Respirační selhání. Status asthmaticus MUDr. V. Zvoníček ARK, FN u sv. Anny

Definice akutní plícní stav ( vyjma COPD) vyžadující aktivní léčbu nespecifický stav různé základní diagnózy: pneumonie, trauma, sepse Acute respiratory failure (ARF) is a common and important indication for critical care with a substantial mortality. It is defined as all acute lung conditions with the exception of obstructive lung disease that require active therapy. ARF is not a specific disease but a reaction to an underlying condition, e.g. trauma, sepsis or pneumonia. Due to different definitions, the incidence and mortality rates for ARF vary across studies. In addition, the underlying condition strongly influences prognosis. The data quoted below are from the Scandinavian study (see reference on the next screen). The incidence of ARF, including acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) was 78 per 100 000 people >15 years of age per year  Ninety-day mortality was close to 40%, independent of whether the condition was defined as ARF, ALI or ARDS  The majority of patients had ARF of pulmonary origin (52%), with pneumonia as the predominant diagnosis (23%

respirační selhání- rozpoznání Anamnéza chronická onemocnění plic a srdce, astma, COPD, kouření, alergeny, infekce, imunosuprese , revmatická onemocnění, neurologická onemocnění ( např. Guillain-Barré), léky (betablokátory), operace plic, genetická onemocnění Kašel Chronický, suchý (může být pleurální), produktivní (infekce) Sputum žluté (leukocyty), nazelenalé (stagnace), nebo nahnědlé (erytrocyty) Hemoptýza Různý stupeň, bronchitis,mitrální stenosa, plicní infarkt, bronchiektazie, karcinom, TBC Dušnost Uvědomování si dechového úsilí v situaci kdy se normálně neuvědomuje, nerovná se hyperpnoe a tachypnoe Cyanosa 50g/1000 ml redukovaného Hb, periferní (velká extrakce O2) nebo centrální (hypoxie) nebo kombinovaná Bolesti na hrudi Onemocnění pariet. pleury Introduction The respiratory system consists of two parts: the upper respiratory tract, which includes the nose (nasal cavity, sinuses), mouth, larynx, and trachea; and the lower respiratory tract which includes bronchi, bronchioles, and alveoli. The respiratory centres in the brain stem (pons and medulla) control the rhythm, rate, and depth of respiration. Respiratory failure represents the most frequent cause of admission to intensive care units (ICUs). Several diseases can be characterised by an impairment of the respiratory system. Similar skills can be learned and used for the diagnosis and treatment of different lung diseases. The aim of this module is to present a systematic and easy approach to patients with respiratory impairments. Monitoring of the respiratory system can be started using simple skills and devices and can be later supported by more sophisticated equipment. ICU staff should be familiar with the most common respiratory monitoring devices and techniques. The baseline investigation is the best guide to planning a diagnostic pathway and for timely assessment of the best treatment for a patient. The differential diagnosis is essential and should be structured on a complete history and an appropriate clinical investigation. Respiratory monitoring is necessary to estimate key prognostic elements and to assess patients' outcome. Regular monitoring of a patient's respiratory system is a sensible guide to measure the efficiency of a given treatment. 1/ How to recognise lung diseases It is fundamental to perform an exhaustive and systematic clinical examination on all patients admitted to the ICU. The initial clinical examination provides a baseline reference. It is essential for the differential diagnosis and treatment planning. See the PACT module on Basic clinical examination . The clinical examination of the respiratory system comprises history taking, physical examination (inspection, palpation, percussion, and auscultation) and, the evaluation of laboratory data and radiological findings. Clinical history The history taking should include the past medical and surgical history, current medications, as well as the presenting complaint. Information about risk factors for lung disease should be obtained while recording the past medical history. A history of current or previous smoking must be noted and a record made of the number of years the patient has smoked, the number of cigarettes per day and the interval since smoking cessation. A history of significant passive exposure to smoke may be a risk factor for neoplasia or an exacerbating factor for airway diseases (such as chronic obstructive lung disease). A history of sleep-disordered breathing is typical in obese patients. The anamnestic data should be collected comparing the patient's subjective feelings with the objective sleep history reported by the family members. The pathologic increase in the PaCO2 (partial pressure of carbon dioxide in the blood) modifies the strength of the history reported by these patients. Obese patients suffering from sleep-disorders complain of headaches in the morning, somnolence during the daytime, and apnoea or shortness of breath during night-time. These disorders are important as predictors of difficult intubations. Exposure to other inhaled agents associated with lung disease must be ascertained. Among these agents are inorganic dusts (especially asbestos and silica) and organic antigens (especially antigens from moulds and animal proteins). Asthma is often exacerbated by exposure to environment allergens or occupational exposure. Patients presenting with a history of severe asthma, or a previous admission to an ICU due to an episode of status asthmaticus, must be considered at high risk for respiratory failure. Emergency or ICU doctors should not delay endotracheal intubation in these patients. See the PACT module on COPD and asthma Exposure to infectious agents can be suggested in previously healthy people having contact with individuals with known respiratory infections (tuberculosis). Healthy people travelling in specific areas of the world can be exposed to pathogens. For an appropriate management plan it is important to obtain a detailed travel history on admission. Respiratory system infections should be suspected in all immunocompromised patients (oncology/haematology patients, transplants, HIV/AIDS). Immunisation status must be evaluated in children and newborn. See the PACT module on Immunocompromised patients Systemic rheumatic diseases (such as rheumatoid arthritis) are sometimes the cause of pleural and parenchymal lung diseases. Patients with a history of motor neurone diseases such as amyotrophic lateral sclerosis, neuromuscular junction diseases such as myasthenia gravis, immune-mediated neuropathies such as Guillain-Barré syndrome, or myopathies, might have multiple admissions to ICUs. These patients are likely to need long-term invasive ventilation. Treatment of non-respiratory disease can be associated with respiratory complications, either because of effects on host defence mechanisms (immunosuppressive agents, chemotherapy drugs) with resulting infection or because of direct effects on the pulmonary parenchyma (amiodarone) or on the airways (β-blockers, angiotensin-converting enzyme inhibitors). Family history is important for evaluating genetic risk factors (cystic fibrosis, α- antitrypsin deficiency, pulmonary hypertension, asthma) and predisposition for lung diseases. The past surgical history should be obtained paying particular attention to all operations performed in the neck, throat and in the thorax of the patient. It is important to exclude lesions of the phrenic nerve after surgery in the cervical region. Pre-operative and postoperative lung capacities should be reported on the patient's record if the history taking is positive for a pneumonectomy, lobectomy or atypical lung resection. Clinical signs/features of respiratory diseases Common manifestations of respiratory diseases on admission are cough, sputum, haemoptysis, dyspnoea (shortness of breath), cyanosis, chest pain, and clubbing of the fingers and toes. Cough Cough is the most frequent of all respiratory symptoms. There are various types of cough. It can be moist or dry depending on whether or not the cough is accompanied by sputum. Chronic cough is defined as a cough persisting in excess of three weeks and is widespread among smokers. Cough associated with inflammation of the pleura (pleurisy) is characte ristically dry and short. Here the act of coughing causes pain owing to the movement of the pleura, and so the cough is cut short by the pain. Cough is accompanied by purulent sputum in bacterial infections. Sputum Sputum varies in amount and character according to the nature and extent of the lung disease. Sometimes in the early stages of disease, sputum may be absent and appears later when the lesion in the respiratory tract has progressed. Yellow sputum usually indicates a large number of white cells and underlying infection. However, light yellow sputum might be seen in patients with asthma because of a high sputum eosinophil count. Green discolouration indicates stagnation of mucus, and red or brownish sputum is caused by the presence of red blood cells. Haemoptysis Haemoptysis of all grades of severity may occur, from slight streaking of the sputum with blood, which is a common symptom in acute and chronic bronchitis, to a massive haemorrhage. Bronchial carcinoma, pulmonary infarction, pulmonary tuberculosis, bronchiectasis and mitral stenosis are the most common causes of massive bleeding. Dyspnoea Dyspnoea occurs as a symptom in a wide variety of lung and heart diseases. It is defined as the subjective state in which the effort of breathing reaches consciousness, usually under circumstances in which a normal person would not be aware of his/her breathing at all (at rest). It should be distinguished from hyperpnoea, where the volume of ventilation is increased, but no abnormal sensation is felt, and tachypnoea, an excessive respiratory rate. In children, respiratory rate must be evaluated according to age. Cyanosis Cyanosis depends on the absolute amount of reduced haemoglobin in the blood. Cyanosis is evident when reduced haemoglobin exceeds 5 g/100 ml. Peripheral cyanosis is due to an excessive extraction of oxygen from the blood when the circulation is impaired by vasoconstriction, low cardiac output or stasis. Central cyanosis is due to oxygen undersaturation of the arterial blood from poor gaseous exchange in the lungs in conditions such as emphysema, pulmonary oedema and pneumonia or when there is a veno-arterial shunt in congenital heart disease. A combination of central and peripheral cyanosis may occur. It is often seen in cardiac failure. Chest pain Chest pain caused by diseases of the respiratory system frequently originates from involvement of the parietal pleura. Chronic or recurrent chest pain may reflect pulmonary vascular or pleural disorders. Clubbing of the fingers and toes Clubbing of the fingers and toes can be found in lung cancer, interstitial lung disease and chronic infections of the thorax such as lung abscess and empyema.

