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Hemodynamics of cardiac tamponade, constrictive pericarditis & restrictive cardiomyopathy
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Hemodynamics of cardiac tamponade, constrictive pericarditis & restrictive cardiomyopathy

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  • The pericardium is composed of two layers,[1,2] the visceral pericardium, a monolayer membrane of mesothelial cells and associated collagen and elastin fibers that is adherent to the epicardial surface of the heart, and the fibrous parietal layer, which is about 2 mm thick in normal humans and surrounds most of the heart. The parietal pericardium is largely acellular and also contains both collagen and elastin fibers. Collagen is the major structural component and appears as wavy bundles at low levels of stretch. With further stretch, the bundles straighten, resulting in increased stiffness. The visceral pericardium reflects back near the origins of the great vessels, becoming continuous with and forming the inner layer of the parietal pericardium. The pericardial space or sac is contained within these two layers and normally contains up to 50 mL of serous fluid.
  • It has a relatively flat, compliant segment transitioning relatively abruptly to a noncompliant segment.Pericardial reserve volume: diff. between the unstressed pericardial volume and the cardiac vol.Thus, the pericardial sac has a relatively small reserve volume.The shape of the pericardial pressure-volume relation accounts for the fact that once a critical level of effusion is reached, relatively small amounts of additional fluid cause large increases in the intrapericardialpressure and have marked effects on cardiac function. Conversely, removal of small amounts of fluid can result in striking benefit.
  • The most common example is RVMI usually in conjunction with IWMI. Here, the right side of the heart dilates markedly and rapidly such that total heart volume exceeds the pericardial reserve volume. As a result of increased pericardial constraint and augmented interaction, left- and right-sided filling pressures equilibrate at elevated levels, and a pulsusparadoxus and kussmaul’s sign are seen.Other conditions with similar effects include acute pulmonary embolus and subacute mitral regurgitation.
  • The most common example is RVMI usually in conjunction with IWMI. Here, the right side of the heart dilates markedly and rapidly such that total heart volume exceeds the pericardial reserve volume. As a result of increased pericardial constraint and augmented interaction, left- and right-sided filling pressures equilibrate at elevated levels, and a pulsusparadoxus and kussmaul’s sign are seen.Other conditions with similar effects include acute pulmonary embolus and subacute mitral regurgitation.
  • These pressure volume curves shows the difference between rapid accum. of small amnt of fluid vs. slow accum. of large amount of fluid.Eventually, however, cardiac output and blood pressure progressively decline. Patients who cannot mount a normal adrenergic response (e.g., those receiving beta-blockers, are more susceptible to the effects of an effusion. Also it should be noted that in terminal tamponade, a depressor reflex with paradoxical bradycardia can supervene in some patients.
  • -6 mm end-insp-3 mm end-exp
  • The absence of chamber collapse in echo is especially useful in excluding tamponade in patients with effusions, but its presence is less well correlated with tamponade than abnormal venous flow patterns are.
  • The right atrial y descent begins when the tricuspid valve opens, that is, when blood is not leaving the heart. Thus, no blood can enter, and the y descent is lost. In contrast, the x descent occurs during ventricular ejection. Because blood is leaving the heart, venous inflow can increase and the x descent is retained. Loss of the y descent can be difficult to discern at the bedside but is easily appreciated in recordings of systemic venous or right atrial pressure and provides a useful clue to the presence of very significant tamponade.
  • The right atrial y descent begins when the tricuspid valve opens, that is, when blood is not leaving the heart. Thus, no blood can enter, and the y descent is lost. In contrast, the x descent occurs during ventricular ejection. Because blood is leaving the heart, venous inflow can increase and the x descent is retained. Loss of the y descent can be difficult to discern at the bedside but is easily appreciated in recordings of systemic venous or right atrial pressure and provides a useful clue to the presence of very significant tamponade.
