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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
V. Respiratory dysregulation
Respiratory dysregulation: tachypnea, bradypnea, apnea, hyperpnea, periodic respiration, terminal respiration (Fig. 17).
Fig. 17. Respiratory control mechanism
The main mechanisms of respiratory regulation disorder are:
1) Excess (↑) or lack (↓) of excitatory afferent effects on the
respiratory center (RC).
2) Excess (↑) inhibitory afferent effects on RC.
3) Direct damage to the RC (as a result, an increase or decrease
in the activity of the RC develops).
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Pathophysiology of breathing and cardiovascular pathology
• Drug overdose: opioids, benzodiazepines, alcohol.
• Cerebral stem hemorrhage, infarction.
• Primary alveolar hypoventilation.
Etiology and pathogenesis of respiratory distress syndrome
Etiology:
Shock (clinical situation accompanied by lower blood pressure):
• infectious causes;
• sepsis syndrome (predominantly from Gram-negative bacte-
ria) with or without;
• persistent hypotension (> 40
% of cases);
• pneumonia (viral, bacterial, fungal, mycobacterial), miliary
tuberculosis;
• bronchiolitis obliterans — organizing pneumonia; Injury:
bruised lung;
Embolism: Fat Emboli; Air Emboli; Blood clots; Amniotic;
fluidembolism Traumatic brain injury (increased intracranial pressure).
• Aspiration (> 30
% of cases).
• Gastric contents.
Drowning (fresh/salt water).
Drug overdose:
• Heroin;
• Methadone;
• Propoxifene;
• Barbiturates, salicylates, thiazides, colchicine.
Inhaled toxins
• Smoke inhalation;
• High oxygen concentrations (iatrogenic);
• Corrosive chemicals (ammonia, sulfur dioxide, chlorine, ni-
trogen dioxide);
• Smoking the free base of cocaine.
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Topic 3. Pathophysiology of external respiration
Radiation.
Hematological disorders:
• Disseminated intravascular coagulation;
• Massive blood transfusion;
• After cardiopulmonary bypass;
• Thrombotic thrombocytopenic purpura;
Metabolic disorders:
• Pancreatitis;
• Uremia;
• Paraquat inward.
Burns.
Cancer.
Anaphylaxis.
Eclampsia.
Radiation pneumonia (Fig. 18, 19).
Trauma and increased permeability of the capillary-alveolar
membrane are permeable to fluid, protein, debris (cellular debris);
platelets and blood cells exit the vessels into the interstitium and
alveoli. Activated neutrophils secrete a variety of products, damage
alveolar cells, and lead to the development of edema, surfactant
inactivation, and hyaline membrane formation.
Causes of acute respiratory failure:
Central nervous system:
• Drug overdose (sedative, sleeping pills, opioids, anesthetics);
• Cerebral vascular pathology (stroke);
• Hypothyroidism;
• Central nervous system infections;
• Brain injury;
• Brain tumour.
Neuromuscular diseases and related disorders:
• Guillain-Barre syndrome;
• Myasthenia gravis;
• Multiple sclerosis;
• Muscular dystrophy;
• Mixedema;
63
Pathophysiology of breathing and cardiovascular pathology
• Polio;
• Polymyositis;
• Drug or toxin-induced (botulism, aminoglycosides, organo-
phosphates, neuromuscular blockers);
• Tetanus;
• Amyotrophic lateral sclerosis;
• Quadriplegia;
• Hemiplegia.
Fig. 18. Pathogenesis of Acute Respiratory Distress Syndrome
64
Topic 3. Pathophysiology of external respiration
Fig. 19. Mechanism of changes in the lungs in RDSV
Chest and diaphragm lesions:
• Trauma (thoracic/abdominal);
• Kyphoscoliosis;
• Upper abdominal or thoracic surgery;
• Pleural effusion;
• Hemothorax/pneumothorax/chylothorax;
• Massive ascites.
Airway lesions:
• Laryngospasm;
• Foreign body aspiration;
• Asthma;
• Acute exacerbation of chronic bronchitis or emphysema.
