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Файл:Pathophysiology of breathing and cardiovascular pathology. Educational and methodological manual
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Topic 3. Pathophysiology of external respiration
(decrease in alveolar ventilation). Hypoventilation often develops
in extrapulmonary diseases, in which the lungs very often remain
healthy.
Two important physiological properties of hypoventilation
should be emphasized. First, it always causes an increase in the
partial pressure of carbon dioxide — P
be easily eliminated by increasing the P
; second, hypoxemia can
CO2
of inhaled air (for exam-
02
ple, by prescribing oxygen inhalation through a breathing mask).
Currently, the definition of forced inspiratory volume (FIV) and
forced vital capacity (FVC) should be considered mandatory in
clinical practice.
Characteristics of hypoventilation parameters:
1) reduction of Respiratory Minute Volume (RMV) due to re-
duction of respiratory rate (RR): (↓) RMV = respiratory volume
× RR (↓);
(RV)
2) hypoxemia;
3) hypercapnia;
4) shift of oxyhemoglobin dissociation curve to the right.
Some causes of hypoventilation
1. Decrease in respiratory center (RC) activity and spinal cord
damage:
— drug-mediated depression of the respiratory center activity
(barbiturates, morphine preparations, etc.), lesions of the medulla
oblongata (with encephalitis, hemorrhage, less often — with neoplasm growth, etc.), spinal cord lesions (for example, displacement
in the upper parts), lesions of cells of the anterior horns of the spinal cord (polio, etc.).
2. Upper airway obstruction:
— ingress of foreign solid objects, liquids into DP lumen;
— impaired drainage function of bronchi and lungs (in hypercrinia, discrinia);
— compression of the upper respiratory tract from the outside;
— thickening of the airway walls;
— bronchial muscle spasm and bronchioles;
— laryngospasm (laryngeal muscle spasm);
— tongue sinking in case of patient's unconscious state.
51
Pathophysiology of breathing and cardiovascular pathology
Characteristics of obstructive hypoventilation measures:
— when the airway lumen decreases, the resistance to air movement along them increases;
— the work of respiratory muscles to overcome resistance increases, especially during exhalation;
— expiratory shortness of breath occurs;
— the reserve exhalation volume (REV) decreases;
— increased residual lung volume;
— Vital Capacity (VC) remains normal for a long time;
— RMV, MV(maximum ventilation) decrease and TiffeneauPinelli index (obstructive disorder index) decrease.
3. Restrictive type of hypoventilation
— extrapulmonary causes:
• disorders of the innervation of the respiratory muscles (for
example, in Guillain-Barre syndrome or diphtheria);
• disorders of neuromuscular transmission (myasthenia, poison-
ing with cholinesterase inhibitors, etc.);
• respiratory muscle lesions (e.
g. progressive muscular dystro-
phy);
• lesions of the supporting structures of the chest (injury, etc.);
— intrapulmonary causes:
• reduced respiratory surface, impaired pulmonary extensibility
(elasticity).
Characteristics of restrictive respiratory failure parameters:
— decrease in total lung capacity and vital capacity, Tiffeneau-
Pinelli index is normal or higher than normal;
— decreases to respiratory volume (RV), decreases the reserve
volume of inhalation (RVI);
— difficulty in breathing — inspiratory shortness of breath occurs;
— the work of respiratory muscles increases, their fatigue occurs;
— decreased Respiratory Minute Volume (RMV), hypoxemia,
hypercapnia were observed in the blood, oxyhemoglobin dissociation curve was shifted to the right.
52
Topic 3. Pathophysiology of external respiration
4. Neuromuscular form of alveolar hypoventilation:
• damage to the nerve innervating the respiratory muscle: Guil-
lain-Barre syndrome;
• neuromuscular junction damage: myasthenia, Lambert-Eaton
syndrome;
• respiratory muscle involvement: Myopathy.
5. Thoracic diaphragmatic form of alveolar hypoventilation:
• Chest wall defects: kyphoscoliosis, thoracoplasty, fibrothorax.
Clinical consequences of hypoventilation:
Effects on the nervous system:
• hypoxemia and hypercapnia;
• acidosis of brain tissue;
• dilation of brain vessels, increase in blood flow, increase in
intracranial pressure (headache appears), increase in permeability
of brain vessels;
• edema of the interstitium;
• reduced diffusion of oxygen from blood into brain tissue;
• brain hypoxia;
• glycolysis is activated;
• acidosis is aggravated; a vicious cycle is formed.
Effects on the circulatory system:
• according to the Euler-Liljestrand reflex, spasm of the pulmonary arterioles develops, pulmonary hypertension appears;
• pulmonary hypertension increases the load on the right ventricle of the heart (the development of right ventricular heart failure
is possible);
• compensatory in hypoxia develops erythrocytosis, increases
blood viscosity, this increases the load on the heart.
