SlideShare una empresa de Scribd logo
1 de 33
Constrictive
Pericarditis
Secrete parlour
Pathology
 Pericardium
 Thickened > 5mm by
CT
 Scarred
 Loss of elasticity
No thickening
28% -CT scan
18% -Histopathology
Ref:Talreja et al,circulation,2003
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
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
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
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
Out of Subject
Respiratory variations
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.
How does normal pericardium response?
Rapid vs slow accumulation
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
Some beautiful features of CP
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
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.
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
CT vs. CP
Clinical
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
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
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
89% senstive for constriction
100% specific.
RCM:
E’ decreases as severity ↑
E’< 8 cm/s.
Respiratory Mitral Inflow & TD of mitral
annulus
HV diastolic flow reversal:CP vs
RCM
VS
Pulmonary Venous flow
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
• 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
Conclude with some comparison
Pericardium failed to relax

Más contenido relacionado

La actualidad más candente

Hypertrophic cardiomyopathy
Hypertrophic cardiomyopathyHypertrophic cardiomyopathy
Hypertrophic cardiomyopathy
Fuad Farooq
 
Bundle branch blocks
Bundle branch blocksBundle branch blocks
Bundle branch blocks
Adarsh
 
Supraventricular tachycardias
Supraventricular tachycardiasSupraventricular tachycardias
Supraventricular tachycardias
Praveen Nagula
 

La actualidad más candente (20)

dialated cardiomyopathies
dialated cardiomyopathiesdialated cardiomyopathies
dialated cardiomyopathies
 
Diastolic Dysfunction 2016
Diastolic Dysfunction 2016Diastolic Dysfunction 2016
Diastolic Dysfunction 2016
 
Hypertrophic cardiomyopathy
Hypertrophic cardiomyopathyHypertrophic cardiomyopathy
Hypertrophic cardiomyopathy
 
Chronic constrictive pericarditis
Chronic constrictive pericarditisChronic constrictive pericarditis
Chronic constrictive pericarditis
 
Bundle branch blocks
Bundle branch blocksBundle branch blocks
Bundle branch blocks
 
Hemodyanmic features of Constrictive pericarditis and Restrictive cardiomyopathy
Hemodyanmic features of Constrictive pericarditis and Restrictive cardiomyopathyHemodyanmic features of Constrictive pericarditis and Restrictive cardiomyopathy
Hemodyanmic features of Constrictive pericarditis and Restrictive cardiomyopathy
 
Sick sinus syndrome
Sick sinus syndrome Sick sinus syndrome
Sick sinus syndrome
 
Supraventricular tachyarrythmias
Supraventricular tachyarrythmiasSupraventricular tachyarrythmias
Supraventricular tachyarrythmias
 
Right bundle branch block
Right bundle branch blockRight bundle branch block
Right bundle branch block
 
Complications of acute mi
Complications of acute miComplications of acute mi
Complications of acute mi
 
Ventricular tachycardia
Ventricular tachycardiaVentricular tachycardia
Ventricular tachycardia
 
Ventricular arrhythmias
Ventricular arrhythmiasVentricular arrhythmias
Ventricular arrhythmias
 
Atrial Fibrillation by Dr. Aryan
Atrial Fibrillation by Dr. AryanAtrial Fibrillation by Dr. Aryan
Atrial Fibrillation by Dr. Aryan
 
Pericardial diseases
Pericardial  diseasesPericardial  diseases
Pericardial diseases
 
Ventricular arrhythmias
Ventricular arrhythmias Ventricular arrhythmias
Ventricular arrhythmias
 
ATRIAL FIBRILLATION
ATRIAL FIBRILLATIONATRIAL FIBRILLATION
ATRIAL FIBRILLATION
 
Echo Mitral Stenosis
Echo Mitral StenosisEcho Mitral Stenosis
Echo Mitral Stenosis
 
Supraventricular tachycardias
Supraventricular tachycardiasSupraventricular tachycardias
Supraventricular tachycardias
 
Mitral stenosis
Mitral stenosisMitral stenosis
Mitral stenosis
 
Long QT Syndrome
Long QT SyndromeLong QT Syndrome
Long QT Syndrome
 

Destacado

Eisenmenger syndrome
Eisenmenger syndromeEisenmenger syndrome
Eisenmenger syndrome
Fuad Farooq
 
