DISTURBANCES OF

RESPIRATION
Normal respiratory pattern is called eupnea.
Respiratory pattern is altered by many ways.
1. Tachypnea: Increase in the rate of respiration
2. Bradypnea: Decrease in the rate of respiration
3. Polypnea: Rapid, shallow breathing resembling
panting in dogs,only the rate of respiration
increases but the force does not increase
significantly.
4. Apnea: Temporary arrest of breathing
• 5. Hyperpnea: Increase in pulmonary ventilation
due to increase in rate or force of respiration.
• 6. Hyperventilation: Abnormal increase in rate
and force of respiration, which often leads to
dizziness and sometimes chest pain
• 7. Hypoventilation: Decrease in rate and force
of respiration
• 8. Dyspnea: Difficulty in breathing
• 9. Periodic breathing: Abnormal respiratory
rhythm
 ASPHYXIA
• Asphyxia is the condition characterized by
combination of hypoxia and hypercapnea,
due to obstruction of air passage.
• It develops in conditions characterized by
acute obstruction of air passage such as:
• 1. Strangulation
• 2. Hanging
• 3. Drowning, etc.
• Effects of asphyxia develop in three stages:
• 1. Stage of hyperpnea
• 2. Stage of convulsions
• 3. Stage of collapse.
• 1. Stage of Hyperpnea
• Hyperpnea is the first stage of asphyxia.
• In this stage, breathing becomes deep and rapid.
• It is due to the powerful stimulation of respiratory
centers by excess of carbon dioxide.
• Hyperpnea is followed by dyspnea and cyanosis.
• Eyes become more prominent.
• 2. Stage of Convulsions
• Stage of convulsions is characterized mainly by convulsions
(uncontrolled involuntary muscular contractions).
• Duration of this stage is less than 1 minute.
• Hypercapnea acts on brain and produces the following
effects:
• i. Violent expiratory efforts
• ii. Generalized convulsions
• iii. Increase in heart rate
• iv. Increase in arterial blood pressure
• v. Loss of consciousness.
• 3. Stage of Collapse
• Stage of collapse lasts for about 3 minutes.
• Severe hypoxia produces the following effects during this
stage:
• i. Depression of centers in brain and disappearance of
convulsions
• ii. Development of respiratory gasping occurs- During
respiratory gasping, there is stretching of the body with
opening of mouth, as if gasping for breath.
• iii. Dilatation of pupils
• iv. Decrease in heart rate
• v. Loss of all reflexes.
• Duration between the gasps is gradually
increased and finally death occurs.
• All together, asphyxia extends only for 5
minutes.
• The person can survive only by timely help
such as relieving the respiratory obstruction,
good aeration, etc.
 CYANOSIS
• Cyanosis is defined as the diffused bluish
coloration of skin and mucus membrane.
• It is due to the presence of large amount of
reduced hemoglobin in the blood.
• Quantity of reduced hemoglobin should be at
least 5 to 7 g/dL in the blood to cause
cyanosis.
 DISTRIBUTION OF CYANOSIS
• It is more marked in certain regions where the
skin is thin.
• These areas are lips, cheeks, ear lobes, nose
and fingertips above the base of the nail.
CONDITIONS WHEN CYANOSIS OCCURS
• 1. Any condition which leads to arterial
hypoxia and stagnant hypoxia.
• Cyanosis does not occur in anemic hypoxia
because the hemoglobin content itself is less.
• It does not occur in histotoxic hypoxia
because of tissue damage.
• 2. Conditions when altered hemoglobin is
formed.
• Due to poisoning, hemoglobin is altered into
methemoglobin or sulfhemoglobin, which
causes cyanosis.
• The cyanotic discoloration is due to the dark
color of these compounds only and not due to
reduced hemoglobin.
• 3. Conditions like polycythemia when blood
flow is slow.
• During polycythemia, because of increased
RBC count, the viscosity of blood is increased
and it leads to sluggishness of blood flow.
• Quantity of deoxygenated blood increases,
which causes bluish discoloration of skin.
• Cyanosis usually occurs only when the
quantity of reduced hemoglobin is about 5
g/dL to 7 g/dL.
• But, in anemia, the hemoglobin content itself
is less.
• So, cyanosis cannot occur in anemia.
 Clinical Classification & Etiology

