Pericardial Disease Flashcards
Class 1 Recommendations for TEE
- Patients with suspected pericardial disease including effusion, constriction, or effusive-constrictive process
- Patients with suspected bleeding in the pericardial space
- Follow-up study to evaluate recurrence of effusion or to diagnose early constriction
- Pericardial friction rub developing in acute MI accompanied by symptoms such as persistent pain, hypotension, and nausea
Pericardial anatomy
Two pericardial layers — sac composed of two serous membranes
•Inner serous layer — visceral pericardium is continuous with the epicardium
•Outer fibrous layer — parietal pericardium functions in a restraint role to prevent the heart from dilating too much and blends with the diaphragm inferiorly and pleural spaces laterally
•The layers meet in areas called “reflections”
-> oblique sinus — surrounds vena cava and pulmonary veins creating a pocket behind the LA
-> transverse sinus — surrounds the great vessels (PA and aorta)
•Normally very thing layers with thin distance between them (2-3 mm thick)
> 4 mm = thickened [inflammation and pericarditis]
Triad: chest pain, pericardial friction rub, elevated ST changes in multiple leads
•Normally < 25 - 50 mL of serous pericardial fluid
Increased fluid —> elevated pericardial pressure —> exceeds diastolic pressures in the chambers —> tamponade and impaired filling
Pericardial function
- Restraint —> prevents excessive dilation —> improved atrioventricular valve function
- Isolates the heart from surrounding structures
- Lubrication function —> normal rotation and translation
- Secretion of biochemical substances: prostacyclin, sympathetic neuronal regulation, coronary vascular tone and cardiac contractility
- Fibrinolytic function
Respirophasic Variation
•Variation in transtricsupid and transmitral inflow that occurs with spontaneous ventilation due to changes in intrathoracic pressure
•Pressure changes are normally transmitted to the pericardial space and cardiac chambers
•Normal spontaneous ventilation — intrathoracic pressures -3 to -6 mmHg
More negative —> increased venous return and enhanced RV filling
•Gradient for RV filling = intracardiac P - pericardial P
…If RAP = 6 and PP = -6 then filling gradient = 12
•Transtricuspid inflow velocities change by ≈ 20%
Increase on inspiration / decrease on expiration
RV SV/VTI/flow increases during inspiration and LV flow decreases — negative pericardial pressure enchanting filling on right side
•Transmitral inflow velocities change by ≈ 10%
Decrease on inspiration / increase on expiration
LV less compliant and d’intensi le so affected less than RV to changes in intrathoracic/pericardial pressures
•Pericardial pressure essentially the same as intrathoracic pressure
End expiration pressure -3 mmHg : less tricuspid inflow and more mitral inflow
End inspiration pressure -6 mmHg : more tricuspid inflow and less mitral inflow
Spontaneous respiration changes
Inspiration / Expiration More - / + intrathoracic pressure Dilation / smush of pulmonary veins Increase / decrease systemic venous return Increase / decrease RV filling & RV SV Decrease / increase RV afterload Decrease / increase LA filling Decrease / increase LV SV Increase / decrease LV afterload
Spontaneous inspiration
- increased gradient for RV filling
- decreased LV filling (pulmonary venous pooling)
- septum shifts from R —> L
- venous return to RA increases —> RV filling increases —> RV SV increases
- negative intrathoracic pressure increases —>pulmonary venous pooling —> decrease LA filling —> decrease LV filling —> decrease LV SV
Spontaneous expiration
- decreased gradient for RV filling (decreased venous return)
- increased LV filling (compresses lungs and pulmonary vasculature)
- venous return to RA decreases —> RV filling decreases —> RV SV decreases
- compression pulmonary vasculature —> increases pulmonary venous return —> increases LA filling —> increases LV filling —> increases LV SV
Positive Pressure Ventilation changes
- In normal, constrictive pericarditis, and tamponade the changes that occur between spontaneous and PPV are opposite
- CP & T there are exaggerated changes with Spont ventilation
- CP has exaggerated changes with both spont ventilation and PPV
- T has decreased variation with PPV —> tremendous decrease in transmitral flow indicating decrease in LV SV
Pericardial Tamponade Pathology
- Fixed cardiac volume, limited cardiac filling
- Increased respiratory variation with spont ventilation
- Decreased respiratory variation with PPV***
- Ventricular interdependence
- Elevated & equalized central venous, pulmonary venous & ventricular DIASTOLIC pressures
- Prominent systolic filling (extenuated Y descent)***
- Inspiratory decrease in intrathoracic pressure NOT transmitted to the heart
- Pulsus paradoxes common***
- Kussmaul’s sign NOT present***
Constrictive Pericarditis Pathology
- Fixed cardiac volume, limited cardiac filling
- Increased respiratory variation with spont ventilation
- Increased respiratory variation with PPV***
- Ventricular interdependence
- Elevated & equalized central venous, pulmonary venous & ventricular DIASTOLIC pressures
- Prominent early filling (exaggerated Y descent)***
- Inspiratory decrease in intrathoracic pressure NOT transmitted to the heart
- Pulsus paradoxes uncommon***
- Kussmaul’s sign common***
Key differences: Tamponade vs CP
Tamponade:
•prominent systolic filling and attenuated Y descent — compression of the heart that is worsened when the heart is the fullest (diastole) therefore diastolic flow impeded severely
•during systole, the ventricle is small so there is accentuated filling of the atria with an attenuated y descent
•lose your y —> then you die !!
