D-Transposition, also known as dextro-Transposition of the great arteries (d-TGA), is a congenital heart defect where the ventricles are connected to the wrong great arteries. Specifically, the aorta arises from the right ventricle while the pulmonary artery arises from the left ventricle. This causes two parallel circulations instead of the normal series circulation. The basic embryological defect is abnormal development of the conus, which prevents normal septal formation between the great arteries. Untreated d-TGA is fatal in infancy due to lack of oxygenated blood to the body. Clinical presentation depends on the degree of mixing between the circulations.
preop TEE assessment of atrial septal defect is very important for making decision for device closure, properly assessed adequate rims of ASD will reduce risk of device embolization to almost nil.
Ventricular tachycardia are difficult to understand. it is classified in to two types. 1. VT in structurally normal heart, 2. VT in heart with structural diseases. I have tried to simplify the VT in structurally normal heart, which may be helpful to many students and learners.
Our concepts of heart disease are based on the enormous reservoir of physiologic and anatomic knowledge derived from the past 70 years' of experience in the cardiac catheterization laboratory.
As Andre Cournand remarked in his Nobel lecture of December 11, 1956, the cardiac catheter was the key in the lock.
By turning this key, Cournand and his colleagues led us into a new era in the understanding of normal and disordered cardiac function in huma
An overview of the normal embryological process of development of the Aortic arch and the clinically relevant anomalies of the aortic arch development. Ideal for Cardiology Fellows.
preop TEE assessment of atrial septal defect is very important for making decision for device closure, properly assessed adequate rims of ASD will reduce risk of device embolization to almost nil.
Ventricular tachycardia are difficult to understand. it is classified in to two types. 1. VT in structurally normal heart, 2. VT in heart with structural diseases. I have tried to simplify the VT in structurally normal heart, which may be helpful to many students and learners.
Our concepts of heart disease are based on the enormous reservoir of physiologic and anatomic knowledge derived from the past 70 years' of experience in the cardiac catheterization laboratory.
As Andre Cournand remarked in his Nobel lecture of December 11, 1956, the cardiac catheter was the key in the lock.
By turning this key, Cournand and his colleagues led us into a new era in the understanding of normal and disordered cardiac function in huma
An overview of the normal embryological process of development of the Aortic arch and the clinically relevant anomalies of the aortic arch development. Ideal for Cardiology Fellows.
Definition:
Also known as Hypoplastic Right Heart Syndrome (HRHS)
It is a rare congenital cardiac lesion characterized by heterogeneous right ventricular development, an imperforate pulmonary valve, and possible extensive ventriculocoronary connections.
It is a type of congenital cyanotic heart disease, a severe form of Tetralogy of Fallot (TOF)
Newborn patients present cyanotic with high desaturation and pulmonary blood flow that depend on patent ductus arteriosus
Tricuspid atresia is a form of congenital heart disease whereby there is a complete absence of the tricuspid valve. Therefore, there is an absence of right atrioventricular connection. This leads to a hypoplastic (undersized) or absent right ventricle.
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
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.
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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
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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2. D -TRANSPOSITION
• Atrioventricular concordance with ventriculo-arterial
discordance
• aorta arises from a morphological RV, and the PA arises
from a morphological LV
• Abnormal spatial relationship of the great arteries
• two circulations in parallel
3. • dextroposition of the bulboventricular loop (ie, the
position of the RV, which is on the right side).
• aorta =right and anterior
• great arteries are parallel rather than crossing
•
4. Basic Embryological defect
• Abnormal development, growth, and
absorption of the distal infundibulum (conus)
• normal conus is subpulmonary, left sided, and
anterior= prevents fibrous continuity between
the pulmonary and tricuspid valve rings
• infundibulum is usually subaortic, right sided,
and anterior= prevents fibrous continuity
between the aortic and tricuspid valve rings
5. Embryology
1. Spiral aortico-pulmonary septum forms but does not
spiral or twist during its partitioning of the truncus
arteriosus
a. Aorta arises from right ventricle
b. Pulmonary trunk arises from the left ventricle
2. a. Systemic – unoxygenated – repeatedly re-circulated
b. Pulmonary - oxygenated - repeatedly re-circulated
6.
7.
8. • 4 truncus and 2 conal cushions develop.
• Dextro- sinistro cushions of both conus and truncus fuse to
form Conotruncal septum.
• Intercalated cushions play an role in formation of semi lunar
valves
Embryology - Septation of conus and truncus.
9. Embryology - Septation of conus and truncus.
• Because the cushions are
dextro-superior and sinistro
inferior in truncus and dextro-
dorsal and sinistro-ventral in
conus union forms a spiral
septum than true lineal
relation.
10. • Aorta will be in connection with RV and PA with LV.
