Pathology of acute respiratory failure

2021-01-27 12:00 AM

Acute respiratory failure is a severe disturbance of blood oxygen exchange; generally, acute respiratory failure is a net decrease in arterial oxygen partial pressure (PaO2) <60 mmHg.

 

Acute respiratory failure

Define

Acute respiratory failure is a severe disturbance of blood oxygen exchange; generally, acute respiratory failure is a net decrease in arterial oxygen partial pressure (PaO2) <60 mmHg, and artery carbon dioxide partial pressure (PaCO2) may be normal or increase.

There are 2 types of acute respiratory failure:

Acute respiratory failure with hypoxia with carbon dioxide retention.

Acute respiratory failure with anaemia with decreased carbon dioxide.

Causes

Causes in the lungs

Acute decompensation of chronic respiratory failure:

Factors that make it easy are bronchopulmonary infections, pulmonary embolism, pneumothorax.

Lung infections:

They occur in healthy lungs and only cause acute respiratory failure when these lung infections have spread to many lobes: bronchitis due to exponential infections, millet TB, malignant viral infections.

Pulmonary oedema:

Acute cardiogenic pulmonary oedema:

All causes of left heart failure: persistent hypertension or hypertension, coronary failure in which myocardial infarction is the most common cause, aortic stenosis, mitral regurgitation, disease myocardium.

Mitral valve stenosis.

Pulmonary artery embolism.

Good upper lung oedema:

Excessive infusion.

Neurological causes: traumatic brain injury, tumour or surgery to touch the brain stem, encephalitis.

Acute pulmonary oedema due to physical damage:

First of all, malignant influenza due to many factors: viral factors, local factors, because the severe forms are mainly found in people who have heart disease, mitral stenosis, especially in the elderly, women have pregnancy; in children with a severe viral infection in the form of bronchiolitis - alveolar inflammation. Less common are due to toxins (hydrogen, carbon oxides, venomous snake venom), septic shock, fat embolism, drowning, Mendelson's syndrome (inhalation of gastric juice due to heartburn).

Severe-threatening asthma, severe acute asthma:

This is a common disease, usually due to improper treatment or in time may be due to the patient's predisposition to severe bronchial asthma.

Acute bronchial obstruction:

This disease is rare, in children can be caused by foreign objects, in adults, it can be caused by tumours, atelectasis may be caused by intubation.

Extra-pulmonary causes

Bar-tracheal obstruction:

This disease is caused by tumours such as a laryngeal tumour, submerged thyroid tumour, neck oesophageal tumour, tracheal tumour; caused by infections such as laryngitis, tetanus; due to a large foreign object.

Pleural effusion:

Less acute respiratory failure if effusion slowly, only causes acute respiratory failure during acute effusion, fluid volume increases rapidly.

Free-form pneumothorax:

Often due to pulmonary tuberculosis, emphysema rupture, congenital, spontaneous (unexplained) gas cocoon rupture, possibly due to rupture of a pulmonary abscess always accompanied by pleural effusion.

Chest injury:

This disease causes fractures of the ribs thereby damaging the pleura and lungs.

Respiratory muscle damage:

Common causes are pre-spinal keratitis, Guillain Barré syndrome with Landry acute paralysis, tetanus, snakebite, poisoning with organic phosphorus-based insecticides, severe myasthenia gravis, and polymyalgia.

Central nervous system damage:

The causes are often traumatic brain injury, drug poisoning, cerebrovascular accident; causes of damage to the respiratory centre.

Mechanism of hypoxia

Reduced alveolar ventilation

The oxygen pressure in the alveoli is determined by the balance between the rate of oxygen loss, the metabolic function of the tissue, and the renewal rate of oxygen by alveolar ventilation. If the alveolar ventilation is abnormally reduced, the oxygen pressure in the alveoli decreases and the oxygen partial pressure in the canal decreases. Alveolar ventilation can be secondary to damage to the respiratory centre (coma, drug poisoning) or deactivation of thoracic-pulmonary activity (pre-spinal horn damage, respiratory muscle damage steam or dominant nerve).

