This first part of the presentation gives a brief about the pathophysiology of supplemental oxygen in patients as well as basics of ventilation in the human body.
Oxygen therapy is an integral part of the treatment of critically ill patients. Maintenance of adequate
oxygen delivery to vital organs often requires the administration of supplemental oxygen,
sometimes at high concentrations. Although oxygen therapy is lifesaving, it may be associated
with deleterious effects when administered for prolonged periods at high concentrations.
Oxygen therapy is an integral part of the treatment of critically ill patients. Maintenance of adequate
oxygen delivery to vital organs often requires the administration of supplemental oxygen,
sometimes at high concentrations. Although oxygen therapy is lifesaving, it may be associated
with deleterious effects when administered for prolonged periods at high concentrations.
Oxygen therapy by Dr Arun Gangadharan
This ppt cover basics of oxygen therapy, its indication and the various methods to give oxygen.
Reference- Fishman's Pulmonary Diseases and Disorders
Oxygen therapy is a treatment that delivers oxygen gas for you to breathe. Overview. You can receive oxygen therapy from tubes resting in your nose, a face mask, or a tube placed in your trachea, or windpipe.
Oxygen therapy by Dr Arun Gangadharan
This ppt cover basics of oxygen therapy, its indication and the various methods to give oxygen.
Reference- Fishman's Pulmonary Diseases and Disorders
Oxygen therapy is a treatment that delivers oxygen gas for you to breathe. Overview. You can receive oxygen therapy from tubes resting in your nose, a face mask, or a tube placed in your trachea, or windpipe.
For my colleagues and medical students out there who need to either read or present the subject of hypoxia in surgical patients. I hope you find this one helpful.
lecture 5: it's good for as to take a breif about how does atmospheric air will pass to our lungs then to blood, for transportation and utilization of oxygen and excretion of carbon dioxide. Many issue are related when gas exchange is performed.
Hypoxia :types , causes,and its effects Aqsa Mushtaq
hypoxia :oxygen defecincy at tissue level.in these slides you are going to in touch with its types ,causes effects.share whatever you wanted to say comment us .
these notes are provided by our loving mam MAM SANIA .thanks to teach us mam :)
This presentation will surely help the general physicians and paediatricians to understand the symptoms of cystic fibrosis and will educate regarding various diagnostic modalities in cystic fibrosis
This presentation gives an in-depth insight of all the recent advances and evidence based treatment of the Bronchiolitis, which is one of the most common cause of hospitalisation in children less than 5 years of age
This second part of the presentation mainly aims at imparting knowledge regarding various oxygen delivery devices with its indication and contra-indications
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
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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.
- 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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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.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
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.
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. Oxygen…..
• Its not just gas……. It’s a medicine.
• Atmospheric air contains 20.95% of oxygen.
160 mmHg
104 mmHg in alveoli
90 – 100 mmHg in blood
3. Brief history:
Joseph Priestly, an English chemist who, although
discovered the oxygen molecule in 1772
In 1885, the first ever recorded use of oxygen was documented for a
medical purpose. This medical procedure was to treat a patient with
pneumonia by Dr. George Holtzapple
In 1917, Jon Scott Haldane invented the gas mask to protect
and treat soldiers who had been affected by dangerous chlorine
gasses during the First World War.
4. It wasn’t until the 1950’s that the first form of portable medical oxygen
therapy was invented. This portable oxygen was used strictly in ambulances
and on the scene of medical emergencies.
Finally, you could own your own oxygen therapy unit in your home
Oxygen concentrators began to shrink, due to the demand by younger and
more active oxygen therapy patients who wanted smaller and more mobile
machines
Presently, oxygen concentrators are small enough to fit in a purse, bring bike riding,
or even store under your seat on an airplane! Nowadays, some concentrators can
weigh less than 3 pounds, others have over 10 hours of battery life, and some
home units have an oxygen output upwards of 10,000 ml per minute!
7. 1.
Fundaments of gas transfer:
• Gases moves from areas of high concentration (or pressure) to
areas of lower concentration (or pressure).
• Partial pressure:
Pressure that each gas would produce if it occupied the
container alone.
• Total pressure of the gas mixture is the sum of the partial
pressures of all the individual gases.
9. 1.
• The decrease in PO2 from air to the mitochondrion is known as
the oxygen cascade.
• It is a normal physiological phenomenon.
• Exaggerated in pathological states:
• Hypoventilation
• Ventilation/ perfusion inequality
• Diffusion abnormality
11. 1.
Atmosphere Alveolus
• Atmospheric pressure: 101 kPa = 760 mmHg
• Oxygen: 21%
• Pressure of Oxygen = 21% of 101 = 21.2 kPa (160 mmHg)
• When we breath in, the air is humidified and warmed by our upper
airway.
• At 37℃, the water vapour in trachea is 6.3 kPa.
• Hence, effective PO2 in trachea:
(101 – 6.3) x 21 / 100 = 19.9 kPa (146 mmHg)
12. As the air reaches alveoli:
19.9 kPa
13.4 kPa
This reduction of PO2 is mainly because of the dilution with CO2
which enters the alveoli from the pulmonary capillaries.
