I'm afraid I don't have enough information to answer these questions. The document provided is an overview of techniques for detecting intracardiac shunts and quantifying cardiac output and shunt flow. It does not include a specific patient case. Could you please provide more details about a patient for me to reference in answering your questions?
Our concepts of heart disease are based on the enormous reservoir of physiologic and anatomic knowledge derived from the past 70 years' of experience in the cardiac catheterization laboratory.
As Andre Cournand remarked in his Nobel lecture of December 11, 1956, the cardiac catheter was the key in the lock.
By turning this key, Cournand and his colleagues led us into a new era in the understanding of normal and disordered cardiac function in huma
Our concepts of heart disease are based on the enormous reservoir of physiologic and anatomic knowledge derived from the past 70 years' of experience in the cardiac catheterization laboratory.
As Andre Cournand remarked in his Nobel lecture of December 11, 1956, the cardiac catheter was the key in the lock.
By turning this key, Cournand and his colleagues led us into a new era in the understanding of normal and disordered cardiac function in huma
Admixture lesions in congenital cyanotic heart diseaseRamachandra Barik
Admixture lesions in congenital cyanotic heart disease
Jaganmohan A Tharakan
Department of Cardiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, India
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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
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
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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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.
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
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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?
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- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
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These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
2. Normal circulation
Left to right shunting of blood as in ASD,VSD and PDA
Unoxygenated blood can be shunted from the right
heart to the left heart - Eisenmenger syndrome
Intracardiac shunts can be either congenital or
acquired e.g., VSD as a complication of myocardial
infarction
3. Detection, localization and quantification of
intracardiac shunts are an integral part of the
hemodynamic evaluation in these patients
4. Intracardiac shunting of blood results when there is an
opening between the right and left heart chambers and
a pressure difference between the connected
chambers
Pressures on the left side of the heart are generally
higher than on the right side so most shunts are
predominantly left to right although right to left and
bidirectional shunts are seen (predominantly in
Eisenmenger syndrome)
5. Many techniques are available for the detection
intracardiac shunts
• Indicator dilution method – Injecting indocyanine
green into a right sided heart chambers and then
monitoring its appearance in the systemic
circulation
• Contrast angiography – Contrast dye is injected into
high pressure chamber of suspected shunt
• Oximetry run – Most frequently used measurement
of the oxygen saturations in various locations in the
venous system and the right heart
6.
7.
8.
9. Basic technique for detecting and quantifying left to
right shunts
Oxygen content or percent saturation is measured in
blood samples drawn sequentially from the pulmonary
artery, right ventricle, right atrium, superior vena cava
and inferior vena cava
A left to right shunt may be detected and localized if a
significant step-up in blood oxygen saturation is found
in one of the right heart chambers
10. Samples need to be acquired with the patient
breathing room air or a gas mixture containing no more
than a maximum of 30% oxygen
Saturation data may be inaccurate in patients breathing
more than 30% oxygen, as a significant amount of
oxygen may be present in dissolved form in the
pulmonary venous sample
Dissolved oxygen is not factored into calculations when
saturations are used and thus pulmonary flow will be
overestimated and the amount of shunt exaggerated
Heart 2001;85:113–120.
11. The simplest way to screen for a left to right shunt is to
sample SVC and pulmonary artery blood and measure
the difference in O2 saturation if >=8%, a left to right
shunt may be present at atrial, ventricular or great
vessel level, and a full oximetry run should be done
12. Samples are obtain (2-mL) from each of the following locations
with the end hole catheter
13. To ensure the results are as accurate as possible, the
samples must be collected as close in time as good
technique permits
Blood samples should not be withdrawn into the
syringe too rapidly, “rapid aspiration increased oxygen
saturations”
Complete mixing of blood is assumed in all chambers
Matta et al. Anesthesiology 1997;86:806–808.