Imbalance between ventilation / perfusion

A mismatch between ventilation and blood flow is responsible for a disturbance in the air exchange in a lung unit; the ventilation / perfusion ratio is close to 1; The pressure of oxygen and carbon dioxide in the alveoli is 100 mmHg and 40 mmHg is close to the partial pressure of oxygen and carbon dioxide in the arteries. If the air is reduced, the ventilation/perfusion ratio: VA / Q is 0 then the oxygen and carbon dioxide pressure in the alveoli and the partial pressure of oxygen and carbon dioxide are nearly equal, the partial pressure of oxygen and gas the carbon dioxide in the veins is 40 mmHg and 45 mmHg.

If perfusion is reduced, then the ventilatory / perfusion ratio tends to be indefinite, the air pressure in the alveoli and in the artery is close to the inhalation pressure (PO2 = 150mmHg, PCO2 = 0). In the lungs, the ventilation/perfusion ratio varies by region and disease. There are 3 unusual types of this billion:

Shunt lung

This abnormality is blood circulation in the arterial system that does not pass through the respiratory zones. The pulmonary shunt was seen in pulmonary oedema, atelectasis.

The shunt effects

This abnormality corresponds to the diffusion of lung units where ventilation is decreased, the rate of ventilation/perfusion is reduced, but the alveoli remain active at least in the early stages of communication with the respiratory tract; hypoxia is caused by a decrease in the oxygen supply of the venous blood. People experience shunt efficacy in pulmonary oedema, acute lung disease, acute bronchitis, chronic bronchitis, pleural effusion.

Effective dead space

Because of this abnormality due to hypoventilation of a unit of the still respirable lung, the ventilation/perfusion ratio tends to be infinite. Pulmonary embolism or destruction (pulmonary artery embolism, emphysema) causes an additional death space in addition to the surgical death space.

The hypoxia is exacerbated when the alveolar number is not involved in the gold gas exchange much; Hyperventilation (compensatory breathing) leads to a decrease in blood carbon dioxide if the air in the alveoli is not trapped during expiration (chronic bronchitis, severe acute bronchial asthma).

Diffusion disorder

Some lung diseases such as fibrosis interstitial lung disease cause damage to the alveolar-capillary membrane, this membrane thickness is> 0.5 (thus reducing the exchange of oxygen gas from the alveoli to the capillaries. Alveolar bloc - capillary causes hypoxaemia to discuss.

Mechanism of change in carbon dioxide in the blood

Carbon dioxide pressure in the alveoli and in the artery changes in the opposite direction of alveolar ventilation. The changes in carbon dioxide production are usually small and play a minor role in the changes in carbon dioxide in the blood.

Reducing blood carbon dioxide

This phenomenon is the result of hyperventilation caused by a lack of blood oxygen.

Increased blood carbon dioxide

This phenomenon is a mismatch of the pulmonary clearance coefficient for carbon dioxide, which corresponds to a decrease in alveolar ventilation.

Clinical

Respiratory rate and amplitude

Hypoxemia and or hyperserotonaemia induce tachypnoea, the breathing rate of about 40 beats/min in conjunction with the contraction of the respiratory muscles, apparent in the upper sternum and rib spaces; In children, bulging nose wings may be attached. In cases of paralysis damage (poliomyelitis, quadriplegia due to spinal cord injury, severe myasthenia gravis ...), the breathing frequency often decreases, the respiratory amplitude is weak, the patient does not cough. OK, thus causing a build-up of phlegm in the bronchi.

Respiratory monitoring is important because bradycardia can be an improvement in blood oxygen exchange but can also be respiratory muscle deterioration, especially in severe acute bronchial asthma.

In laryngotracheal diseases, a combination of dyspnoea is observed.

The team

Purple is the main control sign, appearing on lips, limbs, face or the whole body when haemoglobin is reduced> 50g / l. This corresponds to a saturation of oxygen in the arterial blood is 85%. Purple is more pronounced when haemoglobin blood is higher (chronic respiratory failure); purple is not visible in severe anaemia. Purple is often associated with hyperserotonaemia, violet is accompanied by vasodilation in the extremities, sometimes with sweating.