respirační selhání-vyšetření Inspekce Dechová frekvence, vzor dýchání, zapojování pomocných dýchacích svalů, symetrie dýchání, deformity hrudníku, kyfoskoliosa, uzliny, periferní otoky, náplň jug.žil Palpace Potvrzení viditelných nálezů, symetrie dýchaní, subkutánní emfysem, krepitace Auskultace Oslabené, vymizelé dýchání Abnormální poslech Chrůpky, bronchitické fenomény, třecí šelest Stridor Physical examination The physical examination should be directed both to lung and thoracic abnormalities and to findings that may reflect underlying lung diseases. The patient's temperature should be taken before examining the chest, to look for hypothermia or hyperthermia. The findings on physical examination should be equivalent on both sides of the chest. On inspection the rate and pattern of breathing, as well as the depth and symmetry of lung expansion, are examined. Breathing that is associated with the use of accessory muscles indicates an increase in the work of breathing (see Task 5 ). A note should be made of the rate and character of breathing, the type and severity of coughs and the amount and character of the sputum. Asymmetric expansion of the chest is always due to a localised process affecting one or other lung such as endobronchial obstruction of the airway or phrenic nerve paralysis. Thoracic abnormalities such as kyphoscoliosis and ankylosing spondylitis must be recorded on inspection because of the related decrease in total lung capacity and increase in the risk of pneumonia. Skeletal abnormalities such as an increase in the antero-posterior diameter of the chest could be due to severe emphysema. Enlarged lymph nodes in the cervical and supraclavicular regions should be evaluated, because these could be related to several diseases, including cancer. Peripheral oedema (lower extremities) may be related to pulmonary vascular hypertension, and right ventricular failure. It is wise to consider possible pulmonary hypertension problems in every patient with chronic respiratory failure. In patients with chronic respiratory failure, it is fundamental to look for all the signs of cor pulmonale, and in particular: raised jugular venous pressure (signs of tricuspid regurgitation (TR)), loud S2 and hepatomegaly. If these signs are gross, it is appropriate to perform a transthoracic echocardiogram to look at TR jet velocity and to estimate pulmonary artery (PA) pressures. On palpation, findings observed by inspection may be confirmed. The symmetry of lung expansion can be assessed. The chest wall should be carefully examined for soft tissue abnormalities such as cutaneous lesions, subcutaneous swelling or emphysema (subcutaneous crepitation on palpation), bulging or indrawing of intercostal spaces. The consistency of lymph nodes should be described. By percussion the sound of a normal lung is resonant while the consolidated lung or a pleural effusion is dull, and emphysema is hyperresonant. On auscultation the quality and intensity of breath sounds should be assessed using a stethoscope. The categories of findings include normal breath sounds, decreased or absent breath sounds, and abnormal breath sounds. Normal breath sounds are described as 'vesicular'. Vesicular sounds are smooth, low tone, and widespread over the thorax of normal patients. Vesicular sounds are higher during inspiration and lower (like blowing) during expiration. These sounds are generated by air movements inside and outside the alveoli. Reduced breath sounds reflect reduced airflow to a portion (segment) of the lungs, over-inflation of a portion of the lungs (such as emphysema), air or fluid around the lungs, or sometimes increased thickness of the chest wall. There are several types of abnormal breath sounds: rales, rhonchi, and wheezes are the most common. Rales (crackles or crepitations) are small clicking, bubbling, or rattling sounds in a portion of the lung. They are believed to occur when air opens closed alveoli (air spaces). Rhonchi are sounds that resemble snoring. They are produced when air movement through the large airways is obstructed or turbulent. Wheezes are high-pitched, musical sounds produced by narrowed airways, often occurring during expiration. Wheezing can sometimes be heard without a stethoscope. Pleural friction or rub is a diagnostic sign of pleural inflammation. It is a grating or creaking sound, unaltered by coughing, audible during both inspiration and expiration. Stridor is a specific sound secondary to obstruction of upper airways. Some diseases that most commonly affect the respiratory system, such as sarcoidosis, can have findings on physical examination not related to the respiratory system, including ocular findings (uveitis, conjunctival granulomas) and skin findings (erythema nodosum). Management plans and differential diagnosis should be formulated following the history taking, physical examination, and review of all available laboratory data and radiological findings (X-rays, CT scan, ...).   In your next ten patients check the quality of your history taking and physical examination: how complete are they, how do you judge consistency? Ask your supervisor to observe you while you take a history and perform a physical examination. Investigations Investigations used for the chest include radiological techniques and fibre optic techniques such as bronchoscopy.

