Catherine Jones Practice Educator Respiratory Failure

Have you ever looked after a patient with Respiratory Failure? Most will – very familiar condition on the wards & most days on ICU – pneumonia, post op chest sepsis, pulm oedema, neoro conditions – reduced drive, asthma …

Learning Outcomes Causes of Respiratory Failure Define the term respiratory failure Type 1 Respiratory failure Type 2 Respiratory Failure Adult Respiratory Distress Syndrome

CO2 O2 Major function of airways is to WARM, FILTER & HUMIDIFY AIR The major function of the lung is to get oxygen into the body and carbon dioxide out. Respiratory Failure occurs when Pulmonary system is unable to achieve this to meet metabolic needs of body. O2 in – depends on partial pressure of oxygen, diffusing capacity, perfusion & V/Q CO2 out depends on alveolar ventilation (RR & VT) & deadspace (Anatomical & physiological)

RESPIRATORY FAILURE OCCURS WHEN THE RESPIRATORY SYSTEM IS UNABLE TO MAINTAIN GAS EXCHANGE TO MEET METABOLIC DEMANDS OF BODY CO2 O2 Major function of airways is to WARM, FILTER & HUMIDIFY AIR The major function of the lung is to get oxygen into the body and carbon dioxide out. Respiratory Failure occurs when Pulmonary system is unable to achieve this to meet metabolic needs of body. O2 in – depends on partial pressure of oxygen, diffusing capacity, perfusion & V/Q CO2 out depends on alveolar ventilation (RR & VT) & deadspace (Anatomical & physiological)

Types of Respiratory Failure Oxygenation failure (Type 1) Acute Often life threatening Ventilation failure (Type 2) Chronic (usually) Compensation mechanisms

Type 1 Respiratory Failure British Thoracic Society (2002) Acute Hypoxaemic Respiratory Failure Pa O2 < 8 KPa HYPOXIA Pa CO2 < 6 KPa SaO2 < 92% Life threatening hypoxaemia Impairment to gas exchange normal CO2 can be maintained; CO2 more soluble than oxygen so can perfuse adequately across increased fluid barrier

Causes of Type 1 Respiratory (Oxygenation) Failure Decrease in partial pressure of inspired O2 Ventilation/Perfusion (V/Q) Mismatch Impaired Diffusion Alveolar Hypoventilation

FIO2 Ventilation without perfusion (deadspace ventilation) Hypoventilation Diffusion abnormality Normal Perfusion without ventilation (shunting)

Dead Space Ventilation Each breath will have an element of dead space 2 components: Anatomical: Volume which never meets alveolar/capillary membrane – conducting airways, ETT tube, ventilator tubing & gubbins Alveolar: Volume reaching alveoli which are not perfused so gas exchange cannot occur

Type 2 Respiratory Failure British Thoracic Society (2016) Acute Hypercapnic Respiratory Failure Pa O2 < 8 Kpa Hypoxaemia –mild; easily corrected Pa CO2 > 6.5 Kpa pH < 7.35 SaO2 < 92%

Causes of Type 2 Respiratory (Ventilatory) Failure Insufficient respiratory drive Hypoventilation most common cause of hypercapnia Dead space (wasted ventilation) Structural abnormalities of chest wall Neuro- muscular dysfunction Obesity COPD

Causes of Type 2 Respiratory (Ventilatory) Failure Capacity, Load & Drive: For effective ventilation, respiratory muscle pump must have capacity to sustain ventilation against a given load It also requires a neural drive from central nervous system Severe derangements of load, drive or capacity can lead to development of ventilatory failure

Abnormalities of CAPACITY Not a constant Intrinsic weakness of respiratory muscles = reduced capacity Weakness may be irreversible if due to: Neuromuscular disease (NMD) Weakness may be reversible if due to: Electrolyte disturbance (& malnutrition) Hypoxia Hypercapnia Acidosis 14

Abnormalities of LOAD Load against which the respiratory muscle pump works (& not a constant) Excessive load due to: Reduced compliance of chest wall (e.g. scoliosis) Reduced compliance of lungs (e.g. atelectasis, obstructive airways disease) Changes to load due to: Sputum Fluid retention Increased airflow obstruction Normal circadian physiological changes (loss of upper airway muscle tone during sleep leads to increased upper airway resistance) 15

Abnormalities of DRIVE Neural drive reduced by: Structural & Metabolic abnormalities of respiratory control centre in brain stem Loss of wakefulness drive Chronic nocturnal hypoventilation Sedative drugs 16

Ventilatory Failure Severe derangements of load, drive or capacity (or any combination of these factors) can lead to development of ventilatory failure Acute asthma: respiratory muscle pump (capacity) is working against intolerable load (but normal drive) Sedative drugs: Apnoea (reduced drive) even though lungs (load) and respiratory muscles (capacity) are normal 17

Adult Respiratory Distress syndrome Direct/Indirect Injury to Lungs: Pulmonary Oedema Inflammatory Infiltrates Surfactant Dysfunction Risk factors: Direct: Pneumonia; Aspiration of gastric contents; lung contusion; fat emboli; drowning; inhalational injuries. Indirect: Non-pulmonary sepsis; multiple trauma; massive transfusion; pancreatitis Effects: Hypoxaemia Decreased Compliance Collapse/consolidation Pulmonary hypertension

WHAT MIGHT HELP? Ferguson et al (2012) The Berlin Definition of ARDS an expanded rationale, justification & supplementary material Intensive Care Medicine 38 P. 1573-1582

Final thoughts You will all definitely see lots of respiratory failure with varying degrees of severity. Use your assessment skills to help you understand what has caused… but also what might help…

References British Thoracic Society Standards of Care Committee (2002) Non- invasive ventilation in acure respiratory failure. Thorax; 57: 192 – 211. O’Driscoll et al (2008) Guideline for emergency oxygen use in adult patients. Thorax; 63: Supp VI. Coombs et al (2013) Assessment, monitoring & interventions for the respiratory system. In Mallett, Albarron & Richardson Eds: Critical Care Manual of Clinical Procedures & Competencies. (Wiley & Sons, West Sussex) Intensive Care Foundation (2015) Handbook of Mechanical Ventilation – A Users Guide (Intensive Care Society, London) file:///C:/Users/User/Downloads/Ventilation%20handbook%20(1).p df (downloaded August 2016) 23

Ventilation/Perfusion (V/Q) Matching Distribution of blood flow (Q) and ventilation (V) is closely matched. This minimises physiological dead space & so optimises gas exchange