4 Essential Principles for Treating Respiratory Failure

Acute respiratory failure (ARF) is a severe condition characterized by a drop in oxygen levels in the blood. As a rule, such a situation directly threatens a person’s life and requires immediate professional medical assistance.

Manifestations of ARF are a feeling of suffocation, psycho-emotional agitation and cyanosis. With the progression of acute respiratory failure syndrome, the following clinical picture develops: convulsive syndrome, varying levels of impaired consciousness, and eventually coma.

To determine the severity of acute respiratory failure, the gas composition of the blood is examined, and the cause of its development is also sought. Treatment is based on eliminating the cause of the development of this syndrome, as well as intensive oxygen therapy.

Acute and chronic respiratory failure are common conditions in medical practice associated with damage not only to the respiratory system, but also to other organs.

Why does respiratory failure occur?

Full respiratory function is carried out by several processes:

• ventilation of the alveoli - saturation of lung structures with oxygen (in some diseases, not all alveoli are involved in the breathing process; normally, of course, not all structures are involved in a healthy person - this is called the “dead space” of the lungs, but in patients the “dead space” expands significantly);
• the entry of oxygen into the pulmonary capillaries and the removal of carbon dioxide from them (this process is called perfusion; blood supply is a very important link in breathing; when it is disrupted, gas exchange in the lungs and, accordingly, in all tissues of the body changes);
• exchange of gases (oxygen and carbon dioxide) through the capillary and tissues of various organs (this process is called gas diffusion).

Due to the normal functioning of the lungs, all these processes are carried out, but there are various reasons that do not allow this or that process to occur fully.

Causes from the respiratory tract

The most common cause of respiratory failure is obstruction (obstruction) of the bronchi (airways).

Foreign body obstruction is common in children, but is not uncommon in adults. A foreign body can be understood not only as some objects, but also as biological fluids - mucus, gastric contents. This group also includes breathing problems due to drowning (water entering the respiratory tract).

Swelling of the mucous membrane of the respiratory tract occurs with viral and bacterial infections. In children it is much more common, since the anatomical structure predisposes to this (smaller size of the respiratory tube and, accordingly, rapid narrowing with edema).

Pneumonia is a disease in which respiratory failure is pronounced and severe.

A special place is occupied by diseases that specifically affect the pulmonary structures - bronchitis, emphysema, bronchial asthma, diffuse pulmonary sclerosis, atelectasis, bronchiectasis, etc. All these lesions are chronic in nature (that is, a long development of diseases, decades), in which respiratory failure is chronic and develops gradually. For the patient, sometimes this is not noticeable, since the body gradually adapts to such conditions, and the person does not feel much of a difference, but this, of course, is in the initial stages of the disease.

Causes from the central nervous system

The human brain contains all the vital regulatory centers of the body. The respiratory center is also located in the brain; it is from there that all signals for the lungs, blood vessels, nerves and even the respiratory muscles come. This is how a harmonious breathing function is carried out at the highest level.

What can interfere?

1. Tumor processes - benign or malignant. With a tumor of significant size (for a tumor in the brain, even 0.5 cm is considered significant!), which is located next to the respiratory center and somehow affects it (for example, the center is compressed by the tumor), there may be a breathing disorder (development of respiratory failure).
2. Brain swelling due to injury or intoxication (poisoning). During swelling, the brain can significantly increase in size, which also affects the compression of its structures and centers.
3. A stroke (bleeding) in the brain can also lead to DN.
4. Clinical death, when a person is connected to a ventilator (artificial lung ventilation) due to the inability to breathe independently.

Other violations

Other disorders that cause respiratory failure include: traumatic lesions of the chest (rib fractures, wounds, pneumothorax, hydrothorax); poisoning with toxic substances and gases (FOS - cause paralysis of the respiratory muscles); some dangerous infections (botulism, tetanus paralyze the respiratory muscles with their toxins, often death in these diseases occurs due to respiratory failure).

Of course, these are not all the causes of respiratory failure, but they are the most common and basic.

Causes and mechanisms of development

Atelectasis can cause acute respiratory failure.
ARF is a consequence of various diseases or injuries in which disturbances in pulmonary ventilation or blood flow occur suddenly or progress rapidly.

According to the development mechanism there are:

• hypoxemic;
• hypercapnic type of respiratory failure.

In hypoxemic respiratory failure, sufficient oxygenation of arterial blood does not occur due to impaired gas exchange function of the lungs. The following problems can cause its development:

• hypoventilation of any etiology (asphyxia, aspiration of foreign bodies, tongue retraction, apnea);
• decrease in oxygen concentration in the inhaled air;
• pulmonary embolism;
• atelectasis of pulmonary tissue;
• pneumonia;
• airway obstruction;
• non-cardiogenic pulmonary edema.

Hypercapnic respiratory failure is characterized by an increase in the concentration of carbon dioxide in the blood. It develops with a significant decrease in pulmonary ventilation or with increased production of carbon dioxide. This may occur in the following cases:

• for diseases of a neuromuscular nature (myasthenia gravis, poliomyelitis, viral encephalitis, polyradiculoneuritis, rabies, tetanus) or the administration of muscle relaxants;
• with damage to the central nervous system (traumatic brain injury, acute cerebrovascular accidents, poisoning with narcotic analgesics and barbiturates);
• with pneumothorax or massive pleural effusion;
• in case of chest injury with its immobilization or damage to the diaphragm;
• with convulsive seizures.

Classification of respiratory failure

Respiratory failure according to the pathophysiological process can be of several types:

• respiratory failure of the first type (hypoxemic);
• respiratory failure of the second type (hypercapnic).

Hypercapnic and hypoxemic reflect the concentration of the gas composition (oxygen and carbon dioxide) of the blood. The first type of respiratory failure develops with severe pneumonia, cardiogenic pulmonary edema, and acute respiratory distress syndrome. The second type develops with airway obstruction (COPD, chest deformation, obesity, etc.). The second type of respiratory failure responds better to oxygen therapy than the first.

Respiratory failure can vary in severity:

Degrees of respiratory failure	Partial pressure of oxygen in the blood (oxygen gas pressure) on a vessel (artery)	Oxygen saturation (oxygen saturation of hemoglobin - the oxygen carrier in the blood)
Norm	Greater than or equal to 80	Greater than or equal to 95
1st degree	60 — 79	90 — 94
2nd degree	40 – 59	75 — 89
3rd degree	Less than 40	Less than 75

Development speed

With rapid development and increase in symptoms, acute respiratory failure (ARF) occurs, with slower development - chronic. Acute failure develops over several hours or days. This condition requires immediate medical intervention, since in this condition the body is not able to independently cope with disorders that sometimes occur at lightning speed. Acute respiratory failure without medical intervention can result in the death of the patient.

With chronic respiratory failure, things are different. Over time, the body compensates for the condition, that is, it gets used to working in conditions of insufficient oxygen. For example, the intensity of the kidneys increases - they secrete a larger amount of under-oxidized products, the capillaries are in an expanded state - this makes it easier to exchange gas molecules with tissues, heart contractions become more frequent so that the heart muscle receives a sufficient amount of oxygen.

Phase

The phase of respiratory failure can be compensated and decompensated. The phases are clearly visible during the development of acute respiratory failure. The compensated phase is a state when the body tries to cope with breathing disorders, using its additional reserves - shortness of breath, an increase in heart rate (tachycardia), and the inclusion of auxiliary muscles in the breathing process.

The decompensated phase is a serious condition; it develops when the body’s reserves are depleted; if at this moment you do not intervene (medically) and eliminate the cause of respiratory failure, death occurs.

Mechanism of occurrence

Two mechanisms of disorders in respiratory failure can be distinguished - obstructive and restrictive. The obstructive type is characterized by obstruction of the airways: upper or at the level of bronchi of various sizes. Air may not flow at all when obstructed by a large foreign body, but most often the role is played by too slow filling of the lungs with air. Restrictive disorders are characterized by insufficient expansion of the lung tissue during inspiration (atelectasis, sclerosis, pneumonia, etc.). With any mechanism of disturbance, a state of hypoxia (lack of oxygen) in the body occurs.

Children and ODN

The anatomical structure of all systems of the child’s body, including the respiratory system in children, causes frequent diseases, which are commonly called colds, and leads to health problems such as pneumonia, laryngitis, tracheolaryngitis and the like, accompanied by breathing disorders.

