HEMODYNAMICS OF CARDIAC TAMPONADE,

CP & RCMDR. RAJESH DAS; DM-PDT (2ND YEAR)

PERICARDIUM - ANATOMY• Fibro-serous sac .

• The inner visceral layer– monolayer membrane of mesothelial cells, collagen & elastin fibres.

• Outer parietal pericardium- collagenous fibrous tissue and elastin fibrils.

• Between these 2 layers lies the pericardial space- 10-50ml of fluid- ultrafiltrate of the plasma.

• Drainage of pericardial fluid is via right lymphatic duct and thoracic duct.

FUNCTIONS OF THE PERICARDIUM

1) Effects on chambers.• Limits short-term cardiac chamber distention.

• Facilitates chamber coupling and diastolic interaction.

2) Effects on whole heart.• Maintains the position of the heart relatively constant.

• Lubricates the heart, minimises friction .

3) Mechanical barrier to infection.

FUNCTIONS OF THE PERICARDIUM

• The best-characterized mechanical function → restraining effect on cardiac volume.

• At low applied stresses (physiologic or subphysiologic cardiac volumes) it is very elastic.

• As stretch increases, the tissue fairly & abruptly becomes stiff and resistant to further stretch.

STRESS-STRAIN AND PRESSURE-VOLUME CURVES OF THE NORMAL PERICARDIUM.

PERICARDIUM- PHYSIOLOGY

• Contact pressure exerted on the heart can limit filling when upper limit of normal cardiac volume is exceeded.

• Pericardial contact pressure is more imp for Rt. heart which have a lower filling pressure than the Lt.

• The normal pericardium also contributes to diastolic interaction.

• transmission of intracavitary filling pressure to adjoining chambers.

• Once cardiac volume increases above the physiologic range, the pericardium contributes increasingly to intracavitary filling pressures.• directly → by the ↑ external contact pressure.• indirectly → d/t ↑ diastolic interaction.

• These results in a hemodynamic picture with features of both cardiac tamponade and constrictive pericarditis.

• The most common example is RVMI usually in conjunction with IWMI.• Pulsus paradoxus.• Kussmaul’s sign.

• Chronic cardiac dilation d/t DCM or regurgitant valvular disease

• can result in cardiac volumes well in excess of the normal pericardial reserve volume.

• Despite this, exaggerated restraining effects are not ordinarily encountered.

• This implies that the pericardium undergoes chronic adaptation to accommodate marked ↑ in cardiac volume.

3 POSSIBLE ‘PERICARDIAL COMPRESSION SYNDROMES’:

• Cardiac tamponade• Accumulation of pericardial fluid under pressure and may

be acute or subacute

• Constrictive pericarditis• Scarring and consequent loss of elasticity of the

pericardial sac.

• Effusive-constrictive pericarditis• Constrictive physiology with a coexisting pericardial

effusion.

HEMODYNAMICS OF CARDIAC TAMPONADE

CARDIAC TAMPONADE -- PATHOPHYSIOLOGY

• Cardiac tamponade represents a continuum from an effusion causing minimal effects to full-blown circulatory collapse.

• Clinically, the most critical point occurs when• an effusion reduces the volume of the cardiac

chambers → ↓ CO.

CARDIAC TAMPONADE -- PATHOPHYSIOLOGY

• Determinants of the hemodynamic consequences of an effusion are• the pressure in the pericardial sac and • the ability of the heart to compensate for

elevated pressure.

• The pressure in the pericardial sac depends on:• Volume of fluid• Rate of fluid accumulation• Compliance characteristics of the pericardium.

CARDIAC TAMPONADE -- PATHOPHYSIOLOGY

A. Sudden increase of small amount of fluid.B. Slow accumulation of large amount of fluid.

The cardiac compensatory responses: → ↑ adrenergic stimulation and parasympathetic withdrawal. → tachycardia, increased cardiac contractility & per.

vasoconstriction. → maintain cardiac output and blood pressure for some

time only.