Circulatory sign

Lack of blood oxygen and hyperserotonaemia increase the rate of catecholamine and thus make blood vessels fast, causing the increase in blood pressure and cardiac output, possibly with supraventricular arrhythmias, the post-blood pressure stage may lower.

Signs of acute right ventricular failure

Particularly common in exacerbations of chronic respiratory failure. The main signs are enlarged liver, the cervical venous liver feedback signal, heavier than naturally floating cervical vein (in position 450), these signs decrease when acute respiratory failure decreases.

Psychiatric signs

This sign is only seen in severe acute respiratory failure; it is a state of excitement, struggles, perceptual disturbances such as drowsiness or coma.

Subclinical

Blood gas

Normal:

The PaO2 is 80 - 95 mmHg.

The PaCO2 is 38 - 43 mmHg.

Blood pH is 7.38 - 7.43

The alkaline reserve is 24 - 26 mmol / l.

Pathological:

Anaemia: The PaO2 can be reduced to only 25 mmHg.

Carbonic disorder: will lead to an acid-alkaline balance disorder.

Increased PaCO2: leads to respiratory acidosis, which is compensated for by buffers of the blood and tissue and by renal excretion of H + ions.

In the presence of an acute increase in PaCO2, the buffering mechanism is initially plasma and haemoglobin, then tissue and kidney intervene in phase 2 at 24 hours by increasing H + ion excretion and reabsorption of Na + ions and bicarbonate.

Respiratory acidosis is called compensatory when cellular buffers are used to keep the pH from falling. This compensation is limited by an increase in the bicarbonate of not more than 50 mmol / l.

Reduction of PaCO2: leads to respiratory alkalosis with decreased plasma bicarbonate.

Cardiovascular survey

Right ECG and cardiac catheterization, cardiac Dopler ultrasound to investigate heart damage.

Movie chest

This test should be done to be able to detect the damage in the lung tissue, pleura, mediastinum.

Stage of respiratory failure

Table: Stages of acute respiratory failure.

Symptom

State 1

Phase 2

Stage 3

Stage 4

Shortness of breath

When exertion, when lying in the chest can move

Continuously, the thorax moves with difficulty

Continuously, the chest does not move, the respiratory muscles are still active

Continuously, the respiratory muscles are weak, shallow breathing, breathing disorders

Breathing frequency

times / minute

25-30 when exertion

25 - 30

30 - 40

> 40

 

< 10

The team

When exertion

Lips, head limbs

Face, tissue, head limbs

Body

Sweat

0

±

+ +

+ + +

Circuit times/minute

90 - 100

100 - 110

110 - 120

> 120

Blood pressure

Normal

Normal

High

High or low

Consciousness disturbances

Are not

Are not

Struggling

Lethargic, lethargic

SaO2 (%)

80 - 90

70 - 80

60 - 70

< 60

PaCO2 (mmHg)

40

45 - 55

55 - 70

> 70

blood pH

7,35 - 7,40

7,30 - 7,35

7,25 - 7,30

< 7,25

Reserve alkali

Normal

Normal

Reduction

Reduction

Progression and prognosis

Respiratory failure, if properly treated, can completely recover. During progression, it is possible to have superinfection of the lungs or urinary tract, especially in patients with intubation or urinary incubation.

If treatment is not timely, acute respiratory failure can progress gradually, and the patient can become comatose and die.

The principles of treatment

Clear the airways.

Oxygen therapy.

Endotracheal intubation, tracheostomy, respiratory support.

Anti-infection, superinfection.

Alkaline plasma.

Specific treatment

Respiratory support and release

Clean mouth, throat, nose.

Put the Mayo canuyn to keep from pulling your tongue.

Absorb phlegm, secretions by vacuum.

Wash the bronchi, dilute the phlegm with aerosol, by pumping with 14 ‰ bicarbonate de sodium solution or 9 chlorure de natri solution 2 - 5 ml each time and then aspirate.

Rehydration of water and electrolytes and acid-alkaline balance.

Ensure there is a balance between fluid output and daily intake, avoid dry sputum, bronchial secretions. If respiratory acidosis is present, a cumulative infusion such as sodium bicarbonate is 14

Oxygen therapy

Breathe oxygen:

Oxygen must be moist and warmed prior to use on the patient. Oxygen must pass through a water tank and be heated by ultrasound or heated plates.

