Chris Thompson   USyd Lectures Listing

VENTILATION, VENTILATORS and HUMIDFICATION

INTRODUCTION

Normally, Alveolar Ventilation is unconsciously regulated to maintain constant arterial blood gas tensions (particularly CO2), despite variable levels of oxygen consumption and CO2 production.

Many drugs and techniques used in anaesthesia interfere with control or mechanics of ventilation, and it is the Anaesthetists responsibility to ensure the adequacy of ventilation during the perioperative period.

Ventilation and ventilators are consequently of great importance to the Anaesthetist. Correct use requires a good understanding of basic respiratory physiology as well as how the individual ventilator operates.

I've recently uploaded a plain text abstract and PDF set of slides from a recent talk on ventilators, optimising PEEP and lung recruitment.

NORMAL PHYSIOLOGY

Basic Principles

Venous blood always has a lower PaO2 (40 mmHg or 75% saturated or 15 ml O2/100ml blood) and higher PaCO2 (46 mmHg) than inspired gas (PiO2 150 mmHg, PiCO2 usually 0). Hence there is a partial pressure gradient driving Oxygen in and CO2 out of the pulmonary capillary blood.

Ventilation of the lungs is the pprocess that mixes fresh inspired gas with alveolar gas.

If there is no ventilation at all, there will be no replenishment of oxygen and no removal of CO2. PAO2 will fall and PACO2 will rise towards the venous O2 and CO2 tensions.

After the onset of apnoea, CO2 rises rapidly and within about 30s it is about 50mmHg. This causes nearly all of the air hunger experienced while holding your breath. The subsequent rate of rise of CO2 tension is much slower, thaking 15 minutes or so to reach 80mmHg, because it is very soluble. The rapid response of arterial CO2 to apnoea explains why it is such a good gas for our body to use as the primary control mechanism for ventilation.

In contrast a reservoir of oxygen exists within the alveoli that can maintain acceptable oxygen tensions for about a minute. If the lung volume is adequate, after a deep breath, and in particular if the lung is filled with a higher than usual oxygen partial pressure, acceptable alveolar oxygen tensions can be maintaned for much longer. However, should FRC be reduced, oxygen consumption increased, or collapse likely, the benefit of 'pre-oxygenation' is markedly reduced.

If the ventilation is greater than is needed, then the alveolar gas tensions will be shift closer to inspired gas, ie the CO2 level will be lower, and the oxygen level a little higher.

Non ventilated but perfused (very low V/Q) lung units shunt venous blood to the arterial circulation, causing hypoxaemia that cannot be corrected by increasing FiO2.

The matching of ventilation to perfusion across the majority of alveoli, even in the presence of lung disease, is the key to optimising ventialtion.

Definitions

Ventilation is the process by which Oxygen and CO2 are transported to and from the lungs.

Tidal Volume (Vt) is the amount of gas expired per breath - typically 500ml at rest.

Deadspace Volume (VD) is the sum of the Anatomic Deadspace, due to the volume of the airways (typically 150ml), and Physiologic Deadspace, due to alveoli which are ventilated but not perfused (usually insignificant).

Minute Volume (VE) is the amount of gas expired per minute.

Alveolar Ventilation (VA) is the amount of gas which reaches functional respiratory units (ie, alveoli) per minute. VA = (Tidal Volume - Deadspace) x Respiratory rate

Lung Volumes

  • FRC (Functional Residual Capacity) 2.2l.(supine)
  • TLC (Total Lung Capacity) 6.2l.
  • Maximum Inspiratory Volume 4.0l. above FRC.
  • ERV (Expiratory Reserve Volume) 1.0l. below FRC.
  • RV (Residual Volume) 1.2l.
  • MVV (Maximal Voluntary Ventilation) 150 l/m.

Lung Mechanics

Inspiration

An active process requiring musular effort; 75% diaphragmatic at rest; intercostals used on exertion.

Inspiratory effort causes:

  • Fall in intrapleural pressure
  • Fall in Alveolar pressure
  • Pressure gradient from mouth to alveoli
  • Gas flow down pressure gradient

Maximum inspiratory force sometimes used as an index of resp. effort; if < 20 cmH2O most patients have difficulty

Expiration

Usually a passive process due to lung recoil:

  • Relaxation of inspiratory muscles causes:
  • Intrapleural pressure becomes less negative
  • Alveolar pressure rises
  • Pressure gradient from alveoli to mouth
  • Gas flow down pressure gradient

Respiratory Rate and I:E ratio

Normal respiratory rate is about 15 breaths per minute, increasing markedly with exertion.

