Respiratory
adjustments in special
conditions
By
Dr. MB.Bhat..
In muscular exercise
In Heavy exercise body’s metabolism
increases about 2000% above normal
(compare to high fever it increases only
about 100% above normal)
 Energy store available in the body at this
high level activities is only for 20 seconds.
 For sustaining exercise extra fuel & O2
should be supplied by Respiration & CVS
adjustments.
 O2 consumption increases proportionaly to
severity of exercise up to a maximum

Increased O2 consumption during
exercise is achieved by –
1. Increased pulmonary ventilation
2. Increased O2 diffusion capacity of
lungs (from normal 250 to
4000ml/min)
 [same time CO2 diffusion capacity
also increases from 200 to
8000ml/min)
Factors increasing pulmonary
ventilation
 In
moderate exercise –by increased
depth of respiration
 In severe exercise –by increased
depth & rate of respiration.
Effect of exercise on pulmonary
ventilation









Pulmonary ventilation shows –
With exercise -Abrupt increase –during on-set of exercise
(just before the exercise commence)
Followed by a brief pause
Graded increase –during exercise
proportionate with grade of exercise
Cessation of exercise –
Abrupt slight decrease –immediately after
cessation of exercise
Followed by a brief pause
Followed by graded decline to pre-exercise
level
Abrupt increase with on-set of exercise due to
stimulation of respiratory center by -1.
2.
3.
Anticipatory response – Psychic
stimuli coming from higher center
(From limbic system)
Pyramidal tract impulses via some
collaterals
Afferent impulses from
proprioceptors of muscle, tendon &
joints via collateral of dorsal column
tracts (Lovan reflex)

1.
2.
3.
4.
5.
6.
The graded increase is due to
stimulation of respiratory center by –
Increase in temperature
Increase sensitivity of the respiratory
center to the CO2 (fluctuation of
arterial PCO2 is increased even though
the mean arterial PCO2 remain same)
O2 (even though arterial PO2 in not
decreased)
Humeral effect (even though blood pH,
PCO2 & PO2 remain constant during
moderate exercise)
Increase in plasma K+ level
In vigorous exercise all the above +
Lactic acid
Cessation of exercise
 Abrupt
decrease – due to stoppage
of impulses bombarding respiratory
center (but not coming back to basal
level)
 Graded decline – due to lactic
acedemia -- due to O2 debt –last as
long as 90 minutes
 Magnitude of O2 debt – amount by
which O2 exceeds basal consumption
from the end of exertion until return
to basal level

1.
2.
3.





Extra O2 during this period is used for –
Combine with muscle myoglobin
Resynthesis of ATP & Phosphocreatine
Removalof lactic acid
Fate of lactic acid –
80% converted to glycogen in the liver
20% is metabolized to CO2 & water
During strenuous exercise because of O2
debt the RQ rise to 2.
After cessation because of repayment of
O2 debt the RQ falls to 0.5
Hypoxia
Oxygen deficiency at
tissue level is known as
hypoxia
Classification of hypoxia
1.
2.
3.
4.
Hypoxic hypoxia or Arterial hypoxia
Anemic hypoxia
Stagnant hypoxia or Ischemic
hypoxia or Hypo kinetic hypoxia
Histotoxic hypoxia
Type of hypoxia
Hypoxic
Anemic
Stagnant
Histotoxic
Oxygen content in the blood
Reduced
Reduced
Normal
Normal
Arterial PO2
Reduced
Normal
Normal
Normal
Oxygen carrying capacity
Normal
Reduced
Normal
Normal
Hemoglobin saturation of blood
Reduced
Reduced Normal
or normal
Normal
Rate of blood flow to tissue
Normal
Normal
Reduced
Normal
O2 utilization by tissue
Normal
Normal
Normal
Reduced
A-V O2 difference
More
More
More
Reduced
Cyanosis
General
Not occur Local & Not occur
general
Oxygen therapy
useful
not useful Not
useful
Treatment
oxygen
with
hyperbaric
--
useful
Not
useful
Not useful
Useful
Hypoxic hypoxia
 Seen
in - Physiological condition – High
altitude (alveolar PO2 is decreased)
 Pathological condition – Cardiorespiratory diseases (O2 diffusion
capacity is decreased)
High altitude
Atmospheric pressure decreases in high
altitude
 Concentration of gases everywhere in the
atmosphere is same
 Whereas, partial pressure of the gas
varies.
 Also in the alveoli, the water vapor
pressure is constant (47 mm Hg)
 So PO2 in alveoli = ATP –47 X O2
concentration (20% or 0.2)

