An endocardial cushion defect (ECD) is caused by a failure in the normal development of endocardial cushion tissue during fetal life. This can result in a ventricular septal defect (VSD), atrial septal defect (ASD), and clefts in the mitral and tricuspid valves. A primum ASD in ECD is similar to a secundum ASD, causing enlarged right heart chambers. Complete ECD results in biatrial and biventricular enlargement due to combined effects of ASD and VSD with possible mitral regurgitation. Physical exam findings include enlarged heart, murmurs, and signs of congestive heart failure. ECG may show biventricular
The Norwood procedure is the first of three surgeries required to treat single-ventricle conditions such as hypoplastic left heart syndrome (HLHS). Because the left side of the heart can’t be fixed, the series of surgeries rebuilds other parts of the heart.
The Norwood procedure is performed in the baby’s first or second week of life.to redirect the blood flow.
Three goals for the Norwood procedure:
1, Build a new aorta.
2, Direct blood from the right ventricle through the new aorta and on to the rest of the body.
3, Direct the right ventricle to pump blood to the lungs until the next surgery.
TAPVC defines the anomaly in which the pulmonary veins have no connection with the left atrium. Rather, the pulmonary veins connect directly to one of the systemic veins (TAPVC) or drain in to right atrium.
A PFO or ASD is present essentially in those who survive after birth
When pulmonary veins drain anomalously into the right atrium either because of complete absence of the interatrial septum or malattachment of the septum primum , then it is known as total anomalous pulmonary venous drainage.
When some or all of the pulmonary veins drain anomalously in to RA or its tributaries without being abnormally connected, the terms partially anomalous pulmonary venous drainage (PAPVD) or totally anomalous pulmonary venous drainage (TAPVD) with normal pulmonary venous connections are used.
The Norwood procedure is the first of three surgeries required to treat single-ventricle conditions such as hypoplastic left heart syndrome (HLHS). Because the left side of the heart can’t be fixed, the series of surgeries rebuilds other parts of the heart.
The Norwood procedure is performed in the baby’s first or second week of life.to redirect the blood flow.
Three goals for the Norwood procedure:
1, Build a new aorta.
2, Direct blood from the right ventricle through the new aorta and on to the rest of the body.
3, Direct the right ventricle to pump blood to the lungs until the next surgery.
TAPVC defines the anomaly in which the pulmonary veins have no connection with the left atrium. Rather, the pulmonary veins connect directly to one of the systemic veins (TAPVC) or drain in to right atrium.
A PFO or ASD is present essentially in those who survive after birth
When pulmonary veins drain anomalously into the right atrium either because of complete absence of the interatrial septum or malattachment of the septum primum , then it is known as total anomalous pulmonary venous drainage.
When some or all of the pulmonary veins drain anomalously in to RA or its tributaries without being abnormally connected, the terms partially anomalous pulmonary venous drainage (PAPVD) or totally anomalous pulmonary venous drainage (TAPVD) with normal pulmonary venous connections are used.
A 30-minute talk, presented as part of the weekly teaching activities in Alder Hey Children's Hospital (Liverpool, UK). It addresses PDA evaluation in children - starting with embryology & anatomy with the basis behind physiological closure versus patency after birth. What is the role of echo study in diagnosing/evaluating PDA? Modes used with some clear movies? Its limitations?
Transposition of Great Arteries;TGA,Firas Aljanadi,MDFIRAS ALJANADI
presentation about the Transposition of great arteries.Definition,Epidemiology,History,Embryology,Classification,Anatomy,Coronary arteries,Physiology,natural history,clinical presentation,doagnosis,management.palliative and definitive treatment,Arterial switch operation,atrial switch,senning,mustard,special cases,with VSD ,with PS.
A 30-minute talk, presented as part of the weekly teaching activities in Alder Hey Children's Hospital (Liverpool, UK). It addresses PDA evaluation in children - starting with embryology & anatomy with the basis behind physiological closure versus patency after birth. What is the role of echo study in diagnosing/evaluating PDA? Modes used with some clear movies? Its limitations?
Transposition of Great Arteries;TGA,Firas Aljanadi,MDFIRAS ALJANADI
presentation about the Transposition of great arteries.Definition,Epidemiology,History,Embryology,Classification,Anatomy,Coronary arteries,Physiology,natural history,clinical presentation,doagnosis,management.palliative and definitive treatment,Arterial switch operation,atrial switch,senning,mustard,special cases,with VSD ,with PS.
