3. Why artificial respiration?
To maintain vitality of the nerve centers, heart
To maintain circulation
To stimulate respiratory centers
To help respiratory centers to take-up their own
spontaneous rhythm
5. Schafer’s method
Subject is laid in prone position
Pillow is placed underneath the chest
Head is turned to one side
Operator kneels down by the side of subject facing
towards his head
Two hands are placed on the two sides of the lower part
of the chest
Operator puts his body weight leaning forwards and
presses the loins of the subject
6. Schafer’s method
Increase in the intra-abdominal pressure
Diaphragm pushed up
Air is forced out of lungs
Operator releases the pressure and comes back to erect
position
Abdominal pressure falls
Diaphragm descends
Air enters the lungs (procedure repeated for 12 times a
minute)
8. Sylvester’s method
Subject placed in supine position
Operator kneels at the head end
Holds the two arms of subject
Operator raises the subject’s hands above the head
Folds the hands back upon the chest
Compressing the chest wall
Repeat the movements
Air enters and leaves lungs
10. Holger-Neilson method
Subject placed in prone position
Arms abducted at the shoulders
Elbows remain flexed
Face is turned to one side and rests on hands
Mouth is cleaned after wiping out mucus
Operator kneels down in front of subject facing towards
head
Two hands placed on two sides of the back of the chest
Operator puts his weight on subjects back by leaning
forward – compression of chest – expiration
11. Holger-Neilson method
Subject arms forwards by holding them above the
elbows
Helps in natural inspiration
Process repeated for 10-12 times a minute
13. Mouth-to-mouth method
Subject is laid in the supine position with extended head
Operator sits by side of subjects head
Operator holds the lower jaw of subject by one thumb
and index finger
Clamps the nostrils with the other thumb and index finger
Operator keeps his mouth over the subjects mouth and
exhales forcibly
Inflation of lungs and thorax (positive pressure breathing)
Operator takes off his mouth
Process repeated 10-20 times for minute
14. Eve’s rocking method
Patient tied on a stretcher
Head and feet are alternatively tilted through an
angle of 45 degrees
8-9 movements are carried out per minute
7 seconds per each movement
4 seconds head down - expiration
3 seconds feet down - inspiration
16. Instrumental methods
Negative pressure breathing – alternatively
compressing and relaxing chest wall
Positive pressure breathing – introducing oxygen
directly into the lungs
17.
18.
19. Normal Pressures
Normally atmospheric pressure or barometric
pressure is about 760 mmHg
Out of this, contribution of oxygen is 21% that is
pressure of oxygen is 160 mmHg (out of 760 mmHg)
Alveolar PO2 is 104 mmHg
As per diffusion, the PO2 should be same in
atmosphere and alveoli. Why it is not same?
20. What happens in high altitudes
Pressure of oxygen in the atmosphere drops (less
than 160 mmHg)
Imagine it becomes 130 mmHg
PO2 of alveoli decreases significantly
Imagine it may decrease to 60 mmHg or less
What is the problem??
21. PO2 at high altitude
1. Atmospheric PO2 is 130 mmHg
2. Alveolar PO2 is 60 mmHg
3. PO2 of the Blood entering the lungs is 40 mmHg
4. PO2 of the Blood leaving the lungs is 60 mmHg
5. This is called hypoxemia - abnormally low level of
oxygen in the blood.
22. Effect of hypoxemia
When PO2 less than 60 mmHg (stimulus)
Stimulation of peripheral chemo receptors
Inactivation of potassium channels
Opening of calcium channels
Release of neurotransmitter
Stimulation of nerves (cranial nerves IX and X)
Sends signals to respiratory centers
increase in the frequency of motor signals
23. Effect of hypoxemia
Increase in the frequency of stimulation of
diaphragm
Increase in the contraction
Increase in alveolar ventilation
Increase in the rate and depth of respiration
Tries to bring more air in
Imagine it increases PO2 to 80 mmHg
24. PO2 after hypoxemia effect
1. Atmospheric PO2 is 130 mmHg
2. Alveolar PO2 is 80 mmHg
3. PO2 of the Blood entering the lungs is 40 mmHg
4. PO2 of the Blood leaving the lungs is 80 mmHg
25. What happens to stimulus to
PCR?