Patent ductus arteriosus
Patent ductus arteriosusPatent ductus arteriosus
Patent ductus arteriosus
Ramachandra Barik
 
Diagnosis of diabetes mellitus
Diagnosis of diabetes mellitus  Diagnosis of diabetes mellitus
Diagnosis of diabetes mellitus
Dilek Gogas Yavuz
 
Aortic regurgitation
Aortic regurgitationAortic regurgitation
Aortic regurgitation
Dhinil Dares
 

Destacado (20)

Constrictive Pericarditis
Constrictive PericarditisConstrictive Pericarditis
Constrictive Pericarditis
 
Unstable Angina Pectoris
Unstable Angina PectorisUnstable Angina Pectoris
Unstable Angina Pectoris
 
Pericardial effusion
Pericardial effusionPericardial effusion
Pericardial effusion
 
Ventricular septal defect (vsd)
Ventricular septal defect (vsd)Ventricular septal defect (vsd)
Ventricular septal defect (vsd)
 
Glycated haemoglobin ppt by Basalingappa BG
Glycated haemoglobin ppt by Basalingappa BGGlycated haemoglobin ppt by Basalingappa BG
Glycated haemoglobin ppt by Basalingappa BG
 
Management Of PDA
Management Of PDAManagement Of PDA
Management Of PDA
 
Eisenmenger syndrome
Eisenmenger syndromeEisenmenger syndrome
Eisenmenger syndrome
 
Peripheral Vascular Examination
Peripheral  Vascular  ExaminationPeripheral  Vascular  Examination
Peripheral Vascular Examination
 
Patent ductus arteriosus
Patent ductus arteriosusPatent ductus arteriosus
Patent ductus arteriosus
 
Vsd
VsdVsd
Vsd
 
Cyanosis
Cyanosis Cyanosis
Cyanosis
 
Nursing care of client with Coronary artery disease part 2 of 2
Nursing care of client with Coronary artery disease part 2 of 2Nursing care of client with Coronary artery disease part 2 of 2
Nursing care of client with Coronary artery disease part 2 of 2
 
Acute pericarditis
Acute pericarditisAcute pericarditis
Acute pericarditis
 
Diagnosis of diabetes mellitus
Diagnosis of diabetes mellitus  Diagnosis of diabetes mellitus
Diagnosis of diabetes mellitus
 
ECG: Atrial Flutter
ECG: Atrial FlutterECG: Atrial Flutter
ECG: Atrial Flutter
 
Raynaud's phenomenon
Raynaud's phenomenonRaynaud's phenomenon
Raynaud's phenomenon
 
TRANS ESOPHAGEAL ECHOCARDIOGRAPHY
TRANS ESOPHAGEAL ECHOCARDIOGRAPHYTRANS ESOPHAGEAL ECHOCARDIOGRAPHY
TRANS ESOPHAGEAL ECHOCARDIOGRAPHY
 
Aortic regurgitation
Aortic regurgitationAortic regurgitation
Aortic regurgitation
 
Rheumatic Heart Disease
Rheumatic Heart DiseaseRheumatic Heart Disease
Rheumatic Heart Disease
 
Glucosuria
GlucosuriaGlucosuria
Glucosuria
 

Similar a Constrictive pericarditis

Anaesthetic management of a patient with mitral stenosis put for non-cardiac ...
Anaesthetic management of a patient with mitral stenosis put for non-cardiac ...Anaesthetic management of a patient with mitral stenosis put for non-cardiac ...
Anaesthetic management of a patient with mitral stenosis put for non-cardiac ...
Ankur Khandelwal
 
Anaesthetic management of mitral valvular heart disease
Anaesthetic management of mitral valvular heart diseaseAnaesthetic management of mitral valvular heart disease
Anaesthetic management of mitral valvular heart disease
Dhritiman Chakrabarti
 

Similar a Constrictive pericarditis (20)

Constrictive pericarditis
Constrictive pericarditisConstrictive pericarditis
Constrictive pericarditis
 
Pediatric cardiac-anomalies-part-3
Pediatric cardiac-anomalies-part-3Pediatric cardiac-anomalies-part-3
Pediatric cardiac-anomalies-part-3
 
Pericardial Dse Cath Lab
Pericardial Dse Cath LabPericardial Dse Cath Lab
Pericardial Dse Cath Lab
 
