High altitude physiology involves several physiological responses to hypoxic conditions at increased elevations. Upon acute exposure to high altitude, hypoxic hypoxia causes peripheral chemoreceptors like the carotid bodies to stimulate hyperventilation and tachycardia to increase oxygen delivery. With long term exposure and acclimatization, erythropoiesis increases red blood cell count while higher 2,3-DPG levels reduce hemoglobin's oxygen affinity. Common altitude illnesses include acute mountain sickness, high altitude cerebral edema, and high altitude pulmonary edema, which are treated by descending or using supplemental oxygen. Chronic mountain sickness involves excessive polycythemia.
Altitude physiology typically focuses on people above 2500 m; ∼8000 ft. Altitudes above that are sometimes subdivided into very high (3500–5500 m; ∼11,500–18,000 ft) and extreme (>5500 m; >18,000 ft). An estimated 40 million people travel each year to altitudes >2500 m (∼8000 ft),1 and as many or more travel to altitude for leisure and sports, and work in mines, military or border operations, and the like. Altitude medicine considers the clinical disorders associated with acclimatization by the travelers, workers and migrants, and with adaptation by people with lifetimes or populations with millennia of residence (an estimated 83 million people).
With a hurried ascent, many (∼80%) will report a transient headache (high-altitude headache or [HAH]), and some will develop one of three forms of acute high-altitude illness: acute mountain sickness (AMS) and HAH, high-altitude cerebral edema (HACE), and high-altitude pulmonary edema (HAPE). AMS and HAH are annoying and interfere with activity and work, however, HACE and HAPE can be fatal with mortality rates approaching 30%. Among some residents, chronic mountain sickness (CMS) and right ventricular hypertrophy develop over months to years of residence at altitude. Birth weights are generally lower and the rate of small-for-gestational-age babies and congenital heart defects are higher than that in lowland populations.
Altitude physiology typically focuses on people above 2500 m; ∼8000 ft. Altitudes above that are sometimes subdivided into very high (3500–5500 m; ∼11,500–18,000 ft) and extreme (>5500 m; >18,000 ft). An estimated 40 million people travel each year to altitudes >2500 m (∼8000 ft),1 and as many or more travel to altitude for leisure and sports, and work in mines, military or border operations, and the like. Altitude medicine considers the clinical disorders associated with acclimatization by the travelers, workers and migrants, and with adaptation by people with lifetimes or populations with millennia of residence (an estimated 83 million people).
With a hurried ascent, many (∼80%) will report a transient headache (high-altitude headache or [HAH]), and some will develop one of three forms of acute high-altitude illness: acute mountain sickness (AMS) and HAH, high-altitude cerebral edema (HACE), and high-altitude pulmonary edema (HAPE). AMS and HAH are annoying and interfere with activity and work, however, HACE and HAPE can be fatal with mortality rates approaching 30%. Among some residents, chronic mountain sickness (CMS) and right ventricular hypertrophy develop over months to years of residence at altitude. Birth weights are generally lower and the rate of small-for-gestational-age babies and congenital heart defects are higher than that in lowland populations.
Gas exchange between the alveoli and the pulmonary capillary blood occurs by diffusion, as will be discussed in the next chapter. Diffusion of oxygen and carbon dioxide occurs passively, according to their concentration differences across the alveolar-capillary barrier. These concentration differences must be maintained by ventilation of the alveoli and perfusion of the pulmonary capillaries.
Alveolar ventilation brings oxygen into the lung and removes carbon dioxide from it. Similarly, the mixed venous blood brings carbon dioxide into the lung and takes up alveolar oxygen. The alveolar Image not available. and Image not available. are thus determined by the relationship between alveolar ventilation and pulmonary capillary perfusion. Alterations in the ratio of ventilation to perfusion, called the Image not available., will result in changes in the alveolar Image not available. and Image not available., as well as in gas delivery to or removal from the lung.