• There are two rotations one at conoventricular junction
and other at Conotruncal junction.
• Both rotations are counterclockwise around 110º
Embryology - Rotation and absorption.
11. • Conoventricular rotation brings aorta in continuation with
LV and PA with RV.
• Conotruncal rotation brings the normal position of aorta in
relation to PA ( left and posterior to PA)
Embryology - Rotation and absorption.
12.
13. • selective Resorption of conal septum
• coni which gets selectively resorbed during
development that respective artery is drawn
over LV .
14.
15.
16. 1. Absence of both conoventricular and Conotruncal rotation
2. Persistence of sub aortic and complete resorption of sub
pulmonic coni
17. • abnormal growth and development of the SA
infundibulum and the absence of growth of the SP
infundibulum.
• AV is protruded superiorly and anteriorly by the
development of the SA infundibulum, placing it above
the anterior RV
• Failure of development of the SP infundibulum
prevents the normal morphogenetic movement of the
PV from posterior to anterior and further results in
abnormal PV to MV ring fibrous continuity.
18. • Jatene =TGA and VSD.
• LECOMPTE = direct anastomosis of both great
arteries without interposition of a tube when
the pulmonary bifurcation is transferred in front
of the distal ascending AA.
19. Epidemiology
• 20.1 to 30.5 per 100,000 live births
• 60% to 70%= male
• 5% to 7% of all CHD
• males than in females =3:1
22. • physiologic L-to-R shunt =
volume of the PV blood
recirculating through the lungs
without having passed through
the body
• physiologic R-to-L shunt -
volume of SV blood reentering
the systemic circulation
without having passed through
the lungs.
23. • The net volume of blood
passing from the pulmonary
circulation (LA, LV, PA) to the
systemic circulation (RA, RA,
aorta) represents the
anatomic L-to-R shunt
• The effective systemic blood
flow (i.E., Oxygenated PV
return perfusing the
systemic capillary bed)
24. • The net volume of blood
passing from the systemic
circulation to the pulmonary
circulation represents the
anatomic R-to-L shunt
• The effective PBF (SV return
perfusing the pulmonary
capillary bed).
25. • deficient oxygen supply to the tissues
• excessive right and LV workload.
• incompatible unless mixing at some anatomic
level.
26. Anatomy
• TGA {S,D,D} –
• situs solitus (S)
• (D) looping of the ventricles
• anterior and rightward (D) aorta
27. Great artery relationship
• aortic root - anterior or anterior and to the right of
the pulmonary trunk in a slightly oblique relationship
(S,D,D)
• Less commonly- aorta may be positioned anterior
and to the left (S,D,L).
• rare - aorta is posterior
28.
29. Atria
• normal internal anatomy.
• Right atria is larger , particularly when IVS is
intact.
• Almost always=PFO
• 5% - true secundum ASD
• sinus and AV nodes =usual locations.
30. Right Ventricle
• hypertrophied, and large
• 90% =subaortic conus (infundibulum)
• less wedging of the pulmonary trunk between mitral and
tricuspid valves
• atrioventricular (AV) valves may be at virtually the same level
• 10% of hearts with TGA and IVS= subaortic conus in the RV is
absent or very hypoplastic.
31. Left Ventricle
• infrequently contains an infundibulum (conus
• PV-MV fibrous continuity exists
• RV wall is considerably thicker than normal at birth
and increases in thickness with age.
32. • IVS is intact and no PS -- LV wall is of normal thickness at birth
• less than normal thickness within a few weeks of birth
• thin wall by age 2 to 4
• VSD is present = LV wall thickness increases slightly less than in
the normal heart but remains well within the normal range
during the first year of life
• LV cavity is the usual ellipsoid in shape at birth but soon
becomes banana shaped.
33. Conduction System
• AV node and bundle of His lie in a normal position,
although the AV node is abnormally shaped and may
be partly engulfed in the right trigone
• LBB originates more distally from the bundle of His
• Damage to the bifurcation of the bundle at VSD
closure – CHB
34. Coronary Arteries
• aortic sinuses that face the pulmonary trunk,
regardless of the interrelationships of the great
arteries
• LAD and LCx arise as a single trunk (LCA]) from aortic
sinus 1 and distribute in a normal manner
• RCA = sinus 2 and follows this artery's usual course.
• single coronary artery= sinus 2.
35.
36.
37. • Usual =single ostium in the center of the sinus
• may arise from a double-barreled ostium consisting
of two ostia immediately adjacent to each other and
constituting essentially a single ostium
• At times, the LCA or LAD passes forward between
aorta and pulmonary trunk in an intramural course
to emerge anteriorly.
38. • conus artery frequently arises separately and
from its own ostium in sinus 1. ==considerable
part of the anterior wall of the infundibulum of
the RV.