14. Oximetry method of quantifying shunts loses accuracy
when determining small shunts or in the presence of
high cardiac output (which decreases AVO2 difference)
The magnitude of the step-up varies with the oxygen
carrying capacity of blood
Relationship between the magnitude of step-up and the
shunt flow is nonlinear and with increasing left to right
shunting, a given change in shunt flow produces less of
a change in the saturation step-up
15. Saturation step-ups are increased if
hemoglobin concentration is low or cardiac
output is low
16. Hillis et al. found that the difference between RA and PA
saturations in 980 patients without intracardiac shunts was
2.3% ± 1.7%. In this same population,the difference between
SVC and RA saturations was 3.9% ± 2.4%
Using threshold values of 8.7% and 5.7% respectively,
between SVC to RA and RA to PA as “cut-offs” to identify
patients with intracardiac shunts had excellent sensitivity
and specificity
Am J Cardiol 1986;58:129–132
17. Level of shunt Difference in
O2 saturation
Differential diagnosis
Atrial
(SVC/IVC to RA)
>7% ASD; PAPVD; Ruptured sinus of
Valsalva; VSD with TR; Coronary to
RA fistula
Ventricular
(RA to RV)
>5% VSD; PDA with PR; Primum ASD;
coronary to RV fistula
Great Vessel
(RV to PA)
>5% PDA; AP window; Aberrant coronary
artery origin
Any level
(SVC to PA)
>7% All the above
18. Generally done in two ways
1. The ratio of pulmonary blood flow versus the
systemic blood flow can be calculated (QP/QS)
2. Calculation of actual flow of the shunt by
difference between the pulmonary blood flow
and the systemic blood flow
These two are equal in a normal heart
19. Quantification of shunt size using Qp/Qs is not affected
by hemoglobin concentration and the relationship
between Qp/Qs and shunt flow is linear
20. If a PV has not been entered, systemic arterial oxygen
content may be used if >95%
21. If systemic oxygen saturation is <95% then,
• Must determine whether a right to left intracardiac shunt
is present
• If right to left shunt is present then an assumed value for
pulmonary venous oxygen content of 98% oxygen
capacity should be used
• If no right to left intracardiac shunt is found, then the
observed systemic arterial oxygen saturation should be
used to calculate pulmonary blood flow
22. Oxygen consumption can measured by using the metabolic rate meter
Mixed venous oxygen content must be measured in the chamber
immediately proximal to the shunt
23. Location of shunt as determined
by site of O2 step-up
Mixed venous sample to use in
calculating systemic blood flow
1. Pulmonary artery (e.g., patent
ductus arteriosus)
Right ventricle
2. Right ventricle (e.g., ventricular
septal defect)
Right atrium
3. Right atrium (e.g., atrial septal
defect)
3 SVC + 1 IVC
4
24.
25. These equations are simplified as
Since pulmonary veins are rarely entered during a cardiac cath,
a pulmonary catheter wedge sample or LA sample (if the LA is
entered via an ASD) can be used in its place
Alternatively, arterial saturation can be substituted or an
assumed value of 98% may be used
26. Qp/Qs can be a very useful tool in making decisions
about the need for repair of a shunt
• Qp/Qs of 1–1.5 – observation is generally recommended.
• Qp/Qs ratio of 1.5–2.0 – significant enough that closure (either
surgically or percutaneously) should be considered if the risk of the
procedure is low
• Qp/Qs ratio of greater than 2 – closure (either surgically or
percutaneously) should be undertaken unless there are specific
contraindications
27. If there is no evidence of an associated right to left
shunt, the left-to-right shunt is calculated by
28. Primary indication for the use of techniques to detect
and localize right to left intracardiac shunts is the
presence of cyanosis, or more commonly, arterial
hypoxemia
Right to left shunting is unusual except in the case of
Eisenmenger syndrome
Qp/Qs will be less than 1
29. In right to left shunting, the effective pulmonary flow is
reduced by the amount of the shunt
Flow through the + Flow through the shunt = Flow through the
pulmonary valve aortic valve
30. 1. Angiography:
May demonstrate Right to Left intracardiac shunts
Important in detecting Right to Left shunting owing to
a pulmonary AVF
Although angiography may localize Right to Left