Acute respiratory failure in children is a common pathology that disrupts the regular rhythm of life of the child and his family. Many factors contribute to this. One of the main ones is that all tissues of a child’s body constantly need oxygen for high-quality growth and development. In addition, compensatory systems are still very poorly developed, especially in very young children. Therefore, acute respiratory failure that appears in a small person quickly moves into the third, decompensated stage, which can quickly lead to death. Since the patient’s childhood, including infancy, does not allow him to talk about his problems and feelings, doctors and parents can only carefully monitor his condition in order to notice the symptoms of ARF in time and take measures to eliminate the pathology. Acute respiratory failure in children can be detected by the following visual indicators:

• the child breathes heavily, drawing in the intercostal spaces, areas above the jugular notch and interclavicular spaces;
• the baby's breathing is very loud, noisy, with wheezing or whistling;
• the skin and mucous membranes acquire a bluish tint;
• the child is overexcited compared to his usual state;
• The pulse rate increases by more than 15%.

Even a couple of such signs of ARF serve as an incentive to immediately seek qualified medical help.

Manifestations of respiratory failure

Respiratory failure is always accompanied by certain symptoms. The intensity of these symptoms varies between acute and chronic respiratory failure.

• Shortness of breath (may be with difficulty exhaling or inhaling);
• cyanosis of the skin, limbs (bluish color);
• pale skin;
• tachycardia (increased heart rate).

Acute respiratory failure

Acute respiratory failure is a condition that requires prompt medical attention! ARF occurs with status asthmaticus, pulmonary edema, pulmonary embolism, drug overdose, etc. At the beginning of the development of the process, the patient complains of lack of air, shortness of breath, cyanosis occurs, and heart rate increases. This is the compensatory phase when the victim is conscious.

Then euphoria or excitement appears, breathing becomes more rapid and shallow, cold sticky sweat appears on the face. The change from tachycardia to bradycardia (decreased heart rate) is a poor prognostic sign. When compensatory mechanisms are exhausted, the patient falls into a coma or death occurs.

Chronic

Chronic respiratory failure develops over years. Patients do not pay attention to minor changes for a long time, that is, they adapt to gradual disturbances in the respiratory system. All the symptoms described above are present. For a long time, patients live a normal life with minor deviations from the norm, but as respiratory failure progresses, the condition worsens and the symptoms become noticeable, as they significantly affect the quality of life (inability to perform physical activity, forced position to breathe, feeling of lack of air, etc. .).

Symptoms

Respiratory failure can be acute or chronic. The acute form of the pathology occurs suddenly, develops rapidly and poses a threat to the patient’s life.

In primary failure, the structures of the respiratory tract and respiratory organs are directly affected. Its reasons are:

1. Pain from fractures and other injuries of the sternum and ribs,
2. Bronchoobstruction due to inflammation of the small bronchi, compression of the airways by a neoplasm,
3. Hypoventilation and pulmonary dysfunction
4. Damage to the respiratory centers in the cerebral cortex - head injury, drug or drug poisoning,
5. Respiratory muscle damage.

Secondary respiratory failure is characterized by damage to organs and systems not included in the respiratory complex:

• Blood loss
• Thrombosis of large arteries,
• Traumatic shock state
• Intestinal obstruction,
• Accumulation of purulent discharge or exudate in the pleural cavity.

Acute respiratory failure manifests itself with quite striking symptoms. Patients complain of a feeling of lack of air, shortness of breath, difficulty inhaling and exhaling. These symptoms appear earlier than others. Tachypnea usually develops - rapid breathing, which is almost always accompanied by respiratory discomfort. The respiratory muscles become overstrained and require a lot of energy and oxygen to function.

As respiratory failure increases, patients become excited, restless, and euphoric. They stop critically assessing their condition and the environment. Symptoms of “respiratory discomfort” appear – cough, wheezing, distant wheezing, weakened breathing, tympanitis in the lungs. The skin becomes pale, tachycardia and diffuse cyanosis develop, and the wings of the nose swell.

In severe cases, the skin acquires a grayish tint and becomes sticky and moist. As the disease progresses, arterial hypertension gives way to hypotension, consciousness is depressed, coma and multiple organ failure develop: anuria, gastric ulcer, intestinal paresis, kidney and liver dysfunction.

The main symptoms of the chronic form of the disease:

1. Shortness of breath of various origins;
2. Increased breathing – tachypnea;
3. Blueness of the skin – cyanosis;
4. Increased work of the respiratory muscles;
5. Compensatory tachycardia,
6. Secondary erythrocytosis;
7. Edema and arterial hypertension in later stages.

The tension of the neck muscles and the contraction of the abdominal muscles during exhalation are determined by palpation. In severe cases, paradoxical breathing is detected: when inhaling, the stomach is drawn inward, and when exhaling, it moves outward.

In children, pathology develops much faster than in adults due to a number of anatomical and physiological characteristics of the child’s body. Babies are more prone to swelling of the mucous membrane, the lumen of their bronchi is quite narrow, the process of secretion is accelerated, the respiratory muscles are weak, the diaphragm is high, breathing is more superficial, and the metabolism is very intense.

These factors contribute to impaired respiratory patency and pulmonary ventilation.

Children usually develop an upper obstructive type of respiratory failure, which complicates the course of acute respiratory viral infections, peritonsillar abscess, false croup, acute epiglotitis, pharyngitis, laryngitis and tracheitis. The child’s voice changes, a “barking” cough and “stenotic” breathing appear.

Degrees of development of respiratory failure:

• The first is difficulty in breathing and the child’s anxiety, a hoarse, “rooster” voice, tachycardia, perioral, unstable cyanosis, which increases with anxiety and disappears when breathing oxygen.
• The second is noisy breathing, which can be heard from a distance, sweating, constant cyanosis on a pale background, disappearing in the oxygen tent, cough, hoarseness, retraction of the intercostal spaces, pallor of the nail beds, sluggish, adynamic behavior.
• The third is severe shortness of breath, total cyanosis, acrocyanosis, marbling, pale skin, drop in blood pressure, suppressed reaction to pain, noisy, paradoxical breathing, adynamia, weakened heart sounds, acidosis, muscle hypotension.
• The fourth stage is terminal and is manifested by the development of encephalopathy, asystole, asphyxia, bradycardia, convulsions, and coma.

The development of pulmonary failure in newborns is caused by an incompletely mature surfactant system of the lungs, vascular spasms, aspiration of amniotic fluid with original feces, and congenital anomalies of the respiratory system.

What are the possible complications?

The most unpleasant complication is cor pulmonale. Cor pulmonale develops in chronic respiratory failure due to the fact that when adaptive mechanisms are turned on, a larger volume of blood passes through the heart muscle than it should, and over time it hypertrophies (increases), and excess pressure is transferred to the vessels of the systemic circulation, which leads to subsequently lead to organ disorders (enlarged liver, the appearance of cardiac edema, etc.).

In the lungs themselves, pulmonary hypertension occurs (increased pressure in the capillaries), which is manifested by difficulty breathing, discomfort and swelling of the lung tissue. From the nervous system, sleep disturbances, bad mood, and headaches are possible.

In acute respiratory failure, such disorders do not occur, since this requires a long time. In this case, the worst thing is death!

Features and causes of acute respiratory failure in children

Unfortunately, respiratory failure in children is not considered uncommon in modern medicine, since a similar condition develops in various pathologies. Moreover, some anatomical and physiological features of the child’s body increase the likelihood of such a problem.

For example, it is no secret that in some babies the respiratory muscles are very poorly developed, which leads to impaired ventilation of the lungs. In addition, respiratory failure in children may be associated with narrow airways, physiological tachypnea, and less surfactant activity. At this age, insufficient functioning of the respiratory system is the most dangerous, because the baby’s body is just beginning to develop, and a normal blood gas balance for tissues and organs is extremely important.

Diagnostic procedures for respiratory failure

Acute respiratory failure requires quick action on the part of the doctor; in the case of chronic respiratory failure, the doctor must find out the medical history (what diseases, bad habits there are). Examination of the patient - the color of the skin (cyanosis), changes in the nail phalanges of the fingers in the form of “drumsticks” and “watch glasses” - a sign of hypoxia. Some patients experience shortness of breath even at rest.

General clinical studies

The most important analysis is the determination of the gas composition (oxygen and carbon dioxide) in arterial blood. This method allows you to fairly accurately assess the situation and set the stage of respiratory failure (the table is presented in the classification section). This diagnostic method is used for both chronic and acute respiratory failure. Blood tests can be performed over time to track treatment results. They also examine the pH of the blood and the level of bicarbonates (during the day, there is a shift towards the acidic state and the pH of the blood increases, which greatly affects the metabolism in the body). In the CBC (general blood count), in the chronic form, an increase in the number of erythrocytes (red blood cells, involved in oxygen transport) is observed. UAM (general urinalysis) is basically unchanged, unless there are kidney problems.

Instrumental diagnostics

X-ray of the lungs allows you to identify a large number of pathological conditions (tumor, pneumonia, atelectasis, bronchiectasis, etc.). MRI diagnostics is used to determine circulatory disorders and neoplasms in the brain.

