This document discusses various disturbances of respiration, including abnormal respiratory patterns, apnea, dyspnea, periodic breathing, hypoventilation, hyperventilation, and disturbances related to respiratory gases. It provides definitions and descriptions of these conditions, their causes, types, symptoms, and physiological mechanisms. Key topics covered include eupnea, tachypnea, bradypnea, polypnea, voluntary apnea, deglutition apnea, hypoventilation, hyperventilation, Chyne-Stokes breathing, Biot's breathing, hypoxia, cyanosis, and the physiological effects and treatment of oxygen therapy.
Respiratory Distress in the Small Animal Patientupstatevet
Danielle Berube, DVM, DACVECC
This presentation will review the many differentials for patients presenting in respiratory distress. The lecture will be organized based on anatomic locations within the airway, including upper airway disorders, pulmonary causes of respiratory distress, and diseases of the pleural space. Within each section, we will focus on the physical examination findings, diagnostic options to localize the disorder, and stabilization techniques for the patient. We will also discuss less common causes of respiratory distress such as acute lung injury (ALI), acute respiratory distress syndrome (ARDS), transfusion related acute lung injury (TRALI) and even some examples of nonrespiratory look-alikes.
Respiratory Distress in the Small Animal Patientupstatevet
Danielle Berube, DVM, DACVECC
This presentation will review the many differentials for patients presenting in respiratory distress. The lecture will be organized based on anatomic locations within the airway, including upper airway disorders, pulmonary causes of respiratory distress, and diseases of the pleural space. Within each section, we will focus on the physical examination findings, diagnostic options to localize the disorder, and stabilization techniques for the patient. We will also discuss less common causes of respiratory distress such as acute lung injury (ALI), acute respiratory distress syndrome (ARDS), transfusion related acute lung injury (TRALI) and even some examples of nonrespiratory look-alikes.
It is a short description or short notes on ards, know we can easily know about this superficially.
It is a condition where in the alveoli, the alveoli is filled with fluid and then the gas exchange can't be done properly..
Oxygen therapy has been in use for centuries. Oxygen)(O2) is gas used as a drug/medication and a such should be prescribed and administered in the right manner with regards to presenting indications for it's use[1]; which is always in the case of hypoxaemia[2]. It has side effects and specific risks, but, with objective monitoring and administration, it is a potent therapy for the patient with respiratory condition
Other indications include:
Increased work of breathing
Increased myocardial work and/or Myocardial infarction
Pulmonary hypertension[5]
Pre-oxygenation in induction and difficult intubation.
Pre and post suctioning[6]
Postoperative oxygenation especially in abdominal and chest surgeries[7]
Hyperbaric oxygen therapy indicated in decompression sickness, gas embolism, gas gangrene and carbon monoxide poisoning.
Anaemic Hypoxia : it’s benefits is limited due circulatory deficit[8].
In aerosol drug delivery.
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.
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
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.
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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
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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
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.
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.
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.
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.
3. ABNORMALITY
RESPIRATORY PATTERN.
Eupnoea – normal rate, rhythm & depth
Tachypnoea - increase in the rate of respiration
Bradypnoea - increase in the rate of respiration
Polypnoea - the rapid but shallow breathing
resembling panting in dogs
Tuesday, August 25, 2020
4. ABNORMALITY
RESPIRATORY PATTERN.
Apnoea - temporary cessation of breathing.
Hypoventilation - Decrease in the rate and force
of respiration.
Hyperventilation - Increase in the rate as well as
force of respiration.
Tuesday, August 25, 2020
5. ABNORMALITY RESPIRATORY
PATTERN.
Hyperpnoea - A marked increase in the
pulmonary ventilation due to an increase in rate
and/or force of respiration.
Dyspnoea. When hyperpnoea involves four to
five fold increase in the pulmonary ventilation, an
unpleasant sensation or discomfort is felt.
Periodic breathing - Respiratory pattern
characterized by alternate periods of respiratory
activity and apnoea.
Tuesday, August 25, 2020
7. Voluntary apnoea
Temporary arrest of breathing due to the
voluntary control of respiration also called
breath-holding.
The breath-holding time or apnoea time -- 40−60
s in a normal person, after a deep inspiration.
Tuesday, August 25, 2020
8. Voluntary apnoea
Breaking point is the point at which breathing
can no longer be voluntarily inhibited.