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
presentation will give a idea about management of thoracoabdominal aortic aneurysm, including detail of investigation and treatment options available today.
Infective Endocarditis- surgical indication & principle of surgeryDhaval Bhimani
this presentation is to give idea about surgical indication for Infective Endocarditis and what are the principle of surgery for infective endocarditis.
Neurocognitive function in on pump vs off pump CABGDhaval Bhimani
CABG(coronary artery bypass grafting) is most common operation done in cardiac surgery, this presentation will give idea about neurocognitive dysfunction in on pump vs off pump CABG.
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!
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
Title: Sense of Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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
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.
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.
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.
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.
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
6. Key points
• LA is not enlarged
• Because of increased pulmonary venous return to LA does not stay goes
into RA.
• Absence of LA enlargement is one of the helpful X-RAY findings for
differentiating ASD from VSD.
• Prolong depolarisation of RV because of enlargement lead to RBBB.
• Left to right shunt is silent in ASD. Murmur is because of high flow through
normal pulmonary valve relative stenosis.
• So, heard more in systole, in pulmonary area, (Upper left Sternal border)
7. • Shunt is large more flow through TV relative TV stenosis.
• Wide split S2 ( delayed depolarisation of RV late closure of PV )
• Important:-
1- Infant and small children does not have classical symptom until 3-4
year ??
• Because compliance of RV improve slowly so that any significant shunt
does not occuruntil that age.
2 - CHF is rare in children even in presence of large shunt??
• PA can handle blood flow for longer period without developing CHF
because of no direct systemic flow to PA.
• However, Pulmonary HTN developes by third to fourth decade.
11. Key points
• Acynotic VSD is L R shunt, shunt determined by the size, not the location
of the defect and the level of pulmonary vascular resistance (PVR).
• small VSD large resistance to shunt occurs at the defect, and the shunt
does not depend on the level of PVR normally PVR
• large VSD Minimal resistance shunt depends largely on the level of
PVR. lower the PVR, the greater the magnitude of the left-to-right shunt.
This type of left-to-right shunt is called a dependent shunt.
12. • In VSD, it is the LV that does volume overwork, not the RV. This results
in LV enlargement; the RV does not enlarge.
• WHY ??
• Because the shunt of VSD occurs mainly during systole when the RV
also contracts, the shunted blood goes directly to the PA rather than
remaining in the RV cavity.
• VSD & PDA both has LA,LV enlargement.
13. • Small VSD
• Small flow in shunt (only half arrow) minimal PVR & other changes.
• Murmur is due to shunt itself (regurgitant systolic)
• Moderate VSD
• One arrow shunt significant changes, LVH
• RV is not significant volume pressure load, so no RVH.
• Due to pressure flow across MV leads to relative stenosis of MV
MDM murmur, best at apex.
• PA is mild elevated p2 may be loud.
14. • Large VSD
• Relatively more chamber enlargement due to more flow across
shunt
• Direct pressure to RV RVH.
• Bi-ventricular enalargement in bith ECG & X-ray. Along with LA
enlargement.
A large VSD usually results in CHF in early infancy
15.
16. What if left, Untreated ??
• Irreversible changes take place in the pulmonary arterioles, producing
pulmonary vascular obstructive disease (or Eisenmenger’s syndrome).
• May take years to develop this canges.
• PVR L R Shunt.
• Eventually lead to decrease in LA ,LV size.
• Only RVH remains.
• Cynosis is present.
• S2 is Loud due to PAH.
20. Key points
• Hemodynamics of PDA are similar to those of VSD.
• The magnitude of the left-to-right shunt is determined by
the resistance offered by the ductus (i.e., diameter, length, and
tortuosity)
• when the ductus is small and level of PVR is large
(i.e.,dependent shunt). Similar Of VSD.
21. • Hemodynamic consequences of PDA are similar to those of VSD.
• LA ,LV enlarge same as VSD, Except here Aorta upto level of PDA is
enlarged.
• Continuous murmur
• Small Shunt- No significant changes.
• Moderate shunt-
• LA, LV & PA enlarge, ECG - s/o LVH.
• In addition, there may be an apical diastolic flow rumble as a result of relative
stenosis of the mitral valve. The P2 slightly increases in intensity if it can be
separated from the loud heart murmur.
