intracardiac diastolic pressures are 6 to 12 mmHg may be present.

• May not have a pulsus paradoxus. • A fluid challenge with one liter of isotonic

saline can bring out typical tamponade dynamics.

Treatment Options

Nonsurgical• pericardiocentesis– blind– ECG guided– Echo guided– CT guided

• balloon pericardiotomy

Surgical• subxiphoid• video-assisted

thoracoscopy• pericardial-peritoneal• pericardial window• pericardiectomy

Tx of Cardiac Tamponade• Most require urgent/emergency

pericardiocentesis

– Closed pericardiocentesis• Generally in cath lab but can be at bedside• Subxiphoid approach under echo guidance is most common -

minimizes risk & can assess completeness of fluid removal• Can alternatively use Fluoroscopic guidance• Pigtail catheter often left in place

– Open Pericardiocentesis – May be best for loculated effusions, effusions containing clots or

fibrinous material, and/or effusions that are borderline in size • Allow for bx and creation of a pericardial window for recurrent

effusions

Emergency Bedside Pericardiocentesis• 16- or 18-gauge needle

inserted at angle of 30-45° to the skin, near the left xiphocostal angle, aiming toward the L shoulder

Tx of Cardiac Tamponade – Other Measures

• IVFs, especially if hypovolemic or if diuretics were given for dx of HF

• Temporary inotropic support (Dobutamine, Dopamine)

• Serial echos after draining the fluid

• Analysis of pericardial fluid– Only has a low yield in determining the etiology of pericardial

dz– Can send for specific gravity, pH, glc, LDH, protein, cell count,

cytology, staining & Cx for bacteria, fungi, & TB).

Tx of Recurrent Effusions

• Pericardectomy

• Pericardial-peritoneal shunt

• Pericardiodesis - Steroids, tetracycline, or anti-neoplastic drugs administered into the pericardial space sclerosis of the pericardium

PERICARDIAL CONSTRICTION

• Results from scarring with consequent loss of elasticity of the pericardial sac.

• Compression does not occur until the cardiac volume approximates that of the pericardium, which begins in mid diastole.

• The majority of ventricular filling occurs rapidly in early diastole.

• Impairment in ventricular filling affects both ventricles, almost always equally.

Clinical features

• History

Decreased cardiac output – weakness and fatigue

Fluid retension – peripheral oedema• Examination

Elevated JVP – Kussmaul’s sign may be present(lack of inspir decline in JVP)

Oedema,Pulsativle hepatomegaly,pleural effusion

Pericardial knock

Echocardiography

• Pericardial thickening +/- calcification.Measurements with TOE correlate more strongly.

• Abrupt posterior motion of the ventricular septum in early diastole, due to rapid filling of the more compliant right ventricle.

• Dilation and absent collapse of the inferior vena cava and hepatic veins.

• Atrial enlargement.

Doppler echocardiography • Exaggerated E/A ratio of MV inflow velocity.(High E velocity

on RV and LV inflow due to the abnormally rapid early diastolic filling + the combination of a small volume and rapidly recoiling ventricle).

• Short deceleration time.• Exaggerated respiratory variation in E wave. Mitral inflow

velocity usually falls as much as 25 to 40 percent and tricuspid velocity greatly increases in the first beat after inspiration. This phenomenon,is not present with restrictive CM.

• In suspected constriction volume loading may unmask these features.

• Hepatic veins reveal an expiratory increase in diastolic flow reversal.

Computed tomography & cardiac magnetic resonance imaging

• Pericardial thickening and calcification • The effect of cardiac motion transmitted to the

surrounding pulmonary parenchyma. Failure of the immediately adjacent pulmonary structures to pulsate during the cardiac cycle, in the presence of a regionally or globally thickening pericardium, is virtually diagnostic of constrictive physiology.

• MRI shows pericardial thickening and dilatation of the inferior vena cava

Cardiac catheterization

• Increased right atrial pressure.• Prominent x and y descents in venous and atrial

pressure tracings.• Increased RV end-diastolic pressure, usually to a level

one-third of RV systolic pressure.• "Square root" signs in the RV and LV diastolic

pressure tracings (an early diastolic dip followed by a plateau, often with absent a wave). This finding, also called dip and plateau, reflects rapid early diastolic filling of the ventricles, followed by lack of additional filling due to compression in mid and late diastole.

• Equalization of LV and RV diastolic pressure tracings.

• Discordance between RV and peak LV systolic pressures during inspiration-during peak inspiration, an increase in RV pressure occurs when LV pressure is lowest.

Restrictive Cardiomyopathy

• 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

Differentiation

• History-such as prior pericarditis, a systemic disease predisposing to restrictive cardiomyopathy (eg, diabetes mellitus or amyloidosis).

• pericardial knock favors constriction, but is difficult to distinguish from the third heart sound of heart failure .

• Depolarization abnormalities (such as bundle branch block), ventricular hypertrophy, pathologic Q waves, or impaired atrioventricular conduction strongly favor RCM.

• CXR - Calcification of the pericardium suggests constrictive pericarditis. Mild cardiomegaly is common in both conditions, but more prominent in RCM - atrial rather than ventricular enlargement.

• Thickening of pericardium favors constriction, while thickening of the ventricular wall and septum, abnormal myocardial texture and, to a lesser extent, mitral or tricuspid regurgitation favor RCM.

• Pulmonary HT is frequent in RCM.

• There is no significant respiratory variation in Doppler inflow velocities in RCM.

• Doppler tissue imaging of mitral annulus – constriction more rapid early relaxation and in RCM diastolic velocities are below normal.

• Velocity of propergation of mitral inflow (colour M mode), in constriction normal or high (>55cm/sec) and reduced in RCM.

• Constrictive pericarditis or RCM have reductions in coronary flow reserve and peak hyperemic flow velocity compared to normals .

• Coronary flow in constrictive pericarditis shows a rapid acceleration and more rapid deceleration (velocity half-time <260 msec )of diastolic blood flow compared to RCM.

• RVEDP and LVEDP are equal in constriction, while LVEDP is sometimes higher in RCM.

• Biopsy

EFFUSIVE CONSTRICTIVE PERICARDITIS

• Effusive–constrictive pericarditis is a clinical–haemodynamic syndrome in which there is constriction of the heart by the visceral pericardium in the presence of effusion in free pericardial space.

• The hallmark of effusive–constrictive pericarditis is the demonstration of persistently raised right atrial and end diastolic ventricular pressures after the intrapericardial pressure is reduced to normal levels by removal of pericardial fluid.

clinical clues suggesting..

• Pulsus paradoxus (rare in classical constrictive pericarditis because of the absence of transmission of the inspiratory decline in pressure to the right heart chambers)

• Absence of a pericardial knock

• The Y descent less dominant than expected

• Kussmaul's sign frequently absent

Treatment

• Most cases of constriction require surgical removal of the pericardium, which has a significant operative mortality.25% will have persistent abnormal diastolic filling.

• Mild constriction in patients whose only abnormality is a mild to moderate increase in central venous pressure with little or no edema can be followed.

• Patients with "end-stage" constrictive pericarditis manifest by cachexia, atrial fibrillation, low cardiac outut at rest, and depressed serum albumin level due to protein losing enteropathy show little or no benefit from surgery.

• Effusive constrictive pericarditis is important to recognize since it is the visceral, not the parietal layer, that constricts the heart. Thus, if surgery is required, it is visceral pericardiectomy that must be performed.

Thankyou