Mechanical Ventilation & Strategies for Oxygenation Dawn Oddie

What are we going to talk about? Physiology Ventilation classifications Types of Ventilation Optimising Oxygenation Complications of Ventilation Weaning from Ventilation

Physiology

Where it all happens! 300 million alveoli

Physiology of normal breathing I:E ratio times How do we breathe? Negative pressure Active inspiration Passive expiration Respiratory rate High lung volume (Inhalation) Low lung volume (Exhalation) / Functional residual capacity Tidal volumes

How is normal breathing controlled How do you know, Rate - How fast / slow to breathe? Tidal volume - How big a breathe to take in? I:E ratio – How long to breath in / out for? When to cough / sneeze?

Nervous Control / Chemical Respiratory centre. Reticular formation – brain stem Medullary rhythmicity area Pneumotaxic area / Apneustic area (transition from I to E) Inflation (Hering-Breuer) reflex - Stretch receptors Cortical influences – cerebral cortex giving some voluntary control eg hold breath underwater Central chemosensitive area (pH / H+) – Medulla Peripheral chemoreceptors (CO2 / O2 / H+) – carotid bodies Proprioceptors – joints / muscles Other influences – Baroreceptors / Temp / Pain / stretching the anal sphincter muscle / Irritation of the air passages

Lung Volumes

Respiratory Mechanics- Compliance Compliance is ΔV/ΔP (Change in Volume / change in pressure) Total lung is made up of thoracic and lung compliance Pulmonary compliance (or lung compliance) is the ability of the lungs to stretch during a change in volume relative to an applied change in pressure. Compliance is greatest at moderate lung volumes, and much lower at volumes which are very low or very high. LIP and UIP can be good guides Pulmonary Surfactant increases compliance by decreasing the surface tension of water. The internal surface of the alveolus is covered with a thin coat of fluid. The water in this fluid has a high surface tension, and provides a force that could collapse the alveolus. The presence of surfactant in this fluid breaks up the surface tension of water, making it less likely that the alveolus can collapse inward. If the alveolus were to collapse, a great force would be required to open it, meaning that compliance would decrease drastically.

Respiratory Mechanics- Compliance Low compliance indicates a stiff lung and means extra work is required to bring in a normal volume of air. This occurs as the lungs in this case become fibrotic, lose their distensibility and become stiffer. In a highly compliant lung, as in emphysema, the elastic tissue has been damaged, usually due to their being overstretched by chronic coughing. Patients with emphysema have a very high lung compliance due to the poor elastic recoil, they have no problem inflating the lungs but have extreme difficulty exhaling air. In this condition extra work is required to get air out of the lungs.

Causes of Decreased Intrathoracic Compliance Decreased Chest Wall Compliance Decreased Lung Compliance Obesity Ascites Neuromuscular weakness Flail Chest Kyphoscoliosis Paralysis Scleroderma Pectus Excavatum Tension Pneumothorax Intubation Pulmonary oedema ARDS Connective tissue disease Sarcoidosis Dynamic Hyperinflation Lymphangitis Carcinomatosis

Some Important Physiology V/Q Mismatch Oxygen Cascade Oxyhaemoglobin Dissociation Curve Spirometry Trace

Supply and demand V/Q mismatch Functional alveoli Permeable membranes V = Ventilation P = Perfusion Hypoxic Pulmonary Vasoconstriction Functional alveoli Permeable membranes Circulating volume – with Adequate haemoglobin levels Oxygen saturation of haemoglobin (affinity) Oxygen dissociation Perfusion pressure

When room air just isn’t enough….. Increased metabolic demand V/Q mismatch Damaged alveoli / airways Blocked alveoli Inadequate circulation

Some indications to increase O2 Acute respiratory failure eg pneumonia, asthma, pulmonary oedema, pulmonary embolus Acute myocardial infarction Cardiac Failure Shock Hypermetabolic states eg major trauma, sepsis, burns Anaemia Carbon monoxide poisoning Cardio respiratory resuscitation During / post anaesthesia Pre-suction Suppressant drug eg narcotics Pyrexia (Oxygen consumption increases by 10% for each degree rise)

