Diseases of the respiratory organsThis article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.
In the nose, the air breathed is: – purified (filtering effect of the nasal hairs, particle deposition on the nasal mucus, pharyngeal cilia movement of the epithelium) – warmed (almost to body temperature) – humidified (almost complete saturation with water vapor) Disturbed nasal breathing can therefore cause irritation and dehydration of the bronchial mucosa. This must be taken into account during artificial ventilation (tracheal catheter, tracheal cannula). Impaired nasal breathing can therefore irritation. Cause desiccation of the bronchial mucosa. This must be taken into account during artificial ventilation (tracheal catheter, tracheal cannula).
Self-cleaning of the tracheobronchial system s
occurs due to the
mucous protective film of the trachea and bronchi in conjunction with the pharyngeal Cilia movement of the epithelium (transport velocity 10-15 cm/h).
Components of cigarette smoke inhibit ciliary activity!
Cough and Sneezing are additional reflex triggered purification mechanisms.
Attenuation or elimination of the cough reflex can be life threatening, z. B. Aspiration during anesthesia or coma, or inadequate expectoration in advanced obstructive pulmonary disease.
functions of the lungs
Ventilation includes the Inhalation with ventilation of the alveolar space and the Exhalation. Inhalation takes place actively by contraction of the respiratory muscles, exhalation predominantly passively by elastic restoring forces of the lungs and the rib cage. When exhalation becomes more difficult, the expiratory muscles (abdominal press) become more active. When inspiration is difficult or increased, the scalenus, sternocleidomastoid, and, when the arms are supported, the Mm. pectoralis minor et major as respiratory accessory muscles. The volume of a normal breath is about 500 ml. Of this, the airways (dead space) 150 ml, the compartment of the alveoli 350 ml. At 15 breaths per minute, an alveolar ventilation of about 5 l/min results. The oxygen intake is 300 ml, the CO2 output is 250 ml/min. Under stress, oxygen uptake can increase to 4-5 l/min. The respiratory minute volume to the 15-fold.
Through Diffusion respiratory gases are exchanged between alveolar air and pulmonary capillary blood. Alveolar space. To the capillary blood (◘ Fig. 2.1 ).
Gas exchange occurs through the respiratory membrane, whose Diffusion capacity is dependent on:
Membrane thickness (layers: Fluid film in alveoli, alveolar epithelium, interstitium, basement membrane of capillaries, capillary endothelium)
Membrane surface (is enlarged by alveolar expansion during physical exertion)
Diffusion coefficients (depending on the molecular weight of the gas and its solubility in the membrane; twenty times greater for CO2 than for O2).
Under resting conditions, blood oxygen saturation is complete after less than one-third of the passage time through pulmonary capillaries. Accelerated blood circulation during stress therefore does not affect O2 saturation. Only at the coincidence of load and reduced atmospheric oxygen prere (high altitude air) the arterial O2 saturation decreases, because the reduced O2 prere gradient decreases the diffusion speed. CO2 exchange between alveolar air and capillary blood is very rapid because of the high diffusion rate of this gas and is never impeded by the respiratory membrane.
The pulmonary blood flow has the same size as the cardiac output and is about 5 l/min. Since alveolar ventilation is also 5 l/min, global Ventilation-perfusion ratio of approximately 1. A small portion of cardiac output (1-2%) passes through the lungs bypassing the alveoli. This venous admixture to the arterialized pulmonary venous blood causes the pO2 of the arterial blood (paO2) to drop to 95 mm Hg.
Ventilation and perfusion reach different levels in different parts of the lung (◘ Fig. 2.2 ). Perfusion per unit volume decreases continuously from the base of the lungs to the apex in an upright posture. The same applies to ventilation, but the gradient is not as steep. Consequently, the Ventilation-perfusion ratio from the base to the tip. Relatively little O2 is removed from the alveoli of the tip region and little CO2 is supplied because of the low capillary flow rate. The opposite is true in the highly perfused alveoli of the base of the lung. Despite the uneven distribution of ventilation. perfusion, global oxygen saturation of the pulmonary blood is normally ensured. But disturbances in arterial O2 saturation occur when ventilation-perfusion ratio changes significantly in lung disease. In extreme cases, a ventilated alveolus is not perfused at all (vascular occlusion) or. A perfused alveolus is not ventilated (atelectasis). Compensatory reflex mechanisms ensure that blood flow to poorly ventilated alveoli is throttled, or. that the ventilation of poorly perfused alveoli decreases.
Regulation of respiration
Neuron groups bilaterally in the medulla oblongata and pons:
Dorsal respiratory group: Generates the basic rhythm of respiration by spontaneous inspiratory impulses without stimulated expiration. Receives and responds to afferent signals from peripheral chemoreceptors and various receptors in the lungs. Stimulated by superior centers during stress. Voluntary respiration proceeds via somatic nerves from the cerebral cortex to the respiratory muscles.
Pneumotactic center: Localized in the upper pons. Controls the duration of the inspiratory signal and thus the frequency and depth of breathing. The normal inspiratory signal extends over 2 seconds, so that the diaphragm can lower like a lifting platform and cause a calm inflow of respiratory air.
Ventral respiratory group: Located close to the front and sides of the dorsal respiratory group and inactive during normal resting respiration. Receives impulses from the dorsal respiratory group during increased respiration and then stimulates expiration and, with some neurons, also increases inspiration.
Regulates alveolar ventilation so that gas exchange meets the metabolic needs of the organism and paO2 and paCO2 remain approximately normal, even during exercise. Stimulation of the respiratory center causes increase in respiratory rate and respiratory depth.
Regulation of the respiratory center by stretch receptors of the lungs
The muscle layer in the wall of bronchi and bronchioles is equipped with stretch receptors that shorten inspiration when overstretched. The depth of breathing decreases and the respiratory rate increases. This process, known as the Hering-Breuer reflex, is not involved in the normal control of ventilation in humans, but merely protects against extreme lung distension. It is caused by CO2 (measurand paCO2). hydrogen ions (measured by pH). The respiratory center is stimulated via an adjacent chemosensitive region that responds to hydrogen ions. CO2 reacts with H2O in CSF and brain interstitial fluid to form H2CO3, which dissociates into H + and HCO3 -. This happens most effectively in the cerebrospinal fluid, which contains hardly any acid buffers. The respiratory center is much less sensitive to H ions in the blood because the blood-brain and blood-liquor barriers, which CO2 can pass rapidly, are largely impermeable to H +.
