Pulmonary ventilation
The pulmonary ventilation , just as a fan called, describes the respiration in the meaning lung nbelüftung and the "ability to increase the chest cavity and collapse and thus draw air into it and squeeze out of him." The ventilation enables gas exchange in the alveoli ( respiration , breathing in the second sense of the word) by keeping the oxygen partial pressure high and the carbon dioxide partial pressure low so that oxygen can enter the blood and CO₂ can be exhaled. Ventilation is not a function of the lungs themselves (mammalian lungs have no muscles), but of the diaphragm and the intercostal muscles , which - controlled by the brain via nerves - periodically increase and decrease the volume available in the chest. The structures necessary for ventilation are collectively referred to as breathing pumps ; Diseases of the lungs, the airways or the breathing pump can lead to ventilation disorders and even respiratory insufficiency . The measurement of ventilation parameters for diagnostic purposes is called lung function test ; Tidal volumes and volume flow strengths are determined by spirometry , and possibly also the volume remaining in the lungs after maximum exhalation by body plethysmography .
Pulmonary breathing of vertebrates
respiratory tract
When breathing, air flows into the body through the mouth or nose. When inhaling through the nose, the air is first cleaned, moistened and warmed up by the hairs of the nose and mucous membranes. The breath then passes through the pharynx, past the larynx and vocal folds, into the windpipe. The trachea branches into the two branches of the bronchi, which branch out further and further as bronchioles. In the windpipe, the air is cleaned again by tiny cilia. In the end, the alveoli are located in the lungs, through whose thin membrane oxygen passes into the blood vessels and, conversely, carbon dioxide is released from the blood via the alveolar air into the air.
Breathing Mechanics of Mammals
Breathing mechanics describes the static and dynamic forces that are influenced by lung volumes, airway pressures and flow resistance and counteract the ventilation. The two lungs fill the paired pleural cavity in the thoracic cavity with the exception of a narrow gap . This increases by straightening the ribs ( chest breathing ) and pulling down the muscular diaphragm ( abdominal breathing ). Since the pleural space filled with fluid does not change its volume, the lungs have to follow this expansion and fill with air via the airways. Here, the stretch alveoli against the surface tension of. A soap-like liquid ( surfactant ) reduces this surface tension, on the one hand to relieve the respiratory muscles and on the other hand to avoid the collapse of the smaller blisters. At the same time, elastic fibers prevent the overstretching of already stretched bubbles (for instability in connection with surface tension, see Young-Laplace equation ). The regulation of the bronchioles diameter also contributes to the even ventilation of different parts of the lungs .
When you exhale, the breathing muscles relax and the lungs contract. The pressure in the pleural space usually remains slightly negative. The expiratory auxiliary muscles are only used for forced exhalation during physical exertion, when speaking , singing , coughing or when breathing is difficult .
Dead space ventilation
The conductive airways from the nose / mouth through the throat, trachea and bronchi to the bronchioles form the anatomical dead space , as they are ventilated but no gas exchange takes place there. The anatomical dead space in the adult has a volume of about 150 ml; In diseases such as emphysema , functional dead space is added to the relevant extent , i.e. alveolar space that is not sufficiently supplied with blood for gas exchange. The volume inhaled per period is called the tidal volume and is calculated as the product of the respiratory rate and tidal volume . The respiratory time volume is divided between the alveolar and dead space ventilation; Since the dead space is served first with every breath, rapid and shallow breathing has a negative effect on the alveolar ventilation despite the constant breathing time volume. The alveolar gas mixture is only partially replaced by fresh air with each breath; the ventilation coefficient indicates the volume fraction exchanged per breath.
Breath control in mammals
Breathing is controlled by the brain or the respiratory center in the elongated medulla ( medulla oblongata ). The decisive factor here is the reaction of chemoreceptors to the carbon dioxide content of the blood . If this exceeds a certain threshold value, the respiratory drive begins . Receptors that react to the pH value of the arterial blood and a lack of oxygen are of secondary importance as respiratory stimuli.
