Blood from the placenta is carried to the fetus by the umbilical vein. In humans, less than a third of this enters the fetal ductus venosus and is carried to the inferior vena cava, while the rest enters the liver proper from the inferior border of the liver. The branch of the umbilical vein that supplies the right lobe of the liver first joins with the portal vein. The blood then moves to the right atrium of the heart. In the fetus, there is an opening between the right and left atrium (the foramen ovale), and most of the blood flows through this hole directly into the left atrium from the right atrium, thus bypassing pulmonary circulation. The continuation of this blood flow is into the left ventricle, and from there it is pumped through the aorta into the body. Some of the blood moves from the aorta through the internal iliac arteries to the umbilical arteries, and re-enters the placenta, where carbon dioxide and other waste products from the fetus are taken up and enter the maternal circulation.
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.
Fetal Circulation by Barkha Devi,Lecturer,Sikkim Manipal College of NursingBarkha Devi
This PowerPoint will provide you a short a sweet lecture about fetal circulation. Please give me your feed back .
-Discuss anatomy and physiology of fetal circulation
-Compare and contrast fetal circulation to infant circulation
-Define specialized structures of fetal circulation
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.
Fetal Circulation by Barkha Devi,Lecturer,Sikkim Manipal College of NursingBarkha Devi
This PowerPoint will provide you a short a sweet lecture about fetal circulation. Please give me your feed back .
-Discuss anatomy and physiology of fetal circulation
-Compare and contrast fetal circulation to infant circulation
-Define specialized structures of fetal circulation
Describe the normal fetal circulation and mention the changes that occur in it is placental stage and after birth. Fetal circulation is composed of placenta, umbilical cord, heart and systemic blood vessels.
A major difference between the fetal circulation and postnatal circulation is that the lungs are not used during the fetal stage resulting in the presence of shunts to move oxygenated blood and nutrients from the placenta to the fetal tissue.
At birth, the start of breathing and the severance of the umbilical cord prompt various changes that quickly transform fetal circulation into postnatal circulation.
When the embryo develops into the fetus, it creates a functional cardiovascular system that cooperates with the mother's system.
During birth, there are functional physiological changes that transform the shared system into an individual one for the fetus.
In the fetus main filtration site for plasma nutrients and wastes in the placenta, which is outside of the body cavity.
In adults, the circulation occurs entirely inside the body.
The blood that flow to through the fetus is actually more complicated than after the baby is born (normal heart).
This is because the mother (the placenta) is doing the work that the baby's lungs will do after birth.
The placenta accepts the blood without oxygen from the fetus through blood vessels that leave the fetus through the umbilical cord (Umbilical arteries , there are two of them).
When blood goes through the placenta it pick up oxygwn.
The oxygen rich blood then returns to the fetus via the third vessels in the umbilical cord (Umbilical vein).
The oxygen rich blood that enters the fetus passes through the fetal liver and enters the right side of the heart.
The oxygen rich blood goes through one of the two extra connections in the fetal heart that will close after the baby is born.
The hole between the top two heart chmbers (right and left atrium) is called "Patent Foramen Ovale (PFO).
This hole allows the oxygen rich blood to go form the right atrium to left atrium and then to the left ventricle and out the aorta.
As a result the blood with the most oxygen gets to the brain.
Blood coming back from the fetus's body also enters the right atrium, but the fetus is able to send this oxygen poor blood from the right atrium to the right ventricle (the chamber that normally pumps blood to the lungs).
most of the blood that leaves the right ventricle in the fetus bypass the lungs through the second of the extra fetal connections known as the ductus arteriosus.
The ductus arteriosus sends the oxygen poor blood to the organs in the lower half of the fetal body. This also allows for the oxygen poor blood to leave the fetus through the umbilical arteries and get back to the placenta to pick up oxygen.
Since the patent foramen ovale and ductus arteriosus are normal findings in the fetus, it is impossible to predict whether or not these connections will close normally after birth in a normal fetal heart.
USMLE CVS 008 Fetal and regional circulation anatomy .pdfAHMED ASHOUR
Fetal circulation and regional circulation refer to the distinct patterns of blood flow in the developing fetus and the circulatory pathways within different regions of the body.