Excitation of the respiratory center via the chemoreceptors in the carotid sinus and aortic arch, which is mainly caused by O2 deficiency in the arterial blood (paO2 2 and H + at. When blood prere drops, they increase heart rate and vasomotor tone via sympathetic nervous system.
The most important control variable is paCO2. A pCO2 increase from 40 to 63 mmHg in the alveoli causes a 10-fold increase in ventilation. On the one hand, the paCO2 increase in the blood has a direct respiratory stimulating effect, on the other hand indirectly via respiratory acidosis.
A drop in pH due to increase in fixed acids causes less increase in ventilation as paCO2 decreases due to compensatory hyperventilation. In the pH range 7.3-7.5, the effect on ventilation is 10-fold less than at paCO2 preres between 35 and 60 mmHg.
O2 regulation of respiration via chemoreceptors is usually insignificant because a small decrease in alveolar pO2 does not significantly affect blood oxygen saturation and does not lead to stimulation of chemoreceptors. In addition, hyperventilation induced by O2 deficiency is slowed by the decrease in paCO2 and increase in pH associated with the increase in ventilation. In obstructed ventilation (obstructive emphysema), however, the braking of O2 deficiency stimulation is absent because the respiratory center adapts to elevated CO2 preres. In these situations, O2 deficiency is the major stimulant of respiratory increase, as evidenced by the fact that oxygen ventilation attenuates respiration and increases blood CO2 concentration. Risk of respiratory acidosis and coma.
Even at low atmospheric O2 preres in high altitude climates, respiration is stimulated by chemoreceptors. After 2- to 3-day acclimatization, the respiratory center loses 80% of its sensitivity to changes in paCO2. Consequently, exertion-induced hyperventilation (z. B. During mountaineering) is no longer slowed by a drop in paCO2.
Buffer function of respiration
Breathing counteracts pH shifts in arterial blood by changes in paCO2. Metabolic acidosis can be partially compensated by hyperventilation (exhalation of CO2), and metabolic alkalosis can be partially compensated by hypoventilation (retention of CO2). On the other hand, respiratory acidosis can cause. Alkalosis can be partially compensated metabolically. For a detailed discussion, see the section on acid-base balance (▶ 10.1007/978-3-642-33108-4_3). In healthy athletes, O2 consumption can. CO2 production increases up to 20-fold. During physical exertion, alveolar ventilation immediately adapts to the metabolic increase. Apparently, collateral impulses go from the CNS to the respiratory center with the impulses to skeletal muscles. This respiratory response can be increased by training. Fine regulation of respiration under stress is performed by blood gases. Definition of volumes. Capacities (◘ Tab. 2.1 ):
Tidal Volume (VT): Volume inhaled or exhaled during each normal breath. is exhaled (ca. 500 ml).
Inspiratory Reserve Volume (IRV): Extra volume that can be inhaled beyond the normal respiratory volume (ca. 3000 ml).
Expiratory Reserve Volume (ERV): Extra volume that can still be maximally exhaled at the end of a normal exhalation (approx. 1100 ml).
Residual volume (RV): Volume remaining in the lungs after extreme expiration (approx. 1200 ml).
Functional residual capacity (FRC): Residual volume plus expiratory reserve volume (approx. 2300 ml). FRC is the lung volume at the end of a normal exhalation.
Vital Capacity (VC): The sum of respiratory volume, expiratory reserve volume and inspiratory reserve volume. Depending on age, height, and sex (approx. 4600 ml).
Inspiratory Vital Capacity (IVC): Volume that can be maximally inhaled after slow maximal expiration.
Expiratory vital capacity (EVC): Volume that can be maximally exhaled after maximum inspiration (approx. 5% less than the inspiratory vital capacity).
Forced expiratory vital capacity (FVC): Volume that can be exhaled at the highest possible rate after maximum inhalation. Important for detecting airway obstruction.
Total lung capacity (TC): The maximum lung volume (ca. 5800 ml), reached at deepest inspiration (respiratory volume + inspiratory + expiratory reserve volume + residual volume).
The classic spirometer consists of a drum that is immersed upside down in a water bath and held in place by a counterweight. There is air in the drum, and a tube connects the gas chamber to the mouth. The atemsynchronous raising and lowering of the drum is recorded against time by a pointer on a rotating drum. In ◘ Fig. 2.3 is the diagram of respiratory excursions schematically shown.
Foreign gas dilution method
Used to determine functional residual capacity (FRS), which cannot be detected by simple spirometry. A spirometer of known volume is filled with air to which helium is added at a known concentration. At the end of a normal expiration, the patient is connected to this spirometer and initially continues to exhale forcefully. During this process, the expiratory reserve volume is recorded. This is followed by minutes of resting breathing, during which the helium is diluted in the volume of the FRC. Concentration balance is achieved when the helium concentration in the spirometer does not drop any further. From the degree of helium dilution in the spirometer. spirometer volume, the FRC can be calculated. The method is rarely used today.
Dynamic ventilation variables
Measurements are made with spirographs or integrating pneumotachographs. The latter measure the flow velocity of the air (l/s) during the breathing phases and display it graphically. The
Pneumotachograph consists of an open tube in which there are numerous parallel fins to ensure laminar airflow. Prere receptors are located at the beginning and end of the tube to measure the prere gradient in the tube during the flow. For a given tube diameter, the prere gradients result in the flow velocities. An integrator is used to determine the volume from the flow.
Respiratory rate: Resting value 12-18/min, depending on the depth of breathing.
Respiratory minute volume (AMV): The resting value is approx. 6-8 l/min. Target value calculation: basal metabolic rate × 4.73.
Respiratory threshold (AGW): Maximum Voluntary Ventilation (MVV). Practical implementation: hyperventilation for 10-15 s, conversion to l/min. Normal values: 80-150 l/min.
Forced expiratory one-second volume (FEV 1 ): The volume expired after maximum inspiration during forced expiration in the first second (◘ Abb. 2.3 ). Absolute values depend on body size and age. FEV1 is expressed as a percentage of expiratory forced vital capacity: FEV1/FVC %. It is inversely proportional to expiratory flow resistance.
Flow-volume curve: The pneumotachograph is used to measure the flow velocities (l/s) while measuring the flow volume during the respiratory phases, especially the forced maximal expiration. The flow rate (l/s) is plotted on the ordinate and the respiratory volume on the abscissa. The flow velocities at 25, 50, and 75% of the forced expiratory vital capacity (FVC) can then be read in addition to the maximum (◘ Fig. 2.4 ).