True Cyanosis (increased amount of reduced Hb)—

• Central Type—
• Peripheral Type—
• Mixed Type
• Cyanosis due to abnormal Hb derivatives—
Methemoglobinemia
• Sulfhemoglobinemia
• Central cynosis only occurs when oxygen
saturation of arterial blood is less then 85%
• Peripheral cynosis is due to poor peripheral
circulation and increased oxygen consumption
in peripheral tissues
• In conditions such as cardiogenic shock with
pulmonary edema there may be a mixture of
both types
 REYNAUD’S PHENOMENON
• Fingers became white due to lack of blood
flow then becomes blue as vessels dilate to
keep blood in tissues and finally red as blood
flow returns
• Discriminating feature between central and
peripheral cynosis is obtained from testing the
oxygen saturation of arterial blood
 HYPOXIA
• Hypoxia is defined as deficiency of O2 at the
tissue level.
• Hypoxia is classically divided into 4 categories.
• 1. Hypoxic hypoxia.
• 2. Anemic hypoxia.
• 3. Stagnant hypoxia.
• 4. Histotoxic hypoxia.
 Hypoxic Hypoxia

• When PO2 of arterial blood is reduced, the

hypoxia is called hypoxic hypoxia.
• Mechanism of hypoxia
• In hypoxic hypoxia, PO2 of arterial blood is
decreased, due to which the delivery of O2 to
the tissue is reduced.
• This occurs either due to decreased O2 in the
inspired air or due to diseases of the respiratory
apparatus that decrease O2 supply to the tissue.
• It is seen in following conditions:
• 1. Low PO2 in the inspired air
• Hypoventilation
• Diffusion defect
• Ventilation-perfusion mismatch
 Anemic Hypoxia

• When PO2 of arterial blood is normal, but the

hemoglobin to carry O2 is not adequate in
amount, anemic hypoxia develops.
• Conditions that lead to anemic hypoxia are:
• a. Anemia (decreased Hb concentration in
blood)
• b. Carbon monoxide poisoning
• c. Altered Hb, e.g. Methemoglobin
• The affinity of CO for Hb is about 210 times
greater than the affinity of O2.
• CO combines with hemoglobin to form
carboxyhemoglobin (COHb)
• In CO poisoning, release of CO from COHb is
very slow due the high affinity of CO to Hb
therefore, O2 cannot bind with hemoglobin.
• Thus, in CO poisoning, though the hemoglobin
content is normal, Hb is not available to deliver
O2 to the tissue.
• Hb-dissociation curve shifts to left signifying
the decreased release of O2 from Hb
 Stagnant Hypoxia (Hypoperfusion Hypoxia)