Constrictive Pericarditis:
•prominent early filling and exaggerated y descent: the constriction/shell that surrounds the heart doesn’t impair early diastolic filling so it’s augmented (E wave)
Congenital Problems
- rare
- partial or total absence of the pericardium — heart cant herniate through a partial absence causing constriction / strangulation (uncommon) ; decrease of the restrictive fole of the pericardium with total absence leading to excessive dilation
- Mulibery nanism —> CHF & CP ; muscle, liver, brain, eye, stunted or dwarfed ; characterized by pericardial constriction with growth failure ; rare autosomal recessive
Pericarditis
•inflammation of the pericardium
•triad: chest pain (acute, sharp, radiated to back, pleuritic, positional — worse flat), EKG changes (diffuse ST elevation), pericardial friction rub
•other findings: new/worsening effusion, elevated CRP & ESR, late gadolinium enhancement on cMRI
•etiology:
most often idiopathic (often viral) 42-49%
Infection
Neoplastic
Autoimmune/inflammatory
Post cardiac surgery/intervention 11-37%
Post radiation (mediastinal)
Miscellaneous (drugs, trauma, uremia)
•thickness > 4 mm —> highly suspicious
[normal = 1-2 mm]
Pericardium is not always thick
MRI & CT > TEE > TTE for measuring thickness
•timing: < 3 mos = acute, > 3 mos = chronic
•exaggerated respirophasic variation in both PPV and spont ventilation
CP vs. RICM
CP:
•peak velocity pulmonary venous D wave variation > 18%
•peak velocity TM E wave variation > 10%
•color M-mode prop velocity (Vp) slope > 100 cm/s
•pericardial knock
•BNP < 100
•pericardial thickness > 4 mm
•e’ > 10 cm/s
•annulus reversus: lateral e’ < septal e’
•annulus paradoxus: E/e’ < 15
•reversal of forward venous hepatic flow during spont expiration
•late gadolinium enhancement of pericardium
•LA volume»_space; RA volume
•max septal excursion between inspiration and expiration is greater
•elevation and equalization of diastolic pressures
•ventricular interdependence
•respirophasic variation in SV, peak systolic P, pulse pressure
•respiratory variation in LV systolic pressure-time area
RICM: •tissue doppler e’ < 8 cm/s •S3 •elevated BNP •E/e’ > 15 •reversal of forward venous hepatic flow in spont inspiration •late gadolinium enhancement of subendocardium •Vp < 50 cm/s •LVEDP > RVEDP
Effusions
Symptoms & findings: tachycardia ; chest pain ; fatigue ; dyspnea ; tachypnea ; peripheral edema ; shock: hypotension, cool extremities, decreased UOP ; elevated JVP ; pulsus paradoxus ; effusion, rub, muted sounds ; elevation and equalization of PP and diastolic pressures ; decreased SV and CO ; exaggerated respirophasic variation with spont vent ; decreased variation with PPV ; electrical alternans
Echo findings: effusion (clot or Lou latex) ; IVC plethora (>20 mm & decrease <50% w/ sniff — Se but not Sp) ; enlarged hepatic veins ; RA collapse (systole & diastole) — RA collapse for >1/3 cardiac cycle nearly 100% Se and Sp (can occur in normal patients with low RAP but systolic collapse should never occur) — occurs in diastole when PP > RVP (absence of any chamber collapse >90% NPV) ; ventricular interdependence ; reciprocal respiratory changes in RV & LV volumes ; normal ventricular size ; premature mid-diastolic PV opening (best seen in M-mode)
Pericardial fluid: 0.5 cm (100-200ml) = small 0.5 - 2 cm (200-500ml) = moderate >2 cm (>500ml) = large *clinical presentation depends on volume and time course of accumulation
