Respiratory Failure how the respiratory physicians deal with airway emergencies

Respiratory Failure how the respiratory physicians deal with airway emergencies Dr Michael Davies MD FRCP Consultant Respiratory Physician Respiratory Support and Sleep Centre Papworth Hospital NHS Foundation Trust Physiology of respiratory failure Basics of acute respiratory support Non-invasive ventilation The acutely ill patient with COPD Asthma Morbid obesity The failing heart Acute Respiratory Failure Acute Respiratory Failure Lung Failure I II Pump Failure Lung Failure I Hypoxaemia Hypercapnia Hypoxaemia OXYGEN TRANSPORT NOT TIGHTLY REGULATED PaO 2 < 8kPa PaO 2 > 6kPa PaO 2 < 8kPa The oxygen cascade Supplying more oxygen = easy Improving Tissue Hypoxia = more complex air SUPPLY DELIVERY PaO 2 kpa alveoli capillary arterial tissue cellular Oxygen CPAP Cardiac output functioning alveolar units Hypoxia atmosphere mitochondria Invasive ventilation Haemoglobin

Acute Respiratory Failure PUMP FAILURE II PaCO 2 Alveolar ventilation Pump Failure Hypercapnia PaO 2 > 6kPa INCREASED RESPIRATORY LOAD REDUCED MUSCLE CAPACITY PaCO 2 IS TIGHTLY REGULATED REDUCED NEURAL DRIVE Acute Respiratory Failure CAPACITY MUST MEET DEMAND II Pump Failure Ventilation in REM sleep Ventilation throughout sleep Daytime hypercapnia Hypercapnia Controlled oxygen PaCO 2 Non-invasive ventilation Invasive ventilation Alveolar ventilation The capacity-demand tipping point Pneumonia Previously well PaO 2 6.1, PaCO 2 8.1 ph 7.24, FiO 2 15L Intubate Pneumonia Duchenne Muscular Dystrophy PaO 2 6.9, PaCO 2 8.7 ph 7.29, FiO 2 15L Physio ++ (cough-assist) WHAT IS NON-INVASIVE VENTILATION?

Pressure What is non-invasive ventilation? Spontaneous breathing Pressure IPAP EPAP WHO MAY BENEFIT FROM? SIMPLE RULES OF THUMB TO ASSESS CHANCES OF SUCCESS Time Time 1. Pump failure > lung failure alveolar ventilation 2. Acute-on-chronic > Acute 3. If intubation greatly increases the risk of death. Physiology of respiratory failure Basics of acute respiratory support Non-invasive ventilation The acutely ill patient with COPD Asthma Morbid obesity The failing heart MANAGEMENT OF ACUTE COPD THE ACUTELY HYPERCAPNIC COPD PATIENT Severity, risk stratify, other causes (PE!) Controlled oxygen therapy Improve hypoxaemia first, then CO 2. Repeat ABGs. Bronchodilators, Corticosteroids Antibiotics If increased sputum volume/purulence Respiratory specialist care Non-invasive ventilation The ceiling of therapy? avoid therapeutic nihilism! Discharge planning Rehabilitation Home ventilatory support? A paper that changed UK practice The early use of for acute exacerbations of COPD. (YO study) Plant P, Owen J & M Elliott, Lancet ; 355: 1931-5. Is feasible in the real world? Can it be performed successfully outside the ITU?

Why it is important Why it is important 5 4 p =.2 Control p =.5 Control 5 4 p =.2 Control p =.5 Control Treatment failure In-hospital mortality Treatment failure In-hospital mortality 5 ph > 7.3 ph < 7.3 ph > 7.3 ph < 7.3 CAN BE DELIVERED ON THE WARD. 4 Treatm ent fa ilure In-hos pital mortality Why it is important GREATER BENEFIT IN MILD ACIDOSIS. EARLY IN ACUTE HYPERCAPNIC COPD SAVES LIVES, DECREASES HOSPITAL STAY AND COSTS LESS MONEY THAN STANDARD CARE 5 4 ph > 7.3 ph < 7.3 Treatm ent fa ilure ph > 7.3 ph < 7.3 In-hos pital mortality Decrease in mortality 48 Decreased rate of intubation 59 Decreased hospital stay 3 days Ram FSF et al. Cochrane Database of Systematic Reviews 4. What proportion of COPD patients need? What proportion of COPD patients receive? Not acidotic (75) Not acidotic on repeat ABG (5) Acidotic () Plant P et al. Thorax Acidotic () Roberts CM et al. Thorax 11 Plant P et al. Thorax

