Ventilation-Perfusion Mismatch Optimum gas exchange: Ventilation and perfusion must match each other in all lung regions. Mean ratio of approximately 1 somewhere in the middle of the lung Range of ratios from 0.5 in the bottom of the lung to 5.0 in nondependent way of showing the matching : multicompartmental analysis by a multiple inert gas elimination technique : (MIGET) PAO2 - PaO2 ~ 3 to 5 mm Hg (0.4 to 0.7 kPa) More V/Q mismatch, the PAO2 - PaO2 difference is further increased

Impaired Diffusion Reduces PaO2 can occur if the alveolar-capillary membranes are thickened: fibrosis systemic vascular diseases

Right-to-Left Shunt 2% to 3% of cardiac output in normal In pathologic states, between nearly normal to above 50% of cardiac output Shunt increases to 25%, the rise in PaO2 will be small by giving O2 With a shunt of 30% or greater, almost no effect of added O2 can be seen

Respiratory Function During Anesthesia Anesthesia causes an impairment in pulmonary function either: Breathing spontaneously or Ventilated mechanically FIO2 is maintained at around 0.3 to 0.4. Despite these measures : Mild to moderate hypoxemia: O2 Sat 85% to 90% ~half of all patients undergoing elective surgery. Last few seconds to up to 30minutes. In about 20% of patients O2 Sat below 81% for up to 5 minutes postoperative clinically significant pulmonary complications : 1% to 2% after minor surgery up to 20% after upper abdominal and thoracic surgery

Lung Volume and Respiratory Mechanics During Anesthesia Lung Volume FRC, is reduced by 0.8 to 1.0 L from upright to supine 0.4- to 0.5-L decrease when anesthesia has been induced So,End-expiratory lung volume is reduced from approximately 1.5 to 2 L Muscle paralysis and mechanical ventilation cause no further decrease in FRC.

Compliance and Resistance of the Respiratory System Static compliance(total) is reduced : From 95 to60 mL/cm H2O during anesthesia. Static lung compliance : From a mean of 187 mL/cm H2O awake to 149 mL/cm H2O during anesthesia The possibility increased lung resistance :merely reflects reduced FRC during anesthesia

Atelectasis and Airway Closure During Anesthesia Atelectasis : Atelectasis could not be shown on conventional chest radiography On CT with transverse exposure of the chest: Development of densities in the dependent regions shown during anesthesia Atelectasis appears in approximately 90% of all patients who are anesthetized. 15% to 20% of the lung is regularly collapsed at the base of the lung during uneventful anesthesia After thoracic surgery and cardiopulmonary bypass: More than 50% of the lung can be collapsed even several hours after surgery. There is good correlation between the amount of atelectasis and pulmonary shunt as measured by MIGET.

A regression equation based on 45 patients studied during anesthesia with inhaled anesthetics : Shunt = 0.8 × atelectasis (r =.81, P <.01)

Prevention of Atelectasis During Anesthesia POSITIVE END-EXPIRATORY PRESSURE: Application of 10–cm H2O PEEP will consistently reopen collapsed lung tissue.

Prevention of Atelectasis During Anesthesia MAINTENANCE OF MUSCLE TONE. RECRUITMENT MANEUVERS:

Prevention of Atelectasis During Anesthesia MINIMIZING GAS RESORPTION: Ventilation with pure oxygen after a VC maneuver that reopened collapsed lung: Resulted in rapid reappearance of the atelectasis. But 40% O2 in nitrogen is used atelectasis reappears slowly

Prevention of Atelectasis During Anesthesia POSTANESTHETIC OXYGENATION: Not only preoxygenation promotes formation of atelectasis but: Also the so-called postanesthetic oxygenation at the end of the surgery. This procedure is often combined with suctioning of the airway tree. A VC maneuver followed by a lower O2 concentration, 40%, kept the lung open after Recruitment until the end of anesthesia. Airway Closure As much as 74% of the impaired arterial oxygenation can be explained by atelectasis and airway closure taken together, according to the following equation.

Distribution of Ventilation and Blood Flow During Anesthesia Distribution of Ventilation: Redistribution of inspired gas away from dependent to nondependent has been observed in anesthetized supine humans by isotope techniques. PEEP increases dependent lung ventilation in anesthetized subjects in lateral position Restoration of FRC toward awake level returns gas distribution toward awake pattern. Distribution of Lung Blood Flow: The lowermost portion of the lung, which was atelectatic as evidenced by simultaneous CT, was still perfused. PEEP : reduce QT, Affect PVR Redistribution of blood flow toward dependent lung regions.

Hypoxic Pulmonary Vasoconstriction Several inhaled anesthetics have been found to inhibit HPV in isolated lung No such effect has been seen with intravenous anesthetics (barbiturates). The HPV response may obscured by changes in : Cardiac output, Myocardial contractility Vascular tone Blood volume distribution Blood pH Lung mechanics. With no gross changes in cardiac output, isoflurane and halothane depress the HPV by 50% at a 2 MAC

Ventilation-Perfusion Matching During Anesthesia Dead Space, Shunt, and Ventilation-Perfusion Relationships Both CO2 elimination and oxygenation of blood are impaired : Increased dead space ventilation? Or High V/Q ratios? Impairment in arterial oxygenation is more severe in: Higher ages Obesity Smokers Venous admixture increased during anesthesia to approximately 10% of QT.