Normal I:E ratio at rest and while asleep is 1:2 or less. On exertion the I:E ratio is 1:1. Inspiration is normally an active process (requiring work). Expiration is passive, and usually longer than the time required for exhalation, resulting an a no-flow period. When breathing spontaneously, the work of breathing is minimised by keeping inspiratory times short and tidal volumes low - just enough to get rid of the produced CO2. To minimise collapse, sighs are taken from time to time.

Under anaesthesia, FRC is reduced, resistance increased and collapse is common. Longer than normal inspiratory times may be required forall alveoli to reach inspiratory equilibrium. Expiratory pauses with no gas flow will not contribute to ventilation (no gas is flowing) and may contribute to collapse. All work of respiration is done by the machine.

It is likely that the optimal I:E ratio under anaesthesia is 1:1, not 1:2. A good starting point is a respiratory rate about 12 at an I:E ratio of 1:1. The actual inspiratory and expiratory time should be adjusted so that the gas flow curve in pressure mode shows near complete equilibration both in inspiration and expiration.

Airway Resistance

  • Limits gas flow down airways
  • Due mostly to airway/ETT diameter (fourth power of radius)
  • Normal response to increased resistance is increased effort
  • GA's increase resistance and decrease response, causing hypoventilation
  • Asthmatics have increased resistance due to spans (Rx Beta Agonists etc) and oedema (Rx steroids) and mucus.
  • Optimal airway resistance occurs at normal FRC
  • Under conditions of increased airway resistance, slower respiratory rates are better.

Intrapleural Pressure

  • Normally -7.5 cmH2O at mid-chest level, due to elastic recoil of lung opposed by chest wall.
  • Becomes more negative on inspiration.
  • Less negative at the dependent regions of the lung, reducing alveolar size.

Compliance

"Static" Compliance is a measure of the "stiffness" of lung and chest wall, typically 50 ml/cmH2O in adults and proportionally less in kids. It is usually due equally to lung and chest wall compliances (100 ml/cmH2O each).

Surfactant improves lung compliance, especially at low lung volumes; its absence as in ARDS, results in stiff lungs and a tendency for the alveoli to collapse and fill with fliud.

Lung collapse results in a reduction in available ventilatable lung volume, reducing compliance and causing higher than expected airway pressures.

"Dynamic" compliance includes the extra pressure needed to overcome resistance to airflow, inertia of chest wall, and viscoelasticity of tissues.

Total compliance varies from person to person and from time to time. A ventilator with pressure limited inspiration will deliver varying tidal volumes during an anaesthetic and from patient to patient. Most modern anaesthesia ventilators are of the "Volume Preset" type to minimise this problem.

Work of Breathing

Work = Pressure x Volume

Respiratory work at rest or during exercise is seldom responsible for more than 5% of the total body work. Most of this is used to overcome the lung and chest wall stiffness during inspiration. Work to overcome airway resistance is usually very small, except during exercise or in athsmatics.

Patients with most respiratory diseases have increased respiratory workloads, which may be due to high respiratory rates, stiff lungs, or high airway resistances. When the patient becomes so exhausted that they can no longer keep up the workload, respiratory failure ensues. Anaesthetic machine tubing, one-way valves, and ETTs all increase total resistance and respiratory work, while drugs will diminish respiratory effort, so that the patient with poor respiratory function usually requires ventilating both during and after the operation.

CO2 Elimination

Oxygen Transport

Effect of Shunts

Some venous blood passes through the lungs without equilibration with Alveolar gas. This "Venous Admixture" or "Shunt" subsequently mixes with oxygenated blood in the pulmonary veins, and has the effect of reducing PaO2 and elevating PaCO2.

While the slight rise in PaCO2 can be overcome easily by increasing the ventilation to normal alveoli, the same is not true for PaO2. Normal alveoli can blow off twice as much CO2 as usual if ventilated twice as much normal, but never saturate the blood leaving them any more than 100%.

A pure shunt causes hypoxaemia that DOES NOT correct by increasing inspired oxygen.

A patient with a 50% shunt breathing 100% inspired oxygen will only get a PaO2 of about 60 mmHg, but doubling their ventilation will maintain normocarbia.

Low V/Q ratio

Areas of lung with lower-than-normal ventilation cause hypoxaemia. The blood leaving these areas is part-way between alveolar and mixed venous.

If we reduce the total ventilation of an otherwise normal lung by half, ie give it a global V/Q ratio of 0.5, CO2 levels will rise and eventually reach equilibrium at 80mmHg but the patient will become very hypoxic well before the CO2 levels get high. Increasing inspired oxygen to as little as 30% will, however, completely correct the resulting hypoxaemia.