What proportion of COPD patients receive? (66) British Thoracic Society Audit Data collected from 925 admissions in 61 UK Hospitals (Feb March ) intubated No () COPD >> Acute Pulmonary oedema >>> Other Radiological consolidation in 34 Roberts CM et al. Thorax 11 Plant P et al. Thorax British Thoracic Society Audit Treatment plans 49 as ceiling 14 would intubate 5 palliative intent Discussed with ITU 36 patient / relative supervising cons Outcomes 27 unsuccessful 2.3 later intubated 33 no follow up plan 23 LTOT 9 home What does an acute exacerbation of COPD mean to patients and physicians? Mortality One year survival Risk Stratification? Effective treatment? Discharge meds Rehabilitation Attitudes Patient awareness Learning from Cardiology? AECOPD 25 Rarely Yes No plan Evidence, patchy Nihilism? / exasperation ACUTE MI (75 yrs) 25 Yes Yes Routine bundle Routine Active Yes THE ACUTELY HYPERCAPNIC COPD PATIENT Severity, risk stratify, other causes (PE!) Controlled oxygen therapy Improve hypoxaemia first, then CO 2. Repeat ABGs. Bronchodilators, Corticosteroids Antibiotics If increased sputum volume/purulence Respiratory specialist care Non-invasive ventilation The ceiling of therapy? avoid therapeutic nihilism! Discharge planning Rehabilitation Home ventilatory support?

Clear benefit in COPD, but who else? Severe (hypoxaemic) respiratory failure Intubation increases morbidity and mortality prevents need for intubation ACUTE IN CONDITIONS OTHER THAN COPD Avoid intubation Improve morbidity and mortality? usually no benefit when used in Hypoxaemic Respiratory Failure 8 risk of failure 7 6 Pulmonary fibrosis ARDS extrapulmonary Community acquired pneumonia ARDS - pulmonary 5 Nosocomial Atelectasis 4 Aspiration pneumonia Pulmonary contusion IS UNLIKELY TO HELP A PATIENT WITH ACUTE SEVERE PNEUMONIA. Cardiogenic pulmonary oedema Adapted from Antonelli et al Intensive Care Med 1; 27:1718-1728 EXCEPTION: Pneumonia in the immunocompromised [RESPIRATORY DIALYSIS?] failure may cause harm Acute hypoxaemic respiratory failure + fever + infiltrates. Creating an inappropriate ceiling of therapy Standard treatment (n=26) Standard treatment plus NPPV (n=26) P value Wildman et al.7. BMJ 335: 1132 Treatment failure (intubation) In-hospital mortality 77 46.3 81 5.2 Delaying intubation Demoule A et al. 6 ICM 32; 1756-65 Worst outcomes in haematological malignancy + neutropaenia. Hilbert G et al. NEJM 1; 344(7):481-487.

LIFE-THREATENING ASTHMA Steroids! Pred 4 mg po AND Hydrocort mg iv Continuous nebulised Salbutamol & 4 o Ipratropium Antibiotics +/- po Tamiflu (if <48hr of flu symptoms) MANAGEMENT OF LIFE- THREATENING ASTHMA Fluid resuscitation Magnesium, but benefit only in very severe attacks Aminophylline can be life-saving in acute severe asthma? NOT RECOMMENDED BEYOND BRIEF TRIAL IN ITU BY EXPERIENCED SPECIALISTS. SMALL SCALE CLINICAL STUDY ONLY. Soroksky A et al. Chest 3 ACUTE IN THE MORBIDLY OBESE PATIENT Obesity Trends* Among U.S. Adults 199, 1999, 8 199 1999 Obesity-related acute respiratory failure THINK OF SLEEP-DISORDERED BREATHING Infection? Pre-existing COPD? 8 PE? Cardiac? Acute hypercapnic respiratory failure No Data < 14 15 19 24 25 29 Percentage of adult population with a BMI > Previously unrecognised sleep-disordered breathing?

