The document provides information on the anatomy, physiology, and pathophysiology of the pericardium and pericardial diseases. It discusses the layers of the pericardium, functions of restraining cardiac volume and lubricating the heart. In pathophysiology, it describes cardiac tamponade, constrictive pericarditis, and their differences from restrictive cardiomyopathy. Diagnostic tools including echocardiography and cardiac catheterization are outlined for evaluating pericardial diseases and distinguishing constrictive pericarditis from restrictive cardiomyopathy.
A lecture on the echocardiographic evaluation of hypertrophic cardiomyopathy. Starts with an overview of the topic then a systematic approach to diagnosis and then a differential diagnosis followed by take-home messages and conclusion.
A lecture on the echocardiographic evaluation of hypertrophic cardiomyopathy. Starts with an overview of the topic then a systematic approach to diagnosis and then a differential diagnosis followed by take-home messages and conclusion.
A case of missed diagnosis. Presentation can be in form of heart failure. Differentials can be of Constrictive pericarditis. Restrictive cardiomyopathy/Endomyocardial fibrosis, DCM. This presentation contains clinical presentation, differentials, hemodynamics of cath study, echocardiogrpahy in a case of CP
Day 1 -RESERVE CONPENSATION FAILURE2wb.pptxMkindi Mkindi
There are nearly 100 viruses of the herpes group that infect many different animal species.
Official name of herpesviruses that commonly infect human is Humans herpesvirus (HHV)
herpes simplex virus types 1 (HHV 1)
Herpes simplex virus type 2 (HHV 2)
Varicella-zoster virus (HHV 3)
Epstein-Barr virus, (HHV 4)
Cytomegalovirus (HHV 5)
Human herpesvirus 6 (HHV 6)
Human herpesvirus 7 (HHV 7)
Human herpesvirus 8 (HHV 8) (Kaposi's sarcoma-associated herpesvirus).
Herpes B virus of monkeys can also infect humans
hELMINTHS#corona virus#Aspergillosis#BUGANDO#CUHAS#CUHAS#CUHAS#CELL MEMBRANE TRANSPORT#PHYSIOLOGY#BODY FLUIDS#RENAL PHYSIOLOGY#
Similar to Hemodynamics of cardiac tamponade, constrictive pericarditis & restrictive cardiomyopathy (20)
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
Follow us on: Pinterest
Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Factory Supply Best Quality Pmk Oil CAS 28578–16–7 PMK Powder in Stockrebeccabio
Factory Supply Best Quality Pmk Oil CAS 28578–16–7 PMK Powder in Stock
Telegram: bmksupplier
signal: +85264872720
threema: TUD4A6YC
You can contact me on Telegram or Threema
Communicate promptly and reply
Free of customs clearance, Double Clearance 100% pass delivery to USA, Canada, Spain, Germany, Netherland, Poland, Italy, Sweden, UK, Czech Republic, Australia, Mexico, Russia, Ukraine, Kazakhstan.Door to door service
Hot Selling Organic intermediates
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
HOT NEW PRODUCT! BIG SALES FAST SHIPPING NOW FROM CHINA!! EU KU DB BK substit...GL Anaacs
Contact us if you are interested:
Email / Skype : kefaya1771@gmail.com
Threema: PXHY5PDH
New BATCH Ku !!! MUCH IN DEMAND FAST SALE EVERY BATCH HAPPY GOOD EFFECT BIG BATCH !
Contact me on Threema or skype to start big business!!
Hot-sale products:
NEW HOT EUTYLONE WHITE CRYSTAL!!
5cl-adba precursor (semi finished )
5cl-adba raw materials
ADBB precursor (semi finished )
ADBB raw materials
APVP powder
5fadb/4f-adb
Jwh018 / Jwh210
Eutylone crystal
Protonitazene (hydrochloride) CAS: 119276-01-6
Flubrotizolam CAS: 57801-95-3
Metonitazene CAS: 14680-51-4
Payment terms: Western Union,MoneyGram,Bitcoin or USDT.
Deliver Time: Usually 7-15days
Shipping method: FedEx, TNT, DHL,UPS etc.Our deliveries are 100% safe, fast, reliable and discreet.
Samples will be sent for your evaluation!If you are interested in, please contact me, let's talk details.
We specializes in exporting high quality Research chemical, medical intermediate, Pharmaceutical chemicals and so on. Products are exported to USA, Canada, France, Korea, Japan,Russia, Southeast Asia and other countries.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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.
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.
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).
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
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.
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.
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
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.