Ventricular Septal Defect (VSD) is a developmental defect allowing shunting of blood between the left and right ventricles. It is the most common congenital heart defect, accounting for 25% of cases. VSDs occur when the interventricular septum fails to fuse properly during embryonic development of the heart. Small VSDs often close spontaneously, while large VSDs can cause heart failure if not surgically repaired before irreversible pulmonary damage. Surgical repair has excellent outcomes, restoring a normal heart size and function while preventing complications like Eisenmenger's syndrome.
A cyanotic heart defect is a group-type of congenital heart defects (CHDs). The patient appears blue (cyanotic), due to deoxygenated blood bypassing the lungs and entering the systemic circulation. This can be caused by right-to-left or bidirectional shunting, or malposition of the great arteries.
Cyanotic heart defects, which account for approximately 25% of all CHDs, include:
Tetralogy of Fallot (ToF)
Total anomalous pulmonary venous connection
Hypoplastic left heart syndrome (HLHS)
Transposition of the great arteries (d-TGA)
Truncus arteriosus (Persistent)
Tricuspid atresia
Interrupted aortic arch
Pulmonary atresia (PA)
Pulmonary stenosis (critical)
Eisenmenger syndrome(Reversal of Shunt due to Pulmonary Hypertension) .
Patent ductus arteriosus may cause cyanosis in late stage.
Transposition of the great arteries is a serious but rare heart defect present at birth (congenital), in which the two main arteries leaving the heart are reversed (transposed). The condition is also called dextro-transposition of the great arteries.
A cyanotic heart defect is a group-type of congenital heart defects (CHDs). The patient appears blue (cyanotic), due to deoxygenated blood bypassing the lungs and entering the systemic circulation. This can be caused by right-to-left or bidirectional shunting, or malposition of the great arteries.
Cyanotic heart defects, which account for approximately 25% of all CHDs, include:
Tetralogy of Fallot (ToF)
Total anomalous pulmonary venous connection
Hypoplastic left heart syndrome (HLHS)
Transposition of the great arteries (d-TGA)
Truncus arteriosus (Persistent)
Tricuspid atresia
Interrupted aortic arch
Pulmonary atresia (PA)
Pulmonary stenosis (critical)
Eisenmenger syndrome(Reversal of Shunt due to Pulmonary Hypertension) .
Patent ductus arteriosus may cause cyanosis in late stage.
Transposition of the great arteries is a serious but rare heart defect present at birth (congenital), in which the two main arteries leaving the heart are reversed (transposed). The condition is also called dextro-transposition of the great arteries.
A congenital heart defect is a problem with the structure of the heart. It is present at birth. Congenital heart defects are the most common type of birth defect. The defects can involve the walls of the heart, the valves of the heart, and the arteries and veins near the heart. They can disrupt the normal flow of blood through the heart. The blood flow can slow down, go in the wrong direction or to the wrong place, or be blocked completely.
Doctors use a physical exam and special heart tests to diagnose congenital heart defects. They often find severe defects during pregnancy or soon after birth. Signs and symptoms of severe defects in newborns include
Rapid breathing
Cyanosis - a bluish tint to the skin, lips, and fingernails
Fatigue
Poor blood circulation
Many congenital heart defects cause few or no signs and symptoms. They are often not diagnosed until children are older.
Many children with congenital heart defects don't need treatment, but others do. Treatment can include medicines, catheter procedures, surgery, and heart transplants. The treatment depends on the type of the defect, how severe it is, and a child's age, size, and general health.
Patent Ductus Arteroisus, PDA, Cardiology, Paediatrics, Pedicatrics, Critical Care, Emergency medicine, Medicine, Internal Medicine, MBBD, MD, India, CMC Vellore, Christian Medical College
commonly used for medical students, and helpful to use this ppt to study for them, and also a common man can understand very easily what is coarctation of aorta.
Some babies with tricuspid atresia have other conditions, such as pulmonary stenosis or transposition of the great arteries, that also affect blood flow through their heart. These conditions require treatment, too.
A congenital heart defect is a problem with the structure of the heart. It is present at birth. Congenital heart defects are the most common type of birth defect. The defects can involve the walls of the heart, the valves of the heart, and the arteries and veins near the heart. They can disrupt the normal flow of blood through the heart. The blood flow can slow down, go in the wrong direction or to the wrong place, or be blocked completely.
Doctors use a physical exam and special heart tests to diagnose congenital heart defects. They often find severe defects during pregnancy or soon after birth. Signs and symptoms of severe defects in newborns include
Rapid breathing
Cyanosis - a bluish tint to the skin, lips, and fingernails
Fatigue
Poor blood circulation
Many congenital heart defects cause few or no signs and symptoms. They are often not diagnosed until children are older.
Many children with congenital heart defects don't need treatment, but others do. Treatment can include medicines, catheter procedures, surgery, and heart transplants. The treatment depends on the type of the defect, how severe it is, and a child's age, size, and general health.