• When hypoxia occurs due to decreased blood

flow to the tissues, this is called stagnant
hypoxia (stagnation of flow).
• This is also called hypoperfusion hypoxia, as it
causes decreased perfusion of tissues due to
stagnation of blood flow.
• This is sometimes also called ischemic
hypoxia.
• Hypoxia occurs due to stagnation of blood in
circulation therefore, this is also called
circulatory hypoxia.
• Stagnant hypoxia is seen in:
• 1. Heart failure
• 2. Shock
• 3. Vascular obstruction (that causes specific
organ hypoxia)
 Histotoxic Hypoxia
• When tissue cannot utilize oxygen inspite of normal
O2 supply, the resulting hypoxia is called histotoxic
hypoxia.
• As tissue is unable to utilize O2, the venous tension
of O2 is high.
• Mechanism of hypoxia depends on the cause of
hypoxia.
• 1. Cyanide poisoning: Cyanide inhibits cytochrome
oxidase.
• Therefore, tissue oxidation is paralyzed.
• Diphtheria: In severe diphtheria, diphtheria
toxin inhibits the synthesis of one of the
cytochromes and therefore, prevents O2
utilization..
• Cyanide poisoning is treated by methylene blue
or nitrites.
• They form methemoglobin, which in turn reacts
with cyanide to form Cyanmethemoglobin,
which is a non-toxic compound.
• Hyperbaric O2 therapy is also useful in cyanide
poisoning.
 Effects of Hypoxia
• Hypoxia mainly affects CNS, especially the higher
centers.
• Effects of hypoxia depend on the severity,
duration and type of hypoxia.
• Acute and Subacute Hypoxias
• Features of acute hypoxia resemble acute
alcoholism.
• Impaired judgment and motor incoordination are
major manifestations of acute hypoxia.
• In severe and prolonged hypoxia, brainstem is
depressed and death results from respiratory
failure.
• Anaerobic glycolysis results in formation of
more lactic acid that leads to metabolic
acidosis.
• Stimulation of chemoreceptors by hypoxia
produces hyperventilation and causes
respiratory alkalosis.
• Effects on Cells
• Transcription factors known as hypoxia inducible factors
(HIFs) are produced by hypoxia.
• HIFs have α and β subunits. Normally, in the presence of
adequate oxygen in the tissues, α subunits are rapidly
removed from the cells.
• In hypoxic conditions, dimerization of α and β subunits
occurs in the cells.
• The α-β dimers cause induction of genes that produce
erythropoietin and angiogenic factors.
• 3. This is one of the causes of angiogenesis or
neovascularization in hypoxic tissues.
• Effects on Brain
• Brain tissue is highly sensitive to hypoxia.
• Sudden fall in inspired PO2 to less than 20 mm
Hg, causes loss of consciousness in about 15
seconds.
• If hypoxia continues, death can occur in 4 to 5
minutes.
• Hypoxia of lower intensities, cause the
symptoms similar to that of acute alcohol
intoxication such as disorientation, impaired
judgment, headache, drowsiness etc.
• Chronic Hypoxia
• In chronic hypoxia, polycythemia occurs due
to increased erythropoietin production.
• Local hypoxic vasodilation in the tissue
increases tissue blood flow.
 OXYGEN THERAPY
• Oxygen therapy is indicated in hypoxia. It is
very useful in acute and severe hypoxia,
especially when hypoxia is associated with
dyspnea.
• Oxygen is administered by following methods.
• Using oxygen tent: It is very useful in children,
as they usually do not tolerate mask or
cannula.
• It is also useful in administering hyperbaric
oxygen.
• Using oxygen mask: Oxygen enters the mask
at a higher velocity so that oxygen is drawn
through the holes in the mask.
• Mechanical ventilator: When patient is
semiconscious or comatose, oxygen is
administered from a mechanical ventilator
through an endotracheal or tracheostomy
tube.
• Through an intranasal tube: A cannula is
inserted into the nostril, which is connected
to the oxygen cylinder.
O2 Therapy in Different Forms of Hypoxia