Factors That Influence Respiratory Function During Anesthesia Spontaneous Breathin 1- FRC is reduced 2- Atelectasis (1&2) Same extent in spontaneously breathing as during muscle paralysis. 3- Cranial shift of the diaphrag lower, dependent portion of the diaphragm moved the most, whereas with muscle paralysis, the upper, nondependent part showed the largest displacement. 4-V/Q mismatch, increased from 0.66 to 0.83 and 0.89 from awake to spontaneous breathing and mechanical ventilation. 5-Shunt increased from 1% awake to 11% and 14% with spontaneous breathing and mechanical ventilation.

Increased Oxygen Fraction Air (FIO2 of 0.21): Only small shunts of 1% to 2%, SDQ increased from 0.77 to FIO2 0.5 : Increase in shunt of 3% to 4% FIO to 0.85: Shunt from 7% to 10% Thus, a certain dependence on FIO2 exist: 1-Attenuation of the HPV OR 2- further development of atelectasis and shunt in lung units with low V/Q ratios

Body Position FRC is dramatically reduced by the combined effect of supine position and anesthesia Upright position preserve FRC. But! No clear improvement in oxygenation was noticed Increase V/Q mismatch In anesthetized, paralyzed, lateral and improvement in prone Ventilation distribution is more uniform in anesthetized subjects in prone position.

Age Arterial oxygenation is further impeded with increa 1- Larger percentage of atelect 2- Increasing V/Q mismatch

Obesity Obesity worsens the oxygenation of blood 1- Reduced FRC 2- Promotes airway closure 3- High FIO2 will promote rapid atelectasis Correlations between BMI and: 1- Size of atelectasis during anesthesia and postoperatvely 2- Pulmonary shunt Have been presented Prevention: PEEP or CPAP or FIO2=1 during induction & maintenance ?

Preexisting Lung Disease Smokers and patients with lung disease have impairment of gas exchange: In the awake state Also during anesthesia Considerable V/Q mismatch + large perfusion fraction to LOW V/Q regions Interestingly, smokers with moderate airflow limitation!! May have less shunt as measured by MIGET than healthy subjects : A possible reason( for absence of atelectasis and shunt ) May be chronic hyperinflation.

Regional Anesthesia Type and extension of motor blockade: Extensive blocks include all of the thoracic and lumbar segments: 1- Inspiratory capacity is reduced by 20% 2- Expiratory reserve volume approaches zero Skillfully handled regional anesthesia affects pulmonary gas exchange only minimally. SaO2 and CO2 elimination well maintained during spinal and epidural anesthesia? 1-unchanged relationship of CC and FRC[116] 2-unaltered distributions of ventilation-perfusion ratios (MIGET,epidural anesthesia)

Lung Function After Cardiac Surgery Cardiac surgery produces the largest atelectasis in the postoperative period 1-Both lungs collapsed 2-Patient connected to an extracorporeal pump and oxygenator 3-more than half the lung may be collapsed 1 to 2 days later 4-with a shunt that is around 20% to 30% of cardiac output A recruitment maneuver with airway pressure of 30 cm H2O for a 20 second is sufficient to reopen the collapsed lung Dyhr and coworkers studied 30 patients after cardiac: 1- lung recruitment maneuver (LRM = four 10-second,AWP 45 cm H2O)then ZEEP 2- 12–cm H2O PEEP 3- LRM plus PEEP Recruitment maneuver resulted in true opening of collapsed lung PEEP alone caused hyperinflation of already open alveoli

Respiratory Function During One-Lung Ventilation Oxygenation may be a challenge even during anesthesia. One lung is nonventilated but still perfused, Postoperative period: restoration of lung integrity & V/Q matching may take time

Measures in one lung ventilation Tusman and colleagues tested an “alveolar recruitment strategy” (ARS): 1-Increasing PAP min by min from 25 to 30, 35, finally 40 cm H2O 2- Simultaneously increasing PEEP from 5 to 10, 15, finally 20 cm H2O 3-PAP then reduced of 25 and PEEP to 5 cm H2O This resulted :increase in PaO2 from 217 to 470 mm Hg after ARS: More of the shunt is located in the dependent lung than is generally considered. In another (Tusman ) study,ARS : Improved oxygenation Dead space decreased Slope of the CO2 curve during expiratory VT (phase III) was flatter

Measures in one lung ventilation(cont) PEEP versus ZEEP Thoracic epidural anesthesia Inhaled nitric oxide (NO) alone or in combination with intravenous almitrine Positioning of the patient