Constrictive Pericariditis and mnagement.pptx
Constrictive Pericariditis and mnagement.pptxConstrictive Pericariditis and mnagement.pptx
Constrictive Pericariditis and mnagement.pptx
 
Cardiogenic shock
Cardiogenic  shockCardiogenic  shock
Cardiogenic shock
 
Cardiac tamponade
Cardiac tamponadeCardiac tamponade
Cardiac tamponade
 
Cardiac tamponade
Cardiac tamponadeCardiac tamponade
Cardiac tamponade
 
pulmonary embolism
pulmonary embolismpulmonary embolism
pulmonary embolism
 
DIAGNOSIS AND MANAGEMENT OF ACS copy.pptx
DIAGNOSIS AND MANAGEMENT OF ACS copy.pptxDIAGNOSIS AND MANAGEMENT OF ACS copy.pptx
DIAGNOSIS AND MANAGEMENT OF ACS copy.pptx
 
Chronic constrictive pericarditis
Chronic constrictive pericarditisChronic constrictive pericarditis
Chronic constrictive pericarditis
 
Venous thromboembolism.pptx
Venous thromboembolism.pptxVenous thromboembolism.pptx
Venous thromboembolism.pptx
 
2.8. Pericardial disease.pptx
2.8. Pericardial disease.pptx2.8. Pericardial disease.pptx
2.8. Pericardial disease.pptx
 
Anaesthetic management of a patient with mitral stenosis put for non-cardiac ...
Anaesthetic management of a patient with mitral stenosis put for non-cardiac ...Anaesthetic management of a patient with mitral stenosis put for non-cardiac ...
Anaesthetic management of a patient with mitral stenosis put for non-cardiac ...
 
Pericardial diseases 2020 final
Pericardial diseases 2020 finalPericardial diseases 2020 final
Pericardial diseases 2020 final
 
Acute Pulmonary Embolism: Introduction, Clinical presentation, Classification...
Acute Pulmonary Embolism: Introduction, Clinical presentation, Classification...Acute Pulmonary Embolism: Introduction, Clinical presentation, Classification...
Acute Pulmonary Embolism: Introduction, Clinical presentation, Classification...
 
Anaesthetic management of mitral valvular heart disease
Anaesthetic management of mitral valvular heart diseaseAnaesthetic management of mitral valvular heart disease
Anaesthetic management of mitral valvular heart disease
 
Cardiac tamponade
Cardiac tamponadeCardiac tamponade
Cardiac tamponade
 
Cardiac tamponade Toufiqur Rahman
Cardiac tamponade Toufiqur RahmanCardiac tamponade Toufiqur Rahman
Cardiac tamponade Toufiqur Rahman
 
Peri op management of mitral stenosis patient coming for non cardiac surgery
Peri op management of mitral stenosis patient coming for non cardiac surgeryPeri op management of mitral stenosis patient coming for non cardiac surgery
Peri op management of mitral stenosis patient coming for non cardiac surgery
 
ECHOCARDIOGRAPHY IN CARDIAC TAMPONADE
ECHOCARDIOGRAPHY IN CARDIAC TAMPONADEECHOCARDIOGRAPHY IN CARDIAC TAMPONADE
ECHOCARDIOGRAPHY IN CARDIAC TAMPONADE
 

Más de Ramachandra Barik

Brugada syndrome
Brugada syndromeBrugada syndrome
Brugada syndrome
Ramachandra Barik
 

Más de Ramachandra Barik (20)

Willens's syndrome.pptx
Willens's syndrome.pptxWillens's syndrome.pptx
Willens's syndrome.pptx
 
Intensive care of congenital heart disease.pptx
Intensive care of congenital heart disease.pptxIntensive care of congenital heart disease.pptx
Intensive care of congenital heart disease.pptx
 
Management of Hypetension.pptx
Management of Hypetension.pptxManagement of Hypetension.pptx
Management of Hypetension.pptx
 
CRISPR and cardiovascular diseases.pdf
CRISPR and cardiovascular diseases.pdfCRISPR and cardiovascular diseases.pdf
CRISPR and cardiovascular diseases.pdf
 
Pacemaker Pocket Infection After Splenectomy
Pacemaker Pocket Infection After SplenectomyPacemaker Pocket Infection After Splenectomy
Pacemaker Pocket Infection After Splenectomy
 
