Downloaded 166 times
Echo in pericardial diseases
This document provides an overview of echocardiography in pericardial diseases. It begins with an introduction to pericardial anatomy and pathophysiology. It then discusses various pericardial diseases that can be evaluated by echocardiography, including acute pericarditis, recurrent pericarditis, pericardial effusions, cardiac tamponade, and constrictive pericarditis. For each condition, it describes the echocardiographic findings and techniques used to evaluate the condition. It emphasizes that echocardiography is usually the initial imaging test of choice but that CT or CMR may be needed in some complex cases.
More Related Content
Similar to Echo in pericardial diseases
More from Dr. Murtaza Kamal MRCPCH,MD,DNB,DrNB Ped Cardiology
Echo in pericardial diseases
- 1. ECHO IN PERICARDIAL DISEASES MURTAZAKAMAL SEPT 3, 2019 1
- 2. Scope of thetalk Introduction Anatomy Pathophysiology Diseases 2
- 3. So, lets startwith the pioneer… 3
- 4. Introduction Not only cardiology,rheumatology, oncology, infectious ds Although imaging to confirm initial suspicion—> Sometimes, clinically unsuspected diagnosis+ complementary approach to clinical diagnosis ECHO: 1st line initial imaging tool 4
- 5.
- 6. Anatomy of pericardium Flaskshaped sac: Fibrous (O)+ serosal (I) Serosal: Outer parietal (+ Fibrous)+ Inner visceral (epicardium) Pericardial space Epicardial fat: B/w epi+ myocardium: CA, CV, lymphatics, nerves Thickness: 0.7-1.2mm CT; 1.2-1.7mm CMR: Difference due to inclusion of small amount of physiologic pericardial fluid TTE: Unreliable for thickness 6
- 7.
- 8.
- 9. Lymphatic drainage, vascularsupply and innervation < 50 mm serous fluid: Plasma ultrafiltrate from epicardial+ parietal pericardial capillaries; Prostaglandins from meso+ endothelial cells—> Modulation of cardiac reflexes+ coronary tone—> Drainage by lymphatics on heart surface+ parietal pericardium Arterial supply: Pericardiophrenic+ musculophrenic arteries (Br of ITA+ DTA) Venous drainage: Pericardiophrenic veins—> Superior intercostal veins+ internal thoracic veins—> Innominate veins Nerve innervation: PS supply: Vagus+ Lt RLN, Br from oesophageal plexus Sensory fibers: Phrenic nerve Sympathetic: 1st dorsal ganglion, stellate ganglion and aortic, cardiac and diaphragmatic plexus 9
- 10. Pericardial response toinjury… Exudation of fluid, fibrin, inflammatory cells Healing with organisation: Focal/ diffuse obliteration of pericardial cavity by adhesions b/w vis+ parie pericardium Ch. effusions—> Pericardial thickening Loculated fluid accumulation: Cardiac compression Calcific deposits: Focal/ extensive—> End stage reaction to injury 10
- 11. Response to injurycontinued… 11
- 12. Although not essentialfor life… 12
- 13. Mechanical effects ofpericardium If cut—> Inelastic parietal pericardium retracts—> Exerts pressure on underlying myocardial chambers—> Effect greatest on thinner walled RA+ RV Effect on cardiac chamber pressures magnified by: Rapid rise in total cardiac volume:Exercise, hypervolumia, acute severe valvular regurgitation Increase in pericardial fluid above normal “reserve volume”—> Increases cardiac pressures+ reduces cardiac filling Hypovolumia: Diminishes mechanical effects of pericardium on heart
- 14. Pericardial reserve volume+ P-V relations Pericardial reserve volume <50ml Amount adequate to allow increased rt heart filling with normal inspiration, without increased pericardial restrain+ increased rt heart chamber pressures If marked swings in intra thoracic pressures (acute dyspnea)—> Rt ht filling during inspiration can exceed pericardial reserve volume—> Pericardial constrain + cardiac pressure rise This rt ht overfilling—> decreases lt ht filling—> Ventricular interdependence Chiefly in diastole—> Due to in elastic parietal pericardium (CP, CT, acute cardiac dilatation) 14
- 15.
- 16. P-V relationship: Dependence onrate of effusion 16
- 17.
