This document provides information on duct-dependent congenital heart disease. It begins with references and learning objectives. It then discusses the presentation of duct-dependent lesions, which can include shock, collapse, or heart failure in the first weeks of life. These lesions are classified into three categories: left-sided obstructive lesions, right-sided obstructive lesions, and transposition physiology. Common examples are provided for each category. The document continues by covering topics such as the anatomy and physiology of the ductus arteriosus, diagnostic challenges, methods of diagnosis including pulse oximetry and echocardiography, and differential diagnoses.
Acyanotic heart defects are a class of congenital malformation of the heart. It provides knowledge in detail regarding acyanotic heart defects(VSD &ASD) for B.Sc(N) students.
Drs. Potter and Richardson's CMC Pediatric X-Ray Mastery October CasesSean M. Fox
Drs. Potter and Richardson are interested in education and Pediatric Emergency Medicine. Follow along with the EMGuideWire.com team and Dr. Michael Gibbs as they post these educational, self-guided radiology slides on Pediatric Emergency Medicine Radiology Topics including:
• Scoliosis
• Pneumothorax
• Parapneumonic Effusion
• Cardiomegaly
• Vaping associated lung injury
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
Acyanotic heart defects are a class of congenital malformation of the heart. It provides knowledge in detail regarding acyanotic heart defects(VSD &ASD) for B.Sc(N) students.
Drs. Potter and Richardson's CMC Pediatric X-Ray Mastery October CasesSean M. Fox
Drs. Potter and Richardson are interested in education and Pediatric Emergency Medicine. Follow along with the EMGuideWire.com team and Dr. Michael Gibbs as they post these educational, self-guided radiology slides on Pediatric Emergency Medicine Radiology Topics including:
• Scoliosis
• Pneumothorax
• Parapneumonic Effusion
• Cardiomegaly
• Vaping associated lung injury
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
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.
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.
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Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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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.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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.
2. References
Eric C. Eichenwald, Anne R.Hansen, Camilia R. Martin,
Ann R. Stark.South Asian 8th Edition of Cloherty and
Stark’s Manual of Neonatal Care.wolters kluwer.2017.
Josheph K. Perloff, Ariane J. Marelli, Perloff’s clinical
recognition of congenital heart disease.6th edition.Elsevier
Kleigman, St Geme, Blum, Shah, Tasker, Wilson.Nelson
textbook of pediatrics.21st international edition
Ramesh Agarwal, Ashok Deorari, Vinod Paul, M Jeeva
Sankar, Anu Sachdeva.AIIMS protocols I neonatalogy
volume 1. 2nd edition.Noble.2019
https://indianpediatrics.net/dec2018/dec-1075-1082.htm
https://www.rch.org.au/cardiology/heart_defects
PYW 2
3. “Neonates who present with shock /
collapse/ heart failure in the first few
weeks of life have duct-dependent blood
flow until proved otherwise”.
PYW 3
4. Specific learning objectives
By the end of presentation, we will be able to
Present scenario
Understand anatomy and physiology of PDA.
Define of duct dependent lesion(DDL).
Classify and Pathophysiology of these lesions.
Understand presentation of DDL
Diagnose and differentiate DDL
Manage DDL and referral.
PYW 4
5. Present scenario
Incidence rate of CHD is 8-9/1000 live births, nearly 1.8-
2lacs children are born with CHD each year in India.
Of these, nearly 60,000 to 90,000 suffer from critical CHD
requiring early intervention.
Approximately 10% of present infant mortality in India may
be accounted for by CHD alone.
Lack of awareness & delay in diagnosis is biggest obstacle.
Frontline health workers & primary caregivers are not
sensitized to the problem of CHD.
PYW 5
https://indianpediatrics.net/dec2018/dec-1075-1082.htm
6. Present cont..
78.9- 81.4% Institutional deliveries.
20% of births in India occur at home, and the infant is
likely to die before the critical, ductus-dependent CHD
is diagnosed.
