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RESPIRATORY CHANGES DURING ANESTHESIA AND POSITIVE

PRESSURE VENTILATION

DR DANISH OMAIRMODERATOR- DR FERHAN

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INTRODUCTION• The lung is regularly affected by anesthesia and mechanical

ventilation. • This occurs even in healthy volunteers or patients with no

cardiopulmonary disease, and sometimes the dysfunction can be severe enough to cause life-threatening hypoxemia.

• In patients with preexisting lung disease, gas exchange will be further compromised in comparison to the awake state.

• Knowledge of the functional impairment that will ensue during anesthesia and mechanical ventilation will make possible ventilatory support that should, in the large majority of patients, prevent any disastrous impairment in gas exchange.

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RESPIRATORY FUNCTION DURING ANESTHESIA

• Anesthesia causes an impairment in pulmonary function, whether the patient is breathing spontaneously or is ventilated mechanically after muscle paralysis.

• Impaired oxygenation of blood occurs in most subjects who are anesthetized.

• It has therefore become routine to add oxygen to the inspired gas so that the inspired oxygen fraction (FIO2) is maintained at around 0.3 to 0.4.

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• Despite these measures, mild to moderate hypoxemia, defined as an arterial oxygen saturation of between 85% and 90%, may occur in approximately half of all patients undergoing elective surgery, and the hypoxemia can last from a few seconds to up to 30 minutes.

• About 20% of patients may suffer from severe hypoxemia, or oxygen saturation below 81% for up to 5 minutes.

• Lung function remains impaired postoperatively, and clinically significant pulmonary complications can be seen in 1% to 2% after minor surgery in up to 20% after upper abdominal and thoracic surgery.

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• The first phenomenon that might be seen with anesthesia is loss of muscle tone with a subsequent change in the balance between outward forces (i.e., respiratory muscles) and inward forces (i.e., elastic tissue in the lung) leading to a fall in FRC.

• This is paralleled by an increase in the elastic behavior of the lung (reduced compliance) and an increase in respiratory resistance.

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• The decrease in FRC affects the patency of lung tissue with the formation of atelectasis (made worse with the use of high concentrations of inspired oxygen) and airway closure.

• This alters the distribution of ventilation and matching of ventilation and blood flow and impedes oxygenation of blood and removal of carbon dioxide.

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LUNG VOLUME AND RESPIRATORY MECHANICS DURING ANESTHESIA

• LUNG VOLUME:• FRC is reduced by 0.8 to 1.0 L by changing

body position from upright to supine, and there is another 0.4- to 0.5-L decrease when anesthesia has been induced.

• End-expiratory lung volume is thus reduced from approximately 3.5 to 2 L, the latter being close or equal to RV.

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• The anesthesia per se causes a fall in FRC despite maintenance of spontaneous breathing and the decrease in FRC occurs regardless of whether the anesthetic is inhaled or given intravenously.

• Muscle paralysis and mechanical ventilation cause no further decrease in FRC.

• The average reduction corresponds to around 20% of awake FRC and may contribute to an altered distribution of ventilation and impaired oxygenation of blood.

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• The decrease in FRC seems to be related 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, as during ketamine anesthesia, does not reduce FRC.

• FRC increases with age if weight and height remain unaltered over the years

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COMPLIANCE AND RESISTANCE OF RESPIATORY SYSTEM

• Static compliance of the total respiratory system (lungs and chest wall) is reduced on average from 95 to 60 mL/cm H2O during anesthesia.

• There is a decrease in compliance during anesthesia when compared to awake states.

• There are also studies on resistance of the total respiratory system and the lungs during anesthesia, most of them showing a considerable increase during both spontaneous breathing and mechanical ventilation.

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• This figure shows the cranial shift of diaphragm and a decrease in transverse diameter of thorax contribute to lowered FRC during anesthesia.

• Decreased ventilated volume (atelectasis and airway closure) is a possible cause of reduced lung compliance.

• Decreased airway dimensions by lowered FRC should contribute to increase airway resisitance.

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ATELECTASIS AND AIRWAY CLOSURE DURING ANESTHESIA

• ATELECTASIS: In their classic paper, Bendixen and coworkers proposed “a concept of atelectasis” as a cause of impaired oxygenation during anesthesia.