- 18. Acute pericarditis: Infiltrationof inflammatory cells into pericardium 18
- 19. Instructions for imaging… ECHOrecommended as initial non invasive imaging test—> Accurate to access PEff+ tamponade physiology: Within 24 hrs May appear normal; +nce of PEff consistent with acute pericarditis Increased pericardial brightness, pericardial thickning, abnormal septal bounce suggesting early constriction 3%: Tamponade physiology 19
- 20. ECHO of acutepericarditis 20
- 21. Conditions requiring additionalimaging with CT/ CMR Inconclusive ECHO findings and ongoing clinical concerns Failure to respond promptly to anti inflammatory therapy Atypical clinical presentation Search for specific cause (Malignancy/ TB) Suspition of CP Associated trauma (penetrating injury/ chest injury) Acute pericarditis in setting of acute myocardial infarction, neoplasm, lung/ chest infections, pancreatitis 21
- 22. Recurrent pericarditis Recurrence ofepisodes after latent/ asymptomatic period of 6 weeks Common with acute pericarditis: 1/3rd pts Repeat episodes of primary acute pericarditis (viral reactivation), auto-immune mediated inflammation by pericardial injury from initial/ prior episodes Symptoms similar but less severe; pericardial rub, ECG changes, PEff less likely 22
- 23. PEff Accumulation of fluid> 50 ml: Conditions affecting pericardium, hypothyroidism, end stage renal disease, neoplastic diseases Transudates, exudates, hemopericardium, pyopericardium Definition arbitrary: Small: 50-100 ml (acute pericarditis), Moderate: 100-500 ml, Large: >500 ml (neoplasia, TB, hypothyroidism) Tachycardia, dyspnia, hemodynamically unstable, elevated CVP Drainage of moderate/ large PEff: Symptomatic, purulent pericarditis suspected, CT supervenes, to establish ethology of a hemodynamically insignificant effusion 23
- 24.
- 25. ECHO in PEff Initialprocedure of choice: Minimal delay+ accuracy Physiologic+ hemodynamic effects of PEff M mode: Persistance of echo free space b/w epicardium+ parietal pericardium throughout cardiac cycle Separation only in systole: Normal/ Trivial PEff; both sy+ diastole: >50 ml Lt pleural effusion—> May mimic PEff (PLAX: Fluid b/w descending aorta+ heart—> Pericardial rather than pleural 2D ECHO: Qualitative assessment of size+ distribution, loculated/ density features Epicardial fat: Brighter than myocardium+ moves in concert with heart+ tends to be of uniform thickness; PEff-echolucent+ motionless 25
- 26. ECHO in PEff:Differentiation 26
- 27.
- 28. PEff quantification by2D ECHO… Seen in end diastole: Trivial: Seen in systole only Small: <10 mm Moderate: 10-20 mm Large: >20 mm Very large: >25 mm Exudate PEff: Strands, adhesions, uneven distribution reflecting more inflammatory and complicated nature 28
- 29.
- 30. When to consideradditional imaging? CMT/ CT: Complex located effusions Clot in effusion Localisation, characterisation and quantification of fluid 30
- 31. CT Life threatening, compressescardiac chambers+ inhibits normal filling Elevation+ equalisation of cardiac diastolic + pericardial pressures, reduced CO, exaggerated inspiratory decrease in SBP > 10 mm Hg (PP) Pericardial pressure rises—> Systemic+ PV pressures must increase to maintain cardiac filling Venocardiac gradients continue to decrease as tamponade increases— > Progressive decrease in CO Exhausted compensatory mechanisms—> Preload insufficient to sustain cardiac filling+ coronary and systemic perfusion—> Abrupt drop in HR+ BP (Terminal event) 31
- 32. CT cont… Excessive pericardialfluid raises pressure in all chambers throughout cardiac cycle—> Diminishes cardiac filling + CO Atrial filling from systemic+ pulmonary veins predominates over diastolic filling as pericardial pressure falls mainly during early vent systole, when total cardiac volume is falling due to vent ejection Ventricular diastolic filling reduces due to reduced inflow pressure gradient Ventricular interdependence 32
- 33. CT cont… Mild (asymptomatic)to severe (tachycardia+ marked dyspnea) Hypotention late feature ( highlighted sympathetic tone maintains systemic BP as CO is decreasing) Compensatory mechanisms (tachycardia/ increased systemic venous pressures to maintain cardiac filling/ arterial vasoconstriction) exhaused—> Decrease in arterial pressure+ coronary perfusion —> Cardiac arrest+ death LOW PRESSURE TAMPONADE: Hypovolumia—> Cardiac filling is severely impaired, but equalised pericardial and end- diastolic intracardiac pressures are normal at <10 mm Hg 33