At this point, chemical regulation overcomes the
neural regulation due to an increased arterial
pCO2 and a decreased pO2
Tuesday, August 25, 2020
9. After hyperventilation
Reduced stimulation of respiratory centre
owing to CO2 wash caused by
hyperventilation
Tuesday, August 25, 2020
10. Degluttion apnoea
reflexly during swallowing
(about 0.5 s)
Pharyngeal
phase
• During of swallowing, The fluid or food stimulates the sensory nerve
endings (5th, 9th and10th cranial nerves) around the pharynx.
• Nerve impulses from these irritant receptors, via the swallowing centres
• specifically inhibit the respiratory centre, stopping the breathing at any
point of the cycle
• Deglutition apnoea - Prevent aspiration of fluid or food into the lungs
Tuesday, August 25, 2020
11. Breath holding attacks
Brief period of apnoea
which occur in infants
and young children
and are generally
precipitated by an
emotional distress.
Tuesday, August 25, 2020
13. Sleep apnoea.
The cessation of
breathing for a brief
period (10 s) during
sleep in a normal
individual
Tuesday, August 25, 2020
14. HYPOVENTILATION
A decrease in the rate and force of respiration.
The amount of air moving in and out of lungs is
reduced.
Causes :
Depression of respiratory centres by some drugs.
Partial paralysis of respiratory muscles.
Tuesday, August 25, 2020
15. HYPOVENTILATION
Effects :
Hypoventilation leads on to hypoxia and hypercapnia
(respiratory acidosis), which result in an increase in
rate and force of respiration and the patient may
develop dyspnoea.
Tuesday, August 25, 2020
16. HYPERVENTILATION
An increase in the rate & force of respiration.
The amount of air moving in and out of lungs
is increased.
Causes of hyperventilation are:
During exercise due to stimulation of respiratory
centres by increased pCO2.
Voluntary hyperventilation and
Secondary to hypoxia.
Tuesday, August 25, 2020
17. DYSPNOEA
Difficulty in breathing.
When hyperpnoea involves four to five fold
increase in pulmonary ventilation, an
unpleasant sensation or discomfort is felt.
This type of respiration is called dyspnoea.
Dyspnoea point – height of hyperpnoea at
which dyspnoea appears.
Tuesday, August 25, 2020
18. Predisposing factors
Low vital capacity
Maximum ventilatory volume (MVV) - Patients with
reduced MVV, (Normal value is 120 L/min) are more
predisposed to get dyspnoea.
Breathing reserve (BR) is the difference between
MVV and respiratory minute volume (RMV).
Tuesday, August 25, 2020
19. Predisposing factors
RMV is the volume of air that is taken in or
given out per minute (Normal 500 × 12 = 6
L/min).
Individuals with increased RMV (also called
pulmonary ventilation) by four to five times
get dyspnoea.
Tuesday, August 25, 2020
20. Predisposing factors
Individuals with less breathing reserve are more
prone to get dyspnoea.
BR = MVV − RMV = 114 L/min
Dyspnoeic index (DI) refers to the breathing
reserve percentage of MVV, i.e.
Tuesday, August 25, 2020
21. Predisposing factors
DI = BR × 100/MVV = 100 × 100/120 = 95%
Normal value of DI range from 70% to 95%
Dyspnoea occurs when DI is < 60%.
Tuesday, August 25, 2020
22. Causes
Physiological - severe muscular exercise.
Pathological-
Respiratory disorders, such as bronchial
asthma,emphysema, pneumonia, pulmonary oedema
andpenumothorax, and
Cardiac failure.
Tuesday, August 25, 2020
23. Causes
Metabolic disorders causing dyspnoea are diabetic
acidosis, uraemia and increased H+
concentration.
Metabolic acidosis causes dyspnoea by increasing
the pulmonary ventilation.
Tuesday, August 25, 2020
24. PERIODIC BREATHING.
Characterized by the alternate periods of
respiratory activity and apnoea.
Chynes stokes breathing
Biot’s breathing.
Tuesday, August 25, 2020
25. CHYNES STOKES BREATHING
Periodic type of
breathing in which the
alternate periods of
respiratory activity and
apnoea occur at regular
intervals and
Tuesday, August 25, 2020
26. CHYNES STOKES BREATHING
During the period of
respiratory activity
there is waxing and
waning of tidal volume.