• They had observed a successive decrease in compliance of the respiratory system and a similar successive decrease in arterial oxygenation in both anesthetized humans and experimental animals.

• This was interpreted as formation of atelectasis.

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• Atelectasis appears in approximately 90% of all patients who are anesthetized.

• It is seen during spontaneous breathing and after muscle paralysis and whether intravenous or inhaled anesthetics are used.

• Thus, 15% to 20% of the lung is regularly collapsed at the base of the lung during uneventful anesthesia, before any surgery has even been done.

• Abdominal surgery does not add much to the atelectasis, but it can remain for several days in the postoperative period.

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• It is likely that it is a focus of infection and can contribute to pulmonary complications.

• It may also be mentioned that after thoracic surgery and cardiopulmonary bypass, more than 50% of the lung can be collapsed even several hours after surgery.

• The amount of atelectasis decreases toward the apex, which is mostly spared (fully aerated).

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• There is a weak correlation between the size of the atelectasis and body weight or body mass index (BMI), with obese patients showing larger atelectatic areas than lean ones do.

• Although this was expected, it came as a surprise that the atelectasis is independent of age, with children and young people showing as much atelectasis as elderly patients.

• Another unexpected observation was that patients with COPD showed less or even no atelectasis during the 45 minutes of anesthesia that they were studied.

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• The mechanism that prevents the lung from collapse is not clear but may be airway closure occurring before alveolar collapse takes place, or it may be an altered balance between the chest wall and the lung that counters a decrease in lung dimensions

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PREVENTION OF ATELECTASIS DURING ANESTHESIA

• Several interventions can help prevent atelectasis or even reopen collapsed tissue, as discussed in the following paragraphs:

• 1)PEEP: The application of 10–cm H2O PEEP has been tested in several studies and will consistently reopen collapsed lung tissue.

• This is more likely an effect of increased inspiratory airway pressure than of PEEP per se.

• However, some atelectasis persists in most patients. Whether a further increase in the PEEP will reopen this tissue was not analyzed in these studies.

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• PEEP, however, does not appear to be the ideal procedure.

• First, shunt is not reduced proportionately, and arterial oxygenation may not improve significantly.

• The persistence of shunt may be explained by a redistribution of blood flow toward more dependent parts of the lungs when intrathoracic pressure is increased by PEEP.

• Under such circumstances, any persisting atelectasis in the bottom of the lung receives a larger share of the pulmonary blood flow than without PEEP.

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• Furthermore, increased intrathoracic pressure will impede venous return and decrease cardiac output.

• This results in a lower venous oxygen tension for a given oxygen uptake and reduces arterial oxygen tension.

• Second, the lung recollapses rapidly after discontinuation of PEEP.

• Within 1 minute after cessation of PEEP, the collapse is as large as it was before the application of PEEP.

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• During mechanical ventilation with zero end-expiratory pressure (ZEEP), perfusion goes mainly to the lower lung, but there is still perfusion of the upper lung, with the average distribution to the upper lung being 33% to 40% of total lung perfusion.

• With a general PEEP of 10 cm H2O, perfusion is squeezed down to the lower lung, and there may be almost no perfusion at all in the upper lung.

• This causes a dramatic dead space–like effect.

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• If, on the other hand, PEEP is applied selectively to the lower lung, in this example 10 cm H2O, perfusion might be redistributed to the upper lung so that a more even distribution between the two lungs can be seen.

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2)MAINTENANCE OF MUSCLE TONE

• Use of an anesthetic that allows maintenance of respiratory muscle tone will prevent atelectasis from forming.

• Ketamine does not impair muscle tone and does not cause atelectasis.

• This is the only anesthetic thus far tested that does not cause collapse.

• However, if muscle relaxation is required, atelectasis will appear as with other anesthetics.

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3)RECRUITMENT MANEUVERS• The use of a sigh maneuver, or a double VT, has

been advocated to reopen any collapsed lung tissue.• However, the atelectasis is not decreased by a

double VT or by a sigh up to an airway pressure of 20 cm H2O.

• Not until an airway pressure of 30 cm H2O is reached does the atelectasis decrease to approximately half the initial size.

• For complete reopening of all collapsed lung tissue, an inflation pressure of 40 cm H2O is required.

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• Such a large inflation corresponds to a maximum spontaneous inspiration, and it can thus be called a VC maneuver.