Alveolar ventilation is normally about 4 to 6 L/min and pulmonary blood flow (which is equal to cardiac output) has a similar range, and so the Image not available. for the whole lung is in the range of 0.8 to 1.2. Image not available. However, ventilation and perfusion must be matched on the alveolar-capillary level, and the Image not available. for the whole lung is really of interest only as an approximation of the situation in all the alveolar-capillary units of the lung. For instance, suppose that all 5 L/min of the cardiac output went to the left lung and all 5 L/min of alveolar ventilation went to the right lung. The whole lung Image not available. would be 1.0, but there would be no gas exchange because there could be no gas diffusion between the ventilated alveoli and the perfused pulmonary capillaries.
Oxygen is delivered to the alveolus by alveolar ventilation, is removed from the alveolus as it diffuses into the pulmonary capillary blood, and is carried away by blood flow. Similarly, carbon dioxide is delivered to the alveolus in the mixed venous blood and diffuses into the alveolus in the pulmonary capillary. The carbon dioxide is removed from the alveolus by alveolar ventilation. As will be discussed in Chapter 6, at resting cardiac outputs the diffusion of both oxygen and carbon dioxide is normally limited by pulmonary perfusion. Thus, the alveolar partial pressures of both oxygen and carbon dioxide are determined by the Image not available. If the Image not available. in an alveolar-capillary unit increases, the delivery of oxygen relative to its removal will increase, as will the removal ...
Non respiratory functions of lung ( The Guyton and Hall physiology)Maryam Fida
Besides primary function of gaseous exchange, the respiratory tract is involved in several non respiratory functions of the body
1. OLFACTION
Olfactory receptors present in the mucous membrane of nostril are responsible for olfactory sensation.
2. VOCALIZATION
Larynx alone plays major role in the process of vocalization. Therefore, it is called sound box.
3. PREVENTION OF DUST PARTICLES
Particles, which escape the protective mechanisms
in nose and alveoli are thrown out by cough reflex and sneezing reflex.
4. DEFENSE MECHANISM
Lungs play important role in the immunological defense system of the body.
Defense functions of the lungs are performed by their own defenses and
by the presence of various types of cells in mucous
membrane lining the alveoli of lungs.
These cells are
leukocytes,
macrophages,
mast cells,
natural killer
cells
dendritic cells.
5. MAINTENANCE OF WATER BALANCE
Respiratory tract plays a role in water loss mechanism.
During expiration, water evaporates through the
expired air and some amount of body water is lost by this process.
6. REGULATION OF BODY TEMPERATURE
During expiration, along with water, heat is also lost
from the body. Thus, respiratory tract plays a role in
heat loss mechanism.
5. MAINTENANCE OF WATER BALANCE
Respiratory tract plays a role in water loss mechanism.
During expiration, water evaporates through the
expired air and some amount of body water is lost by this process.
6. REGULATION OF BODY TEMPERATURE
During expiration, along with water, heat is also lost
from the body. Thus, respiratory tract plays a role in
heat loss mechanism.
I am a medical student. I have one friend who is persuing his MBBS degree in Taishan Medical UNiversity. I got these notes from him.
These notes are by Dr. Bikesh, He is a famous lecturer of TMU.
These notes have helped me a lot and i also watch his lecture videos , which are great; highly simple and huge content.
I am uploading with Renal physiology. If you want some other topics i would upload for you.
"Let the Knowledge be spread" Dr. Bikesh
Gas exchange between the alveoli and the pulmonary capillary blood occurs by diffusion, as will be discussed in the next chapter. Diffusion of oxygen and carbon dioxide occurs passively, according to their concentration differences across the alveolar-capillary barrier. These concentration differences must be maintained by ventilation of the alveoli and perfusion of the pulmonary capillaries.
Alveolar ventilation brings oxygen into the lung and removes carbon dioxide from it. Similarly, the mixed venous blood brings carbon dioxide into the lung and takes up alveolar oxygen. The alveolar Image not available. and Image not available. are thus determined by the relationship between alveolar ventilation and pulmonary capillary perfusion. Alterations in the ratio of ventilation to perfusion, called the Image not available., will result in changes in the alveolar Image not available. and Image not available., as well as in gas delivery to or removal from the lung.