Tuesday, August 25, 2020
27. Causes
Physiological
Voluntary
hyperventilation,
High altitude and
During sleep in some
normal individuals
especially infants.
Pathological
Chronic heart failure,
Brain damage,
Uraemia and
Poisoning by
narcotics.
Tuesday, August 25, 2020
28. Mechanism of development.
Voluntary hyperventilation
Heart failure.
Left ventricular failure → Pulmonary
congestion →Hypoxia → Stimulation of
respiratory centres → Increased ventilation
→ Increased alveolar pO2 and decreased
pCO2 → Decreased arterial pCO2.
Tuesday, August 25, 2020
29. Mechanism of development.
As in heart failure circulation time is prolonged, so
it takes longer than normal time for the blood with
low pCO2 to reach the brain and cause apnoea by
inhibiting respiratory centre.
Tuesday, August 25, 2020
30. Mechanism of development.
Since in heart failure the pulmonary congestion is
continuously present, so hypoxia is maintained and
the above described cycle of apnoea followed
respiratory activity that keeps on repeating till the
heart failure is treated or alveolar pCO2 comes back
to normal.
Tuesday, August 25, 2020
31. Brain damage
Increased sensitivity of central
chemoreceptors to CO2 → Hyperventilation
→ CO2 washout → Apnoea → Accumulation
of CO2 → Increased pCO2 →Hyperventilation
→ Cycle of respiratory activity and apnoea
continues.
Tuesday, August 25, 2020
32. BIOT’S BREATHING.
Ataxic breathing is a
type of periodic
breathing showing
alternate periods of
respiratory activity
and apnoea.
Tuesday, August 25, 2020
33. BIOT’S BREATHING.
Characteristics
It occurs at irregular
intervals,
There is no waxing and
waning of tidal volume
during the period of
respiratory activity and
It can never occur
physiologically.
Tuesday, August 25, 2020
34. Causes.
when medulla is involved in disorders, such
as meningitis, head injury, medullary
compressions like pontine haematomas or
cerebellopontine herniation.
Most common cause - Central medullary
lesions
So, it is rare in cerebral ischaemia, which has
to be bilateral to infarct the central medulla
Tuesday, August 25, 2020
38. Causes
Decreased oxygen tension (pO2) of the
arterial blood,
Decreased oxygen carrying capacity of the
blood,
Decreased rate of blood flow to the tissue or
Decreased utilization of oxygen by the tissue
cells.
Tuesday, August 25, 2020
39. Types
Hypoxic hypoxia,
Anaemic hypoxia,
Stagnant hypoxia and
Histotoxic hypoxia.
Tuesday, August 25, 2020
40. Symptoms
It depends upon
Rapidity of
development of
hypoxia,
Severity of hypoxia
and
Effectiveness of the
body’s compensatory
mechanisms.
Tuesday, August 25, 2020
42. Fulminant
A severe hypoxia developing very fast, i.e.
which occurs within seconds after exposure
to an arterial O2 tension of less than 20 mm
Hg.
Tuesday, August 25, 2020
43. Fulminant
It results in: Unconsciousness within 15–20 s
due to lack of O2 supply to brain and Brain
death may follow in 4–5 min.
Tuesday, August 25, 2020
44. Acute
By exposure to arterial
O2 tensions of 25–40
mm Hg (e.g. as would
occur at altitudes of
18,000−25,000 ft).
Symptoms
Lack of co-ordination,
Slowed reflexes,
Slurring of speech,
Overconfidence and
eventually,
Unconsciousness, coma
& death.
Tuesday, August 25, 2020
45. CHRONIC
Due to the exposure to
low pO2 (40−60 mm
Hg) for long periods
(e.g. as would occur
after stay for extended
period of time at
altitudes of
approximately
10,000−18,000 ft)
Symptoms
Severe fatigue,
Dyspnoea,
Shortness of breath,
Respiratory
arrhythmias (e.g.
Cheyne–Stokes
breathing).
Tuesday, August 25, 2020
46. Signs of hypoxia
Cyanosis
Tachycardia
Tachypnoea
Tuesday, August 25, 2020
47. Cyanosis
Bluish discolouration of
skin and mucous
membrane caused by
the presence of more
than 5 g of
deoxyhaemoglobin/100
mL of the capillary
blood.