Research of respiratory functions. Various respiratory parameters are studied (FVD, PSV, VC, FVC, TEL, Tiffno index). All these abbreviations indicate one or another volume in the lungs when inhaling or exhaling, the volume that remains in the lungs, etc. Any of these indicators has its own norm; if you deviate from it, you should talk about respiratory failure. Such tests help to suspect respiratory problems in the early stages.

An ECG (electrocardiogram of the heart) is used to monitor cardiac function and to diagnose conditions such as PE (pulmonary embolism).

Steps in the development of ODN

The degree of acute respiratory failure is important to consider both in the treatment of the condition and in making a prognosis and preventing possible complications. Experts identify several characteristic stages in the development of the pathological condition:

• The initial stage is the stage of silence. Like many diseases, respiratory failure at the first stage does not make itself felt, without showing any significant symptoms that can be felt by a person. The invisibility of breathing problems is determined by compensatory mechanisms. One can suspect ARF only because shortness of breath or increased breathing occurs during physical activity.
• The second stage is called subcompensatory. It is characterized by the depletion of mechanisms that compensate for insufficient breathing, so shortness of breath appears even at rest; breathing takes a long time to recover after physical effort. The patient becomes characterized by a posture in which it becomes much easier for him to breathe. In this case, attacks of manifestation of the pathology are accompanied by dizziness and rapid heartbeat.
• The third stage is decompensated. Those mechanisms that could completely compensate for disturbances in the respiratory system are exhausted and cannot help; the skin and mucous membranes turn blue, the level of oxygen in the blood and blood pressure decrease. The patient may fall into a state of psychomotor agitation. This phase of ARF requires immediate medical intervention with the use of certain medications and medical procedures. If help does not come, then the person’s condition deteriorates sharply, and respiratory failure enters the terminal stage.
• Terminal is an extreme degree of problem of the respiratory system, it is characterized by a strong decrease in the level of oxygen that enters the blood, the patient develops cold sweat, breathing is shallow and very frequent, the pulse is weak, the so-called threadlike. Loss of consciousness, anuria, and hypoxic cerebral edema may develop. Unfortunately, this stage of respiratory failure in most cases ends in death.

This gradation of pathology is typical for cases of breathing disorders caused by diseases of the respiratory system, for example, pneumonia. If destruction, blockage, or disruption of the impulse conductivity of the respiratory center occurs, then the stages of ARF are confused and displaced. Thus, the initial stage is practically or completely absent, the second stage is minimal in duration, and acute respiratory failure abruptly progresses to the third stage. Research and observations have revealed that in elderly people, due to age-related tissue characteristics, they are content with less oxygen; the subcompensation stage can last much longer than in young and middle-aged people. But in children, a decompensatory period begins almost immediately, since all systems and tissues of the growing body are in dire need of constant replenishment of oxygen and removal of carbon dioxide. If the cause of the development of acute respiratory failure is eliminated in time - the foreign body is removed from the larynx, allergic edema is relieved, the necessary medications or manipulations are used, then all stages of ARF are reversed, returning the patient's respiratory functionality.

Treatment

Treatment of any respiratory failure is based on the following principles:

• restoration of airway patency (removal of foreign bodies, tumor removal, surgical treatment of abscesses, bronchiectasis, etc.).
• ensuring the supply of sufficient oxygen (oxygen therapy, ventilator);
• infusion therapy (droppers - Ringer's solution, saline solution, etc.).
• treatment of the underlying disease (without eliminating the cause, you cannot achieve a positive result!).

Patients with acute respiratory failure require resuscitation measures; they continue treatment in intensive care and resuscitation wards. Patients with chronic respiratory failure can be treated on an outpatient basis (at home), or in a hospital if their condition worsens or if medication adjustments are required and the dynamics of treatment are determined.

Breathe - don't breathe!

A complex physiological, biochemical, physical process on which the work of all organs, systems and, undoubtedly, human life depends is breathing. It is largely responsible for metabolism and homeostasis - the procedure for converting some substances into others and at the same time maintaining the stability of the body and all its structures taken together. A person’s breathing problems can arise for completely different reasons; in one case or another, only specialists using different techniques and means can help. But it is worth understanding that violations of this process are very dangerous, as they can lead to irreversible changes in tissues and organs. The causes of acute respiratory failure can also be different, although the condition itself requires urgent care in any case.

Prognosis for respiratory failure

The prognosis for respiratory failure is different in each specific case. For example, with myasthenia gravis (a disease in which the respiratory muscles do not function) the mortality rate is high, death can occur within a year. For pneumonia, after complete recovery (treatment with antibacterial drugs), the prognosis is favorable and often without consequences. Patients with COPD and bronchial asthma can maintain a normal condition for a long time with the help of medications.

Each specific case and each individual patient has its own prognosis, since the concept of respiratory failure includes groups of different diseases and cannot be said unambiguously.

Diagnostics

Diagnosis of respiratory failure begins with studying the patient’s complaints, collecting an anamnesis of life and illness, and identifying concomitant pathologies. Then the specialist proceeds to examine the patient, paying attention to the cyanosis of the skin, rapid breathing, retraction of the intercostal spaces, and listens to the lungs with a phonendoscope.

To assess the ventilation capacity of the lungs and the function of external respiration, functional tests are performed, during which the vital capacity of the lungs, the peak volumetric rate of forced expiration, and the minute volume of respiration are measured. To assess the work of the respiratory muscles, inspiratory and expiratory pressure in the oral cavity is measured.

Laboratory diagnostics include the study of acid-base balance and blood gas composition.

Additional research methods include radiography and magnetic resonance imaging.

Prevention

Prevention of this condition includes:

• full examination for existing diseases affecting respiratory function;
• compliance with the recommendations of the attending physician (medicines, physical treatment);
• giving up bad habits (smoking, alcohol, drugs);
• work and rest schedule;
• prevention of viral and bacterial diseases;
• compliance with personal safety rules (applies to traumatic injuries to the chest);
• elimination of carcinogenic factors (factors influencing the development of tumors in the brain and lungs, for example, some medications, ionizing radiation, chemical compounds).

The listed prevention methods cannot cover the entire list of diseases and suggest how to avoid them. Your doctor will give you more specific rules of conduct; if you have symptoms of respiratory failure, be sure to consult a doctor!

About the chronic form of insufficiency

Unlike the acute form of failure, the contractility of the heart in the chronic course decreases very slowly. Therefore, all of the above symptoms are not pronounced; they are often manifested by one sign, for example, shortness of breath during physical exertion.

An important sign of chronic pulmonary heart failure is an increase in pressure in the pulmonary circulation, and then in the large one. As a result, severe swelling occurs, primarily in the legs. The swelling is symmetrical, of a dough-like consistency, located on the ankles and back of the feet. In the initial stages of failure, they completely disappear at night, since it is easier for the heart to pump blood when the body is in a horizontal position. Then the swelling becomes permanent and the liver swells. Hypertension also occurs in the pulmonary circulation, since the blood entering there is retained there. This occurs due to the weak contractility of the main muscle - the myocardium of the left ventricle, as well as weakness of the left atrium. The result of this is a wet cough, which can lead to pulmonary edema or an attack of cardiac asthma.

Cardiac asthma appears as shortness of breath, abundant moist wheezing appears in the lungs, breathing becomes difficult when inhaling, and becomes bubbling. As pulmonary edema develops, pink foam appears and progressive suffocation occurs. One of the oldest ways to treat pulmonary edema and cardiac asthma is to sit, lower your legs into a basin of hot water, and apply tourniquets to your arms and legs for a short time. All these measures were aimed at reducing the flow of venous blood to the heart and reducing the manifestations of cardiac asthma.

In conclusion, it is worth mentioning the reasons for the development of chronic pulmonary heart failure. Their list is extensive: on the part of the heart - these are congenital and acquired defects, valvular defects, bacterial endocarditis. On the part of the lungs, these are chronic obstructive diseases, severe pneumosclerosis, effusion pleurisy and other conditions. If symptoms such as shortness of breath on exertion, pain in the heart, cough and swelling in the legs appear, you should immediately consult a therapist or cardiologist to find out the reasons. After all, untimely treatment leads to the appearance of chronic tissue hypoxia, which significantly worsens the prognosis.

Treatment of the disease

In acute forms of insufficiency, therapy is carried out in intensive care conditions, since the patient’s serious condition poses a threat to his life. Inhalation of an oxygen mixture is used through a mask or by installing a nasal catheter. This helps saturate the blood with oxygen molecules and mitigate the manifestations of hypoxia on body tissue. In severe cases, the patient is transferred to artificial ventilation.