Understanding these circulation patterns is crucial for comprehending the physiological adaptations that occur during fetal development and in the various regions of the body after birth.
After birth, the circulatory system undergoes significant changes, such as closure of the foramen ovale and ductus arteriosus, leading to the establishment of the adult circulatory pattern.
Embark on a captivating exploration of #FetalCirculation in this presentation. Delve into the intricacies of the developing cardiovascular system, understanding how the fetus receives oxygen and nutrients for optimal growth within the womb. Uncover the role of critical structures such as the ductus venosus and foramen ovale in facilitating unique circulatory patterns. Gain insights into the transition from fetal to neonatal circulation and its crucial significance for newborns. This presentation provides a comprehensive overview of the physiological marvel that sustains life before the first breath.
Wellens syndrome. Wellens syndrome (also referred to as LAD coronary T-wave syndrome) refers to an ECG pattern specific for critical stenosis of the proximal left anterior descending artery. The anomalies described occur in patients with recent anginal chest pain, and do not have chest pain when the ECG is recorded.
Congenital defects can put a strain on the heart, causing it to work harder. To stop your heart from getting weaker with this extra work, your doctor may try to treat you with medications. They are aimed at easing the burden on the heart muscle. You need to control your blood pressure if you have any type of heart problem.
Changing your lifestyle can help control and manage high blood pressure. Your health care provider may recommend that you make lifestyle changes including:
Eating a heart-healthy diet with less salt
Getting regular physical activity
Maintaining a healthy weight or losing weight
Limiting alcohol
Not smoking
Getting 7 to 9 hours of sleep daily
CRISPR technologies have progressed by leaps and bounds over the past decade, not only having a transformative effect on
biomedical research but also yielding new therapies that are poised to enter the clinic. In this review, I give an overview of (i)
the various CRISPR DNA-editing technologies, including standard nuclease gene editing, base editing, prime editing, and epigenome editing, (ii) their impact on cardiovascular basic science research, including animal models, human pluripotent stem
cell models, and functional screens, and (iii) emerging therapeutic applications for patients with cardiovascular diseases, focusing on the examples of Hypercholesterolemia, transthyretin amyloidosis, and Duchenne muscular dystrophy.
A post-splenectomy patient suffers from frequent infections due to capsulated bacteria like Streptococcus
pneumoniae, Hemophilus influenzae, and Neisseria meningitidis despite vaccination because of a lack of
memory B lymphocytes. Pacemaker implantation after splenectomy is less common. Our patient underwent
splenectomy for splenic rupture after a road traffic accident. He developed a complete heart block after
seven years, during which a dual-chamber pacemaker was implanted. However, he was operated on seven
times to treat the complication related to that pacemaker over a period of one year because of various
reasons, which have been shared in this case report. The clinical translation of this interesting observation
is that, though the pacemaker implantation procedure is a well-established procedure, the procedural
outcome is influenced by patient factors like the absence of a spleen, procedural factors like septic measures,
and device factors like the reuse of an already-used pacemaker or leads.
Transcatheter closure of patent ductus arteriosus (PDA) is feasible in low-birth-weight infants. A female baby was born prematurely with a birth weight of 924 g. She had a PDA measuring 3.7 mm. She was dependent on positive pressure ventilation for congestive heart failure in addition to the heart failure medications. She could not be discharged from the hospital even after 79 days of birth, and even though her weight reached 1.9 kg in the neonatal intensive care unit. We attempted to plug the PDA using an Amplatzer Piccolo Occluder, but the device failed to anchor. Then, the PDA was plugged using a 4-6 Amplatzer Duct Occluder using a 6-Fr sheath which was challenging.
Accidental misplacement of the limb lead electrodes is a common cause of ECG abnormality and may simulate pathology such as ectopic atrial rhythm, chamber enlargement or myocardial ischaemia and infarction
A Case of Device Closure of an Eccentric Atrial Septal Defect Using a Large D...Ramachandra Barik
Device closure of an eccentric atrial septal defect can be challenging and needs technical modifications to avoid unnecessary complications. Here, we present a case of a 45-year-old woman who underwent device closure of an eccentric defect with a large device. The patient developed pericardial effusion and left-sided pleural effusion due to injury to the junction of right atrium and superior vena cava because of the malalignment of the delivery sheath and left atrial disc before the device was pulled across the eccentric defect despite releasing the left atrial disc in the left atrium in place of the left pulmonary vein. These two serious complications were managed conservatively with close monitoring of the case during and after the procedure.