Piccolo Duct Occluder.pdf
Piccolo Duct Occluder.pdfPiccolo Duct Occluder.pdf
Piccolo Duct Occluder.pdf
 
MISPLACED ECG LEADS.pptx
MISPLACED ECG LEADS.pptxMISPLACED ECG LEADS.pptx
MISPLACED ECG LEADS.pptx
 
A Case of Device Closure of an Eccentric Atrial Septal Defect Using a Large D...
A Case of Device Closure of an Eccentric Atrial Septal Defect Using a Large D...A Case of Device Closure of an Eccentric Atrial Septal Defect Using a Large D...
A Case of Device Closure of an Eccentric Atrial Septal Defect Using a Large D...
 
Arrythmia-IV.pptx
Arrythmia-IV.pptxArrythmia-IV.pptx
Arrythmia-IV.pptx
 
Arrythmia-III.pptx
Arrythmia-III.pptxArrythmia-III.pptx
Arrythmia-III.pptx
 
Arrythmia-II.pptx
Arrythmia-II.pptxArrythmia-II.pptx
Arrythmia-II.pptx
 
Arrythmia-I.pptx
Arrythmia-I.pptxArrythmia-I.pptx
Arrythmia-I.pptx
 
Trio of Rheumatic Mitral Stenosis, Right Posterior Septal Accessory Pathway a...
Trio of Rheumatic Mitral Stenosis, Right Posterior Septal Accessory Pathway a...Trio of Rheumatic Mitral Stenosis, Right Posterior Septal Accessory Pathway a...
Trio of Rheumatic Mitral Stenosis, Right Posterior Septal Accessory Pathway a...
 
Anticoagulation therapy during pregnancy
Anticoagulation therapy during pregnancyAnticoagulation therapy during pregnancy
Anticoagulation therapy during pregnancy
 
Coronary guidewire
Coronary guidewireCoronary guidewire
Coronary guidewire
 
Intracoronary optical coherence tomography
Intracoronary optical coherence tomographyIntracoronary optical coherence tomography
Intracoronary optical coherence tomography
 
Brugada syndrome
Brugada syndromeBrugada syndrome
Brugada syndrome
 
A roadmap for the human development
A roadmap for the human developmentA roadmap for the human development
A roadmap for the human development
 
Intra aortic balloon pump
Intra aortic balloon pumpIntra aortic balloon pump
Intra aortic balloon pump
 
Left ventricular false tendons
Left ventricular false tendonsLeft ventricular false tendons
Left ventricular false tendons
 

Último

Call Girls Bhubaneswar Just Call 9907093804 Top Class Call Girl Service Avail...
Call Girls Bhubaneswar Just Call 9907093804 Top Class Call Girl Service Avail...Call Girls Bhubaneswar Just Call 9907093804 Top Class Call Girl Service Avail...
Call Girls Bhubaneswar Just Call 9907093804 Top Class Call Girl Service Avail...
Dipal Arora
 
Call Girls Aurangabad Just Call 8250077686 Top Class Call Girl Service Available
Call Girls Aurangabad Just Call 8250077686 Top Class Call Girl Service AvailableCall Girls Aurangabad Just Call 8250077686 Top Class Call Girl Service Available
Call Girls Aurangabad Just Call 8250077686 Top Class Call Girl Service Available
Dipal Arora
 

Último (20)

Call Girls Tirupati Just Call 8250077686 Top Class Call Girl Service Available
Call Girls Tirupati Just Call 8250077686 Top Class Call Girl Service AvailableCall Girls Tirupati Just Call 8250077686 Top Class Call Girl Service Available
Call Girls Tirupati Just Call 8250077686 Top Class Call Girl Service Available
 
Call Girls Bhubaneswar Just Call 9907093804 Top Class Call Girl Service Avail...
Call Girls Bhubaneswar Just Call 9907093804 Top Class Call Girl Service Avail...Call Girls Bhubaneswar Just Call 9907093804 Top Class Call Girl Service Avail...
Call Girls Bhubaneswar Just Call 9907093804 Top Class Call Girl Service Avail...
 
