Mechanical Ventilation 101 Dr Paul Healey ICU Fellow John Hunter Hospital Newcastle

Outline What is mechanical ventilation ? History of mechanical ventilation. Why do we mechanically ventilate patients ? Modes of mechanical ventilation ? Setting the ventilator Trouble shooting ventilation Refractory Hypoxaemia When to extubate the patient ?

Mechanical ventilation Is a method to mechanically assist or replace spontaneous ventilation. Is a supportive therapy. Two main divisions of mechanical ventilation Negative pressure ventilation Positive pressure ventilation

Polio epidemic – Copenhagen 1952

Positive pressure ventilation

Mechanical ventilation Positive pressure ventilation Non-invasive ventilation (NIV) modes: Continuous Positive Airways Pressure (CPAP) Bi-level Positive Airways Pressure (BiPAP) Invasive positive pressure ventilation (IPPV) modes: Volume Control Ventilation (VCV) Pressure Control Ventilation (PCV) Pressure Support Ventilation (PSV)

Case study Mr CS – 75 year old male, weighs 80kg. Background IHD, Ex-smoker 20 years ago, Type II DM, AF. Day 4 post Hartmans procedure for colorectal cancer, severe abdominal pain and fever. Anastamotic leak on CT scan. Commenced on IV Tazocin. Taken to OT and had extensive washout of abdomen and stoma formed. Abdomen is closed. Currently ventilated in OT on FiO2 50% PCV-VG 14 x 480mL, with PEEP of 6cmH2O. Vital signs: HR 115, BP 110/50 on 0.2mcg/kg/min of Noradrenaline, SaO2 96%, temperature 38.8 degrees. Last ABG: pH 7.32, PaO2 92mmHg, PaCO2 35mmHg, Lactate 2.2mmol/l and BE -5.3mmol/l What is the reason for mechanically ventilating this patient ?? What are the risks of mechanical ventilation ??

Why do we mechanically ventilate patients ? Indications for mechanical ventilation Impaired level of consciousness Potential airway compromise Respiratory failure Hypoxaemic Hypercapnoeic Work of breathing and fatigue Cardiac failure

Risks of mechanical ventilation 1. Respiratory Complications Infection Ventilator Associated Events Ventilator Induced Lung Injury (VILI) Barotrauma Volutrauma Atelectotrauma Gas trapping and intrinsic PEEP Oxygen toxicity 2. Non-respiratory complications Haemodynamic compromise Raised ICP Reduced urine output Ventilator induced lung injury Excessive inflation pressurem Mechanical tissue damage Inflammation – mechano-signaling due to tensile forces Overstretching of lung units Shear force at junction of open and collapsed tissue Repeated opening and closing of small airways under high pressure

Modes of ventilation

Modes of invasive ventilation Nomenclature Triggering – what initiates a breath Ventilator Patient Inspiration Volume Pressure Cycling – what determines change from inspiration to expiration Time Flow Exhalation Passive process due to lung elastic recoil

Modes of ventilation Classification based on patient triggering: 1. Mandatory ventilation modes 2. Spontaneous ventilation modes 3. Adaptive ventilation modes Mandatory modes in the past did not allow triggering. Now they do. Spontaneous modes in the past did not allow back up ventilation, but now they do. Adaptive ventilation modes are a combination of mandatory, and spontaneous modes that adapt to the

Modes of ventilation 1. Mandatory ventilation modes Volume control ventilation (VCV) Pressure control ventilation (PCV) Synchronised Intermittent Mandatory Ventilation (SIMV)

Ventilator waveforms

Volume Control Ventilation

Modes of ventilation 1. Mandatory modes Volume control ventilation All breaths given are the same preset volume Advantages Relatively simple to set Guaranteed minute ventilation Rests respiratory muscles Disadvantages Historically, no patient triggering Ventilator-patient dysynchrony Reduced lung compliance will result in increased pressures and potential barotrauma