1.
13. PAO2 here is calculated by Alveolar Gas Equation:
1.
RQ = respiratory quotient
i.e. ratio of CO2 production to O2 consumption
value – 0.8
14. Alveolus Blood
• In an ideal situation termed as “Perfect Lung”, the PO2 of pulmonary
venous blood would be equal to the PO2 in the alveolus.
• But this does not happen…..
2 main factors which are responsible for this “Alveolar-Arterial difference”
• Ventilation / Perfusion mismatch (d/t increased dead space or shunt)
• Slow diffusion across the alveolar – capillary membrane
1.
16. Present Concept:
• V & Q are both gravity dependent.
• Both variables increase down the lung.
• Perfusion shows about a 5 fold difference between the top
and bottom of lung.
• Ventilation shows about a 2 fold difference:
• Alveoli are relatively more distended towards the base because of
the negative pressure created by the underlying diaphragm.
1.
20. Diffusion:
• Oxygen diffuses from the alveolus to the capillary until the
PaO2 is equal to that in the alveolus.
• Total time when blood flows around the alveoli allowing gas
exchange – 0.75 sec.
• But normally, gas exchange is complete by the time the blood
has passed about one third of the way along the pulmonary
capillary.
• In normal lung, gas exchange takes in 0.25 sec.
1.
22. In normal lung, during exercise:
• There is increase in:
• Cardiac output
• Blood flow around the alveoli
Hence the time for gas exchange is decreased (yet complete)
1.
Maintain the increased oxygen
demands of the body
23. Now consider a diseased lung, with an already compromised
alveolar-capillary membrane……
The time taken for gas to transfer from alveoli to capillary is
prolonged in resting state itself
1.
24. And now when this diseased lung is exposed to exercise or
stressful condition,
1.
Hypoxemia develops
Eg. Alveolar Fibrosis
25. 1.
Fick’s Law
Rate of transfer of a gas through
a sheet of tissue
⍺
Difference in the partial pressures of
the gas on either side of the tissue
Area of tissue
Solubility of the gas
Tissue thickness
1
1
Square root of molecular weight
27. 1.
Hypoxic Pulmonary Vasoconstriction
• Pulmonary blood vessels have a unique property to respond to
hypoxia by vasoconstriction.
• Hence reducing blood flow to the under-ventilated areas.
• Protective mechanism
29. 1.
Oxygen carriage by the blood:
• O2 is carried in 2 forms:
• Combined with hemoglobin (98%)
• Dissolved in plasma (2%)
• 1 gm Hb 1.34ml O2
• 1 litre blood with Hb 15 gm/dl 200 ml O2
• As compare to this, only 3ml O2 is dissolved in each litre of
plasma
30. Oxygen Delivery
Adequacy of oxygen delivery to the tissue depends on 3 factors:
• Hemoglobin concentration
• Cardiac output
• Oxygenation
1.
32. 1. Oxygen delivery (ml O2 / min) =
= Cardiac output (lit / min) x Hb concentration (gm / L) x
1.34 (ml O2 in gm of Hb) x % Saturation
= 5000 x 200 / 1000
= 1000 ml O2 / min
33. Hypoxemia & Hypoxia :
Definitions:
Hypoxemia:
Low levels of oxygen in the blood (low blood oxygen saturation or
content)
Hypoxia:
Inadequate oxygen in tissue for normal cell and organ function.
Hypoxemia leads to Hypoxia (not always)
2.
34. Types of Hypoxia
Hypoxemia is the most common cause of Hypoxia (but not the
only cause)
Hypoxemia without hypoxia:
If the patient compensates for low PAO2 by increasing
oxygen delivery (increasing cardiac output).
Hypoxia without hypoxemia:
If the oxygen delivery to the tissue is impaired or if the
tissue is not able to extract oxygen effectively from blood.
3.
36. Hypoxic Hypoxia
Also known as:
• Hypoxemic Hypoxia
• Arterial Hypoxia
Results from insufficiency of oxygen available to the lungs or
decreased oxygen tension
3.
38. Mechanisms:
• Decreased PaO2
• V/Q mismatch in the lungs causing a widened A-a gradient.
V/Q mismatch responds to Oxygen therapy.
• Increased pulmonary shunt, i.e. perfusion without gas
exchange. Shunts do not respond to Oxygen therapy.
3.
39. Causes:
Low oxygen tension in inspired air:
• High altitude
• Breathing in closed space
Respiratory disorder with decreased pulmonary ventilation:
• Asthma
• Pneumothorax
• Sleep apnea
• Bulbar poliomyelitis
3.
41. Anemic Hypoxia:
Hypoxia in which arterial pO2 is normal but the amount of
hemoglobin available to carry oxygen is reduced
3.
42. Reduced tissue oxygenation as a consequence of low Hb or
Hemoglobin with abnormal oxygen carrying capacity.
Causes:
• Decreased number of RBC’s
• Decreased Hb content in blood
• Formation of altered Hb
• Combination of Hb with gases other than O2 and CO2
3.