Thus hypoxaemia due to hypoventilation can be easily corrected with supplemental oxygen, whereas that due to true shunt will not correct no matter how much oxygen is administered.

Control of Ventilation

Effects of Anaesthesia

  • Impaired control of ventilation. Volatile agents almost totally abolish hypoxic responses, narcotics, sedatives, anaesthetics impair CO2 responses
  • Increased Deadspace (equipment and physiological)
  • Increased work of ventilation due to:
    • Increased circuit and airway resistance
    • Decreased lung compliance
  • Increased shunt and low V/Q areas, leading to hypoxia, due to:
    • Atelectasis of dependent parts of the lung
    • Impaired sputum clearance (cilia, atropine, sedation, pain)
    • Decreased FRC
  • More rapid onset of hypoxaemia with apnoea

Collapse, atelectasis and low V/Q areas are common under anaesthesia. As little as 30-40 seconds of apnoea in an oxygen rich environment can cause significant collapse. Recruitment manouvres can expand collapsed lungs, but PEEP alone cannot. However, after recruitment, optimal PEEP can maintain an 'open lung' and prevent or minimise subsequent collapse.

Recruitment manouvres under anaesthesia can cause hypotension, especially in hypovolaemic or elderly patients, and will increase venous pressure, so they should be performed at an appropriate moment and perhaps with transient vasopressure support.. Typical approaches are to manually valsalva for 30s to 30-40 cmH2O pressure, or to keep ventilating as usual but add say 20-25 of PEEP for about 30s with a maximul pressure limitation of about 45. The time component is essential. Frequently compliance will improve by about 1/3 after recruitment. Hypoxia in the recovery room or PACU is much less of a problem if the patient's lungs are recruited before the end of surgery, if the patient is extubated sitting up, and if periods of apnoea in high oxygen environments are avoided. This is of particular importance with obese patients

ARTIFICAL VENTILATION

Classification

  • Mouth-to-Mouth/mask/ett etc
  • IPPV - "Conventional" Mechanical Ventilation
  • PCV - Pressure Control Ventialtion
  • IMV - Intermittent Mandatory (Volume) Ventilation
  • MMV - Mandatory Minute Ventilation (amount of ventilation is automatically adjusted byt he ventilator to ensure a constant minute volume).
  • SIMV -- Synchronised IMV ("Assisted") - inspirations are brought forward in time (within a limited time window) if the patient makes a triggering effort.
  • PRVC - Pressure Regulated Volume Controlled (volume preset pressure ventilation; machine alters pressure on a breath by breath basis to generate the tidal volume set by the user)
  • BiPAP - Two-level CPAP (pt can breathe during inspiration and expiration)
  • PS - Pressure Support - positive pressure applied to the airway when an inspiratory trigger is detected and released once expiration is detected (typically by a fall in flow rate to less than 25% of the peak inspiratory flow.
  • APRV - Airway Pressure Release Ventilation - kind of long-period inverse BiPAP where the high pressure is held for an extended period of time.
  • J et Ventilation (Sanders Injector)
  • HFV - High-Frequency Ventilation
  • HFO - High-Frequency Oscilation
  • HFJV - High-Frequency Jet Ventilation
  • PEEP - Positive End-Expiratory Pressure
  • CPAP - Constant Positive Airway Pressure (pt can breathe duting expiration)
  • NPV - Negative Pressure Ventilation
  • TRIO - Tracheal Insufflation of Oxygen
  • Apnoeic oxygenation

Effects of Artifical Ventilation

Respiratory:

  • Decreased PaCO2 due to increased Alveolar Ventiilation
  • Improved PaO2 (see previous graphs)
  • Intrapleural Pressure less negative
  • Work of breathing reduced
  • Decreased lung water
  • Optimum PEEP increases alveolar size, FRC, reduces compliance, reduces shear stress, etc
  • Hazards associated with intubation, paralysis or sedation, equipment failure.

Cardiovascular:

  • Pressure gradient for venous return decreased whenever intrathoracic pressure rises
  • CVP and peripheral venous pressure rise
  • Reduced RV filling and increased RV afterload; opposite effects on LV . Note that pulmonary vascular resistance is minimised at optimal / normal FRC and increases with both lung distension and collapse.
  • Cardiac Output may fall, particularly in hypovolaemic patients, causing reflex increase in contractility, heart rate, MVO2, vasoconstriction to augment venous pressure, reduced mixed venous oxygen tension, which may worsen aterial PO2

Renal

  • Decreased renal function due to fall in Cardiac Output & Renal perfusion
  • Increased ADH due to decreased central venous wall tension

Pressure Support, CPAP or BiPAP

PEEP alone is not good for spontaneous breathing, because the patient cannot breathe 'in' easily in the expiratory phase. Simple PEEP generators are just an APL type valve occluding the expiratory limb, with the bag as a poor pressure reservoir. These simple systems will maintain FRC during controlled ventilation but markedly increase the work of breathing during spontaneous respiration.