Trio of Rheumatic Mitral Stenosis, Right Posterior Septal Accessory Pathway a...Ramachandra Barik
A 57-year-old male presented with recurrent palpitations. He was diagnosed with rheumatic mitral stenosis, right posterior septal accessory pathway and atrial flutter. An electrophysiological study after percutaneous balloon mitral valvotomy showed that the palpitations were due to atrial flutter with right bundle branch aberrancy. The right posterior septal pathway was a bystander because it had a higher refractory period than the atrioventricular node.
Percutaneous balloon dilatation, first described by
Andreas Gruentzig in 1979, was initially performed
without the use of guidewires.1 The prototype
balloon catheter was developed as a double lumen
catheter (one lumen for pressure monitoring or
distal perfusion, the other lumen for balloon inflation/deflation) with a short fixed and atraumatic
guidewire at the tip. Indeed, initially the technique
involved advancing a rather rigid balloon catheter
freely without much torque control into a coronary
artery. Bends, tortuosities, angulations, bifurcations,
and eccentric lesions could hardly, if at all, be negotiated, resulting in a rather frustrating low procedural success rate whenever the initial limited
indications (proximal, short, concentric, noncalcified) were negated.2 Luck was almost as
important as expertise, not only for the operator,
but also for the patient. It is to the merit of
Simpson who, in 1982, introduced the novelty of
advancing the balloon catheter over a removable
guidewire, which had first been advanced in the
target vessel.3 This major technical improvement
resulted overnight in a notable increase in the procedural success rate. Guidewires have since evolved
into very sophisticated devices.
Optical coherence tomography-guided algorithm for percutaneous coronary intervention. Vessel diameter should be assessed using the external elastic lamina (EEL)-EEL diameter at the reference segments, and rounded down to select interventional devices (balloons, stents). If the EEL cannot be identified, luminal measures are used and rounded up to 0.5 mm larger for selection of the devices. Optical coherence tomography (OCT)-guided optimisation strategies post stent implantation per EEL-based diameter measurement and per lumen-based diameter measurement are shown. For instance, if the distal EEL-EEL diameter measures 3.2 mm×3.1 mm (i.e., the mean EEL-based diameter is 3.15 mm), this number is rounded down to the next available stent size and post-dilation balloon to be used at the distal segment. Thus, a 3.0 mm stent and non-compliant balloon diameter is selected. If the proximal EEL cannot be visualised, the mean lumen diameter should be used for device sizing. For instance, if the mean proximal lumen diameter measures 3.4 mm, this number is rounded up to the next available balloon diameter (within up to 0.5 mm larger) for post-dilation. MLA: minimal lumen area; MSA: minimal stent area;NC: non-compliant
Brugada syndrome (BrS) is an inherited cardiac disorder,
characterised by a typical ECG pattern and an increased
risk of arrhythmias and sudden cardiac death (SCD).
BrS is a challenging entity, in regard to diagnosis as
well as arrhythmia risk prediction and management.
Nowadays, asymptomatic patients represent the majority
of newly diagnosed patients with BrS, and its incidence
is expected to rise due to (genetic) family screening.
Progress in our understanding of the genetic and
molecular pathophysiology is limited by the absence
of a true gold standard, with consensus on its clinical
definition changing over time. Nevertheless, novel
insights continue to arise from detailed and in-depth
studies, including the complex genetic and molecular
basis. This includes the increasingly recognised
relevance of an underlying structural substrate. Risk
stratification in patients with BrS remains challenging,
particularly in those who are asymptomatic, but recent
studies have demonstrated the potential usefulness
of risk scores to identify patients at high risk of
arrhythmia and SCD. Development and validation of
a model that incorporates clinical and genetic factors,
comorbidities, age and gender, and environmental
aspects may facilitate improved prediction of disease
expressivity and arrhythmia/SCD risk, and potentially
guide patient management and therapy. This review
provides an update of the diagnosis, pathophysiology
and management of BrS, and discusses its future
perspectives.