 At
10,000ft (3000m) alveolar PO2 is
60 mm Hg –Hb saturation maybe
normal
 At 12,000ft (3700m), mental
irritability appears (first hypoxic
symptom)
 At 18,000ft (5500m), hypoxic
symptoms are severe
 At 20,000ft (6100m)consciousnes lost
in 20 seconds & death occurs in 4 to 5
minutes (PO2 is only 20 mm Hg)
Hypoxic symptoms at high altitude








Less severe hypoxic symptoms –
Acute mountain sickness --
Many individuals first arrive at high altitude develop
“transient mountain sickness” –acute mountain sickness
The syndrome develops 8 to 24 hours after arrival & last 4
to 8 days
Symptoms of acute mountain sickness are –
Mental symptoms --Irritability, mental aberrations such as
impaired judgment, dis-orientation, excitement,
drowsiness, loss of sense of time, loss of sensibility,
Other systemic symptoms -- dulled pain & headache,
breathlessness, dizziness, insomnia, fatigue, Cheyne-Stoke
breathing is common during sleep
–anorexia, nausea, vomiting, tachycardia, palpitation,
retinal hemorrhage (after healing no visual defect);
 Severe
hypoxic symptoms –
 1. Hypertension (proportionate to
severity
of chemoreceptor drive)
 2. High-altitude cerebral edema –due
to low PO2 –arteriolar dilation –
increase capillary pressure –increase
transudation of fluid into brain tissue
 Due to Cerebral edema – ataxia,
disorientation, in extreme case coma &
death
 3.
High-altitude pulmonary edema –is
a patchy edema of lungs due to
pulmonary hypertension (due to low
PO2), Left atrial pressure is normal
 Cough with pink frothy sputum
 Increased pulmonary capillary
pressure along with polycythemia
cause increased right heart work &
right ventricular hypertrophy.
Chronic mountain sickness
(Monge’s disease)
 Disease
of long term residents at
high altitude
 These people develop –manifestation
of superimposed pulmonary disease
with - Fatigue, reduced exercise tolerance,
severe hypoxemia & polycythemia
Acclimatization (Increase altitude tolerance)
Compensatory mechanisms develop over a period of
time to tolerate high altitude

1.
2.
‘Mechanisms are –
Hyperventilation –due to hypoxic action
through peripheral chemoreceptor
Increased sensitivity to CO2 (after 4
days) —due to
--outward movement of HCO3 from
;
--active transport of H+ ions into CSF;
--development of lactic acidosis in the brain
All these decrease pH in CSF that stimulate
respiration through central chemoreceptor


1.
2.
3.
4.
5.
6.
3. Polycythemia – dueto
erythropoietin (within 2 to 3 days) –
due to hypoxia –sustain as long as
stay in high altitude
Others –
Increase number of capillaries in
peripheral tissues
Increase mitochondria
Increase cytochrome oxidase in the
tissue
Increase myoglobin level
Increase MBC (up to 200L/min) as air
is less dense
Kidney secrete alkaline urine
Hypoxic hypoxia in pathological
condition
Lung failure (or) Gas-exchange failure –
 Pulmonary fibrosis
 V/Q imbalance –Shunt –Congenital heart
diseases –Tetralogy of Fallot (Blue baby) –
Right to left shunt
 Pump failure (or) Ventilation failure –
 Respiratory muscles fatigue
 Mechanical defects cause atelectasis
 Depression of respiratory center –by
morphine & other drugs