CPAP means 'constant positive airway pressure', typically meaning that the ventilator can maintain constant airway pressure during the expiratory phase, so that the patient can breathe in at any time during the expiratory phase without the airway pressure falling below the CPAP level. Patients that require PEEP while breathing spontaneously require a CPAP generator.

BiPAP refers to maintaining constant airway pressure during both inspiration and expiration. This is a variant of Pressure Control ventilation in which the patient can breathe in and out during any phase of respiration.

Common BiPAP modes have the ventilator synchronise both inspiration and expiration to patient effort. Inspiration usually commences on detection of a patient-generated trigger (typically flow or pressure). The ventilator switches to expiration when the flow rate during inspiration falls below the peak flow rate (tyically below 25% of peak flow).

Pressure Support ventilation modes under anaesthesia are forms of BiPAP often with a fall-back in case of apnoea. Dräger Pressure Support machines will dynamically switch in and out of a fixed rate form of BiPAP ('apnoea mode') at a predertmined rate whenever apnoea occurs.

The advantages of BiPAP/Pressure Support are

  • Patient can breathe spontaneously; paralysis not always required
  • Optimum CPAP inspiratory support reduces work of breathing
  • CO2 levels are generally lower than without support
  • Intrapleural pressure generally not as high as for IPPV so less depression of C.O.

Optimising PEEP or CPAP during controlled ventilation is relatively easy. When a ventilatiator is in Pressure Control Mode the tidal volume resulting from a given differential airway pressure is proportional to lung compiance. Improved tidal volume at the same differential pressure indicate an improvement in lung compliance. If the inspiratory and expiratory times are long enough for alveolar equilibration, optimal PEEP (in a mechanical sense) is that which results in the greatest tidal volume at a given differential airway pressure.

After recruitment, PEEP should always be optimised. The ideal setting may change.

My approach to recruitment and PEEP optimisation is to:

  • Put the ventilator into Pressure Support Mode, rate of 8, I:E ratio 1:1
  • Set a differential pressure so that the tidal volume is say 0.5ml/kg
  • Ramp up the PEEP in steps (keeping the same differential pressure), noting tidal volume at each step
  • Hold the PEEP at say 20-25 for 30s
  • Ramp it down at the same steps, noting improved tidal volumes due to recruitment.
     

Ventilators

Classification

  • TYPE OF VENTILATION
    • Positive ie modern ventilators
    • Negative ie iron lung type
       
  • OTHER CAPABILITIES
    • PEEP - positive pressure at the end of inspiration (but not necessarily maintaind)
    • CPAP - maintaining positive pressure throughout expiration even with spontaneous breathing
    • Pressure Control - modes in which the primary control of inspiratory depth is inspiratory pressure, not volume. Keeping pressure constant throughout inspiration may improve gas distribution within the lung because long time constant alveoli will 'see' an opening pressure throughout the whole of inspiration
    • Pressure Support / BiPAP - see above
    • Synchronisation with spontaneous breathing, ie SIMV, PS etc
    • MMV or other 'targeted' automated modes intended to automatically adjust ventilator settingst o maintain patients within acceptable limits
    • Tube Compensation (Airway pressure shift up and down in proportion to flow to reduce work of breathing)
    • Voume preset but pressure regulated /(autoflow in Dräger machines) is when the volume is set as per standard volume control / IPPV but the actual airway pressure is held constant throught inspiration as in Pressure Control modes. This is slightly more efficient than standard IPPV
    • Specialised high frequency ventilation eg, HFV/HFO/HFJV etc.
       