Patent Ductus Arteroisus, PDA, Cardiology, Paediatrics, Pedicatrics, Critical Care, Emergency medicine, Medicine, Internal Medicine, MBBD, MD, India, CMC Vellore, Christian Medical College
commonly used for medical students, and helpful to use this ppt to study for them, and also a common man can understand very easily what is coarctation of aorta.
Some babies with tricuspid atresia have other conditions, such as pulmonary stenosis or transposition of the great arteries, that also affect blood flow through their heart. These conditions require treatment, too.
congenital heart disease is a heart defect, it is caused by the exposure of teracogenic substances during pregnancy ,it may lead to the congenital defect .
ACYANOTIC DISEASE- Non cyanotic heart diseasesNelsonNgulube
ETIOLOGY AND EPIDEMIOLOGY
Congenital heart disease occurs in 8 per 1,000 births. The spectrum of lesions ranges from asymptomatic to fatal. Although most cases of congenital heart disease are multifactorial, some lesions are associated with chromosomal disorders, single gene defects, teratogens, or maternal metabolic disease (see Table139-2).
Congenital heart defects can be divided into three pathophysiological groups (Table 143.1).
1. Left-to-right shunts
2. Right-to-left shunts
3. Obstructive, stenotic lesions
Acyanotic congenital heart disease includes left-to-right shunts resulting in an increase in pulmonary blood flow (patent ductus arteriosus [PDA], ventricular septal defect [VSD], atrial septal defect [ASD]) and obstructive lesions (aortic stenosis, pulmonary stenosis, coarctation of the aorta), which usually have normal pulmonary blood flow.
VENTRICULAR SEPTAL DEFECTEtiology and Epidemiology
The ventricular septum is a complex structure that can be divided
into four components. The largest component is the muscular
septum. The inlet or posterior septum comprises endocardial
cushion tissue. The subarterial or supracristal septum com
prises conotruncal tissue. The membranous septum is below
the aortic valve and is relatively small. VSDs occur when any of these components fail to develop normally (Fig. 143.1). VSD,
the most common congenital heart defect, accounts for 25% of all congenital heart disease. Perimembranous VSD
Congenital heart disease is a general term for a range of birth defects that affect the normal way the heart works. The term "congenital" means the condition is present from birth.
The lecture is for medical student. It is from Dr RUSINGIZA Emmanuel, MD, senior lecture at UR( UNIVERSITY OF RWANDA) .
It will help to understand heart diseases in newborn, infants and children.
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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.
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
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
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
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.
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.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
2. Definition
VSD is a developmental
defect in the interventricular
septum allowing shunt
between the left & right
ventricles.
3. Development
➔ At 4-8 weeks of gestation, the single ventricular chamber is
effectively divided into two chambers.
➔ This division is accomplished with the fusion of the
membranous portion of the interventricular septum, the
endocardial cushions, and the bulbous cordis.
➔ Failure of development or fusion of one of the above
components during morphogenesis of the embryonic heart
results in a VSD in the corresponding component.
4. Epidemiology
➔ Most common cardiac malformation.
➔ It accounts for 25% of all congenital heart disease.
➔ VSDs are the most common lesion in many chromosomal
syndromes, including trisomy 13 (Patau syndrome), trisomy
18 (Edwards syndrome), trisomy 21 (Down syndrome).
5. Types
According to location of the defect:
1. Perimembranous (most common)
2. Muscular or Trabecular
3. Outlet VSD (Supracristal/ Infundibular)
4. Inlet VSD (AV canal type)
6. Types
According to size of the defect:
1. Small (<5 mm)
2. Moderate (5-10 mm)
3. Large (>10 mm)
According to haemodynamic status:
1. Restrictive: Small defect, shunt is limited.
2. Non-restrictive: Large defect, shunt is not limited.
7. Pathophysiology
➔ The pathophysiologic effects of a VSD derive from the
effects of the left-to-right shunt.
➔ A left-to-right shunt at the ventricular level has following
hemodynamic consequences:
◆ Increased LA & LV volume load > LA & LV hypertrophy
◆ Excessive pulmonary blood flow > Pulmonary HTN
◆ Reduced systemic cardiac output
8. Pathophysiology
Eisenmenger’s syndrome
Left to Right shunt
Increased pulmonary blood flow
Endothelial dysfunction & pulmonary vascular remodeling
Increased pulmonary vascular resistance
Inversion of shunt: Right to Left
9. Natural History
➔ Spontaneous closure occurs in about 50% of cases by 1
year.
➔ Congestive Cardiac Failure (CCF) develops in large VSD
after 8 weeks of age.
➔ In a large VSD, the shunt may reverse as early as 6-12
months of age, but Eisenmenger’s syndrome does not get
established till the teenage years.
➔ Rarely, Infective endocarditis develop in VSD patients.