Atelectasis –Collapse of the alveoli

1.
2.
3.
Causes –
Surfactant deficiency
Obstruction of bronchus & bronchioles –
alveoli beyond point of obstruction
collapse –leading to more negative
intrapleural pressure –pulls mediastinum
towards affected side
Pneumothorax –air in the interstitial
space –intrapleural pressure equal to
atmospheric pressure –Push the
mediastinum towards normal side
Asthma
 Obstructive
type of respiratory
disease
 Due to air way obstruction – due to
 Air way hypersensitivity –due to –
Allergy
 Attack usually occurs in morning &
also during exercise
 Treatment –
 β2 adrenergic agonists
 Administration of steroids
Emphysema
Obstructive type of respiratory disease
 Degenerative potentially fatal disease
 Lungs are voluminous & inelastic with
widespread destruction of alveolar walls &
pulmonary capillaries
 Most common cause heavy cigarette
smoking
 Smoking increase PAM which attracts
leucocytes –which release protease
enzymes & O2 free radicals –destroy lung
tissues
 Smoking also decrease α1antitrypsin –
which destroy protease enzymes

Features of Emphysema
1.
2.
3.
4.
5.
6.
7.
8.
9.
Barrel-shaped chest
Work of breathing (both inspiration &
expiration is laboured)
Compliance (normal o.25 to 0.9L/mm Hg)
FRC (normal 3L to 8L)
FVC duration (normal 4 to 8second)
FEV1 (normal 3.2L to 0.75L)
Physiological dead space (doubled)
Physiological shunt
O2 diffusion capacity (1/5th)
9. Arterial PO2 (even goes to 50 mm Hg)
10. Arterial PCO2 (goes up to 60 mm Hg)
11. Hb saturation (only 80 to 85%)
12. Plasma HCO3 (compensatory acidosis)
13. Polycythemia (due to hypoxia)
14. Pulmonary hyperventilation
15. Right ventricular hypertrophy
(Cor Pulmonale)
Here respiratory drive is due to hypoxia.
So O2 treatment is not recommended
Anemic hypoxia
 Seen
in
 Anemia –only in severe anemia;
where Hb deficiency is marked
(because in hypoxic condition
increase 2,3-DPG level shift O2
dissociation curve to right)
 Carbon-monoxide poisoning
Stagnant hypoxia
 Due
to slowing of circulation
 Local –vasoconstriction due to cold
or obstruction to venous outflow; &
peripheral circulatory failure
 General – cardiac failure
Histotoxic hypoxia
 Seen
in cyanide poisoning
 Cyanide inhibit cytochrome oxidase &
other iron containing enzymes
 Treatment –Administration of
methylene blue or nitrates (oxidizing
agents)
 –oxidized Hb to methemoglobin
which react with cyanide to form
cyanmethemoglobin, a non-toxic
compound
 Hyperbaric O2 therapy is useful
Cyanosis
Bluish coloration of skin, nail beds, ear
lobe, lips, fingers & mucus membrane due
to presence of HHb >5gm/dl
 Local cyanosis or Peripheral cyanosis –
seen in stagnant hypoxia due to exposure
of cold, circulatory failure
 Signs –patients may be cold & blue,
peripheral pulses difficult to feel
 Central cyanosis – seen in hypoxic
hypoxia
 Signs –patients extremities are warm &
pulsatile, rapid blood flow, increase heart
rate & pulse pressure and vasodilation



1.
2.
3.

Before cyanosis readily apparent; the Hb
saturation of O2 must fall below 80% &
PO2 45 mm Hg.
Cyanosis does not occur in –
Anemic hypoxia –due to low Hb content
CO poisoning –COHb is cheery red
Histotoxic hypoxia –O2 utilization is less
so HHb is also less
High circulatory level of methemoglobin
also produce discoloration of skin similar
to cyanosis
O2 therapy
 Useful
in treatment of
 Hypoxic hypoxia (except in shunt
condition)
 Cyanosis
 Only limited value in treatment of –
 Anemic, Stagnant & Histotoxic
hypoxia
Hyperbaric oxygen therapy










Exposure of O2 with high pressure
Advantage –markedly increase dissolved O2
content in blood
Used in treatment of –
CO poisoning, Cyanide poisoning, Congenital
cardiac disease (right to left shunt)
Gas gangrene
Very severe blood loss anemia
Diabetic leg ulcers & other wounds that are slow
to heal
Rescue of skin flaps & grafts in which circulation
is marginal,
Primary treatment for decompression sickness &
air embolism
Radiation induced tissue injury
Oxygen toxicity
Due to production of superoxide anions (O2—)—
oxygen free radicals & H2O2, also – due to
decrease surfactant production & lung
macrophages in high PO2.
 Safe level –gas mixture contain O2 <80% (can
administer even 24 hours for years)
 When gas mixture contain O2 >80% to 100%
(& 2 to 3 ATP) –can tolerate only up to 5 hours
(Hyperbaric O2 treatment)
 When above administered >8 hours –
respiratory irritation, sub-sternal distress, nasal
congestion, sore throat & coughing