CARDIAC TAMPONADE -- PATHOPHYSIOLOGY

• As fluid accumulates:• Lt and Rt -sided atrial and ventricular diast. pressures

↑.• and equalize at a pressure similar to that of

pericardial pressure(15-20 mm Hg ).

NORMAL PERICARDIAL PHYSIOLOGY

• Normal pericardial pressure is always subatmospheric, i.e.,

normal range: -5 to +5 cm of water.

Normally transmural pressure > 0 at all times.

Transmural pressure across any cardiac chamber: (Intracavitary pressure) - (Intrapericardial pressure)

CARDIACTAMPONADE -- PATHOPHYSIOLOGY

• Transmural pressure (IC-IP) is zero/ neg.

• Cavity collapse → when local transmural gradient become negative.

• Thus, the pericardial pressure dictates the intracavitary pressure.

CARDIACTAMPONADE -- PATHOPHYSIOLOGY

• the transmural pressures ↓ → progressive ↓ cardiac volumes.

• small EDV → small stroke volume.

• compensatory increases in contractility → ↓ ESV.

ABSENCE OF Y DESCENTIN CARDIAC TAMPONADE

• Normally – biphasic venous return to the heart-

• at the vent ejection (x descent)

• at early diastole-when the TV open (y descent).

• In severe tamponade the total heart volume is fixed.

• Elevated IP prresure THROUGHOUT cycle except momentary relief in early systole.

ABSENCE OF Y DESCENTIN CARDIAC TAMPONADE

• Thus, blood can enter the heart only when blood is simultaneously leaving.

• The right atrial y descent when blood is not leaving the heart → no blood can enter → y descent is lost.

• X wave occurs during ventricular systole-when blood is leaving from the heart- hence preserved.

PULSUS PARADOXUS

• Intraperi pressure (IPP) tracks- intrathoracic pressure.

• Inspiration:

→ -ve intrathoracic pressure is transmitted to the pericardial space

→ ↓ IPP

→ ↑ blood return to the right ventricle

→ ↑ right ventricular volume & shifting of IVS towards the LV

→ ↓ left ventricular volume

→ ↓ LV stroke volume.

• ↓ blood pressure (>10mmHg) during inspiration.

PULSUS PARADOXUS

Other factors:

• ↑afterload- Owing to an increase in the relative difference between left ventricular end-diastolic and aortic pressure.

• Traction on the pericardium caused by descent of the diaphragm → ↑ pericardial pressure.

CT VS. CP

• Both CT & CP have ventricular interdependence and exaggerated resp. variation of TV or MV inflow.

• Then why pulsus paradoxus is not common in CP??.

• Cardiac tamponade → Coupled constraint on LV & RV → greater ventricular interdependence• Increased inspiratory filling of the RV results in highly coupled reduction in

filling of the LV (hence pulsus paradoxus)

• CP → Uncoupled constraint → has less effect on ventricular interdependence.• but more prominently reduces the effective elastance of the thin-walled RV

(hence the Kussmaul sign).

CT VS. CP

•CT without Pulsus paradoxus:• Already increased filling press LV• AR, LV dysfunction.

•Equilibration of volume in RV & LV:• ASD

•Tamponade without RV collapse:• Pt having PAH

LOW PRESSURE TAMPONADE

• Intravascular volume low in a preexisting effusion

•Modest ↑ in pericardial pressure can compromise already ↓ SV

•Dialysis patient

•Diuretic to effusion patient

• Pats with blood loss and dehydration

• JVP- normal & pulsus paradoxus- absent.

EFFUSIVE CONSTRICTIVE PERICARDITIS

• Failure of RAP to decline by atleast 50% to a level ≤10 mm Hg after pericardial pressure reduced to 0 by aspiration of fluid.

• Radiation or malignancy, TB

•Often need pericardiectomy

CONSTRICTIVE PERICARDITIS&

RESTRICTIVE CARDIOMYOPATHY

CONSTRICTIVE PERICARDITIS

CP- PATHOPHYSIOLOGY

• impairment of both RV and LV filling• EARLY DIASTOLIC filling rapid (↑ RAP + suction due to ↓ ESV)

• filling abruptly halted in mid and late diastole.