10. Clinical Features:
➔ In small defect:
◆ Usually asymptomatic
◆ Normal growth and development.
◆ Incidental detection of a pansystolic murmur at left 3rd
and 4th intercostal spaces.
11. Clinical Features:
➔ Symptoms appear in large defect:
◆ Dyspnoea
◆ Feeding difficulties
◆ Poor weight gain
◆ Easy fatigability
◆ Profuse perspiration
◆ Recurrent respiratory tract infections
◆ Cyanosis is usually absent in early stage
12. Clinical Features:
➔ General examination:
◆ Appearance: Sick looking, often malnourished.
◆ Tachypnoea
◆ Tachycardia
◆ Blood pressure: Normal
◆ JVP: May be raised in CCF
◆ Pedal oedema: May be present in Heart Failure
13. Clinical Features:
➔ Precordium examination:
◆ Inspection:
● Hyperdynamic
● May be bulged
◆ Palpation:
● Apex beat is thrusting, shifted to the left.
● Left parasternal heave may be present.
● Thrill may be present in tricuspid area.
● Palpable P2 may be present.
14. Clinical Features:
➔ Precordium examination:
◆ Auscultation:
● 1st & 2nd heart sounds are audible in all 4 areas
● A harsh, pansystolic murmur (Grade 4/6) best heard
at lower left sternal border at the 3rd, 4th & 5th
intercostal spaces.
● The murmur may radiate to the right lower sternal
border. Intensity varies based on the size of the
VSD and pulmonary vascular resistance.
15. Investigations:
➔ Chest X-ray:
◆ In small defects: May be normal.
◆ In large defects:
● Cardiomegaly.
● Increased pulmonary vascular markings.
16. Investigations:
➔ ECG:
◆ Normal in small defect.
◆ Left ventricular hypertrophy in large VSD
◆ Biventricular hypertrophy when associated with
pulmonary hypertension.
◆ P wave may be notched when there is left atrial
enlargement.
17. Investigations:
➔ Echocardiogram:
◆ Shows location & size of the defect.
◆ Shows direction of blood flow.
➔ Cardiac catheterization:
◆ Measurement of intracardiac & intravascular oxygen
content defines the magnitude & direction of shunting.
18. Treatment:
➔ Counselling:
◆ For small defects:
● Reassurance of parents
● Encouraged to live a normal life
● No restrictions on physical activity
◆ For large defects:
● Parents should be counselled about its
complications & prognosis.
19. Treatment:
➔ Medical Management:
◆ Adequate nutrition
◆ Maintenance of good dental hygiene
◆ Antibiotic prophylaxis against Infective Endocarditis
◆ Treatment of CCF:
● Loop diuretics: Frusemide
● ACE inhibitors: Enalapril, Captopril
● Inotropic agents: Digoxin
20. Treatment:
➔ Surgical Management:
◆ As 50% of VSD close spontaneously by 1st year,
patients with small & moderate defects should be kept
in regular follow-up to observe spontaneous closure.
◆ In patients with large defects, surgical repair has to be
done before irreversible damage to the pulmonary
vasculature occurs.
21. Treatment:
➔ Indication of surgery:
◆ At any age: Patients with large defect in whom clinical
symptoms & failure to thrive can not be controlled
medically.
◆ <6 months: If patient develops CCF which does not
respond to decongestive therapy.
◆ After 6 months: Large defects with pulmonary
hypertension, even if the symptoms are controlled by
medication.
22. ➔ Indication of surgery:
◆ Significant L-R shunt with Qp : Qs > 2 : 1
◆ Patients with a Supracristal VSD of any size should be
operated because of high risk for aortic valve
regurgitation.
➔ Contraindication of surgery:
◆ Large VSD with predominant Right to Left shunt
◆ Small VSD with no CCF and Qp : Qs < 1.5 : 1
➔ Risk of surgery: The rate of surgical mortality is < 2%
23. Prognosis:
➔ The results of primary surgical repair are excellent and
complications leading to long term problems are rare.
➔ After surgical obliteration of left to right shunt:
◆ The hyperdynamic heart becomes quiet
◆ Cardiac size decreases toward normal
◆ Thrills & murmurs are abolished
◆ Pulmonary arterial hypertension regresses
➔ The long term prognosis after surgery is excellent.
24. Complications
Complications of VSD:
➔ Congestive cardiac
failure
➔ Eisenmenger’s
syndrome
➔ Aortic regurgitation
Complications of surgery:
➔ Infection
➔ Post operative
hemorrhage
➔ Pulmonary hypertension
➔ Valve injury
➔ AV block
➔ Residual VSD
25. VSD & Endocarditis
According to the most recent recommendations of the
American Heart Association-
➔ Unrepaired VSDs don't require endocarditis prophylaxis,
➔ After the VSD is successfully closed, preventive treatment
is needed only during a six-month healing period.