The Human Developmental Cell Atlas (HDCA) initiative, which is part of the Human Cell Atlas, aims to create a comprehensive reference map of cells during development. This will be critical to understanding normal organogenesis, the effect of mutations, environmental factors and infectious agents on human development, congenital and childhood disorders, and the cellular basis of ageing, cancer and regenerative medicine. Here we outline the HDCA initiative and the challenges of mapping and modelling human development using state-of-the-art technologies to create a reference atlas across gestation. Similar to the Human Genome Project, the HDCA will integrate the output from a growing community of scientists who are mapping human development into a unified atlas. We describe the early milestones that have been achieved and the use of human stem-cell-derived cultures, organoids and animal models to inform the HDCA, especially for prenatal tissues that are hard to acquire. Finally, we provide a roadmap towards a complete atlas of human development.
The treatment of patients with advanced acute heart failure is still challenging.
Intra-aortic balloon pump (IABP) has widely been used in the management of
patients with cardiogenic shock. However, according to international guidelines, its
routinary use in patients with cardiogenic shock is not recommended. This recommendation is derived from the results of the IABP-SHOCK II trial, which demonstrated
that IABP does not reduce all-cause mortality in patients with acute myocardial infarction and cardiogenic shock. The present position paper, released by the Italian
Association of Hospital Cardiologists, reviews the available data derived from clinical
studies. It also provides practical recommendations for the optimal use of IABP in
the treatment of cardiogenic shock and advanced acute heart failure.
Left ventricular false tendons (LVFTs) are fibromuscular
structures, connecting the left ventricular
free wall or papillary muscle and the ventricular
septum.
There is some discussion about safety issues during
intense exercise in athletes with LVFTs, as these
bands have been associated with ventricular arrhythmias
and abnormal cardiac remodelling. However,
presence of LVFTs appears to be much more common
than previously noted as imaging techniques
have improved and the association between LVFTs
and abnormal remodelling could very well be explained
by better visibility in a dilated left ventricular
lumen.
Although LVFTsmay result in electrocardiographic abnormalities
and could form a substrate for ventricular
arrhythmias, it should be considered as a normal
anatomic variant. Persons with LVFTs do not appear
to have increased risk for ventricular arrhythmias or
sudden cardiac death.
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.
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
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
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.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
Follow us on: Pinterest
Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
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
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
4. Contents
• Embryology of heart
• Anatomy fetal circulation
• Physiology of fetal circulation
• Transition from fetal to infant circulation
• Compared fetal to infant circulation
• Impact of fetal circulation on various congenital heart during
intrauterine life and during transition
5. FETAL CIRCULATION
• The term usually encompasses the entire fetoplacental circulation,
which includes the umbilical cord and the blood vessels within the
placenta that carry fetal blood
8. – Formed by the overlapping
edge of the septum secundum
against the ruptured upper
portion of the septum
primum.
– Acts like a flap valve for
preferential blood flow from
the right atrium to the left
atrium.
Foramen Ovale
9. • Blood column in IVC inlet (to RA)
• hits the interatrial ridge, the crista
dividens
left arm Right arm
fills the ‘windsock’ TV
Foramen Ovale RV
LA
• Foramen Ovale
10. – Connects the left branch of the
pulmonary trunk to arch of
aorta(beyond the origin of left
subclavian artery)
– It protects the lungs from circulatory
overloading.
– Less oxygenated blood in Pulmonary
artery flows through Ductus
Arteriosus to descending aorta and
then to placenta foroxygenation
Ductus Arteriosus
11. Vena-caval Circulation
Superior Vena Cava
• Drains the upper part of the
body,including the brain (15% of
combined ventricular output).
• Most (95%)of SVC blood goes
to the Right Ventricle.
•SVC SpO2- 40%
Inferior Vena Cava
• Drains lower part of body and
placenta (70% of combined
ventricular output)
• Most of IVC blood is directed to
the LA through Foramen ovale.