Tuesday, August 25, 2020
48. Cyanosis is not a reliable sign
of hypoxia
Anaemic patients may never develop cyanosis,
because of an inadequate haemoglobin
concentration.
Cyanosis does not occur in histotoxic hypoxia
either because the O2 saturation of haemoglobin
is normal.
Tuesday, August 25, 2020
49. Cyanosis is not a reliable sign
of hypoxia
In contrast, patients with polycythaemia may be
cyanotic as a result of high concentration of
haemoglobin, even though their tissues are
adequately oxygenated and further.
Methaemoglobin, with its slate-grey colour, can
also impart a bluish colour to tissues
Tuesday, August 25, 2020
50. Tachycardia
Occurs as a peripheral
chemoreceptor reflex
response to the low
arterial oxygen tension
Tuesday, August 25, 2020
51. Tachypnoea
Presents in the hypoxic hypoxia where arterial
pO2 is low, but absent in both anaemic hypoxia
and
Stagnant hypoxia in which the arterial pO2 is
normal
Tuesday, August 25, 2020
53. Physiological basis of oxygen
therapy in hypoxia
O2 therapy is not of much help in treatment
of hypoxia because diffusion across
respiratory membrane depends upon the
partial pressure of gases, so alveolar pO2 can
be increased by:
Inhalation of 100% pure oxygen or
Inhalation of 100% pure oxygen at high barometric
pressure
called hyperbaric oxygen therapy
Tuesday, August 25, 2020
54. Oxygen therapy with 100% pure oxygen at
atmospheric pressure, i.e. at 760 mm Hg
Oxygen therapy is useful
In atmospheric hypoxia,
In hypoventilation hypoxia and
In hypoxia due to an impaired respiratory
membrane diffusion.
Tuesday, August 25, 2020
55. Oxygen therapy with 100% pure oxygen at
atmospheric pressure, i.e. at 760 mm Hg
Oxygen therapy is of limited value
In an anaemic hypoxia, stagnant hypoxia and
hypoxic hypoxia caused by the physiological or
anatomical shunts.
Tuesday, August 25, 2020
56. Oxygen therapy with 100% pure oxygen at
atmospheric pressure, i.e. at 760 mm Hg
Oxygen therapy is of no use in the histotoxic
hypoxia because in this type of hypoxia, the tissue
metabolic enzyme system is simply incapable of
utilizing the oxygen that is delivered.
Tuesday, August 25, 2020
57. Hyperbaric oxygen therapy (inhalation of
100% pure
oxygen at high barometric pressure)
Advantages - increases the amount of dissolved
O2 in plasma and is therefore unaffected by the
haemoglobin concentration.
Tuesday, August 25, 2020
58. Indications of hyperbaric O2
therapy
ACarbon monoxide poisoning
Anaemic hypoxia (due to severe anaemia)
Decompression sickness and air embolism
Wounds with poor blood supply
Stagnant hypoxia (very limited value)
Tuesday, August 25, 2020
59. Side effects of 100% O2 (O2
toxicity)
Due to the conversion of molecular oxygen
into active oxygen, i.e. superoxide anion (O–2),
which is free radical, and H2O.
Irritation of airways
Bronchopneumonia
Nervous system complication
Tuesday, August 25, 2020
60. Complications in newborn
infants
Retinopathy of prematurity (old name
retrolental fibroplasia),
Retinal neovascularization and proliferation of
fibrovascular tissue ultimately forming an opaque
retrolental mass, leading to bilateral permanent
blindness.
Tuesday, August 25, 2020
61. Complications in newborn
infants
Bronchopulmonary dysplasia is
characterized by the formation of lung cysts
and opacities.
Tuesday, August 25, 2020
62. HYPERCAPNIA.
An increase in the arterial pCO2 (normal
value 40 mm Hg) associated with the
respiratory acidosis
Tuesday, August 25, 2020
63. Causes
Defective elimination of CO2 as occurs in:
Reduced pulmonary ventilation and
Reduced effective alveolar ventilation
Accidental inhalation of CO2 in persons working
in breweries and refrigeration plants.
Tuesday, August 25, 2020
64. Signs & symptoms
Hyperpnoea -- Due to the stimulation of
respiratory centre through central
chemoreceptors.