The expansion of the lungs is also recorded via the sensitive fibers of the vagus nerve . If this exceeds a certain level, the respiration is limited by reflex .
Measurements in humans
The essential parameters of lung ventilation are the respiratory rate and the tidal volumes . The average number of inhalations and exhalations per minute (the breathing rate ) is at rest
Age | Breaths per minute |
---|---|
Adults | 11-15 |
Teenagers | 16-19 |
School child | 20th |
small child | 25th |
infant | 30th |
Newborn | 40-50 |
An adult inhales about 0.5 liters (tidal volume ) in one breath .
The minute ventilation is the sum of all tidal volumes within one minute. Understood as liters per minute:
Example: 4.2 l / min = 12 / min × 0.35 l
The dead space volume is the amount of air that is not actively involved in gas exchange, so in breathing in the gas-conducting system (space between mouth and alveoli) "stops". When an adult breathes about 500 ml at rest, the dead space corresponds to about 30% of the total tidal volume, i.e. H. about 150-200 ml.
The adult breathing pressure is normally around 50 mbar, with a maximum of around 160 mbar.
Disruptions
Classification according to ICD-10 | |
---|---|
R06 | Breathing disorders |
R06.1 | Stridor |
R06.2 | Pulling breathing |
R06.3 | Periodic breathing |
R06.4 | Hyperventilation |
R06.5 | Mouth breathing |
R06.6 | Singultus |
R06.7 | Sneeze |
R06.8 | Other and unspecified breathing disorders |
ICD-10 online (WHO version 2019) |
The feeling of being unable to breathe is called shortness of breath or, in medical terminology, dyspnea ; it arises when the respiratory drive cannot be satisfied. In addition to the ventilation disorders shown here, a lack of oxygen in the inhaled air and all disorders of the gas transport in the body are possible causes, including disorders of diffusion in the lungs ( respiratory disorders), insufficient pumping function of the heart or reduced oxygen transport capacity in the event of a deficiency in the red blood pigment ( anemia ) . The respiratory disorders are summarized in the ICD-10 under the symptoms affecting the circulatory system and the respiratory system as R06 .
Ventilation disturbances cause an excessively high CO₂ partial pressure ( hypercapnia ) and, secondarily, an excessively low oxygen partial pressure ( hypoxia ), both in the alveoli and in the blood. The increased CO₂ partial pressure in the blood disrupts the acid-base balance : there is an overacidification caused by carbon dioxide , the respiratory acidosis . Both the acidosis and the high CO₂ partial pressure itself represent a respiratory stimulus. In the case of chronic ventilation disorders (classic example: COPD ), this stimulus decreases over time and the respiratory drive increasingly depends on the oxygen partial pressure ; those affected now tolerate a higher CO₂ partial pressure, which protects them from respiratory arrest due to overloading the breathing pump.
A complete cessation of breathing - also voluntarily - is called apnea . Deep breathing is called hyperpnea , shallow hypopnea . An increased respiratory rate is called tachypnea , a decreased one is called bradypnea . Hyperventilation refers to ventilation that exceeds the need, hypoventilation to ventilation that is not needs-based. Adequately increased ventilation means increased breathing .
