respiratory failure - clinical medicine, Schemes and Mind Maps of Clinical Medicine

Download respiratory failure - clinical medicine and more Schemes and Mind Maps Clinical Medicine in PDF only on Docsity! Respiratory failure SC2 Medicine 2021/22 Common Medical Presentations RCSI Learning outcomes At the end of this session, students should be able to: • Describe the components of an ABG • Differentiate between types of respiratory failure • Understand the mechanisms underlying type one and two respiratory failure • Interpret common respiratory ABG abnormalities • Generate a treatment plan for T1 and T2RF Case 1 1. What else do you want to know? 2. Is he in respiratory failure? Case 1 1. What else do you want to know? 2. Is he in respiratory failure? Not enough information to answer this. Why? Case 1 1. What else do you want to know? 2. Is he in respiratory failure? Not enough information to answer this. Why? You need an ABG PaO2 <8kPa on room air The Respiratory System The human respiratory system is a series of organs responsible for taking in oxygen and expelling carbon dioxide. The primary organs of the respiratory system are lungs, which carry out this exchange of gases as we breathe. Feb 12, 2018 Other receptors (e.g., pain) and emotional stimuli acting through the hypothalamus Respiratory centers (medulla and pons) ‘Stretch receptors in lungs Copyright2001 Benjamin Cummings, an imprint of Addison Wesley Longman, Inc. ‘Chest wall Shnodtte tissue, itercastal muscsee) RCSI Respiratory failure Failure to oxygenate _J PaO2 <8kPa T1RF — Respiratory failure Lung failure Pump failure Gas exchange failure Ventilatory failure manifested by manifested by hypoxaemia hypercapnia RCSI Respiratory failure Failure to ventilate PaO2 <8kPa PaCO2 >6kPa T2RF What else is on an ABG? The usuals • pH: 7.35-7.45 • PaCO2 4.7-6.0 kPa • HCO3 22-26 mmol/l • PaO2: 11-13 kPa • Lactate Other useful stuff. . . • ‘sO2’: Hb Saturation • Glucose • Chloride • Sodium • Potassium Case 2 • A 55-year-old man self refers to the ED complaining of malaise, SOB and productive cough. • He is a non-smoker. He reports a prodrome of myalgia, arthralgia, fatigue and coryzal symptoms. • On examination, crackles are audible at the right base and percussion note is dull. • HR 112 BP 110/65 Temp. 38.1 RR 20 Sp02 91% on room air ABG Results • pH 7.45 (7.35- 7.45) • PaO2 7.2kPa (11-13 kPa) • PaCO2 3.5 kPa (4.7-6.0 kPa) • HCO3 24mmol/L (22-26mmol/l) • Lactate 1.8 V/Q matching 1. V = ventilation 2. Q = perfusion 3. Normally some variation in VQ as you move from apices to bases. V/IQ mismatch From pulmonary artery Airway Alveolus Impaired f ventilation => Alveolocapillary membrane To Hypoxemia Normal W/O pulmonary vein Low WO Blocked Impaired ventilation perfusion Alveolar Collapsed alveolus Hypoxemia Shunt (very low) W/Q dead space Hypoxemia High W/Q RCSI Type one respiratory failure PaO2< 8kPa Acute on Chronic Acute Chronic Case 2 Management • Sepsis six • Supplemental O2 (91% of room air) • IV fluids • Antibiotics • Bronchodilators • +- steroids Management Supplemental O2 What are your options? Nasal Cannulae Venturi mask 100% Non-rebreather Continuous positive airway pressure (CPAP) Nasal high flow (NHF) Non-invasive ventilation (NIV / BIPAP) Management Supplemental O2 What are your options? Nasal Cannulae Venturi mask 100% Non-rebreather Continuous positive airway pressure (CPAP) Nasal high flow (NHF) Non-invasive ventilation (NIV / BIPAP) Case 3 • O/E: HR 120, Temp 37C, BP 120/60, RR 20, SaO2 80% on R/A. • O/Ausc: Bibasal coarse crackles. Pitting sacral and ankle oedema bilaterally. CXR ABG on room air • pH 7.40 (7.35 – 7.45) • PaO2 6.5 kPa (11-13) • PaCO2 5kPa (4.7 - 6) • HCO3 26mmol/L (22 – 26) • Lactate 1.5 Problem list 1. Hypoxia: T1RF, CCF background – EF 40%. Crackles & lower limb oedema 2. Alveolar shadowing consistent with pulmonary oedema 3. ?cardiac ischaemia / arrhythmia – ECG required Treatment T1RF What are your options? Nasal Cannulae Venturi mask 100% Non-rebreather Continuous positive airway pressure (CPAP) Nasal high flow (NHF) Non-invasive ventilation (NIV / BIPAP) Treatment T1RF What are your options? Nasal Cannulae Venturi mask 100% Non-rebreather Continuous positive airway pressure (CPAP) Nasal high flow (NHF) Non-invasive ventilation (NIV / BIPAP) CXR Room air ABG Ph 7.22 (7.35 – 7.45) PaCO2 14kPa (4.7 – 6) PaO2 6.8 kPa (11 – 13) Sa02 79% (>94%) HCO3 38 (22 – 26) • What’s the pattern? • What’s the mechanism? PROBLEM LIST 1. Known COPD with an exacerbation 2. Hypoxia / T2RF – saturation 82% RA / PaO2 6.8 kPa Target oxygen saturations (88-92%) & method of O2 delivery ABG suggests acidosis with chronic CO2 retention (increased HCO3) 3. Bronchospasm / wheeze Steroids, Bronchodilators 4. Low GCS / drowsy secondary to acidosis – ventilation problem Consider how this can be reversed / treated T2RF: Why does it happen? Remember: 2 Functions of the respiratory system 1. Gas exchange: Oxygenation 2. Elimination of metabolic waste (CO2) : Ventilation The patient with high CO2 must be hypoventilating as they aren’t eliminating metabolic waste appropriately Ventilation and CO2 share an inverse relationship ↑ Ventilation = ↓ CO2 ↓ Ventilation = ↑ CO2 T2RF: Why does it happen? • Ventilation is comprised of RR and Tidal volume (much like cardiac output comprises HR and stroke volume) – Tidal volume is the volume of air that moves in or out of the lungs with each breath • Alterations in either RR or Tidal volume alter ventilation and therefore CO2 • To relate to case 4: – She presented with RR of 28/min – But we know she has ↑ CO2 – Therefore, she must have a low tidal volume NIV artificially increases Tidal volume which in turn increases ventilation and decreases CO2 NIV / BiPAP Mechanism of action IPAP: Inflates EPAP: Recruits collapsed alveoli for gas exchange The Difference = Pressure Support