  • The second characteristic hemodynamic finding is the paradoxical pulse, an abnormally large decline in systemic arterial pressure during inspiration (usually defined as a drop of >10 mm Hg in systolic pressure).Other causes of pulsusparadoxus include CP, PE and pulmonary disease with large variations in intrathoracicpressure (tension pneumothorax, ac. sev. Asthma). In severe tamponade, the arterial pulse is impalpable during inspiration. The mechanism of the paradoxical pulse is multifactorial, but respiratory changes in systemic venous return are certainly important.In tamponade, in contrast to constriction, the normal inspiratory increase in systemic venous return is retained. Therefore, the normal decline in systemic venous pressure on inspiration is present (and Kussmaul sign is absent). The increase in right-sided heart filling occurs, once again, under conditions in which total heart volume is fixed and left-sided heart volume is markedly reduced to start. The IVSshifts to the left in exaggerated fashion on inspiration, encroaching on the LV such that its stroke volume and pressure generation are further reduced. Although the inspiratory increase in right-sided heart volume (preload) causes an increase in RV stroke volume, this requires several cardiac cycles to increase LV filling and stroke volume and to counteract the septal shift. Other factors that may contribute to the paradoxical pulse include increased afterload caused by transmission of negative intrathoracic pressure to the aorta and traction on the pericardium caused by descent of the diaphragm, which increases pericardial pressure. Associated with these mechanisms are the striking findings that left- and right-sided heart pressure and stroke volume variations are exaggerated and 180 degrees out of phase
  •  Reverse pulsusparadoxus (inspiratory rise of arterial pressure) may be noted in hypertrophic cardiomyopathy, intermittent positive pressure ventilation and isorhythmic AV dissociation.
  • The pericardial constraint of the left and right ventricles in cardiac tamponade is coupled by uniform liquid pressure on the heart, whereas it is uncoupled in constriction given regional differences in surface pressure Coupled constraint (tamponade) produces greater ventricular interdependence, so that increased inspiratory filling of the right ventricle results in highly coupled reduction in filling of the left ventricle (hence the occurrence of pulsusparadoxus), whereas uncoupled constraint (constriction) has a more modest effect on ventricular interdependence but more prominently reduces the effective elastance of the thin-walled right ventricle (hence the Kussmaul sign, an increase in right atrial pressure during inspiration (Grossman).Elastance is a measure of the tendency of a hollow organ to recoil toward its original dimensions upon removal of a distending or compressing force.Compliance is the ability of a hollow organ to distend and increase volume with increasing transmural pressure or the tendency of a hollow organ to resist recoil toward its original dimensions on application of a distending or compressing force.
  •  It is assumed that equilibration of flow across the atrial septal defect prevented paradoxical pulse. Patients with a large atrial septal defect and tamponade do not manifest a paradoxical pulse.
  • Restrictive physiology is characterised by impediment to ventricular filling caused byIncreased ventricular stiffness-RCMIncreased pericardial restraint-CCPConstrictive pericarditis and restrictive cardiomyopathy share clinical features and hemodynamic findings:Preserved systolic function.Grade III diastolic dysfunction.Elevation and equalization of diastolic pressuresDip and plateau pattern in Ventricular pressure tracing.
  • The mean normal pericardial thickness in adults is 1.2 ± 0.8 mm (two standard deviations [SD])a pericardial thickness >3.5 mm indicates pathologic thickening, whereas any thickness >6 mm is specific for pericardial constriction. – grossman.
  • Otto. Textbook of Clinical Echocardiography, 3rd Edition, 2004.
  • Otto. Textbook of Clinical Echocardiography, 3rd Edition, 2004.
  • Feigenbaum’s-Under normal circumstances,peak velocity of mitral inflow varies by 15% or less with respiration and tricuspid inflow by 25% or less. However, up to 20% of ptwith constriction do not exhibit typical respiratory changes, most likely because of markedly increased LA pressure or possibly a mixed constrictive-restrictive pattern due to myocardial involvement by the constrictive process. In patients without typical respiratory mitral-tricuspid flow findings, examination after maneuvers that decrease preload (head-up tilt, sitting) can unmask characteristic respiratory variation in mitral E velocity. Similar patterns of respiratory variation can be observed in COPD, RVinfarction,pul. embolism, and pleural effusion. Superior vena caval flow velocities are helpful in distinguishing CP from COPD. Patients with pulmonary disease display a marked increase in inspiratory superior vena caval systolic forward flow velocity, which is not seen in constriction. (less than 20 cm/sec respiratory variation in superior vena cava systolic velocity)
  • Feigenbaum’s Echocardiography, 7th ed
  • CP:With insp: minimal increase in HV S & D.With exp: decreased diast. Flow & increased reversal.RCM: blunted S/D ratio, increased insp. Reversal of dias flow.