• Hypoxic Hypoxia
• As hypoxia is due to decreased PO2 of arterial
blood, oxygen therapy is very useful in hypoxic
hypoxia.
• In such conditions, administration of O2
increases the pressure gradient between
alveoli and the blood that facilitates O2 entry
into the blood.
• O2 therapy is harmful in states of depressed
respiratory centers:
• Though O2 therapy is beneficial in most forms of
hypoxic hypoxia; it is harmful to subjects with
depressed respiratory centers.
• In such subjects, blood PCO2 is high that depresses
the respiratory centers and their breathing is
maintained by stimulation due to hypoxia.
• When 100% O2 is administered to these subjects, this
stimulatory effect by hypoxia is abolished that results
in further respiratory depression.
• Anemic Hypoxia
• Oxygen therapy increases O2 content of blood
by increasing the quantity of dissolved oxygen
in the blood.
• Thus, it helps in providing supply of extra O2 to
tissue.
• In CO poisoning, hyperbaric O2 is useful as it
facilitates dissociation of CO from Hb and
increases the transport of O2 in dissolved state.
• Stagnant Hypoxia
• O2 therapy is not much useful as blood flow to
the tissue is decreased in stagnant hypoxia.
• Histotoxic Hypoxia
• Tissue is unable to utilize O2. Hence, O2
therapy is not very beneficial.
• However, hyperbaric O2 therapy benefits by
displacing the chemical bound to Hb.
• Hyperbaric O2 therapy means, administration
of 100% O2 at increased pressure.
• However, 100% O2 at high pressure facilitates
the onset of oxygen toxicity.
 Effect of 100% O2 Therapy
• The effects depend on the duration of therapy
with pure O2, and the pressure at which O2 is
delivered.
• When, administered at 4 atmospheres,
symptoms develop in half an hour, and if
administered at 6 atmospheres, the features
develop in just few minute
• CNS Effects
• Nausea, irritability, dizziness, disorientation,
muscle twitching and convulsions.
• In severe cases person becomes comatose.
• Hyperbaric therapy decreases ATP and GABA
content of brain.
• Respiratory System
• Congestion and irritation of airway increases
tracheobronchial secretion, and decrease
surfactant synthesis.
• This also causes pulmonary edema and
atelectasis.
• Special Sense
• Ringing in the ears (tinnitus), blurring of vision, loss
of equilibrium, and retrolental fibroplasia in
newborn that results in premature retinopathy.
• Visual defects also occur due to formation of
opaque vascular tissue in the eye.
• If given for a longer period, 100% O2 causes
bronchopulmopary dysplasia and lung cysts,
especially in infants treated for respiratory distress
syndrome.
• With pure O2 therapy, oxidizing free radicals
like super oxide anion (O2−), and hydrogen
peroxide (H2O2) accumulate in the body in
excess amounts.
• They oxidize the polyunsaturated fatty acids
and destroy the cellular enzymes.
• As a result, toxic effects due to O2 therapy
develop.
 ABNORMAL RESPIRATIONS
• Periodic Breathing
• Cyclical repetition of apnea and shallow
breathing (like hyperpnea) in normal
individuals is called periodic breathing.
• This is typically seen following voluntary
hyperventilation performed for 2 to 3 min.
• Apnea occurs due to removal of CO2 during
hyperventilation that removes the CO2 drive
on ventilation.
• Cheyne-Stokes Respiration
• Periodic breathing that occurs in diseases and
abnormal condition is called Cheyne-Stokes
respiration.
• Though it occurs in deep sleep in some normal
persons, it is more common in congestive
cardiac failure, uremia and brain diseases.
• The patients have increased sensitivity to CO2
due to disruption of neural pathways.
• Accumulation of CO2 causes hyperventilation
that lowers PCO2.
• Decreased PCO2 removes the CO2-drive on
ventilation and produces apnea, which
consequently increases the PCO2 again.
• The increased sensitivity of respiratory
mechanism to PCO2 produces hyperventilation
and the cycle continues.
• Cheyne-Stokes respiration is seen in:
• Premature infants.
• Unacclimatized persons at high altitude.
• During deep sleep in some people.
• Heart failure.
• Renal failure.
• Kussmaul Breathing
• The pattern of respiration seen in diabetic
ketoacidosis is called Kussmaul breathing
(described by Kussmaul).
• Accumulation of metabolic acids such as
acetoacetic acid and β-hydroxy butyric acid
produces metabolic acidosis that stimulates
respiratory centers.
• This leads to rapid and deep respiration or ‘air
hunger as described by Kussmaul.
• Biot’s Respiration
• In this type of abnormal breathing, 3 to 4 cycles
of normal respiration is followed by abrupt
onset of apnea
• Before apnea, usually deep gasps occur.
• It is seen in meningitis, diseases affecting
medulla of the brain, increased intra cranial
pressure, morphine poisoning and damage to
the brainstem.
• Sleep Apnea Syndrome
• In adult sleep apnea syndrome, marked loss of tone
of pharyngeal muscles occurs during REM sleep
causing obstruction of airway during inspiration.
• This produces apnea.
• The person wakes up and breathes normally for
sometimes and sleeps again to have another bout of
apnea.
• Thus repeated apnea occurs during sleep.
• These people develop morning headache and fatigue
due to frequent apnea in the night.
• Sleeplessness occurs during the day.
• Sudden Infant Death Syndrome
• Sudden infant death syndrome (SIDS) is
believed to be a type of sleep apnea in
premature infants.
• Loss of rhythmic activity of the respiratory
center leads to apnea in sleep and causes death
of the infant.
• It is also common in mothers who are chronic
smokers.
• Hysteric Hyperpnea
• Spontaneous hyperpnea of sudden onset
occurs in patients with hysteria.
• This results in washing out of CO2 leading to
alkalosis and convulsions.
• This is treated by allowing the patient to
breath into a facial mask till he recovers.