5 Physiology of normal breathing I:E ratio timesHow do we breathe?Negative pressureActive inspirationPassive expirationRespiratory rateHigh lung volume (Inhalation)Low lung volume (Exhalation) /Functional residual capacityTidal 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 stemMedullary rhythmicity areaPneumotaxic area / Apneustic area (transition from I to E)Inflation (Hering-Breuer) reflex - Stretch receptorsCortical influences – cerebral cortex giving some voluntary control eg hold breath underwaterCentral chemosensitive area (pH / H+) – MedullaPeripheral chemoreceptors (CO2 / O2 / H+) – carotid bodiesProprioceptors – joints / musclesOther influences – Baroreceptors / Temp / Pain / stretching the anal sphincter muscle / Irritation of the air passages
9 Respiratory Mechanics- Compliance Compliance is ΔV/ΔP (Change in Volume / change in pressure)Total lung is made up of thoracic and lung compliancePulmonary 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 guidesPulmonary 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.
12 Some Important Physiology V/Q MismatchOxygen CascadeOxyhaemoglobin Dissociation CurveSpirometry Trace
13 Supply and demand V/Q mismatch Functional alveoli Permeable membranes V = VentilationP = PerfusionHypoxic Pulmonary VasoconstrictionFunctional alveoliPermeable membranesCirculating volume – withAdequate haemoglobin levelsOxygen saturation of haemoglobin (affinity)Oxygen dissociationPerfusion pressure
14 When room air just isn’t enough….. Increased metabolic demandV/Q mismatchDamaged alveoli / airwaysBlocked alveoliInadequate circulation
15 Some indications to increase O2 Acute respiratory failure eg pneumonia, asthma, pulmonary oedema, pulmonary embolusAcute myocardial infarctionCardiac FailureShockHypermetabolic states eg major trauma, sepsis, burnsAnaemiaCarbon monoxide poisoningCardio respiratory resuscitationDuring / post anaesthesiaPre-suctionSuppressant drug eg narcoticsPyrexia (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 metabolismProduction of lactic acidIncreasing metabolic acidosisLow pHLow HCO3Negative base excessCell 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 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 = mls / min
19 HaemoglobinIntracellular 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 oxygenPrimary 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 HaemoglobinAverage 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
21 The transfusion debate… Risks of vs Reduced oxygentransfusion carrying capacity
22 Factors affecting carriage Timing of haemoglobin uptake and release of oxygen affected by,Partial pressure of oxygen (PaO2)TemperatureBlood pHPartial 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 thisdecrease in pressure is: in agiven volume of air, there arefewer molecules present. Thepercentage of those moleculesthat are oxygen is exactly thesame: 21%.The problem is that there arefewer molecules of everythingpresent, 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 partialpressures) 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 PressurePartial 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 wallsPP 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 ofHaemoglobin (Y axis) and partial pressure ofarterial 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 linearSlope steeply progressive between 1.5 – 7kPa (area of most rapid uptake and delivery of oxygen to and from haemoglobin), then plateaus out between 9 – 13.5kPaHaemoglobin 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 P50P50 is conventional measure of haemoglobin affinity for oxygenIncreased P50 indicates a right shift of the standard curve – meaning larger partial pressure necessary to maintain a 50% oxygen saturation
32 Factors influencing the position of oxygen dissociation curve To the right,HyperthermiaAcidosis (pH)Increased pCO2Endocrine disordersCurve shifts to left,HypothermiaAlkalosisDecreased pCO2Carbon monoxideGenerally a shift to the,Right will favour unloading of oxygen to the tissuesLeft will favour reduced tissue oxygenation
33 Factors influencing the position of oxygen dissociation curve - explained To the rightAs pH declines (acidosis) the affinity of haemoglobin for oxygen reduces. Result – less oxygen is bound while more oxygen is unloadedBohr effectTo the leftTemperature – 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 = 8.0kPa30mmHg = 4.0kPa
35 The oxygen cascade Transport has three stages (steps), By gas exchange in the lungsPartial pressure gradient of oxygen (PaO2) in alveoli 13.7kPaPartial pressure gradient of oxygen (PaO2) in pulmonary capillaries 5.3kPaTransport of gases in the bloodPartial pressure gradient of oxygen (PaO2) in arterial blood 13.3kPaMovement from blood into the tissuesPartial pressure gradient of oxygen (PaO2) in tissues 2.7kPaMitochondrial 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.
42 NIV - BiPAP IPAP / PS / ASB EPAP Inspiratory assistance with each spontaneous breathEPAPExpiratory 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 patientInhalation replenishes alveolar gasBalance needed between O2 replenishment and CO2 removal
45 Ventilators – What do they need to do… Mechanical ventilators are flow generatorsMust be able to,ControlCyclingTriggeringBreathsFlow patternMode or breath pattern
46 Ventilator strategyAim to achieve adequate minute volume with the lowest possible airway pressure
47 Ventilator Classification ControlHow the ventilator knows how much flow to deliverCan be,Volume controlled (volume limited, volume targeted) & pressure variablePressure controlled (pressure limited, pressure targeted) & volume variableDual controlled (volume targeted (guaranteed) pressure limited
48 Ventilator Classification CyclingHow the ventilator switches from inspiration to expiration (the flow has been delivered – how long does it stay there?)Time cycled e.g. pressure controlled ventilationFlow cycled e.g. pressure supportVolume cycled. The ventilator cycles to expiration once a set tidal volume has been delivered.