Fortunately, the rate of hospital deliveries have
increased due to several incentivized schemes by the
Govt of India.
Ductus-dependent CHD may still escape detection as
babies are often discharged earlier.
PYW 6
https://indianpediatrics.net/dec2018/dec-1075-1082.htm
7. Present cont..
Predischarge screening of newborns by pulse oximetry,
which may pick up these CHDs, is often not practiced,
especially in rural & semi-urban centers.
Lack of follow up care.
Delay in referral results in poor outcomes as co-
morbidities may have already set in.
The risks of developing hypothermia and hypoglycemia
during long, unsupervised transport further adds to the
already serious condition of the infants with CHD.
PYW 7
https://indianpediatrics.net/dec2018/dec-1075-1082.htm
8. Patent ductus arteriosus
Short circuit channel between the
pulmonary artery and the aorta in the fetus, which
bypasses the lungs to distribute oxygen received
through the placenta from the mother’s blood.
It normally closes once the baby is born and the
lungs inflate, separating the pulmonary and
systemic circulations, thus converting parallel
circulation into series.
PYW 8
Josheph K. Perloff, Ariane J. Marelli, Perloff’s clinical recognition of congenital heart
disease.6th edition.Elsevier
9. • Functional closure of the ductus arteriosus
occurs within 10-15 hours after birth in
healthy infants born at term.
• This occurs by abrupt contraction of the medial
smooth muscular wall of the ductus arteriosus.
• Multiple factors are responsible for the
closure of ductus arteriosus. Ex- Po2, GA,
PGE2 , etc.
Patent cont…
Josheph K. Perloff, Ariane J. Marelli, Perloff’s clinical recognition of congenital heart
disease.6th edition.Elsevier
PYW 9
10. Patent cont…
Increase in the partial pressure of oxygen (PO2) from
25mmHg(in utero) to 50mmHg after lung expansion is
the strongest stimulus.
Decrease in PGE2.
Anatomic closure completes by end 2-3 weeks.
Starting of ductus closure is the cause for deterioration
in these lesions.
PYW 10
Josheph K. Perloff, Ariane J. Marelli, Perloff’s clinical recognition of congenital
heart disease.6th edition.Elsevier
11. Definition
These are critical congenital heart disease (cCHD), in
which the permeability of the ductus arteriosus is
mandatory in order to maintain systemic and
pulmonary perfusion after birth.
These are most important d/d for newborns who are
going to collapse in and around day3.
Critical congenital heart disease (cCHD) is the most
common reason for acute cardiac failure in the neonatal
period.
PYW 11
12. Introduction
Incidence- 25% of all CHDs, nearly 25% mortality in
first year life.
The distribution of cCHD differs from the distribution
of CHDs in general.
Left sided heart obstructions have the largest share
with 30–40%, followed by complete transposition of
the great arteries (approx. 30%) and right sided heart
obstructions (20–30%).
PYW 12
https://indianpediatrics.net/dec2018/dec-1075-1082.htm
13. Classification
These duct dependent lesions are classified into 3
categories
1) Left sided obstructive lesions
(Duct dependent systemic circulation)
2) Right sided obstructive lesions
(Duct dependent pulmonary circulation)
3) Transposition physiology
(Duct dependent systemic and pulmonary
circulation)
PYW 13
Eric C. Eichenwald, Anne R.Hansen, Camilia R. Martin, Ann R. Stark.South Asian 8th Edition of
Cloherty and Stark’s Manual of Neonatal Care.wolters kluwer.2017
14. Duct dependent
lesions
Duct dependent
systemic
circulation
1) HLHS
2) Interrupted Aortic
arch
3) Severe Coarctation
of Aorta
4) Critical Aortic
stenosis
5) Shone complex
Transposition
physiology
Transposition
of great
arteries
Duct dependent
pulmonary
circulation
1) Severe pulmonary
stenosis
2) PA with intact IVS
3) Tricuspid atresia
4) Severe Ebstein
Anamoly
5)Severe TOF
PYW
14
Eric C. Eichenwald, Anne R.Hansen, Camilia R. Martin, Ann R. Stark.South Asian
8th Edition of Cloherty and Stark’s Manual of Neonatal Care.wolters kluwer.2017
15. Hypoplastic left heart syndrome
PYW
15
Ductus arteriosus
https://www.rch.org.au/cardiology/heart_defects
24. Severe Tetrology of Fallot
PYW 24
https://www.rch.org.au/cardiology/heart_defects
25. Diagnostic gap
Newborns with duct dependent lesions are going to
present to ED between birth to 1st week of life, usually
with nonspecific symptoms.
