Pathology of chronic respiratory failure

2021-01-28 12:00 AM

The causes of chronic respiratory failure are many and varied, possibly in the respiratory apparatus and outside the respiratory system.


Chronic respiratory failure is a condition in which the oxygen needed by the body cannot be supplied or used during rest or exertion.

In fact, chronic respiratory failure is diagnosed in the presence of chronic disturbances in the blood gases, decreased PaO2 and increased PaCO2.


The causes of chronic respiratory failure are many and varied, possibly in the respiratory apparatus and outside the respiratory system.

People distinguish 3 types of chronic respiratory failure: obstruction, restriction and coordination.

Chronic obstructive respiratory failure

Chronic obstructive pulmonary disease (COPD):

A medical condition of chronic bronchitis or emphysema with limited airflow. This obstruction occurs slowly with the increased bronchial response and may not be reversible or partially reversible.

The main causes of chronic obstructive pulmonary disease are smoking, followed by passive inhalation, environmental pollution, mid-respiratory pollution, and occupational pollution.

There are 4 pathophysiological features of chronic obstructive pulmonary disease:

Airway obstruction:

As a result of the destruction of the medial parenchyma is the result of a decrease in antiprotease in which a decrease (1 - antitrypsin and/or an increase in protease that is neutrophil elastase is an enzyme that breaks down the alveolar walls, causing bronchitis, reduced hairy epithelium and increased secretion of mucus.

Due to airway changes: due to chronic inflammation, oedema, proliferation and proliferation of mucus cells, an increase in the number and diameter of airway microchips, hypertrophy and hyperplasia smooth mechanical layer of the air path.

Increased activity of the respiratory centre: to maintain a necessary level of alveolar ventilation.

Respiratory muscle abnormality: due to increased stimulation from the respiratory centre, geometrical changes in the respiratory muscles, adverse metabolic factors, and muscle fatigue.

Abnormalities between ventilation and perfusion: capillary shunt due to obstruction of the air passages (decreased VA / Q) and alveolar death space due to emphysema (increased VA / Q).


Especially the progression is prolonged, heavy, and irreversible.

Upper respiratory tract congestion:

Do u, narrow due to scarring.

Chronic respiratory distress in and out of the lungs

In the lungs:

Severe sequelae spread to 2 sides (pulmonary fibrosis).

Diffuse interstitial lung diseases causing fibrosis: drug allergies, toxins, after radiation therapy, Sarcoidosis disease.

Lung resection.

Chronic interstitial pulmonary oedema (heart failure).

In the chest:

Pleural thickening, chronic pleural effusion.

The heart is too big.

From the abdomen and chest wall:

Diaphragmatic hernia.

Lots of ascites.

Due to muscles and nerves:

Myopathy affects the respiratory muscles.

The central nervous system damage affects the respiratory muscles: keratitis before spinal cord, lateral sclerosis atrophy, encephalitis, stroke, Parkinson's disease ...

Lesions to the respiratory centre, receptors transmit to the centre:

Central: Hypothyroidism, mucosal oedema, metabolic alkalosis.

Receptor: Diabetic neuropathy.

Path to the centre: Transverse myelitis, scattered sclerosis ...

Combined chronic respiratory failure


Chronic bacterial diffuse pneumonia is common, or TB.

Mechanism of pathogenesis

Reduce the PaO 2

The most important objective disorder, known as chronic hypoxaemia, when a PaO2 less than 70 mmHg occurs persistently during the stable period. Chronic hypoxia becomes ominous from a PaO2 level = 55 mmHg.

Reduced oxygen transport:

Oxygen transport to tissues depends on cardiac output (Q) and on the oxygen capacity of the arterial blood (CaO 2).

TO2   = Q x CaO2

CaO2 depends on the amount of oxygen that is, on the amount of usable haemoglobin and on the oxygen saturation.

In the case of severe hypoxia (PaO2 <50 mmHg, SaO2 <85%), CaO2 decreases TO2 decrease. However, a decrease in the PaO2 is usually balanced by an increase in the concentration of haemoglobin (secondary polycythaemia). As a result, oxygen transport is usually not affected much except during acute respiratory failure or during periods of severe hypoxaemia such as during sleep.