Pneumoperitoneum(CO2) 1-Hypercapnia and acidosis 2-Decreased cardiaccontractility 3-Sensitization of the myocardium to the arrhythmogenic effects of catecholamines 4-Systemic vasodilation 5-Even long-lasting postoperative effects on breathing control 6-Decreased FRC and VC 7-Formation of atelectasis 8-Reduced respiratory compliance 9-Increased peak airway pressure Nonetheless, shunt is reduced and Sao2 is mostly improved ? Paradox: more atelectasis and less shunt !! CO2 may enhance HPV,may be the mechanism of the paradox

Physiotherapy Physiotherapy may do more harm than good As large an inspiration as possible and As early in the postoperative period as possible are : Two important factors in preventing postoperative lung complications. Deep inspiration is done with or without a device for forced breathing

Normal Sleep Ventilation is affected by sleep Significant reduction in VT and inspiratory drive Minute ventilation falls by 5% to 16% most marked during REM. Decrease FRC (REM) Breathing pure oxygen would also lead to the formation of atelectasis.

CO 2 Transport Carbon dioxide transport: Carbon dioxide transport: –~9% dissolved in plasma –~13% as carbamino compounds  Most combined with Hb –~78% converted to HC0 3 -  CO 2 + H 2 O  H 2 CO 3  H + + HCO 3 - Haldane effect Haldane effect –Inverse relationship between amount of Hb-O 2 and CO 2 carrying capacity of blood  Hb binds and transports more CO 2 than O 2  Hb buffers more H + than Hb-O 2 –Promotes conversion of CO 2 to HCO 3 - via carbonic anhydrase reaction

Key Concepts O 2 mostly transported in blood bound to hemoglobin O 2 mostly transported in blood bound to hemoglobin If the P O2 increases Hb binds O 2 If the P O2 increases Hb binds O 2 If P O2 decreases Hb releases O 2 If P O2 decreases Hb releases O 2 CO 2 mostly transported in blood as HCO 3 - CO 2 mostly transported in blood as HCO 3 - Lesser amounts of CO 2 are bound to Hb or dissolved in plasma Lesser amounts of CO 2 are bound to Hb or dissolved in plasma

Respiratory centers (p. 848) Basic rhythm of ventilation controlled by medullary rhythmicity area (medulla oblongata) Basic rhythm of ventilation controlled by medullary rhythmicity area (medulla oblongata) Inspiratory area (Dorsal Resp.Group) Inspiratory area (Dorsal Resp.Group) –determines basic rhythm of breathing –causes contraction of diaphragm and external intercostals Expiratory area (Ventral Resp. Group) Expiratory area (Ventral Resp. Group) –Inactive during normal quiet breathing –Activated by inspiratory area during forceful breathing –Causes contraction of internal intercostals and abdominal muscles

Respiratory centers Transition between inhalation and exhalation controlled by: Transition between inhalation and exhalation controlled by: –Pneumotaxic area  located in pons  inhibits inspiratory area of medulla to stop inhalation –Breathing more rapid when pneumotaxic area active –Apneustic area  located in pons  stimulates inspiratory area of medulla to prolong inhalation

Regulation of Respiratory centers Basic rhythm of ventilation coordinated by inspiratory area of respiratory centre, but modified by: Basic rhythm of ventilation coordinated by inspiratory area of respiratory centre, but modified by: –Cortical influences  Voluntary control over breathing –Hypothalamus and limbic system  Emotional stimuli –Proprioceptors  Upper motor neurons of primary motor cortex also stimulate inspiratory area –Inflation (Hering-Breuer) reflex  Stretch receptors in walls of bronchi and bronchioles –Inhibit inspiratory and apneustic areas  causes exhalation to begin to protect against overinflation –Chemoreceptors  Increased PCO 2, or reduced pH or PO 2 causes chemoreceptors to stimulate inspiratory area of respiratory centre

Problem solving Josh hyperventilates for several minutes before diving into a pool. Shortly after he enters the water he blacks out and almost drowns. What caused this to happen? Josh hyperventilates for several minutes before diving into a pool. Shortly after he enters the water he blacks out and almost drowns. What caused this to happen?

Regulation of Respiratory centers Rhythm of ventilation also modified by: Rhythm of ventilation also modified by: –Temperature   temp =  ventilation (and vice versa)  sudden cold stimulus may cause apnea –Pain  Sudden severe pain can cause apnea  Prolonged somatic pain increases respiratory rate  Visceral pain may slow respiratory rate –Irritation of airways –Blood pressure   BP =  ventilation (and vice versa) –Attempt to reduce venous return via respiratory pump?

Effects of smoking Smoking reduces respiratory efficiency Smoking reduces respiratory efficiency –Deposits tar & other chemicals –swelling of mucosal lining and increased production of mucus  Impedes airflow –destroys cilia and inhibits their movement  Reduces removal of excess mucus and debris Smokers lungs Bodies The exhibition March 2006

Smoking –Nicotine constricts terminal bronchioles  Reduces airflow into and out of lung –CO binds irreversibly to Hb  Reduces blood oxygen carrying capacity –Destruction of elastic fibers (prime cause of emphysema)  Reduced lung compliance  Collapse of small bronchioles during exhalation –traps air in alveoli during exhalation  Reduces efficiency of gas exchange