Sn of the clinical examination in the first days of life
for detection of cCHD is <50%.
Possible symptom-free interval is due to the delayed
change from fetal to neonatal circulatory physiology.
The sensitivity of prenatal diagnostics for critical heart
defects is reported to be up to a maximum of 51% .
PYW 25
26. Diagno cont..
Fetal CVS physiology with a R -> L shunting through
foramen ovale (FO) and ductus arteriosus (DA) with a
high Rp and low systemic vascular resistance (Rs) allows
to a large extent a normal fetal development.
Umbilical clamp placement terminates the placental
circulation.
This transition from the fetal parallel to the adult serial
circulation might lead to a life-threatening condition in
the presence of critical heart defects.
PYW 26
27. Diagno cont..
Open DA and FO can lead to inconspicuous clinical
findings in newborns with critical CHD. This period is
therefore also referred to as “diagnostic gap”.
Pulse oximetry screening is a proposed method by
which this postnatal “diagnostic gap” should be
reduced.
PYW 27
28. Presentation of duct depedent
SBF lesion
The symptoms range from signs of acute cardiac
failure up to the complete picture of a cardiogenic
shock.
Tachypnea is the early and therefore leading symptom,
followed by tachycardia, prolonged CRT, hypotension,
pallor and profound shock.
Usually referred due to acute cardiogenic shock or any
other degree of cardio-vascular failure.
PYW 28
29. Present cont…
Inaudible murmur is not a criteria for exclusion, but
disappearance of previously audible murmur points for
urgent intervention.
H/o diagnosed cardiac diseases in ANC and fetal
Doppler.
PYW 29
30. Present cont…
Newborns with critical aortic valve stenosis are mostly
symptomatic within the first week of life.
A critical aortic coarctation mostly within the first 4
weeks with a typical history of a “3-week-old baby
referred, after failure of a sepsis therapy.”
In a newborn whose condition worsens clinically in the
first days of life, d/d of a cCHD must always be considered
in addition to the suspected diagnosis of sepsis.
PYW 30
31. Presentation of duct depedent
PBF lesion and TGA
Incremental cyanosis is the main & common symptom
followed by varying degree of respiratory distress due to
under perfused lungs, not benefited by O2
administration.
Right heart failure- dyspnea, hepatomegaly, raised JVP
and dependent edema.
Shock and metabolic acidosis.
PYW 31
32. Present cont…
“The cause of a cyanotic but vital newborn is a heart
defect until the opposite is proven”.
Most critical part is to rule out duct dependent lesion in
all cases of cardiovascular collapse in few first weeks of
life.
Ask relevant history and progression of condition, history
of CHD in siblings or unexplained deaths in past
postnatal periods and lastly Pulse oxymetry.
PYW 32
33. Diagnosis
ABC – stabilize newborn
History and clinical examination
Presentation coincides with ductal closure.
GPE- Vitals, Four limb SpO2 + BP, JVP
Detailed Cardiovascular examination -Single S2,
murmur and crepts
Hepatomegaly + edema
Hyperoxia test – for all cases
PYW 33
34. Pulse oxymetry (Pox)
Universal screening with Pox and should be a part of
standard neonatal care.
Measurement of oxygen saturation by pulse oxymetry
provides much easier, noninvasive and reliable
assessment of hypoxemia.