Alveolar ventilation is normally about 4 to 6 L/min and pulmonary blood flow (which is equal to cardiac output) has a similar range, and so the Image not available. for the whole lung is in the range of 0.8 to 1.2. Image not available. However, ventilation and perfusion must be matched on the alveolar-capillary level, and the Image not available. for the whole lung is really of interest only as an approximation of the situation in all the alveolar-capillary units of the lung. For instance, suppose that all 5 L/min of the cardiac output went to the left lung and all 5 L/min of alveolar ventilation went to the right lung. The whole lung Image not available. would be 1.0, but there would be no gas exchange because there could be no gas diffusion between the ventilated alveoli and the perfused pulmonary capillaries.
Oxygen is delivered to the alveolus by alveolar ventilation, is removed from the alveolus as it diffuses into the pulmonary capillary blood, and is carried away by blood flow. Similarly, carbon dioxide is delivered to the alveolus in the mixed venous blood and diffuses into the alveolus in the pulmonary capillary. The carbon dioxide is removed from the alveolus by alveolar ventilation. As will be discussed in Chapter 6, at resting cardiac outputs the diffusion of both oxygen and carbon dioxide is normally limited by pulmonary perfusion. Thus, the alveolar partial pressures of both oxygen and carbon dioxide are determined by the Image not available. If the Image not available. in an alveolar-capillary unit increases, the delivery of oxygen relative to its removal will increase, as will the removal ...
Non respiratory functions of lung ( The Guyton and Hall physiology)Maryam Fida
Besides primary function of gaseous exchange, the respiratory tract is involved in several non respiratory functions of the body
1. OLFACTION
Olfactory receptors present in the mucous membrane of nostril are responsible for olfactory sensation.
2. VOCALIZATION
Larynx alone plays major role in the process of vocalization. Therefore, it is called sound box.
3. PREVENTION OF DUST PARTICLES
Particles, which escape the protective mechanisms
in nose and alveoli are thrown out by cough reflex and sneezing reflex.
4. DEFENSE MECHANISM
Lungs play important role in the immunological defense system of the body.
Defense functions of the lungs are performed by their own defenses and
by the presence of various types of cells in mucous
membrane lining the alveoli of lungs.
These cells are
leukocytes,
macrophages,
mast cells,
natural killer
cells
dendritic cells.
5. MAINTENANCE OF WATER BALANCE
Respiratory tract plays a role in water loss mechanism.
During expiration, water evaporates through the
expired air and some amount of body water is lost by this process.
6. REGULATION OF BODY TEMPERATURE
During expiration, along with water, heat is also lost
from the body. Thus, respiratory tract plays a role in
heat loss mechanism.
5. MAINTENANCE OF WATER BALANCE
Respiratory tract plays a role in water loss mechanism.
During expiration, water evaporates through the
expired air and some amount of body water is lost by this process.
6. REGULATION OF BODY TEMPERATURE
During expiration, along with water, heat is also lost
from the body. Thus, respiratory tract plays a role in
heat loss mechanism.
I am a medical student. I have one friend who is persuing his MBBS degree in Taishan Medical UNiversity. I got these notes from him.
These notes are by Dr. Bikesh, He is a famous lecturer of TMU.
These notes have helped me a lot and i also watch his lecture videos , which are great; highly simple and huge content.
I am uploading with Renal physiology. If you want some other topics i would upload for you.
"Let the Knowledge be spread" Dr. Bikesh
Changes in Respiratory System with Various Physiological ConditionsAnand Bansal
Topics - High-Altitude Physiology, Deep Sea Diving And Effects Of Increased Barometric Pressure, Changes In Respiratory System During Pregnancy, Physiological Changes Of Repiratory System With Exercise, Physiological Changes Of Respiratory System With Aging
Operation “Blue Star” is the only event in the history of Independent India where the state went into war with its own people. Even after about 40 years it is not clear if it was culmination of states anger over people of the region, a political game of power or start of dictatorial chapter in the democratic setup.
The people of Punjab felt alienated from main stream due to denial of their just demands during a long democratic struggle since independence. As it happen all over the word, it led to militant struggle with great loss of lives of military, police and civilian personnel. Killing of Indira Gandhi and massacre of innocent Sikhs in Delhi and other India cities was also associated with this movement.