PCV

Modes of ventilation 1. Mandatory modes Pressure control ventilation All breaths have same preset inspiratory pressure and time Advantages Simple to set Avoids high inspiratory pressures Rests respiratory muscles Disadvantages Historically, no patient triggering Change in lung compliance results in change in tidal volumes No guaranteed minute ventilation

SIMV

SIMV

Modes of ventilation 1. Mandatory modes SIMV Advantages Disadvantages - Mandatory VCV or PCV with triggered PSV Advantages Better patient-ventilator synchrony Guaranteed minute ventilation Allows patient triggering and possible weaning Disadvantages - More complicated mode with multiple settings

PSV

Modes of ventilation 2. Spontaneous ventilation modes Pressure support ventilation Provides a set inspiratory and expiratory pressure during patient initiated breathing Inspiration ends when inspiratory flow falls to a preset level (usually 25%) Advantages Maintains full spontaneous ventilation Better ventilator-patient synchrony Weaning mode of ventilation Disadvantages Historically no back-up ventilation Changes in patient effort and lung compliance effect tidal volumes

PRVC Ventilator will adjust pressure by 3cmH2O to aim for TV. The SERVO-i will restart with the start-up sequence should one of the following criteria occur: - if the delivered Vt is 50% less than the set Vt, or when the Upper pressure limit is exceeded during 3 consecutive breaths If the measured Insp. Tidal Volume is more than 1.5 times higher than the set Tidal Volume, the breath is interrupted and the next breath is delivered with 25% reduced pressure compared with the previous breath. However, the maximum pressure decrease is 20 cmH2O. If the patient suddenly coughs during an inspiration, and if the pressure reaches the set Upper pressure limit, then the ongoing inspiration will be cut off and the next breath is delivered with the same pressure as the previous breath. TUTORIAL English

Mechanical ventilation 3. Adaptive ventilation modes Assist Pressure regulated volume control PCV - VG

Case study Mr CS – 75 year old male, weighs 80kg. Background IHD, Ex-smoker 20 years ago, Type II DM, AF. Day 4 post Hartmans procedure for colorectal cancer, severe abdominal pain and fever. Anastamotic leak on CT scan. Commenced on IV Tazocin. Taken to OT and had extensive washout of abdomen and stoma formed. Abdomen is closed. Currently ventilated in OT on FiO2 50% PCV-VG 14 x 480mL, with PEEP of 6cmH2O. Vital signs: HR 115, BP 110/50 on 0.2mcg/kg/min of Noradrenaline, SaO2 96%, temperature 38.8 degrees. Last ABG: pH 7.32, PaO2 82mmHg, PaCO2 35mmHg, Lactate 2.2mmol/l and BE -5.3mmol/l How are you going to set the ventilator ?? What other information would you want to know ??

Setting the ventilator FiO2 Mode Triggering Tidal volume Inspiratory pressure PEEP Respiratory rate Inspiratory time I:E ratio Inspiratory flow Alarm settings Peak pressure PEEP Minute ventilation

How to set a ventilator FiO2 Mode Triggering Begin at 100% and wean as quickly as able to < 60% Mode Volume controlled ventilation Set tidal volume 6 – 8 mL/kg Pressure controlled ventilation Set inspiratory pressure 10 – 20 cmH2O Triggering Flow triggering : 1 – 5 L/min Pressure triggering: -0.5 to -2.0 cmH2o Inspiratory pressure (Plateau) Aim < 30 cmH2O. VCV or SIMV = plateau pressure PCV = Sum of PEEP and Inspiratory pressure PEEP Start with 5-10 cmH20 Respiratory rate Start at 10 – 12 breaths per minute Inspiratory time Normal 0.8 – 1.3 seconds I:E ratio Normally 1:2 Increase in obstructive airways disease (COPD/Asthma) Inspiratory flow 40 – 60 L/min