1. When alveolar PO2 is 80 mmHg
2. PO2 of the Blood entering the lungs is 40 mmHg
3. PO2 of the Blood leaving the lungs is 80 mmHg
4. The movement PO2 increases to 80 mmHg, the
stimulus to PCR goes away
5. No stimulation to DRG and respiration slowdown
26. PCO2 at high altitude
1. As we move to high altitudes, PCO2 also decreases
slightly
2. Say Atmospheric PCO2 decreased to 25 mmHg
3. Alveolar PCO2 is 25 mmHg
4. PCO2 of the Blood entering the lungs is 45 mmHg
(pressure gradient increased)
5. PCO2 of the Blood leaving the lungs is 25 mmHg (more
CO2 goes out)
6. PCO2 decreases in the blood (very bad??)
28. CO2 – Normal Mechanism
CO2 easily cross Blood brain barrier
When PCO2 increases in interstitial fluid of medulla
and CSF, the CO2 reacts with water of the tissues and
forms carbonic acid
Carbonic acid dissociates and releases hydrogen ions
Hydrogen ions stimulates the chemo sensitive area
and thus respiration
29. CO2 –Mechanism at high altitude
PCO2 decreases
Decrease in H+ ions
Inhibition of central chemo receptors
Inhibition of DRG
Inhibition of VRG
Decrease in the frequency of action potentials
Decrease in the alveolar ventilation
Decrease in the rate and depth of respiration
30. What is happening
Initially there is hypoxemia
Increase in ventilation
Brings PO2 back to normal
In this process more CO2 moves out
PCO2 decreases
Inhibition of CCR
Decrease in the ventilation
OPPOSITE ACTIONS
31. Lost more CO2 from body?
If we breath out more CO2
Respiratory alkalosis
PH is very high due to low PO2
32. How your body deals this condition?
Acclimatization
Kidney comes into the role
kidney consists of intercalated cells
When PH increases in blood (decrease in H+ ions)
Intercalated cells pumps H+ ions out (into blood)
Increase in H+ ions (PH back to normal)
Stimulation of CCR
Stimulation of respiratory centers
Increase in the rate and depth of respiration
33. Is this enough?
No …. Not enough
Kidney again comes into the role
When the PO2 decreases (hypoxia)
When PH increases in blood (decrease in H+ ions)
Hypoxia inducing factor is released from PCT
Production of hormone - erythropoietin
Stimulation of bone marrow
Increase in RBC (polycythemia) – increase in HB
Increase in oxygen carrying capacity
34. Is this enough?
No …. Not enough
Due to polycythemia there is increase in the
perfusion
Due to hypoxemia there is increase in the
ventilation
Increase in ventilation and perfusion
Good V/P coupling there
Efficient gaseous exchange
35. Is this enough?
Yes for short periods stay
If stay for longer periods angiogenesis takes place
Angiogenesis - formation of new blood vessels
36. Angiogenesis
In high altitude PO2 decreases
Less oxygen supply to tissues
Endothelial cells of blood vessels releases
vascular endothelial growth factor (VGF)
Sprouts blood vessels
More blood vessels
Angiogenesis
37. Is this enough?
If stay still very longer periods the shape of chest
wall also changes to large or barrel shape.
Increase in the diffusion capacity due to increase in
the pulmonary capillary blood volume and increase
in the lung air volume.
In permanent natives of high altitudes, the number
of mitochondria and cellular enzymes is plentiful
than the sea level habitants. (cellular
acclimatization)
38. Acclimatization
1. Increase in the rate and depth of respiration
2. Increase in the RBC (polycythemia)
3. Normal V/P ratio (efficient gas exchange)
4. Angiogenesis
5. Change in shape of chest
39. How long it takes to climb Everest
1. Entire climb takes 6-9 weeks
2. First week – arrive to base camp
3. Next 3-4 weeks – going up and down the
mountain to establish camps with food, fuel and
oxygen
4. Acclimatization process can not be rushed
40. If you climb Everest very fast???
Acclimatization will not takes place
Cerebral edema
Pulmonary edema
Called as Acute mountain sickness
41. Cerebral edema at high altitude?
Low PO2 in systemic circulation
Vasodilation of blood vessels
Increase in the blood flow through cerebral blood
vessels
More fluid loss
Increase in fluid accumulation
Cerebral edema
42. Cerebral edema at high altitude?
Increase in intra cranial pressure
Head ache
Increase in Pulse rate
Herniation of brain that compresses the respiratory
centers
Death
43. What medications should I carry?
Acetazolamide (inhibits carbonic anhydrase) and
increases CO2 (stimulates RC)
Mannitol (relieves cerebral edema)
Dexamethasone (steroid) – relieves cerebral
edema
Oxygen supplements
44. pulmonary edema at high altitude?
