4. Effusive-constrictive
pericarditis
Constrictive pericarditis Cardiac tamponade
JVP remain elevated
despite lowering of the
pericardial pressure to
near zero with peri-
cardiocentesis
Rapid y descent
appears
No inspiratory decline
in RAP
Thickened ,scarred
and consequent loss
of the normal elasticity
of the pericardial sac
Typically chronic
Variants
Subacute
Transient
occult constriction
Acute
Subacute
Accumulation of
pericardial fluid under
pressure
Variants
Low pressure
(occult)
Regional
tamponade
5. What went wrong
Normal pericardium Pericardium in constriction
The normal pericardium can stretch to
accommodate physiologic changes in cardiac
volume
Keep up with intra thoracic pressure
Inelastic, resulting in minimal ability to adapt
to volume changes
Cardiac filling is impeded by an external
force(constriction)
Pathophysiologic
Entry and exit of external volume is
handled by enhanced ventricular
interdependence= exaggerated
coupling
Pericardial space has no communication
with intra thoracic pressure change
6. A little more
Normal pericardium Constriction
With a normal pericardium,
intrathoracic pressure decreases
during inspiration, leading to an
increase in venous return to the right
heart and transient increase in right
ventricular chamber size. Because the
normal pericardium accommodates the
increased venous return by expanding,
this increase in venous return does not
impair left ventricular filling or
influences to bare minimum
Upper limit of cardiac volume is constrained
Intrathoracic pressure is not transmitted to the heart chambers
Pericardium does not expand to accommodate increased venous return to
the right heart during inspiration
PCWP fall but not LVEP in inspiration, leading to a reduction in LV volume
Ventricular filling thrives on interdependence
Compression does not occur until the cardiac volume approximates that of
the pericardium, which begins in mid-diastole
Early diastolic filling is even more rapid than normal
Ventricular filling occurs in early diastole with little or no filling subsequently
Stroke volumes are reduced
7. Tuberculosis is the most common cause in
INDIA
Idiopathic or viral – 42 to 49 percent
Post-cardiac surgery – 11 to 37
percent
Post-radiation therapy – 9 to 31
percent, primarily after Hodgkin
disease or breast cancer
Connective tissue disorder – 3 to 7
percent
Postinfectious (tuberculous or purulent
pericarditis) – 3 to 6 percent
Miscellaneous causes (malignancy,
trauma, drug-induced, asbestosis,
sarcoidosis, uremic pericarditis) – 1 to
10 percent
Idiopathic/viral – 0.76 cases per 1000
person-years
Connective tissue/pericardial injury
syndrome – 4.40 cases per 1000
person-years
Neoplastic pericarditis – 6.33 cases
per 1000 person-years
Tuberculous pericarditis – 31.65 cases
per 1000 person-years
Purulent pericarditis – 52.75 cases per
1000 person-years
10. You know all of them
The " a " wave corresponds to right Atrial contraction and
ends synchronously with the carotid artery pulse. The peak
of the 'a' wave demarcates the end of atrial systole.
The " c " wave corresponds to right ventricular Contraction
causing the tricuspid valve to bulge towards the right
atrium.
The " x " descent follows the 'a' wave and corresponds to
atrial relaxation and rapid atrial filling due to low pressure.
The " x' " (x prime) descent follows the 'c' wave and occurs
as a result of the right ventricle pulling the tricuspid valve
downward during ventricular systole. (As stroke volume is
ejected, the ventricle takes up less space in
pericardium, allowing relaxed atrium to enlarge). The x' (x
prime) descent can be used as a measure of right ventricle
contractility.
The " v " wave corresponds to Venous filling when the
tricuspid valve is closed and venous pressure increases
from venous return - this occurs during and following the
carotid pulse.
The " y " descent corresponds to the rapid emptying of the
atrium into the ventricle following the opening of the
tricuspid valve.
11. How does normal pericardium response?
Rapid vs slow accumulation
12. Transmural pressure gradient
(TPG)
Normal pericardial pressure is -5 to +5 mmHg
RVEDP or LVEDP minus intra-pericardial
pressure=TPG
Normal Transmural pressure gradient is zero
Negative in Tamponade
Positive in CP
14. Features……
Increased right atrial pressure
Prominent x and y descents of venous in atrial pressure tracings
Kussumal's sign
Increased RV end-diastolic pressure, usually to a level one-third or more of RV systolic
pressure
"Square root" signs in the RV and LV diastolic pressure tracings A greater inspiratory fall in
pulmonary capillary wedge pressure compared to left ventricular diastolic pressure
Equalization of LV and RV diastolic plateau pressure tracings, with little separation with
exercise, since filling, and therefore diastolic pressure, in both ventricles is constrained by the
inelastic pericardium
Mirror-image discordance between RV and peak LV systolic pressures during inspiration,
another sign of increased ventricular interdependence
During peak inspiration, an increase in RV pressure occurs when LV pressure is lowest
15. Pulsus Paradoxus not in CP
Normally intrapericardial pressure 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.
16. Kussumal’s sign +ve in CP
Kussumal’s Sign is no reduction of mean
column height JVP in inspiration
RV fills only in early diastole irrespective of
respiratory phase
Because no communication between
pericardial space and intra thoracic pressure
change
20. 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.
21. Echo Doppler- mitral inflow:
Constriction
1. RV and LV inflow show
prominent E wave due to
rapid early diastolic filling
2. Short deceleration time of E
wave as filling abruptly stops
3. Small A wave as little filling
occurs in late diastole
following atrial contraction
4. E/A ratio >1.5:1
5. DT<160ms
6. IVRT: <60ms
22. Echo Doppler- mitral inflow: RCM
Early disease E<A.
Late disease: E>A
Constant IVRT
23. Respiratory Mitral Inflow velocity
IN CP:
Mitral peak E velocity >25 %
increase in exp.
IN RCM:
velocity varies by <10%.
24. 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
89% senstive for constriction
100% specific.
RCM:
E’ decreases as severity ↑
E’< 8 cm/s.
28. 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).
29. Right & Left Heart
Catheterization
Dip and plateau pattern in diastolic waveform (square root
sign)
Constrictive pericarditis
Restrictive cardiomyopathy
RV ischemia
30. Right & Left Heart
Catheterization
RVSP < 35-45 mm
Hg
RVEDP / RVSP >
1/3
LVEDP-RVEDP < 5
• PASP = RVSP very high(>55 - 60 mm
Hg)
• RVEDP / RVSP < 1/3
• LVEDP-RVEDP > 3-5 mm Hg
CP RCM
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 intrathoracic pressure (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 IVS shifts 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
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, 7th edRespiratory changes in LV and RV pressures measured with micromanometer catheters in a patient with CP (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.