How to Make a Field invisible in Odoo 17Celine George
It is possible to hide or invisible some fields in odoo. Commonly using “invisible” attribute in the field definition to invisible the fields. This slide will show how to make a field invisible in odoo 17.
Honest Reviews of Tim Han LMA Course Program.pptxtimhan337
Personal development courses are widely available today, with each one promising life-changing outcomes. Tim Han’s Life Mastery Achievers (LMA) Course has drawn a lot of interest. In addition to offering my frank assessment of Success Insider’s LMA Course, this piece examines the course’s effects via a variety of Tim Han LMA course reviews and Success Insider comments.
A Strategic Approach: GenAI in EducationPeter Windle
Artificial Intelligence (AI) technologies such as Generative AI, Image Generators and Large Language Models have had a dramatic impact on teaching, learning and assessment over the past 18 months. The most immediate threat AI posed was to Academic Integrity with Higher Education Institutes (HEIs) focusing their efforts on combating the use of GenAI in assessment. Guidelines were developed for staff and students, policies put in place too. Innovative educators have forged paths in the use of Generative AI for teaching, learning and assessments leading to pockets of transformation springing up across HEIs, often with little or no top-down guidance, support or direction.
This Gasta posits a strategic approach to integrating AI into HEIs to prepare staff, students and the curriculum for an evolving world and workplace. We will highlight the advantages of working with these technologies beyond the realm of teaching, learning and assessment by considering prompt engineering skills, industry impact, curriculum changes, and the need for staff upskilling. In contrast, not engaging strategically with Generative AI poses risks, including falling behind peers, missed opportunities and failing to ensure our graduates remain employable. The rapid evolution of AI technologies necessitates a proactive and strategic approach if we are to remain relevant.
The French Revolution, which began in 1789, was a period of radical social and political upheaval in France. It marked the decline of absolute monarchies, the rise of secular and democratic republics, and the eventual rise of Napoleon Bonaparte. This revolutionary period is crucial in understanding the transition from feudalism to modernity in Europe.
For more information, visit-www.vavaclasses.com
Embracing GenAI - A Strategic ImperativePeter Windle
Artificial Intelligence (AI) technologies such as Generative AI, Image Generators and Large Language Models have had a dramatic impact on teaching, learning and assessment over the past 18 months. The most immediate threat AI posed was to Academic Integrity with Higher Education Institutes (HEIs) focusing their efforts on combating the use of GenAI in assessment. Guidelines were developed for staff and students, policies put in place too. Innovative educators have forged paths in the use of Generative AI for teaching, learning and assessments leading to pockets of transformation springing up across HEIs, often with little or no top-down guidance, support or direction.
This Gasta posits a strategic approach to integrating AI into HEIs to prepare staff, students and the curriculum for an evolving world and workplace. We will highlight the advantages of working with these technologies beyond the realm of teaching, learning and assessment by considering prompt engineering skills, industry impact, curriculum changes, and the need for staff upskilling. In contrast, not engaging strategically with Generative AI poses risks, including falling behind peers, missed opportunities and failing to ensure our graduates remain employable. The rapid evolution of AI technologies necessitates a proactive and strategic approach if we are to remain relevant.
2. Hypoxia
•defined as deficiency of oxygen at the
tissue level. Types
• Hypoxic hypoxia
• Anemic hypoxia
• Stagnant hypoxia
• Histotoxic hypoxia
3. • Hypoxic hypoxia- PO2 of arterial
blood is reduced.
• Eg. high altitude, ascend rapidly to
3000m or 10,000 ft hypoxia develops
due to decline in alveolar PO2 to about
60mmHg.
4. Chemoreceptor- Carotid Bodies
• Special features
- receive unusually high blood flow
- high metabolic rate
• easily detect minor changes in P02, PC02 and pH of
blood.
-Type 1- glomus cells
-Type 2- sustentacular cells
• Glomus cells- chemosensitive cells,
neuroectodermal in origin, structurally resemble
chromaffin cells of adrenal medulla, cytoplasm
containing catecholamines.
• Dopamine is released from glomus cells in response to
hypoxia - acts on D2 receptors present on membrane
of 9th nerve ending and triggers AP in carotid sinus
nerve
5.