Carrying out resuscitation measures in acute forms of cardiac failure

The following drugs are administered intravenously:

• thrombolysis drugs (streptocaniasis, actilisis) - for thromboembolism of the pulmonary artery trunk and its branches to dissolve the blood clot and restore blood flow;
• atropine relaxes the smooth muscle muscles of the bronchi, thereby improving respiratory function;
• papaverine reduces vascular tone, expands their lumen, normalizes pressure in the pulmonary circulation;
• anticoagulants (warfarin, heparin) prevent thrombosis of blood vessels and cavities of the heart, thin the blood;
• aminophylline normalizes the contractile function of the myocardium and reduces the manifestations of respiratory disorders.

In the case of a chronic form of incompetence, the underlying ailment is treated. Anti-inflammatory drugs, bronchodilators to dilate the bronchi, and hormonal drugs are prescribed. To treat pathologies of the heart and lungs, treatment is used that is used for heart failure:

• potassium-sparing diuretics (veroshpiron, triampur) remove stagnant fluid from the body;
• cardiac glycosides (digitalis) improve myocardial function;
• selective beta blockers (bisaprolol, atenolol) normalize high blood pressure;
• drugs that stimulate the vasomotor center (caffeine, camphor) are prescribed for respiratory depression;
• cardioprotectors (mildronate) protect myocardial and vascular cells from destruction as a result of hypoxia;
• potassium and magnesium preparations (panangin) improve metabolic reactions in the cells of damaged tissues.

In case of severe erythrocytosis, bloodletting is performed in an amount of 280-400 ml, followed by replacement of the blood volume with low-density solutions (saline solution, rheopolyglucin). They recommend giving up bad habits and prescribe a low-fat, salt-free diet. To maintain normal heart function, reduce the amount of fluid consumed, limit vigorous physical activity and stressful situations.

Heart failure with severe signs of pulmonary hypertension requires timely diagnosis and treatment. Constant monitoring and supportive courses of therapy help avoid severe complications and increase the life expectancy of patients.

Pathogenesis [edit | edit code ]

The pathogenesis of most cases of DN is based on alveolar hypoventilation.

With all types of DN, due to a lack of oxygen in the blood and hypoxia, compensatory reactions of organs and tissues develop. The most common developments are erythrocytosis, hyperhemoglobinemia and an increase in minute volume of blood circulation. In the initial stage of the disease, these reactions compensate for the symptoms of hypoxia. With significant disturbances in gas exchange, these reactions can no longer compensate for hypoxia and themselves become the causes of the development of cor pulmonale.

Obstructive respiratory failure [edit | edit code]

Obstructive DN

associated with bronchial obstruction. The pathogenesis of obstructive DN is based on narrowing of the bronchial lumen.

Reasons for narrowing of the lumen of the bronchi:

• bronchospasm,
• allergic edema,
• inflammatory edema,
• infiltration of the bronchial mucosa,
• blockage of the bronchi with phlegm,
• sclerosis of the bronchial walls,
• destruction of the frame of the bronchial walls.

The narrowing of the lumen of the bronchi causes an increase in resistance to air flow in the bronchi. An increase in resistance to air flow leads to a decrease in its speed exponentially. Compensation for the decrease in air flow speed occurs due to significant additional efforts of the respiratory muscles. The reduction in the lumen of the bronchi is complemented by a natural narrowing during exhalation, so with obstructive DN, exhalation is always difficult.

Due to an increase in bronchial resistance during exhalation, an involuntary shift of the respiratory pause into the inhalation phase occurs. This displacement occurs with the help of a lower position of the diaphragm and inspiratory tension of the respiratory muscles. In this case, inhalation begins with inspiratory stretching of the alveoli and the volume of residual air increases.

In the initial stage of disease development, the shift in the respiratory pause is functional in nature. Subsequently, atrophy of the alveolar walls occurs due to compression of the capillaries by high pressure during exhalation. As a result of atrophy of the alveolar walls, secondary pulmonary emphysema develops and the displacement of the respiratory pause becomes irreversible.

Due to the increase in bronchial resistance, there is a significant increase in the load on the respiratory muscles and an increase in the duration of exhalation. The duration of exhalation in relation to the duration of inhalation can increase to 3:1 or more. Thus, 3/4 of the time the respiratory muscles do the hard work of overcoming bronchial resistance. With severe obstruction, the respiratory muscles can no longer fully compensate for the decrease in air flow.

Also, for 3/4 of the time, high intrathoracic pressure compresses the capillaries and veins of the lungs. Compression of capillaries and veins leads to a significant increase in resistance to blood flow in the lungs. An increase in resistance to blood flow causes secondary hypertension of the pulmonary circulation. Hypertension subsequently leads to the development of cor pulmonale.

Diagnostic features

If this disease develops, the patient should be observed by two specialists: a cardiologist and a pulmonologist. Making a diagnosis begins with collecting a detailed history, when the patient talks about his complaints, bad habits, previous illnesses, working conditions and lifestyle, etc.

The next stage is listening to the heart, determining its boundaries using percussion, and measuring pressure. With right ventricular hypertrophy, muffled tones are detected, accompanied by increased pulmonary pressure, strong heartbeat and decreased blood pressure. If congestion in the lungs is observed, then signs of arterial hypertension may appear against their background.

After this, instrumental diagnostics are prescribed, the purpose of which is to accurately determine the nature of the pathology:

1. X-ray of the sternum. Allows you to determine possible pathologies of the lung tissue when the mediastinum grows to the right.
2. Echocardiography. One of the main diagnostic methods by which functional deviations in the operation of the valve apparatus are determined. Also, during the study, the specialist can identify changes in cardiac output and assess the correctness of myocardial contractions.
3. CT. This procedure is used to in-depth study those areas of the lungs and heart that have undergone changes.
4. Angiography. Necessary for visualizing the lumen of the vessel, its shape, identifying blood clots and various atherosclerotic changes.
5. Electrocardiography. Allows you to determine the conductivity and excitability of the organ. In this way, areas of cardiac muscle hypertrophy, rhythm disturbances and ischemic foci are identified. If doubts arise, specialists additionally conduct research using the Holter apparatus.
6. Catheterization with pressure gauge. Necessary for determining pressure in large vessels and cavities of the heart. The procedure is very important in the treatment of thrombosis, since in this way agents are introduced into the vessels to help break down blood clots.
7. Spirometry, through which it is possible to determine the degree of respiratory failure.

Diagnosis is advisable in the early stages of the disease. With timely detection of pathology, it is possible to prevent the development of irreversible changes in the myocardium, kidneys, liver, lungs and brain. If a patient develops concomitant diseases that lead to cardiopulmonary disorders, then the examination should be carried out at the preclinical stage of pathology development.

Causes

Pulmonary hypertension leads to a violation of the enrichment of blood in the alveoli with oxygen. As a result, the myocardium of the right ventricle increases cardiac output in order to reduce tissue hypoxia (lack of oxygen). Over time, due to excessive stress, the muscles of the right side of the heart grow.

There are several groups of factors that cause the disease:

Bronchopulmonary factors include:	chronic bronchitis, bronchiolitis obliterans; pulmonary enphysema; extensive pneumonia; sclerosis of lung tissue; bronchial asthma; chronic suppurative processes in pathologically altered bronchi. The disease can develop with tuberculosis and pulmonary sarcoidosis.
Vascular factors include:	pulmonary artery atherosclerosis; tumor in the middle parts of the chest cavity; compression of the “right heart” by an aneurysm; pulmonary arteritis; pulmonary artery thrombosis.
The disease can cause deformities of the diaphragm and chest:	curvature of the spine in the lateral and anteroposterior direction (kyphoscoliosis); polio; ankylosing spondylitis; impaired innervation of the diaphragm.

Under the influence of vascular factors, the arteries narrow. This occurs due to blockage by a blood clot or thickening of the vascular walls due to the inflammatory process.

In medical practice, the disease most often develops against the background of:

• pneumosclerosis;
• pulmonary vasculitis;
• emphysema;
• thromboembolism;
• pulmonary edema;
• pulmonary artery stenosis.