Low PO2 in pulmonary circulation
Vasoconstriction of blood vessels
Blood is diverted to medium constricted or normal
blood vessels
Increase in blood flow
Increase in leak of fluid
Accumulation of fluid
Pulmonary edema
45. Chronic mountain sickness
Seen in individuals who stays for long at high altitudes
Polycythemia increases viscosity of blood and decreases
the blood flow to the tissues ( oxygen delivery decreases)
All alveoli now becomes low oxygen state, so
vasoconstriction of all pulmonary blood vessels results in
increase in the arterial pressure and failure of right side of
heart.
Poorly oxygenated blood
These individuals recover within days or weeks when they
are moved to low altitudes
46. Deep sea diving
Descending beneath the sea, the pressure
increases tremendously
To prevent collapse of lungs, air must be supplied at
very high pressures
This will expose the blood in the lungs to extremely
high pressure – hyper-barism
Beyond certain limits, these high pressures cause
major alterations in the body physiology and can be
lethal
47. Physiological effects of deep sea
diving
Nitrogen narcosis at high nitrogen pressure
Oxygen toxicity at high pressure
Carbon dioxide toxicity due to deep sea diving
48. Nitrogen narcosis
At the sea level pressure, the nitrogen has no significant
effect on body functions
When the diver remains beneath the sea for an hour or
more and breathing compressed air, the depth at which
the first symptom occurs is 120 feet
At 120 feet, diver begins to be jovial
At 150-200 feet, he becomes drowsy
At 200-250 feet, his strength wanes considerably (
unable to do required work)
Beyond 250 feet, he becomes useless
49. Nitrogen narcosis
Similar as alcoholic intoxication
Also called raptures of the depths
Mechanism is same as any other gas anesthetics
Nitrogen dissolves in the fatty substances in the
neural membranes, alters the neuronal excitability
50. Oxygen toxicity at high pressures
When PO2 of blood increases (say 100 mmHg), there
will be increase in the dissolved oxygen in addition to
that bound to hemoglobin
Extremely high PO2 (when oxygen is breathed at high
pressures) is detrimental to body tissues
Causes brain seizures and coma in 30-60 minutes
These seizures occurs with out warning sign and are
lethal
Nausea, muscle twitchings, dizziness, disturbance of
vision, irritability and disorientation
51. Oxygen toxicity at high pressures
Molecular oxygen converts into active form of oxygen called
oxygen free radicals
One of the most important form of oxygen free radicals is
super oxide free radical and other is peroxide free radical
Even at normal PO2, these free radicals will be continuously
formed
Body is equipped with enzymes to remove these free radicals
(oxidases, catalases, superoxide dismutase)
But when PO2 is above the critical levels, there will be
excessive oxygen free radicals
52. Oxygen toxicity at high pressures
Free radicals oxidizes the polyunsaturated fatty
acids that are essential components of many of cell
membranes
Also oxidizes cellular enzymes and damages the
cellular metabolic processes
Nervous tissues are highly susceptible due to
high lipid content
Most lethal effect of oxygen toxicity is brain
dysfunction
53. Carbon dioxide toxicity
Depth alone does not increase the rate of CO2 production in
the body
As long as diver continues to breath normal tidal volume and
expires the CO2 as it is formed, Alveolar PCO2 will be
normal.
In certain types of diving gear, diving helmet and some type
of rebreathing apparatus, CO2 will build up.
Beyond 80 mmHg PCO2, the respiratory centers will be
depressed.
Respiratory acidosis, narcosis, lethargy and even anesthesia.
54. Decompression sickness
If a diver stays longer periods beneath the sea,
nitrogen is dissolved in the body
If he comes to surface suddenly, nitrogen bubbles
are formed in the body fluids (intra or extra cellular)
Cause minor to serious damage to any area of the
body
This is called as Decompression sickness
Also called as Bends, compressed air sickness,
Caisson disease, Diver’s paralysis, Dysbarism
55. Symptoms of Decompression
sickness
Gas bubbles blocks many blood vessels in different
tissues
Tissue ischemia and death
In 85-90% of people, pain in the joints and muscles
of legs and arms (bends)
In 5-10% of people, paralysis, dizziness or
unconsciousness
in 2% of people, chokes, shortness of breath,
pulmonary edema and death
56. Prevention and management of
Decompression sickness
Slow ascent
Tank decompression
Using helium oxygen mixture in spite of nitrogen
Why??
57. Why helium??
Has only one-fifth of narcotic effect of nitrogen
The amount of helium dissolves in the body is less
when compared to nitrogen
Low density of helium keeps the airway resistance
minimum (work of breathing less)
58. SCUBA
Self Contained Under Water Breathing Apparatus
Designed by French explorer Jacques Cousteau
Advantage- Only required amount of air enters the
mask and on expiration, the air can not go back to
tank but instead is expired into the sea
Limitation – only limited time one can remain
beneath water