Static compliance is defined as the change in volume of the lungs per unit change in prere (ml/cmH2O resp. l/kPa) and thus a
measure of the distensibility of the lungs. For lung expansion, the intrapleural prere authoritative. This is the negative prere (suction), which is necessary to prevent collapse of the lungs. With breath held, there is a difference between the retraction force of the lungs. The negative intrapleural prere acting on the lung surface a balance. If the negative intrapleural prere is increased during inspiration, the volume increase of the lung per centimeter of water column (or kPa) (negative) prere increase is proportional to the distensibility of the lung. Methodically, the change in intrapleural prere during inspiration is measured by means of a balloon probe in the lower esophagus instead of in the pleural space (esophageal prere method).
Compliance is the quotient of inhaled volume and the prere difference between the beginning and end of inspiration. Normal values: men 0.21 l/cmH2O (kPa) and women: 0.17 l/cmH2O (kPa).
Compliance is inversely proportional to the elastic restoring forces of the lungs. These are composed of one third of the elastic force of the lung tie, and two thirds of the elastic force emanating from the surface tension of the fluid film in the alveoli. Surface tension reduced. Collapse of the alveoli prevents.
A pathological decrease in compliance leads to an increase in work of breathing, since more (negative) prere must be applied to fill the stiff lung with the same volume. It is often found in restrictive lung diseases, but can also occur in acute changes such as edema, pneumonia and ARDS.
Compliance is decreased in pulmonary fibrosis and premature infants with surfactant deficiency, increased in emphysema.
Bronchial flow resistance (Resistance )
Air movement in the airways is generated by a prere gradient between the external air and the alveolar space. At the end of normal expiration, the alveolar prere is equal to the atmospheric prere of the external air because no air is flowing. With the onset of inspiration, the alveolar prere becomes negative due to thoracic expansion on the part of the respiratory muscles. There is a prere gradient from the outside to the inside, which disappears again at the end of inspiration. With the onset of expiration, the alveolar prere rises above the atmospheric prere of the outside air due to compression of the alveoli; a prere gradient from the inside to the outside is created. The respiratory flow rate (V) in l/s is proportional to the prere gradient (ΔP) between the external air and the alveolar space and inversely proportional to the endobronchial flow resistance (R):
The Resistance is defined as the prere difference between alveolar air and external air required to allow 1 liter of air/second to flow in the bronchial system. It can be determined by different methods.
During spontaneous breathing on the pneumotachograph, the airway is closed at the mouth 2-5×/s for less than 0.1 s. In the occlusion phase, the oral prere equals the alveolar prere. The respiratory flow intensity is measured during the opening phase. Somewhat more complex is oscillometry, in which a rapid small alternating flow is introduced into the air stream at the mouthpiece. The resistance of the airways is determined from the ratio of alternating prere to alternating flow.
The patient is enclosed in the whole-body plethysmograph, an airtight chamber (◘ Fig. 2.5 ). While breathing in it, the changes in ventricular prere and, by means of a pneumotachograph, the respiratory flow rate are measured and both are recorded on an XY recorder. When the chest expands during inspiration, a negative prere (suction) is created in the alveoli and a corresponding positive prere in the chamber, both of which disappear by the end of inspiration because the displaced chamber air has then flowed into the lungs. During expiration, conversely, an overprere is created in the alveoli. A negative prere is created in the chamber. The greater the flow resistance, the more the preres in the chamber give way, respectively. in the alveoli differs from the initial position. The prere flow diagram recorded by the recorder during a breathing cycle shows a loop shape (resistance loop) with inspiration in the upper right quadrant and expiration in the lower left quadrant (◘ Fig. 2.6a ). The steeper the axis of the loop, the smaller the resistance. To determine the absolute value of the resistance, it must be known which alveolar prere change corresponds to a defined change in the ventricular prere. To determine this relation, the chamber prere is registered against the mouth prere after closing the breathing tube, because then mouth prere and alveolar prere coincide (◘ Fig. 2.6b ). The patient is panting during these measurements (respiratory excursions without airflow). In adults, resistance values above 3.0 cm H2O (= 0.3 kPa/l/s) are considered pathological (◘ Fig. 2.7 ). The thoracic gas volume can also be calculated from the prere changes during hechel breathing, because the volume changes can be derived from the prere changes in the chamber.
Evidence of ventilatory distribution disorders
In ventilatory distribution disorders, the lungs are not ventilated uniformly. There is a coexistence of hyper-. Hypoventilated alveoli. One of the detection methods is the expiratory CO2 prere curve (◘ Abb. 2.8 ).
Diffusion capacity, also known as transfer factor, is defined as the volume of gas that can be transferred from the alveoli to the blood at a prere gradient of 1 mmHg per minute. passes into the erythrocytes. It must pass through the alveolocapillary membrane (tie barrier) and the blood with its liquid and solid components (blood barrier). The normal value for O2 diffusion capacity during quiet respiration is 21 ml O2/min/torr. This value is reduced in the case of diffusion disturbances due to thickening of the respiratory membrane (pulmonary fibrosis, congested lung) and in the case of reduction of the total diffusion area (emphysema, lung resections). Practice too costly. Susceptibility to disturbances. Therefore, one determines the diffusion capacity for CO, whose partial prere in pulmonary capillary blood can be set equal to zero because of the strong affinity of CO for hemoglobin and whose alveolar partial prere is consequently equal to the prere gradient at the respiratory membrane.
The inhalation draw technique is currently the standard procedure. It is based on CO diffusion during an apnea time of 10 seconds. For this, a CO-containing mixed gas is deeply inspired (to total capacity) after maximal expiration. After apnea, expiratory air contains less CO than inspiratory air. The difference is a measure of CO transfer. The calculation requires knowledge of the alveolar volume at apnea time. The inspiratory dilution of carbon monoxide. For this purpose, a small concentration of helium is added to the mixed gas, the transfer of which is negligible.
In this equilibrium method, the patient breathes an air mixture containing 0.1% carbon monoxide for a few minutes. CO concentration in the breath is determined using a gas chromatograph, z. B. CO-Uras.
respiratory gases and blood pH
Blood gas analysis and blood pH determination provide the most important data for assessing global lung function. However, your results will also depend on the condition of your cardiovascular system (z. B. Shunt vitiation) and from acid-base balance (acidosis, alkalosis).
