Disturbances of respiration

DR NILESH KATE
MBBS,MD
PROFESSOR
ESIC MEDICAL COLLEGE, GULBARGA.
DEPT. OF PHYSIOLOGY
DISTURBANCES
OF
RESPIRATION

OBJECTIVES.
 Abnormality respiratory pattern.
 Apnoea
 Dyspnoea
 Periodic breathing.
 Hypoventilation
 Hyperventilation.
 Disturbances related to respiratory gases.
 Hypoxia
 Asphyxia
 Hypocapnia
 Hypercapnia.
 Carbon monoxide poisoning

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

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.

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.

APNOEA
 Def – Temporary
cessation of breathing.
 Types
 Voluntary apnoea
 After hyperventilation
 Degluttion apnoea
 Breath holding attacks
 Adrenaline apnoea
 Sleep apnoea.

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.

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

After hyperventilation
 Reduced stimulation of respiratory centre
owing to CO2 wash caused by
hyperventilation

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

Breath holding attacks
 Brief period of apnoea
which occur in infants
and young children
and are generally
precipitated by an
emotional distress.

Adrenaline apnoea
 After injection of high doses of adrenaline

Sleep apnoea.
 The cessation of
breathing for a brief
period (10 s) during
sleep in a normal
individual

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.

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.

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.

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.

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).

 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.

 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.

 DI = BR × 100/MVV = 100 × 100/120 = 95%
 Normal value of DI range from 70% to 95%
 Dyspnoea occurs when DI is < 60%.

Causes
 Physiological - severe muscular exercise.
 Pathological-
 Respiratory disorders, such as bronchial
asthma,emphysema, pneumonia, pulmonary oedema
andpenumothorax, and
 Cardiac failure.

Causes
 Metabolic disorders causing dyspnoea are diabetic
acidosis, uraemia and increased H+
concentration.
 Metabolic acidosis causes dyspnoea by increasing
the pulmonary ventilation.

PERIODIC BREATHING.
 Characterized by the alternate periods of
respiratory activity and apnoea.
 Chynes stokes breathing
 Biot’s breathing.

CHYNES STOKES BREATHING
 Periodic type of
breathing in which the
alternate periods of
respiratory activity and
apnoea occur at regular
intervals and

CHYNES STOKES BREATHING
 During the period of
respiratory activity
there is waxing and
waning of tidal volume.

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.

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.

 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.

 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.

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.

BIOT’S BREATHING.
 Ataxic breathing is a
type of periodic
breathing showing
alternate periods of
respiratory activity
and apnoea.

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.

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


DISTURBANCES RELATED TO
RESPIRATORY GASES.
 Hypoxia
 Asphyxia
 Hypocapnia
 Hypercapnia
 Carbon monoxide poisoning.

HYPOXIA
 Deficiency of oxygen
supply at the tissue
level.

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.

Types
 Hypoxic hypoxia,
 Anaemic hypoxia,
 Stagnant hypoxia and
 Histotoxic hypoxia.

Symptoms
 It depends upon
 Rapidity of
development of
hypoxia,
 Severity of hypoxia
and
 Effectiveness of the
body’s compensatory
mechanisms.

Depending on severity…….
 Fulminant
 Acute
 chronic

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.

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.

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.

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).

Signs of hypoxia
 Cyanosis
 Tachycardia
 Tachypnoea

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.

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.

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

Tachycardia
 Occurs as a peripheral
chemoreceptor reflex
response to the low
arterial oxygen tension

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

Physiological compensatory
responses to chronic hypoxia
 Accommodation
and
 Acclimatization

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

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.

 Oxygen therapy is of limited value
 In an anaemic hypoxia, stagnant hypoxia and
hypoxic hypoxia caused by the physiological or
anatomical shunts.

 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.

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.

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)

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

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.

Complications in newborn
infants
 Bronchopulmonary dysplasia is
characterized by the formation of lung cysts
and opacities.

HYPERCAPNIA.
 An increase in the arterial pCO2 (normal
value 40 mm Hg) associated with the
respiratory acidosis

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.

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.

HYPOCAPNIA
 Reduced pCO2 is usually associated with
respiratory alkalosis,
 Causes.
 Hypocapnia occurs due to hyperventilation

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.

Clinical stages of acute
asphyxia
 Stage I – stage of Hyperpnoea
 Stage II – stage of central excitation
 Stage III – stage of central depression.

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.

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.

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

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.

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),

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

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

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

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).

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.

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

Symptoms of CO poisoning
 Headache and nausea
 Loss of consciousness
 Death may occur when Haemoglobin is 50%
saturated with CO.

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.

Disturbances of respiration

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