Broadly SpO2 < 95% represent hypoxemia and at this
cut off it reaches high specificity of 99.9% and a
sensitivity of 75% for detecting cyanotic CHD.
PYW 34
35. Pulse cont…
All four limb pulse oxymetry is mandatory before they
are declared free of hypoxemia.
Preferably POx screening should be done after 24hrs of
age or shortly before discharge if less than 24hrs of age
to decrease false positivity due to respiratory problmes.
PYW 35
36. SpO2 in right hand & foot after
24hrs
>95% in all limbs
Pre & post duct diff
< 3%
POxS is negative
Critical CHD is
unlikely
Routine
neonatal care
90-94% in either of
the limbs
Pre & post ductal diff
> 3%
POxS is
intermediate
Repeat 3 times 1hr
apart
<90% in either of
limbs
POxS is positive
Critical CHD is
likely
Pediatric cardilogy
consultation
PYW 36
37. Hyperoxia test
Most sensitive and specific tool in the initial
evaluation of the all neonate with suspected critical
congenital heart disease, in sites with timely no access
to echocardiography.
Determine Pao2 while the infant is on room air.
Give 100% O2 for 10–20 min by mask/hood/ ET
Obtain an arterial blood gas level while the infant is
breathing 100% oxygen.
PYW 37
38. Hyper cont..
PaO2 Test result Interpretation
> 250mmHg Passed Eliminates critical structural cyanotic
heart disease
Possible respiratory/ CNS /normal
100-
250mmHg Intermediate
Structural heart disease with complete
intracardiac mixing
Hypoplastic left heart syndrome
< 100mmHg Failed Most likely due to intracardiac right-to-
left shunting and is virtually diagnostic
of cyanotic congenital heart disease in
absence of clear-cut lung disease
PYW 38
39. Diagnosis cont..
X ray chest and ECG
ABG.
Echocardiography as soon as possible.
Septic workup- CBC, CRP and blood culture.
PYW 39
41. Echocardiography
Gold standard investigation.
To study anatomy of heart disease.
Physiologic alterations.
Size of duct, extent of constriction.
Flow across various shunts and Doppler.
Guide for further management.
PYW 41
42. Differential Diagnosis
Cardivascular disease
Acyanotic CHD with presure overload
Acyanotic CHD with volume overload
Duct dependent lesion with decreased systemic/
pulmonary/ both blood flow
Cardiomyopathies
Tachy and brady arrythmias
Mycarditis and hypovolumia.
PYW 42
46. Management
Initial resuscitation
For the neonate who presents with evidence of
decreased cardiac output or shock, initial attention is
devoted to the basics of advanced life support.
Stabilize airway & maintain adequate ventilation to
maintain SpO2 75-85%.
Reliable vascular access is essential, including an
arterial line.
In the neonate, this can most reliably be
accomplished through the umbilical vessels.
PYW 46
47. Volume resuscitation and Ionotrpes
Inotropic support-
Dopamine can be expected to increase MAP,
improve ventricular function, and improve urine
output at doses of <10micro g/kg/min.
Dobutamine- in few studies showed favourable
results compared to dopamine
Combination of low dose dopamine +
dobutamine
Upgrade ionotropes for desired improvement.
PYW 47
48. Manage cont..
Supportive measures
Detection and Management of hypoglycemia,
hypocalcemia, hypothermia and metaboilic
acidosis
CCF and its management
PYW 48
49. Recommendation
Continuous infusion of prostaglandin-E1 in low
dosage of 0.005–0.01 micro g/kg/min is never
wrong.
Treatment should immediately be started in any
newborn, whose condition worsens clinically in
the first days of life; in particular, if the
cardiovascular system cannot be immediately
analyzed by echocardiography.
This recommendation is also true, when sepsis is
suspected or even confirmed by laboratory data.