• IVC SpO2 -Inlet- 70%
Distal- 35%
12. Fetal Pulmonary Circulation
• Fetal lung does not serve gas exchange function.
• MPA continues as Ductus and RPA and LPA arise as branches.
• PVR is high and PBF is low (10 % of CCO). This helps to reduce workload
of fetal heart.
Causes – - Thick muscular layer
• decreased NO synthetase ,Adrenomedullin
• increased endothelin 1 ,Leukotriens
• mechanical – fluid filled alveoli
• PVR – In early gestation-> extremely high : small number of small arteries
In last half of gestation-> decreases progressively : growth of new
arteries and an overall increase in cross section.
Mean PAP - increases progressively with gestation and at term is about
50 mm Hg, exceeds mean aortic blood pressure.
15. Fetal Blood volume• The blood volume - fetus: 10-12% of BW
Adult: 7-8% of BW
• The main reason for this difference is the large pool of blood contained within
the placenta; a volume that reduces as gestation progresses.
• Compared with adults, the fetus is capable of much faster regulation and
restoration of the blood volume due to high diffusion rates between fetal
compartments.
• Placental Blood flow regulation:
Endothelin and prostanoids vasoconstriction
Nitric oxide vasodilation.
No neural vascular regulation, and
Catecholamines - Little effect.
16. 20
5 4.5
55
25
6
0
10
20
30
40
50
60
SBP DBP UVP
MID GESTATION TERM GESTATION
Fetal Blood Pressure
Johnson P, Maxwell DJ, Tynan MJ, Allan LD. Intracardiac
pressures in the human fetus. Heart 2000;84:59e63.
17. Fetal Cardiac performance
• The myocardium grows by cell division until birth, and growth beyond birth
is due to cell enlargement.
• The density of myofibrils increases particularly in early pregnancy and the
contractility continues to improve during the second half of pregnancy.
• Fetal and neonatal myocardial cells
• are smaller in diameter
• contain relatively more non-contractile mass (primarily mitocondria,
nuclei & surface membrane).
• force of generation , extent and velocity of shortening arelow
• stiffness and water content of ventricular myocardium are high
18. Fetal Cardiac Output
• The cardiac output of the fetus is expressed in terms of the total output of
both ventricles—the combined Cardiac output (CCO).( Because of Parallel
circulation)
• Right ventricular output is about 1.3 times the left ventricular flow.
• During fetal life the right ventricle
• -is pumping against systemic blood pressure
• -is performing greater volume of work than LV.
• The fetal and neonatal heart has limited ability to increase CO in presence
of increased preload or afterload.
• CO determinants-
-HR ( Most important determinant)
-SV- Frank starling mechanism, Adrenergic drive
19. Changes in blood flow to various organs during
the latter half of gestation.
Maternal Physiology during Pregnancy & Fetal & Early Neonatal Physiology: Current
Diagnosis & Treatment: Obstetrics & Gynecology, 11e
|
20. Physiology of Foetal Hb
• Approximately 80% of foetal
haemoglobin is Hb F.
Oxygen Uptake Facilitated by
-Low P50 of Hb F
- Lower content of 2,3-DPG of
Hb F.
Oxygen Delivery Maintained by
-High CCO, high haemoglobin
concentrations , and more O2
content (despite the relatively
low partial pressures of oxygen.
-Lower Foetal pH (normal values
7.25-7.35) than in adults.
21. Response of fetal circulation to stress• Acute hypoxic insult
Autonomic
Responses
Activates a chemoreflex mediated by the carotid
bodies - vagal effect - reduced heart rate and a
sympathetic vasoconstriction
Endocrine
Responses
• Early-
adrenaline and noradrenaline, RAAS
• maintaining vasoconstriction (a-
adrenergic),
• increasing heart rate (b-adrenergic)and
• reducing blood volume with
renin release and increased
angiotensin II concentration
Delayed-
• Increased concentrations of adrenocorticotrophic
hormone, cortisol, atrial natriuretic peptide,
neuropeptide Y and adrenomedullin
22. Watershed Areas in Fetal Circulation
• Isthmus aortae –
• As a watershed between the aortic arch and the ductus arteriosus
• Retrograde flow ( DA to Ascending aorta) in LV obstructive lesions
• An Indicator of placental compromise
• Left portal vein-
• As a watershed between umbilical vein and main portal vein
• Retrograde flow (Main portal vein to Umbilical vein) in compromised placental venous
return.