• Because a VC maneuver may result in adverse cardiovascular events, the dynamics in resolving atelectasis during such a procedure was analyzed.

• It was found that in adults with healthy lungs, inflation of the lungs to +40 cm H2O maintained for no more than 7 to 8 seconds may re-expand all previously collapsed lung tissue.

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4)MINIMIZING GAS RESORPTION

• Ventilation of the lungs with pure oxygen after a VC maneuver that had reopened previously collapsed lung tissue resulted in rapid reappearance of the atelectasis.

• If, on the other hand, 40% O2 in nitrogen is used for ventilation of the lungs, atelectasis reappears slowly, and 40 minutes after the VC maneuver only 20% of the initial atelectasis had reappeared.

• Thus, ventilation during anesthesia should be done with a moderate fraction of inspired oxygen (e.g., FIO2 of 0.3 to 0.4) and should be increased only if arterial oxygenation is compromised.

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• The striking effects of oxygen during anesthesia raised the question of whether “preoxygenation” during induction of anesthesia has an effect on the formation of atelectasis.

• Breathing of 100% O2, just for a few minutes before and during commencement of anesthesia, increases the safety margin in the event of difficult intubation of the airway with prolonged apnea.

• However, there turned out to be a price for it. • Avoidance of the preoxygenation procedure

(ventilation with 30% O2) eliminated atelectasis formation during induction and subsequent anesthesia.

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• Preoxygenation can also be provided without producing atelectasis if undertaken with continuously increased airway pressure, as with continuous positive airway pressure (CPAP).

• By applying CPAP of 10 cm H2O, Rusca and associates could induce anesthesia on 100% O2 without any substantial atelectasis formation.

• This technique might provide the greatest safety without atelectasis formation but it requires a tight system and might be complicated in clinical practice.

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AIRWAY CLOSURE

• In addition to atelectasis, intermittent closure of airways can be expected to reduce the ventilation of dependent lung regions.

• Such lung regions may then become “ low Va/Q ” units if perfusion is maintained or not reduced to the same extent as ventilation.

• Airway closure increases with age, as does perfusion to “low- Va/Q ” regions.

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• Because anesthesia causes a reduction in FRC of 0.4 to 0.5 L, it may be anticipated that airway closure will become even more prominent in an anesthetized subject.

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DISTRIBUTION OF VENTILATION DURING ANESTHESIA

• Redistribution of inspired gas away from dependent to nondependent lung regions has been observed in anesthetized supine humans by isotope techniques.

• With the use of a radiolabeled aerosol and SPECT, ventilation was shown to be distributed mainly to the upper lung regions, and there was a successive decrease down the lower half of the lung.

• Moreover, there was no ventilation at all in the bottom of the lung, a finding corresponding to the distribution of atelectasis that was simultaneously observed by CT .

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• PEEP increases dependent lung ventilation in anesthetized subjects in the lateral position, so the distribution of ventilation is more similar to that in the awake state.

• Similar findings of more even distribution between the upper and lower lung regions have also been made in supine anesthetized humans after previous inflation of the lungs, similar to PEEP.

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DISTRIBUTION OF LUNG BLOOD FLOW DURING ANESTHESIA

• A successive increase in perfusion down the lung, from the ventral to the dorsal aspect, was seen, with some reduction in the lowermost region.

• PEEP will impede venous return to the right heart and therefore reduce cardiac output.

• It may also affect pulmonary vascular resistance, although this may have less of an effect on cardiac output.

• In addition, PEEP causes a redistribution of blood flow toward dependent lung regions.

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• By this means, upper lung regions may be poorly perfused, thereby causing a dead space–like effect.

• Moreover, forcing blood volume downward to the dorsal side of the lungs may increase fractional blood flow through an atelectatic region.

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HYPOXIC PULMONARY VASOCONSTRICTION

• Several inhaled anesthetics have been found to inhibit HPV in isolated lung preparations. However, no such effect has been seen with intravenous anesthetics (barbiturates).

• The HPV response may thus be obscured by simultaneous changes in cardiac output, myocardial contractility, vascular tone, blood volume distribution, blood pH and CO2 tension, and lung mechanics.

• In studies with no gross changes in cardiac output, isoflurane and halothane depress the HPV response by 50% at a MAC of 2 .

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EFFECTS OF ANESTHETICS ON RESPIRATORY DRIVE

• Spontaneous ventilation is frequently reduced during anesthesia.

