Transcript Pathophysiology of breathing

Pathophysiology of external
breathing. Hypoxia
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Reasons for respiratory dysfunction
• Dysfunction of the respiratory neurons;
• Chest pathology
• Respiratory muscles and diaphragm
pathology;
• Injure of pleura;
• Obstructive lung disease;
• Restrictive lung disease.
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• The pathological
factors impair
metabolism,
structure and
function of nerve
cells.
• They are hypoxia,
hypoglycemia,
toxic agents,
inflammatory
processes in the
brain tissue,
compression of
the medulla,
traumas,
circulatory
disorders in the
brain.
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Neurochemical
respiratory
control system
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Investigation of terminal breathing in
experiment
• 1 – normal breathing;
• 2 – apneustic breathing
after cutting both vagal
nerves and brain between
pneumotaxic and
apneustic centers;
• 3 – gasping after cutting
under dorsal respiratory
group;
• 4 – an arrest of breathing
after cutting medulla
under respiratory neurons.
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Pathological Patterns of Breathing
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Eupnea - normal breathing movements
Bradypnea - decreased rate of breathing
Hyperpnea - increased breathing movement
Polypnea – increased rate and decreased depth
of breathing
Apnea - arrested breathing
Periodic breathing
Terminal breathing
Asphyxia - inability to breathe
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Bradypnea
• Bradypnea – decreased rate of breathing, cased by lack
of impulsation from respiratory neurons, that leads to
hypoventilation.
• Bradypnea is observed in hypertension (reflexes from
carotid sinus baroreceptors), in increased ventilatory
resistance, inhibition of respiratory neurons by
hypoxia, effect of narcotic drugs to brain that decrease
the sensitivity of the respiratory neurons to pH or CO2
in CSF, functional impaction of nervous system
(neurosis, hysteria).
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Hyperpnea
• Hyperpnea - increased breathing movement.
• Hyperpnea is a result of intensive nerve or
humoral stimulation of respiratory neuronal
area (lack of pO2 in ihaled air, extra pCO2 in
ihaled air, anemia, acidosis).
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Polypnoe
• Polypnea – increased rate and decreased depth of
breathing because of changed activity of respiratory
neurons by reflex regulation.
• Polypnea revealed in fever, functional impaction of
nervous system (hysteria), injure of lungs (atelectasis,
pneumonia, impaired perfusion), pain syndrome in
body organs engaged in ventilatory function.
• Polypnea affects breathing in such a manner that
ultimately sufficient O2 uptake and CO2 release can no
longer be guaranteed.
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Apnea
• Apnea - an arrest of breathing lasting a few
seconds. It is more likely in the presence of a
metabolic alkalosis because decrease pCO2 in
blood (after artificial lung ventilation), giving
adrenalin in blood, inhibition of respiratory
neurons (as a result of hypoxia, toxic effects,
organic pathology of the brain) .
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Periodic breathing
• Cheyne–Stokes breathing is irregular. The depth of
breathing periodically becomes gradually deeper and then
gradually more shallow. It is caused by a delayed response
of respiratory neurons to changes in blood gases resulting
in an overshooting reaction. It occurs when there is
hypoperfusion of the brain, or when breathing is regulated
by a lack of oxygen (hypoxiaї, uremia, immature infants).
• Biot breathing consists of a series of normal breaths
interrupted by long pauses. It is an expression of damage to
respiratory neurons. Gasping also signifies a marked
disorder in the regulation of breathing (meningitis,
encephalitis).
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Terminal breathing
• In terminal conditions the apneustic breathing and
severe gasping are revealed.
• Apneustic breathing consist of prolonged spastic
inhales, interrupted by brief exhalations (impaired
connections of apneustic, pneuvmotaxic centers and
vagal nerve).
• Severe gasping characterized by gradually decreased
rate and depth of inhales because of arrest of
resperatory neurons activity above dorsal and ventral
respiratory group in medulla (in agony of death,
terminal period of asphyxia).
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Short wind
• Short wind – increased breathing because of subjective
feeling lack of air, when excitatory influences to
respiratory neurons are more intensive, then
pathological effects.
• (in loss of diffusion area, lack of perfusion,
inflammation and activation of reflexes from irritant
receptors in pneumonia, decreased impulsation from
baroreceptors in aorta and carotids in blood loss,
shock; increased impulses from chemoreceptors in
hypoxia, hypercapnia, acidosis, overstratching
respiratory muscles because of decreased lung elastic
recoil, obstruction of upper respiratory pathways.
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Acute deficiency of breathing
• Acute deficiency of breathing develops in
some minutes to hours and progressing
rapidly.
• The main pathological mechanisms are
hypoxemia, hypercapnia, acidosis, central
nerve control disturbances. Acute deficiency
of breathing can result in coma.
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Chronicle deficiency of breathing
• Chronicle deficiency of breathing is
characterized by gradual enhance of
hypoxemia and hypercapnia.
• Pathological disturbances in chronicle
deficiency of breathing are less intensive, than
in acute deficiency of breathing due to
activation of compensatory mechanisms.