Modern automated, computer-controlled micro-pH/blood gas analyzers measure blood gases and pH with special electrodes after entering a blood sample from the arterialized earlobe. They provide the following parameters: paO2 (arterial O2 partial prere), paCO2 (arterial CO2 partial prere), pH, plasma bicarbonate, base excess, O2 saturation and O2 content of the blood. Normal values for men. Women 75-100 mmHg. When lying down the means-. Limits about 5 mmHg lower than in standing position.
SaO2 (O2 saturation )
Percentage saturation of hemoglobin in arterial blood with oxygen. Normal values for both sexes 95-98 %. In the steep part of the dissociation curve, a relatively small increase in paO2 leads to a large increase in O2 saturation, an effect that explains the benefit of O2 inhalation in hypoxic patients.
The amount of O2 bound to hemoglobin at full oxygen saturation in vol.% (ml O2/100 ml blood). Calculated from the hemoglobin content: 1 g Hb binds 1.34 ml O2. With a Hb content of 16 g/100 ml blood, the O2 capacity is 21.4 Vol%. Physically dissolved oxygen reaches only 0.29% by volume at a respiratory pO2 of 95 mmHg.
Decreased paO2 partial prere in blood. Causes: O2 deficiency in respiratory air (altitude climate), ventilatory disorders, ventilation-perfusion ratio disorders, diffusion disorders, right-to-left shunt.
Decreased amount of O2 per unit volume of blood, compared to the O2 content of the blood of a normal person under the same atmospheric conditions.
Causes: As in hypoxia, also in anemia and CO intoxication. May be partially compensated by secondary (compensatory) polycythemia when pO2 is decreased.
Measurement of paCO2 and pH with calculation of base
paCO2: Normal values for men 35-45 mmHg, for women 32-42 mmHg.
Hypocapnia: Decreased paCO2, always due to hyperventilation.
Hypercapnia : Increased paCO2 partial prere, always due to alveolar hypoventilation.
pH normal values: Men: 7.34-7.44; women 7.35-7.45. The range of variation is smaller in the individual than in the collective.
Plasma bicarbonate : Current concentration of bicarbonate in plasma.
Normal values: 22-26 for men, 20-24 mmol/l for women.
In primary metabolic alkalosis (pH>7.45, paCO2 increased by compensatory hypoventilation)
Compensatory in respiratory acidosis (pH aCO2 increased by primary hypoventilation)
in metabolic acidosis (pH aCO2 lowered by compensatory hyperventilation)
Compensatory in respiratory alkalosis (pH>7.45, paCO2 lowered by primary hyperventilation)
Standard bicarbonate: Concentration of bicarbonate in blood plasma equilibrated with a gas of 40 mmHg pCO2 and 100 mmHg pO2 at 37 °C. Normal values: For males. Women 22-26 mmol/l.
Further explanations about the acid-base balance in ▶ 10.1007/978-3-642-33108-4_3.
Ergometry : blood gas analysis during dosed exercise
Measure paO2, paCO2, and pH during graded exercise on a cycle ergometer or treadmill.
During aerobic dynamic work up to about 50% of maximal oxygen uptake capacity (VO2max), paO2 increases slightly because additional alveoli are ventilated (increase in ventilation-perfusion quotient). The paCO2 and pH remain constant because the increased CO2 is exhaled.
With further increasing load, anaerobic energy is also required in addition to aerobic energy, and lactate is produced during the extraction of this energy. While paO2 still increases somewhat, lactate decreases bicarbonate levels. In order to slow down the pH drop, more CO2 is exhaled by increasing ventilation, which leads to a drop in paCO2. When the pH has dropped to about 7.24, inhibition of muscle contraction occurs due to acidosis, and the absolute limit of exertion is reached.
At rest, paO2 is decreased and paCO2 is also decreased by compensatory hyperventilation. Under stress, paO2 continues to decrease, while paCO2 increases to normal values due to increased attack of CO2.
At rest, decreased paO2, paCO2 normal or decreased. Under exercise, increase in paO2 due to improvement in ventilation-perfusion quotient; decrease in paCO2 due to lactic acidosis. At rest, lowered paO2. Increased paCO2 (because CO2 is insufficiently exhaled). paO2 may normalize under exercise, paCO2 remains elevated.
Measurement of O2 uptake (VO2) and CO2 output (VCO2) under pH control during increasing exercise on a cycle ergometer or treadmill. For this purpose, the respiratory minute volume is determined with a pneumotachograph and the gas concentrations in the inhaled and exhaled air are determined with sensors.
Anaerobic threshold: VO2 and VCO2 increase in a 1:1 ratio during the aerobic phase. Respiratory quotient (RQ) is 1. The anaerobic threshold is reached as soon as VCO2 starts to increase more than VO2 due to lactate formation. RQ (VCO2/VO2) becomes>1.
Continuous output limit (working capacity): It is reached when lactic acidosis is no longer compensated ventilatory and pH begins to decrease. At this point, VCO2 decreases slightly while respiratory minute volume increases exponentially.
Maximum oxygen uptake capacity: Defined as the O2 uptake at a pH of 7.25 or. Exhaustion. In lung diseases. Heart failure, maximum O2 uptake is markedly reduced. In lung disease and heart failure, maximum O2 uptake is significantly reduced. Untrained young men reach 3.600 ml/min, trained athletes 4.000 ml/min, marathon runner 5.100 ml/min. The maximum oxygen uptake capacity increases with the number of mitochondria in the skeletal muscles, because that is where the oxidation processes take place.
ARDS (adult/acute respiratory distress syndrome)
Unpleasant sensation of inadequate effort in breathing. Described by the patient as air hunger, shortness of breath, breathlessness, breath pinching, labored breathing, shortness of breath, and in extreme cases, a feeling of suffocation.
Sensation dyspnea can be caused by at least 3 mechanisms:
Increased work of breathing: Due to increased effort for adequate breathing in obstructive and restrictive ventilatory disorders, especially pulmonary congestion (reduced compliance due to blood overfilling resp. Edema formation in the lungs). Mediated by afferent, via the N. vagus-led impulses from joint, tendon and muscle receptors of the chest wall. Shortness of breath during and after exhaustive physical exertion is also felt, but as a normal phenomenon without alarming.