Means of breathing oxygen.

A nasal bath is often used.

Most often the end of a cannula with multiple holes placed not exceeding the posterior nostril (length is the distance between the nose and the earlobe).

Nasal spray can be used for volumes from 1 to 6 litres/minute, often used in cases of mild or moderate respiratory distress.

Point:

Breathe pure oxygen.

Applied in very few cases such as cardiac arrest, heavy bleeding.

Oxygen-enhanced breathing air.

Patients with normal or decreased blood carbonic concentrations: In all hypoxia, the PaO2 decreases below 65 mmHg, oxygen is provided with an output of 4-6 litres/min by nasal inhalation or in other cases for more severe hypoxia, use an oxygen mask.

In patients with chronically high blood carbonic concentrations: those with chronic respiratory failure, the oxygen supply in patients with chronic respiratory failure is as low as 1-3 litres/min, breathing intermittently and controlled concentration of gases in the blood.

Endotracheal intubation

Point:

When there are upper respiratory tract problems such as oedema, laryngeal injury, lethargy causing a drop of the tongue.

When need to reduce dead space to increase alveolar ventilation, respiratory support, need oxygen, mechanical ventilation.

When there is an increase in blood carbon dioxide.

When it is necessary to protect the respiratory tract, prevent inhalation is wrong.

Methods

There are two methods.

Nasal endotracheal intubation:

Also known as intubation, is a commonly used method, especially for infants, nursing infants and children, especially in tetanus and in medical resuscitation. The patient is placed in an improved Jackson posture: lying on his back, with his shoulders resting 5-7 cm in height to moderate neck rest or a half-sitting position, especially when afraid of blood, pus, fluid ... from the diseased lung to the side that.

Oral intubation:

The patient is placed in the same position as above: Jackson posture or half-sitting. Give oxygen for several minutes before insertion.

Usually, the tube is not placed for more than 3 days.

Open the trachea

Point:

As indicated for intubation or inability to insert the tube or when needing to be placed for more than 3 days.

Method:

High tracheostomy: easier to see trachea.

Low tracheostomy.

Complications can occur with intubation and tracheostomy:

Accident when placing:

Bleeding, laryngeal oedema, tracheal perforation, glottic spasm, cardiac arrest.

Accidents after placing:

Site infections, pneumonia, ulcers, necrosis of the trachea, oesophageal leakage, vocal cord damage, atelectasis, pneumothorax, mediastinal airflow, subcutaneous airflow.

Respiratory support

Manual respiratory aids:

The breathing air supplied to the patient is outdoor air.

Glossy type: Ambu, Canister.

Pockets: Ranima, Drager.

Breathing machine:

Point:

Mechanical ventilation is used when conventional respiratory support methods are ineffective.

The three major types of patients correspond to three different degrees of carbon dioxide in the blood. Each type of patient needs a different way of modulating CPR:

The first type of patient: one with a large increase in carbon dioxide with a decrease in blood oxygen, such as acute decompensation of chronic respiratory failure, oxygen must start with a low volume, then gradually increase. Up but very slowly, the maximum oxygen delivery (FiO2) is in the beginning.

The second type of patient: is the type of developing hyperserotonaemia, this patient can breathe completely normal with FiO2 about 50%.

The third type of patient: the type with a decrease in blood carbon dioxide. Phenomenon pulmonary hyperaemia after hypoxemia. However, due to underlying lung disease, the increase in respiration did not lead to an increase in the PaO2. As a result, the patient gets worse, and oxygen debt becomes worse and worse.

There are 5 types of ventilators:

The ventilator generates cycles based on frequency.

The ventilator generates cycles based on volume.

The ventilator generates cycles based on pressure.

The ventilator creates a cycle based on the airflow.

The ventilator creates a mixed cycle.

Anti-bacterial infection:

The bacteria that cause superinfection are usually Streptococcus pneumoniae, Haemophilus influenza, Staphylococcus aureus, Klebsiella pneumonia, etc., so appropriate antibiotics must be given.

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