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Damage to the chest
• The contamination of air
in the pleural cavity is
called pneumothorax
(opened, closed,
valvular).
• If air can enter the
pleural cavity and go out
by place of trauma, this
is opened
pneumothorax.
• In case of shift the
damaged tissues the air
cannot go out the
pleural cavity and closed
pneumothorax develops.
• When mild tissues in the
place of trauma permit
entering of air and
prevent outflow of air
from the pleural cavity,
the valvular
pneumothorax develops.
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Damage of the respiratory muscles
• Damage of motoneurons of spinal cord that control respiratory
muscles may occur due to inflammatory and degenerative
processes (with amyotrophic lateral sclerosis, poliomyelitis,
syringomyelia), due to intoxication (strychnine, tetanus toxin).
• Violation of the conduction impulses in the peripheral nerves that
supply respiratory muscles can occur because of inflammation,
vitamin deficiency, trauma. Diaphragmatic nerve lesion leads to
paralysis of the diaphragm, which manifests its paradoxical
movements according to changes in pressure in the chest cavity at the inhalation diaphragm rises, at the exhale – gets plant.
Violation of neuromuscular transmission of impulses occurs in
myasthenia, botulism, introduction of muscle relaxants. In all
these cases, the ventilation function get disturbed.
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• When obstructive respiratory insufficiency, airway can
be broken due to their narrow, leading to increased
resistance to air movement (when inhaled forensic
particles, thickening of the walls of airways due to
inflammation, muscle spasm of the larynx, bronchial
compression due to swelling, inflammation, enlarged
thyroid gland .)
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Causes of bronchial asthma
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Mechanism that limits maximal expiratory flow rate
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Emphysema
• In emphysema the lungs
lose their elasticity and
stretch considerably with
less transpulmonary
pressure, so there is lack of
pressure from within
bronchioles - their
clearance decreases,
increases resistance to air
movement, difficult
breath.
• Exhalation becomes active
due to decreased elasticity
of the lungs, the pressure
increases and bronchioles
collapse, so alveoli are
filled with residual air. 21
The alveoli filled with residual air
because of emphysema
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Pathology of the
lung in end-stage
cystic fibrosis
Key features are:
• the widespread
mucus impaction
of airways and
bronchiectasis (U);
• small cysts (C);
• hemorrhagic
pneumonia in
lower lobe.
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Atelectasis
• Atelectasis
caused by
airway
obstruction
and
absorption of
air from the
involved lung
area on the
left and by
compression
of lung tissue
on the right.
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Atelectasis
• The right lung of
an infant (left
side of photo) is
pale and
expanded by air,
whereas the left
lung is collapsed.
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Asphyxia
• The first stage is characterized by deep and rapid breathing
with a predominance of inspiratory phase (inspiratory dyspnea).
• In the second stage begins a gradual decline in respiration rate
against the background of deep respiratory movements. Phase
exhalation prevails over the inspiratory phase (expiratory
dyspnea).
• In the third stage of the frequency and depth of respiratory
movements decreased steadily up to a complete stop breathing.
After a short term of absent respiration (preterminal pause)
several rare deep respiratory movements are observed (terminal
or agonic, breathing).
• Stimulation of breathing at the beginning of asphyxia
associated with direct and reflex excitation of carbon dioxide and
respiratory center hipoksemichnoyu blood. With the growth
inhibition of hypoxic brain come the respiratory center and
complete paralysis of its functions. The appearance of terminal
respiration explained by the excitation of neurons of the caudal
medulla oblongata.
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Obstruction of larynx leads to hypoxia
А – normal larynx; В – Obstruction of larynx
from edema caused by croup.
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Violation of ventilation-perfusion ratio
• To maintain the gas composition of blood it is important
to not only the absolute value of alveolar ventilation, but
the proper balance between ventilation and perfusion
lung. The amount of blood flowing through the lungs for 1
min, equal to 4.5-5 liters, approximately corresponds to
the value cardiac output.
• The optimal ratio of alveolar ventilation and perfusion
lung is 0.8 (4 l/ 5 l). It may vary upward or downward. In
both cases, normal blood gas composition can not
provide.
• The predominance of ventilation pressure of oxygen in
the alveoli in blood is sufficient, but blood carry out too
much carbon dioxide (hipokapniya). If, however,
ventilation is slower than perfusion, hypoxemia and
hypercapnia occur.
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Acute respiratory distress syndrome (ARDS)
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Hypoxia
Hypoxia occurs when O2 transport from ambient air to the
cell is impaired.
There may be several causes:
• In exogenous (hypoxic) hypoxia the hypoventilation
reduces the diffusion gradient to venous blood and thus
impairs O2 uptake.
• In respiratory (hypoxic) hypoxia reduced diffusing capacity
prevents equilibration of gas concentrations in alveoli and
capillary blood.
• In hemic hypoxia reduced O2 uptake capacity of the blood.
• In circulative hypoxia circulatory failure impairs O2
transport in the cardiovascular system.
• In hystotoxic (tissue) hypoxia the tissue diffusion is
impaired.
