Presentation on theme: "RESPIRATORY PHYSIOLOGY DURING ANESTHESIA"— Presentation transcript:
1RESPIRATORY PHYSIOLOGY DURING ANESTHESIA Presenter – Hitesh GuptaModerater – Dr Anil Ohri
2Anesthesia - impairment in pulmonary function whether patient is breathing spontaneously or ventilated mechanically after muscle paralysis.20% of patients may suffer from severe hypoxemia(spo2 81% for up to 5 minutes)
3GA producesFall in FRCFall in lung complianceUneven distribution of ventilationIncreased physiological dead spaceIncreased P(A-a)O2
4FRC reduced by0.8 to 1.0 L - changing body position from upright to supineanother 0.4- to 0.5-L - when anesthesia is given.Muscle paralysis and mechanical ventilation cause no further decrease in FRC.average reduction corresponds to around 20% of awake FRC
5Cranial shift of diaphragm and a decrease in transverse diameter of the thorax contribute to lowered functional residual capacity (FRC).Decreased ventilated volume (i.e. in atelectasis and airway closure ) is a possible cause of reduced lung compliance (CL).Decreased airway dimension by the lowered FRC should contribute to increased airway resistance (Raw).
6Causes of reduced FRC General anesthesia: due to loss of respiratory muscle tone, which shifts the balance between the elastic recoil force of the lung and the outward force of the chest wall to a lower chest and lung volume.Maintenance of muscle tone( ketamine anesthesia) does not reduce FRCSupine Position:FRC decreases by LDiaphragm cephalad displacement
7. Immobility, excessive intravenous fluid administration: Dependent areas below the heart (zone3-4) are susceptible to edemathis will happen after being immobile (5 hour or more) in supine position with excess volume administration
8. Surgical position: Supine : FRC Trendelenburg: FRC Steep trendelenburg: FRCLateral decubitus : FRC in dependent lung and FRC in un dependent lung (overall FRC )Lithotomy : FRC more than supineProne : FRCProne> lateral decubitus > supine > lithotomy> trendelenburg> steep trendelenburg
9Ventilation pattern:Rapid shallow breathing occurs due to reduced compliance - FRCThis can be prevented byPeriodic large mechanical inspirationSpontaneous sighPeep
10Tracheal tube (low or high pressure cuffs any place in trachea) . Decreased removal of secretion:Increasing viscosity & slowing mucocilliary clearanceTracheal tube (low or high pressure cuffs any place in trachea)High FiO2Low moistureLow temperatureHalogenated anesthetics
11Compliance and Resistance of the Respiratory System Static compliance(lungs and chest wall) is reduced – from 95 to 60 mL/cm H2O during anesthesiastatic lung compliance- 187 mL/cm H2O awake to 149 mL/cm H2O during anesthesiaResistance( total respiratory system and lungs)increases both spontaneous breathing and mechanical ventilationincreased lung resistance reflects reduced FRC during anesthesia
12Causes of decreased lung compliance Atelectasis15% to 20% of lung is collapsed at the base of lung during uneventful anesthesia.thoracic surgery and cardiopulmonary bypass > 50% of the lung can be collapsed.decreases towards apex of lungincreases with BMI but is independent of ageCOPD patients show less atelectasisRisk factors:High FiO2Low V/Q ratioLonger time exposure of high FiO2 to low V/Q
13ZONE A – ventilation > perfusion resulting in dead space like effect ZONE B – perfusion > ventilation leading to low Va/Q and caused impaired oxygenation of blood due to intermittent airway closureZONE C – there is complete cessation of ventilation (atelectasis) but still perfusion is there (shunt)
14Prevention of atelectasis Positive end expiratory pressure (PEEP)Application of 10 cm water PEEP can open collapsed lung but it recollapses on cessation of peepGen PEEP of 10 cm H2O squeezes perfusion to lower lungSelective application of PEEP to lower lung might lead to redistribution to upper lung
15Maintenance of muscle tone Anesthetic that allows maintaince of respiratory muscle tone will prevent atelectasis e.g ketaminePacing of diaphragm through phrenic nerve stimulation prevents atelectasis ,but is too complicated
16Recruitment maneuvers Sigh maneuverDouble VTairway pressure of 30 cm of H2O decrease atelectasis by 50 % of initial sizefor complete reopening 40 cm of H2O is req.
17Prevention of atelectasis VC maneuverVital capacity maneuver is the volume inflated to the maximum breath by the awake subject before anesthesia.Inflation of lungs to +40 cm H2O maintained for no more then 7 to 8 sec re expand all previously collapsed lung tissue
18Prevention of atelectasis Minimising gas resorption100% O2 - collapse reappears faster but using 40% O2 in nitrogen, atelectasis appears slowlyAvoidance of preoxygenation procedure (ventilation with 30% O2) eliminates atelectasis formation during induction and subsequent anesthesiaCPAP of 10 cm H2O can prevent atelectasis even with 100 % O2
19Prevention of atelectasis Postanesthetic oxygenationPostanesthetic oxygenation (100% O2) 10 minutes before termination of anesthesia together with a VC maneuver at the end of anesthesia will not protect against atelectasis at the end of anesthesiaVC maneuver followed by a low O2 concentration, 40% keeps the lung open after recruitment until end of anesthesia.