• sinus node artery =atrial switch (Mustard or
Senning) = arises from the RCA close to its origin
and passes superiorly and rightward, usually
partly embedded in the most superior portion of
the limbus of the atrial septum, where it can be
damaged if this portion of the atrial septum is
widely excised
39.
40.
41. Coexisting Anomalies
• 50% =no other anomaly except a PFO or a PDA.
• VSD =-40% to 45%.
1. - perimembranous (conoventricular 33%)
2. - AV canal (inlet septum 5%)
3. - muscular (27%)
4. - malalignment (30%)
5. - conal septal hypoplasia type (5%)
42. Ventricular Septal Defect
• Conoventricular defects of the several different
varieties
• some hearts with conoventricular VSDs=outlet
(conal, infundibular) septum is malaligned and fails
to insert within the Y of the septal band
• septum may be displaced leftward= LVOTO
• Rightward=n RV (subaortic) obstruction.
43. • conal septum is displaced to the right= pulmonary
trunk may be biventricular in origin and over a
juxtapulmonary VSD and may be associated with
subaortic stenosis or aortic arch obstruction (arch
hypoplasia, coarctation, or interruption).
• Occasionally the VSD is juxta-aortic and associated
with a malaligned but nondisplaced conal septum.
• The conal septum may be absent and the VSD is
then juxta-arterial (doubly committed).
44.
45.
46. LV Outflow Tract Obstruction
• subpulmonary obstruction
• dynamic or anatomic
• 0.7% of patients with TGA and intact ventricular septum
• 20% of patients born with TGA and VSD
• apparent or develop after birth in other patients,
• overall prevalence of 30% to 35%.
• Dynamic type of LVOTO, developing in patients with TGA and intact ventricular
septum= leftward bulging of the muscular ventricular septum secondary to
higher RV than LV pressure.
47. Subpulmonary Stenosis or LVOTO
• Fixed
-Circumferrential fibrous membrane /diaphragm
- Fibromuscular ridge
- Herniating tricuspid leaflet tissue
- Anomalous MV septal attachments
- Tissue tags from membranous septum
• Dynamic-associated with SAM
48.
49.
50. Subaortic Obstruction
• Rightward and anterior displacement of the infundibular
septum
- hypoplasia
- coarctation
- interruption
Asso. RV hypoplasia & tricuspid valve anomalies
51. Aortic Obstruction
• discrete (coarctation, or less often interrupted aortic
arch)
• distal arch hypoplasia.
• 7% to 10% of TGA and VSD.
• more frequent when the VSD is juxtapulmonary and
the pulmonary trunk is partly over the RV in
association with rightward and anterior displacement
of the infundibular septum and with some subaortic
narrowing.
• associated coarctation= underdevelopment of the RV
sinus is more common.
52. Patent Ductus Arteriosus
• PDA-more common
• Persistence of a large PDA for more than a few
months = increased prevalence of pulmonary
vascular disease.
53. • PDA is present at age 1 week =half
• thereafter the prevalence falls rapidly.
• When patent, the ductus is small (less than 3 mm in diameter)
in two thirds of patients =little influence on natural history.
• Large = LV output is increased and hypoxia lessens=heart
failure
• acute and often early closure of the ductus --sudden increase
in hypoxia and clinical deterioration = decreased mixing at
ductus level but also at atrial level because of the fall in left
atrial pressure that results from decreased pulmonary venous
return.
54. TV anomalies
31%
Functionally imp 4%
Ratio of tricuspid to mitral anulus circumference is less than 1
in 50%
normal hearts this ratio -greater than 1
55. TV anomalies
• Straddling/overriding of chordae
• Overriding of the tricuspid annulus
• Abnormal chordal atatchments
• Dysplasia
• Accessory tissue
• Double orifice
57. Juxtaposition of atrial appendages
• Both appendages or left + part of right are adjacent
• 2-6%
• dextrocardia, VSD, bilateral infundibulum, right
ventricular hypoplasia and tricuspid stenosis or
atresia.
• Imp in BAS
58.
59. Right Aortic Arch
• 5%
• more common when there is an associated
VSD than when the IVS
• associated leftward juxtaposition of the atrial
appendages.
60. Bronchopulmonary Collateral Circulation
• > 30% of infants with TGA under 2 years of age
• functionally and freely communicate with the pulmonary vascular bed
proximal to the pulmonary capillary bed
• Potential intercirculatory (systemic-to-pulmonary) mixing pathway,
• accelerated and more widespread PVD
• Persistence of a significant BPC circulation after surgical repair - large
enough left-to-right shunt – CCF - warrant catheter embolization
61. • contribution to PBF from the BPC circulation
enters the pulmonary vascular circuit distal to the
usual catheter sampling sites
• true mixed PA saturation present at the
precapillary level cannot be sampled
• falsely high PA oxygen saturation and blood flow
calculation will result
• A modest BPC Circulatation(20%) to the pulmonary
precapillary blood flow can result in 30%
overestimation of PBF.