Effect of insufficient oxygen Reduced oxygen supply leads to cellular shift from aerobic to anaerobic metabolism Production of lactic acid Increasing metabolic acidosis Low pH Low HCO3 Negative base excess Cell death / system wide failure

What is oxygen What percentage of oxygen is in atmospheric air? In normal circumstances with a average respiratory rate sufficient to meet metabolic demands Oxygen delivery (mls O2/min) = Cardiac output (litres/min) x Hb concentration (g/litre) x 1.31 (mls O2/g Hb) x % saturation   Oxygen Consumption = 200 - 250 mls / min

Haemoglobin

Haemoglobin Intracellular protein contained within erythrocytes (red blood cells) Made up of 2 pairs of polypeptide chains (2Alpha, 2 Beta), each bound to a haem group that contains iron. Each molecule of haemoglobin can combine with 4 molecules of oxygen Primary vehicle for oxygen transportation in the blood (small amount in plasma Approx 1.5-3%) Each haemoglobin molecule has a limited capacity for holding oxygen molecules. How much of that capacity that is filled by oxygen bound to the haemoglobin at any time is the oxygen saturation (SaO2)

Haemoglobin Average 70Kg Adult = 900g of circulating haemoglobin (Hb 14-18g/dl) 1g Haemoglobin can carry 1.34ml oxygen Example, 10g/dl with an average 5l circulating volume = 500g total body haemoglobin If fully saturated 500 x 1.34 = 670ml of oxygen (Only approx 25% unloads leaving venous sats (SvO2) 70-75% - useful in times of higher metabolic demand etc

The transfusion debate… Risks of vs Reduced oxygen transfusion carrying capacity

Factors affecting carriage Timing of haemoglobin uptake and release of oxygen affected by, Partial pressure of oxygen (PaO2) Temperature Blood pH Partial Pressure of Carbon dioxide (PaCO2)

Partial Pressure - effect of Altitude At sea level we live under a layer of air that is several miles deep – the atmosphere. The pressure on our bodies is about the same as 10 metres of sea water pressing down on us all the time. At sea level, because air is compressible, the weight of the air around us compresses making it denser. As you go up a mountain, the air becomes less compressed and therefore thinner.

Partial Pressure - effect of Altitude The important effect of this decrease in pressure is: in a given volume of air, there are fewer molecules present. The percentage of those molecules that are oxygen is exactly the same: 21%. The problem is that there are fewer molecules of everything present, including oxygen. So why is this an issue?

Partial Pressure of gases In a mixture of ideal gases, each gas has a partial pressure which is the pressure which the gas would have if it alone occupied the volume. The total pressure of a gas mixture is the sum of the partial pressures of each individual gas in the mixture. Dalton's law (also called Dalton's law of partial pressures) states that the total pressure exerted by a gaseous mixture is equal to the sum of the partial pressures of each individual component in a gas mixture.

Partial Pressure Partial pressure (PP) is a way of describing how much of a gas is present. All gases exert pressure on the walls of their container as gas molecules bounce constantly of the walls PP is also used to describe dissolved gases. In this case, the PP of a gas dissolved in blood is the PP that the gas would have, if the blood were allowed to equilibrate with a volume of gas. When blood is exposed to fresh air in the lungs, it equilibrates almost completely so that the PP of oxygen in the air spaces in the lungs is equal to the partial pressure of oxygen in the blood. PP of arterial blood is slightly less than PP of oxygen in lungs – due to physiological shunt (some blood passing through lungs without encountering an air space)

Partial Pressure of gases The partial pressure of a gas dissolved in a liquid is the partial pressure of that gas which would be generated in a gas phase in equilibrium with the liquid at the same temperature. The partial pressure of a gas is a measure of thermodynamic activity of the gas's molecules. Gases will always flow from a region of higher partial pressure to one of lower pressure; the larger this difference, the faster the flow. Gases dissolve, diffuse, and react according to their partial pressures, and not necessarily according to their concentrations in a gas mixture.