Case study Mr CS – 75 year old male, weighs 80kg. Background IHD, Ex-smoker 20 years ago, Type II DM, AF. Day 4 post Hartmans procedure for colorectal cancer, severe abdominal pain and fever. Anastamotic leak on CT scan. Commenced on IV Tazocin. Taken to OT and had extensive washout of abdomen and stoma formed. Abdomen is closed. Currently ventilated in OT on FiO2 50% PCV-VG 14 x 480mL, with PEEP of 6cmH2O. Vital signs: HR 115, BP 110/50 on 0.2mcg/kg/min of Noradrenaline, SaO2 96%, temperature 38.8 degrees. Last ABG: pH 7.32, PaO2 82mmHg, PaCO2 35mmHg, Lactate 2.2mmol/l and BE -5.3mmol/l How are you going to set the ventilator ?? What other information would you want to know ??

Setting the ventilator FiO2 Mode Triggering Tidal volume Inspiratory pressure PEEP Respiratory rate Inspiratory time I:E ratio Inspiratory flow Alarm settings Peak pressure PEEP Minute ventilation

What is the evidence ??

Ventilation modes - evidence A single RCT and 3 observational trials There were no statistically significant differences in mortality, oxygenation, or work of breathing PCV lower peak airway pressures a more homogeneous gas distribution (less regional alveolar over distension) improved patient-ventilator synchrony earlier liberation from mechanical ventilation than volume-limited ventilation VCV it can guarantee a constant tidal volume, ensuring a minimum minute ventilation Most studies comparing pressure-limited and volume-limited ventilation used a square wave (constant flow) pattern for both modes. When volume-limited mechanical ventilation with a ramp wave (decelerating flow) pattern was compared to pressure-limited ventilation, lower peak airway pressures were no longer an advantage of pressure-limited ventilation

Evidence for ventilation

The trial was stopped after the enrollment of 861 patients because mortality was lower in the group treated with lower tidal volumes than in the group treated with traditional tidal volumes (31.0 percent vs. 39.8 percent, P=0.007), NORMAL MORTALITY RATE OF 40 – 60%

Twenty articles (2822 participants) were included. Meta-analysis using a fixed-effects model showed a decrease in lung injury development (risk ratio [RR], 0.33; 95% CI, 0.23 to 0.47; I2, 0%; number needed to treat [NNT], 11), and mortality (RR, 0.64; 95% CI, 0.46 to 0.89; I2, 0%; NNT, 23) in patients receiving ventilation with lower tidal volumes.

Evidence for ventilation 2013

In this multicenter, double-blind, parallel-group trial, we randomly assigned 400 adults at intermediate to high risk of pulmonary complications after major abdominal surgery to either nonprotective mechanical ventilation or a strategy of lung-protective ventilation. The primary outcome was a composite of major pulmonary and extrapulmonary complications occurring within the first 7 days after surgery.

Evidence for ventilation –FACCT trial 2006

Trouble shooting ventilation

Case study Mr CS – 75 year old male, weighs 80kg. Background IHD, Ex-smoker 20 years ago, Type II DM, AF. Day 4 post Hartmans procedure for colorectal cancer, severe abdominal pain and fever. Anastamotic leak on CT scan. Commenced on IV Tazocin. Taken to OT and had extensive washout of abdomen and stoma formed. Abdomen is closed. Vital signs: HR 115, BP 110/50 on 0.2mcg/kg/min of Noradrenaline, SaO2 96%, temperature 38.8 degrees. The nursing staff come to you after one hour and show you the following ABG: pH: 7.21, PaO2 82mmHg, PaCO2 58mmHg, Lactate 2.1mmol/l, BE -5.2mmol/l How will you adjust the ventilator ??