 When
exposed above >24 to 48 hours
–cause lung damage, pulmonary
edema, diminished vital capacity (due
to absorption atelectasis), due CNS
effect convulsion preceded by nausea,
ringing in the ear & twitching of face
 In children –
 Bronchopulmonary dysplasia,
Retrolental fibroplasia –formation of
opaque vascular tissue in eyes
(retinopathy of pre maturity)
Hypercapnea
 Occurs
in –
 Various forms of pump failure
 Febrile state –For each 1oC rise in
temperature, the CO2 production by
13%
 High carbohydrate food intake
 Symptoms of large excess of CO2 in
blood –CO2 narcosis – Depression of
CNS –leads to confusion, diminished
sensory activity, in extreme case –
coma, respiratory depression &
death
Hypocapnia
 Occurs
due to hyperventilation
 Leads to –
 Alkalosis
 Vasoconstriction
 Reduction in Cerebral blood flow (by
30%)
 Cerebral ischemia –cause dizziness &
parenthesis
Asphyxia
 Existence
of acute hypercapnia &
hypoxia together due to closed
airway breathing
 Leads to improper aeration of blood
 Occur in –
 Drowning
 Hanging
 Pneumothorax
Effect of asphyxia
Stage 1 –Stage of hyperpnoea –
 duration 1 min
 Features –
 Rate & depth of respiration increased
 Respiratory efforts are Violent
 Dyspnea results
 Initially both inspiratory & expiratory
movements are increased
 Later expiratory movements are more
pronounced
 Unconsciousness marked end of this stage
 Cause –due to hypercapnea












Stage 2 –Stage of central excitation –
duration 1 to 2 minutes
Expiratory movements are still more pronounced
with each expiration, the whole body enters into
convulsion
Saliva secretion & vomiting occurs
Blood pH decreases –acidosis (accumulation of
lactic acid due to convulsion)
Increased wide spread sympathetic stimulation
Signs of central excitations appear – such as
Increase heart rate & BP;
Pupillary constriction (myosis)
Exaggeration of reflexes
Cause –hypercapnia, hypoxia & acidosis
 Stage
3 –Stage of central depression  Duration 2 to 3 minutes
 Expiratory convulsion ceased
 Replaced by slow deep spasmodic
inspiration –individuals stretches out
& open mouth wide as if gasping for
breath (gasping type of breathing)
 Signs of central depression appear –
 Pupillary dilation (mydriasis)
 Abolition of reflexes
 Decreased HR & BP and vasodilation
As this stage is progressed interval
between successive gasping longer
 Cause –direct hypoxic effect on respiratory
& other brain centers which is depressive.
 Asphyxiated victim can still be saved by
artificial respiration
 Victim may develop ventricular fibrillation
due to hypoxic myocardial damage & high
circulatory catecholamine
 If artificial respiration is not started –
 At the end of 4 to 5 minutes of stage 3,
the victim dies.

Periodic breathing
 When
breathing is non-rhythmic &
irregular, it is said to be periodic
breathing
 Two types
 Cheyne-Stoke breathing –Regularly
irregular type of periodic breathing
 Biot’s breathing –Irregularly irregular
type of periodic breathing
Cheyne-Stoke breathing
Occurrence of waxing & waning type of respiration
with a period of apnea in between last for few
seconds to few minutes & then the cycle repeats
1.
Physiological
High altitude
2.
After hyperventilation
3.
In deep sleep
2.
4.
In anesthetic condition
3.
5.
Quite common

infants
in healthy

1.
Pathological
Congestive heart
failure
Uremia
Elevating intracranial
pressure
Biot’s breathing
 Varying
breathing time alternate with
apnoeic periods of different lengths
 Transition from periods of activity to
apnea & back are abrupt
 Occurs only in pathological conditions
affect CNS –such as meningitis
Dyspnea