Zobrazovací metody RTG hrudníku CT hrudníku Ultrazvuk hrudníku Rutinní vyšetření u respiračního selhání Nemusí odhalit: COPD, malé léze ( <1 cm), plicní embolii, počínající pneumonii, fibrosu plic Odlišnosti ICU RTG Ležící pacient, předozadní, srdce a mediastinum je o 15% širší, pleurální tekutina je více rozlita, distorze plicní vaskulatury CT hrudníku Zhodnocení plicní patologie, zhodnocení mediastina, staging nádorů, High resolution CT ke zhodnocení intersticiálního postižení, zhodnocení aorty a cév, CT angiografie. Ultrazvuk hrudníku Zhodnocení pleurálních výpotků, drenáž hrudníku Bronchoskopie Ke zhodnocení dýchacích cest a odběr vzorků (BAL) Imaging techniques for the chest The plain chest radiograph The plain chest radiograph is the most common radiological investigation in anaesthetic and intensive care practice. A number of studies have shown that daily chest radiographs frequently demonstrate new, unexpected, or changing abnormalities, which result in changes in therapy. The plain radiograph is used both to provide anatomical information and to evaluate changes in the heart and lungs. In addition it provides important data about abdominal contents just below the diaphragm (e.g. gut, gas under the diaphragm) and the anatomy or state of the airway. On the other hand overinterpretation of subtle changes on chest X-rays due to a change in exposure or technique may lead to erroneous assumptions (e.g. diagnosis of pulmonary oedema in particular). Almost all intubated patients require a daily chest radiograph. A chest radiograph should be routinely obtained after the insertion of a subclavian or internal jugular central venous catheter, to confirm the correct placement of the catheter and to exclude a pneumothorax. Some physicians perform a chest X-ray after any intubation to exclude any complications. In all other patients, chest radiographs should be ordered only when needed. See the PACT module on Clinical imaging Everyone should be able to make an instant diagnosis of life-threatening conditions such as pneumothorax as well as use radiological investigations to confirm the safe placement of endotracheal tubes, nasogastric tubes, chest drains or vascular catheters. It is important to realise that a normal chest X-ray does not rule out the following chest pathologies. Diseases with no or minimal radiological features: Obstructive airway disease (e.g. asthma, moderate emphysema, bronchitis, bronchiolitis) Small lesions (e.g. masses of <1 cm diameter, endobronchial lesions without collapse or consolidation) Pulmonary emboli without infarction Early stages of infection/pneumonia Pulmonary fibrosis (early) Interpretation of a bedside film is fraught by numerous pitfalls. In addition, a portable chest radiograph may be difficult to interpret due to poor positioning of the patient. Because lateral chest films cannot easily be obtained in the ICU, abnormalities in the posterior costophrenic area, within the mediastinum and adjacent to the spine, can be missed.   What are the differences between X-rays performed in the ICU and those taken in the radiology department? Most X-rays performed on the critically ill are done in the ICU using mobile equipment with the patient in a bed. As such, these films are suboptimal, and this should be borne in mind when making comparisons with those taken in the radiology department, or with previous films. The chest radiograph in the ICU is antero-posterior (AP) rather than postero-anterior (PA) as in the radiology department. On the AP view, the heart and the mediastinum are about 15% wider than on an upright PA chest radiograph, because of the increased distance of the heart from the film. Further magnification can also be due to the fact that the portable radiography is performed with the X-ray tube closer to patients. A false cardiomegaly or a wide mediastinum are often erroneously presumed. What is the position of choice for performing chest X-rays in the ICU? What are limitations to achieving this position? Patients, if possible, should be in the sitting or semi-erect position. This is necessary because pleural effusion can easily be missed in the supine position. Fluids track posteriorly, resulting in a diffuse haziness of the lung fields. Fluid collections can be confirmed by ultrasonography. The pulmonary vasculature is distorted because blood no longer flows preferentially to the lower lobes in all supine patients. Bedside, changes in the lung blood flow can mimic signs of congestive heart failure. Every effort should be made to position the patient upright. The main limit to this could be haemodynamic instability, cervical and spine fracture and hip fractures. See the PACT modules on Clinical imaging and Respiratory failure The chest radiograph should be studied systematically: first the quality of images and the patient's position; then the location of all tubes and catheters, together with the evaluation of ribs, vertebrae, lung parenchyma, pleura, mediastinum, and diaphragm; and lastly the assessment of signs of extra-alveolar air. Computed tomography Use of the computed tomography (CT) scan in the diagnosis of lung diseases includes the following indications: Investigation of pulmonary pathology Assessment of the mediastinum Tumour staging Interventional procedures such as biopsy High-resolution CT technique is used to assess interstitial pulmonary disease Assessment of thoracic trauma Assessment of aorta and blood vessels CT pulmonary angiography for suspected embolism Pre-operative assessment of airway involvement by mediastinal masses CT is a very useful and frequently employed technique in intensive care medicine. Conventional CT scan and high-resolution computed tomography (HRCT) are both used for evaluating aortic dissection, pleural disease and mediastinum masses, but HRCT is better for studying diffuse infiltrative lung diseases (e.g. immunocompromised patients with pulmonary infiltrates). Spiral CT is most helpful in evaluating lesions at, or near, the diaphragm (less motion artefact), vascular structures (main pulmonary arteries in suspected pulmonary embolism), and small pulmonary nodules. For more