Oxygen dissociation curve Dissociation curve relates oxygen saturation of Haemoglobin (Y axis) and partial pressure of arterial oxygen (X axis) in the blood

Dissociation curve explained Extent of oxygen binding to haemoglobin depends on PaO2 of blood, but relationship not precisely linear Slope steeply progressive between 1.5 – 7kPa (area of most rapid uptake and delivery of oxygen to and from haemoglobin), then plateaus out between 9 – 13.5kPa Haemoglobin almost completely saturated at 9kPa – further increases in partial pressure of oxygen will result in only slight rises in oxygen binding

Oxygen dissociation curve The partial pressure of oxygen in the blood at which haemoglobin is 50% saturated (26.6mmHg) is known as the P50 P50 is conventional measure of haemoglobin affinity for oxygen Increased P50 indicates a right shift of the standard curve – meaning larger partial pressure necessary to maintain a 50% oxygen saturation

Oxygen dissociation curve Increased affinity Reduced Affinity

Factors influencing the position of oxygen dissociation curve To the right, Hyperthermia Acidosis (pH) Increased pCO2 Endocrine disorders Curve shifts to left, Hypothermia Alkalosis Decreased pCO2 Carbon monoxide Generally a shift to the, Right will favour unloading of oxygen to the tissues Left will favour reduced tissue oxygenation

Factors influencing the position of oxygen dissociation curve - explained To the right As pH declines (acidosis) the affinity of haemoglobin for oxygen reduces. Result – less oxygen is bound while more oxygen is unloaded Bohr effect To the left Temperature – as body temp falls the affinity of haemoglobin for oxygen increases. Result – more oxygen is bound while less oxygen is unloaded

mmHg vs. kPa Both measures commonly in use The kiloPascal: A pressure of one thousand pascals (1 kPa) is about 10.2 cm H2O or about 7.75 mmHg. Atmospheric pressure is about 1034 cmH2O or 101.9 kPa. The useful approximations are 1000 cm H2O or 100 kPa. mmHg to kPa: To convert pressure in mmHg to kPa, divide the value in mmHg by 7.5. Eg. 60mmHg = 8.0kPa 30mmHg = 4.0kPa

The oxygen cascade Transport has three stages (steps), By gas exchange in the lungs Partial pressure gradient of oxygen (PaO2) in alveoli 13.7kPa Partial pressure gradient of oxygen (PaO2) in pulmonary capillaries 5.3kPa Transport of gases in the blood Partial pressure gradient of oxygen (PaO2) in arterial blood 13.3kPa Movement from blood into the tissues Partial pressure gradient of oxygen (PaO2) in tissues 2.7kPa Mitochondrial pressure 0.13-1.3kPa

Oxygen delivery to tissues…. The amount of oxygen bound to the haemoglobin at any time is related to the partial pressure of oxygen to which the haemoglobin is exposed. Eg in lungs at the alveolar-capillary interface, partial pressure of oxygen is high so oxygen readily binds. As the blood circulates to other body tissue in which the partial pressure of oxygen is less the haemoglobin releases the oxygen into the tissues. Haemoglobin cannot maintain its full bound capacity in the presence of lower oxygen partial pressures.

Supplementing Oxygen Nasal cannula Fixed performance mask Variable performance mask Non rebreathe reservoir Tracheostomy mask Tents / head boxes Bag valve mask CPAP – nasal / facial or hood BiPAP – IPAP / EPAP Intubation and mechanical ventilation

Indicators for initiating mechanical ventilation?

Types of positive pressure ventilation Non invasive Invasive

CPAP / PEEP / EPAP Pressure applied at end of expiration to maintain alveolar recruitment Airway pressure kept positive Beware of gas trapping (autoPEEP) in non compliant lungs

CPAP

NIV - BiPAP IPAP / PS / ASB EPAP Inspiratory assistance with each spontaneous breath EPAP Expiratory resistance

The science of mechanical ventilation is to optimise pulmonary gas exchange; the art is to achieve this without damaging the lungs

What is a Mechanical Ventilator? Generates a controlled flow of gas in and out of a patient Inhalation replenishes alveolar gas Balance needed between O2 replenishment and CO2 removal

Ventilators – What do they need to do… Mechanical ventilators are flow generators Must be able to, Control Cycling Triggering Breaths Flow pattern Mode or breath pattern

Ventilator strategy Aim to achieve adequate minute volume with the lowest possible airway pressure

Ventilator Classification Control How the ventilator knows how much flow to deliver Can be, Volume controlled (volume limited, volume targeted) & pressure variable Pressure controlled (pressure limited, pressure targeted) & volume variable Dual controlled (volume targeted (guaranteed) pressure limited

Ventilator Classification Cycling How the ventilator switches from inspiration to expiration (the flow has been delivered – how long does it stay there?) Time cycled e.g. pressure controlled ventilation Flow cycled e.g. pressure support Volume cycled. The ventilator cycles to expiration once a set tidal volume has been delivered.

