The gas exchange is measured by various means, including diffusing capacity for carbon monoxide, pulse oximetry and arterial blood gas samples. Diffusion capacity of carbon monoxide with the diffusion capacity of carbon monoxide (DLCO) is the ability of gases measured to diffuse through the alveolar epithelium and capillary endothelium from the alveoli in the erythrocytes. The DLCO depends not only on the area and thickness of the blood-air barrier, but also by the volume of blood in the pulmonary capillaries. The distribution of alveolar ventilation and affects the measurement. The DLCO is measured at end expiration in the expiration air; it allowed to the patient a small amount of carbon monoxide (CO) inhale, hold your breath and exhale. The measured DLCO should the alveolar volume (determined by the helium dilution technique) and is related to the hematocrit of the patient. DLCO is absolutely indicated in ml / min / mm Hg and relative percentage of the setpoint. States reduce the DLCO In primary diseases of the lung vessels as primary pulmonary hypertension and pulmonary embolism the DLCO is reduced. Diffusely distributed lung diseases such as emphysema, and pulmonary fibrosis lead to a reduction of DLCO and alveolar ventilation (VA). Even in patients with prior lung resections the DLCO is reduced because the total volume of the lungs is reduced. If the DLCO However, the VA based (n. D. Ed .: DL CO / VA = Krogh index K CO), it is normal to increase, since the remaining portions are perfused lung enhanced. Anemic patients have decreased DLCO values, but based on the Hb normal sind.Zustände, DLCO DLCO increase over the reference value can occur with heart failure in patients because of increased pulmonary venous pressure and -arterielle probably leads to the recruitment of additional small pulmonary vessels. Also in patients with “erythrocythemia” the DL CO is increased due to the increased hematocrit and viscosity increase, which pulls on the increased perfusion pressure increased vessel recruitment by itself. The DLCO is increased in patients with alveolar hemorrhage, because the beaten into the alveoli erythrocytes can also bind CO. Also asthmatics may have higher DLCO. Although this increase in suspected vascular recruitment is attributed to some data suggest that it can also arise due to wachstumsfaktorstimulierter neovascularization. Clinical Calculator: DVT probability: Guidelines for the primary medical treatment, including D-dimer Clinical Calculator: Correction of the expected value of the carbon monoxide diffusing capacity (DLCO) for anemia pulse oximetry Based on the absorption of originating from LEDs light, at a clip or tape finger or earlobe be attached to the transcutaneous oximetry O2 saturation (SpO2) is determined by capillary blood. The determined values ??are usually very accurate and correlate within a 5% difference with the measured arterial O2 saturation (SaO2). Less accurate measurements may fail, in which the signal level may be lower in patients with highly pigmented skin or nail polish and in patients with arrhythmias, hypotension or profound systemic vasoconstriction. In addition, in the pulse oximetry only oxyhemoglobin and reduced hemoglobin can be detected, but no other Hb variants (such. As carboxyhemoglobin, methemoglobin). These variants are considered oxyhemoglobin and lead to falsely high SpO2 values. Arterial blood gas analysis, arterial blood gas analyzes (ABGA) are carried out for accurate measurement of PaO2, PaCo2 and arterial pH. This is adapted to the body temperature variables allow a calculation of the HCO3-mirror (which can be determined directly in venous blood) and SaO2. A ABGA also provides accurate values ??for carboxyhemoglobin and methemoglobin levels. Usually, the A. is to dotted radial. Since an arterial puncture in rare cases, leading to thrombosis, and hypoperfusion of the distally facing tissue, Allen-test should be performed to ensure sufficient collateral circulation. These ulnar artery and radial artery be pressed simultaneously until the hand fades away visible. Subsequently, the ulnar artery is released while the radial artery remains closed. If the entire hand again rosy within 7 seconds after release of the ulnar artery, a sufficient perfusion through the ulnar artery is proved. Under sterile conditions, the 22- is introduced distal to the palpable maximum radial pulse to 25-needle a heparinized syringe and easily advanced proximally into the artery can be aspirated to pulsating blood. The syringe plunger is usually sufficient to push back the systolic blood pressure. After removal of 3-5 ml blood, the needle is quickly withdrawn and fixed pressure on the puncture site exerted to bring the bleeding rapidly to a standstill. At the same time ABGA sample is put on hold in order to reduce the O2 consumption and CO2 production leukocyte, and sent to the