information see the PACT module on Clinical imaging . CT scanning in ALI/ARDS Acute lung injury/ acute respiratory distress syndrome (ALI/ARDS) can be studied using X-rays and CT images. Desai SR. Acute respiratory distress syndrome: imaging of the injured lung. Clin Radiol 2002; 57(1): 8-17. Review. PMID 11798197 ARDS can be derived from two pathogenetic pathways: a direct insult to lung cells (pulmonary ARDS, ARDSp) or indirectly (extrapulmonary ARDS, ARDSexp). The radiological (X-rays and CT scan) pattern in ARDSp is characterised by a prevalent alveolar consolidation while the ARDSexp by a prevalent ground-glass opacification. More information regarding ARDS can be found in the PACT module on Respiratory failure and in the following references. Gattinoni L, Pelosi P, Suter PM, Pedoto A, Vercesi P, Lissoni A. Acute respiratory distress syndrome caused by pulmonary and extrapulmonary disease. Different syndromes? Am J Respir Crit Care Med 1998; 158(1): 3-11. PMID 9655699 Desai SR, Wells AU, Suntharalingam G, Rubens MB, Evans TW, Hansell DM. Acute respiratory distress syndrome caused by pulmonary and extrapulmonary injury: a comparative CT study. Radiology 2001; 218(3): 689-693. PMID 11230641 Gattinoni L, Caironi P, Pelosi P, Goodman LR. What has computed tomography taught us about the acute respiratory distress syndrome? Am J Respir Crit Care Med 2001; 164(9): 1701-1711. Review. No abstract available. PMID 11719313 These measurements require a multidisciplinary approach CT scanning can be used to assess positive end-expiratory pressure (PEEP)-induced alveolar recruitment. This is classically achieved by quantifying the decrease in non-aerated lung parenchyma on a single juxtadiaphragmatic section. This approach is known as the Gattinoni method. As described by Gattinoni and co-workers, alveolar recruitment is assessed on a single CT section located 1 cm above the diaphragmatic cupola and computed as the decrease in the weight of non-aerated lung parenchyma between zero end-expiratory pressure (ZEEP) and PEEP. Gattinoni L, Pelosi P, Crotti S, Valenza F. Effects of positive end-expiratory pressure on regional distribution of tidal volume and recruitment in adult respiratory distress syndrome. Am J Respir Crit Care Med 1995; 151(6): 1807-1814. PMID 7767524 Gattinoni's approach ignores the alveolar recruitment occurring in poorly aerated areas of the lung. Malbouisson and co-workers suggested a new CT method in which PEEP-induced alveolar recruitment is computed as the volume of gas penetrating in poorly and non-aerated lung regions following PEEP. Malbouisson LM, Muller JC, Constantin JM, Lu Q, Puybasset L, Rouby JJ; CT Scan ARDS Study Group. Computed tomography assessment of positive end-expiratory pressure-induced alveolar recruitment in patients with acute respiratory distress syndrome. Am J Respir Crit Care Med 2001; 163(6): 1444-1450. PMID 11371416 Magnetic resonance imaging Magnetic resonance imaging (MRI) requires special ventilation and monitoring equipment, because of the strong magnetic field. Some indications for MRI extend beyond those for CT scanning. MRI usually does not require the use of intravenous contrast agents to identify blood vessels. It is possible to differentiate between a dilated pulmonary vessel and a hilar mass without using contrast. The reason is that flowing blood has no signal on MRI images and consequently appears black. The following list gives the indications for using MRI rather than CT: Evaluation of thoracic aorta Evaluation of mediastinal masses/Pancoast tumour Evaluation of lymph nodes Evaluation of vascular lesions such as arteriovenous malformations MRI can be used for the assessment of lung ventilation. Kauczor HU, Hanke A, Van Beek EJ. Assessment of lung ventilation by MR imaging: current status and future perspectives. Eur Radiol 2002; 12(8): 1962-1970. Epub 2002 May 24. Review. PMID 12136314 Other techniques Ultrasound - The role of ultrasound in chest radiology is limited to pleural pathology and to the guided placement of thorax drains in localised pleural effusions. van der Werf TS, Zijlstra JG. Ultrasound of the lung: just imagine. Intensive Care Med 2004; 30(2): 183-184. Epub 2003 Dec 19. No abstract available. PMID 14685657Full text (pdf) Radionuclide scanning - Radionuclide scanning and pulmonary angiography are used to detect pulmonary embolism. The two standard types of radionuclide scans in the lungs are perfusion and ventilation scans. These are used to detect and study pulmonary embolism. Spiral CT has largely replaced radionuclide scanning for this indication. Pulmonary angiography - This is performed by rapid injection of contrast media into the pulmonary arterial circulation with serial radiographic exposure. The procedure is invasive and not without risk. The main indication is congenital vascular abnormalities. Spiral CT has largely replaced angiography for initial diagnosis of pulmonary embolism. Whatever the benefits of proposed interventions, they must outweigh the risks of transporting the critically ill patient and those posed by the procedures themselves. See the PACT module on Transportation and the following reference. Shirley PJ, Bion JF. Intra-hospital transport of critically ill patients: minimising risk. Intensive Care Med 2004; 30(8): 1508-1510. Epub 2004 Jun 9. PMID 15197442Full text (pdf) Bronchoscopy Bronchoscopy is the process of direct visualisation of the tracheobronchial tree. Although bronchoscopy is now performed almost exclusively with flexible fibre optic instruments, rigid bronchoscopy still has a role in selected circumstances and under general anaesthesia. What reasons could lead ICU doctors to use a rigid bronchoscope? One reason to use a rigid bronchoscope is the need of a large suction channel, for retrieval of a foreign body or suctioning of a massive haemorrhage. Bronchoscopy is useful in some settings for visualising abnormalities of the airways and for obtaining a variety of samples from either the airway or the pulmonary parenchyma. The bronchoscope may provide the opportunity for diagnosis as well as treatment. For more information regarding the use of bronchoscopy