Pulmonary parenchymal diseases:
• Lung contusion;
• Aspiration;
• Pneumonia;
65
Pathophysiology of breathing and cardiovascular pathology
• Interstitial lung disease;
• Emphysema;
• Pulmonary ibrosis;
• Acute respiratory distress syndrome;
• Infant respiratory distress syndrome;
• Pulmonary emboli (blood, fat, air, amniotic fluid);
• Cardiac and non-cardiac pulmonary edema;
• Shock.
Increase in CO
generation:
2
• Fever;
• Infectious Diseases;
• Hyperthyroidism;
• Medicines.
SITUATIONAL TASKS
Clinical case №
1
Patient N., 28 years old, complains of periodic, mainly daytime, episodes of shortness of breath with difficulty exhaling, accompanied first by coughing, then the appearance of whistling
wheezing.
History: first noted the appearance of attacks 4 months ago, after suffering an acute viral disease. Previously, there were no such
symptoms, although she often had respiratory infections (more
than four times a year). The first attacks appeared during the period
of work in the hairdresser. Since then, they have been repeated no
more than once a week during working hours. Nocturnal episodes
of difficulty breathing does not note. When studying concomitant
diseases, it was found that in childhood she suffered from diathesis,
from the age of 14 during the flowering of poplars she noted the
appearance of itching in the eyes and mucous discharge from the
nose, sneezing. I did not contact the doctor earlier about the treatment of allergies. Self-administered suprastin if necessary. Doesn't
smoke. Alcohol is not abused.
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Topic 3. Pathophysiology of external respiration
Objective: the patient is emotionally labile. Height 174 cm,
weight 66 kg, waist girth 76 cm. Skin of ordinary color, warm and
wet to the touch. The skin turgor is normal, there is no smell of
acetone from the mouth. NPV 20 per minute. Vesicular breathing
in the lungs, no wheezing. Pulse 70 per minute, rhythmic, moderate
filling and tension. The boundaries of relative dullness of the heart
are normal. Heart tones are loud, rhythmic, heart rate 70 per minute. BP 110/70 mm Hg.
Questions:
1. Highlight and justify syndromes, identify the presenter.
2. Indicate the etiological factors for the occurrence of attacks.
3. Describe the pathogenesis of symptoms.
4. List the anamnestic data confirming the possibility of dysp-
nea attacks in this patient and their origin.
5. Assign additional examinations.
6. Specify main link of pathogenesis (MLP):
I. Alveolar ventilation disorder.
II. Diffusion disorder
III. perfusion disorder. Blood bypass.
IV. Disorders of ventilation-perfusion ratio.
V. Dysregulation of respiration.
VI. Combination of pathogenetic factors.
Answer:
1. Based on complaints, it can be concluded that an attack of
bronchial obstruction syndrome has developed.
2. Contact with environmental allergens (poplar down, professional allergens — aerosols (varnishes and paints in a hairdresser)
provokes the development of bronchial obstruction.
3. Complaints are related to bronchospasm, mucus hypersecretion and inflammatory edema of the bronchial mucosa.
4. Attacks of periodic bronchial obstruction indicate an allergic
nature in individuals prone to atopy. A history of diathesis and pollinosis during poplar flowering indicates a genetic predisposition to
atopy.
67
Pathophysiology of breathing and cardiovascular pathology
5. Scarification intradermal tests with possible allergens (plant
pollen, whose flowering occurs in May, the month-time of poplar
flowering). In order to detect bronchial hyperreactivity, a study of
the function of external respiration (determination of FEV
(forced
1
exhalation volume in the first second) and a change in FVC (forced
vital capacity of the lungs).
6. I. Alveolar ventilation disorder
Comments. These complaints are related to the presence of episodes of bronchial obstruction in the patient against the background of genetic predisposition to atopy.
Possible diagnosis: Bronchial asthma, persistent course.
Clinical case №
2
Patient N., 42 years old, presents complaints of: shortness of
breath with difficulty exhaling when walking in a flat area (notes
that it is slower than the faces of his age group), cough in the morning after getting out of bed, periodic excretion of sputum mucosa,
as well as weakness, lethargy, decreased performance.
History: Cough in the morning celebrates over the past five
years. He contacted the doctor once about the appearance of cough
with purulent sputum against the background of acute respiratory
infection. Acute bronchitis was diagnosed. He received antibiotic
treatment, after which he noted an improvement in well-being.