6. Hypoxia
• major stimulus for activation of
peripheral chemoreceptors.
• Mechanisms of less rise in ventilation when
PO2 falls from 100 to 60 mmHg:
-Hb is less saturated with 02- Oxy Hb is a
stronger acid- fall in arterial P02- fall in H+
inhibits respiration.
- Increased ventilation due to hypoxia
decreases PCO2 that in turn inhibits
ventilation.
• Response is most effective at P02 less
than 60 mm Hg- hypoxic drive.
7. • Hypoxia inhibits K+ channel.
• The accumulation of K+ in the glomus cell
results in depolarization activates voltage
gated Ca+
channels. ↑Ca influx causes
neurotransmitter secretion that stimulates
the afferent nerve.
• Mechanism: (inhibits K+ channels)
- Heme-containing protein loses its 02
- Hypoxia increases cAMP
- Hypoxia inhibits mitochondrial NADPH
oxidase
8. The French
physiologist Paul Bert
first recognized that
the harmful effects of
high altitude are
caused by low oxygen
tension.
9.
10. Mount Everest
29,028 ft (8848mt)
• Atmospheric
Pressure=255mm
Hg
• PO2= 53mmHg
• Inspired PO2
=44mmHg
Unacclimatized
person
• Unconscious in
45 seconds
• Dead in 4 to 6 mins
11. Physiologic changes in High
Altitude
I) Acute responses (accommodation)
II)Long term responses (acclimatization)
Accomodation
• Refers to immediate reflex adjustments of
respiratory and cardiovascular system to
hypoxia
Acclimatization
• Refers to changes in body tissues in
response to long term exposure to hypoxia
12. Accommodation at high altitude
Immediate reflex responses of the body to acute
hypoxic exposure.
Hyperventilation
• Decrease arterial PO2 → stimulation of peripheral
chemoreceptors → increased rate & depth of
breathing
Tachycardia
• Also stimulate peripheral chemo. receptors →
increase Cardiac output → increase oxygen
delivery to the tissues.
Increased 2,3-DPG conc. in RBC
• within hours, ↑deoxy-Hb conc. → locally ↑pH → ↑2,3-
DPG
13. Acclimatization at high altitude
• Various physiological readjustments and
compensatory mechanisms in body that
reduces the effects of hypoxia in
permanent residents at high altitude.
14.
15. RESPONSES TO HYPOBARIC HYPOXIA
Ventilatory Adaptations
• Hyperventilation - ↓alveolar CO2 in order
to
↑PAO2
• Sensor- Carotid body- afferent activity
↑, PaO2 falls <60 mm Hg.
• stimulated by decreasing the
[ATP]/[ADP][Pi] ratio.
17. THE PULMONARY CIRCULATION
• Moderate-to-severe pulmonary
hypertension
• supplied with sympathetic &
parasympathetic fibers- regulation of
vasomotor tone
• altitude is a model of whole lung
hypoxic, hypocapnic pulmonary
vascular vasoconstrictive responses
18. FLUID HOMEOSTASIS
• Dermal edema is seen in faces
• Pulmonary edema, cerebral edema,
and peripheral edema are the
hallmarks of disease.
19. ERYTHROPOIESIS AND HEMOGLOBIN
AFFINITY
• ↑ RBC occurs -acute exposure ↑ in
EPO synthesis in response to HIF-1
and HIF-2
• ↑ ventilation- ↓ PACO2, PaCO2 and arterial
[H+]; concomitantly, serum levels of 2,3-DPG
↑
• While the reductions in PaCO2 and [H+] –
↑ hemoglobin affinity for O2, ↑ in 2,3-DPG
diminish the affinity.
20. COMMON CLINICAL DISORDERS OF
HIGH ALTITUDE
• HIGH-ALTITUDE HEADACHE
• ACUTE MOUNTAIN SICKNESS
• HIGH-ALTITUDE CEREBRAL
EDEMA
• HIGH-ALTITUDE PULMONARY
EDEMA
• CHRONIC MOUNTAIN
SICKNESS
21. HIGH-ALTITUDE HEADACHE
• very common
• exacerbated by insufficient hydration in
the setting of increased water loss with
hyperventilation, overexertion, and
insufficient energy intake
• Vasodilation may also contribute.