62. Fetal circulation
• compatible with normal fetal survival and relatively
normal gestational development.
• course of fetal circulation is modified
• right side of the heart ejects blood directly into the
ascending aorta
• RV ejects into the descending aorta via the PDA in normal
• cardiac and CNS structures similar in size and weight to
control values
• increased numbers and size of pancreatic islet cells
• increased weight of the adrenal cortex
•
63. Neonatal transition
• After birth, the PVR falls
• PBF and LA pressures increase
• more or less normal neonatal transitional physiology
• SVR increases because of removal of the low-resistance placental
circulation
• With TGA= RA pressures are increased( contrast to normal) and the
similarity of atrial pressures tends to keep the PFO open (incompetent
valve), with resulting bidirectional shunting
• TGA with IVS- ductus arteriosus is often widely patent after birth.
• Early after birth, when PVR is still high, there is bidirectional ductal flow:
• systole, LV–PA–ductus–-descending aorta
• diastole, aorta–ductus–PA.
64. Natural history
• 1st week-30%
• 1st month-50%
• 1st year-90%
• Depends on the degree of shunting
• Moderate PS improves survival
65. Survival
• all varieties
• 55% survive 1 month
• 15% survive 6 months
• 10% survive 1 year.
• Mean life expectancy = 0.65 year
• 4 years for those who survive to 12 months
• 6 years for the few who survive for 18
months
• Thereafter, life expectancy declines rapidly.
66. ]TGA and essentially intact ventricular septum
80% at 1 week
only 17% at 2 months
4% at 1 year
better when there is a true ASD.
TGA and important VSD
• 91% at 1 month
• 43% at 5 months
• 32% at 1 year
• lower when the patient has a very large Qp.
67. • large VSD and aortic obstruction (coarctation, interrupted arch)
• Lethal
• all patients die within a few months with severe heart failure.
• In patients with TGA, VSD, and LVOTO, early survival is still
better, reaching 70% at 1 year and 29% at 5 years, because in
many LVOTO is only moderate initially.
• Leibman and colleagues found that PDA increased risk of early
death in all subsets of patients. This is particularly the case when
the ductus is large.
68.
69. CLINICAL COURSE IN COMPLETE TGA
• CYANOSIS,
• HYPOXEMIC DETERIORATION,
• HEART FAILURE WITH EARLY DEATH
Inter circulatory mixing
70. CLINICAL FEATURES
• Symptoms and clinical presentation - degree of mixing
• high degree of mixing and large PBF- Qp, SaO2 may be near normal,
and unless there is pulmonary venous hypertension, symptoms are
minimal.
• When mixing is minimal= SaO2 is low and symptoms of hypoxia are
severe
• Adequate mixing =communications of reasonable size at atrial,
ventricular, or great artery levels
• Factors that reduce Qp, such as LVOTO and increased PVR= reduce
mixing and increase cyanosis.
71. • Reverse differential cyanosis
– TGA with a PDA and PA-to-aorta shunting
– complex TGA malformation including an aortic
arch anomaly, such as COA or IAA.
– TGA with suprasystemic PVR.
72. CLINICAL SPECTRUM
1. TGA (IVS or small VSD) with increased PBF
and small ICS
2. TGA (VSD large) with increased PBF and large
ICS
3. TGA (VSD and LVOTO), with restricted PBF
4. TGA (VSD and PVOD), with restricted PBF
73. Essentially TGA IVS
(Poor Mixing)
• infants with out a VSD or with a VSD 3 mm or less in
diameter.
• PFO or naturally occurring ASD +
• Cyanosis - half these infants within the first hour of life
• 90% within the first day and is rapidly progressive.
• critically ill with tachypnea and tachycardia and dies
from hypoxia and acidosis without appearance of frank
heart failure.
74. • rapid downhill course is usually obviated with a
naturally occurring ASD of adequate size because
cyanosis is less severe.
• surviving infants, appearance of moderate or severe
dynamic LVOTO -- increasing cyanosis and hypoxic
spells, even after an adequate atrial septostomy
• patients are of average birth weight and in good
general condition although with severe cyanosis
• Clubbing of fingers and toes is absent and generally
does not appear unless the infant survives to about age
6 months
• There is mild increase in heart and respiratory rates
75. • The heart is not hyperactive, and the liver is barely
palpable
• faint mid- systolic ejection-type murmur is present along
the midleft sternal edge in less than half these infants
• more prominent with organic or dynamic LVOTO, first
appearing at age 1 or 2 months with the dynamic form
and then gradually increasing in intensity.
• The second heart sound is unremarkable (often
apparently single or narrowly split).