Ventilator Classification Triggering What causes the ventilator to cycle to inspiration. Ventilators may be…… Time triggered Cycles at set frequency as determined by the rate Pressure triggered Ventilator senses the patients inspiratory effort by sensing a decrease in baseline pressure Flow triggered Constant flow through circuit – flow-by. Ventilator detects a deflection or change in this flow. Requires less work from the patient than pressure triggered

Ventilator Classification Breaths Mandatory (controlled) – determined by the respiratory rate Assisted E.g. synchronised intermittent mandatory ventilation (SIMV) Spontaneous No additional assistance during inspiration e.g. CPAP

Ventilator Classification Flow pattern Sinusoidal (normal breathing) Decelerating (inspiration slows as alveolar pressure increases) Constant (flow continues at a constant rate until set tidal volume is delivered) Accelerating (not used in clinical practice)

Ventilator Classification Mode or Breath Pattern CMV Volume Assist-Control (caution with sensitivity) Synchronised Intermittent Mandatory Ventilation – SIMV Pressure support High frequency ventilation BiPAP/BILEVEL – airway pressure release ventilation Proportional assist ventilation Automatic tube compensation Enhance patient interactivity

Methods of Ventilation Synchronised Intermittent Mandatory Ventilation – SIMV Pressure Control Volume control Pressure regulated volume control Pressure support Continuous positive airway pressure (CPAP)

Waveforms

So the problem is this If the patient is hypoxic then they need O2 If still hypoxic then they need +ve pressure If still hypoxic then you need to increase the Ti time (at the expense of the Te time) Adjustment of the I:E ratio (did) mean increased sedation as it was impossible to breath with the flipped ratio. New modes have now been developed to allow spontaneous ventilation on adjusted I:E ratios e.g. BIPAP and APRV

Biphasic Positive Airway Pressure

BIPAP / APRV (Airway pressure release ventilation)

Why is mechanical ventilation bad for you?

Problems with Mechanical Ventilation

Problems with Intubation

Problems with Intubation Bypass natural protective mechanisms – moisten, filter, warm Plastic tubing – airway trauma, vocal cord damage Pressure sores – oral or from cuff Mouth care! Need sedation

Sedation and Ventilation Good Points Reduced pain Reduced stress Easier to nurse Better for relatives Less chance of lines falling out Bad Points Increased pneumonia risk Venous thrombosis Pressure area problems Hypotension Prolonged ICU stay Better for relatives Increased barotrauma

Problems with Prolonged Ventilation Barotrauma Volutrauma Oxygen Toxicity Pneumonia (VAP) Sheer Stress – flow delivery

Barotrauma – pressure Air leak from alveoli situated near respiratory bronchioles 10 – 20% of ventilated patients Predisposing factors Frequent +ve pressure breaths Infection ARDS Hypovolaemia

Volutrauma - volume Excessive stretch in the absence of excessive airway pressure. If alveoli cannot over distend they are less likely to be damaged Not just a mechanical problem but also a local and generalised inflammatory response. C.f. IL-6 levels in ARDS Net lung protection study.

