Cardiopulmonary failure: clinical features, diagnosis and treatment

Cardiopulmonary failure is a decompensated stage of cor pulmonale, which occurs with acute or chronic right ventricular heart failure. The occurrence of pathology is associated with impaired blood circulation in the vessels of the lungs, which is accompanied by a decrease in blood oxygen saturation.

There are two main forms of cardiopulmonary failure - acute and chronic. The acute form in most cases occurs as a result of asthma, emphysema or massive thromboembolism. Clinical signs appear several hours after a sharp increase in arterial pressure. The chronic form is characterized by slow development with an increasing clinical picture (it can develop over several months or years).

There are several types of cardiac pulmonary failure, which differ in their characteristic symptoms. Among them: cerebral, anginal, respiratory, abdominal and collaptoid type of pathology. The cerebral type is characterized by signs of encephalopathy (for example, drowsiness and lethargy or, on the contrary, excitability and aggressiveness). Some patients complain of headaches and dizziness.

The anginal type is characterized by the appearance of severe pain in the area (with no irradiation) and a feeling of lack of oxygen. The progression of the respiratory type is accompanied by the appearance of shortness of breath, cough and cyanosis of the skin. The abdominal type is characterized by painful sensations and a feeling of nausea. Without further treatment, stomach ulcers may occur. The collaptoid type is accompanied by a persistent increase in blood pressure, tachycardia and general weakness. In this case, patients experience pallor of the skin.

Circulatory failure depends on two main factors: a decrease in the contractile force of the muscular membrane of peripheral vessels and a decrease in the contractility of the muscular organ. If the first factor significantly predominates, then we are talking about vascular circulatory failure, and if the second predominates, we are talking about chronic heart failure.

The left and right sections of the muscular organ are responsible for blood circulation. When one of these sections is damaged, isolated or predominant lesions appear, respectively, on the left or right half of the muscular organ. Based on this, left ventricular failure and right ventricular failure are distinguished.

From an anatomical and functional point of view, the lungs and heart have a close relationship. This explains the fact that when one organ is damaged, negative consequences subsequently affect the other. Depending on which of these organs is more affected, pulmonary-cardiac and cardiopulmonary failure are distinguished.

There are two main phases – compensation and decompensation. In the compensation stage, the muscular organ is able to cope with its load and work. But this does not always happen: over time, a period comes when its internal reserves are completely exhausted, resulting in a decompensation phase. In this phase, the muscular organ is no longer able to cope with the load.

Causes of cardiopulmonary failure

Causes of SLN:

• bronchial asthma
• obstructive bronchitis
• chronic obstructive pulmonary disease (COPD)
• pulmonary tuberculosis
• emphysema
• systemic connective tissue disorders (collagenosis)
• pulmonary embolism
• Deformations of the chest and spine (kyphoscoliosis)
• trauma, including pneumothorax
• arthritis
• polio
• botulism
• vasculitis
• pneumoconiosis (accumulation of solid particles of silicates and coal dust in the lung tissue)
• tumors
• major lung surgery

Risk factors for developing CHF:

• arrhythmias
• arterial hypertension
• overdose of certain drugs
• smoking
• injecting drugs
• valvular heart defects
• severe obesity
• immunodeficiency states

Mechanism of development of SLI

SLN often develops as a complication after diseases that lead to pulmonary hypertension and right-sided heart failure. The first version of the development of SLN begins with a pathology of the lungs, leading to an increase in the stiffness and density of the lung tissue, which is why the right ventricle requires more effort for systole. Subsequently, its wall hypertrophies, and the cavity expands, forming the so-called “pulmonary heart” (CP). Another variant of pathogenesis is associated with the progression of left ventricular heart failure to the last stage, as a result of which blood stagnates in the large and then small circle, increasing the pressure in the pulmonary vessels.

How to determine the severity of respiratory failure

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To definitively diagnose the disease and its stage, it is enough to determine the level of blood gases.

Early diagnosis of DN includes examination of external respiration, identification of obstructive and restrictive disorders.

An examination for suspected DN necessarily includes spirometry and peak flowmetry, and arterial blood is taken for analysis.

The algorithm for determining respiratory failure consists of the following diagnostic criteria:

• oxygen tension (Pa) - lower than 45-50;
• carbon dioxide tension is higher than 50-60 (indicators in mmHg).

There is a low likelihood that a patient will undergo a blood gas test without good reason. Most often, diagnosis is carried out only when the pathology has manifested itself in the form of obvious

signs.

