ACUTE RESPIRATORY FAILURE (ARF)

DR. NADIIA RAHMAT

The Upper Respiratory System:

-nasal cavity
-nasopharynx
-oropharynx with oral cavity

The lower respiratory tract includes:

- larynx (although sometimes it is also

referred to the upper tract),
- trachea,
- Bronchus
- lungs.
Non-respiratory functions
of the lung
•The lung, with its unique ability to distend and recruit pulmonary
vasculature, acts as a reservoir of blood, fine tuning preload to the left
heart to optimize cardiac output.
•The lung acts as a filter against endogenous and exogenous emboli,
preventing them from accessing systemic circulation.
•Pulmonary epithelium forms the first line of defence against inhaled
particles.
•Pulmonary endothelial cells are responsible for uptake, metabolism, and
biotransformation of several exogenous and endogenous substances.
•Pulmonary metabolic capacity is easily saturated, but pulmonary
endothelial binding of some drugs alters their pharmacokinetics.
Acute respiratory failure
(ARF) is a polyetiological
condition characterized by a
pronounced violation of the
transport of oxygen (O 2) to
tissues and the removal of
carbon dioxide (CO 2) from
the body, which, at maximum
stress, have all compensatory
systems of the body.
Classification of Respiratory failure
 Etiology
Acute and chronic diseases of the respiratory system

Diseases of the heart with blood congestion in the pulmonary circulation

Disorders in the central nervous system, respiratory muscles, and nerves

Critical conditions (shock, collapse, coma).

 Causes of Acute Hypoxemic
Respiratory Failure
Diffuse lung
Most frequent
injury
- Cardiogenic (hydrostatic or high pressure)
edema - Sepsis and systemic inflammatory response
- Left ventricular failure (with ischemic heart syndrome
disease, cardiomyopathy, valve damage) - Aspiration of acidic stomach contents
- Volume overload (especially with comorbid - Multiple transfusions for hypovolemic shock
kidney and heart disease)
- Edema with increased capillary permeability
with low blood pressure (ARDS)
 Less common causes
Drowning
Pancreatitis
Air or fat embolism
Cardiopulmonary shunt
Drug reaction or overdose
Leukoagglutination
Inhalation trauma
Infusion of biologically active substances (for example,
interleukin-2)
Edema of unspecified or mixed etiology
After straightening of the atelectasized lung
Neurogenic, after seizure
Associated with treatment aimed at relaxing
the musculature of the uterus
High-rise
Alveolar bleeding
Connective tissue diseases
Thrombocytopenia
Bone marrow transplant
Immunodeficiency infection
Focal lung lesions
Lobar pneumonia
Lung contusion
Atelectasis of the lung lobe
ARDS is acute respiratory distress syndrome.
 Pathogenesis
Violations of the ventilation-perfusion relationship

Violations Violations Decreased

of perfusion
Restrictive Violations blood flow
ventilation
of
diffusion Obstruction

Increase
in Thickening
intermembrane or decreased
Dysregulatory
spaces permeability of
Hurdle membranes:
utflow of blood alveoli,
capillaries,
erythrocytes
The main methods used in the diagnosis
of respiratory failure are:

• physical examination of the patient;

• spirometry;
• determination of blood gas composition
• Rg /CT (computed tomography of chest)
• ECG
Respiratory - increased breathing;
- increased heart rate;
distress - loss of consciousness;
- lowering blood pressure;
symptoms - dyspnea;
- paradoxical movements of the chest;
- cough;
- the participation of the auxiliary respiratory muscles;
- swelling of the veins in the neck;
- fright;
- blue discoloration of the skin;
- chest pain;
- stopping breathing.
 Severity of RD
According to the severity, the following types of respiratory failure are
distinguished:
First degree. The partial pressure of oxygen in arterial blood is 60 to 79
mm Hg. According to pulse oximetry data, this corresponds to 90 - 94%.
Second degree. The oxygen partial pressure is from 40 to 59 mm Hg
(75 - 89% of the norm).
Third degree. The oxygen partial pressure is less than 40 mm Hg.
(less than 75%).
Pneumonia is an acute infectious disease of predominantly
bacterial etiology, characterized by focal lesions of the respiratory
parts of the lungs and the mandatory presence of intraalveolar
exudation
Etiology. The development of pneumonia is of great importance:
 