- 34. CT associated withcardiac surgery Early: <24 h: Surgical bleeding, cardio-pulmonary bypass induced coagulopathy—> Should be suspected when ever haemodynamic compromise Late: >5-7 days: Excessive mediasinal drainage, post craniotomy syndrome (occurs after days to weeks, with PEff+ inflammatory component) During PPV: The mitral inflow patterns show very minimal respiratory variation—> Can be missed 34
- 35. ECHO in CT Emergency Regardlessof effusion size: CT is potentially lethal PEff, dilated IVC+ hepatic veins (elevated systemic venous pressures), LV with decreased ED+ ES dimensions, reduced stroke volume+ CO Rt heart diastolic chamber collapse when pericardial pressures exceeds intra cardiac pressures, inspiratory septal bounce into LV, respiratory changes in doppler flow velocity recordings 35
- 36. Echo of CTcont… RV diastolic diameter increases during inspiration, LV diastolic diameter decreases, with opposites seen during expiration 36
- 37. Echo of CTcont… > 90% pts: IVC plethora Dilated IVC (>2.1cm) with <50% reductio in diameter during inspiration—> Elevation in systemic venous pressure which occurs as pericardial pressure increases intracardiac pressures Dilatation of hepatic veins 37
- 38. ECHO of CTcont… RA+ RV collapses during their relaxation phase when intracavitatory pressure reaches its lowest value and transiently falls below pericardial pressures Atria: Indentation starts near peak of R wave Ventricles: Early diastole after end of T wave Duration of RA collapse >1/3rd of cardiac cycle: 100% Sn+Sp for clinical cardiac tamponade Absence of any cardiac chamber collapse:>90% negative predictive value for clinical cardiac tamponade 38
- 39. ECHO of CTcont… Inspiratory bounce of IVS into LV during inspiration: Not specific- Seen in cases with PP (Pul embolism, COPD, dyspnea due to metabolic disorders) Inspiratory septal bulge may be absent with CT in: LVH, pre existing markedly elevated LV filling pressures 39
- 40. ECHO in CTcont… 40
- 41. Doppler flow velocityrecordings… TV+ PV velocities by doppler increases with inspiration; MV+ AV simultaneously decreases In normal conditions: Change in peak E wave mitral flow velocity: 5% Hepatic. Venous flow velocity with PW: High PPV (82%) + NPV (88%)-Cannot be evaluated in 1/3rd patients 41
- 42.
- 43.
- 44. CP cont… Increased pericardialthickness suggested by parallel motion of visceral + parietal pericardium, separated by a echo free space IVC: Absence of a dilated IVC in a patient without recent diuresis should call into question the diagnosis of hemodynamically significant CP 44
- 45. M Mode ECHOof CP 45
- 46. Doppler flow velocityrecordings… High early (E) velocity, shortened deceleration time, reduced atrial wave (A) %tage respi variation: (Expi-Inspi)/ Expi MV: 25% TV: 40% Hepatic vein diastolic flow reversal increases with expiration, reflecting ventricular interaction+ dissociation of intracardiac+ intrathoracic pressures 46
- 47. CP cont… Usually +velinear relationship b/w E/e’ ratio and LA pressure, which is useful for assessing LA pressure in cardiomyopathy, is reversed in CP: Annulus paradoxes Medial e’ increases progressively as severity of constriction becomes worse. Lateral mitral annular e’ is usually lower than e’ from medial annulus: Annulus reversus Annulus reversus: Tethering of lateral mitral annulus to thickened pericardium After pericardectomy, lateral + medial mitral annulus normalises 47
- 48. Strain imaging Reduced: Circumferential strain Tortion Earlydiastolic untwisting Unchanged: GLS 48
- 49.
- 50. Effusive CP Occurs whenpericardial fluid accumulates b/w a thickened, oedematous or fibrotic parietal+ visceral pericardium Hallmark: Elevated RA pressure, elevated RV+ LV EDPs with associated dip+ plateau ventricular waveforms, respiratory inter ventricular dependence—> Occuring after pericardiocentesis 50
- 51. Congenital absence ofpericardium Case reports/ small series Isolated (65%), associated with other congenital disorder 5 types: Complete absence of entire pericardium Complete absence of rt/lt sided pericardium Partial: lt/ rt sided MC: Complete absence of lt pericardium Young, male patient with non specific symptoms of chest pain, dyspnea, palpitation Laterally displaced apical impulse, migratory apical pulsations, ESM may be present due to excessive heart motion 51
- 52. Congenital absence ofpericardium cont… Partial left sided defects: Greatest risk—> compression, herniation, strangulation of cardiac chambers, great vessels or coronaries ECHO: Unusual imaging windows Appearance of an enlarged RV Excessive cardiac motion Abnormal IVS motion Tear drop cardiac shape: Elongation of atrium + widening of ventricles 52
- 53. Take home message Echoinitial test CMR/ CT needed when poor window, complexity not handled by echo, tissue characterisation needed-edema or inflammation 53
- 54.