76. ECG
• often normal at birth.
• By the end of the first week -- persistence of
an upright T wave in right precordial leads
indicates abnormal RV hypertrophy, and right-
axis deviation predominates.
• When important LVOTO is present or PVR
elevated, ECG evidence indicates biventricular
hypertrophy.
77. CXR
• • An oval- or egg-shaped cardiac silhouette with a
narrow superior mediastinum
• Mild cardiac enlargement
• Moderate pulmonary plethora
• first week of life-CXR may be normal, or occasionally
cardiac enlargement may be more marked.
• narrow mediastinum - great artery positions and by
shrinkage of the thymus, usually associated with stress,
and the plethora is caused by the increase in Qp.
• Plethora is less marked -LVOTO.
78. CXR
• TGA/IVS
(a) oval or egg-shaped cardiac silhouette with
narrow superior mediastinum
(b) mild cardiomegaly
(c) increased pulmonary vascular markings
79.
80. D TGA
CHEST X RAY IN DIAGNOSIS OF CARDIAC
CONDITIONS
81. Large VSD, Large PDA, or Both (Good Mixing)
• Presentation -latter half of the first month
• mild cyanosis
• signs of HF -PVH and myocardial failure
• Tachycardia, tachypnea, important liver enlargement,
and moist lung bases
• heart is more active
• larger than in the poor-mixing group
• large VSD =moderate-intensity pansystolic murmur
along the lower left sternal edge that may not be
present initially.
82. • apical middiastolic murmur or gallop rhythm
• narrow splitting
• accentuation of p2
• large PDA-continuous murmur, bounding
pulses, and an apical middiastolic murmur are
=less than half the patients, even when the
ventricular septum is intact.
83. • more cardiomegaly
• more plethora
• wider superior mediastinum than in the poor-mixing
group.
• ECG =BVH
• persistent large VSD=Q wave in V6.
• Isolated LV hypertrophy =RV hypoplasia with
tricuspid valve overriding
• Development of PVD = reduction in Qp and less
plethora, particularly in the peripheral lung fields, as
well as reduced heart size, but these features
generally appear after the neonatal period.
84. • coarctation with VSD and PDA= femoral
pulses are usually normal because the
coarctation is preductal and ductus arteriosus
large.
• Rarely, differential cyanosis can occur, with
cyanosis confined to the upper torso.
85. Large VSD and LVOTO (Poor Mixing without High PBF)
• least common of the three TGA groups
• decreased Qp and poor mixing
• PVH and associated symptoms and signs do not
develop
• Heart failure is -- not present.
• cyanosis is severe from birth.
86. • heart is not overactive
• pulmonary ejection murmur
• single S2
• apical gallop or middiastolic murmur
• near normal-sized heart with normal or
ischemic lung fields.
• ECG-biventricular hypertrophy.
87. TGA VSD Pulmonary Vascular Disease
• simple TGA= PVOD rarely develops in the first few months of life
• After 6 to 24 months=prevalence increases to 10% to 30%.
• TGA and moderate or large VSD= PVD develops more rapidly, as it
does in those with persistently large PDA
• Among those dying at about age 6 months, 25% have developed
severe pulmonary vascular disease (grade 3 or greater), and 50% of
infants dying by age 12 months have developed it.
88. Echocardiography
• dynamic LVOTO
• leftward deviation of the VS
• abnormal fluttering and premature closure of the PV
• SAM of the mitral leaflet
• prolonged diastolic apposition of the AML to the septum.
• coronary arteries=number, origin, major branching pattern, ,
intramural course.
89. Coronary artery anatomy;
Morphologic details of pulmonary or
subpulmonary obstruction;
VSD number, site, and size;
Great vessel alignments in relation to the
VSD and outlet septum;
Type and severity of aortic arch
abnormalities
Inter atrial communication
90.
91.
92.
93. The RAA lies posterior and to the left of the GA and anterior to the LA.
The posterior portion of the atrial septum (a) is oriented normally; the anterior portion (b) is
oriented transversely and parallel to the anterior chest wall.
The atrial septum curves toward the right. The LA and RPV wrap around the posterosuperior
aspect of the RA
94. Cardiac Catheterization and
Cineangiography
• SBF and PBF and pressures, including those across the
LVOT.
• Using appropriate views, cineangiography demonstrates
the cardiac connections and great artery positions
position and number of VSDs site of any LVOTO the size
and function of AV valves, size and function of both
ventricles, and presence of other cardiac anomalies.
95. Indications of cardiac catheterization
• hemodynamically unstable and rquire BAS.
• physiologic and anatomic data is required
concerning coronary artery, the VSD, degree of
LVOTO.
• complex cardiac anomalies like CoA, interrupted
aortic arch.