Trouble shooting ventilation We need to increase minute ventilation Minute ventilation = TV x RR

Trouble shooting ventilation Dead space ventilation - Excess tubing, especially in paediatrics 2. Tidal volume Aim 6-8 mL/kg Risk of barotrauma if plateau pressure > 30cmH2O Risk of volutrauma 3. Respiratory rate Aim for < 30 Monitor for gas trapping, dynamic hyperinflation and intrinsic PEEP

Trouble shooting ventilation

Trouble shooting ventilation

Case study Mr CS – 75 year old male, weighs 80kg. Background IHD, Ex-smoker 20 years ago, Type II DM, AF. Day 4 post Hartmans procedure for colorectal cancer, severe abdominal pain and fever. Anastamotic leak on CT scan. Commenced on IV Tazocin. Taken to OT and had extensive washout of abdomen and stoma formed. Abdomen is closed. Vital signs: HR 130, BP 90/50 on 0.3mcg/kg/min of Noradrenaline, SaO2 96%, temperature 38.8 degrees He is ventilated in ICU, and adjustments made after the last ABG. The nursing staff come to you later that shift stating the patient has desaturated to 85% and shows you the following ABG: pH 7.30, PaO2 52mmHg, PaCO2 40mmHg, lactate 2.0mmol/l, BE -5.1mmol/l How will you manage this ??

Trouble shooting ventilation Hypoxaemia Most patients need SaO2 90-94% at the most, some only 88-92% (chronic respiratory disease) What to do ??

Patient is still hypoxic !

Trouble shooting ventilation Increase FiO2 Increase mean alveolar pressure Main determinant of oxygenation Can be increased by increasing Inspiratory pressure or tidal volume Inspiratory time PEEP Increase PEEP Maintains open alveoli and reduces shunt

What if SaO2 is still only 85% ??

Refractory hypoxaemia

Refractory hypoxaemia 1. Recruitment maneuvers Is a high pressure inflation maneuver aimed at temporarily raising the transpulmonary pressure above levels typically obtained with mechanical ventilation. Purpose is to overcome the high “opening pressures” of diseased and collapsed alveoli. By opening alveoli, this increases the area available for gas exchange and oxygen transfer. Open collapsed lung tissue so it can remain open during tidal ventilation with lower pressures and PEEP, thereby improving gas exchange and helping to eliminate high stress interfaces Although applying high pressure is fundamental to recruitment, sustaining high pressure is also important Methods of performing a recruiting maneuver include single sustained inflations and ventilation with high PEEP

Spectrum of Regional Opening Pressures (Supine Position) Small Airway Collapse 10-20 cmH2O Inflated Superimposed Pressure Consolidation  Alveolar Collapse (Reabsorption) 20-60 cmH2O = Lung Units at Risk for Tidal Opening & Closure

met the inclusion criteria for this review (the total number of included participants was 1170). All trials included a recruitment manoeuvre as part of the treatment strategy for patients on mechanical ventilation for ARDS or ALI. However, two of the trials included a package of ventilation that was different from the control ventilation in aspects other than the recruitment manoeuvre. The intervention group showed no significant difference on 28-day mortality (RR 0.73, 95% CI 0.46 to 1.17, P = 0.2). Similarly there Recruitment manoeuvreswas no statistical difference for risk of barotrauma (RR 0.50, 95% CI 0.07 to 3.52, P = 0.5) or blood pressure (MD 0.9 mm Hg, 95% CI -4.28 to 6.08, P = 0.73). Recruitment manoeuvres significantly increased oxygenation above baseline levels for a short period of time in four of the five studies that measured oxygenation. There were insufficient data on length of ventilation or hospital stay to pool results.

