ICU patients (as well as other patients) can (<90% O2 saturation) develop without respiratory disorders during their hospital stay hypoxia. The hypoxia in patients with pre-existing respiratory disorders is discussed in the relevant chapters. Etiology Numerous disorders can cause hypoxia (eg, dyspnea, respiratory failure, see table. Some reasons for the drop in oxygen saturation). Nevertheless, the acute hypoxia in hospitalized patients can be traced back without pulmonary disease on a small selection of causes. These causes can be divided into: Disorders of ventilatory impairment of oxygenation Some reasons for the drop in oxygen saturation mechanism examples disorders of ventilation Decreased respiratory drive Restricted mental status (eg caused by head injuries, oversedation, sepsis, shock or stroke.) Airway obstruction bronchospasm dislocation de s endotracheal tube laying of airways or endotracheal tube through secretion Severe pain in the chest and / or abdomen rib fractures thoracic or Abdomenoperation disorders oxygenation Pulmonary causes acute respiratory distress syndrome (ARDS) atelectasis, pneumonia, pneumothorax, pulmonary embolism, pulmonary contusion, aspiration Nichtpulmonale causes Iatrogenic fluid overload congestive heart failure (z. B. Clarification The total volume administration during hospitalization, and especially the last 24 hours has to be detected by exacerbation of the underlying disease or acute myocardial infarction) in order to detect a volume overload. administered for sedation substances must be checked for dosing out. While significantly hypoxia (O2 saturation <85%) is the same time as these considerations initiate treatment. History Sudden onset of dyspnea and hypoxia can always initially suspect a pulmonary embolism. Often this takes in patients with positive pressure ventilation. Fever, chills and productive cough (or increased secretion) suggestive of pneumonia. In anamnestic evidence of cardiopulmonary disease (asthma, COPD, heart failure) may be a deterioration in the respective pre-existing conditions. Symptoms and signs of myocardial infarction may indicate an acute valvular insufficiency, pulmonary edema or cardiogenic shock. Unilateral pain of a limb must be thinking of a deep vein thrombosis, possibly together with a pulmonary embolism. A previous severe trauma or sepsis, which requires a significant resuscitation can think of ARDS. In vorausgegangenem Toraxtrauma is suspected to Lungenkontusion.Körperliche investigation openness of the airways, respiratory strength and scope of the breathing must be evaluated immediately. In ventilated patients relocation or dislocation is ruled out of the tube. The results are interpreted as follows: the unilateral reduction of the respiratory sound together with a transparent lung surface in the X-ray image makes a pneumothorax likely. In rales and fever more of a pneumonia can be assumed. This can be caused in a intubation in the right main bronchus. Distended neck veins with rales over both lung areas indicate a volume overload with pulmonary edema, cardiogenic shock, pericardial tamponade (often without crackles) or acute valvular insufficiency. Jugular venous distension in bright lung fields, or one-sided decrease in respiratory noises and axis deviation of the trachea speak for a tension pneumothorax. Bilateral edema of the dependent body sections are found in heart failure. Unilateral edema however, correspond to the image of deep vein thrombosis. Therefore, the possibility of pulmonary embolism must in these cases be considered. Wheezing can auscultate (typical of asthma or allergic reaction, but rarely with pulmonary embolism or heart failure) when bronchospasm. Increasing consciousness disorders can be caused by hypoventilation. Basically tests hypoxia is first of all determined on the basis of pulse oximetry. In patients following should occur: A chest x-ray (. Eg to check for pneumonia, pneumonia, pleural effusion, pneumothorax or atelectasis) ECG (to check for cardiac arrhythmias or ischemia) Arterial blood gas analysis (for confirmation of hypoxia and evaluate the adequacy of ventilation) A performed by an intensive care physicians at the bedside echocardiography (monitoring and analysis of intensive care patients: Portable echocardiography) can be used to detect a hemodynamically significant pericardial effusion or a reduced global left ventricular function until a formal echocardiography can be performed. An elevated level of natriuretic peptide (BNP) in the serum of the brain (B-type) can help to distinguish heart failure from other causes of hypoxia. remains the diagnosis remains unclear, the examination process must be continued in view of a pulmonary embolism (pulmonary embolism (PE): Diagnosis). When intubated patients, bronchoscopy is advised to rule out a relocation of the tracheobronchial tree by mucus (or to remove such material). Therapy Revealed causes of hypoxia are treated as elsewhere in the MSD Manual shown. Persists hypoventilation, then a mechanical ventilation in the form of non-invasive positive pressure ventilation or a subsequent endotracheal intubation is required (respiratory failure and mechanical ventilation). A prolonged hypoxia makes the supplementary O2 administration necessary. O 2 therapy The required height of the O2 content of the inspiration air is obtained from the arterial blood gas analysis or pulse oximetry. The aim is to ensure a PaO2 between 60 and 80 mmHg (or 92-100% oxygen saturation), without reaching the region of the O2 toxicity. To these limits sufficient O2 supply can be guaranteed to the tissues. Since the oxyhemoglobin dissociation curve has a sigmoidal curve, the O2 supply decreases with an increase in PaO 2> 80 mmHg to very little. Therefore, this area is less significant for oxygenation. Lowest utmost O2 (FiO2), which still leads to an acceptable PaO 2 should be selected. The toxicity of O2 concentration and time dependent. Longer-term increases over a FiO2 of 60% cause inflammatory changes, alveolar infiltration and possibly pulmonary fibrosis. A FiO 2> 60% should always be avoided if this is not essential for the survival of the patient. If the FIO2 below 60%, this will contrast well tolerated for a long time. A FiO 2 <40% can be administered both via nasal probe or via a face mask. Nasal tubes provide an O2 flow of 1-6 l / min. As with 6 l / min of the nasopharynx is sufficiently filled, higher flow rates have no further use. However, simple face masks and nasal probes do not allow delivery of an accurate FIO2. This is due to the inconsistent admixture of O2 in the air due to leaks and mouth breathing. With masks of the type of Venturi masks a fairly accurate O2 concentration can still be offered. Clinical Calculator: prognostic criteria for pancreatitis Clinical Calculator: Conversion of units for oxygen release a FiO 2> 40% makes the use of an O2 mask with a reservoir which is filled with oxygen from the O2 source required. In typical non-rebreathing mask the patient 100% O2 inhaled from a reservoir; However, a rubber valve ensures during exhalation that the exhaled air is discharged into the environment. Thus, the addition of CO2 and water vapor by the inhaled O2 can be prevented. However, due to leaks these masks offer only a FiO2 of more than 80-90%. Summary Hypoxia can be caused by disorders of ventilation and / or oxygenation and is first usually detected by pulse oximetry. In these patients a chest x-ray, an electrocardiogram and a blood gas analysis should be made (to confirm the hypoxia and to evaluate the adequacy of ventilation). If the diagnosis remains unclear, tests should be taken into consideration pulmonary embolism. (H i. E. 92- 100% saturation) O2 It should be given as required to a PaO2 between 60 and 80 mmHg to maintain, in addition, the cause should be treated.