22. • Large Shunt:-
• marked cardiomegaly and increased pulmonary vascular markings
are present
• LVH, & occasionally LAH in ECG.
• The free transmission of the aortic pressure to the PA produces
pulmonary hypertension and RV hypertension, with resulting RVH on
the ECG.
• ECG shows BVH and LAH, as in a large VSD.
• The continuous murmur is present, with an apical diastolic rumble
owing to relative mitral stenosis. The P2 is accentuated in intensity
due to pulmonary hypertension.
23. What if left, Untreated ??
• Irreversible changes take place in the pulmonary arterioles, producing
pulmonary vascular obstructive disease (or Eisenmenger’s syndrome).
• As in VSD, Eventually lead to decrease in LA ,LV size.
• Only RVH remains.
• Cynosis is present, but only in lower half of body.
• ECG- RVH, NO LVH.
• No continuous murmur, only S2 is single & Loud due to PAH.
25. Introduction
• During fetal life, the endocardial cushion tissue contributes to the closure of both
the lower part of the atrial septum (i.e., ostium primum) and the upper part of
the ventricular septum in addition to the formation of the mitral and tricuspid
valves.
• The failure of normal development of this tissue may be either complete or
partial.
• A simple way of understanding the complete form of endocardial cushion defect
(ECD) is that the tissue in the center of the heart is missing, with resulting VSD,
the primum type of ASD, and clefts in the mitral and tricuspid valves.
• In the partial form of the defect, only an ASD is present in the ostium primum
septum (primum type of ASD), often associated with a cleft in the mitral valve.
26. primum-type ASD
• Hemodynamic abnormalities of primum-type ASD are similar to those of secundum-type
ASD, in which the RA and RV are dilated with increased pulmonary blood flow.
• The cleft mitral valve is usually insignificant from a hemodynamic point of view because
blood regurgitated into the LA is immediately shunted to the RA, thereby decompressing
the LA.
• The physical findings are also similar to those of secundum ASD: a widely split and fixed
S2, a systolic ejection murmur at the upper left sternal border, and a mid-diastolic
rumble of relative tricuspid stenosis at the lower left sternal border.
• Systolic murmur of mitral regurgitation (MR) is occasionally present.
27. ECG
• RBBB, mild RVH.
• One exception, which is important in
differentiating between the two types of
ASDs, is the presence of a “superior” QRS
axis or left anterior hemiblock (with the QRS
axis in the range of −20 to −150 degrees) in
primum-type ASD.
• It occurs as a result of the primary
abnormality in the development of the
bundle of His and the bundle branches.
28. complete ECD
• Hemodynamic changes seen with complete ECD are the sum of the
changes seen in ASD and VSD.
• There is volume overload of the LA and LV as in VSD and partially due
to MR. In addition, it has volume overload of the RA and RV as in ASD.
• The result is biatrial and biventricular enlargement.
• he magnitude of the left-to-right shunt in complete ECD is
determined by the level of PVR (i.e., dependent shunt).
29. ECG &
Clinical
findings
• BVH and occasional biatrial hypertrophy (BAH)
• “Superior” QRS axis is also characteristic of
ECD.
• Hyperactive precordium
• Regurgitant systolic murmurs of VSD and MR,
• Loud and narrowly split S2 (because of PAH),
• Apical or tricuspid diastolic rumble (or both),
and
• Signs of CHF.
• Those who survive infancy may develop pulmonary
vascular obstructive disease, as already discussed for
large VSD and large PDA
30. DIRECT COMMUNICATION BETWEEN THE LV AND RA
• This may occur as part of ECD (or as an isolated defect unrelated to
ECD).
• The direction of the shunt is from the high-pressure LV to the low-
pressure RA.
• The magnitude of the shunt is determined by the size of the defect,
regardless of the state of PVR; blood shunted to the RA must go forward
through the lungs even if the PVR is high.
• This type of shunt, which is independent of the status of PVR, is called
an obligatory shunt.
31. • When an LV-RA shunt is present as part of complete ECD, CHF may occur
within a few weeks, which is earlier than in the usual VSD.
• The enlarged chambers are identical to those of the complete form of
ECD.
• Therefore, the chest radiographs and ECG findings are similar to those
seen in complete ECD.
• Physical findings also resemble those of complete ECD, although the
holosystolic murmur (resulting from the LV-RA shunt) may be more
prominent at the mid-right sternal border.