• Thus, inhaled anesthetics, as well as barbiturates for intravenous use, reduce sensitivity to CO2.

• The response is dose dependent and entails decreasing ventilation with deepening anesthesia.

• Anesthesia also reduces the response to hypoxia. • Attenuation of the hypoxic response may be

attributed to an effect on the carotid body chemoreceptors.

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• The effect of an anesthetic on respiratory muscles is nonuniform.

• Rib cage excursions diminish with deepening anesthesia.• The normal ventilatory response to CO2 is produced by

the intercostal muscles, with no clear increase in rib cage motion with CO2 rebreathing during halothane anesthesia.

• Thus, the reduced ventilatory response to CO2 during anesthesia is due to impeded function of the intercostal muscles.

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FACTORS THAT INFLUENCE RESPIRATORY FUNCTION DURING ANESTHESIA

1)SPONTANEOUS BREATHING:• FRC is reduced to the same extent during anesthesia,

regardless of whether a muscle relaxant is used, and atelectasis occurs to almost the same extent in anesthetized spontaneously breathing subjects as during muscle paralysis.

• Furthermore, the cranial shift of the diaphragm, as reported by Froese and Bryan in their classic paper, was of the same magnitude both during general anesthesia with spontaneous breathing and with muscle paralysis, even though a difference in movement of the diaphragm from the resting position was noted.

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• Thus, during spontaneous breathing, the lower, dependent portion of the diaphragm moved the most, whereas with muscle paralysis, the upper, nondependent part showed the largest displacement.

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2)INCREASED OXYGEN FRACTION(FiO2)

• Anjou-Lindskog and associates induced anesthesia on air (FIO2 of 0.21) in middle-aged to elderly patients during intravenous anesthesia before elective lung surgery and found only small shunts of 1% to 2%.

• When FIO2 was increased to 0.5, an increase in shunt of 3% to 4% was noticed.

• In another study on elderly patients during halothane anesthesia , an increase in FIO2 from 0.53 to 0.85 caused an increase in shunt from 7% to 10% of cardiac output.

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3)BODY POSITION

• Supine : when conscious person changes from erect to supine position, FRC decreases by 0.5-1L, because abdominal viscera press against the diaphragm and 4 cm cephaloid shift of diaphragm occurs.

• During anesthesia, cephaloid shift of diaphragm is due to muscle paralysis.

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• During IPPV, gas moves along the line of least resistance, to the less congested and more compliant substernal units of the superior lungs are inflated preferentially .

• Gravity increases perfusion of dependent i e posterior lung segments.

• Spontaneous ventilation favors dependent lung segments and controlled ventilation favors independent i e anterior segments.

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• Prone : compression of abdominal and thorax decreases total lung compliance and increase work of breathing.

• Mechanical ventilation in prone position improves oxygenation in ALI/ARDS, as it re-aerates the dorsal lung units.

• Lateral decubitus: there is decrease volume of dependent lung but there is increase in perfusion. Decrease ventilation to dependent lung in anesthesized patients.

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• Tredlenberg: decrease in lung capacities due to shift of abdominal viscera, increase V/Q mismatch and atelectasis, decrease FRC and pulmonary compliance.

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4)AGE

• It is well known that arterial oxygenation is further impeded with increasing age of the patient.

• Shunt and formation of atelectasis does not increase with age in adults.

• In contrast, there appears to be increasing V/Q mismatch with age, with enhanced perfusion of low VA/Q regions both in awake subjects and when they are subsequently anesthetized.

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• Thus, the major cause of impaired gas exchange during anesthesia at ages younger than 50 years is shunt, whereas at higher ages mismatch.

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5)OBESITY• Obesity worsens the oxygenation of blood.• A major explanation appears to be a markedly

reduced FRC, which promotes airway closure to a greater extent than in a normal subject.

• The use of high inspired oxygen concentrations will promote rapid atelectasis formation behind closed airways.

• The shorter time until desaturation during induction of anesthesia, as observed in morbidly obese patients, may also be prevented by PEEP or CPAP.

• This can be explained by the increase in lung volume by PEEP or CPAP so that more oxygen is available for diffusion into the capillary blood.

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PRE-EXISTING LUNG DISEASE

• Smokers and patients with lung disease have more severe impairment of gas exchange in the awake state than healthy subjects do, and this difference also persists during anesthesia.