laboratory. (N. D. Talk .: The capillary blood gas analysis [usually from the hyperemic earlobe] somewhat too low Pa supplies compared to ABGA O2 values, but correlated well overall with the arterial measured values. In terms of simple, low-risk and minimally invasive implementation should be given in routine operation [except in patients in shock] capillary of the BGA preference over the arterial BGA) hypoxemia oxygenation means a decreased arterial oxygen partial pressure (PO2). under hypoxia is meant a reduced tissue PO2 Using a ABGA hypoxemia can be accurately examined. Hypoxemia is usually defined as a PaO2 so low that the SaO2 drops below 90% (i. E. PaO2 <60 mm Hg). Pathological Hb derivatives (eg. B. methemoglobin), elevated body temperature, lower pH and higher 2,3-diphosphoglycerate levels reduce the Hb O2 saturation, although the PaO2 yet sufficient, according to oxyhemoglobin dissociation curve (oxyhemoglobin dissociation curve.) would. Oxyhemoglobin dissociation curve. The arterial oxygen saturation is related to PO2. PO2 at 50% saturation (P50) is usually 27 mmHg. The dissociation is increased hydrogen ions (H +) - shifted concentration, increased erythrocyte 2,3-diphosphoglycerate (DPG), elevated temperature (T) and increased PCO2 to the right. Decreased values ??of H +, DPG, temperature and PCO2 move the curve to the left. Hb, which is characterized by a shift of the curve to the right, has a reduced affinity for O2, and Hb, which is characterized by a shift of the curve to the left, has an increased affinity for O2. The causes of hypoxemia can be divided based on whether the alveolar-arterial PO2 gradient [(A-a) Do 2], which is defined as the difference between the O2 voltage and (PaO 2) and PaO 2 increases or is normal. The PAO2 is calculated as follows: where FIO2 the fraction of inspired O2 is (. For example, 0.21 in room air) is Patm the ambient air pressure (eg, 760 mmHg at sea level.) PH2O is the partial pressure of water vapor (usually 47 mmHg ), PaCO2 of the measured partial pressure of arterial CO2 and R is the respiratory Quotiente, which is believed that it is a normal diet at a resting patient 0.8. Clinical Calculator: Aa gradient at sea level and at ambient air is FiO 2 = 0.21 and (Aa) DO2 can be simplified as follows: where (Aa) DO2 is <20 normally, but (with age because of the age-related deterioration of the lung function) and increasing FIO2, however, increases (since the O2} -Plasmagehalt with increasing FIO2 to the physical O2 solubility increases further, although the Hb is saturated at a PaO 2 of about 150 mmHg to 100%). The assumptions that the normal (A-a) DO2 value <(2.5 + [FIO2 × years of life]) or less than the absolute value of FiO2 (e.g., <21 at room temperature;. <30 at 30% FiO2) , this Effekte.Hypoxämie correct with increased (Aa) DO 2 this situation is caused by low ratio of ventilation / perfusion (V / Q) (a kind of mismatch between V / Q) right-to-left shunt Stark limited diffusion capacity a low V / Q ratio is one of the more common causes of hypoxemia and plays a causal role in COPD and asthma. In the healthy lung perfusion ventilation is locally well adapted because the arterioles react with alveolar hypoxia with vasoconstriction (n. D. Übers .: Euler Liljestrand reflex). In diseases dysregulation leads to perfusion of the alveoli, which are only ventilated incomplete (V / Q mismatch). This venous blood flows through the pulmonary capillaries, without reaching a normal PaO 2. can vonO2 additional administration hypoxemia on the bottom of a low V / Q ratio by raising the PAO2 improve, even though the increased (A-a) DO2 persists. Right-left shunts are an extreme example of a low V / Q ratio. By shunts deoxygenated pulmonary arterial blood reaches bypassing ventilated areas of the lung directly the left heart. The shunt may be in the lung in the form of abnormal connections between the arterial and venous pulmonary circulation or by intracardiac compounds (eg. As patent foramen ovale) arise. Hypoxemia due to right-left shunt can not be improved through additional O2 administration is. A restricted diffusion capacity occurs rarely isolated on; it is usually accompanied by a low V / Q ratio. Since the Hb is completely saturated already at a fraction of the time, which is the blood, the alveolar air in combination with O2, occurs hypoxemia by a limited diffusion capacity only when the cardiac output is increased (z. B. on exertion), wherein low air pressure (eg. as at high altitudes), or when> 50% of the lung are destroyed. It is increased as in a low V / Q ratio of (A-a) DO2. However, PaO 2 can be raised quickly by increasing the FIO2. Hypoxemia can be due to limited diffusion capacity through additional O2 administration verbessern.Hypoxämie with normal (Aa) DO 2 This situation is caused by hypoventilation Low partial pressures of inspired O2 (PIO2) By hypoventilation (decreased