43. Stagnant / Circulatory Hypoxia:
Also known as “Ischemic Hypoxia”.
Hypoxia in which the blood flow to the tissues is so low or slow
that adequate oxygen is not delivered to them despite a normal
arterial pO2.
3.
44. Pathophysiology:
• Decreased Cardiac output:
Extremely low cardiac output (cardiogenic shock)
causes a decreased mixed venous oxygen tension that does not
permit complete oxygenation of the blood during pulmonary
gas exchange.
• Increased non-pulmonary shunting:
In certain diseases (cirrhosis), large amounts of
blood flow bypass the entire lungs preventing gas exchange.
3.
46. Histotoxic Hypoxia
Inability of the tissues to use oxygen, even in the absence of
hypoxemia.
Cyanide Poisoning:
Cyanide interferes with the aerobic cellular
metabolism by destroying the oxidative enzymes completely
paralyzing the cytochrome oxidase system
3.
48. Increases affinity of Hb to Oxygen.
Decreased oxygen delivery to the tissue
Eg: CO poisoning,
Massive blood transfusion
3.
49. Comparison of types of hypoxias:
Types of
Hypoxia
Arterial
pO2
Hb count Blood
flow to
tissue
Arterial O2
content
Arterial
Hb O2
saturation
A-V PO2
difference
Cyanosis Stimulation
of
peripheral
chemo-
receptors
Hypoxic Normal Normal
+ +
Anemic Normal Normal Normal Absent Absent
Stagnant Normal Normal Normal Normal More than
normal
Absent
+
Histo-toxic Normal Normal Normal Normal Normal Less than
normal
Absent
+
3.
50. Detection of Hypoxemia
Numerous ways to measure whether oxygenation is impaired:
1. Arterial oxygen saturation (SpO2 & SaO2)
2. Arterial oxygen tension (PaO2)
3. A-a oxygen gradient
4. PaO2/FiO2 (P/F ratio)
5. a-A oxygen ratio
6. Oxygenation index
4.
51. Arterial Oxygen saturation:
SaO2 – direct measurement of the percent of oxyhemoglobin in
blood using lab tests on arterial blood.
SpO2 – non-invasive measurement of the percent of saturated
hemoglobin in the capillary bed using pulse-oximetry or
co-oximetry.
SpO2 does not measure the molecules like carboxyHb or
methHb.
4.
52. Oxygen content of arterial blood (CaO2) includes bound and
dissolved oxygen and is calculated as:
CaO2 = (1.34 x Hb concentration x SaO2) + (0.0031 x PaO2)
4.
Oxygen combined with Hb Oxygen dissolved in Plasma
53. Pulse Oximetry:
4.
Works on the principle of spectral analysis for measurement of oxygen saturation, i.e.
detection and quantification of components in solution by their unique light absorption
characteristics.
Light emitting diodes of red and infra-red lights – 660 & 940 nm wavelength
54. • The blood, tissue and bone at the site of application absorb much of the
light.
• Some light passes through the extremity which is sensed by the sensor
on the opposite side.
• By calculating the absorption at the 2 wavelengths, the processor can
compute the proportion of Hb which is oxygenated.
• Oximetry depends on the pulsatile flow and produces a graph of the
quality of flow.
• It measures the functional saturation (saturation of Hb capable of
carrying oxygen).
• It assumes that there are no non-functional Hb in the arterial blood and
measures the O2 saturation as:
% Saturation = HbO2 / HbO2 + Hb
4.
55. Arterial Oxygen tension (PaO2)
• Small amount of oxygen that diffuses from the alveolus into
the plasma.
• Measured by arterial blood gas.
• Normally at room air its value is >80 mmHg.
• Cannot be calculated by non-invasive method.
4.
56. A-a oxygen gradient:
• Alveolar to arterial oxygen gradient.
• It is the difference between the amount of oxygen in the
alveoli and the amount of oxygen in the plasma.
A-a oxygen gradient = PAO2 – PaO2
Alveolar gas equation:
4.
57. Normal A-a gradient varies with age:
A-a gradient = 2.5 + 0.21 x age in years
• A-a gradient increases with higher FiO2.
• With higher FiO2, both PAO2 & PaO2 increase.
• However, PAO2 increases disproportionately causing increase
in the gradient.
4.
58. P/F ratio:
• Most commonly used to measure oxygenation in ventilated
patients.
• Normal value – 300 to 500
• < 300: abnormal gas exchange
• < 200: Acute lung injury
• < 100: ARDS
4.
59. a-A oxygen ratio:
PaO2 / PAO2
It predicts the change in PaO2 that will result when the FiO2 is
changed.
Lower limit of normal: 0.77 – 0.82
Most reliable when FiO2 is less than 55%.
4.
60. Oxygenation Index:
• Used in the recent guidelines to grade the severity of ARDS
OI = (MAP x FiO2 / PaO2 ) x 100
• Normal: < 4
• Mild ARDS: 4 – 8
• Moderate ARDS: 8 – 16
• Severe ARDS: > 16
• Requires ECMO: > 20
4.