1.
2.
3.
4.
Difficulty in breathing; where breathing
becomes consciousness
Causes –
Reflex stimulation of respiratory centers
either through central or peripheral or
both chemoreceptors.
Hypersensitivity of the Hering-Breuer
reflex
Hypoxic conditions
Restriction of the action of the
diaphragm or inter-costal
5.
6.
7.
8.
9.
Acidosis
Increased metabolism
Nervous conditions such as emotional
disturbance, neurasthenia, hysteria,
encephalitis, cerebral tumor, cerebral
hemorrhage or cerebral edema
Various pulmonary diseases
Cardiac Dyspnea –mitral stenosis
Effects of increased barometric
pressure (Under water breathing)
Ambient pressure increases by 1ATP for
every 10m (33ft) of depth in sea water or
10.4m of depth in fresh water
 But work of breathing is increased as
density of gas is increased
 To overcome this, divers breath gas or air
at increased pressure from pressurized
chamber (Caisson chamber)
 At high pressure, gases including inert gas
equilibrium with body fluid & tissue
increases diffusion & soluble capacity of
gas

 Among
excess of gas content in the
body - Excess of O2 can be utilized by the body
 Excess of CO2 can be expired out
 Excess of N2 pose problem
 Total volume of N2 in the body at sea
level is one liter; whereas at 300ft
depth, 10L
 N2 solubility is high in fatty tissue
Decompression sickness
[Dysbarism]
[Caission disease]
[Bent knee paralysis]
Symptoms takes place to a diver, if he
ascends rapidly from underwater to surface
 In underwater breathing, due to high
pressure, volume of gas equilibration
(content) in body fluid & tissue is more.
 In surface, as pressure is normal, excess
gas equilibrates at high pressure begins to
come out as bubbles.

Small bubbles –no physiological disturbance
 Formation of large bubbles (if ascends
rapidly) –which when,
 Coming out in the region of joints –Bends –
pain around joints
 Enter in pulmonary circulation –Chokes –a
feeling of shortness of breath often
accompanying cough
 Enter coronary circulation –myocardial
damage –heart attack
 Enter in cerebral circulation –leads to
neurological symptoms such as -
Neurological symptoms are –
 Parenthesis
 Itching
 Deafness
 Impaired vision
 Vestibular disturbance
 Even stroke (Diver’s paralysis)
 In extreme case patient may collapse &
die

Prevention –
 Slow ascending has enough timeto prevent
bubbles from being unduly large
 Wearing SCUBA gear (Self-Contained
Underwater Breathing Apparatus)
 Treatment –
 Recompression in a pressure chamber
followed by slow decompression
 Note – Half-time for elimination of N2 –
From blood is 2 minutes; from muscle 20
minutes & from fat 60 minutes.

Artificial respiration
 Useful
in–
 Acute asphyxia due to drowning
 CO or other forms of gas poisoning
 Electrocution
 Anesthetic accidents
The purpose of giving artificial respiration is - To maintain the gaseous interchange, the
vitality of the nerve centers, as well as that of
the heart.
 It also helps to maintain circulation.
 It is expected that after sometime, the
respiratory centers will start functioning
spontaneously.
 During artificial respiration, the alternate
inflation and deflation of lungs reflexly
stimulate the respiratory centers, and revive
the spontaneous respiration

Methods of artificial respiration
 I.
Manual methods &
 II. Instrumental methods
Manual methods

1.
2.
3.
4.
5.
The different types of manual methods are-Schafer’s method- Subject in prone position;
Head tilted side; Operator-side by
Holger-Nielsen method (Arm-lift back
pressure method) –Subject in prone
position, hands folded rested under head;
Operator –head end
Sylvester’s method —subject in supine
position, Operator at head end
Mouth-to-mouth method –better than others
Eve’s rocking method
Instrumental methods
Negative pressure breathing method –
 By alternately compressing and relaxing
the chest wall –
 Drinker’s method
 Bragg-Paul’s method
 Positive-pressure breathing –
 By introducing air or oxygen directly into
the lungs –
 Continuous inflation method
 Intermittent inflation method

END
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