  • RCM:S/D ratio: <0.5.No resp. variation in D.CP:Decreased S & D wave with insp. Opp with exp.
  • Grossman’s cardiac catheterisation, 7thh ed
  • Grossman’s cardiac catheterisation, 7thh ed
  • Grossman’s cardiac catheterisation, 7thh ed
  • Grossman’s cardiac catheterisation, 7thh ed
  • Grossman’s cardiac catheterisation, 7thh ed
  • Grossman’s cardiac catheterisation, 7th edRespiratory changes in LV and RV pressures measured with micromanometer catheters in a patient withCP(left) and in a patient with RCM (right).Peak inspiration is indicated in beat 2 in each cardiac cycle.In the pt with CP, there is a discordant change in LV and RV syst.pressures during respiration: LV syst. pressure falls to its minimum value during peak inspiration simultaneously with an increase in RV syst. pressure to its highest value in the cardiac cycle.These findings indicate the presence of ventricular interdependence owing to the constricting pericardium, and suggest that as LV filling and stroke volume decreases, there is a corresponding increase in RV filling and stroke volume.In contrast, in the patient with cardiomyopathy (right), there are concordant changes in LV and RV pressures during respiration.
  • Braunwald’s 9th ed.
  • Transcript

    • 1. DR. RAJESH DAS; DM-PDT (2ND YEAR)
    • 2. 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.
    • 3. 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.
    • 4. 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.
    • 5. STRESS-STRAIN AND PRESSURE-VOLUME CURVES OF THE NORMAL PERICARDIUM.
    • 6. 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.
    • 7. • 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.
    • 8. • 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.
    • 9. 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.
    • 10. HEMODYNAMICS OF CARDIAC TAMPONADE
    • 11. 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.
    • 12. 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.
    • 13. 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.
    • 14. 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 ).
    • 15. 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)
    • 16. 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.
    • 17. CARDIACTAMPONADE -- PATHOPHYSIOLOGY • the transmural pressures ↓ → progressive ↓ cardiac volumes. • small EDV → small stroke volume. • compensatory increases in contractility → ↓ ESV.
    • 18. ABSENCE OF Y DESCENT IN 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.
    • 19. ABSENCE OF Y DESCENT IN 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.
    • 20. 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.
    • 21. 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.
    • 22. 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).
    • 23. CT VS. CP
    • 24. •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
    • 25. 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.
    • 26. 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
    • 27. CONSTRICTIVE PERICARDITIS & RESTRICTIVE CARDIOMYOPATHY
    • 28. CONSTRICTIVE PERICARDITIS
    • 29. 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.
    • 30. NORMAL- RESPIRATORY VARIATIONS
    • 31. CP- RESPIRATORY VARIATIONS
    • 32. 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
    • 33. 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
    • 34. 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.
    • 35. 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
    • 36. ECHO DOPPLER- MITRAL INFLOW: RCM • Early disease E<A. • Late disease: E>A • Constant IVRT
    • 37. RESPIRATORY MITRAL INFLOW VELOCITY IN CP: • Mitral peak E velocity >25 % increase in exp. IN RCM: • velocity varies by <10%.
    • 38. 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.
    • 39. RESPIRATORY MITRAL INFLOW & TD OF MITRAL ANNULUS CP vs. RCM
    • 40. HV DIASTOLIC FLOW REVERSAL CP RCM VS
    • 41. PULM. VENOUS FLOW
    • 42. 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..
    • 43. 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.
    • 44. 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).
    • 45. RIGHT & LEFT HEART CATHETERIZATION • Dip and plateau pattern in diastolic waveform (square root sign) • Constrictive pericarditis • Restrictive cardiomyopathy • RV ischemia
    • 46. 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
    • 47. RV- LV DISCORDANCE VS. CONCORDANCE CP RCM
    • 48. TO SUM UP……..
    • 49. THANK YOU