20Airway Resistance Increase airway resistance, leads to airway collapse Factors:Decreases in FRCETTUpper and lower airway passagesExternal anesthesia apparatus
21Uneven distribution of ventilation Right > leftNondependent > dependentPEEP increases dependent lung ventilation
22Distribution of Lung Blood Flow(Perfusion) Uneven distributionBase> apexsuccessive increase in perfusion down the lung, from the ventral to the dorsal aspect.PEEP impede venous return to the right heart and therefore reduce cardiac output.PEEP causes a redistribution of blood flow toward dependent lung regions.By this upper lung regions may be poorly perfused,causing a dead space–like effect.
23V/Q ratios V/Q ratio: 0.8 Shunt: V/Q ratio =0, perfusion only Dead space: V/Q ratio =infinity, ventilation onlyPerfusion increases at a greater rate than ventilationApical area: higher V/Q ratioBasal area: lower V/Q ratio (shunt)
25during anesthesiaincreased VA /Q mismatchincreased Venous admixture (approx 10% cardiac output).increased alveolar dead space
26Hypoxic Pulmonary Vasoconstriction Normally PaO2 decrease will cause HPVinhaled anesthetics inhibit HPV . Aggravate an existing V/Q mismatchno such effect seen with intravenous anesthetics (barbiturates)isoflurane and halothane depress the HPV response by 50% at 2 MACDirect: nitroprusside ,NTG, Isoproterenol ,inhaled anesthetics, hypocapniaIndirect: MS , fluid overload, high fio2 , hypothermia ,emboli, vasoactive drugs, lung disease
27Effect of depth of anesthesia on respiratory drive Inhaled anaesthetics and barbiturates reduce sensitivity to CO2 and the effect is dose dependent.due to impeded function of intercoastal musclesAnaesthesia also reduces response to hypoxia due to effect on carotid body receptors
28Effect of depth of anesthesia on respiratory pattern Less than MACvary from excessive hyperventilation to breath holding1 MAC (light anesthesia)regular pattern with larger VT than normalMore deepend inspiration pause (hitch) – active and prolong expiration
29Effect of depth of anesthesia on respiratory pattern More deep (moderate)faster and more regular – shallow –no pause – Inspiration = ExpirationDeepNarcotic- N2O : Deep and slowVolatiles : rapid & shallow (panting)Very deepall inhaled drugs : gasping-jerky respiration – paradoxical movement of chest-abdomen (only diaphragmatic respiration) just like airway semi obstruction or partial paralysis
30Effect of depth of anesthesia on spontaneous minute ventilation Minute ventilation decreases progressively as depth of anesthesia increasesET CO2 increases as depth of anesthesia increasesIncrease of CO2 caused by halogenated anesthetics(<1.24 MAC) enflurane > desflurane =isoflurane > sevoflurane > halothane(>1.24 MAC) enflurane = desflurane > isoflurane > sevofluraneVentilation response to CO2 increase is decreasedApnea threshold is increased
31Factors That Influence Respiratory Function During Anesthesia Spontaneous BreathingFRC is reduced to the same extent during anesthesiaatelectasis occurs to almost the same extent in anesthetized spontaneously breathing subjects as during muscle paralysis.
32Increased Oxygen Fraction As Fio2 is increased, shunt is also increasedexplained by attenuation of HPV response with increasing Fio2 or further development of atelectasis and shunt in lung units with low VA /Q ratiosBody PositionFRC is reduced in supine positionLateral position causes severe impairment in arterial oxygenation in some patients.ventilation distribution was more uniform in anesthetized subjects who were in the prone position
33Age arterial oxygenation is impeded with increasing age of the patient shunt is independent of age 23 to 69 yearsThere is increasing VA /Q mismatch with agemajor cause of impaired gas exchange during anesthesia at ages younger than 50 years is shunt, whereas at higher ages mismatch becomes increasingly important.
34Obesity worsens the oxygenation of blood markedly reduced FRC, which promotes airway closure to a greater extent than in a normal subjectPEEP , CPAP or near-VC inflations followed by PEEP ventilation
35Preexisting Lung Disease Smokers and patients with lung disease have severe impairment of gas exchange in the awake state as well as during anesthesiasmokers with moderate airflow limitation have less shunt, however, considerable Va /Q mismatch with a large perfusion fraction to low Va /Q regionsReason - chronic hyperinflation which changes the mechanical behavior of the lungs and their interaction with the chest wall such that the tendency to collapse is reducedthese low Va /Q ratios can be converted over time to resorption atelectasis.
36Regional Anesthesiaextensive blocks (thoracic and lumbar segments)- inspiratory capacity is reduced by 20% and expiratory reserve volume approaches zero.Diaphragmatic function is often spared, even in sensory block up to the cervical segments.Arterial oxygenation and carbon dioxide elimination are well maintained