Labratorní vyšetření Parciální tlak kyslíku v arteriální krvi paO2 Norma 13,3 kPa (100mmg) Hypoxie pod 8 kPa Obsah kyslíku v krvi CaO2 =(SaO2 x Hb x 1.34) + (0.003 x PaO2) DO = CaO2 *CO PaCO2 Odráží zejména produkci CO2 a alveolární ventilaci Hyperkapnie zejména při poklesu alveolární ventilace Hyperkapnie také při snížení plicní perfůze a tluštění alveolo-kapilární membrány (paCO2 -EtCO2 >5 mmHg)

Pulzní oxymetrie , saturace O2 Měří absorbanci světelného signálu fluktující části krve (pulzní) Vyjádřena v procentech oxygenovaného hemoglobinu, norma >96% Pokles po 90% představuje velký pokles paO2 (O2 disociační křivka) Neinvazivní standardní monitorace Limitace: normální hodnoty u otravy CO, neměří při poruchách prokrvení (šok), méně přesný při poklesu saturace pod 83% The pulse oximeter is a two-wavelength oximeter that determines the fluctuating component of the light absorbance signal (analogous to an AC amplifier). Arterial pulsations are associated with changes in blood volume that produce phasic changes in the intensity of transmitted light. This eliminates errors created by light reflection in nonpulsatile structures such as extravascular tissues and (nonpulsating) veins. The pulse oximeter can distinguish only two haemoglobin species: haemoglobin and oxyhaemoglobin. If there are significant quantities of other haemoglobin species, for example, methaemoglobin (MetHb) or carboxyhaemoglobin (COHb), the two-wavelength SaO2 measurement can be enhanced by a four-wavelength haemoximeter ruling out the MetHb or COHb fraction. Pulse oximeters record light transmission through pulsating arteries only. When and why do I have to use pulse oximetry? Determination of arterial O2 saturation The need to measure the response of arterial oxyhaemoglobin saturation to therapeutic intervention or to a diagnostic procedure (e.g. bronchoscopy) Superior detection of hypoxaemic episodes Non-invasive Low morbidity and high patient satisfaction Less expensive than blood gas measurement Hyperbilirubinaemia has been shown not to affect the accuracy of SpO2 readings. Changes in pH, temperature, and 2,3-diphosphoglycerate concentration alter the PO2-SaO2 relationship and may result in misleading calculations of oxyhaemoglobin saturation. Limitations of pulse oximetry: Motion artefact Abnormal haemoglobins (primarily COHb and MetHb) Exposure of measuring probe to ambient light during measurement Low perfusion states Skin pigmentation Nail polish or nail coverings with finger probe Inability to detect saturations below 83% with the same degree of accuracy and precision seen at higher saturations

Kapnografie Průběh a kvantifikace vydechovaného CO2 End tidal CO2, EtCO2 Obstrukce expirace Zástava oběhu Normální kapnografie

ARDS acute respiratory distress syndrome ALI acute lung injury akutní nástup respiračního selhání nové bilaterální infiltráty na RTG plic nepřítomnost levostranného selhání klinicky diagnostikovaného nebo PAOP < 18 mmHg hypoxemie paO2/FiO2<200 mmHg =ARDS paO2/FiO2<300 mmHg =ALI ALI je lehčí formou ARDS The definition of ARDS that is now generally accepted is from the North American – European consensus committee (NAECC) presented in 1994. ARDS is defined as an inflammatory process in the lungs with:   An acute onset of respiratory failure   New onset bilateral infiltrates on frontal chest radiograph   Absence of left ventricular failure (clinically diagnosed or a pulmonary artery wedge pressure <18 mmHg) Hypoxaemia with a ratio between the partial pressure of oxygen in the arterial blood and the fraction of inspired oxygen (PaO2/FiO2) <27 kPa (200 mmHg) independent of the positive end-expiratory pressure (PEEP)-level ALI is defined by the same criteria except that the PaO2/FiO2 ratio is between 27 kPa (200 mmHg) and 40 kPa (300 mmHg).