Refractory hypoxaemia 2. Inhaled prostacyclin Nebulised prostacylin (PGI-2) given continuously via an ultrasonic nebuliser attached to the inspiratory limb of the ventilator. An alternative to inhaled Nitric Oxide which is expensive and requires scavenging set-up. Prostacyclin (PGI2), generic name epoprostenol (brand name Flolan) is a member of the family of lipid molecules known as eicosanoids. PGI2 is a naturally occurring prostaglandin that has vascular smooth muscle relaxant and has anti-inflammatory properties (it inhibits platelet aggregation and neutrophil adhesion). It is synthesized by vascular endothelial and smooth muscle cells within the lung and has an in vivo half-life of three to six minutes (Jain 2006). PGI2 is a potent vasodilator of the systemic and pulmonary vasculature resulting in reduction of right and left heart afterload (Siobal 2004) and can be administered by different routes such as: intravenous for pulmonary hypertension, and inhalational preparations for ALI and ARDS. Inhaled PGI2 appears to improve oxygenation; lower pulmonary vascular resistance (PVR) andmean pulmonary arterial pressure (MPAP); and reduce pulmonary shunt fraction (Siobal 2004). It might have potential benefits in resolving hypoxaemia from ALI or ARDS and in the treatment of pulmonary hypertension and right heart failure, similar to the indications for inhaled nitric oxide (Siobal 2004).

Refractory hypoxaemia 3. Prone ventilation Has been studied in severe ARDS Complex process with safety issues Risk of extubation Risk of removing lines Pressure areas OH and S Homogenise transpleural pressure Compression – reduced compression from heart + abdomen Improved recruitment Increase in FRC Decreased shunt Benefit Improved oxygenation in 60-80% patient, even on return to supine position

PROSEVA trial 2013 severe ARDS to undergo prone-positioning sessions of at least 16 hours or to be left in the supine position. Severe ARDS was defined as a ratio of the partial pressure of arterial oxygen to the fraction of inspired oxygen (Fio2 ) of less than 150 mm Hg, with an Fio2 of at least 0.6, a positive end-expiratory pressure of at least 5 cm of water, and a tidal volume close to 6 ml per kilogram of predicted body weight.

Refractory hypoxaemia 4. High frequency oscillatory ventilation Specialised equipment Respiratory rates of 5 -15 Hz Mean airway pressures of 30cmH2O Tidal volumes smaller than dead space ! Effective at rescue oxygenation

OSCILLATE trial Canada and Saudi Arabia

On the recommendation of the data monitoring committee, we stopped the trial after 548 of a planned 1200 patients had undergone randomization. The two study groups were well matched at baseline. The HFOV group underwent HFOV for a median of 3 days (interquartile range, 2 to 8); in addition, 34 of 273 patients (12%) in the control group received HFOV for refractory hypoxemia. Patients in the HFOV group received higher doses of midazolam than did patients in the control group (199 mg per day [interquartile range, 100 to 382] vs. 141 mg per day [interquartile range, 68 to 240], P<0.001), and more patients in the HFOV group than in the control group received neuromuscular blockers (83% vs. 68%, P<0.001). In addition, more patients in the HFOV group received vasoactive drugs (91% vs. 84%, P = 0.01) and received them for a longer period than did patients in the control group (5 days vs. 3 days, P = 0.01).

OSCAR trial United Kingdom

There was no significant between-group difference in the primary outcome, which occurred in 166 of 398 patients (41.7%) in the HFOV group and 163 of 397 patients (41.1%) in the conventional-ventilation group (P = 0.85 by the chi-square test). After adjustment for study center, sex, score on the Acute Physiology and Chronic Health Evaluation (APACHE) II, and the initial Pao2 :FIo2 ratio, the odds ratio for survival in the conventional-ventilation group was 1.03 (95% confidence interval, 0.75 to 1.40; P = 0.87 by logistic regression

Refractory hypoxaemia 5. Extracorporeal Membrane oxygenation (ECMO) Involves gas exchange via an extracorporeal circuit. Can support the lungs alone (V-V ECMO) or the heart and lungs (V-A ECMO) Significant risks and costs

CESAR trial In this UK-based multicentre trial, we used an independent central randomisation service to randomly assign 180 adults in a 1:1 ratio to receive continued conventional management or referral to consideration for treatment by ECMO. Eligible patients were aged 18–65 years and had severe (Murray score >3·0 or pH <7·20) but potentially reversible respiratory failure. Exclusion criteria were: high pressure (>30 cm H#O of peak inspiratory pressure) or high FiO# (>0·8) ventilation for more than 7 days; intracranial bleeding; any other contraindication to limited heparinisation; or any contraindication to continuation of active treatment. The primary outcome was death or severe disability at 6 months after randomisation or before discharge from hospital. Primary analysis was by intention to treat.