PYW 49
50. Key points in the treatment of suspected or
confirmed CHD with duct-dependent SBF:
Reopening of the arterial duct
(initially high PGE1 dosage, rapid reduction)
Reduction of diastolic left to right shunt across a non-
obstructive right-left-shunting DA;
Avoidance of inadequate measures resulting in the
reduction of the Rp;
Reduction of Rs without jeopardizing adequate
perfusion pressures;
Rapid transfer of the patient to a pediatric cardiac
center.
PYW 50
51. Prostaglandin E1
PGE1 has been used since the late 1970s to
pharmacologically maintain patency of the ductus
arteriosus in patients with duct-dependent systemic or
pulmonary blood flow.
PGE1 must be administered as a continuous parenteral
infusion.
The usual starting dose is
0.05 to 0.1 μg/kg/minute.
PYW 51
52. Prosta….
The response to PGE1 is often immediate if patency of
the ductus arteriosus is important for the hemodynamic
state of the infant.
Failure to respond to PGE1 may mean that the initial
diagnosis was incorrect, the ductus arteriosus is
unresponsive to PGE1 or the ductus is absent.
PYW 52
53. Prosta….
In most infants, the ductus will reopen within 30
minutes to 2 hours after starting PGE1 evidenced by
PO2 values typically rise 20-30 mm Hg.
Once the ductus has opened, the dose can usually be
reduced to 0.002-0.05 mcg/kg/min.
Therapy is continued until balloon atrial septostomy
or cardiac surgery is performed.
PYW 53
54. Preparation of Prostaglandin E1
Add 1 Ampule
(500 μg/1 mL)
to
Concentratio
n
(μg/mL)
mL/hour × Weight (kg)
Needed to Infuse 0.1
μg/kg/minute
200 mL D10% 2.5 2.4
100ml D10% 5 1.2
50ml D10% 10 0.6
PYW 54
56. Urgent cardiac intervention
Balloon atrial- septostomy (Rashkind procedure)
Live-threating hypoxemia can be effectively treated by
atrial septum manipulation.
Compromised systemic blood flow due to duct
obstruction by transcatheter stenting, pulmonary run
off by bilateral surgical pulmonary banding.
Critical aortic coarctation by balloon angioplasty as
bridging procedure to surgical repair.
PYW 56
57. Balloon atrial- septostomy
This procedure may be performed either in an
intensive care unit under echocardiographic guidance
or in the cardiac catheterization laboratory under
fluoroscopic guidance.
Similarly, either the femoral vein or the umbilical
vein can be used for the venous approach.
PYW 57
59. Refferal
A well-prepared rapid transfer of the patient to a
pediatric cardiac center is the most important measure
for appropriate disease specific cardiac intervention by
expert.
Continuous monitoring of all vitals.
Monitoring of hypoglycemia, hypothermia and
ongoing medication.
Well organized cardiac care ambulance with trained
health care professional.
PYW 59
60. Preventive measures
Antenatal diagnosis of cardiac defects by USG, fetal
Echo and doppler in suspected newborn demise in
past.
Immunization with rubella vaccine.
A newborn with critical CHD should be delivered in a
pediatric heart center (PHC), if possible.
In case of a postnatal diagnosis, transfer to a PHC
should be immediately prepared.
Pulse oxymetry.
Educate front line health workers.
PYW 60
61. Take home message
Careful postnatal examination.
Universal screening for CHD
Mandatory use of pulse oxymetry, no new-born
should be discharged without POx.
POx screening preferably after 24hrs & if
abnormal 2D Echo and doppler by expert.
Any neonate who is detoriating in 1st few weeks of
life, should be started with PGE1 even in case of
proved sepsis.
PYW 61
62. Take cont…
Remember left sided obstructive lesions presents
with shock, where as right sided obstructive
lesions presents with cyanosis & features of CCF.
Any newborn who comes to ED with shock/CCF in
1st few weeks, should be resuscitated first,
followed by PGE1 and transfer of pateint to
pediatric cardiac centre.
All newborn with sepsis/ respiratory distress
should be evaluated for cCHD and 2D ech.
PYW 62