• pulmonary vascular resistance in TGA with VSD
96. • oxygen saturation in the pulmonary artery is
always higher than in the aorta.
97. • TV - selective RV injection in the frontal or
RAO views by noting intra-atrial bulging of the
leaflets during ventricular systole and during
diastole by the negative silhouette of the
orifice as nonopacified blood enters the
ventricle
• Continuity of the anterior leaflet of the MV
with the PV = four-chamber long-axial or LAO
views in diastole when the anterior leaflet is
noted to form the posterior wall of the LVOT.
98. Catheterization
PAP
PBF(and PVR ); ( overestimate PBF and
underestimate PVR)
Coronary artery anatomy;
Morphologic details of pulmonary or
subpulmonary obstruction;
VSD number, site, and size;
Great vessel alignments in relation to the VSD
and outlet septum;
Type and severity of aortic arch abnormalities
99. Coronary artery anatomy
• Selective transvenous CAG or antegrade aortic
root angiography with distal balloon occlusion of
the ascending aorta.
» balloon angiographic catheter introduced transvenously, is
positioned in the ascending aorta
» balloon is inflated with CO2 and stabilized in the ascending
aorta.
» 0.5 and 1.0 mL/kg of contrast medium are injected over 1
second
» balloon is deflated immediately after the injection.
100. • Balloon occlusion aortography
with extreme caudal
angulation of the anterior-
posterior camera, - laid-back
aortogram .
• visualization of both the
proximal ostia and distal
distribution of the coronary
arteries in the same plane of
view
101. Medical management
• hemodynamic stabilization
• correction of physiological aberrations caused
by cyanosis and poor perfusion.
• Correction of acid base balance, maintainance
of normothermia, prevention of hypoglycemia.
105. Balloon Atrial Septostomy
• profound hypoxemia
• when corrective surgery must be delayed.
• catheter should be advanced across the foramen ovale
into the LA or a PV and the position of the tip
established with certainty in the LA prior to proceeding
• posterior position of the tip in the lateral or LAO view or
entry of the catheter into a PV
106. • balloon is inflated with diluted angiographic
contrast medium to 12 to 15 mm diameter
• rapidly withdrawn across the atrial septum with
an abrupt, short tug
• balloon and interatrial septum are displaced
toward the inferior vena cava, and the septum
primum flap of the fossa ovalis is ruptured as
the balloon is carried in a single movement
from the left atrium to the right atrial-inferior
vena caval junction.
107. The catheter should be advanced immediately and
the balloon pushed cephalad out of the IVC orifice
into the RA toward the SVC to verify crossing the
septum and to avoid obstruction to IVC return while
the balloon is being deflated.
This same procedure should be repeated several
times with increasing balloon volumes so that
withdrawal of the balloon, inflated tensely to a
diameter of 15 mm, is achieved without much
resistance being perceived at the atrial septum level.
108.
109. COMPLICATIONS
• Atrial wall, Pulmonary vein, inferior vena caval
perforation or tears or AV valve damage.
• Intracardiac rupture of the balloon.
• Air embolism
• CNS complications
110. Difficulties
• older infants, particularly those with
TGA/VSD=thickened interatrial flap =catheter equipped
with an extendable blade
• markedly thick atrial septum, a new defect (separate
from the foramen ovale) -transseptal needle and
dilated with an 8- to 15-mm-diameter balloon
angioplasty catheter (Brockenbrough angioplasty).
111.
112. Surgical Creation of ASD
• Blalock & Hanlon operation or one of its
modifications –
• historical footnote
• excision of the posterior aspect of the IAS.
• oxygen saturation levels modestly higher than BAS
• mortality risks <3% to 5%.
113. Pulmonary Artery Banding
large VSD without LVOTO
To prevent
Heart failure
Pulmonary vascular disease
Present Indications
complex/multiple VSDs
Coexisting medical conditions that cause a delay in
surgery
To train LV before switch in TGA/IVS
114. Partial Venous Return Repair (Baffes)
• connecting the IVC to the LA with a homograft or
synthetic conduit and concurrently detaching the
right pulmonary veins and directly transferring them
to the RA.
• This results in an obligate, effective shunt at the
atrial level.
• Subsequently, some of these patients had a modified
Mustard type of atrial repair to achieve complete
physiologic correction.
115. Aims of surgery
1.To make the parallel circulations into series. So
that oxygenated blood goes to aorta and
deoxygenated blood goes to pulmonary trunk.
2.Correction of other cardiac anomalies like VSD,
PDA, TR, AORTIC OBSTRUCTION, LVOTO.
3.To provide a near normal functional status to
patients.