Symptoms of the disease may appear suddenly. In this case, they are distinguished by rapid development and a vivid clinical picture. In the acute form of the disease, emergency medical care and placement in the intensive care unit are required. Acute cardiopulmonary failure occurs: with sudden spasms or thrombosis of the pulmonary trunk; extensive pneumonia; asthmatic status; accumulation of air or liquid in the pleural cavity; severe form of incompetence of the bicuspid heart valve; chest injuries; impaired operation of the prosthetic valve. Under the complex influence of unfavorable factors, hemodynamics are sharply disrupted. This manifests itself in the form of insufficient blood circulation of the “right heart”. Read also:  Expectorants for children and adults: how they work, differences, names The disorder is accompanied by the following symptoms: rapid breathing; decreased blood pressure; in the acute form, collapse may occur; shortness of breath, difficulty breathing; enlarged veins in the neck; lack of air, suffocation; cold extremities; bluish coloration of the skin; cold sweat; chest pain. The acute form of the disease may be accompanied by pulsation in the epigastric region of the dilated right ventricle. The x-ray shows an increase in the mediastinum to the right and upward; the electrocardiogram shows overload of the “right heart”. When listening to the heart, ri and muffled tones are clearly revealed. In case of acute blockage of the pulmonary artery by a thrombus, pulmonary edema and pain shock rapidly develop, which can lead to rapid death.
Symptoms depend on the stage of the disease. In the compensated form of the pathology, symptoms characteristic of high pressure in the pulmonary circulation are revealed. Chronic pulmonary heart failure can develop over several years. It appears as: fatigue; pulsations in the epigastrium; bluish tint of fingertips and nasolabial area; dizziness; rapid heartbeat.
Decompensated form	It is accompanied by increasing symptoms and leads to irreversible consequences in all tissues and organs. Signs of a progressive disease include: shortness of breath at rest, worsening when lying down; ischemic pain in the heart area; enlargement of the veins in the neck, which persists when inhaling; decreased blood pressure, tachycardia; bluish skin tone; enlarged liver, heaviness on the right side; swelling that cannot be treated. With increasing death of all tissues (terminal state), serious damage to the brain and kidneys develops. These processes are expressed in the form of lethargy, apathy, impaired mental functions, and cessation of urine output. In the blood, due to a lack of oxygen, the concentration of hemoglobin and red blood cells increases.

Treatment and observation of a patient with SLN

Cardiopulmonary failure is a chronic disease that requires lifelong treatment. Under the influence of correctly prescribed medications, symptoms decrease, which significantly improves the quality of life. It is important to treat not only SLN, but also its cause. For most patients, treatment consists of dietary adjustments, medications, and surgical interventions.

The main medications used to treat SLN:

• ACE inhibitors - dilate blood vessels, lower blood pressure, improve blood flow and reduce stress on the heart
• Angiotensin receptor blockers - the principle of action is similar to previous drugs. Prescribed for intolerance to ACE inhibitors
• Beta blockers – slow down heart rate
• Thrombolytic drugs - for conservative treatment of pulmonary embolism
• Glucocorticoids and cytostatic drugs - for the treatment of connective tissue pathology
• Anti-tuberculosis drugs - for appropriate pathology
• Mucolytic drugs - optimize the viscosity of sputum and promote its discharge
• Diuretics – remove fluid that forms swelling, thereby lowering blood pressure and improving breathing
• Aldosterone antagonists – act like diuretics
• Digoxin – strengthens heart contractions, reducing their frequency
• Nitroglycerin – improves blood flow in the myocardium
• Statins – used to treat atherosclerosis
• Anticoagulants - used to reduce blood clotting properties

The drugs are selected individually and require several visits to the doctor to calibrate (titrate) the effective dosage. It is very important to use them regularly and not stop taking them on your own.

Treatment options

Currently, treatment of cardiopulmonary insufficiency is carried out:

• diuretics;
• cardiac glycosides
• beta blockers;
• surgical intervention;
• bloodletting;
• folk healing.

Diuretic drugs

Treatment with diuretics helps eliminate excess fluid that accumulates in the body as a result of decreased contractility of the heart. Hydrochlorothiazide is an effective and inexpensive diuretic. It stabilizes blood pressure and removes excess fluid.

Furosemide is an immediate and stronger drug. It is usually taken in the morning on an empty stomach with regular monitoring of electrolyte-salt balance. Since important microelements are removed from the body along with the liquid. The effect of the drug lasts 6 hours. It can be used even with weak kidney function. Furosemide helps to quickly relieve swelling and removes excess fluid well. Another effective diuretic drug that can help get rid of swelling and remove excess fluid is ethacrynic acid.

Beta blockers

Treatment of the disease with beta blockers improves the functioning of the left ventricle of the heart, normalizes blood circulation, and helps relieve swelling.

The most effective beta blockers are propranolol and timolol. They have adrenergic-selective properties and eliminate almost all the symptoms of this disease. Treatment with metoprolol is also considered effective. Because it has maximum cardioselectivity and eliminates all signs of the disease.

Surgical intervention

Cardinal treatment is applicable if the disease is severe. The most common treatments are atrial septostomy, thromboendarterectomy, or organ transplantation.

Atrial septomy is necessary to reduce pressure in the right atrium and pulmonary artery. Thrombendarterectomy is used to remove blood clots from the lungs. Transplantation is used if treatment by other means has not given the desired effect.

Bloodletting

This treatment involves removing a certain amount of blood from the bloodstream. Up to 400 ml of blood is released from the sufferer’s body. With this method of rescuing the disease, the patient’s blood pressure decreases, excess fluid is eliminated, and swelling disappears.

Glycosides

The most effective glycoside that is common in Russia is digoxin. Glycosides are positive inotropic agents that improve the quality of life of patients suffering from pulmonary-cardiac insufficiency.

Glycosides are prescribed in small doses. Using cardiac glycosides, patients seek hospitalization less often.

Folk remedies

Treatment with folk remedies should be carried out only after consultation and doctor’s prescriptions. Because this disease is very serious and dangerous.

The main remedy for this disease is simple wormwood. It normalizes blood circulation, eliminates pain, and removes excess fluid. You need to prepare a decoction of wormwood and take it before meals every day, three-quarters of a glass.

Another equally effective remedy is a decoction of nettles. Hand baths should be made with this decoction. Timed treatment lasts 10 minutes every day

Pumpkin juice is also an excellent remedy for this disease.

You must always remember that folk recipes alone cannot be used to treat heart and lung diseases; moreover, some medications cannot be used simultaneously with herbal ones due to a possible increase in side effects.

Pulmonary edema

Acute pulmonary failure can be complicated by the development of pulmonary edema. This is the release of a significant volume of blood into the lung tissue. The attack develops suddenly, regardless of the time of day. The onset is characterized by sudden suffocation, and a rapid deterioration in the patient’s condition is observed:

• shortness of breath intensifies, the patient lacks air, there is cyanosis of the skin of the face and limbs, cold sweat;
• consciousness is impaired - this can be either motor excitement or stupor, up to complete loss of consciousness;
• breathing is noisy, bubbling, pink foam is released;
• if the attack occurs against the background of myocardial infarction or myocarditis, cardiogenic shock may develop.

Treatment tactics for acute forms of the disease

The complexity of the disease lies in the fact that the development of pulmonary hypertension leads to a decrease in the volume of oxygen-rich blood that flows to all internal organs and tissues, including the heart.
This condition forces the cardiac myocardium of the right ventricle to reflexively increase the release of blood in order to artificially compensate as much as possible for the insufficient amount of oxygen in tissues and organs.

A long period of such work of the heart myocardium leads to its overload and the build-up of myocardial muscle tissue.

This period is called compensatory. The long course of the disease depletes the strength and resources of the heart, and compensatory processes are significantly weakened. A period of decompensation begins, which entails irreversible changes in the functioning of the cardiac myocardium.

With a long course of pathology, the right parts of the heart build up muscle mass due to constant overload. This period is called compensated and does not lead to the development of complications. With further progression of the disease, compensatory mechanisms fail and irreversible changes in the heart develop - the stage of decompensation.

In modern medicine, the following reasons for the development of pulmonary heart failure are identified:

1. Presence of bronchopulmonary diseases.
2. bronchiolitis or chronic bronchitis;
3. emphysema;
4. severe pneumonia;
5. pneumosclerosis;
6. tuberculosis;
7. bronchial asthma;
8. bronchiectasis.
9. Vascular diseases:
10. atherosclerosis of pulmonary vessels;
11. inflammation of the mediastinum;
12. pulmonary aneurysm;
13. pulmonary vasculitis;
14. thrombosis of the pulmonary arteries.
15. Deformation of the diaphragm or sternum:
16. kyphoscoliosis;
17. ankylosing spondylitis;
18. violation of contraction of the diaphragm;
19. polio.

As a result of the influence of factors of pulmonary vascular disease, the arteries become clogged with blood clots, which leads to their narrowing. Thickening of the walls of the arteries as a result of the formation of a tumor on them is also possible.

There are often cases when cardiopulmonary failure develops rapidly (acute form). In this case, urgent medical attention is necessary. The reasons for the development of the acute form include the following:

• formation of spasm or blood clots on the walls of the arteries of the lungs;
• damage to a large percentage of the lungs;
• asthma;
• accumulation of fluid or air in the pleural cavity (pneumothorax);
• severe form of mitral heart valve disease;
• sternum injury.

In this case, circulatory disturbances rapidly develop in the right half of the heart.

