Post on 07-May-2015
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……..
THANK YOU