  • INSPIRATORY FLOW GENERATOR
    • Turbine / blower (Dräger Primus)
    • Proportional solenoid (Most ICU ventilators, GE anaesthetic machines)
    • Piston (Dräger Primus etc)
    • In-circuit blower (Dräger Zeus)
    • Bellows / levers (Auto-hand)
    • Constant flow via adjustable needle valve +/- venturi (Ulco, Bird, other simple ventilators)
    • Self-inflating bag (field apparatus)
       
  • CYCLING (reason inspiration commences)
    • Automatic
      • Time (control / apnoea modes)
    • Patient triggered - ie SIMV, BiPAP, Pressure Support
      • Flow triggers - tyically 2-5 l/min in adults, adjustable
      • Pressure triggers - require a fall in airway pressure
    • Manually triggered
       
  • INSPIRATION LIMIT
    • Time (most control modes, ie Ti is set by the operator)
    • Flow (Pressure Support and BiPAP modes terminate inspiration when flow falls to a specified % below peak)
  • INSPIRATORY FLOW PATTERN
    • Fixed rate (classical IPPV) +/- inspiratory hold
    • Decelerating (Constant-pressure generators or venturi-driven devices, ie Ulco)
    • Programmable
    • Sinusoidal (Piston driven)
       
  • CONTROL TECHNOLOGY
    • Pneumatic +/- Magnetic (Bird)
    • Fluidic Logic (Ulco )
    • Electronic (most modern ventilators)
  • POWER REQUIREMENTS CONTROLS

Use in Anaesthesia

  • Aim for normocarbia or slight hypocarbia
  • Usually Volume preset IPPV devices
  • Tidal volume and rate adjusted to suit patient (CO2 analysers useful)

With CO2 absorber ON:

  • All inspired gas is free of CO2
  • Effective ventilation depends only on Ventilator settings
  • Very low Fresh Gas Flows may be used in the circle circuit

With the CO2 absorber OFF:

  • Provided that the ventilator settings deliver normal alveolar ventilation, the effective ventilation depends on Fresh Gas Flow.
  • CO2 rebreathing occurs

Hazards

  • Disconnection from circuit
  • Failure to deliver ventilation
  • Barotrauma

Monitoring Ventilation

  • Colour of the Patient
  • Watching the chest move
  • Precordial/Oesophageal Stethoscope +/- telemetry
  • Listening to sound of ventilator
  • Measurement of Circuit Parameters, such as pressure or tidal volume
  • Measurement of Patient Parameters, such as ETCO2, SpO2, chest wall impedance,etc

 

HUMIDIFICATION

Physics

  • Vapour - Gas Phase of a liquid below boiling point
  • Aerosol/Mist - suspension of fine droplets of a liquid in a gas
  • Absolute Humidity - amount of water vapour per unit of gas (mg/l)
  • Relative Humidity - Absolute humidity of the sample as a % of the absolute humidity of fully saturated gas at the same temperature

Measurement of Humidity

  • Dew Point Hygrometer
  • Hair Hygrometer
  • Wet/Dry thermometer
  • Humidity Sensors
  • Measurement of water used by humidifier

Physiology

The nose is a very efficient humidifier:

  • 60% RH at the post-nasal space
  • 5% RH in the mouth
  • 100% at 37 degC in the bronchi

Mouth-breathing is less efficient (60% RH in the upper trachea)

Heat and water loss through the nose is minimised by cooling on inspiration and warming on expiration.

Humidification is required to maintain of ciliary activity, prevent squamous epithelial changes (Mucosal changes in 2-3 hours), prevent dehydration and thickening of secretions and possible ETT obstrucion, minimise atelectasis and tracheitis, and to decrease heatloss

Methods

ANAESTHETIC CIRCUIT CONSIDERATIONS

  • Cylinder gas is completely dry, and tracheal intubation bypasses the nose
  • Waters CO2 absorber heats and humidifies gas very effectively
  • Circle CO2 absorbers are of slight benefit only
  • Bain circuit allows some warming but very little humidification

HEAT AND MOISTURE EXCHANGERS

  • Relatively cheap
  • 70%-80% effective humidification
  • Increased deadspace, resistance, risk of disconnection

HUMIDIFIERS

Up to 100% humidification, essential for longterm respiratory care or if drying of excessive secretions occurs despite HME's. Modern types heat both the water bath and patient hose to prevent rainout. Disadvantages:

  • Cost
  • Potential for leaks, disconnection
  • Drowning if tipped
  • Source of infection
  • Unreliable
  • Airway burns
  • Increased airway resistance

EQUIPMENT

FISHER & PAYKEL

  • Water heated to 37°C , servo controlled hose heaters in newer units to prevent 'rain-out'.

GRANT - NICHOLAS

  • Water heated to 45°C , hose servo to 37°C. Inefficient at >10l/min flows

BOURNS

  • Basic Kettle type

NEBULISERS

  • Produce aerosols with humidity depending on temperature.
  • Air is usually cooled by the droplets ->cold wet air
  • Most useful for drug delivery

 


Last updated Monday, August 08, 2016
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