Hypoventilation is common in the obese and not usually recognised. 15 consecutive medical admissions no prior lung disease TIPS FOR USING IN THE OBESE PATIENT More EPAP (6-). More IPAP (often 25+). Central apnoeas. PaCO2 with BMI PaCO 2 less than 6 kpa 18 month mortality 9 PaCO 2 more than 6 kpa (31) 18 month mortality 23 ECHO -? RV function A sleep history. (Epworth Sleepiness score, snoring, witnessed apnoeas). Refer for sleep opinion (?OSAS). Nowbar et al. Am J Med 4; 116:1-7 Ventilatory support for the failing heart? RESPIRATORY SUPPORT IN LIFE-THREATENING ACUTE HEART FAILURE Pre-load After-load Alveolar recruitment Functional Residual Capacity Inspiratory muscle unloading for acute pulmonary oedema? 3CPO STUDY RESULTS 8 Volume 359:142-51 More rapid resolution of metabolic abnormalities and respiratory distress. No change in 7-day or -day mortality. CPAP or similar. CPAP usually easier. Gray A et al. NEJM 8; 359:142-51

Acute pulmonary oedema vs. acute-on-chronic exacerbation of heart failure Summary Physiology of respiratory failure Basics of acute respiratory support Framework for appropriate treatment Sys.BP >14 CPAP / Nitrates No diuretics Sys.BP -14 Sys.BP < Nitrates CPAP / Diuretics Fluid chall.? Inotropes / Pressors Chatti R et al Heart Fail Rev 7 The acutely ill patient with AECOPD (acute lung attack) Asthma Morbid obesity The acutely failing heart for acute respiratory failure Good evidence CPAP Acute hypercapnic COPD Infection in immunocompromised Obesity-related ventilatory failure Acute cardiopulmonary oedema CONCLUSIONS Applying acute MI management principles would improve the outcomes of acute lung attacks. The revolution has Improved acute COPD care. Exposed some patients to risk. ITU only caution! TRIALS OF Post-extubation ventilatory failure Acute hypoxaemic resp failure Acute asthma clinical trial needed Providing an acute service properly needs Investment but is cost-effective Integration with other departments ADDITIONAL CONTENT The following slides do not form part of the presentation but are included for completeness. Starting a patient upon is a straightforward process but there is no substitute for actually doing this. If you are responsible for patients with respiratory failure on the acute take, then I would strongly urge you to take the time to do this. WHAT MACHINE? LESS IMPORTANT THAN EXPERTISE VPAP I (YO study) Pressure Support Most (current) Pressure Control Complex (future) Volume-assured

WHAT MASK? Any full face mask in the acute situation. Standard masks Total full face masks Helmets good for pre-hospital and postoperative CPAP HOW TO START NON-INVASIVE VENTILATION Team expertise, staffing levels, location. Practical teaching - if you are expected to do something, you should have appropriate training. Set-up the kit away from the patient. Encourage slower breathing to coordinate with the ventilator. You are trying to reduce anxiety and prevent rapid shallow breathing. This would cause failure to trigger ventilation and poor tolerability. Simply reducing the trigger sensitivity may cause autotriggering. HOW TO START NON-INVASIVE VENTILATION makes sense in hypercapnia PaCO 2 = (VCO 2 / VA)k Start at low settings (IPAP 12, EPAP 4) and work up. You are aiming to reduce acidosis / hypercapnia. Increasing pressure (IPAP) will increase the volume applied and reduce CO2. Watch closely at the start Has chest wall movement improved? Repeat ABGs. Have you improved ventilation? INCREASED RESPIRATORY LOAD REDUCED MUSCLE CAPACITY REDUCED NEURAL DRIVE less likely to reverse hypoxia (hypoventilation not typical cause of hypoxia) PAO 2 = PiO 2 - (PACO 2 / RQ) PiO 2 = partial pressure of inspired O 2 V/Q inequality Shunt Hypoventilation Cardiac output functioning alveolar units Hypoxia Diffusion defect Haemoglobin