mechanical ventilation & strategies for oxygenation

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Mechanical Ventilation & Strategies for Oxygenation

Dawn Oddie

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What are we going to talk about?

Physiology Ventilation classifications Types of Ventilation Optimising Oxygenation Complications of Ventilation Weaning from Ventilation

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Physiology

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Where it all happens!

300 millio

n alveoli

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Physiology of normal breathing

How do we breathe?

Low lung volume (Exhalation) / Functional residual capacity

High lung volume (Inhalation)

Negative pressureI:E ratio times

Tidal volumes

Respiratory rate

Active inspiration Passive expiration

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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?

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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

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Lung Volumes

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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.

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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.

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Causes of Decreased Intrathoracic Compliance

Decreased Chest Wall Compliance

Decreased Lung Compliance

ObesityAscitesNeuromuscular weaknessFlail ChestKyphoscoliosisParalysisSclerodermaPectus Excavatum

Tension PneumothoraxIntubationPulmonary oedemaARDSConnective tissue diseaseSarcoidosisDynamic HyperinflationLymphangitis Carcinomatosis

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Some Important Physiology

V/Q Mismatch Oxygen Cascade Oxyhaemoglobin Dissociation Curve Spirometry Trace

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Supply and demand

V/Q mismatch– 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

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When room air just isn’t enough…..

Increased metabolic demand

V/Q mismatch – Damaged alveoli /

airways– Blocked alveoli– Inadequate

circulation

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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)

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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

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What is oxygen

What percentage of oxygen is in atmospheric air?

In normal circumstances with a average respiratory rate sufficient to meet

metabolic demandsOxygen 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

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Haemoglobin

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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)

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Haemoglobin

Average 70Kg Adult = 900g of circulating haemoglobin (Hb 14-18g/dl)

1g Haemoglobin can carry 1.34ml oxygenExample,10g/dl with an average 5l circulating volume =

500g total body haemoglobinIf 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

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The transfusion debate…

Risks of vs Reduced oxygen transfusion carrying capacity

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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)

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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.

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Partial Pressure - effect of Altitude

The important effect of this decrease in pressure is: in agiven 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 everythingpresent, including oxygen.

So why is this an issue?

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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.

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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)

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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.

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Oxygen dissociation curve

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

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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

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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

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Oxygen dissociation curve

Reduced AffinityIncreased affinity

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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 tissuesLeft will favour reduced tissue oxygenation

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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

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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

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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

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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.

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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

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Indicators for initiating mechanical ventilation?

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Types of positive pressure ventilation

Non invasive

Invasive

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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

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CPAP

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NIV - BiPAP

IPAP / PS / ASB– Inspiratory assistance with each

spontaneous breath

EPAP– Expiratory resistance

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The science of mechanical ventilation is to optimise pulmonary gas

exchange; the art is to achieve this without damaging the lungs

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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

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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

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Ventilator strategy

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

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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

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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.

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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

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Breaths– Mandatory

(controlled) – determined by the respiratory rate

– AssistedE.g. synchronised intermittent mandatory

ventilation (SIMV)

– SpontaneousNo additional assistance during inspiration

e.g. CPAP

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Ventilator ClassificationFlow 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)

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Ventilator ClassificationMode 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

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Methods of Ventilation

Synchronised Intermittent Mandatory Ventilation – SIMV

Pressure Control Volume control Pressure regulated volume control Pressure support Continuous positive airway pressure

(CPAP)

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Waveforms

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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

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Biphasic Positive Airway Pressure

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BIPAP / APRV (Airway pressure release ventilation)

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Why is mechanical ventilation bad for you?

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Problems with Mechanical Ventilation

Mechanical Ventilation

IntubationProlonged Ventilation

Ventilator Induced Lung Injury

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Problems with Intubation

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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

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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

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Problems with Prolonged Ventilation

Barotrauma Volutrauma Oxygen Toxicity Pneumonia (VAP) Sheer Stress – flow delivery

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Barotrauma – pressure Air leak from alveoli

situated near respiratory bronchioles

10 – 20% of ventilated patients

Predisposing factors– Frequent +ve pressure

breaths– Infection– ARDS– Hypovolaemia

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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.

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Volutrauma

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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

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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

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Oxygen toxicity

Central nervous system– Visual changes, ringing in ears, nausea,

twitching, irritability, dizziness, convulsions

Pulmonary– Lungs show inflammation / scarring

(ARDS) and pulmonary oedema Retinopathic

– Retinal damage

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Other Complications

Decreased cardiac output

Pneumonia (VAP) Psychological problems Endotracheal tube

complications– Laryngeal injury– Tracheal stenosis– Tracheomalacia– Endobronchial intubation– Sinusitis

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Suctioning and Mechanical Ventilation

Causes Lung de-recruitment due to– Disconnection from the ventilator

Loss of PEEPWorse V/Q mismatch

– Suctioning procedure itselfHigh negative pressure decreases lung

volumeWorse if the suction is open

Suction only when clinically indicated / Pre oxygenate / Minimal suction pressure / limit suction time

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Prone Positioning

What a nightmare! Can dramatically

alter oxygenation Also

– Induces a uniform V/Q distribution

– Promotes alveolar recruitment

– Promotes secretion drainage

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Prone Positioning

Debate about outcome in the most hypoxic

Complications,– Manual Handling– Accidental Extubation– Pressure sores– Facial Oedema– Line disconnection

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Gattinoni et al (2001) NEJM 345 (8): 568

Oxygenation Survival

Improved oxygenation, but not overall survival rate

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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

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HFOV for ARDS in AdultsDerdak 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

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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.

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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

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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

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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

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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

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Your Patient is Hypoxic So What Do You Do

Decide– How much time to you have?– What resources are available– Is escalation appropriate

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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

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Scenarios

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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

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Case

70 year old gentleman

Sudden SOB HR 150 bpm RR 50 FiO2 0.21






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Case

55 year old Rescued from

smoke filled room PaO2 7 on FiO2

85%






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THE ENDTHE END

mechanical ventilation & strategies for oxygenation

Documents

high lung compliance

volume change

stiff lung

pressuretotal lung

compliant lung

normal volume of air

volume relative

moderate lung volumes