• An Indicator of placental compromise
• Foramen Ovale-
• Between RA and LA
• Normally Left arm ( wind sock effect) and Right arm.
• In cases with increased venous return (e.g. arterio-venous malformation), an increased
volume of blood is diverted to the right side
23. Overview of fetal circulatory dynamics
Parallel arrangement of two main arterial systems and their respective
ventricles.
Presence of shunts. (in the venous system, heart & arterial system.)
High impedance and low flow of pulmonary circulation.
Low impedance and high flow of placental circulation.
Mixing of venous return and preferential streaming.
Most oxygenated blood from the umbilical vein perfuses the brain and heart
preferentially by shunting across Ductus Venosus & Foramen Ovale.
Lesser oxygenated blood perfuses the lower body by shunting across the
DuctusArteriosus.
25. Fetal vs. Infant Circulation
• Fetal
• Low pressure system
• Right to left shunting
• Lungs non-functional
• Increased pulmonary resistance
• Decreased systemic resistance
• Infant
• High pressure system
• Left to right blood flow
• Lungs functional
• Decreased pulmonary resistance
• Increased systemic resistance
27. • Blood from the placenta is carried to the fetus by the umbilical vein. In
humans, less than a third of this enters the fetal ductus venosus and is
carried to the inferior vena cava, while the rest enters the liver proper from
the inferior border of the liver. The branch of the umbilical vein that
supplies the right lobe of the liver first joins with the portal vein. The blood
then moves to the right atrium of the heart. In the fetus, there is an
opening between the right and left atrium (the foramen ovale), and most
of the blood flows through this hole directly into the left atrium from the
right atrium, thus bypassing pulmonary circulation. The continuation of this
blood flow is into the left ventricle, and from there it is pumped through
the aorta into the body. Some of the blood moves from the aorta through
the internal iliac arteries to the umbilical arteries, and re-enters the
placenta, where carbon dioxide and other waste products from the fetus
are taken up and enter the maternal circulation
28. • Some of the blood entering the right atrium does not pass directly to
the left atrium through the foramen ovale, but enters the right
ventricle and is pumped into the pulmonary artery. In the fetus, there
is a special connection between the pulmonary artery and the aorta,
called the ductus arteriosus, which directs most of this blood away
from the lungs (which are not being used for respiration at this point
as the fetus is suspended in amniotic fluid).
29. Placenta
• The circulatory system of the mother is not directly connected to that
of the fetus, so the placenta functions as the respiratory center for
the fetus as well as a site of filtration for plasma nutrients and wastes.
Water, glucose, amino acids, vitamins, and inorganic salts freely
diffuse across the placenta along with oxygen. The uterine arteries
carry blood to the placenta, and the blood permeates the sponge-like
material there. Oxygen then diffuses from the placenta to the
chorionic villus, an alveolus-like structure, where it is then carried to
the umbilical vein.
30. Circulation at Materno Placental Level
umbilical
arteries
umbilical Veins-
chorionic villi
intervillous space
Maternal venules Maternal Arterioles
31. Circulation at Materno Placental Level
umbilical
arteries
umbilical
Veins
chorionic villi
intervillous space
Maternal
venules
Maternal
Arterioles
32. Fetal hemoglobin (HbF)
the developing fetus also employs a different type of oxygen transport
molecule in its hemoglobin from that when it is born and breathing its
own oxygen. Fetal hemoglobin enhances the fetus' ability to draw
oxygen from the placenta. Its oxygen-hemoglobin dissociation curve is
shifted to the left, meaning that it is able to absorb oxygen at lower
concentrations than adult hemoglobin. This enables fetal hemoglobin
to absorb oxygen from adult hemoglobin in the placenta, where the
oxygen pressure is lower than at the lungs. Until around six months'
old, the human infant's hemoglobin molecule is made up of two alpha
and two gamma chains (2α2γ). The gamma chains are gradually
replaced by beta chains until the molecule becomes hemoglobin A with
its two alpha and two beta chains (2α2β)
33. Blood pressure
It is the fetal heart and not the mother's heart that builds up the fetal blood pressure to drive its blood through the fetal circulation
Intracardiac pressure remains identical between the right and left ventricles of the human fetus
The blood pressure in the fetal aorta is approximately 30 mmHg at 20 weeks of gestation, and increases to ca 45 mmHg at 40 weeks
of gestation. The fetal pulse pressure is 20 mmHg at 20 weeks of gestation, increasing to ca 30 mmHg at 40 weeks of gestation
The blood pressure decreases when passing through the placenta. In the arteria umbilical, it is 50 mmHg. It falls to 30 mmHg in the
capillaries in the villi. Subsequently, the pressure is 20 mm Hg in the umbilical vein, returning to the heart.