shunts, it does not permit quantification
31. 2. Oximetry :
The site of Right to Left shunts may be localized if blood
samples can be obtained from a pulmonary vein, LA, LV
and aorta
The pulmonary venous blood of patients with arterial
hypoxemia caused by an intracardiac Right to Left shunt is
fully saturated with oxygen
Site of a Right to Left shunt may be localized by noting
which left heart chamber is first to show desaturation (i.e.,
a step-down in oxygen concentration)
32. e.g., If LA blood oxygen saturation is normal but
desaturation is present in the LV and in the systemic
circulation, the Right to Left shunt is across a VSD
33. The only disadvantage of this technique is that a
pulmonary vein and the left atrium must be entered
• This is not as easy in adults as it is in infants, in whom the left
atrium may be entered routinely by way of the foramen ovale
34. Simplified approach to the calculation of
simultaneous right-to-left and left-to-
right (also known as bidirectional) shunts
makes use of a hypothetic quantity
known as the effective blood flow, the
flow that would exist in the absence of
any left-to-right or right-to-left shunting
35. Oxygen content = hemoglobin × 1.36 × percent saturation
The approximate left-to-right shunt then equals Qp - Qeff, and
the approximate right-to-left shunt equals Qs - Qeff
36. Pulmonary circulation is characterized by high flow, low
pressure and low resistance system
Normal pulmonary systolic pressures are 18-25 mm Hg, end
diastolic pressure ranges from 6-10 mm Hg and mean
pulmonary arterial pressures of 10-16 mm Hg
Pulmonary hypertension is define as mean pulmonary
artery pressure (MPAP) >25 mm Hg at rest or > 30mmHg on
exercise or systolic pulmonary artery pressure >30 mm Hg
Pulmonary artery pressure increase in response to increase
on LA pressures, pulmonary vascular resistance and cardiac
output
37. The pulmonary vasculature is a dynamic system and is
subject to many mechanical, neural and biochemical
influences
Pulmonary vascular resistance provides general
information about the pulmonary circulation but this
must be interpreted in the context of the clinical
situation and other hemodynamic data obtained during
cardiac catheterization
38. Expressed in Woods unit (1WU=1mm Hg/L = 80
dynes/cm3
)
Normal value is < 3 WU or 150 – 250 dynes/sec/cm3
PVR is one sixth SVR
39. Factors increases PVR
• Hypoxia
• Hypercapnia
• Increased sympathetic tone
• Polycythemia
• local release of serotonin
• Mechanical obstruction by multiple pulmonary emboli
• Precapillary pulmonary edema
• Lung compression (pleural effusion, increased
intrathoracic pressure via respirator)
40. Factors that decreases PVR:
• Oxygen
• Adenosine
• Isoproterenol
• Inhaled nitric oxide
• Prostacyclin infusions
• High doses of calcium channel blockers
41. Pulmonary vasoreactivity can be checked with the help
of
• 100% oxygen
• Adenosine
• Epoprostenol
• Inhaled nitric oxide
42.
43. Positive response is define as:
• 20% fall in pulmonary artery pressure and PVR or
decrease in mean pulmonary artery pressure of 10
mm Hg to an absolute value of less than 40 mm Hg
without in decrease in cardiac output
These are the patient who are most benefited from
corrective procedure and calcium channels
blockers
44. The ratio between pulmonary vascular resistance and
systemic vascular resistance (resistance ratio) can be
used as a criterion for operability in dealing with
congenital heart disease
• Normally, this ratio is <0.25
• Values of 0.25 to 0.50 indicate moderate pulmonary vascular
disease
• Values greater than 0.75 indicate severe pulmonary vascular
disease
• When the PVR/SVR resistance ratio equals 1.0 or more, surgical
correction of the congenital defect is considered
contraindicated because of the severity of the pulmonary
vascular disease
45. Q 1. What is the level of shunt?
Q 2. What is the direction of shunt?
Q 3. What is diagnosis?
Q 4. What is Qp/Qs
46. Q 1.What is the level of shunt?
Q 2.What is the direction of shunt?
Q 3.What is diagnosis?
Q 4.What is Qp/Qs?
47. Q 1. What is the level of shunt?
Q 2. What is the direction of shunt?
Q 3. What is diagnosis?
Q 4. What is Qp/Qs
48. Q 1.What is the level of shunt?
Q 2.What is the direction of shunt?
Q 3.What is diagnosis?
Q 4.What is Qp/Qs