1. Mechanical Ventilation & Strategies for Oxygenation
Dawn Oddie

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

3. Physiology

4. Where it all happens!
300 million alveoli

5. 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

6. 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?

7. 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

8. Lung Volumes

9. 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.

10. 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.

11. 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

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

13. 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

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

15. 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)

16. 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

17. 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 = mls / min

18. Haemoglobin

19. 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)

20. 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

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

22. 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)

23. 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.

24. 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?

25. 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.

26. 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)

27. 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.

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

29. 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

30. 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

31. Oxygen dissociation curve
Increased affinity
Reduced Affinity

32. 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

33. 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

34. 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 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

35. 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 kPa

36. 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.

37. 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

38. Indicators for initiating mechanical ventilation?

39. Types of positive pressure ventilation
Non invasive
Invasive

40. 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

41. CPAP

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

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

44. 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

45. 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

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

47. 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

48. 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.

49. 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

50. 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

51. 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)

52. 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

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

54. Waveforms

55. 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

56. Biphasic Positive Airway Pressure

57. BIPAP / APRV (Airway pressure release ventilation)

58. Why is mechanical ventilation
bad for you?

59. Problems with Mechanical Ventilation

60. Problems with Intubation

61. 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

62. 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

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

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

65. 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.

66. Volutrauma

67. 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

68. 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

69. 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

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

71. 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

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

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

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

75. 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

76. 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

77. 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.

78. 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

79. 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

80. 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

81. 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

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

83. 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

84. Scenarios

85. 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

86. 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

87. 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

88. THE END