alveolar ventilation) of PAO2 be lowered and the PaCO2 elevated; characterized the PaO2 falls. For pure hypoventilation (A-a) DO2 is normal. Among the causes of hypoventilation include decreased respiratory rate or depth (z. B. due to neuromuscular diseases, obesity per magna or medication overdose or compensation of metabolic alkalosis) or increasing the dead space ventilation in patients who have already reached the limit of the maximum ventilation (eg. B. exacerbation of severe COPD). The due hypoventilation hypoxia responsive to the administration of additional O2, however, may increase of any possible hypercapnia. Reduction of PIO2 is another rare cause of hypoxemia that occurs in most cases at high altitudes. Although the FIO2 does not change with increasing altitude, the ambient air pressure decreases exponentially; characterized PIO2 also decreases. For example, the PIO2 amounts to only 43 mmHg at the top of Mt. Everest (height, 8848 m [29,028 ft]). The (A-a) DO2 value remains normal. Hypoxia stimulates the respiratory drive, alveolar ventilation increases and decreases PaCO2. This type of hypoxemia responds to the administration of additional O2 an.Kohlendioxid The PCO2 is held physiologically between 35 and 45 mmHg. There is a dissociation of CO2, similar to that of O2, however, which is approximately linear in the range of physiological PaCO2 values. A pathological PCO2 almost always accompanied by respiratory disorders (unless he joins compensate for a metabolic abnormality) and disorders of acid-base balance associated. Clinical Calculator: Arterial blood gas interpretation TreeCalc hypercapnia hypercapnia means PCO2> 45 mmHg. The causes of hypercapnia are the same as those of hypoventilation (hypoxemia with normal (A-a) DO 2). Disorders that increase the CO2 production (. Eg hyperthyroidism, fever), can – should you be associated with an inability to increase the Ventialation also corresponds to a hypercapnia führen.Hypokapnie hypocapnia PCO2 <35 mmHg hypocapnia is always carried hyperventilation on the floor of pulmonary (eg. B. pulmonary edema or -embolie), cardiac (eg. B. heart failure), metabolic (z. B. acidosis), drug-induced (z. B. ASS, progesterone), or the central nervous system in question (mentally z. B. infection, tumor, hemorrhage, increased intracranial pressure, n. d. Talk .:) caused disease or physiological conditions (eg. as pain, pregnancy). Hypocapnia will increase bronchoconstriction directly and lower the thresholds for cerebral or myocardial ischaemia, possibly by changes in acid-base Status.Carboxyhämoglobinämie CO binds with a 210-fold higher affinity for Hb than O2 and thus prevents the O2 transport. Clinically toxic carboxyhemoglobin levels usually occur after inhalation of exhaust gases or smoke inhalation, although also include cigarette smoking measurable levels. Patients with CO poisoning (Kohlenmonxidvergiftung) often have nonspecific symptoms such as malaise, headache and nausea. Since poisonings occur frequently in cooler months (due to the increased use of highly flammable oil heaters in enclosed spaces), the symptoms can be confused with those of viral respiratory infections such as influenza. Therefore, the differential diagnosis should think of the possibility of CO poisoning and, if indicated, are determined the carboxyhemoglobin levels; in venous blood COHb can be measured directly, an arterial sample is unnecessary. The treatment consists in the administration of 100% O2 (thus the half-life of the carboxyhemoglobin is reduced), and sometimes in the use of a hyperbaric chamber. Tips and risks Carboxyhämoglobinspiegel can be measured directly from one-venous arterial sample is not required. Methemoglobinemia methemoglobin is Hb, in the divalent (Fe2 +) to trivalent iron (Fe3 +) is oxidized. Methemoglobin transported no O2, and normal HbO2 dissociation curve is shifted to the left, causing the release of O2 is reduced in the tissue. methemoglobinemia is caused by certain drugs (eg. B. dapsone, local anesthetics, nitrates, primaquine, sulfonamides) or less frequently by certain chemicals (eg. as aniline dyes, benzene derivatives). The methemoglobin levels either directly by CO-Oximetry (where light is emitted in four different wavelengths and methemoglobin, COHb, Hb and HbO2} can be determined) is measured, or the difference between the calculated from the measured PaO2 O2 saturation and directly measured SaO2 calculated. Most commonly, patients with asymptomatic methemoglobinemia cyanosis. In severe cases, the O2 supply is so severely restricted that symptoms of tissue hypoxia occur such. B. confusion, sore throat and myalgia. Therapeutically, it is enough usually to end the gift of the causative drug or exposure to the triggering chemical. Rarely are methylene blue (a reducing agent; 1-2 mg / kg of a 1% solution are slowly i.v. administered) or exchange transfusion is needed.