Carbon dioxide narcosis develops when
arterial pCO2 increases above 50 mm Hg.
Tuesday, August 25, 2020
65. HYPOCAPNIA
Reduced pCO2 is usually associated with
respiratory alkalosis,
Causes.
Hypocapnia occurs due to hyperventilation
Tuesday, August 25, 2020
66. ASPHYXIA
Condition in which hypoxia (decreased pO2)
is associated with hypercapnia (increased
pCO2).
Causes
Strangulation,
Drowning,
Acute tracheal obstruction (due to entry of food or
due to choking) and
Paralysis of diaphragm as in acute poliomyelitis.
Tuesday, August 25, 2020
67. Clinical stages of acute
asphyxia
Stage I – stage of Hyperpnoea
Stage II – stage of central excitation
Stage III – stage of central depression.
Tuesday, August 25, 2020
68. Stage I – stage of Hyperpnoea
last for 1 min.
Increase in the rate and depth of respiration
with more pronounced expiratory effort,
Dyspnoea, cyanosis and sudden prominence
of eyeballs.
Tuesday, August 25, 2020
69. Stage I – stage of Hyperpnoea
last for 1 min.
Occurs due to sudden and powerful stimulation of
respiratory centres by acutely occurring rise in
pCO2.
O2 lack is not yet enough to stimulate ventilation.
Tuesday, August 25, 2020
70. Stage II – stage of central excitation
lasts for 1 min.
Occurs due to excess CO2 stimulating the centres
directly and lack of O2 stimulating the centres
reflexly
Expiration becomes more violent,
Heart rate is increased,Systemic blood pressure
rises due to widespread
Tuesday, August 25, 2020
71. Stage II – stage of central excitation
lasts for 1 min.
Vasoconstriction, Pupils are constricted,
All the reflexes are exaggerated,
Convulsions occur due to excess of pCO2 and
Consciousness is lost.
Tuesday, August 25, 2020
72. Stage III – stage of central
depression.
Occurs due to direct effect of O2 lack on vital
centres causing their inhibition.
Convulsions disappear,
Respiration becomes slow and finally it becomes
gasping (shallow and with low frequency),
Tuesday, August 25, 2020
73. Stage III – stage of central
depression.
Heart rate is decreased,Blood pressure falls,
Pupils are dilated, All the reflexes are abolished,
The whole body lies still, Duration between the
gasps is gradually increased and Finally, the death
occurs
Tuesday, August 25, 2020
74. DROWINING
Asphyxia - cause of death in only 10% cases of
drowning.
occurs initially due to breath-holding and after
the breaking in effect due to the severe
laryngospasm induced by first gasp of water
Tuesday, August 25, 2020
75. DROWINING
Flooding of lungs with water - occurs
in 90% cases of drowning.
The muscles of glottis relax and allow entry of
water into the lungs
Tuesday, August 25, 2020
76. Types of drowning
Fresh water drowning is associated with
rapid absorption of water (since it is
hypotonic) into the circulation, which causes
plasma dilution and intravascular haemolysis.
Sea water drowning is associated with
hypovolaemia due to draining of water from
the circulation into the lungs (since the sea
water is hypertonic).
Tuesday, August 25, 2020
77. CARBON MONOXIDE
POISONING
Gas present in exhaust of gasoline engines,
coal mines, gases from deep wells and
underground drainage systems.
Toxic effects - Anaemic hypoxia and
derangement of cellular metabolic system.
Tuesday, August 25, 2020
78. CARBON MONOXIDE
POISONING
Anaemic hypoxia- Carbon monoxide having 200
times more affinity than O2 for haemoglobin
combines with it to form carboxyhaemoglobin
It does not allow the haemoglobin to take up
oxygen from the alveolar air and The presence of
carboxyhaemoglobin decreases the release of
oxygen from haemoglobin
Tuesday, August 25, 2020
79. Symptoms of CO poisoning
Headache and nausea
Loss of consciousness
Death may occur when Haemoglobin is 50%
saturated with CO.
Tuesday, August 25, 2020
80. Treatment of CO poisoning
Immediate termination of exposure to carbon
monoxide,
Immediate hyperbaric 100% O2 therapy and
Administration of air with few percent of CO2 to
stimulate the respiratory centres.
Tuesday, August 25, 2020