49 Ventilator Classification TriggeringWhat causes the ventilator to cycle to inspiration. Ventilators may be……Time triggeredCycles at set frequency as determined by the ratePressure triggeredVentilator senses the patients inspiratory effort by sensing a decrease in baseline pressureFlow triggeredConstant 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 BreathsMandatory(controlled) – determined by the respiratory rateAssistedE.g. synchronised intermittent mandatory ventilation (SIMV)SpontaneousNo additional assistance during inspiration e.g. CPAP
51 Ventilator Classification Flow patternSinusoidal (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 PatternCMVVolume Assist-Control (caution with sensitivity)Synchronised Intermittent Mandatory Ventilation – SIMVPressure supportHigh frequency ventilationBiPAP/BILEVEL – airwaypressure release ventilationProportional assist ventilationAutomatic tube compensationEnhance patient interactivity
55 So the problem is this If the patient is hypoxic then they need O2 If still hypoxic then they need +ve pressureIf 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
61 Problems with Intubation Bypass natural protective mechanisms – moisten, filter, warmPlastic tubing – airway trauma, vocal cord damagePressure sores – oral or from cuffMouth care!Need sedation
62 Sedation and Ventilation Good PointsReduced painReduced stressEasier to nurseBetter for relativesLess chance of lines falling outBad PointsIncreased pneumonia riskVenous thrombosisPressure area problemsHypotensionProlonged ICU stayBetter for relativesIncreased barotrauma
64 Barotrauma – pressureAir leak from alveoli situated near respiratory bronchioles10 – 20% of ventilated patientsPredisposing factorsFrequent +ve pressure breathsInfectionARDSHypovolaemia
65 Volutrauma - volumeExcessive stretch in the absence of excessive airway pressure.If alveoli cannot over distend they are less likely to be damagedNot just a mechanical problem but also a local and generalised inflammatory response.C.f. IL-6 levels in ARDS Net lung protection study.
67 VentilatorsAim to achieve adequate minute volume with the lowest possible airway pressureHigh PEEP levels 10 – 20 (open lung)Permissive hypercapniaPatient specific tidal volume 6 – 7ml/KgImproved 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 / secretionsCOPD – respiratory driveToxic – 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, convulsionsPulmonaryLungs show inflammation / scarring (ARDS) and pulmonary oedemaRetinopathicRetinal damage
71 Suctioning and Mechanical Ventilation Causes Lung de-recruitment due toDisconnection from the ventilatorLoss of PEEPWorse V/Q mismatchSuctioning procedure itselfHigh negative pressure decreases lung volumeWorse if the suction is openSuction only when clinically indicated / Pre oxygenate /Minimal suction pressure / limit suction time
72 Prone Positioning What a nightmare! Can dramatically alter oxygenation AlsoInduces a uniform V/Q distributionPromotes alveolar recruitmentPromotes secretion drainage
73 Prone Positioning Debate about outcome in the most hypoxic Complications,Manual HandlingAccidental ExtubationPressure soresFacial OedemaLine disconnection
74 Gattinoni et al (2001) NEJM 345 (8): 568 SurvivalOxygenationImproved oxygenation, but not overall survival rate
75 High-Frequency Oscillatory Ventilation in Adults Seems a nice idea3 – 10 Hz oscillation‘Tidal volume’ less than normalLess opening and closing of lungsWell established in neonatal and paediatric populationIssues,Patients need heavy sedation / NMJ blockadeDrop in preloadTransport not possibleClinical Ex difficultLittle 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 trial148 patientsHFOV n = 75Conventional Ventilation n = 73Outcome 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 survival37% versus 52%P = 0.102Big 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 QuestionsIdeal timing of the interventionProne positionNitric OxideWhen do you discontinueLong term effects on lung functionUse of volume recruitment methods
79 ECMOIt 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 Failure180 patientsUse 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 DecideHow much time to you have?What resources are availableIs escalation appropriate
83 Your Patient is Hypoxic - What Do You Do? Increase the supply of OxygenDrive it into the lungsGet the lungs in the best shape possibleMake sure blood is getting to the lungsReduce the metabolic demand for oxygen
85 Case 44 year old lady 11/7 post intubation for pneumonia. Trachy. FiO2 .3, PO2 11Sudden SOBFiO2 1.0, Sats 80%Increase the supply of OxygenDrive it into the lungsGet the lungs in the best shape possibleMake sure blood is getting to the lungsReduce the demand for oxygen
86 Case 70 year old gentleman Sudden SOB HR 150 bpm RR 50 FiO2 0.21 Increase the supply of OxygenDrive it into the lungsGet the lungs in the best shape possibleMake sure blood is getting to the lungsReduce the demand for oxygen
87 Case 55 year old Rescued from smoke filled room PaO2 7 on FiO2 85% Increase the supply of OxygenDrive it into the lungsGet the lungs in the best shape possibleMake sure blood is getting to the lungsReduce the demand for oxygen