• pressure rises mid to late diastole.

• ↑ventricular interdependence

• dissociation of thoracic and cardiac chamber pressures• Kussmaul’s sign.

• decreased LV filling with inspiration and increased RV filling.

NORMAL- RESPIRATORY VARIATIONS

CP- RESPIRATORY VARIATIONS

ECHOCARDIOGRAPHIC EVALUATION OF CP

• Preferred modality for assessing the pericardium and pericardial disease.

• Less reliable than MR or CT for pericardial thickening, calcification, or constriction

• Still employed as initial diagnostic test

• Recommended by the ACC/AHA

M-MODE: CONSTRICTION

• Septum-• Abnormal Rapid

movements- notching in early diastole.

• Post LV wall-• Abrupt postr motion in

early diastole and flat in remaining diastole

• IVC and hepatic vein dilatation

2D: CONSTRICTION

• Increased echogenicity of the pericardium from thickening

• May see effusion (effusive-constrictive)

• Septal bounce

• Abrupt septal shift toward LV in early diastole and bounce back toward RV following atrial contraction.

ECHO DOPPLER- MITRAL INFLOW: CONSTRICTION

• RV and LV inflow show prominent E wave due to rapid early diastolic filling

• Short deceleration time of E wave as filling abruptly stops

• Small A wave as little filling occurs in late diastole following atrial contraction

• E/A ratio >2

• DT<160 ms,

• IVRT: <60 ms. Respiratory variation.

ECHO DOPPLER- MITRAL INFLOW: RCM

• Early disease E<A.

• Late disease: E>A

• Constant IVRT

RESPIRATORY MITRAL INFLOW VELOCITY

IN CP:

• Mitral peak E velocity >25 % increase in exp.

IN RCM:

• velocity varies by <10%.

TISSUE DOPPLER OF MITRAL ANNULUS

Constrictictive pericarditis:• Annular paradox:

• E’ increases as severity of CP increase(as increased filing pressure).

• Peak E’ ≥ 8 cm/s: (rajagopalan, N. At al. AJC 2001.)

• 89% senstive for constriction

• 100% specific.

RCM:• E’ decreases as severity ↑.

• E’< 8 cm/s.

RESPIRATORY MITRAL INFLOW & TD OF MITRAL ANNULUS

CP vs.RCM

HV DIASTOLIC FLOW REVERSAL

CP RCM

VS

PULM. VENOUS FLOW

CARDIAC CATHETERIZATION

• Confirm

• Assess severity

• Differentiate from RCM

• Exclude major co-existing causes of increased RAP e.g.- PAH

• CAG- to exclude localized constriction causing coronary pinching..

RIGHT HEART CATHETERIZATION: ABNORMALITIES IN RA TRACING

M or W waves…• Seen in both pericardial

constriction & RCM. Also seen in RV ischemia or CHF.

DIFFERENCE ?• Inspiratory rise or lack

of decline in RA pressure (Kussmaul’s Sign) in CP.

• Normal respiratory variation in mean RAP is seen in RCM.

RIGHT HEART CATHETERIZATION:

• Equalization of pressures• < 5 mm hg difference

between mean RA, RV diastolic, PA diastolic, PCWP, LV diastolic and pericardial pressures in CP.

•Diagnostic for CP (also seen in tamponade).

RIGHT & LEFT HEART CATHETERIZATION

• Dip and plateau pattern in diastolic waveform (square root sign)

• Constrictive pericarditis

• Restrictive cardiomyopathy

• RV ischemia

RIGHT & LEFT HEART CATHETERIZATION

• RVSP < 35-45 mm Hg

• RVEDP / RVSP > 1/3

• LVEDP-RVEDP < 5 mm Hg.

• PASP = RVSP very high(>55 - 60

mm Hg)

• RVEDP / RVSP < 1/3

• LVEDP-RVEDP > 3-5 mm Hg

CP RCM

RV- LV DISCORDANCE VS. CONCORDANCE

CP RCM

TO SUM UP……..

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