Effect on the respiratory system
• pulmonary hypertension, pulmonary edema;
• acidosis causes bronchospasm, decreased surfactant production, increased mucus secretion, decreased mucociliary cleansing;
• respiratory muscle fatigue.
All this leads to even more pronounced hypoventilation, a vi-
cious circle in the pathogenesis of DN closes (Fig. 14).
53
Pathophysiology of breathing and cardiovascular pathology
Fig. 14. Pathogenesis of idiopathic pulmonary fibrosis
Alveolar hyperventilation
Physiological hyperventilation is due to the metabolic needs
of the body due to increased metabolism (for example, during
muscle work, emotional stress).
Pathological hyperventilation occurs with an increase in respiratory center (RC) activity, which is inadequate to the needs of
the body in these conditions:
— direct damage to RC;
— excess (↑) exciting afferent influences on RC;
— passive hyperventilation.
54
Topic 3. Pathophysiology of external respiration
Characteristics of pathological hyperventilation indicators:
1) Increased Respiratory Minute Volume (RMV) by increasing
respiratory rate (RR): ↑ RMV = ↑RR
· RV;
2) Change in arterial blood gas composition:
— hypocapnia (gas alkalosis),
— there may be some increase in O2 tension in arterial blood;
3) Shift of the oxyhemoglobin dissociation curve to the left;
4) Hypocalcemia, since Ca2
+
goes into bone tissue in exchange
for hydrogen ions under alkalose conditions as compensation.
Clinical implications of pathological hyperventilation:
Respiratory paralysis. Spasm of the brain vessels (dizziness,
fainting, decreased attention, memory impairment, irritability, sleep
disorder, nightmare dreams, feeling anxious, threats, etc.). Due to
hypocalcemia, paresthesia, increased neuromuscular excitability
are observed (inclination to seizures up to tetania, there may be
tetanus of the respiratory muscles, laryngospasm, etc.)
Tachycardia and other arrhythmias:
— due to hypocalcemia;
— due to coronary spasm (due to hypocapnia).
Hypotension:
— due to vasomotor center depression (due to spasm; cerebral
vessels);
— due to arrhythmias.
II. Diffusion disorder
Diffusion disorder is manifested by mismatch of capillary and
alveolar P
. However, in some diseases, the thickness of the alveo-
02
lo-capillary membrane increases, which is accompanied by a slowdown in the diffusion of gases through it (in fibrotic alveolitis).
There is a significant expansion of the walls of the alveoli. If hypoxemia develops at rest, then during physical exertion its degree
will increase, since the duration of blood contact with air decreases.
Diffusion disorders accompanied by hypoxemia, especially
pronounced with exercise, can develop in a number of diseases,
55
Pathophysiology of breathing and cardiovascular pathology
including asbestosis, sarcoidosis, fibrotic alveolitis (including idiopathic), interstitial pneumonia, lung damage in diffuse connective
tissue diseases (including systemic scleroderma, rheumatoid arthritis, systemic lupus erythematosis, granulomatosis Wegener, Goodpasture syndrome). In all of the above diseases, the distance from
the alveolar lumen to the red blood cells, which diffuse gases must
pass, can increase (sometimes only in certain parts of the lungs),
and thereby the duration of oxygen diffusion through the alveolarcapillary barrier
III. Lung perfusion disorder
• Pulmonary edema pathogenetic factors:
— increased hydrostatic pressure in capillaries (the most common cause of pulmonary edema, often complicating the course of
heart diseases — acute myocardial infarction, left ventricular insufficiency in hypertension, mitral valve damage);
— increased permeability of capillaries (inhalation or supply of
toxins from the blood, sepsis, toxic effect of oxygen under the influence of ionizing radiation, ARDS.);
— reduced lymphatic drainage (increased central venous pressure, metastatic lymphangitis (Lymphangitis Carcinomatosa);
— reduced pressure in the interstitia (rapid removal of pleural
effusion or pneumothorax, increased airiness of the lung);
— reduced colloidal osmotic pressure (hypoalbuminemia due
to excess fluid transfusion).
In the development of pulmonary edema, two stages are distin-
guished.
1. Interstitial edema.
Increased fluid outflow from the lungs through the lymph vessels. Fluid accumulation in the perivascular and peribronchial
space (as a cuff compresses these formations). X-ray contouring of
interstitial slits. The function of external respiration is practically
unchanged.
56
Topic 3. Pathophysiology of external respiration
2. Alveolar edema.
Often accompanied by severe shortness of breath and orthopnea. Possible departure of pink foamy sputum. Pronounced darkening of pulmonary fields on X-ray diffraction pattern. Severe hypoxemia.
Pulmonary embolism (PE).