obstruction
- Obstruction of the upper respiratory tract → difficult inspiration
- Swelling due to inflammation (e.g. croup , epiglottitis , allergy )
- Foreign body aspiration
- tumor
- obstructive sleep apnea syndrome
- Vocal cord dysfunction
- Strangle
- Narrowing of the lower airways → difficult expiration
- bronchial asthma
- COPD (severe chronic bronchitis, possibly combined with emphysema as a respiratory disorder)
Restriction
- Pulmonary fibrosis (consequence of various interstitial lung diseases )
- Pneumothorax , pleural effusion , pleural rind
- Deformities of the chest (z. B. ankylosing spondylitis , kyphoscoliosis ), severe obesity , last pregnancy sdrittel
Neuromuscular Diseases
- Diaphragmatic paralysis due to a lesion of the phrenic nerve , paraplegia from C4 or higher (fatal if not immediately ventilated)
- Myasthenia gravis , Guillain-Barré syndrome , ALS (cause of death if treatment is discontinued in the end-stage)
- Substances that act on the neuromuscular endplate (e.g. muscle relaxants , the snake venom bungarotoxin )
Respiratory drive disorders
The function of the respiratory center in the brain stem can be disturbed in different ways; In the worst case, central respiratory paralysis occurs . In addition to hypopnea and apnea, pathological forms of breathing such as Biot breathing , Cheyne-Stokes breathing or gasping can result.
- Poisons, drugs, medications (e.g. opioids )
- Pressure (lower entrapment as a result of increased intracranial pressure )
- Ischemia from cardiac arrest , hanging, or strangling
Disturbances in the acid-base balance are compensated if possible by increased or decreased ventilation, the resulting hyperventilation or hypoventilation is also the result of a changed respiratory drive, which in this case represents an adequate response. The Kussmaul breathing is typical of diabetic ketoacidosis .
Further
therapy
If a more causal treatment is not possible, ventilatory disorders are treated by ventilation through a mask or tube , and a donation of breath serves as an immediate life-saving measure . Oxygen administration is not the first choice; In the case of COPD, it can be helpful in that it spares the chronically overloaded breathing pump.
Endobronchial intubation can lead to unilateral ventilation as a so-called incorrect intubation (as part of emergency care or induction of anesthesia ). The diagnosis can be made by auscultation if the absence of ventilation sounds is found in the non-ventilated lungs. The risk of such incorrect intubations is particularly present in children (due to the short windpipe ).
See also
Individual evidence
- ↑ Joachim Frey : Physiology of breathing. In: Ludwig Heilmeyer (ed.): Textbook of internal medicine. Springer-Verlag, Berlin / Göttingen / Heidelberg 1955; 2nd edition, ibid. 1961, pp. 603-605.
- ↑ Thomas Pasch, S. Krayer, HR Brunner: Definition and parameters of acute respiratory insufficiency: ventilation, gas exchange, respiratory mechanics. In: J. Kilian, H. Benzer, FW Ahnefeld (ed.): Basic principles of ventilation. Springer, Berlin a. a. 1991, ISBN 3-540-53078-9 , 2nd, unchanged edition, ibid 1994, ISBN 3-540-57904-4 , pp. 93-108; here: pp. 100-104.
- ↑ Peter Lotz: Anatomy and Physiology of the Respiratory Tract. Pp. 20-25.
- ↑ Peter Lotz: Anatomy and Physiology of the Respiratory Tract. In: J. Kilian, H. Benzer, FW Ahnefeld (ed.): Basic principles of ventilation. Springer, Berlin a. a. 1991, ISBN 3-540-53078-9 , 2nd, unchanged edition, ibid 1994, ISBN 3-540-57904-4 , pp. 3–45; here: pp. 19–21.
- ↑ Thomas Pasch , S. Krayer, HR Brunner: Definition and parameters of acute respiratory insufficiency: ventilation, gas exchange, respiratory mechanics. In: J. Kilian, H. Benzer, FW Ahnefeld (ed.): Basic principles of ventilation. Springer, Berlin a. a. 1991, ISBN 3-540-53078-9 , 2nd, unchanged edition, ibid 1994, ISBN 3-540-57904-4 , pp. 93-108; here: pp. 95-101.
- ^ Fiorenzo Conti: Fisiologia Medica. Vol. 2, Edi-Ermes, Milan 2005, ISBN 88-7051-282-7 .
- ↑ Peter Scheib: Anesthesia, intensive medicine, intensive care . Elsevier, Urban & Fischer, 2004, ISBN 978-3-437-25717-9 ( p. 477 ).