Case study Mr CS – 75 year old male, weighs 80kg. Background IHD, Ex-smoker 20 years ago, Type II DM, AF. Day 4 post Hartmans procedure for colorectal cancer, severe abdominal pain and fever. Anastamotic leak on CT scan. Commenced on IV Tazocin. Taken to OT and had extensive washout of abdomen and stoma formed. Abdomen is closed. He has been ventilated in ICU for 5 days. He had a brief period of hypoxaemia due to bibasal atelectasis. It resolved with a recruitment maneuver and increased PEEP. He has been on PSV for 24 hours, with settings FiO2 30%, Inspiratory pressure 10cmH2O and PEEP 5cmH2O. His vital signs are: HR 90, BP 130/70, SaO2 98%, temperature 37.2 degrees His latest blood gas shows: pH 7.38, PaO2 95mmHg, PaCO2 39mmHg, lactate 0.7mmol/L and BE 1.0mm0l/L How will you assess him for extubation ?? Should you extubate him onto NIV ??

Assessment for extubation 1. Disease process Has disease process that required MV resolved Complications – sepsis, transfusion Pain – especially with thoracotomy, laparotomy Fluid balance : ideally cummulative balance < 3L 2. Airway Grade of intubation How patient was intubated Presence of cuff leak Appropriate assistance available

Assessment for extubation 3. Neurological Awake and co-operative Pain controlled Weakness 4. Respiratory Ventilator support – ideally PSV < 10/5cmH2O RR <30 Vital capacity > 10mL/kg Cough Secretion load – small load Rapid shallow breathing index (f/Vt) <100 Review of CXR 5. Cardiovascular Stable cardiac rhythm Minimal ionotrope/vasopressor requirement

Extubation onto NIV We identified 16 trials, predominantly ofmoderate to good quality, involving 994 participants,mostwith chronic obstructive pulmonary disease (COPD). Compared with IPPV weaning, NPPV weaning significantly decreased mortality. The benefits for mortality were significantly greater in trials enrolling exclusively participants with COPD (risk ratio (RR) 0.36, 95% confidence interval (CI) 0.24 to 0.56) versus mixed populations (RR 0.81, 95% CI 0.47 to 1.40). NPPV significantly reduced weaning failure (RR 0.63, 95% CI 0.42 to 0.96) and ventilator-associated pneumonia (RR 0.25, 95% CI 0.15 to 0.43); shortened length of stay in an intensive care unit (mean difference (MD) -5.59 days, 95% CI -7.90 to -3.28) and in hospital (MD -6.04 days, 95%CI -9.22 to -2.87); and decreased the total duration of ventilation (MD -5.64 days, 95% CI -9.50 to -1.77) and the duration of endotracheal mechanical ventilation (MD - 7.44 days, 95% CI -10.34 to -4.55) amidst significant heterogeneity. Noninvasive weaning also significantly reduced tracheostomy (RR 0.19, 95% CI 0.08 to 0.47) and reintubation (RR 0.65, 95% CI 0.44 to 0.97) rates. Noninvasive weaning had no effect on the duration of ventilation related to weaning

Conclusion Modes of ventilation How to set the ventilator Mandatory Spontaneous Adaptive How to set the ventilator Evidence for ventilator strategies Trouble shooting ventilation Refractory Hypoxia Assessment for extubation