Clinical course of the disease

HF can have an acute onset and a chronic course. The signs are:

• Dyspnea (shortness of breath) during exercise or at rest, suffocation
• Weakness, lethargy
• Swelling of the feet, ankles and legs
• Swelling of the neck veins
• Pain in the right hypochondrium
• Cardiopalmus
• Inability to perform usual physical activities
• Persistent cough with light-colored or pinkish sputum
• Need to urinate at night
• Ascites
• Loss of appetite or nausea
• Inability to concentrate, absent-mindedness
• Chest pain relieved by taking aminophylline
• Sudden attacks of suffocation with coughing and discharge of foamy pink sputum

Emergency medical attention is necessary if the patient experiences:

• Chest pain
• Loss of consciousness or severe weakness
• Fast or irregular heartbeat associated with shortness of breath, dizziness, or chest pain
• Sudden cough with pink sputum or coughing up blood
• Bluishness around the mouth, tip of the nose and fingers

If you have already been diagnosed with heart failure or another cardiac disease and experience the symptoms described above, seek medical help.

How are respiratory failure classified by severity?

The main criteria on which the classification is based are the measurement of blood gas balance, primarily the partial pressure of oxygen

(PaO2), carbon dioxide in arterial blood, as well as blood oxygen saturation (SaO2).

When determining the severity, it is important to identify the form in which the disease occurs.

DN shapes depending on the nature of the flow

There are two forms of DN - acute and chronic.

Differences between the chronic form and the acute form:

• chronic form of
  DN - develops gradually, may not have symptoms for a long time. Usually appears after an untreated acute form;
• acute
  DN - develops quickly, in some cases symptoms appear within a few minutes. In most cases, the pathology is accompanied by hemodynamic disturbances (indicators of blood movement through the vessels).

The disease in a chronic form without exacerbations requires regular monitoring of the patient by a doctor.

Acute respiratory failure is more dangerous than chronic respiratory failure and requires immediate treatment.

Classification according to severity includes 3 types of chronic and 4 types of acute forms of pathology.

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Severity of chronic DN

As DN develops, the symptoms become more complex and the patient’s condition worsens.

Diagnosing the disease at the initial stage simplifies and speeds up the treatment process.

Symptoms in chronic deficiency are not as intense as in the acute form.

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How is acute respiratory failure classified?

There are 4 degrees of severity of acute DN:

I degree

. It is characterized by shortness of breath (may appear on inhalation or exhalation), increased heart rate.

• PaO2 - from 60 to 79 mm Hg;
• SaO2 - 91-94%.

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II degree

. The skin is marbled, bluish. Convulsions are possible, consciousness becomes darkened. When breathing, even at rest, additional muscles are activated.

• PaO2 - 41-59 mm Hg;
• SaO2 - from 75 to 90%.

III degree

. Shortness of breath: sharp shortness of breath is replaced by attacks of respiratory arrest, a decrease in the number of breaths per minute. Even at rest, the lips retain a rich bluish tint.

• PaO2 - from 31 to 40 mm Hg;
• SaO2 - from 62 to 74%.

IV degree

. State of hypoxic coma: breathing is rare, accompanied by convulsions. Possible respiratory arrest. Cyanosis of the skin of the whole body, blood pressure at a critically low level.

• PaO2 - up to 30 mm Hg;
• SaO2 - below 60%.

IV degree corresponds to a terminal condition and requires emergency assistance.

In the body of a healthy person, PaO2 is above 80 mm Hg, the level of SaO2 is above 95%.

If the indicators are outside the normal range, this indicates a high risk of developing respiratory failure.

Diagnostics

To make a diagnosis, the doctor must perform the following actions and analyze the results of the following studies:

• Collecting anamnesis - what complaints are bothering you, when they appeared, how they change under the influence of stress or medications; presence of concomitant diseases
• Examination – presence of edema, dilated veins on the anterior abdominal wall and neck
• Physical examination - auscultation and percussion of the lungs determines the level of fluid in the pleural cavity without the use of x-rays. Tapping the cardiac borders allows you to assess the size of the heart, especially the right half. Listening to murmurs is necessary to diagnose valve defects and changes in the density and structure of lung tissue.
• General clinical tests - blood for cellular composition, lipids, protein, glucose, bilirubin, coagulogram and others.
• Assessment of blood gas composition - percentage of oxygen and carbon dioxide.
• Study of external respiration function (spirography)
• X-ray of the chest - provides information about the condition of the chest organs
• Electrocardiogram
• ECHO-KG
• Catheterization of the right ventricle to measure pressure in the branches of the pulmonary artery
• Lung biopsy
• CT, MRI of the chest - visualize the size, structure of the heart and its relationship with neighboring organs, as well as the structure of the lungs and the condition of the pleural cavity.
• Angiography of the pulmonary vessels - allows you to evaluate the patency of the arteries by introducing an iodine-containing substance through a catheter under the control of an X-ray machine.

2. Reasons

Let's return to the definition given at the beginning of the article. Oxygen is delivered to all structures, tissues and cells of the body in a chemically bound form, as a compound with iron-containing hemoglobin, a high-molecular protein of red blood cells (erythrocytes).