Abnormal constellation of blood gases: Stimulation of the respiratory center by arterial hypoxia (altitude climate, diffusion disorders), hypercapnia (hypoventilation in respiratory muscle paresis and pulmonary afflictions) and acidosis (diabetic coma).
Psychogenic factors: Emotionally induced stimulation of the respiratory center with ventilation exceeding metabolic needs, which can lead to hyperventilation tetany. mostly patients with anxiety neurosis.
The symptom dyspnea can be further differentiated according to the following criteria:
Quality: Asthmatics report wheezing and expiratory, but also inspiratory dyspnea. Suffocation sensation in pulmonary edema, massive pleural effusions, and respiratory muscle paralysis.
Time trend: The following categories must be distinguished:
sudden and dramatic (in minutes): Pneumothorax, large pulmonary embolism, acute pulmonary edema, aspiration
Acute (in hours): pneumonia, acute pulmonary infiltration (allergic alveolitis), asthma, left ventricular failure
subacute (over days): Pleural effusion, bronchial carcinoma, subacute pulmonary infiltration (z. B. Sarcoidosis)
Chronic (lasting months or years): chronic airway obstruction, diffuse pulmonary fibrosis, non-pulmonary causes (anemia, hyperthyroidism)
intermittent: Bronchial asthma, left ventricular failure, recurrent pulmonary emboli
Differentiation between pulmonary and cardiac dyspnea according to physical examination findings, chest x-ray, and spirometry. Cardiac causes are indicated by ECG (acute infarction), echocardiography (left heart failure) and an increase in BNP or. NT-ProBNP to be recorded in serum.
Causal according to underlying disease. Symptomatic: nasal tube oxygenation, for pulmonary congestion i.v. Loop diuretics.
Increased total ventilation in relation to energy metabolism.
Primary hyperventilation: Increased ventilation during psychogenic stimulation of the respiratory center (anxiety, pain, excitation). Leads to hypocapnia. Respiratory alkalosis.
In the case of hypoxia due to diffusion disorders. The respiratory center is stimulated via peripheral chemoreceptors.
In diabetic acidosis to slow pH drop.
Increased ventilation during physical work is not hyperventilation.
Total ventilation decreased in relation to energy metabolism.
Primary hypoventilation: In respiratory insufficiency with elevated paCO2 and respiratory acidosis.
Compensatory hypoventilation: For CO2 retention in metabolic alkalosis (pH rise inhibits the respiratory center).
Alternating periods of hyperpnea (with increases and decreases in depth of breath at normal respiratory rate) and apnea (◘ Abb. 2.9a ).
Delayed blood transport from the lungs to the respiratory center in the brainstem. As a result, breathing continues even though the pCO2 in the pulmonary venous blood has already decreased to a greater extent. When arterial blood with low paCO2 reaches the respiratory center, apnea occurs. Causes of flow delay: heart failure with enlargement of the left ventricle, vitiation, circulatory shock. During apneic phases, paO2 decreases while paCO2 increases. The subsequent increase in ventilation comes from the paCO2 effect on the respiratory center. Causing the paO2 effect on the chemoreceptors. O2 ventilation can eliminate the latter component. Also direct lesions of the respiratory center (intracranial prere, etc.).) can lead to Cheyne-Stokes respiration. On several breaths of equal distance. Equal amplitude followed by apneic pause. Duration of cycles is variable (◘ Fig. 2.9b ).
Direct damage to the respiratory center due to trauma, compression, ischemia, etc.
Blue coloration of skin and visible mucous membranes due to increased capillary blood content of reduced hemoglobin.
Reduced hemoglobin (Hb red.) has an intense blue intrinsic color, which is much stronger than the red color of oxyhemoglobin. The decisive factor is not the relative but the absolute concentration of reduced hemoglobin:
mild cyanosis: Hb red. 3-4 g/100 ml of blood
Severe cyanosis: Hb red. 5 g/100 ml blood and more
In polycythemia, a relatively small decrease in blood O2 saturation is sufficient to cause cyanosis; in anemia, O2 undersaturation must be greater than in normal blood. Rarely, cyanosis occurs due to methemoglobin formation. According to the mechanism of origin, 2 forms of cyanosis are distinguished:
Central cyanosis: Results from a decrease in arterial O2 saturation, z. B. respiratory insufficiency. It affects skin (lips, cheeks, nail bed) and mucous membranes (tongue). In cardiac and pulmonary right-to-left shunt, it increases under physical stress.
Peripheral cyanosis: Results from increased O2 depletion of capillary blood of the skin in the presence of decreased arterial blood flow and slow blood flow.
Causes: Vasoconstriction due to cold exposure, arterial spasm (Raynaud's disease), arterial embolism (skin pallor with cyanotic component), cardiovascular insufficiency with compensatory cutaneous vasoconstriction, and venous congestion.
Obstruction means narrowing of the airway.
Distinguished between 2 forms:
Endobronchial obstruction: Lumen narrowing due to mucosal swelling, secretions, and spasm of bronchial muscles (favored by β-receptor blockers). Occurs in
Asthma and chronic obstructive bronchitis Before.
Lumen narrowing As a result of reduction of the elastic traction forces of the lung tie that keep the bronchi open. Occurrence: in Emphysema.
Abnormal Bronchial collapse by chronic bronchitis.
Compression from outside Due to malignancies.
Obstruction impairs respiratory mechanics, ventilation, and pulmonary circulation. It can thereby lead to severe dysfunction of the lungs and right heart.
Changes in ventilation and respiratory mechanics
The obstruction-related increase in bronchial flow resistance increases the work of breathing. Since expiration is passive (due to the retraction force of the lung) at rest, even in severe obstruction, the lung must be pre-expanded inspiratory to increase the retraction force. In severe obstruction, expiration is so slowed that it is interrupted by inspiration before reaching normal resting volume. Hyperinflation of the lungs occurs with an increase in functional reserve capacity, which favors emphysema formation in a weakened lung structure. With secondary loss of lung elasticity, residual volume decreases. Consequently, total capacity too. While inspiration during obstruction is facilitated by the retractive force of the lung tie acting radially on the bronchi, forced expiration, i.e., physical exertion, results in a significant increase in flow resistance due to compression of the small bronchi. Compensatory use of expiratory respiratory muscles causes end-expiratory intrapleural preres to become positive during workload, whereas in healthy individuals they remain below atmospheric prere. Respiratory rate increases at the expense of respiratory depth. The result is exertional dyspnea, in severe cases resting dyspnea.
