Approach to type 2 Respiratory Failure

Approach to type 2 Respiratory Failure

Changing Nature of NIV Not longer just the traditional COPD patients Increasingly Obesity Neuromuscular Pneumonias 3 fold increase in patients with Ph 7.25 and below

Impact Changing guidelines Increased complexity Increased number of patients Decreased threshold for initiation Lower capacity for ITU to help Higher demands on nursing staff

Resp Failure Type 1 Failure of Oxygenation Type 2 Failure of Ventilation Hypoventilation Po2 <8 Pco2 >6 PH low or bicarbonate high

Ventilation Adequate Ventilation Breathe in deeply enough to hit a certain volume Breathe out leaving a reasonable residual volume Breath quick enough Tidal volume and minute ventilation

Response to demand Increase depth of respiration Use Reserve volume Increase rate of breathing General increase in minute ventilation More gas exchange

Failure to match demand Hypoventilation Multifactorial Can't breathe to a high enough volume Can't breath quick enough Pco2 rises Po2 falls

Those at risk COPD Thoracic restriction Central Neuromuscular Acute aspects Over oxygenation Pulmonary oedema

Exhaustion Complicates all forms of resp failure Type one will become type two Needs urgent action Excessive demand Unable to keep up Resp muscle hypoxia

Exhaustion Muscles weaken Depth of inspiration drops Residual volume drops Work to breath becomes harder Spiral of exhaustion Pco2 rises, Po2 drops

Type 2 Respiratory Failure Management

Identifying Those at Risk Pre-existing conditions Acute factors Bronchoconstriction/Pulmonary oedema Hypoxia Superimposed problems Metabolic acidosis Low cardiac output

Recognising the problem Pick them up early- plan escalation Confusion Flap Signs of exhaustion Agitation, High HR, High BP Sweaty

Why are they in type two? Don t assume Multifactorial Examination- wheeze, opiods, oedema EARLY x-ray- Pneumothorax ECG- Myocardial infarction Bloods- Metabolic, BM, TSH

Simple Measures Reduce work of breathing Sit them up- 45 degree angle Good sputum clearance Enough oxygen- 88-92%? hypoxia will kill you first Avoid resp depressants Max cardiac output

Treat underlying cause Bronchospasm Reduces air trapping and V/Q mismatch Lots of nebs, magnesium, aminophyline Pleural disease drain pneumothorax/effusions Cardiac output fluids/inotropes

Non Invasive Ventilation Augmenting patients breathing without an ET tube Maximises Inspiratory volume (maintains tidal volume) Stops airway collapse Can control rate of breathing Reduces the work of breathing

NIV Bilevel positive pressure ventilation Maintaining the volume in the lungs between two ideal levels Applies pressure at maximum ventilation (ipap) Applies pressure at maximum expiration to splint airways (epap)

NIV- Does it work Up to 70% reduction in work of breathing Improved mortality over invasive ventilation Reduced Invasive ventilation Hospital mortality Length of stay Mortality static over 10 years Effective in the elderly

Role of NIV Support tiring patient at early stage Treat type two resp failure to avoid invasive ventilation Ceiling of treatment when invasive ventilation is inappropriate Palliation

Timing of NIV Is the PH <7.35 Is the Pco2 >6.5 (i.e. do they have a respiratory acidosis) Is their oxygen appropriate for the patient? Have you treated the correctable factors for 30-60mins? If so consider starting NIV

Timing of NIV Maximise for an hour? Mild to Moderate Acidosis COPD 20% will improve Delay of more than hour is harmful Delay in other patient groups Poorer outcomes

Timing of NIV Maximise one hour if Simple copd exacerbation Ph 7.25 or above Capacity for review in one hour Capacity for immediate initiation of NIV No signs of exhaustion

Contra indications to NIV Very few No longer Low ph Low GCS Mainly indications for Invasive ventilation Facial injuries Poor upper airway Uncontrolled bowel obstruction- NG tube

Who should be invasively ventilated 1) Reversible pathology 2) Remains active 3) Reasonable muscle bulk And don t forget 4) Patients wishes Contact early!!

Decision Time Is this patient more appropriate for consideration for immediate invasive ventilation? Poor upper airway very hypoxic severe sepsis bowel obstruction Not PH or decreased GCS

Decision Time Is the patient suitable for NIV but should be considered for ITU if fails NIV? Protect respiratory muscles Prevent VAP Protect against muscle wasting Protect against ITU Psychosis Patients do better on NIV

NIV as a Trial Best done in ITU Ph < 7.15 Decreased GCS Confusion Pneumonia Delayed intubation = increased mortality Make decisions early and be proactive

Special Circumstances Pulmonary Oedema Works May not keep them alive long term Asthma Just don't Pneumonia If not for ITU

Where to NIV? Initiation shouldn t be delayed Specialist Unit Appropriate staffing Trained Nurses Capacity to do regular obs 2-1 nursing Level 2-3

Setting up Mode Bilevel/bipap/pressure support Ipap High pressure used to fill the lung Epap Low pressure use to keep lungs open Difference Ipap and Epap = Tidal volume

IPAP Vs EPAP IPAP controls depth of ventilation Bigger gap between ipap and epap = deeper ventilation Therefore IPAP controls PCO2 EPAP overcomes stiff and noncompliant lungs and airways EPAP and help oxygenation

Rule of thumb Initial settings Start IPAP -15 EPAP 3 Review patient clinically. Is their chest rising? Is their heart rate and BP improving? Are they working less hard to breath? If not titrate up IPAP in 2cm increments

Rule of thumb Are their sats low? Is their chest barely moving? Is the apnoea alarm buzzing at you? If any of yes to any of these increase both the EPAP and IPAP by 2 increments. Once your happy repeat ABG in 1 hour

Oxygen Continue to aim 88-92% Supply oxygen through mask or tubing Difficult to predict how much they need Machine looses a lot of oxygen Patient is ventilating better Start high and titrate down

Failing on NIV High respiratory rate, High BP High pulse Agitation Working hard to breath with accessory muscles Sweating

Pco2 not coming down Inadequate ventilation Assess airway Sit patient up Treat underlying cause Increase IPAP Repeat ABG

Po2 Poor Maximise ventilation Increased inspired Oxygen Increase EPAP and IPAP until chest rising Treat underlying cause Reassess for pneumothorax/mucus plugging

Conclusion Changing nature of patients Reduce work of breathing Early planning-?itu Early initiation-?wait until acidotic Very few contraindications