The factors that provoked the disease have a direct impact on its rate of development and the manifestation of symptoms. For example, in the acute form of the disease the following symptoms appear:

• frequent and heavy breathing;
• a sharp drop in blood pressure;
• dyspnea;
• swelling of veins in the neck;
• the patient experiences a lack of air (suffocation);
• blue discoloration of the upper and lower extremities or nasolabial area;
• the human body becomes covered with cold and sticky sweat;
• feeling of severe pain in the sternum.

In addition to these symptoms, strong pulsation in the epigastric region of the right cardiac ventricle is also often observed.

On the electrocardiogram you can notice large overloads of the right cardiac ventricle and atrium.

During the listening process, you can clearly hear that the heart is beating in a gallop rhythm in muted tones.

The development of thromboembolism in a patient can lead to pulmonary edema and death.

The chronic course of cardiopulmonary failure develops gradually. This period can take from several days to a year. This form of the disease usually has the following symptoms

• the occurrence of shortness of breath during heavy physical overload;
• pulsation in the epigastric region;
• blue discoloration of fingertips or nasolabial area;
• severe dizziness;
• frequent contraction of the heart.

If the decompensated stage of the disease occurs, the symptoms sharply intensify, which leads to the formation of irreversible processes in the patient’s body. In this case, you can see the following picture:

• a person has severe shortness of breath, even at rest, which increases significantly when he assumes a horizontal position;
• pain in the heart area of ​​an ischemic nature;
• the veins in the neck swell. When inhaling, the swelling increases;
• blood pressure decreases;
• the skin turns blue over the entire area;
• the liver is enlarged, there is pain in the right hypochondrium;
• swelling appears in the lower extremities.

If the patient is not provided with timely and correct treatment, hypoxia can provoke toxic brain damage or nephropathy. This condition is manifested by a person’s weakness, lethargy, constant feeling of drowsiness and apathy. A general blood test shows an increase in the level of hemoglobin and red blood cells.

The development of cardiopulmonary failure requires consultation with specialists in several fields (pulmonologist and cardiologist).

First of all, you need to ask the patient about the course of the disease, the speed of its development, the symptoms that he observes, and ask about the lifestyle that he leads. Find out what bad habits he has. Find out in what conditions the person works. After this, the heart and lungs are carefully listened to, and blood pressure is measured.

Treatment of cardiopulmonary failure can begin only after the following methods of examining the patient:

• x-ray of the heart and lungs (makes it possible to determine the presence of changes in the lungs or thickening of the mediastinum);
• tomography (allows for a more in-depth study of the stage of development of pathologies of the heart and lungs);
• echocardiography (using this method you can determine the presence of changes in the heart valves or thickening of the walls of the cardiac myocardium);
• electrocardiography (will help determine the level of conductivity of the cardiac myocardium);
• angiography (will help identify the development of thickening or blood clots in the veins, vessels or arteries of the lungs and heart);
• spirometry (will determine the degree of development of respiratory failure).

The symptoms of the disease should be paid attention to as early as possible, since the success of treatment depends on the stage of development at which diagnosis begins. This must be done when the disease is at a mild stage of development of deficiency. Don't neglect your health. Your life depends on it. Be healthy!

The term cardiopulmonary failure refers to a combined disorder of the respiratory and vascular systems. The basis of this pathological process is an increase in pressure in the vascular system of the small circle, which is responsible for gas exchange between the blood and the environment.

According to its clinical course, this condition can be acute, when symptoms arise and increase over a short period of time, or chronic, in which symptoms become noticeable only after several years.

Causes

Acute cardiopulmonary failure is usually the result of an urgent situation and requires immediate medical intervention.

• its thrombosis or spasm;
• thromboembolism from the veins or heart cavity;
• exacerbation of bronchial asthma or status asthmaticus;
• sharply developed total pneumonia;
• pneumothorax or hydrothorax (usually hemothorax), which in most cases results from trauma.

In addition to pathological changes in the respiratory system, the root cause of pulmonary hypertension may be associated with disruption of the heart muscle.

Most often, such changes are caused by sudden onset of severe mitral valve insufficiency. Rupture of the papillary muscles usually occurs as a result of acute myocardial ischemia or infarction. Traumatic injury is also possible. Another cause may be dysfunction of the prosthetic valve, which is usually associated with thrombosis and infection.

With acquired valvular disorders, pressure also usually increases gradually. The same can be said about unexpressed, slowly progressing congenital conditions.

Symptoms

Symptoms of acute cardiopulmonary failure are usually more pronounced than in its chronic course. These include:

• shortness of breath (shallow breathing, its frequency reaches 40 per minute and higher);
• a feeling of lack of oxygen, reaching the point of suffocation;
• cyanosis caused by hypoxia and venous stagnation;
• cold or sticky sweat due to centralized blood circulation;
• collapse resulting from a sudden decrease in systemic pressure;
• pain in the sternum, which is associated with ischemia and changes in heart size.

Chronic pulmonary heart failure has less pronounced clinical signs, which are associated with the gradual development of hypertension in the pulmonary vessels.

In the first stages, there are usually no symptoms, as changes are compensated due to left ventricular hypertrophy. Subsequently, they begin to appear only during periods of pronounced activity.

At the final stage, the manifestations of the disease are noticeable even in a state of complete rest.

The last two signs appear with secondary changes occurring in the heart under the influence of the underlying disease.

Diagnostics

Diagnosis of this condition begins with examining the patient and asking about his well-being and complaints. For a more detailed assessment, an instrumental examination is carried out:

• X-ray of the lungs, which reveals both diseases of the respiratory system and changes in heart size;
• Breast CT is performed if necessary if the diagnosis remains doubtful after radiography;
• Ultrasound of the heart allows you to determine the degree of dysfunction of this organ;
• catheterization and invasive manometry accurately determines pressure in the pulmonary artery and heart cavities;
• The ECG reflects secondary changes in advanced cases.

Treatment

In acute conditions, treatment should be carried out in a hospital, often in intensive care. The patient must remain calm and breathe an oxygen-enriched mixture. This is usually done using humidified gas delivered through nasal cannulas or a face mask. In severe cases, tracheal intubation and artificial ventilation are performed.

Treatment

• papaverine dilates blood vessels and reduces the severity of hypertension;
• aminophylline helps stabilize heart contractions and reduce the degree of respiratory failure;
• atropine is administered to dilate the bronchi by relaxing their smooth muscle cells;
• anticoagulants are effective in the presence of thrombosis;

Smoking Stress
Shortness of breath is one of the most important signs of heart failure

Surgery

Sometimes surgical treatment methods are necessary to treat the initial disease, such as:

• Thrombembolectomy for pulmonary embolism
• Sympathectomy
• Removal of a lung tissue tumor
• Heart and lung transplantation
• Balloon atrial septostomy

Palliative treatment

In severe and advanced cases, existing treatment methods are not effective, and cardiopulmonary failure progresses.

In this case, it is necessary to take active steps to maintain a decent quality of life for a person in a special clinic (hospice) or at home.

Recommendations for lifestyle changes:

• Stop smoking
• Weight control and maintaining a healthy diet
• Regularly checking your feet and ankles for swelling
• Limiting salt intake
• Vaccination against influenza and pneumonia
• Limiting alcohol intake
• Reducing stress levels
• Physical activity
• Monitoring the implementation of your prescriptions (creating a schedule, carrying the required amount of medications with you)
• Discuss taking additional medications, dietary supplements, vitamins with your doctor
• Keeping a diary to monitor weight, diuresis, blood pressure, fluids drunk and medications taken, and other important notes.

Main signs of the disease

You can understand that pulmonary failure is developing if you know what kind of disease it is and how it manifests itself.

The main symptoms of the disease include:

• Shortness of breath (regardless of its intensity);
• Headaches that bother patients mainly in the morning;
• Increased frequency of contractions of the heart muscle;
• Insomnia;
• Reduced pressure levels;
• Vomiting, nausea;
• Blueness of the skin;
• Memory problems;
• Changes in breathing (the depth and frequency of inhalations/exhalations changes);
• Participation of auxiliary muscles in the breathing process.

Patients complain of suffocation and severe shortness of breath. Problems with consciousness and memory are caused by a lack of oxygen in the bloodstream and the accumulation of carbon dioxide in excessive quantities. In severe cases, this causes loss of consciousness or coma.

The most dangerous sign is a drop in respiratory rate: if the patient takes less than 12 breaths per minute, this indicates the beginning of the process of respiratory arrest.

If such signs appear, you should understand how the disease is diagnosed and treated.

To determine the cause of the above symptoms, you need to:

• Find out complaints;
• Collect anamnesis;
• Assess the acid-base and gas composition of the blood;
• Do spirometry;
• Send the patient for an x-ray.

If signs of pulmonary failure appear, the patient is sent to a medical facility for inpatient treatment.