116. Definitive Repair
1. The atrial level : Senning or Mustard sx
2. Great artery level : Arterial switch operation or jatene
operation
117. Atrial switch
• Removal of the atrial septum
• redirection of the SV pathways to LV
• PV blood to RV
• Senning operation= rerouting by infolding of the atrial walls
• Mustard =synthetic or pericardial tissue
• modifications of the Mustard = trouser-shaped baffle, with
the legs anastomosed to the SVC & IVC inflows.
120. PHYSIOLOGIC CORRECTION (ATRIAL
SWITCH)
• atrial switch operations may be delayed for a few
weeks to several months after birth (and balloon
atrial septostomy).
126. Results and Sequelae of Physiologic
Correction
• 10-year survival rates of 85% to 90%.
(a) residual intra-atrial shunts,
(b) caval and pulmonary venous obstructions,
(c) right ventricular dysfunction,
(d) tricuspid valve insufficiency, and
(e) arrhythmia.
127. • Trivial leaks -10% to 20% of patients,
• Significant leaks requiring reoperation -(1 to 2%).
• RV dysfunction to some extent and dysrhythmias
=late concerns
128. • Progressive loss of NSR and increase in atrial
rhythm disturbances
• Gradual time-related decrease in sinus rhythm
• sinus rhythm at 1 year was 72%, at 5 years
56%, at 10 years 50%, and at 13 years 43%
131. • functional adequacy of the LV??
• Adequate LV muscle mass .
1. Early infancy
2. Nonrestrictive PDA,
3. Surgically remediable or dynamic LVOTO
4. Delayed decrease in PVR and persistent PAH
5. A large, nonrestrictive VSD.
• Definitive early (neonatal) one-stage arterial
repair >> early palliation with PA banding and
later arterial switch surgery.
132. Pre requisite
• LV pressure should be near systemic levels
• switch should be performed shortly after birth
(i.e., before 2 weeks of age).
• LV pressure is low= PA banding, either with or
without a shunt, for 7 to 10 days ( rapid, two-
stage switch operation) or for 5 to 9 months
133. 1. absolute LV systolic pressure that is
appropriate for age,
2. A LV pressure at cardiac catheterization = >70%
systemic levels (left to RV ratio >0.7), or
3. LV muscle mass that is within the normal range
for BSA
EMPIRICAL CRITERIA FOR LV SIZE
134.
135. Pre-op
• Coronary artery pattern amenable to transfer to the
neoaorta without distortion or kinking.
• Risk is high when the left main or LAD coronary
artery passes anteriorly between the aorta and the
PA.
• LV inflow and outflow tracts must be free of
significant structural abnormality
• RVOT should be free of significant stenosis.
136. Anatomic variants that may impact operative
mortality include
– intramural course of a coronary artery
– retropulmonary course of the left coronary
artery
– Multiple VSDs
– Coexisting abnormalities of the aortic
– Straddling AV valves
– Longer duration of global myocardial ischemic
(cross-clamp)
– prolonged circulatory arrest times
137. • great arteries are transected
• reanastomosis of the distal aortic segment to the
proximal pulmonary artery (neo aortic root).
• Transfer of the coronary arteries to this pulmonary
segment =excision from the aortic sinus with a cuff of
adjacent aortic wall
• proximal aortic segment (neopulmonary root) connected
to the distal PA segment
• Maneuver of lecompte - passes the anterior aorta
posterior to the bifurcation of the pulmonary artery
138. • aorta is transected, pulmonary trunk is
transected just proximal to its bifurcation
• aortic button around the orifice of the left
main coronary artery is excised from its sinus,
and this is inserted into the left facing sinus of
the neoaorta (originally,pulmonary trunk).
142. Complications
• PA stenosis at the site of reconstruction - 5% to 10%
• CHB- 5% to 10%.
• AR
– late complication > 20% of patients especially PA banding
– unequal size of the pulmonary cusps that leads to eccentric
coaptation
• Coronary artery obstruction
– myocardial ischemia, infarction, and even death.
143.
144. TGA with Low LV Pressure
PA banding ..
Long preparation period.
Rapid two stage switch.
LV function may be extremely impaired following
banding.( systemic-to-PA shunt is frequently placed to
ensure adequate PBF )
interval period between banding and correction = low
output syndrome.
Clinical improvement coincides with improvement in LV
function such that anatomic correction can be performed
within 7 to 10 days in most cases.
145. OTHER INNOVATIVE APPROACHES
• Percutaneously adjustable band
• Partial balloon occlusion of the MPA with a
percutaneously placed balloon-tipped catheter
• Systemic-to-PA shunting alone
• Primary arterial switch with LV assist in the
perioperative period.
146. Anatomic Correction without Coronary
Translocation
• DAMUS, KAYE, AND STANSEL
• arterial level repair without coronary
translocation.
• children with TGA and coronary artery
patterns not suitable for transfer
• patients with DORV (Taussig bing type) with
severe subaortic stenosis.