Erythropoiesis reaction (secondary polycythaemia vera):

The erythropoietic reaction is beneficial by allowing adequate oxygen transport but is harmful by increasing blood viscosity and thus contributing to increased pulmonary vascular resistance leading to the development of arterial hypertension lung.

Chronic effects on the brain:

Chronic hypoxia causes neurological and mental abnormalities such as attention and memory disorders, difficulty with abstract thinking, skilful behaviour, and simple movement disorders.

Effects on hemodynamic:

Chronic hypoxia increases pulmonary vascular resistance due to strong spasm; hypertrophy increases smooth muscle in the artery wall, causing pulmonary artery hypertension and right heart burden. The heart compensates for this increase in burden increasing systolic frequency and output to ensure oxygen supply. It should be noted that pulmonary hypertension is an adaptive mechanism, helping to select a number of capillaries for good perfusion, improving the ventilatory / perfusion relationship.

Mechanical ventilation disturbances

In chronic obstructive respiratory failure:

In chronic obstructive respiratory failure, the first second maximum expiratory volume (VEMS) decreases, and the Tiffeneau ratio (VEMS / CV%) decreases.

In limited respiratory failure:

Lung volume decreases, total lung capacity (CPT) decreases, and lung relaxation decreases, making it harder to breathe in.

Contact ventilation-perfusion V / Q

Increase short-cut efficiency.

Increases dead space significantly.

Reduce the PaO2 and increase the PaCO2.

Operation of respiratory centres

The respiratory centre in patients with chronic respiratory failure is no longer stimulated by the chronically elevated PaCO2, only remaining active by stimulating hypoxia, so when high doses of oxygen are given to breathe, the respiratory centre is inhibited. . increase CO2.

Clinical symptoms

Meticulous questions must be asked to determine the time and severity of exertion of breathlessness, coughing up coughs, smoking addiction, as well as the pollution of the patient's living or working environments such as inhaling toxins and dust.

In addition to individual indications of individual etiologies, signs of chronic respiratory distress may be apparent.

Purple and difficulty breathing

Purple, the presence of SaO2 gas is below 85% (normal above 95%). Shortness of breath when the lack of oxygen is already severe (severe slowly due to natural progression or sudden due to superinfection).

Behavioural disorders

Behavioural disturbances occurring when a PaCO2 is above 50-55 mmHg can progress spontaneously incrementally or suddenly due to an easy cause such as respiratory depression. Patients with irritability, headache, and disturbed consciousness may be euphoric or moody and may tremble in a coma alert due to increased CO2.

Chronic heart mark

Due to lack of oxygen and due to increased CO2: purple (Note clearly when accompanied by reactive increased erythrocytes), signs of right ventricular failure.

More important are the earlier mild symptoms

Often caution is required to detect, often in obstructive chronic respiratory failure.

Shallow tachypnoea with dilated thorax is intended to compensate for hypoxia and limit atelectasis of small bronchi due to deep exhalation.

Tensile mark indicates an increase in pleural negative pressure due to obstruction of the airway.

Increases the contraction of the trapezoidal muscles, enlarging these muscles when breathing in

Tight lips exhalation: the purpose of reducing the pressure difference between the alveoli and the mouth alleviates the collapsed bronchi.

Chest dilatation and HOOVER mark (decrease in diameter across the lower chest when inhaled).

Fire match blasting:

Open your mouth to a burning match more than 50 cm away.

Stick a rotten match on a fire 100 cm away. If not turned off, there is a risk of chronic respiratory failure.


Explore respiratory function

In chronic obstructive respiratory failure: There is a decrease in FEV1, FEV1 / FCV.

In limited chronic respiratory failure: lung volume decreases, total lung capacity (CPT) decreases, pulmonary relaxation decreases.

Blood gas

Called chronic respiratory failure when the PaO2 is below 65-70 mmHg and the PaCO2> 45 mmHg.

In moderate chronic respiratory failure:

The PaO2 is even greater than 60 mmHg.

And or the PaCO2 is less than 50 mmHg.

SaO2 ≡ 90%.

With blood pH and normal Hct.

In severe chronic respiratory failure.

The PaO2 is less than 60 mmHg.

And or the PaCO2 is less than 50 mmHg.

SaO2 is less than 90%.

With low pH and increased Hct.