Changes in distribution
Airway obstruction results in regional decreased ventilation of alveoli with decrease in ventilation-perfusion quotient. First the paO2 drops, in severe cases with global alveolar hypoventilation there is also an increase in paCO2 and respiratory acidosis.
Increase in pulmonary flow resistance
The distributional disturbance associated with the obstruction causes reflex vasoconstriction in the poorly ventilated lung districts, which can result in pulmonary hypertension with right-sided insufficiency. Predominantly expiratory wheezing. Hum over all lung segments.
Spirometry: Decrease in forced expiratory one second volume (FEV1) and FEV1/FVC(%) ratio. In severe cases, FVC is also decreased. Decrease in maximal expiratory flow rate. Abnormal flow-volume curve. At rest, increased resistance values on whole-body plethysmography. With the interrupter or oscillation method. Increase of the residual volume (RV). Of functional residual capacity (FRC). This leads to an increase in total capacity.
Blood gas determination: Evidence of partial or global respiratory insufficiency as a consequence of obstruction (▶ below).
Restriction means decreased distensibility of the lung or chest wall.
In case of severe thoracic deformities, massive obesity, pneumothorax, pleural effusions, pulmonary congestion, pulmonary edema, atelectasis, massive pneumonia and diffuse fibrosis processes (tuberculosis, sarcoidosis, pneumoconioses, cystic fibrosis, radiation fibrosis, idiopathic pulmonary fibrosis).
Increase the work of breathing by making inspiration more difficult. Decrease in lung ventilation due to limitation of inspiration. Distribution disturbances due to inhomogeneity of ventilation, in severe cases respiratory insufficiency.
volume measurements: Reduction in inspiratory vital capacity, residual volume, and total capacity. The absolute value of the forced expiratory one second volume (FEV1) is reduced, but the quotient FEV1/FVC% is normal, because there is no obstruction.
Compliance Determination: Decreased values, in pulmonary causes with increased, in pleural and thoracic causes of restriction with normal transpulmonary prere.
Blood gas determination: Evidence of secondary respiratory insufficiency (▶ below).
Disorders of the ventilation-perfusion ratio, d. h. Balance between ventilation. Perfusion of alveoli with impairment of gas exchange.
Ventilatory distribution disorder
Primary disorder of ventilation with decreased ventilation-perfusion quotient (obstructive and restrictive ventilation disorders of all types) or cessation of ventilation (atelectasis, pneumothorax, compression by effusions).
Circulatory distribution disorders
Primary disruption of lung perfusion from various causes (z. B. due to pulmonary embolism) and in intrapulmonary shunts.
The imbalance between ventilation and perfusion, already present in the normal lung but functionally inconsequential, is greatly exacerbated by most generalized lung diseases and occlusions of the pulmonary vessels. Both O2 uptake and CO2 excretion are impeded. The latter can be compensated by compensatory hyperventilation of normally ventilated. Perfused lung districts are compensated for. Because capillary blood O2 saturation is already near maximum in normally ventilated alveoli, it can be increased only to a limited extent by hyperventilation. Hypoxemia results, which in severe cases can only be improved by increasing the oxygen partial prere of the breathing air, i.e. by oxygen supply via nasal probe.
A distribution disorder is present when paO2 is decreased while paCO2 is normal or decreased. In milder cases, paO2 normalizes during exercise by increasing ventilation and perfusion while compensating for inhomogeneities. An abnormal expiratory CO2 prere curve also indicates distributional disturbances (◘ Fig. 2.8 ). Application of ventilation scintigraphy with 133 xenon. The perfusion scintigraphy with 99m Tc microspheres.
Respiratory disorders due to reduction of O2 diffusion capacity of the lung.
According to the determinants of O2 diffusion capacity, the following classification results:
Alveocapillary block: Lengthening of the diffusion distance between the alveolar wall and erythrocytes. Occurs in interstitial pulmonary fibrosis, interstitial pneumonia and pulmonary congestion. Less significant for hypoxia than the distributional disturbance that often exists at the same time.
Reduction of the gas exchange area: In pulmonary emphysema, alveolar cell carcinoma and as a consequence of pneumectomy.
Anemia: Reduces the O2 uptake capacity of the blood. In case of CO intoxication it is blocked.
Diffusion disorders are usually combined with distribution disorders. They concern only O2 diffusion, since CO2 diffuses very easily. Hypoxemia triggers compensatory hyperventilation.
Determination of CO transfer factor, which is decreased (▶ above). In emphysema, compliance is simultaneously increased because of loss of elasticity.
Critical hypoxemia with a paO2 aCO2. Only below a paO2 of 60 mmHg does the arterial O2 saturation drop below 90%. In any case, the main threat to the organism comes from hypoxemia.
Type I: Acute hypoxemic respiratory failure
Primarily, arterial oxygen uptake in the lungs is decreased (paO2 2 normal or increased exhaled. Only when the compensatory increase in ventilation leads to exhaustion of the respiratory muscles does hypoventilation result with an increase in paCO2. Occurs when the alveoli are flooded with fluid from the following causes:
Pulmonary edema due to congestion in the small circulation in heart failure
Pulmonary edema without prere increase in the left atrium in ARDS (Acute Respiratory Distress Syndrome), which may be due to primary lung injury from sepsis, pneumonia, gastric juice aspiration, multiple blood transfusions, and pancreatitis.
Type II: Ventilatory type
The primary is alveolar hypoventilation , which leads to the decrease in paO2 and increase in paCO2, that is, global respiratory insufficiency. The increase of paCO2 to>50 mmHg is associated with an equal increase of pCO2 in the alveolar air, which, according to the alveolar gas formula, decreases the pO2 in the alveolar air. The oxygen uptake is additionally impaired. Mechanisms of ventilatory insufficiency are:
Central respiratory stimulation disorders due to overdosed sedatives, brainstem damage, sleep apnea disorders, hypothyroidism
Weakness or paralysis of the respiratory muscles in myasthenia gravis, amyotrophic lateral sclerosis, Guillain-Barre syndrome, phrenic lesion, myopathy, hypokalemia, botulism
Exhaustion of respiratory muscles due to increased work of breathing with decreased compliance of the lungs (alveolar edema, atelectasis) or chest wall (extreme kyphoscoliosis, ◘ Abb. 2.10 ), pneumothorax, pleural effusions, diaphragmatic hypertension, and in increased bronchial flow resistance (COPD)
Respiratory insufficiency due to extensive atelectasis, usually perioperative, with hypoxemia and increased work of breathing. Mechanism of origin: decrease in residual volume under general anesthesia. As a result, collapse of the dependent parts of the lungs.