Premium Call Girls Cottonpet Whatsapp 7001035870 Independent Escort Service
Premium Call Girls Cottonpet Whatsapp 7001035870 Independent Escort ServicePremium Call Girls Cottonpet Whatsapp 7001035870 Independent Escort Service
Premium Call Girls Cottonpet Whatsapp 7001035870 Independent Escort Service
 
Best Rate (Hyderabad) Call Girls Jahanuma ⟟ 8250192130 ⟟ High Class Call Girl...
Best Rate (Hyderabad) Call Girls Jahanuma ⟟ 8250192130 ⟟ High Class Call Girl...Best Rate (Hyderabad) Call Girls Jahanuma ⟟ 8250192130 ⟟ High Class Call Girl...
Best Rate (Hyderabad) Call Girls Jahanuma ⟟ 8250192130 ⟟ High Class Call Girl...
 
Night 7k to 12k Navi Mumbai Call Girl Photo 👉 BOOK NOW 9833363713 👈 ♀️ night ...
Night 7k to 12k Navi Mumbai Call Girl Photo 👉 BOOK NOW 9833363713 👈 ♀️ night ...Night 7k to 12k Navi Mumbai Call Girl Photo 👉 BOOK NOW 9833363713 👈 ♀️ night ...
Night 7k to 12k Navi Mumbai Call Girl Photo 👉 BOOK NOW 9833363713 👈 ♀️ night ...
 
The Most Attractive Hyderabad Call Girls Kothapet 𖠋 9332606886 𖠋 Will You Mis...
The Most Attractive Hyderabad Call Girls Kothapet 𖠋 9332606886 𖠋 Will You Mis...The Most Attractive Hyderabad Call Girls Kothapet 𖠋 9332606886 𖠋 Will You Mis...
The Most Attractive Hyderabad Call Girls Kothapet 𖠋 9332606886 𖠋 Will You Mis...
 
Call Girls Bangalore Just Call 8250077686 Top Class Call Girl Service Available
Call Girls Bangalore Just Call 8250077686 Top Class Call Girl Service AvailableCall Girls Bangalore Just Call 8250077686 Top Class Call Girl Service Available
Call Girls Bangalore Just Call 8250077686 Top Class Call Girl Service Available
 
Call Girls Guntur Just Call 8250077686 Top Class Call Girl Service Available
Call Girls Guntur  Just Call 8250077686 Top Class Call Girl Service AvailableCall Girls Guntur  Just Call 8250077686 Top Class Call Girl Service Available
Call Girls Guntur Just Call 8250077686 Top Class Call Girl Service Available
 
Call Girls Dehradun Just Call 9907093804 Top Class Call Girl Service Available
Call Girls Dehradun Just Call 9907093804 Top Class Call Girl Service AvailableCall Girls Dehradun Just Call 9907093804 Top Class Call Girl Service Available
Call Girls Dehradun Just Call 9907093804 Top Class Call Girl Service Available
 
VIP Hyderabad Call Girls Bahadurpally 7877925207 ₹5000 To 25K With AC Room 💚😋
VIP Hyderabad Call Girls Bahadurpally 7877925207 ₹5000 To 25K With AC Room 💚😋VIP Hyderabad Call Girls Bahadurpally 7877925207 ₹5000 To 25K With AC Room 💚😋
VIP Hyderabad Call Girls Bahadurpally 7877925207 ₹5000 To 25K With AC Room 💚😋
 
(Low Rate RASHMI ) Rate Of Call Girls Jaipur ❣ 8445551418 ❣ Elite Models & Ce...
(Low Rate RASHMI ) Rate Of Call Girls Jaipur ❣ 8445551418 ❣ Elite Models & Ce...(Low Rate RASHMI ) Rate Of Call Girls Jaipur ❣ 8445551418 ❣ Elite Models & Ce...
(Low Rate RASHMI ) Rate Of Call Girls Jaipur ❣ 8445551418 ❣ Elite Models & Ce...
 
Call Girls Siliguri Just Call 8250077686 Top Class Call Girl Service Available
Call Girls Siliguri Just Call 8250077686 Top Class Call Girl Service AvailableCall Girls Siliguri Just Call 8250077686 Top Class Call Girl Service Available
Call Girls Siliguri Just Call 8250077686 Top Class Call Girl Service Available
 
Call Girls Ooty Just Call 8250077686 Top Class Call Girl Service Available
Call Girls Ooty Just Call 8250077686 Top Class Call Girl Service AvailableCall Girls Ooty Just Call 8250077686 Top Class Call Girl Service Available
Call Girls Ooty Just Call 8250077686 Top Class Call Girl Service Available
 
Top Rated Bangalore Call Girls Mg Road ⟟ 9332606886 ⟟ Call Me For Genuine S...
Top Rated Bangalore Call Girls Mg Road ⟟   9332606886 ⟟ Call Me For Genuine S...Top Rated Bangalore Call Girls Mg Road ⟟   9332606886 ⟟ Call Me For Genuine S...
Top Rated Bangalore Call Girls Mg Road ⟟ 9332606886 ⟟ Call Me For Genuine S...
 