• Bacterial infection:
- gram-positive flora (pneumococcus, streptococcus, staphylococcus);
- gram-negative flora (hemophilic bacillus, Klebsiella,
Enterobacteriaceae, Escherichia coli, Proteus, Pseudomonas,
Legionella, Chlamydia).
• Mycoplasma.
• Viral infection (influenza, parainfluenza, herpes viruses).
• Fungal infection.
 Pathogenesis
The main pathogenetic links in the development of pneumonia are:

• Penetration of the causative agent of pneumonia into the lung tissue by inhalation, bronchogenic,
hematogenous and lymphogenous routes.
• Changes in the local bronchopulmonary defense system: mucociliary transport,
bronchopulmonary immune system, nonspecific resistance factors (lysozyme, lactoferrin,
b-lysine, IgA, interferon; surfactant system).

IgA
b-lysine
lactoferrin
lysozyme
• Development under the influence of infection of a local inflammatory process and its spread
through the lung tissue, which depends on the type of pathogen.
• Sensitization to infectious agents and the development of hyperergic, normo - hypoergic
reactions, the formation of immune complexes, their interaction with complement, the release of
inflammatory mediators.
• Increased platelet aggregation, disorders in the microcirculation system.
• Neuro-trophic disorders of the bronchi and lungs.
• Increased oxidation of lipids of cell membranes, activation of endogenous phospholipases, a decrease in the
effect of antioxidants, which leads to damage to the structure and dysfunction of cell membranes.
Classification of pneumonia
Depending on the characteristics of infection:
• Community-acquired pneumonia (synonyms "community-acquired", "generalized",
"outpatient"), which arose outside the hospital.
• Intrahospital (nosocomial, nosocomial), which occurred ≥48 hours after the patient was
admitted to the hospital in the absence of any infectious disease during the incubation
period at the time of hospitalization.
• Aspiration pneumonia.
• Pneumonia in persons with severe immunosuppression (congenital immunodeficiency,
HIV infection, iatrogenic immunosuppression).
 There are small and large criteria for the severe
course of community-acquired pneumonia

Small criteria:
• respiratory rate ≥30 in 1 min;
• impaired consciousness, oxygen
saturation <92% (according to pulse
oximetry data), pO2 <60 mm Hg..;
• systolic blood pressure <90 mm Hg. •
bilateral or multifocal lung lesions,
signs of decay, pleural effusion.
Big criteria:
• the need for artificial ventilation;
• rapid progression of focal-infiltrative
changes in the lungs (increase in the size
of infiltration> 50% within the next 2
days);
• septic shock or the need to administer
vasopressors for ≥4 hours;
• acute renal failure (amount of urine <80
ml in 4 hours or serum creatinine level>
0.18 mmol / l in the absence of chronic
renal failure).

A severe course of community-based pneumonia is evidenced

by the presence of ≥2 small or 1 large criteria in the patient,
each of which significantly increases the risk of death.
Complex treatment of severe pneumonia:
• Immunosubstitution therapy: native or freshly frozen human blood plasma 100-200 ml for 3 days, human
immunoglobulin 6-10 g / day, simultaneously intravenously.
• Detoxification therapy: saline solutions (physiological, Ringer's, etc.) 1000-3000 ml, 5% glucose solution
400-800 ml / day, Neohemodesis 400 ml / day. The solutions are administered under the control of central
venous pressure or diuresis.
• Correction of microcirculatory disorders: sodium heparin 20,000 U / day, dextran + sodium chloride
(Rheopolyglucin) 400 ml / day. Clexan 1 mg/kg, fraxiparini 0,3-0,4 ml
• Correction of dysproteinemia: human albumin 100-500 ml / day (depending on blood counts), nandrolone 1
ml once every 3 days № 3.
• Oxygen therapy: oxygen through a mask, catheters, mechanical ventilation depending on LN.
• Corticosteroid therapy: only in case of infectious toxic shock, infectious toxic damage to the kidneys, liver,
bronchial obstruction, etc. Prednisolone is administered at a dose of 60-90 mg IV or equivalent doses of other
drugs on a situational basis. The amount and duration of administration is determined by the severity of the
condition.
• Bronchodilator therapy: theophylline 5-10 ml of 2.4% solution 2 times a day intravenously drip,
ipratropium bromide 2-4 breaths 4 times a day, ipratropium bromide + fenoterol 2 breaths 4 times a day;
expectorants (ambroxol - 100 mg / day, acetylcysteine ​- 600 mg / day); glucocorticosteroids (see above).
Expectorants and bronchodilators during intensive care are administered through a mixer during oxygen
therapy.
• Antioxidant therapy: ascorbic acid 1.5-2 g / day orally, rutoside 1.5-2 g / day orally.
• Antienzyme drugs: aprotinin 10,000 U / day and other drugs for 1-3 days with the threat of abscess
formation.
For the treatment of community-based and hospital-acquired pneumonia, mainly 5 groups of antibiotics
are used:

1. Penicillins.
2. Cephalosporins are divided into 4 generations depending on the spectrum of antimicrobial activity
3. Macrolides
4. Fluoroquinolones
 Diagnostic program
1. Visual examination, determination of the etiological factor, assessment of the general
condition of the patient, auscultation and percussion of the lungs.
2. Mandatory measurement of heart rate, blood pressure, CVP (central vein
catheterization)
3. Laboratory examination:
- measurement of indicators of arterial blood gases, CBS and lactate;
- general analysis of blood and urine;
- coagulogram;
- blood chemistry;
- ECG.
4. Chest X-ray.
ARDS is a syndrome of acute pulmonary insufficiency that occurs as a response to local or systemic
tissue hypoxia, ischemia and reperfusion, with a multifactorial etiology. The inflammatory process in the
lungs is associated with many factors: the activation of polymorphonuclear neutrophils, endothelial cells,
the production of free oxygen radicals. In the pathogenesis, the main role is played by uncorrected
pulmonary edema due to damage to the alveolar-capillary membrane.
The pathogenesis of ARDS is not well understood. Below are the main pathogenetic links of its development.

1. Under the influence of various factors, a large number of activated leukocytes and platelets accumulate in the
pulmonary capillaries and interstitial tissue of the lungs, which secrete many biologically active substances
(proteinases, prostaglandins, lipid peroxidation products, leukotrienes, etc.), which damage the alveolar epithelium and
vascular epithelium, change the tone and reactivity of the vessels. From the circulating blood, leukocytes enter the area
of ​the inflammatory process in the lungs, which leads to infiltration of the lung parenchyma.

2. Biologically active substances sharply increase vascular permeability, there is a pronounced penetration of plasma
and erythrocytes into the alveoli and interstitial tissue with the development of pulmonary edema and atelectasis.

3. There is hypoventilation of the alveoli against the background of a significant deficiency of surfactant. The
elasticity of the alveolar wall decreases, which leads to discoid atelectasis, shunting of venous blood into the arterial
bed, disruption of the relationship between ventilation and perfusion, impaired diffusion of oxygen and carbon dioxide
with the development of hypoxia, hypercapnia.

4. Increased pressure in the pulmonary artery is a characteristic sign of the disease in the absence of pathology of the
circulatory system.
Ventilation modes in patients with ARDS:
1. The effectiveness of a protective ventilation strategy has been proven, which includes:
tidal volume = 6 - 7 ml / kg and PEEP = 6 - 10 cm H2O; plateau pressure <35 cm water
column PaCO2 can be maintained at a level that does not affect hemodynamics and patient
consciousness - safe hypercapnia mode.
2. Active kinetotherapy: be sure to turn the patient on his stomach (hemodynamic instability, as well as severe
traumatic brain injury, fractures of the spine, pelvic bones may be a contraindication). There are no recommendations
on the rotation regimen yet, but it is important to start kinetotherapy from the first days of mechanical ventilation, to
turn it over at least 2 times for 4 - 6 hours per day, provided that the patient is well tolerated, the time the patient can
be on his stomach can be long. If it is not possible to turn the patient on his stomach, mandatory turns to the sides
with a change in body position at least after 2 hours.
3. You can apply a "recovery maneuver", which consists in periodically inflating the lungs for 40 - 45 s by
increasing the PEEP, or tidal volume.
4. If it is impossible to maintain blood oxygenation at a safe oxygen concentration (FiO2 <0.6), an inverted
ventilation mode with an increase in the inhalation / exhalation ratio> 0.5 is possible.
5. Systematically carry out reorganization of FBS.
Indications for the use of extracorporeal membrane oxygenation:
PaO2 <10 cm H2O or SaО2  85-90% at FiО2 = 1 and PEEP 50mm Hg.
Intratracheal administration of an artificial surfactant.
Anti-inflammatory therapy: glucocorticoids in the first stages of
ARDS are not shown and worsen the results of treatment, only
with late ARDS (proliferative stage) small doses are shown
(methylprednisolone 2-3 mg / kg per day); nonsteroidal anti-
inflammatory drugs are not indicated.