Respiratory failure in shock due to hypoperfusion of respiratory muscles requiring up to 40% of cardiac output under respiratory distress and going into O2 deficit.
Symptoms of hypoxia
Drowsiness, disorientation, confusion, agitation, aggressiveness, disturbances of intelligence as well as clinical-physical findings such as tachypnea or hypopnea, tachycardia, mild hypertension, cyanosis, peripheral vasoconstriction, less frequently bradycardia and hypotension.
Symptoms of hypercapnia
Lack of concentration, fatigue, muscle weakness, respiratory acidosis.
Treatment of the underlying disease as far as possible.
To eliminate hypoxemia of vital importance. May not be used for fear of CO2 anesthesia. Respiratory acidosis should be refrained from. Application via face mask or nasal probe. With the nasal probe, an oxygen fraction in the inspiratory breath (FiO2) of 0.24-0.35 can be achieved with an O2 flow of 1-6 l/min. Intoxication symptoms (tracheobronchitis, atelectasis, respiratory failure) begin only above a FiO2 of 0.6. The paO2 should be brought to>60 mmHg.
Noninvasive respiratory support
Partial or complete mechanical ventilation without endotracheal intubation via nasal or face mask. Indicated for hypoventilation with hypercapnia due to weakness of respiratory muscles. inspiration is induced with compressed air, expiration is spontaneous. The breaths are triggered by the patient's breathing effort or the ventilator according to the set frequency. Breathing volume can be applied volume or prere controlled. This is assisted ventilation in which spontaneous breathing is preserved. Volume-controlled is IPPV (Intermittend Positive Prere Ventilation ), prere-controlled is BIPAP (Biphasic Positive Airway Prere Ventilation ).
Invasive respiratory assistance
Machine assisted or controlled ventilation via endotracheal tube.
Access routes: Orotracheal, nasotracheal, tracheostomy (after dilatation tracheostomy)
Indications: Respiratory failure, severe respiratory insufficiency
Prere-controlled ventilator: Ventilation up to a given airway prere, then passive expiration. The respiratory volume is dependent on thoracopulmonary compliance. Depending on the airway resistance.
Volume-controlled ventilator: The breath volume and the maximum allowed peak prere are preselected. Airway prere adjusts to volume requirements within limits.
Lung transplantation is the last therapeutic option in the final stage of most non-malignant lung diseases. In 2010, 298 lung transplantations were performed in Germany, distributed among 13 centers. Transplant frequency is limited worldwide by the shortage of organ donors.
Most commonly used in the following underlying diseases:
chronic obstructive pulmonary disease (39%)
cystic fibrosis (10%)
Idiopathic pulmonary hypertension (4%)
Unilateral lung transplantation (SLTx): Only one lung is transplanted. The recipient's second lung is left in place.
Bilateral or double-lateral lung transplantation (DLTx): Both lungs are transplanted.
Heart-lung transplantation (HLTx): heart and both lungs of the donor are transplanted en bloc.
bilateral transplantation is necessary in cases of bronchiectasis, because the bronchial infection could spread to the transplant. Heart-lung transplantation is mandatory in Eisenmenger's syndrome with complex cardiac anomalies and in cases where lung and heart disease are end-stage. Cor pulmonale does not need to be replaced because the right ventricle recovers after transplantation. For the remaining lung diseases, SLTx or DLTx are acceptable. The latter achieves prolonged survival in COPD and α1-antitrypsin deficiency.
Prerequisite for transplantation is blood group compatibility between donor and recipient according to ABO criteria. HLA compatibility remains out of time-. Donor deficiency not taken into account. Patients with appropriate severity of lung disease are initially placed on a waiting list at the transplant center and are monitored there until transplantation. The waiting time is about 2 years. The age limit for transplantation is 65 years of age. Age.
Absolute contraindications: Florid infections, malignant tumor disease, addictive behavior including nicotine use during the last 6 months.
Relative contraindications: cachexia, severe obesity, mechanical ventilation (except intermittent self-ventilation), HIV infection, renal insufficiency, chronic viral hepatitis (B or C), liver cirrhosis, heart failure (for lung transplantation), symptomatic osteoporosis, neurological, neuromuscular and psychiatric diseases, systemic diseases with relevant extrapulmonary manifestations, psychosocial problems, poor compliance with previous therapy.
Compared to other organ transplants, lung transplantation requires particularly intensive immunosuppression, which must be continued for life. The following are used
Triple combination from a Calcineurin inhibitor (ciclosporin, tacrolimus), a Inhibitor of T-cell proliferation (azathioprine, mycophenolate, sirolimus) and Prednisolone.
Rejection reactions: Acute form most common during first 3 months after transplantation. Recognizable by fatigue, fever, hypoxemia and very sensitive to drop in one-second capacity (FEV1). Chronic rejection manifests as bronchiolitis-obliterans syndrome . In acute rejection, methylprednisolone (1 time 500-1.000 g/day for 3 days). Monoclonal antibodies against T lymphocytes.000 g/day for 3 days) and monoclonal antibodies against T lymphocytes. In case of chronic rejection intensification resp. conversion of immunosuppression, possibly. Retransplantation.
Infections: Mostly bacterial respiratory infections with gram-negative pathogens, pneumococcus and hemophilus. Cytomegalovirus infections are the second most common.
Malignancies: Increased risk of squamous cell carcinoma and lymphoma. Successful transplantation restores cardiopulmonary function. Thus, the quality of life is also impressively improved regardless of the previous disease. The ergospirometric exercise capacity is reduced after unilateral. Bilateral lung transplantation not significantly different. However, exercise capacity remains reduced, and less than half of the recipients take up full- or part-time employment.
Survival rates Vary relatively little among underlying diseases:
Most frequent causes of death in the first year after transplantation are technical problems during surgery, graft failure due to ischemic damage, and infections. Acute rejection and CMV infections occur fairly frequently in the first year but are rarely fatal. After the first year, most deaths are due to chronic rejection and infection.
Acute respiratory distress syndrome (ARDS )
Rapid onset of severe dyspnea with hypoxemia and diffuse pulmonary infiltrates leading to acute respiratory failure, also known as acute respiratory failure.