ARDS, ALI- etiologie primární, plícní sekundární, extrapulmonální aspirace do plic, pneumonie, kontuze plic. inhalace toxických plynů, tonutí sekundární, extrapulmonální generalizovaná aktivace mediátorů a buněk zánětu sepse nekróza a trauma tkání (pancreatitis, trauma, velký operační výkon) šokové stavy ALI/ARDS is an acute inflammatory condition in the lungs and not a disease in itself, and is therefore always due to an underlying disease process. The pulmonary inflammation is caused by:   A direct (primary or pulmonary) injury to the lungs or   An indirect (secondary or extra-pulmonary) injury ALI/ARDS due to a direct injury comprises 70-80% of all cases, with pneumonia as the most important single cause (40-50% of all cases). Other common direct causes are aspiration of gastric contents, pulmonary contusion, inhalation of toxic gases and near drowning. Indirect ALI/ARDS is caused by systemic inflammation with generalised activation of mediators, inflammatory cells and endothelium due to infection (sepsis, peritonitis), tissue ischaemia (necrosis, pancreatitis) or tissue damage (trauma, cardio-pulmonary bypass, major surgery and some intoxications). Animal experiments and recent clinical studies have shown that ALI/ARDS might also be due to, or be accentuated by inadequate mechanical ventilation. The independent risk factors for ARF are old age, infection and neurological disease. Because ALI/ARDS is due to an underlying disease process, its treatment together with the patient’s concomitant diseases and genetic disposition are major determinants for the course of the lung condition and its outcome.

Klinické známky ARDS, ALI postupně 3 fáze: nekardiogenní plícní edém, zánět (nebakteriální), fibrosa pokles poddajnosti plic, snížení funkční reziduální kapacity, kolaps a zalití alveolů tekutinou, atelektázy- převážně basálně, dependentně intrapulmonální arteriovenosní shunt Plícní manifestace a symptomy cyanosa tachypnoe dyspnoe chrůpky mimo plícní manifestace příznaky základního onemocnění: trauma, šok …. ALI/ARDS, like all other inflammatory processes, develops over time, in at least three phases.  An initial acute first phase of some days to a week characterised by noncardiogenic pulmonary oedema due to capillary leakage.  A second phase of one to two weeks with an inflammatory reaction and organisation of the oedema (hyaline membranes).  A third phase in which fibrosis and structural changes in lung tissues dominate. However, fibrosis and organisation of the oedema may start very early in the process, so that the three phases overlap to some extent. The pulmonary symptoms are due to the pathophysiological alterations on the lungs of ALI/ARDS. The interstitial and alveolar oedema formation causes the extravascular lung water (EVLW) to rise, resulting in increased stiffness of the lungs (reduction of compliance), decrease in functional residual capacity as well as increased intrapulmonary shunting. These changes are augmented by development of basal compression atelectasis produced by the weight of the wet heavy lung. The tendency to atelectasis formation is exaggerated by increased intra-abdominal pressure, which is common in secondary ALI/ARDS. The clinical signs are minor initially but become more marked with the progress of the ALI/ARDS process. Clinical manifestations and symptoms Clinical manifestations and symptoms may be divided into:  Pulmonary, caused by ALI/ARDS and  Extra-pulmonary, caused by the underlying disease Pulmonary manifestations and symptoms The changes are clinically evident as:  Cyanosis due to hypoxaemia  Tachypnoea  Dyspnoea due to a higher work of breathing in order to compensate for an impaired gas exchange  High-pitched crackles heard in all lung fields Extra-pulmonary manifestations and symptoms The underlying process might dominate the clinical picture in the early phase of ALI/ARDS. In trauma, local signs, pain and circulatory shock are prominent and in sepsis, fever and laboratory and clinical signs of impaired perfusion are important manifestations.

ARDS- labor. a RTG diagnostika hypoxemie, hypokapnie, později hyperkapnie a respirační acidosa, pokles poddajnosti respiračního systému bilaterální infiltráty Ascertain the diagnosis: laboratory tests and imaging diagnostics According to the definitions, the diagnosis of ALI/ARDS is established by:  The medical history: acute onset of respiratory failure in combination with an underlying condition which has the potential to initiate a pulmonary inflammation.  A recent frontal chest radiograph showing bilateral infiltrates.  A clinical examination (and medical history), echocardiography or pulmonary artery catheterisation (PCWP <18 mmHg) excluding significant left ventricular heart failure.  An arterial blood sample together with measurement of FiO2, showing a PaO2/FiO2 ratio <27 kPa for the diagnosis of ARDS and between 27 and 40 kPa for the diagnosis of ALI. Early in ALI/ARDS, the blood gas might, in addition to hypoxaemia, show slight hypocapnia due to an increased ventilatory drive induced by increased stiffness of the lungs. In addition, the patient is usually apprehensive and might therefore hyperventilate. Respiratory acidosis develops rather late in the process and signals imminent respiratory failure. Metabolic acidosis may be seen, but this is not commonly caused by ALI/ARDS but by the underlying process (sepsis or tissue hypoperfusion). The other laboratory test results are usually non-specific and dependent on the underlying disease. It is common to find signs of inflammation and coagulopathy. In the patient on the ventilator, lung mechanics show a low compliance of the respiratory system.

