RESPIRATORY PHYSIOLOGY DURING ANESTHESIA Presenter – Hitesh Gupta Moderater – Dr Anil Ohri

Anesthesia - 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)

GA produces Fall in FRC Fall in lung compliance Uneven distribution of ventilation Increased physiological dead space Increased P(A-a)O2

FRC reduced by 0.8 to 1.0 L - changing body position from upright to supine another 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

Cranial 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).

Causes 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 FRC Supine Position: FRC decreases by 0.8-1.0L Diaphragm cephalad displacement

. Immobility, excessive intravenous fluid administration: Dependent areas below the heart (zone3-4) are susceptible to edema this will happen after being immobile (5 hour or more) in supine position with excess volume administration

. Surgical position: Supine : FRC Trendelenburg: FRC Steep trendelenburg: FRC Lateral decubitus : FRC in dependent lung and FRC in un dependent lung (overall FRC ) Lithotomy : FRC more than supine Prone : FRC Prone> lateral decubitus > supine > lithotomy> trendelenburg> steep trendelenburg

Ventilation pattern: Rapid shallow breathing occurs due to reduced compliance - FRC This can be prevented by Periodic large mechanical inspiration Spontaneous sigh Peep

Tracheal tube (low or high pressure cuffs any place in trachea) . Decreased removal of secretion: Increasing viscosity & slowing mucocilliary clearance Tracheal tube (low or high pressure cuffs any place in trachea) High FiO2 Low moisture Low temperature Halogenated anesthetics

Compliance and Resistance of the Respiratory System Static compliance(lungs and chest wall) is reduced – from 95 to 60 mL/cm H2O during anesthesia static lung compliance- 187 mL/cm H2O awake to 149 mL/cm H2O during anesthesia Resistance( total respiratory system and lungs)increases both spontaneous breathing and mechanical ventilation increased lung resistance reflects reduced FRC during anesthesia

Causes of decreased lung compliance Atelectasis 15% 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 lung increases with BMI but is independent of age COPD patients show less atelectasis Risk factors: High FiO2 Low V/Q ratio Longer time exposure of high FiO2 to low V/Q

ZONE 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 closure ZONE C – there is complete cessation of ventilation (atelectasis) but still perfusion is there (shunt)

Prevention of atelectasis Positive end expiratory pressure (PEEP) Application of 10 cm water PEEP can open collapsed lung but it recollapses on cessation of peep Gen PEEP of 10 cm H2O squeezes perfusion to lower lung Selective application of PEEP to lower lung might lead to redistribution to upper lung

Maintenance of muscle tone Anesthetic that allows maintaince of respiratory muscle tone will prevent atelectasis e.g ketamine Pacing of diaphragm through phrenic nerve stimulation prevents atelectasis ,but is too complicated

Recruitment maneuvers Sigh maneuver Double VT airway pressure of 30 cm of H2O decrease atelectasis by 50 % of initial size for complete reopening 40 cm of H2O is req.

Prevention of atelectasis VC maneuver Vital 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

Prevention of atelectasis Minimising gas resorption 100% O2 - collapse reappears faster but using 40% O2 in nitrogen, atelectasis appears slowly Avoidance of preoxygenation procedure (ventilation with 30% O2) eliminates atelectasis formation during induction and subsequent anesthesia CPAP of 10 cm H2O can prevent atelectasis even with 100 % O2

Prevention of atelectasis Postanesthetic oxygenation Postanesthetic 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 anesthesia VC maneuver followed by a low O2 concentration, 40% keeps the lung open after recruitment until end of anesthesia.

Airway Resistance Increase airway resistance, leads to airway collapse Factors: Decreases in FRC ETT Upper and lower airway passages External anesthesia apparatus

Uneven distribution of ventilation Right > left Nondependent > dependent PEEP increases dependent lung ventilation

Distribution of Lung Blood Flow(Perfusion) Uneven distribution Base> apex successive 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.

V/Q ratios V/Q ratio: 0.8 Shunt: V/Q ratio =0, perfusion only Dead space: V/Q ratio =infinity, ventilation only Perfusion increases at a greater rate than ventilation Apical area: higher V/Q ratio Basal area: lower V/Q ratio (shunt)

during anesthesia increased VA /Q mismatch increased Venous admixture (approx 10% cardiac output). increased alveolar dead space

Hypoxic Pulmonary Vasoconstriction Normally PaO2 decrease will cause HPV inhaled anesthetics inhibit HPV . Aggravate an existing V/Q mismatch no such effect seen with intravenous anesthetics (barbiturates) isoflurane and halothane depress the HPV response by 50% at 2 MAC Direct: nitroprusside ,NTG, Isoproterenol ,inhaled anesthetics, hypocapnia Indirect: MS , fluid overload, high fio2 , hypothermia ,emboli, vasoactive drugs, lung disease

Effect 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 muscles Anaesthesia also reduces response to hypoxia due to effect on carotid body receptors

Effect of depth of anesthesia on respiratory pattern Less than MAC vary from excessive hyperventilation to breath holding 1 MAC (light anesthesia) regular pattern with larger VT than normal More deep end inspiration pause (hitch) – active and prolong expiration

Effect of depth of anesthesia on respiratory pattern More deep (moderate) faster and more regular – shallow –no pause – Inspiration = Expiration Deep Narcotic- N2O : Deep and slow Volatiles : rapid & shallow (panting) Very deep all inhaled drugs : gasping-jerky respiration – paradoxical movement of chest-abdomen (only diaphragmatic respiration) just like airway semi obstruction or partial paralysis

Effect of depth of anesthesia on spontaneous minute ventilation Minute ventilation decreases progressively as depth of anesthesia increases ET CO2 increases as depth of anesthesia increases Increase of CO2 caused by halogenated anesthetics (<1.24 MAC) enflurane > desflurane =isoflurane > sevoflurane > halothane (>1.24 MAC) enflurane = desflurane > isoflurane > sevoflurane Ventilation response to CO2 increase is decreased Apnea threshold is increased

Factors That Influence Respiratory Function During Anesthesia Spontaneous Breathing FRC is reduced to the same extent during anesthesia atelectasis occurs to almost the same extent in anesthetized spontaneously breathing subjects as during muscle paralysis.

Increased Oxygen Fraction As Fio2 is increased, shunt is also increased explained by attenuation of HPV response with increasing Fio2 or further development of atelectasis and shunt in lung units with low VA /Q ratios Body Position FRC is reduced in supine position Lateral position causes severe impairment in arterial oxygenation in some patients. ventilation distribution was more uniform in anesthetized subjects who were in the prone position

Age arterial oxygenation is impeded with increasing age of the patient shunt is independent of age 23 to 69 years There is increasing VA /Q mismatch with age major cause of impaired gas exchange during anesthesia at ages younger than 50 years is shunt, whereas at higher ages mismatch becomes increasingly important.

Obesity worsens the oxygenation of blood markedly reduced FRC, which promotes airway closure to a greater extent than in a normal subject PEEP , CPAP or near-VC inflations followed by PEEP ventilation

Preexisting Lung Disease Smokers and patients with lung disease have severe impairment of gas exchange in the awake state as well as during anesthesia smokers with moderate airflow limitation have less shunt, however, considerable Va /Q mismatch with a large perfusion fraction to low Va /Q regions Reason - chronic hyperinflation which changes the mechanical behavior of the lungs and their interaction with the chest wall such that the tendency to collapse is reduced these low Va /Q ratios can be converted over time to resorption atelectasis.

Regional Anesthesia extensive 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

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