Most embols entering the lungs form when blood clots located
in the deep veins of the lower extremities are fragmented. In addition, they can form in the right heart and in the veins of the pelvic
organs. Occasionally, non-thrombotic embols (for example, fat particles, air, amniotic fluid) can enter the lungs.
Pathogenetic factors of PE:
1. Blood stagnation.
2. Disorders in the blood coagulation system.
3. Pathological changes in the vascular wall.
Clinic PE:
— fine particle embolism is not diagnosed, pulmonary hypertension develops in case of repeated thromboembolism;
— embolism with medium-sized particles is accompanied by
pain in the chest, shortness of breath, a small subfebrilitate, bloody
sputum may escape when coughing, pleural friction noise may appear, there are no or minimal pathological changes during lung
X-ray, areas with reduced blood flow are detected during lung
scintigraphy;
— massive embolism is accompanied by hemodynamic collapse, manifested by shock; pallor, pain in the central part of the
chest; dangerous to the life of the patient.
Pulmonary hypertension
An increase in pulmonary artery pressure above 15 mm. Hg is
called pulmonary hypertension.
There are two main types of pulmonary hypertension: primary
(idiopathic) and secondary. Primary pulmonary hypertension
(PPH) is relatively rare (1300 per 1 million people), more often in
women, progresses rapidly. The prognosis is unfavorable, and medical treatment is usually ineffective.
57
Pathophysiology of breathing and cardiovascular pathology
Pathogenetic factors of secondary pulmonary hypertension:
1. Increased pressure in the left atrium.
2. Increased blood flow in the lungs. Blood flow in the lungs
increases in congenital heart defects.
3. Increased pulmonary vessel resistance.
This mechanism causes pronounced pulmonary hypertension
most often:
— vasospastic, mainly developing in alveolar hypoxia, for example at high altitude. in addition, hypertension develops by this
mechanism in chronic bronchitis and emphysema. transient vasoconstriction after thromboembolism causes serotonin, and in a number of diseases (for example, neurogenic pulmonary edema), the
release of catecholamines is important. in addition (for example, in
bronchial asthma), other mediators also matter (Fig. 15, 16).
Fig. 15. Pathogenesis of obstructive changes in bronchial asthma
58
Topic 3. Pathophysiology of external respiration
Fig. 16. Principles of pathogenetic treatment of bronchial asthma
— obstructive (similar to thromboembolism). in addition, fat
particles, air, amniotic fluid, tumor cells can clog vessels. in schistosomiasis, a pronounced reaction develops to colonization of
small arteries by parasites.
— obliterating (for example, in pulmonary emphysema), accompanied by partial destruction of the capillary channel. in addition, this mechanism can be activated in various arteritis, for example nodular polyarteritis. in rare cases (for example, in venoocclusive disease), damage to small veins is noted.
Consequences of pulmonary hypertension:
— formation of pulmonary heart (right ventricular hypertro-
phy) and right-sided heart failure. Manifestations of pulmonary
hypertension due to thromboembolism.
— non-respiration and chest pain.
To confirm the diagnosis, a ventilation and perfusion scan can
be performed.
• Blood bypass.
This disorder implies the passage of part of the venous blood
directly into the arterial channel, bypassing the ventilated areas of
the lungs while maintaining blood flow.
59
Pathophysiology of breathing and cardiovascular pathology
Etiology:
— developmental anomalies;
— pneumonia (impaired ventilation-perfusion ratio);
— acute respiratory distress syndrome;
— in congenital heart defects (atrial or interventricular septum
defects) or non-infection of the arterial duct, the shunts are located
outside the lungs. In this case, the pressure in the right parts of the
heart should exceed that in the left parts; otherwise, the shunt will
occur from left to right. It is very important for clinical practice
that the described changes are observed only with blood bypass
grafting. If inhalation of pure oxygen is prescribed during bypass,
the P
in the arterial blood will increase, but will not reach normal
02
values. With hypoxemia due to the other three causes (hypoventilation, impaired diffusion, impaired ventilation-perfusion ratio),
breathing with pure oxygen leads to an increase in blood P
to al-
02
most physiological level.
IV. Violation of ventilation-perfusion ratio (VPR)
By this term is meant a violation of the interaction of ventilation of the lungs and perfusion of blood through the vascular network of the lungs, which leads to the inefficiency of the entire gas
exchange system.
VPR — primary pathogenesis link in:
— hypoxemia in COPD;
— interstitial and vascular (pulmonary embolism — PE, etc.)
lung diseases.
Disorder of VPR is diagnosed after exclusion of three other
causes of hypoxemia: hypoventilation, diffusion disorder, blood
bypass.
Please note: normally, in almost all parts of the lungs, ventilation and circulation processes occur in such a way that the ventilation-perfusion ratio is ~ 1.
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