Etiology

The main reason for the progression of pulmonary failure in humans is damage to the external respiratory apparatus at its various levels:

• neuromuscular system. The causes of the progression of pulmonary failure can be various infectious or neurological diseases that have a damaging effect on the central nervous system and disrupt the physiological mechanisms of impulse transmission from the brain to the muscles of the respiratory apparatus. Such pathologies include botulism, myasthenia gravis, etc.;
• respiratory center and central nervous system. In this case, the reasons for the progression of pulmonary failure may be brain damage of varying severity, the use of potent drugs, disorders of blood circulation in the brain, etc.;
• rib cage. Pulmonary failure can be caused by scoliosis, pneumothorax and accumulation of excess exudate in the pleural cavity;
• damage to the airways: laryngeal edema, bronchial embolus, asthma, COPD;
• alveoli. Pulmonary insufficiency often manifests itself as the main symptom of pulmonary edema, pneumonia, as well as ailments characterized by the proliferation of connective tissue in the lungs.

Airway obstruction in children

The parainfluenza virus often causes acute stenosing laryngotracheitis in children, which results in respiratory failure.
One of the most common causes of acute DN in children is considered to be airway obstruction, which prevents normal gas exchange. This condition may be based on various diseases and injuries.

In acute epiglottitis, at the onset of the disease, symptoms of an acute respiratory infection (fever, intoxication, impaired phonation, sore throat) dominate. However, within a few hours they progress to complete obstruction of the larynx. In this case, the child is in a forced position (sitting with the cervical spine maximally extended) with stridor breathing and profuse salivation. His condition is assessed as serious and requires emergency medical care.

Stenosing laryngotracheitis occurs in preschool children in the first 24-48 hours of a respiratory infection (influenza, parainfluenza, adenoviral infection). The direct cause of respiratory disorders is swelling of the larynx below the level of the glottis, which leads to a decrease in the diameter of the airways and an increase in resistance to air flow. As the pathological process progresses, gas exchange may be impaired with the development of hypoxemia, accumulation of carbon dioxide in the body, and even asphyxia.

The first symptoms of the disease are hoarseness and paroxysmal cough (the so-called barking cough). As the swelling increases, inhalation becomes difficult, breathing becomes noisy, and auxiliary muscles are actively involved in it. The severity of clinical manifestations depends on the degree of stenosis:

• at grade 1, the child experiences inspiratory shortness of breath and general anxiety;
• 2nd degree is manifested by stridor breathing (which can be heard at a distance), agitation, unstable cyanosis, retraction of the pliable parts of the chest during inspiration;
• at grade 3, suffocation becomes more pronounced, breathing becomes arrhythmic, consciousness becomes confused; constant acrocyanosis and heart rhythm disturbances appear;
• Grade 4 is characterized by shallow breathing, diffuse cyanosis, bradycardia, coma and asphyxia.

The effectiveness of therapeutic measures for stenosing laryngotracheitis depends on the timeliness of their implementation. For grade 1-2 stenosis, corticosteroids, antibiotics, and oxygen therapy are sufficient. With increasing respiratory failure, the doses of hormones increase, and there may be a need for tracheal intubation and mechanical ventilation.

In some cases, the normal flow of air in the respiratory tract is hampered by acute bronchial obstruction syndrome, which is observed in the following pathological conditions:

• obstructive bronchitis and bronchiolitis;
• pneumonia;
• bronchial asthma;
• poisoning with phosphorus compounds, etc.

The main mechanisms of bronchial obstruction in these diseases are:

• spasm of bronchial smooth muscle fibers;
• bronchial dyskinesia;
• pronounced swelling of their walls;
• increased secretion of mucous secretion by the bronchial glands;
• its accumulation in the lumen of the bronchi and drying into crusts.

Obstructive bronchitis is more often detected in young children, bronchiolitis - mainly in children of the first year of life. The disease has an acute onset with fever, shortness of breath and restlessness. Dry whistling rales are heard above the surface of the lungs against the background of weakened breathing.

An acute attack of bronchial asthma also leads to the development of respiratory failure. Clinically, it is manifested by difficulty or wheezing, difficulty in exhaling, and spasmodic cough. The severity of the attack may vary. In severe cases, patients are excited, frightened, and occupy a forced position. Wheezing can be heard from a distance. Severe expiratory shortness of breath is observed. In order to stop this attack, bronchodilators and corticosteroids for inhalation are prescribed. In severe cases, it is necessary to resort to systemic administration of steroid hormones and intensive therapy.

conclusions

Not all diseases that lead to the development of cardiopulmonary failure are reversible, but the right treatment can reduce symptoms to a minimum. Lifestyle changes such as regular physical activity, healthy eating, reducing dietary salt, reducing stress and excess weight improve prognosis and quality of life.

The only way to prevent the development of SLN is to control the underlying disease and follow the instructions of the attending physician.

The following sources of information were used to prepare the material.

• Insomnia
• Chest pain
• Headache
• Labored breathing
• Cough
• Memory impairment
• Heart rhythm disturbance
• Impaired consciousness
• Dyspnea
• Low blood pressure
• Gagging
• Blueness of the skin
• Nausea
• Rapid pulse

Pulmonary failure is a condition characterized by the inability of the pulmonary system to maintain normal blood gas composition, or it is stabilized due to severe overstrain of the compensatory mechanisms of the external respiration apparatus. The basis of this pathological process is a violation of gas exchange in the pulmonary system. Because of this, the required volume of oxygen does not enter the human body, and the level of carbon dioxide constantly increases. All this causes oxygen starvation of organs.

In pulmonary failure, the partial oxygen tension in the blood decreases below 60 mmHg. Art. At the same time, an increase in the partial tension of carbon dioxide is observed. Its indicators exceed 45 mm Hg. Art. This pathological syndrome can begin to progress in people from different age categories. Gender is not characteristic of him.

Symptoms of cardiopulmonary failure

In the case of destruction of the heart muscle, its contractility decreases, which affects the total amount of blood pumped.

Malfunctions of the heart lead to the following pathologies:

1. Hypoxia of various organs due to a reduced amount of oxygen obtained from the blood.
2. Congestion in the lungs, which does not allow the patient to use their full volume when breathing.
3. Pathologies associated with stagnation of fluid in the lungs, which are combined with heart failure. The syndrome includes several dangerous disorders.

The following symptoms appear:

1. Dizziness that begins for no apparent reason, even at rest.
2. Shortness of breath with little physical exertion.
3. Decreased performance, inability to perform habitual actions that did not seem difficult before the onset of the pathology.
4. Paleness of the skin in the area of ​​the nasolabial triangle and fingers of the upper extremities.

1. Pulmonary artery thrombosis.
2. Pneumonia.
3. Exacerbation of asthma.
4. Mitral valve dysfunction.
5. Malfunction of a previously transplanted artificial valve.
6. In the case of the development of many unfavorable factors, signs of severe circulatory failure are possible.

The following symptoms appear:

1. Breathing is accelerated, it is impossible to take a deep breath.
2. A sharp decrease in pressure. If timely assistance is not provided, there is a risk of collapse.
3. Dyspnea.
4. Decreased temperature of the extremities.
5. Blueish skin tone.
6. Profuse sweating.
7. Pain syndrome in the chest.

Signs of chronic cardiopulmonary failure appear as a result of hypertension in the pulmonary circulation. This process gradually intensifies, development occurs over a long period of time. Patients live without developing negative symptoms for several months or years.

From time to time, patients notice the following symptoms:

1. Shortness of breath, which worsens when playing sports.
2. During physical activity, fatigue occurs within a few hours after the start of a work shift or at an important event.
3. Frequent appearance of a bluish tint of the skin in the area of ​​the fingertips and nasolabial triangle.
4. Increased heart rate.
5. If pulmonary heart failure is accompanied by decompensation, the negative manifestations gradually intensify, leading to dangerous processes in the organs. You may notice the following signs of the disease:
6. Shortness of breath does not leave a person even at rest. The attack may intensify if the patient moves to a horizontal position.
7. The pain syndrome increases as a result of the progression of ischemia.
8. Swelling of neck veins.
9. Decrease in blood pressure, development of tachycardia.
10. Blueish skin tone.
11. Enlarged liver, discomfort in the right hypochondrium.
12. The swelling does not subside with the use of standard medications and folk remedies.

If the condition worsens, the functions of the brain and kidneys may be depressed. The person becomes lethargic, apathetic, and signs of increased drowsiness are noticeable. The condition is dangerous due to decreased diuresis and other disorders in organs that are difficult to restore when using medications. With hypoxia, the amount of hemoglobin and red blood cells in the blood increases.

The first group of causes includes more than 20 known nosologies and accounts for 80% of all cases of cor pulmonale. The most common among them are diseases that interfere with the air filling of the alveoli: obstructive bronchitis, EB, bronchial asthma, lobar pneumonia, fibrosing alveolitis, pulmonary tuberculosis, pneumoconiosis, pneumosclerosis, Beck's sarcoidosis, cystic fibrosis, polycystic pulmonary disease.