ARDS , CT

Diff. dg kardiální plícní edém hypervolemie plicní embolie Zvýšený plnící tlak, onemocnění srdce , není inflamace, diagnosticky: ECHO, plicní katetr, piCCO atd. hypervolemie Pozitivní bilance tekutin, odpověď na diuretika plicní embolie Přetížení pravé komory, ECHO, CT picní angografie. Although pulmonary embolism can result in severe hypoxaemia, the main pulmonary manifestation is an increased physiological dead space (which might be seen as a sudden decrease in the end-tidal CO2 fraction). The hypoxaemia can usually be reversed by giving oxygen via a mask. D-dimers are elevated, but this finding is also common in ALI/ARDS. A chest radiograph will sometimes indicate decreased filling of the pulmonary vessels and no oedema and echocardiography may show right ventricular failure and dilation. Definite diagnosis could be obtained by ventilation/perfusion scintigraphy, spiral computed tomography or pulmonary angiography (gold standard). Cardiogenic oedema and fluid overload may give a similar radiographic and clinical picture as in ALI/ARDS. However, the medical history is important. Cardiogenic oedema develops in patients with an acute or chronic cardiac history without any recent inflammatory process. Furthermore, the filling pressures are elevated. A definite diagnosis is obtained by echocardiography. In the fluid overloaded patient after surgery the fluid balance during the anaesthesia and surgery is positive and the filling pressures are elevated. The patient responds quickly to small doses of diuretics. However, since ALI/ARDS might be caused by surgery or surgical complications it is important to be vigilant in patients with respiratory symptoms after surgical procedures.

ventilační podpora u ARDS, ALI Cíle saturace O2>90%, paO2 >8 kPa pH 7,2-7,4 protektivní ventilace prevence ventilatory induced injury- VILI inspirační tlak menší než 32 (35) cm H2O PEEP - positive end expiratory pressure, pozitivní tlak na konci výdechu Strategy of ventilatory support (lung protective ventilatory strategy) See also the PACT module on Mechanical ventilation The goal for ventilatory therapy in ARF is to provide an adequate gas exchange (usually PaO2 >8 kPa, oxygen saturation of haemoglobin in arterial blood (SaO2) >90% and pH 7.2-7.4) without causing additional iatrogenic damage to lungs and other organs, i.e. a lung protective ventilatory strategy. In this context it is important to recognise that a ventilator can only replace the work done by respiratory muscles and not the gas exchange function of the lungs. However, by using lung recruitment manoeuvres, positive end-expiratory pressure and changing the inspired oxygen concentration, gas exchange may be improved and supported.

zahájení ventilace u ARDS , ALI okamžitě při těžkém progredujícím stavu respirační frekvence 30-35/min paO2 =7-8 kPa při O2 maskou vzestup paCO2 , nebo pH <7,3 Spotřeba kyslíku a produkce CO2 stoupá o 6-10% na 1°C When to initiate ventilatory support? Initially, the symptoms in ARF may be subtle. They may become more pronounced with time as a consequence of lung function deterioration as well as an increased metabolism with higher demand for oxygen and increased production of carbon dioxide.  All patients with ARF should immediately receive oxygen via a mask.  If hypoxaemia persists and the clinical condition does not improve rapidly more active measures are urgent.  If the patient has concomitant conditions, compromising cardiopulmonary function, active measures should be considered early. The mean inspired oxygen concentration via a standard face mask is only 40-50% with 10-15 l O2 /min The patient’s clinical condition is more important than the values obtained by blood gas analysis in deciding when to start ventilator treatment.  If the patient is fully awake, haemodynamically stable and is not fatigued there is no immediate need of ventilator support even if blood gases may indicate slight hypoxaemia. However, because almost all patients with ARDS require some form of ventilatory support, ventilator therapy should always be considered early in the disease process.  If the patient is exhausted, has a respiratory rate above 30-35/min, blood gases indicate hypoxaemia (PaO2 <7-8 kPa) on oxygen via mask, an increasing carbon dioxide pressure in the arterial blood (PaCO2) or pH is below 7.3 (showing that the patient cannot maintain a normal pH by spontaneous breathing) ventilator therapy should be initiated expediently.  If the patient is haemodynamically unstable but can maintain PaO2 above 8 kPa on oxygen via mask, haemodynamic support is indicated under careful ventilatory monitoring before invasive ventilatory support (intubation) is initiated. Oxygen consumption and CO2 production increase by 6-10% per °C

ventilace u ARDS většinou intubace a umělá plícní ventilace , UPV neinvazivní ventilace NIV (= ventilace maskou bez intubace) pokud pacient při vědomí, kooperativní hemodynamicky stabilní není vyčerpaný okamžité ukončení NIV a intubace pokud nedojde ke zlepšení za hodinu Non-invasive ventilation (NIV) with continuous positive airway pressure (CPAP) may be considered in otherwise stable patients with hypoxaemia and without CO2 retention. Non-invasive positive pressure ventilation (NIPPV) is otherwise the preferred method in patients with ARF. NIPPV can only be considered if the staff members are experienced with the method and if the patient is:  Fully conscious  Cooperative  Haemodynamically stable  Tolerant of short periods without ventilatory support  Able to take adequately large breaths  Not fatigued

indikace intubace a UPV u respiračního selhání obecně těžká hypoxemie , paO2 < 6-7 kPa respirační acidosa , pH 7,2, pCO2 9-10 kPa bezvědomí, nebo porucha vědomí s neschopností udržet průchodné dýchací cesty CNS postižení akutní chirurgický výkon The indications for intubation in ARF are:  Inadequate gas exchange with non-invasive means (oxygen via mask or NIV) or  When NIV is contraindicated or believed to be insufficient, e.g.  Severe hypoxaemia (PaO2 <6-7 kPa)  Severe respiratory acidosis (pH <7.2, PCO2 > 9-10 kPa)  Semi-or unconsciousness or unable to keep upper airways free  Concomitant central nervous system compromise (head injury, brain oedema due to meningitis or intracerebral bleeding, spinal injury)  Acute surgery