34. Flow
• The blood flow through the umbilical cord is approximately 35 mL/min at
20 weeks, and 240 mL/min at 40 weeks of gestation. Adapted to the weight
of the fetus, this corresponds to 115 mL/min/kg at 20 weeks and 64
mL/min/kg at 40 weeks. It corresponds to 17% of the combined cardiac
output of the fetus at 10 weeks, and 33% at 20 weeks of gestation.
• Endothelin and prostanoids cause vasoconstriction in placental arteries,
while nitric oxide causes vasodilation. On the other hand, there is no neural
vascular regulation, and catecholamines have only little effect.
36. The change from fetal to
postnatal circulation happens
very quickly.
Changes are initiated by baby’s first breath.
37. The first breath:
Pulmonary alveoli open up:
– pressure in pulmonary tissues decrease.
– Blood from right heart rushes to fill the alveolar capillaries.
– Pressure in right side of heart ↓.
– Pressure in the left side of the heart ↑ (as more blood is returned
from pulmonary tissue via pulmonary veins to the LA).
38. Conversion of the fetal to the adult circulation
requires
–Increase of pulmonary blood flow to a level necessary
for adequate gas exchange
-Eliminating the umbilical–placental circulation
–separation of the left and right sides of the heart by
closure of fetal channels.
39. Perinatal circulatory transition
↑ Pulmonary Blood Flow
↑Oxygenation
Removal of the low-resistance
placental circulation
Increase in systemic vascular
resistance.
Mechanical expansion of
lungs
Increase in arterial PO2
Rapid Decrease In Pulmonary
Vascular Resistance
Ductus
Arteriosus
Constriction
↑ Lt.AtrialFlow
↓Foramen Ovale
Shunt
F.O. Closure
40. Umbilical arteries → Umbilical ligaments
Umbilical vein → Ligamentum teres
Shunt Functional
closure
Anatomical
closure
Ductus
arteriosus
10 – 96 hrs
after birth
2 – 3 wks
after birth
Formamen
ovale
Within several
mins after birth
One year
after birth
Ductus
venosus
Within several
mins after birth
3 – 7 days
after birth
41. Foramen Ovale Closure
– After birth, the foramen ovale closes by apposition of the left and right atrial flaps bordering
the opening.
– Decreased flow from placenta & IVC to hold open foramen and;
– Increased pulmonary blood flow & pulmonary venous return to left heart causing pressure in
the LA > RA.
– Premature closure of the foramen in utero may cause hypoplasia of the left side of the heart
because only a minimal amount of blood would reach the left atrium.
42. Ductus Arteriosus Closure
• Factors favouring :
O2- most important factor , At PO2- 50 mm Hg, By Direct effect (O2 Sensitive K channel
inhibition=> Voltage sensitive Ca Channels activation)/ Indirect effect- on decreasing PG E2 &
prostacyclin secretion.
prostaglandin antagonists- highest in third trimester and is enhanced by glucocorticoids and fetal
stress.
Increased Bradykinin and Decreased NO.
43. Contd…
• Immediately after birth: (Functional closure)
• contraction and cellular migration of the medial smooth muscle in
the wall of DA
• functional closure within 12 hours after birth in full-termhuman infants.