The second group of factors affects damage to the pulmonary vascular bed. In most cases, the formation of cardiopulmonary failure is preceded by pulmonary embolism, compression of the pulmonary veins and pulmonary artery by tumor formations, pulmonary vasculitis, and sickle cell anemia.

The third group of causes includes conditions accompanied by limited mobility of the chest and diaphragm.

these include various deformations of the chest and curvature of the spine (kyphosis, kyphoscoliosis), massive pleurisy, multiple rib fractures, ankylosing spondylitis, Pickwick's syndrome (obesity-hypoventilation). Impaired mobility of the diaphragm is characteristic of chronic neuromuscular diseases (myasthenia gravis, poliomyelitis), botulism, paresis and paralysis of the diaphragm. Diseases of the second and third groups together cause cor pulmonale in 20% of cases.

Cardiopulmonary failure can have an acute, subacute and chronic course. Thus, acute cor pulmonale always has a decompensated character, subacute and chronic - it can occur both with the presence of right ventricular failure and without it.

The development of acute cardiopulmonary failure usually occurs against the background of massive pulmonary embolism, valvular pneumothorax, mediastinal emphysema, and status asthmaticus. Acute pulmonary hypertension is formed within several hours due to a sharp and sudden increase in pressure in the pulmonary artery, accompanied by expansion of the cavity (dilatation) of the right ventricle and thinning of its walls.

Cardiopulmonary failure can occur in various clinical types: respiratory, cerebral, anginal, abdominal, collaptoid variant with a predominance of certain symptoms. In the clinic of the respiratory form of decompensated drugs, shortness of breath, episodes of suffocation, cough, wheezing, and cyanosis predominate.

With the cerebral variant, signs of encephalopathy come to the fore: excitability, aggressiveness, euphoria, sometimes psychosis or, on the contrary, drowsiness, lethargy, apathy. Dizziness and persistent headaches may bother you; in severe cases, fainting, convulsions, and decreased intelligence occur.

The anginal type of cardiopulmonary failure resembles the clinical picture of angina pectoris with characteristic severe pain in the heart area without irradiation and suffocation. The abdominal version of decompensated LS occurs with epigastric pain, nausea and vomiting, and sometimes the development of gastric ulcers caused by hypoxia of the gastrointestinal tract.

In other cases, the picture of acute cardiopulmonary failure may not unfold so rapidly. Shortness of breath is accompanied by chest pain associated with breathing, hemoptysis, and tachycardia. With progressive right ventricular failure, severe pain occurs in the right hypochondrium, caused by enlargement of the liver and stretching of its fibrous membrane. Due to increased central venous pressure, swelling of the neck veins appears.

Chronic cardiopulmonary failure develops gradually and is a reflection of blood stagnation in the venous system of the systemic circulation. Exercise tolerance decreases, shortness of breath is constant. Note the blueness of the nasolabial triangle, tip of the nose, chin, ears, and fingertips. Attacks of chest pain (pulmonary “angina pectoris”) occur, which are not relieved by taking nitroglycerin, but decrease after the administration of aminophylline.

Patients with chronic cardiopulmonary failure note fatigue, fatigue, and drowsiness. Fainting may occur during physical activity. Decompensation of chronic drugs is also indicated by heaviness and pain in the right hypochondrium, nocturia, and peripheral edema. In the later stages, edema syndrome, hydrothorax, ascites, and cardiac cachexia are detected.

The most valuable laboratory criteria for cardiopulmonary failure are blood gas indicators: decreased p02, increased pCO2, respiratory acidosis. Chest X-ray can detect not only lung damage, but also signs of cardiomegaly and pulmonary hypertension. Pulmonary angiography and ventilation-perfusion lung scintigraphy are indicated for suspected pulmonary embolism.

The study of respiratory function in cardiopulmonary failure is used to assess the nature and severity of ventilation disorders and identify bronchospasm. Electrocardiography in acute LS allows one to reliably determine signs of overload of the right heart, and in chronic LS - to identify direct and indirect markers of right ventricular hypertrophy.

EchoCG serves as the main non-invasive method to assess intracardiac hemodynamics, determine the size of the heart cavities and the wall of the right ventricle, and determine the degree of pulmonary hypertension. In some cases, if it is impossible to establish the fact of increased pressure in the pulmonary artery, catheterization of the right heart is resorted to. Sometimes, to verify the genesis of cardiopulmonary failure, a transbronchial or transthoracic lung biopsy is performed.

Decompensation of drugs should be differentiated from heart defects, cardiosclerosis, dilated cardiomyopathy and other cardiac pathologies.

Treatment of acute cardiopulmonary failure caused by pulmonary embolism is carried out in the ICU. The most important components of treatment are oxygen therapy, relief of pain, thrombolytic therapy (urokinase, streptokinase, tissue plasminogen activator), anticoagulant (heparin, warfarin) and antiplatelet therapy (pentoxifylline). In some cases, surgical tactics are indicated - thromboembolectomy from the pulmonary artery.

In case of cardiopulmonary failure that has developed against the background of bronchopulmonary pathology, the principles of therapy are determined by the underlying disease. Thus, in the case of COPD and bronchial asthma, bronchodilators, mucolytics, and expectorants are used; for pulmonary tuberculosis - specific anti-tuberculosis antibiotics; for interstitial lung diseases - glucocorticoids, cytostatics, interferon, etc.

Treatment

Posture for pulmonary failure

Forced pose with elbows on a chair

• 1st class CHF. It is considered the mildest form of the disease - when going up to the 3rd floor or higher, shortness of breath appears. Otherwise, the person feels normal, activity is normal;
• Class 2 is already quite easy to detect even in rural areas - when climbing to the first floor, shortness of breath begins, as with fast walking. Morning swelling appears. The heart is enlarged, which becomes noticeable even on a chest x-ray;
• 3rd class - a serious condition in which shortness of breath occurs during any physical activity;
• 4th grade - shortness of breath at rest, the condition constantly worsens (even to death).

Treatment should be lifelong under periodic medical supervision

Acute form

Right ventricular failure

It can also occur as a complication of myocardial infarction or myocarditis. Its manifestations, in addition to shortness of breath and increasing suffocation, are:

• cyanosis of the face and fingers;
• the swollen neck veins are clearly visible, especially when inhaling;
• swelling of the legs, face, abdominal wall up to ascites;
• enlarged liver, pulsation in the epigastrium is observed.

Classification of HDN

Considering the possible causes of this condition, the following types of respiratory failure can be distinguished:

1. Bronchopulmonary (developing during pathological processes in the respiratory tract and lung tissue).
2. Centrogenic (associated with dysfunction of the respiratory center).
3. Neuromuscular (caused by disorders of the respiratory muscles and motor nerves).
4. Thoradiaphragmatic (occurs when there are disturbances in the biomechanics of breathing due to impaired mobility of the chest, its damage or deformation).

Bronchopulmonary respiratory failure occurs much more often than its other types, in turn it is divided into the following types:

1. Restrictive (occurs due to diffuse obstruction of the patency of small bronchi).
2. Obstructive (associated with a decrease in respiratory surface area or limited lung excursion).
3. Mixed (combines characteristics of types 1 and 2).

Therapeutic measures

Treatment of the pathological condition is carried out in a hospital setting so that doctors have the opportunity to monitor the patient’s condition. Therapy should only be comprehensive, only then will it be possible to achieve positive dynamics:

• treatment of the underlying disease that provoked the pathology. In this case, treatment is carried out for heart failure, respiratory diseases, etc.;
• oxygen therapy. It must be included in the treatment plan in order to maintain blood gas composition at the required level;
• postural drainage;
• vibration massage of the sternum is a treatment method that ensures normal bronchial patency;
• prescription of pharmaceutical agents that dilute sputum;
• Ventilation This treatment method is indicated for stage 2 insufficiency;
• tracheal intubation. Carried out if there is no positive dynamics, but there is a high risk of suffocation.

Acute respiratory failure
ICD-10	J 96 96.
ICD-10-CM	J96.0
ICD-9	518.81 518.81
ICD-9-CM	518.81 [1] [2] and 518.83 [2]
DiseasesDB	6623
eMedicine	med/2011
MeSH	D012131

Respiratory failure

(DN) is a pathological condition in which the maintenance of normal blood gas composition is not ensured or it is achieved due to more intense work of the external respiration apparatus and heart, which leads to a decrease in the functional capabilities of the body. It should be borne in mind that the function of the external respiration apparatus is very closely related to the function of the circulatory system: in case of insufficiency of external respiration, increased work of the heart is one of the important elements of its compensation.