• Interestingly, smokers with moderate airflow limitation may have less shunt than lung-healthy subjects do.

• Thus, in patients with mild to moderate bronchitis who were to undergo lung surgery or vascular reconstructive surgery in the leg, only a small shunt was noticed.

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• In patients with chronic bronchitis studied by MIGET and CT, no or very limited atelectasis developed during anesthesia and no or only minor shunt.

• However, a considerable Va/Q mismatch was seen with a large perfusion fraction to low Va/Q regions.

• A possible reason for the absence of atelectasis and shunt in these patients may be 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.

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REGIONAL ANESTHESIA

• The ventilatory effects of regional anesthesia depend on the type and extension of motor blockade .

• With extensive blocks that include all of the thoracic and lumbar segments, inspiratory capacity is reduced by 20% and expiratory reserve volume approaches zero.

• Diaphragmatic function, however, is often spared, even in cases of inadvertent extension of subarachnoid or epidural sensory block up to the cervical segments.

• Skillfully handled regional anesthesia affects pulmonary gas exchange only minimally.

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• Arterial oxygenation and carbon dioxide elimination are well maintained during spinal and epidural anesthesia.

• This is in line with the findings of an unchanged relationship of CC and FRC and unaltered distributions of ventilation-perfusion ratios during epidural anesthesia.

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LUNG FUNCTION AFTER CARDIAC SURGERY

• Cardiac surgery produces the largest atelectasis in the postoperative period .

• Cardiac surgery is generally undertaken with both lungs collapsed and the patient connected to an extracorporeal pump and oxygenator.

• If no precautions are taken in the immediate postoperative period, the lung will recruit slowly, and more than half the lung may be collapsed 1 to 2 days later with a shunt that is around 20% to 30% of cardiac output.

• A recruitment maneuver consisting of inflating the lungs to an airway pressure of 30 cm H2O for a 20-second period is sufficient to reopen the collapsed lung.

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• This lower airway pressure will do the same job as 40 cm H2O in patients undergoing abdominal surgery because the maneuver is undertaken with an open chest before closure and return to mechanical ventilation.

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RESPIRATORY FUNCTION DURING ONE LUNG VENTILATION

• In lung surgery, oxygenation may be a challenge even during anesthesia.

• One lung is non-ventilated but still perfused, and in the postoperative period, restoration of lung integrity and ventilation/perfusion matching may take time .

• The technique of one-lung anesthesia and ventilation means that only one lung is ventilated and provides oxygenation of blood, as well as elimination of carbon dioxide from the blood.

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• Persisting perfusion through the nonventilated lung causes a shunt and decreased PaO2 .

• However, the dependent, ventilated lung will also contribute to the impeded oxygenation by formation of atelectasis in the dependent regions.

• There are reasons to also consider a recruitment maneuver in one-lung ventilation (OLV).

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• The alveolar recruitment strategy(ARS) maneuver was executed by increasing peak airway pressure minute by minute from 25 to 30, 35, and finally 40 cm H2O and simultaneously increasing PEEP from 5 to 10, 15, and finally 20 cm H2O.

• Airway pressure was then reduced to a peak of 25 and PEEP to 5 cm H2O.

• This resulted in an increase in PaO2 from 217 to 470 mm Hg after ARS.

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• Shunt can be seen in lower lung during two- lung ventilation, but both in lower lungs and in all of upper lung during one- lung ventilation.

• In one- lung ventilation, upper non ventilated lung will act as a shunt region as well as lower part of dependent lung.

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RESPIRATORY EFFECTS OF IPPV WITH ZEEP OR PEEP

• IPPV results in minor changes in the spatial distribution of ventilation which is only relevant in pts with ALI.

• PEEP increases lung volume, re expands collapsed alveoli and therefore improves ventilation in these areas.

• Both delivery of IPPV and PEEP results in apparatus deadspace which may or may not influence the overall deadspace.

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• There is slight worsening of V/Q ratios with IPPV but this is often not significant.

• PEEP increases FRC whilst IPPV with ZEEP does not .

• IPPV and PEEP do not change oxygenation in healthy pts but may have significant benefits in decreased pts, as it increases FRC above closing capacity, reducing airway resistance and improving recruitment and maintaining patency in alveolar units.

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