However, he continued to worry about coughing in the morning
and releasing a small amount of sputum. The patient smokes from
the age of 16, in the last ten years to 20—30 cigarettes per day.
Cardiovascular disease denies. Contacts with patients with tuberculosis deny. Allergies to medicines, food products, animal hair denies.
Objectively: asthenic physique, height 184 cm, weight 82 kg,
waist girth 88 cm. Skin of ordinary color, warm to the touch. The
examination revealed thickening of the end phalanges of the fingers of the hands and flattening of the nail plate. The skin turgor is
68
Topic 3. Pathophysiology of external respiration
normal, there is no smell of acetone from the mouth. NPV 22 per
minute. In the lungs, hard breathing, dry wheezing of high and low
timbre. Pulse 65 per minute, rhythmic, satisfactory filling and tension. The left border of relative dullness is 1.5 cm inward from the
midclavicular line. Heart tones are loud, rhythmic, heart rate 65 per
minute. BP 130/80 mm Hg.
Questions:
1. Highlight and justify syndromes, identify the presenter.
2. Describe the mechanism of complaints.
3. Identify the key factors of history in the development of the
described clinical situation.
4. Specify the leading diagnostic method and data required to
confirm the hypothesis about the nature of the disease.
5. Formulate a preliminary diagnosis and specify diagnostic
criteria.
6. Specify MLP:
I. Alveolar ventilation disorder, broncho-pulmonary form, obstructive.
II. Diffusion disorder.
III. perfusion disorder. Blood bypass.
IV. Disorders of ventilation-perfusion ratio.
V. Dysregulation of respiration.
VI. Combination of pathogenetic factors.
Answer:
1. According to the complaints, the following syndromes were
identified: asthenic, bronchial obstruction, respiratory failure. The
leading syndrome is bronchial obstruction.
2. Partially irreversible air flow restriction.
3. The patient has a long smoking experience with a large
number of cigarettes, the patient's age (over 40 years old) and slow
progression of symptoms in the history from cough to shortness of
breath also matter. Smoking is a key factor.
4. Spirometry is the gold standard and the leading diagnostic
method for assessing the degree of bronchial obstruction. To confirm the hypothesis of limiting air flow, a decrease in FEV
ratio of FEV
/ FVC less than 70 % is important.
1
and a
1
69
Pathophysiology of breathing and cardiovascular pathology
5. Given the presence of shortness of breath, slow progression
of symptoms, mature age of the patient and the presence of a risk
factor — smoking, it can be assumed that the patient has chronic
obstructive pulmonary disease. It is possible to clarify the severity
of the disease based on spirometry data.
6. Specify MLP:
I. Alveolar ventilation disorder, bronchopulmonary form, ob-
structive.
Clinical case №
3
Patient N., 32 years old, presents complaints about: pain in the
right half of the chest, worsening during breathing, coughing and
decreasing in position on the sick side, the impossibility of deep
inhalation due to pain, as well as weakness, decreased performance, dry cough and fever up to 37.8
°C.
Medical history: Suffered an acute respiratory illness two
weeks ago. The first symptoms were fever, nasal congestion. I didn't see a doctor. He independently took paracetamol with an increase in temperature, drank tea with raspberries and, with nasal
congestion, used vasoconstrictor drops — naphthysine. The condition did not improve, there was a dry cough, shortness of breath
and pain in the right half of the chest, which became the reason for
seeing a doctor. Cardiovascular disease denies. Contacts with patients with tuberculosis deny. Allergies to medicines, food products, animal hair denies. Doesn't smoke.
Objectively: Skin of ordinary color, warm to the touch. The
examination revealed a lag in the right half of the chest in the act of
breathing. NPV 24 per minute. In the lower parts of the lungs on
the right, noise is detected, which is heard on inhalation and exhalation, does not change localization during coughing and is preserved during a sample with simulated breathing. Pulse 65 per minute, rhythmic, full, intense. The left border of relative dullness is
1.5 cm outside the midclavicular line. Heart tones are loud, rhythmic, heart rate 65 per minute. BP 120/85 mm Hg.
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