Direct damage to the alveolar epithelium
Due to pneumonia, aspiration of gastric contents, pulmonary contusion, near drowning, or toxin inhalation.
Indirect lung injury
Sepsis, severe injuries (multiple fractures, head trauma, burns), multiple transfusions, pancreatitis, intestinal infarction, heart-lung machine surgery. High risk with trauma plus sepsis.
Permeability increase in alveoli due to inflammatory damage of endothelial cells of alveolar capillaries and alveolar epithelial cells. Thereby accumulation of protein-rich fluid in the alveoli and interstitium. Triggered by proinflammatory cytokines (tumor necrosis factor-α, interleukins 1 and and leukotrienes. Effector cells are recruited and activated, especially neutrophils, which are sequestered in the lungs and release toxic O2 metabolites. Precipitates of aggregated proteins and detritus form in alveoli, and microthrombi form in capillaries. Atelectasis occurs due to destruction of surfactant.
Dyspnea and tachypnea begin 12-36 h after the precipitating event, rarely a few days later. The exudative phase lasts about 7 days. Increasing hypoxemia develops (paO2 2. The ratio paO2/FiO2 decreases to 2 is the O2 fraction of inspired air, which is increased by O2 breathing during intensive therapy. To achieve a paO2 of 90 mmHg, the oxygen fraction must be>0.45. X-ray of the lungs shows opacities in the lower two-thirds of the lungs as well as atelectasis.
It lasts from 7.-21. Day. Neutrophilic infiltrates change to predominantly mononuclear infiltrates. In the favorable case, new alveolar cells form, producing surfactant again and initiating resolution of the infiltrates, which may ultimately lead to full healing. On the other hand, the secretion of alveolar type III collagen signifies the transition to fibrosis.
Characterized by extensive ductal and interstitial fibrosis with remodeling of the lung architecture to emphysema-like bullous structures and corresponding decrease in compliance. Intimal proliferation in the small pulmonary vessels leads to severe pulmonary hypertension, often with a lethal outcome.
Under intensive care intensive treatment of the precipitating disease. Mechanical ventilation is usually used to relieve the respiratory muscles. Necessary to eliminate hypoxemia. To avoid overdistension of the ventilated upper lung districts, the respiratory volume should not exceed 6 ml/kg. Ventilation is alternated with positive end-expiratory prere (PEEP) in prone and supine position for better lung development. FiO2 should be as prognostic as possible
The lethality of ARDS is 41-65 %. Most patients die from the underlying disease or from final multiorgan failure. Sleep apnea is the intermittent interruption of respiratory flow at the nose. mouth for at least 10 seconds. Duration of interruption is most 20-30 s and may reach 2-3 min. If there are symptoms of the disease, it is called sleep apnea syndrome.
Affects about 4% of men and 2% of middle-aged women.
Two pathogenetically quite different forms of sleep apnea are to be distinguished:
Obstructive sleep apnea: By far the most common form, in which airway obstruction occurs in the pharyngeal region during the apnea phase with respiratory movements of the thorax.
Central sleep apnea: In central apnea, the central respiratory drive ceases.
Obstructive sleep apnea syndrome
Upper airway collapse during sleep due to reduction in electromyographic activity of upper airway muscles. The seat of obstruction is usually the pharynx. Other mechanisms: collapse of the lateral wall of the oropharynx, sinking back of the tongue against the soft palate and the posterior pharyngeal wall. Most patients are moderately to severely overweight. In them, sleep apnea is likely to be facilitated by retraction of the heavy mandible. An additional risk factor is heavy alcohol consumption. Patients with severe hypertrophy of the tonsils, with micrognathia and retrognathia are also predisposed. In many cases, computed tomography has demonstrated narrowing of the oropharyngeal lumen in patients without striking abnormalities.
During the apnea phase, pO2 in alveolar air and arterial blood decreases, while paCO2 increases. Finally, an arousal stimulus emanates from the chemoreceptors, which does not lead to full consciousness but to normalization of ventilation. Patients do not register this semi-awake state and report in the morning that they slept well. In reality, their sleep was more or less fractionated and therefore not regenerative. Up to 500 apnea episodes can occur per night.
Most important consequence of sleep apnea is intermittent O2 deficit. It can be measured by continuous measurement of arterial oxygen saturation (SaO2) using ear oximetry. In long apnea phases, the SaO2 can drop below 60%, corresponding to a paO2 2 is a measure of the severity of obstructive sleep apnea. In a larger patient collective, values between 62 and 96% have been registered. The most important variables for the drop in SaO2 are awake paO2, lung volume, and percent sleep time in apnea.
Cardiovascular reactions are vagus-induced sinus bradycardia, nocturnal hypertension, increase in diastolic ventricular filling and thus increase in afterload due to negative prere in the thorax, but above all pulmonary hypertension due to hypoxic vasoconstriction in the pulmonary circulation. In severe cases, cor pulmonale results with polyglobulia and right-sided insufficiency. Extreme vagal tone can result in asystole of up to 13 seconds. Myocardial O2 deficiency results in severe cases of tachycardic arrhythmias, including fatal ventricular fibrillation. Neuropsychiatric disorders occur due to the lack of regenerative sleep. Caused by intermittent cerebral hypoxia.
Almost all patients are snorers, but by far not all snorers have obstructive sleep apnea. The leading symptom is a pronounced daytime sleepiness in patients who do not complain of insomnia. The spouse should be asked about respiratory episodes. In milder cases, only unexplained fatigue is complained of. In addition, there is poor concentration, intelligence decline, personality changes, and behavioral disturbances. In severe cases, cyanosis results from polyglobulia, liver swelling, and edema. Attention should be paid to tonsil size and jaw abnormalities. Long-term ECG should be used to look for nocturnal arrhythmias.
Screening with nocturnal ear oximetry
In most cases, an intermittent drop in SaO2 is found. In case of large lung volume and shorter apnea phases the findings can be approximately normal.
Allows a reliable diagnosis, assessment of severity, and differentiation from central sleep apnea (◘ Fig. 2.11 ). Should be performed in every suspected case. Continuous measurements in the sleep laboratory: EEG, electrooculogram, and chin EMG; also, at the mouth and nasal openings, respiratory flow (z. B. Breathing activity by induction plethysmography. The SaO2 by ear oximetry. With a balloon probe in the esophagus, the inspiratory prere drop in the thorax can also be registered.