1 Pathophysiological principles of respiratory insufficiency, oxygen therapy and mechanical ventilation MUDr. MSc. Michal Šitina, PhD. Department of pathological physiology, MUNI Department of anaesthesia and intensive care medicine, FNUSA Biostatistics, ICRC-FNUSA 2 Contents 1. Basics of respiratory (patho)physiology 2. Principles of mechanical ventilation 3. Applied pathophysiology of MV in clinical cases 4. Exact analysis of mechanisms of respiratory insufficiency 3 Mechanisms of respiratory insufficiency 4 Mechanics of spontaneous breathing ▪ pressure in area of lips approx. 0 ▪ active inspiration ▪ diaphragm, intercostal muscles ▪ negative intrapleural pressure ▪ spontaneous expiration ▪ positive intrapleural pressure 5 Important quantities and terms ▪ FiO2 (21 %) ▪ PaO2 (> 80 mmHg, hypoxemia vs. hypoxia) ▪ PaCO2 (35-45 mmHg, hypo/normo/hypercapnia) ▪ tidal volume (≈500 ml) ▪ respiratory rate (≈ 12-16/min) ▪ anatomic dead space (150 ml) 6 Physical principles ▪ resistance▪ compliance▪ pressure vs. pressure difference 7 Respiratory insufficiency ▪ type 1 – oxygenation dysfunction - hypoxemia without hypercapnia ▪ type 2 – ventilation dysfunction – hypercapnia with hypoxemia Mechanisms of respiratory insufficiency ▪ global hypoventilation ▪ impaired diffusion across alveolocapillary membrane ▪ dead space ▪ intrapulmonary (or extrapulmonary) shunt ▪ ventilation-perfusion (V/Q) mismatch 8 Mechanisms of respiratory insufficiency ▪ hypoventilation, diffusion, dead space, shunt, V/Q mismatch Capnometry ▪ monitoring of breathing ▪ 100 % verification of correct tracheal intubation 9 PaCO2 x EtCO2 = CO2-gap ▪ increased with pulmonary pathology x x 10 11 Oxygen therapy ▪ oxygen delivery ▪ principle: increased FiO2 ▪ corrects hypoxemia ▪ no correction or impairment of hypercapnia ▪ sometimes almost no effect 12 Oxygen therapy ▪ Why impairment of hypercapnia? ▪ Why sometimes almost no effect? 13 Principles of mechanical ventilation 14 Mechanical ventilation ▪ ventilation using ventilator replacing a part or a whole work of breathing of a patient ▪ therapeutic goals ▪ correction of hypoxemia ▪ correction of hypercapnia ▪ decrease in work of breathing ▪ hemodynamic stabilisation ▪ airways protection ▪ performance of an operation ▪ … 15 Principle of mechanical ventilation ▪ active inspiration ▪ positive pressure in airways created by ventilator ▪ passive expiration ▪ just as in spontaneous breathing 16 Principle of mechanical ventilation 17 What can we set on the ventilator? ? FiO2 PEEP rate of breathing duration ration of inspirium/exspirium tidal volume inspiratory pressure level of triggering 18 What do we monitor? SaO2 blood gas analysis EtCO2 pressure flow volume 19 Monitoring of MV Analysis of MV curves ▪ modes of MV ▪ volume controlled ▪ pressure controlled ▪ pressure support ▪ SIMV ▪ … 20 21 volume controlled ventilation (CMV) ▪ we set ▪ breath rate ▪ tidal volume ▪ length of inspirium ▪ length of inspiratory pause 22 volume controlled ventilation (CMV) ▪ we set ▪ breath rate ▪ tidal volume ▪ length of inspirium ▪ length of inspiratory pause 23 PCV 24 PCV 25 Curves of MV 26 CPAP/PSV 27 PCV versus PSV PEEP (positive end-expiratory pressure) ▪ the lowest pressure in airways ▪ prevents alveolar collapse (called atelectasis) ▪ both too low and too high values are harmful ➢ it is necessary to find the optimal value 28 Influence of PEEP on lung aeration 29 30 p-V curve and PEEP 31 p-V curve and PEEP 32 Effects on cardiovascular system ▪ decreases venous return and subsequently the cardiac output ▪ affects pulmonary hypertension and so the right ventricle function ▪ can help the failing left ventricle ▪ decreases oxygen consumption in respiratory muscles Effects on other systems ▪ significant influence on acid-base balance (CO2) ▪ decreases renal blood flow and so promotes fluid retention ▪ increases intraabdominal pressure and reduces splanchnic perfusion ▪ can