• The second stage : (Anatomical closure)
• completed by 2 to 3 weeks in human infants
• produced by infolding of the endothelium,
• disruption and fragmentation of the internal elasticlamina
• proliferation of the subintimal layers
• hemorrhage and necrosis in the subintimal region.
44. Contd..
In PRETREM: ( Delayed Closure)
The responsiveness of the ductal smooth muscle to oxygen is related to the gestational age
of the newborn.
- decreased sensitivity to oxygen-induced contraction ( Not due to lack of smooth muscle
development)
- persistently high levels of PGE2
-Low PaO2 in preterm neonate ( due to immature lung)
- Deficient in K+ channels.
45. Ductus venosus Closure
• The shunt obliterates within 1-3 weeks of birth in term infants
• Takes longer time in :
• premature births
• persistent pulmonary hypertension
• various forms of cardiac malformations.
• As in DA, PGE1 may keep it open , thromboxane may close it .
• In contrast to the DA where increased oxygen tension triggers the closure, no O2
trigger for DV.
46. Changes in Pulmonay Circulation
• With initiation of pulmonary ventilation:
• pulmonary vascular resistance decreases rapidly
• pulmonary blood flow increased by eightfold to tenfold.
• mean pulmonary arterial blood pressure is half systemic by 24 hours of age.
• Morphologic changes (vascular remodeling, muscular involution, and rheologic
changes) in the pulmonary vessels result in a permanent fall in pulmonary vascular
resistance.
– most striking change is a decrease in the thickness of the smooth muscle layer in the
small arteries.
– Adult levels of PVR and PAP reached by 2-6 weeks.
48. Contd..
Regulation of PVR-
• state of oxygenation
• the production of vasoactive substances:
– oxygen modulates the production of
both prostacyclin and endothelium-
derived nitric oxide (EDNO).
– Direct potassium channel activation
– Physical expansion
– Changes in alveolar surface tension
49. Post natal changes in various circulatory
beds
Coronary Blood flow Decreases dramatically as the oxygen content increases.
Cerebral circulation -DO-
Cutaneous blood flow Decreases(<= Cutaneous vasoconstriction )
Hepatic blood flow Falls rapidly f/b a surge ( on day 7,250 ml/minute /100 g )
50. Changes in Cardiac output
• The left ventricle in the fetus pumped blood mostly to the upper part of the body and brain
• After birth, LV must deliver the entire systemic cardiac output (450 ml/kg/min) (almost 200%
increase in output)
• This marked increase in left ventricular performance is achieved through a combination of
hormonal and metabolic signals, including an INCREASE IN :
• -The level of circulating catecholamines and
• -The myocardial receptors (β-adrenergic)
(through which catecholamines have their effect)
51. Contd..
• Improved diastolic function
due to removal of compression
by maternal organs and uterus
causes increased cardiac filling
and hence the cardiac output.
• Systemic blood pressure: After
an initial slight fall in systemic BP,
progressive rise occurs with
increasing age.
• Heart rate: Elimination of
Placental circulation => Increase
in systemic vascular resistance=>
Baroreceptor response =>
Slowing of HR
52. FETAL NEWBORN
Gas exchange Placenta Lungs
RV,LV circuit Parallel Series
Pulmonary circulation Vasoconstricted Dilated
Fetal myocardium
Contractility,Compliance Less Good
Dominant ventricle Right Left
Change in Structure Umbilical vein
Umbilical artery
Ductus venosus
Ductus arteriosus
Foramen ovale
Ligamentum teres
Medial umb ligament
Ligamentum venosum
Ligamentum arteriosum
Fossa ovalis
53. Adaptation to extrauterine life
• At birth, when the infant breathes for the first time, there is a
decrease in the resistance in the pulmonary vasculature, which
causes the pressure in the left atrium to increase relative to the
pressure in the right atrium. This leads to the closure of the foramen
ovale, which is then referred to as the fossa ovalis. Additionally, the
increase in the concentration of oxygen in the blood leads to a
decrease in prostaglandins, causing closure of the ductus arteriosus.
These closures prevent blood from bypassing pulmonary circulation,
and therefore allow the neonate's blood to become oxygenated in the
newly operational lungs.