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Hypoxic hypoxia
Blood parameters
Oxygen capacity of blood
In Vol %
Contens О2 , Vol %
Arterial blood
Saturation О2
pО2, mm Hg
Contens О2 , Vol %
Venous blood
Saturation О2
pО2, mm Hg
Arterial-venous difference
In О2
Norm
Hypoxic
hypoxia
20
20
19
95
100
14,8
74
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14,8
74
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10,6
53
21
4,2
4,2
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Hemic hypoxia
Blood parameters
Oxygen capacity of blood
In Vol %
Contens О2 , Vol %
Arterial blood
Saturation О2
pО2, mm Hg
Contens О2 , Vol %
Venous blood
Saturation О2
pО2, mm Hg
Arterial-venous difference
In О2
Norm
Hemic
hypoxia
20
10
19
95
100
14,8
74
41
9,5
95
100
5,3
53
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4,2
4,2
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Circulative hypoxia
Blood parameters
Oxygen capacity of blood
In Vol %
Contens О2 , Vol %
Arterial blood
Saturation О2
pО2, mm Hg
Contens О2 , Vol %
Venous blood
Saturation О2
pО2, mm Hg
Arterial-venous difference
In О2
Norm
Circulative
hypoxia
20
20
19
95
100
14,8
74
41
19
95
100
10,6
53
28
4,2
8,4
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Tissue hypoxia
Blood parameters
Oxygen capacity of blood
In Vol %
Contens О2 , Vol %
Arterial blood
Saturation О2
pО2, mm Hg
Contens О2 , Vol %
Venous blood
Saturation О2
pО2, mm Hg
Arterial-venous difference
In О2
Norm
Tissue
hypoxia
20
20
19
95
100
14,8
74
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19
95
100
18
90
80
4,2
1,0
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Causes of Alkalosis
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Causes of Acidosis
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The damage of nervous system by hypoxia
• In the early stages of hypoxia structural changes in
nerve tissue are reversible. If to continue hypoxia, the
structure and function of neurones will be disturbed.
Neurons of the cerebral cortex live without oxygen for
no longer than 5-6 min, even under normal conditions
they are on the verge of hypoxia.
• The narrowing of the vessels at cerebral
atherosclerosis causes atrophy and glial sclerosis in
brain substance, which is expressed clinically senile
forgetfulness.
•The neurons of the cerebellum are damaged easily.
More stable and breathing vasomotor centers, they
can withstand a complete cessation of blood supply for
30 min. Spinal cord saves hours of livelihoods during
hypoxia. As a result of inhibition of the respiratory
center appears periodic breathing.
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Myocardial injury during hypoxia
• Second place for sensitivity to hypoxia has the heart.
On the contraction of the muscle fibers spent half the
energy generated by them, as hypoxia, accompanied
by an energy deficit, dramatically reduces myocardial
contractile function. In addition, an excess of calcium in
cardiac myocites retards their relaxation, shortens
diastole and further reduces their contractile ability.
• Conductive system of the heart as a whole more
resistant to hypoxia, compared with the contractile
myocardium. Resistance is increasing its divisions from
the base to the apex of the heart. The most enduring
Purkinje cells, which provided energy primarily due to
oxygen-free glycolysis. The sharp decrease in
myocardial blood supply leads to dystrophic and
necrotic changes, life-threatening.
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Compensatory reactions during hypoxia
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•
•
•
Breathing
Haemodynamic
Hemic
Tissue
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Respiratory compensatory reactions (bronchial asthma)
There is shortness of breath pochaschenym and depth,
resulting in inhibition of the respiratory center appears periodic
breathing
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Haemodynamic compensatory reactions
• tachycardia;
• increase in stroke volume of blood due to the
action of adrenaline on cardiac betaadrenoreceptors;
• increase in cardiac output;
• acceleration of blood flow;
• peripheral vascular constriction and
vasodilatation in vital organs, i.e. centralization of
blood circulation, redistribution of blood to the
heart, brain, lung, while limiting the blood supply
to muscles, intestines, skin, spleen.
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Hemic compensatory reaction
• The blood reactions primarily increase the oxygen capacity
of blood. For hypoxia characteristic polycythaemia, i.e.
increasing the number of erythrocytes per unit volume of
blood. Initially, this occurs due to release of erythrocytes
from the depot, which perform the function of capillaries of
the skin, liver, spleen, lungs. Normally there are up to 45%
of blood.
• If prolonged hypoxia, stimulated erythropoiesis in red
bone marrow. This condition stimulates erythropoietin,
secreted mostly by the kidneys. They act on erythropoietic
cells and make them proliferate and differentiate into
mature erythrocytes. At the same time increases the
synthesis of haemoglobin, and charge it to each
erythrocyte becomes larger. In addition, the increased
affinity of haemoglobin for oxygen in the lungs and
decreases - in the tissues.
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Tissue compensatory reaction
Reactions of tissue type are aimed:
• to reduce the need for oxygen (decrease in
basal metabolism),
• maximum utilization of oxygen from the blood
(respiratory chain enzyme activation),
• obtain energy in anoxic processes (activation
of glycolysis).
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