147. MPA is transected and
anastomosed to the
ascending aorta.
coronary arteries are perfused
in a retrograde fashion
native aortic valve may be left
intact
VSD (if present) is closed to
direct lv blood to the native
pulmonary (neoaortic) valve
RV to PA conduit is placed to
establish a normal series
circulation
148.
149. Innovative Techniques for anatomic correction with out
Coronary Translocation
• Creation of aortopulmonary tunnel (aubert
procedure)
• Baffling the LV outflow to the nontranslocated
coronary ostia with a patch of native aorta or
pericardium.
• The entire aortic root may be translocated to the
left ventricle with biventricular outflow tract
reconstruction.
150. Transposition of the Great Arteries (VSD and LVOTO)
with Restricted Pulmonary Blood Flow
• Neonates with TGA, VSD, and severe PS or
atresia have diminished PBF.
• They represent a relatively small proportion
(5% to 8%) of the neonatal TGA population.
• Clinical findings are similar to those in the
infant with TOF with severe PS or atresia, and
the cyanosis is extreme from birth
151.
152. Surgery for TGA with Associated LVOTO
• In some neonates, a palliative systemic-to-PA
shunt (Gore-Tex interposition shunt or classic
BT shunt) may be performed, with intracardiac
correction carried out at a later age.
• Alternatively, corrective surgery can be
performed in early infancy
153.
154. RASTELLI OPERATION
• intraventricular repair ++ extracardiac RV to PA
conduit.
• TGA with large VSD and extensive LVOTO -
complete bypass of the LVOTO and an anatomic
correction of the transposition pathology
• operative survival =95%
• midterm survival =90%
155.
156.
157. complications
1. Unfavorable anatomic variants,
-- restrictive VSD
– anomalous TV connections to the infundibular septum that
prevent baffling the LV to the anterior aorta.
2. Residual VSD,
3. Late unexpected death,
4. myocardial dysfunction .
5. ??Functional longevity of the valved conduits.
Improved results are noticeable with fresh or cryopreserved
homograft-valved conduits compared with the previously
used dacron heterograft structures
158. Complications
• conduit obstruction (especially in those containing porcine
heterograft valves)
• complete heart block (rarely occurs).
• This conduit needs to be replaced as the child grows.
159.
160. REV
Applicable to younger patients ,
Avoidence of Prosthetic extrcardiac conduit,
Avoidence of intracardiac Tunnel Obstruction.
• REV approach allows
1. Complete repair earlier in infancy,
2. Is feasible in patients with anatomic
contraindications to the rastelli operation,
3. reduce the need for reoperation and the prevalence
of residual pulmonary outflow tract obstruction
4. The lifelong implications of pulmonary regurgitation
following this newer operative approach require
continued investigation
161.
162.
163. • This operation involves
1. Performing a high, anterior RV incision
2. Radical excision of the outlet septum to create
an unobstructed anterior RV cavity;
3. Establishing a short and direct intraventricular
tunnel from the LV to the aorta
4. Closure of the pulmonary artery orifice;
5. Reimplantation of the transected (and usually
anteriorly translocated) PA directly onto the RV
outflow cavity without a prosthetic conduit
164. Surgery for TGA/VSD and PVOD
• PVR>10 U or grade 4 (H-E) histologic changes is a
CI to VSD closure.
165.
166. SURGICAL OPTIONS DTGA
Anatomy Surgical options Comments
TGA/IVS Physiologic repair
Senning or Mustard
Usually elective, neonatal-1 yr
Anatomic repair (primary)
Arterial switch (Jatene)
Neonatal period, usually within 2 wk
of age
TGA/IVS with prolonged low
LV pressure
Physiologic repair
Senning or Mustard
Usually elective, 1 mo to “1 yr
Anatomic repair (delayed)
Two-stage arterial switch
Long preparation period (Yacoub)
Rapid two-stage switch (Jonas)
TGA/VSD Physiologic repair
Senning or mustard with VSD
closure
Poor long-term results
Anatomic repair
Arterial switch with VSD closure
Usually neonatal repair; PAB
occasionally (multiple VSDs)
Interventricular baffle repair Not all VSDs suitable
Damus-“Kaye-“Stansel: VSD closure
(LVto’PA); proximal PA to Ao
Used when coronary translocation
impossible aortic valve closure
167. TGA/VSD/PS VSD closure (LV to Ao), RV to
PA conduit (Rastelli)
Palliative systemic-to-pulmonary
shunt frequently performed
Conduit replacement frequently
necessary
VSD closure (LV to Ao),
anterior translocation of PA with
direct connection to RV: REV
procedure (Lecompte)
Long-term pulmonary
regurgitation
TGA/PVOD Physiologic repair, palliative
Anatomic repair, palliative
Symptomatic improvement