• Acetaminophen or ibuprofen with
hydration will improve this symptom
22.
23. ACUTE MOUNTAIN SICKNESS
• occurs after 4 to 36 hours of
altitude exposure.
• headache (usually frontal), nausea,
vomiting, irritability, malaise, insomnia,
and poor climbing performance.
• Sleep-disordered breathing
• self-limited
26. ACUTE MOUNTAIN SICKNESS
• most common and useful self
administered - determine the severity of
AMS.
• 1 (mild)
• 4 (severe)
• 10 and > (very severe)-
immediate intervention
27. ACUTE MOUNTAIN SICKNESS
Risk Factors
• the altitude and speed of ascent
• Old age
• history of migraine, persistence of a
patent foramen ovale, Down syndrome,
congenital pulmonary abnormalities,
perinatal pulmonary vascular insult, and
Holmes–Adie syndrome, a rare disorder
of autonomic control.
29. ACUTE MOUNTAIN SICKNESS
Preacclimatization in hypobaric
chambers and normobaric hypoxic rooms
- risk of acquiring altitude illness.
• key element- elevation change per day to
less than 400 m/d.
Prophylactic administration
• acetazolamide (250 mg at bedtime or 125
mg bid)
• Corticosteroids (dexamethasone at a dose
of 4 mg every 6 hours)
30. ACUTE MOUNTAIN SICKNESS
• sildenafil and tadalafil
• Adequate hydration -2 L of extra fluid per
day is a common rule of thumb.
• A suggested rule is that above 3000 m
(10,000 ft), ascent should be at a rate less
than 300 m (1000 ft) per day, with a “rest”
day (i.e., no additional ascent) every 3
days.
31. ACUTE MOUNTAIN SICKNESS
Treatment
• self-limiting and usually lasts about 3
days- not mandatory.
• Descend
• Acetazolamide- first-line
treatment; dexamethasone
• Temazepam is effective in reducing
recurrent central apnea.
32. HIGH-ALTITUDE CEREBRAL EDEMA
Symptoms
• Dizziness
• Severe unbearable headache
• Vomiting
• Ataxia
• Positive Romberg sign
• Somnolence, stupor, and changes in
pupillary responsiveness- onset of a fatal
stage.
• coma and mortality
34. Awaiting Evacuation
• Supplemental oxygen.
• portable hyperbaric chamber- life-saving.
• Dexamethasone (4–8 mg), IM in severe
cases, or orally in less severe cases-
reduce cerebral edema (repeated every 6
hrs)
36. HIGH-ALTITUDE PULMONARY EDEMA
• symptoms are like pulmonary edema at
sea level.
• Prevalence 0.5% to 2.0%
Mechanism
• migration of fluid into extravasal space
through endothelial damage along with
shear stresses produced by increased
cardiac output and pulmonary artery
pressure.
38. HIGH-ALTITUDE PULMONARY EDEMA
Prevention
• Nifedipine prophylactically (SR 20 mg twice
daily prior to ascent, then three times daily)-
smooth muscle relaxation.
• inhaled β-agonist
Treatment
• Descent is critical for survival
• Nifedipine (10 mg sublingually)
• sildenafil and tadalafil
• portable hyperbaric chamber
39. CHRONIC MOUNTAIN SICKNESS
or Monge's disease
• Excessive erythrocytosis associated with a lower oxygen
saturation and hypoxic ventilatory response with relative
hypercapnia are the main features of CMS
• defining feature is extreme polycythemia, with Hb conc., > 23
g/dL & hematocrits >83%.
• Poor exercise tolerance.
• Patients may have vague neuropsychological complaints-
• Headache,
• Dizziness,
• Somnolence,
• Fatigue,
• Difficulty in concentration,
• Loss of mental acuity,
• Irritability, Depression, Hallucinations
40. CHRONIC MOUNTAIN SICKNESS
• more common in males, middle & later
life.
• Descent to sea level is the
definitive treatment.
• Phlebotomy and administration
of supplemental oxygen are
beneficial
• Medroxyprogesterone - some success
• Acetazolamide – lacking in prevention.