The immediate cause of acute hypoxia as systemic oxygen starvation is either blood deficiency as such, or a drop in blood pressure and a slowdown in hemodynamics, or a lack of bound oxygen in the blood - hypoxemia. In any case, the reduction or cessation of tissue oxygenation, i.e. tissue respiration (which can happen even if external respiration is preserved, if we understand by this the motility of the respiratory muscles and the gas exchange function of the lungs) is one way or another connected with blood oxygen.

There are primary and secondary ODN.

Primary develops due to failures, blockages or difficulties in external breathing. The most common direct cause is mechanical obstruction or obstruction of the airways of various sizes (larynx, trachea, bronchi, small terminal bronchioles) due to spasm, accumulation of mucus or pus, foreign body entry, filling with water, compression from the outside, rapid edema (inflammatory, allergic, toxic , autoimmune). Acute respiratory failure can result from lung damage due to severe thoracic trauma, as well as functional failure of pulmonary gas exchange tissues and structures.

External respiration can also be suppressed during painful and electric shocks, severe head injuries, neuromuscular disorders, overdoses of drugs, muscle relaxants, analeptics (stimulants of the cerebral respiratory center and vascular tone).

Secondary acute respiratory failure develops for reasons that do not affect the external respiratory system. Such reasons include blood deficiency conditions, hemodynamic disorders and hypoxemia of extrapulmonary etiology (hypovolemic shock, heart attack, thromboembolism in the pulmonary artery, various types of anemia, vascular collapse, high-altitude sickness, hypercapnia, etc.).

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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.

How are the severity of pathology in children determined?

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DN in a child usually occurs in an acute form. The main differences between pathology in adults and children are different levels of blood gas parameters.

If signs of DN 3 and 4 severity are detected, the child requires emergency hospitalization and intensive care. Treatment of children with mild DN (stages 1 and 2) is possible at home.

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.

Stages and symptoms of CHF

In Russian medicine, two classifications of chronic heart failure are used: classification of chronic circulatory failure N.D. Strazhesko, V.Kh. Vasilenko and the functional classification of the New York Heart Association. In diagnosing the disease, the indicators of both systems are taken into account.

Classification by N. D. Strazhesko, V. Kh. Vasilenko (1935)

The patient's condition is assessed by the number and severity of clinical manifestations of the disease.

Stage 1

Initial, latent circulatory failure, manifested only during physical activity (shortness of breath, palpitations, excessive fatigue). With rest, these phenomena disappear. Hemodynamics are not impaired.

Stage 2

Severe, prolonged circulatory failure, hemodynamic disturbances (stagnation in the pulmonary and systemic circulation), dysfunction of organs and metabolism are also expressed at rest. Working capacity is sharply limited.

Period 2a

• Hemodynamic disturbances are moderate, and dysfunction of any part of the heart is noted (right or left ventricular failure).

Period 2b

• Severe hemodynamic disturbances, involving the entire cardiovascular system, severe hemodynamic disturbances in the small and large circles.

Stage 3

Ultimate, dystrophic. Severe circulatory failure, persistent changes in metabolism and organ functions, irreversible changes in the structure of organs and tissues, pronounced dystrophic changes. Complete loss of ability to work.

The structure of the human circulatory system: arteries are marked in red, veins are marked in blue.

Functional classification of the New York Heart Association

Adopted in 1964 by the New York Heart Association (NYHA). This classification is used to describe the severity of symptoms; on its basis, four functional classes of the disease (FC) are distinguished.

• First class FC

  . There are no restrictions on physical activity. Normal physical activity does not cause excessive shortness of breath, fatigue, or palpitations.

• Second class FC

  . Slight limitation in physical activity. Comfortable state at rest. Normal physical activity causes excessive shortness of breath, fatigue, or palpitations.

• Third class FC

  . Explicit limitation of physical activity. Comfortable state at rest. Less physical activity than usual causes excessive shortness of breath, fatigue, or palpitations.

• Fourth grade FC

  . Inability to perform any physical activity without discomfort. Symptoms may be present at rest. With any physical activity, discomfort increases.

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.

Disease prevention

In order to prevent pathology, all risk factors that can provoke it should be eliminated. If any negative symptoms appear, it is important to consult a doctor in order to promptly diagnose and treat lung or heart disease. Also, experts recommend leading a healthy lifestyle (not smoking or drinking alcohol), engaging in moderate physical activity and eating right. The diet should be balanced with a predominance of fresh vegetables and fruits.

In order to prevent the development of acute cor pulmonale, patients diagnosed with varicose veins and atrial fibrillation are prescribed indirect anticoagulants. If there are blood clots in the veins, a vena cava filter is often installed. It is a small device that is installed into the lumen of the inferior vena cava. With its help, detached blood clots do not enter parts of the heart muscle and the pulmonary artery system.