UPV u ARDS VCV nebo PCV FiO2 co nejnižší inspirační tlaky mezi 30-35 cm H2O dechový objem 6-8 ml/kg ideální váhy recruitment- otevření kolabovaných alveolů PEEP 8-15 cm H2O prevence kolapsu, může způsobit hyperinflaci zdravých alveolů nastavuje se podle: dosažení nejlepší oxygenace, nebo nejlepší compliance nebo podle tabulek recruitment manévry (krátkodobé zvýšení tlaků, otevřít plící a nechat otevřenou) prone position

Další terapie léčba základního onemocnění prevence hypervolemie- pokud lze tak spíš restrikce tekutin nutrice ATB jen při infekci steroidy NE v akutní fázi (zvažovaný ve fázi fibrózy) rescue terapy: Extracorporeal Membrane Oxygenation surfaktant – u dětí

Komplikace barotrauma při UPV pokles kardiálního výdeje infekce , ventilátorová pneumonie VILI

COPD, asthma

základní patofyziologie limitace expiračního toku plynů při vzestupu rezistence malých cest dýchacích hyperinflace alveolů, plic expirace příliš dlouhá (asthma) , dynamická hyperinflace kolaps dýchacích cest (COPD) air trapping podání kyslíku u COPD může zvýšit paCO2 odstranění hypoxického stimulu, zrušení plicní hypoxické vazokonstrikce exacerbace je nutnost změny terapie při zhoršení kašle, dušnosti či produkci sputa The chain of events The hallmark of COPD is a mainly irreversible expiratory airflow limitation caused by either an increase in the resistance of the small conduction airways, or an increase in lung compliance due to emphysematous lung destruction, or both. The product of resistance and compliance (the ‘time constant’, reflecting the time necessary for lung emptying) is always increased in COPD patients, and is best reflected by measurements of the FEV1 (the maximal volume that can be expired in one second) and its ratio to the forced vital capacity (FEV1/FVC). There are two pathophysiological mechanisms leading to hyperinflation:  Increased airway resistance, which impedes airflow and can lead to so-called dynamic hyperinflation if expiratory time is too short to exhale the whole tidal volume (predominant in asthma). We will refer to this as ‘without expiratory flow limitation (EFL)’ or ‘without EFL’ during normal, quiet tidal volume expiration.  Airway collapse, leading to an airflow stop in the airway concerned and potentially to so-called air-trapping (predominant in COPD); we will refer to this as ‘with expiratory flow limitation’ or ‘with EFL’ during normal, quiet tidal volume expiration. There is no universal answer. According to the American Thoracic Society, an exacerbation of COPD is an event in the natural course of the disease characterised by a change in the patient's baseline dyspnoea, cough and/or sputum beyond day-to-day variability, sufficient to warrant a change in management.

hyperinflace , autoPEEP tlak v alveolech na konci výdechu pozn. na ventilátoru se měří externí PEEP, autoPEEP lze změřit aplikací expirační pauzy

COPD, asthma

Klinický nález COPD astma- život ohrožující stav únava paradoxní torakoabdominální dýchání zapojení pomocných svalů respirační acidosa astma- život ohrožující stav tiché dýchání zmatenost ,koma bradykardie, hypotenze PEFR neměřitelný neschopnost mluvit tachykardie >120/min >30 dechů /min pokles systolického tlaku během inspirace >20 mmHg Clinical findings (COPD) Drowsiness, intercostal retractions, paradoxical thoraco-abdominal movements, and use of auxiliary muscles are important clinical findings in assessment of exacerbation severity. The best predictor of impending respiratory exhaustion is the occurrence of respiratory acidosis, and in particular its progression over time. It is of paramount importance to perform an arterial blood gas analysis, and to compare the results to the results of previous analyses, if available. Clinical findings (asthma) Immediately life-threatening clinical features are: Silent chest, weak respiratory efforts and cyanosis Confusion or coma Bradycardia and hypotension Peak expiratory flow rate (PEFR) unmeasurable Clinical signs of severe asthma are: Inability to complete sentences in one breath Respiratory rate (RR) >30/min Tachycardia >120/min PEFR <50% of predicted normal or of best normal if known (<200 l/min if not known) Arterial paradox (the fall in systolic pressure on inspiration) >20 mmHg See also the figure on page 109 of the NAEPP Expert Panel Report 2 (1997).

PACT ESICM

Terapie, astma inhalační bronchodilatancia kortikoidy (asthma) O2 ventilační podpora Heliox MgSO4 ketamin inhal anestetika

Asthma. Short-acting b2-agonist

Asthma , anticholinergika

Ashtma, iv terapie- poslední mžnost

Asthma - kortikoidy

Indikace ventilační podpory COPD (2 příznaky nejméně) dyspnoe, použití akcesorních svalů hyperkapnická acidosa více než 25 dechů/min Astma -zhoršení příznaků udržení oxygenace změna vědomí změna řeči, polohy pokles dechové frekvence The indications for ventilatory support (two out of three should be present) include:  At least moderate dyspnoea, with use of accessory muscles and paradoxical abdominal motion  Hypercapnic acidosis (pH <7.35)  Respiratory frequency >25 breaths per minute In asthma, the primary goal of intubation and mechanical ventilation is to maintain oxygenation and prevent respiratory arrest; thus intubation should not be deferred too long, but should rely on worsening of clinical signs (changes in alertness, speech and posture as well as respiratory rate decrease, for instance). Once a decision to intubate has been made, the goal is to gain rapid and complete control of the patient’s cardiorespiratory status. The most experienced physician available should handle the intubation.

Závěr lepší je noc na ICU než 100 let v hrobě

UPV, astma, COPD problém hyperinflace , vysoké inspirační tlaky- riziko barotraumatu astma PEEP 0 COPD PEEP 5 zkrátit inspirium (I:E) permisivní hyperkapnie