Volutrauma

Ventilators Aim to achieve adequate minute volume with the lowest possible airway pressure High PEEP levels 10 – 20 (open lung) Permissive hypercapnia Patient specific tidal volume 6 – 7ml/Kg Improved inverse ratio capabilities

Oxygen – the risks Highly flammable Compressed Dry gas – Think humidification! Blindness in neonates (overgrowth of blood vessels) Drying of mucus membranes / secretions COPD – respiratory drive Toxic – inflammation / scarring after 40hrs with 100% Dry eyes

Oxygen toxicity Central nervous system Pulmonary Retinopathic Visual changes, ringing in ears, nausea, twitching, irritability, dizziness, convulsions Pulmonary Lungs show inflammation / scarring (ARDS) and pulmonary oedema Retinopathic Retinal damage

Other Complications Decreased cardiac output Pneumonia (VAP) Psychological problems Endotracheal tube complications Laryngeal injury Tracheal stenosis Tracheomalacia Endobronchial intubation Sinusitis

Suctioning and Mechanical Ventilation Causes Lung de-recruitment due to Disconnection from the ventilator Loss of PEEP Worse V/Q mismatch Suctioning procedure itself High negative pressure decreases lung volume Worse if the suction is open Suction only when clinically indicated / Pre oxygenate / Minimal suction pressure / limit suction time

Prone Positioning What a nightmare! Can dramatically alter oxygenation Also Induces a uniform V/Q distribution Promotes alveolar recruitment Promotes secretion drainage

Prone Positioning Debate about outcome in the most hypoxic Complications, Manual Handling Accidental Extubation Pressure sores Facial Oedema Line disconnection

Gattinoni et al (2001) NEJM 345 (8): 568 Survival Oxygenation Improved oxygenation, but not overall survival rate

High-Frequency Oscillatory Ventilation in Adults Seems a nice idea 3 – 10 Hz oscillation ‘Tidal volume’ less than normal Less opening and closing of lungs Well established in neonatal and paediatric population Issues, Patients need heavy sedation / NMJ blockade Drop in preload Transport not possible Clinical Ex difficult Little research until now

HFOV for ARDS in Adults Derdak et al (2002) Am J Resp & Crit Care Med Vol 166. pp. 801 – 808 Multi-centre randomised control trial 148 patients HFOV n = 75 Conventional Ventilation n = 73 Outcome measure was survival without mechanical ventilation at 30 days

HFOV for ARDS in Adults Derdak et al (2002) Am J Resp & Crit Care Med Vol 166. pp. 801 – 808 Non significant trend towards higher survival 37% versus 52% P = 0.102 Big improvement in PaO2/FiO2 (p = 0.008) in HFOV.

HFOV for ARDS in Adults Derdak et al (2002) Am J Resp & Crit Care Med Vol 166. pp. 801 – 808 Unanswered Questions Ideal timing of the intervention Prone position Nitric Oxide When do you discontinue Long term effects on lung function Use of volume recruitment methods

ECMO It involves connecting the internal circulation to an external blood pump and artificial lung. A catheter placed in the right side of the heart carries blood to a pump, then to a membrane oxygenator, where gas exchange of O2 and CO2 takes place. The blood then passes through tubing back into the patient's veins or arteries. Patients are anticoagulated

CESAR Trial (recruited 2001 – 2006) (reported 2008) Conventional Ventilation or ECMO for Severe Adult Respiratory Failure 180 patients Use of ECMO results in 1 extra survivor for every 6 patients treated

Your Patient is Hypoxic So What Do You Do Remember “Air goes in and out and blood goes round and round” That just getting air into the lungs may not be enough

Your Patient is Hypoxic So What Do You Do Decide How much time to you have? What resources are available Is escalation appropriate

Your Patient is Hypoxic - What Do You Do? Increase the supply of Oxygen Drive it into the lungs Get the lungs in the best shape possible Make sure blood is getting to the lungs Reduce the metabolic demand for oxygen

Scenarios

Case 44 year old lady 11/7 post intubation for pneumonia. Trachy. FiO2 .3, PO2 11 Sudden SOB FiO2 1.0, Sats 80% Increase the supply of Oxygen Drive it into the lungs Get the lungs in the best shape possible Make sure blood is getting to the lungs Reduce the demand for oxygen

Case 70 year old gentleman Sudden SOB HR 150 bpm RR 50 FiO2 0.21 Increase the supply of Oxygen Drive it into the lungs Get the lungs in the best shape possible Make sure blood is getting to the lungs Reduce the demand for oxygen

Case 55 year old Rescued from smoke filled room PaO2 7 on FiO2 85% Increase the supply of Oxygen Drive it into the lungs Get the lungs in the best shape possible Make sure blood is getting to the lungs Reduce the demand for oxygen

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