increase intracranial pressure ▪ „motor“ of multiorgan failure Effects of MV on other systems Ventilator induced lung injury (VILI) !!! inappropriate ventilation can damage lungs 33 How can MV damage lungs? ▪ large distension tears pulmonary structures ▪ econdary inflammatory reaction and fibrosis ▪ danger of lung perforation in thin areas -> pneumothorax ▪ shear forces on the boundary of ventilated and nonventilated areas of lungs ▪ elimination of natural immune barriers ▪ ventilator-associated pneumonia ▪ risks of intubation and airway management ▪ promotion of muscle weakness of critically ill patients ▪ necessary sedation 34 35 Non-invasive ventilation ▪ just as mechanical ventilation, but ▪ patient is not (deeply) sedated ▪ airways are not secured ▪ impossible to use high PEEP or inflation pressures ▪ short-term or repeated usage ▪ typical indications ▪ acute COPD exacerbation ▪ moderate cardiogenic pulmonary edema ▪ intermittent support after extubation 36 PSV at NIV Administration of prostacyclin ▪ prostacyclin causes dilatation of pulmonary arterioles and thus reduces pulmonary hypertension ▪ can be inhaled or administered intravenously ▪ in patients with respiratory insufficiency, just one of both routes of administration improves respiratory insufficiency which one and why? 37 38 Applied pathophysiology of MV in clinical cases 39 MV in clinical cases ▪ Pulmonary edema by acute myocardial infarction ▪ COPD exacerbation ▪ Intubation and MV by polytrauma ▪ Massive pulmonary embolism ▪ ARDS – COVID-19 pneumonia 40 Pulmonary edema by acute myocardial infarction 41 Interstitial vs. alveolar pulmonary edema 42 Pulmonary edema by acute myocardial infarction 43 Acute exacerbation of COPD COPDnorma 44 Acute exacerbation of COPD 45 COPD exacerbation 46 Auto-PEEP 47 Major trauma 48 Intubation and MV by polytrauma 49 Pulmonary embolism – angio CT 50 Pulmonary embolism - echocardiography 51 Massive pulmonary embolism 52 ARDS – COVID-19 pneumonia ▪ protective ventilation ▪ permissive hypercapnia (pH >7.2) ▪ prone position High-flow nasal oxygen53 High-flow nasal oxygen (HFNO) ▪ just as nasal cannula, but ▪ humidified oxygen up to 60 l/min ▪ FiO2 up to 100 % ▪ high flow of gases builds up excess pressure in upper airways and so the PEEP 2-4 cmH2O ▪ better tolerated than NIV ▪ similar indications as NIV ▪ moderate COVID-19 pneumonia ▪ acute COPD exacerbation ▪ moderate cardiogenic pulmonary edema ▪ intermittent support after extubation ECMO54 Extracorporeal membrane oxygenation (ECMO) ▪ extracorporeal circuit ▪ up to complete substitute of lungs (VV-ECMO) or heart and lungs (VA-ECMO) ▪ construction based on pump and oxygenator ▪ in oxygenator blood and air/oxygen come to contact over a membrane ▪ Indication ▪ reasonable chance of solution of the basic problem (as e.g. cure of COVID pneumonia) or bridge-to- transplantation ECMO55 Extracorporeal membrane oxygenation (ECMO) variants ECMO56 Principle of membrane oxygenator Apneic ventilation ▪ apneic test of brain death 1. the patient breathes O2 through the mask, creating an oxygen reserve in the lungs 2. general anaesthesia and muscle relaxation 3. the patient is not breathing, but we continue to administer O2 How long does it take for the patient to desaturate? The lung O2 reserve (5 l) would be sufficient for a maximum of 20 min at 250 ml O2 /min. Up to 60 minutes!! 1+1 = 3 ?? 57 58 Apnoic ventilation Apnoic ventilation59 60 Life-threatening respiratory disorders ▪ Cardiogenic pulmonary edema ▪ Non-cardiogenic pulmonary edema – ARDS ▪ Severe pneumonia ▪ Exacerbation of COPD/asthma ▪ Tension pneumothorax ▪ Upper airway obstruction ▪ Allergic edema ▪ Laryngitis ▪ Epiglotitis ▪ Aspiration ▪ Massive pulmonary embolism ▪ Coma with secondary asphyxia ▪ Acute neuromuscular disorders ▪ Myasthenia gravis ▪ Syndrome Guillain-Barré ▪ Thorax trauma ▪ Lung contusion ▪ Block rip fracture ▪ Massive hemothorax ▪ Massive haemoptysis