Several other parameters are of diagnostic value in the heart of chronic lung


Measurement of pre-capillary pulmonary artery pressure: more sensitive than ECG, normally 13-18mmHg, measured directly and outside each acute or superinfection.



It is the severity of chronic respiratory failure that determines this treatment. The aetiology, whether obstructive or restrictive ventilation or due to alveolar-capillary diffusion disorders, is only an adjunct to treatment.

The severity of chronic respiratory failure is indicated mainly by PaO2, SaO2 and PaCO2, in addition to blood pH, alkaline reserve, Hct.

Treatment of moderate chronic respiratory failure

60 mmHg <PaO2 <70 mmHg and or 43 mmHg <PaCO2 <50 mmHg.

Blood pH, normal Hct.

SaO2 = 90%

General measures:

Stop smoking completely and permanently.

Remove patients from natural or occupational air pollution.

Eliminate any foci of respiratory tract infections, especially the sinuses and teeth, which is the common source of the infection.

Change to a better climate.

Reducing obesity limits ventilation.

Symptomatic treatment:

Prevention of bronchopulmonary superinfection.

Vaccines against influenza and some bacteria that easily cause infections.

Strongly appropriate treatment for all bronchopulmonary superinfection episodes, appropriate antibiotic treatment, strong, well-tolerated in the lungs as antibiotic Macrolide: Roxithromycin [Roxid], Rulid, 150 mg, 2 tablets/day 2 times], or a Cephalosporine antibiotic (Cephadroxil [Opedroxyl, Oracefal], 500 mg, 3 capsules/day, divided into 3 times, for more than 8 days.

Sputum digestion:

Mainly by motor therapy: thoracic flapping followed by sputum practice with maximum effort, proper breathing exercise, utilizing the cooperation of diaphragm force and abdominal wall muscles.

Mucolytics such as Acetylcysteine ​​(Acemuc) 200 mg, 3 packs/day in 3 divided doses.

Mucoid-regulating drugs such as Ambroxol (Mucosolvan), 30 mg, 3 tablets/day, in 3 divided doses.


As a primary, long-term means of treatment, whether or not respiratory function is detected with bronchospasm.

Theophylline fast (100mg Theophylline tablet) or slow (Theodur tablet, 200 mg or 300 mg), 10-15 mg / kg / day, if using fast type, divide 3-4 times, if using slow type, it is 2-3 times.

Salbutamol fast (Ventolin tablets, 2 mg or 4 mg) or slow (Volmax tablets, 4 mg or 8 mg), 0.2 - 0.3 mg / kg / day, if using fast type, divide 3 times, if using type If slow, divide 2 times.


Sedatives, sleeping pills because they can inhibit the respiratory centre.

Some drugs are ineffective, even dangerous, such as corticosteroids, respiratory stimulants (because they only fatigue the respiratory muscles, increase stimulation), and prolonged anticoagulation.

Treatment of severe chronic respiratory failure

PaO2 <60 mmHg and or PaCO2> 50 mmHg.

Low blood pH, increased Hct.

SaO2   < 90%.

The above treatment measures are thoroughly applied.

Medicines that improve oxygen exchange:

Almitrine bimesilate (Vectarion) 15 mg, 3 tablets / day, in 3 divided doses.

Oxygen therapy:

It is very necessary to maintain the PaO2 in the range of 60-80 mmHg, give oxygen at a low flow rate of 0.5 to 1.5 litres/min to avoid inhibition of the respiratory centre, usually about 1l / min.

This oxygen must be done with the right technique: must put the nasopharynx nasal bath quite deeply, the oxygen must pass through a clean water bottle, measured the flow accurately, closely monitored, preferably with blood gas, at first measuring blood 2 times/week, then 1 time/month.

Daily breathing time 12-15 hours/day to ensure the normalization of key factors such as pulmonary artery pressure, Hct and reduce exercise dyspnoea.

Breathing machine:

When none of the above measures worked

Some treatments are conservative

Corticoids: Use in severe bronchial asthma, chronic obstructive pulmonary disease

Cardiac Drugs: Digoxin in the presence of heart failure, however, such arrhythmias are more harmful than beneficial.

Diuretics: As Furosemide can cause alkalosis, inhibiting the respiratory centre (alkalosis is due to increased hydrogen ion excretion and bicarbonate reabsorption).