Top Rated Hyderabad Call Girls Erragadda ⟟ 9332606886 ⟟ Call Me For Genuine ...
Top Rated  Hyderabad Call Girls Erragadda ⟟ 9332606886 ⟟ Call Me For Genuine ...Top Rated  Hyderabad Call Girls Erragadda ⟟ 9332606886 ⟟ Call Me For Genuine ...
Top Rated Hyderabad Call Girls Erragadda ⟟ 9332606886 ⟟ Call Me For Genuine ...
 
Call Girls Cuttack Just Call 9907093804 Top Class Call Girl Service Available
Call Girls Cuttack Just Call 9907093804 Top Class Call Girl Service AvailableCall Girls Cuttack Just Call 9907093804 Top Class Call Girl Service Available
Call Girls Cuttack Just Call 9907093804 Top Class Call Girl Service Available
 
Call Girls Coimbatore Just Call 9907093804 Top Class Call Girl Service Available
Call Girls Coimbatore Just Call 9907093804 Top Class Call Girl Service AvailableCall Girls Coimbatore Just Call 9907093804 Top Class Call Girl Service Available
Call Girls Coimbatore Just Call 9907093804 Top Class Call Girl Service Available
 
Call Girls Agra Just Call 8250077686 Top Class Call Girl Service Available
Call Girls Agra Just Call 8250077686 Top Class Call Girl Service AvailableCall Girls Agra Just Call 8250077686 Top Class Call Girl Service Available
Call Girls Agra Just Call 8250077686 Top Class Call Girl Service Available
 
Call Girls Aurangabad Just Call 8250077686 Top Class Call Girl Service Available
Call Girls Aurangabad Just Call 8250077686 Top Class Call Girl Service AvailableCall Girls Aurangabad Just Call 8250077686 Top Class Call Girl Service Available
Call Girls Aurangabad Just Call 8250077686 Top Class Call Girl Service Available
 
Call Girls Service Jaipur {9521753030} ❤️VVIP RIDDHI Call Girl in Jaipur Raja...
Call Girls Service Jaipur {9521753030} ❤️VVIP RIDDHI Call Girl in Jaipur Raja...Call Girls Service Jaipur {9521753030} ❤️VVIP RIDDHI Call Girl in Jaipur Raja...
Call Girls Service Jaipur {9521753030} ❤️VVIP RIDDHI Call Girl in Jaipur Raja...
 

Constrictive pericarditis

  • 2. Pathology  Pericardium  Thickened > 5mm by CT  Scarred  Loss of elasticity
  • 3. No thickening 28% -CT scan 18% -Histopathology Ref:Talreja et al,circulation,2003
  • 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
  • 19. 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
  • 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.
  • 25. Respiratory Mitral Inflow & TD of mitral annulus
  • 26. HV diastolic flow reversal:CP vs RCM VS
  • 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
  • 31. RV- LV discordance vs. concordance CP RCM
  • 32. Conclude with some comparison

Notas del editor

  1. 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 &gt;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
  2. Otto. Textbook of Clinical Echocardiography, 3rd Edition, 2004.
  3. Otto. Textbook of Clinical Echocardiography, 3rd Edition, 2004.
  4. 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)
  5. Feigenbaum’s Echocardiography, 7th ed
  6. CP:With insp: minimal increase in HV S &amp; D.With exp: decreased diast. Flow &amp; increased reversal.RCM: blunted S/D ratio, increased insp. Reversal of dias flow.
  7. RCM:S/D ratio: &lt;0.5.No resp. variation in D.CP:Decreased S &amp; D wave with insp. Opp with exp.
  8. Grossman’s cardiac catheterisation, 7thh ed
  9. Grossman’s cardiac catheterisation, 7thh ed
  10. Grossman’s cardiac catheterisation, 7thh ed
  11. 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.
  12. Braunwald’s 9th ed.