Respiratory Physiology and Anesthesia Module 1

''What is the difference between ventilation and respiration?''

Ventilation is the movement of gases or the air exchange,
basically the exchange of air from the atmosphere to the alveoli
and vice versa.
Respiration is the gas exchange or at the tissue level,
the exchange of carbon dioxide and other products of respiration
of the cells and tissues to oxygen supplied by the lungs through the blood.
External respiration is between the atmosphere and the lungs up to the alveoli.
Internal respiration is after gas exchange, that means permeability through
the alveolar membrane to the blood and the hemodynamics carrying
oxyhemoglobin to all the tissues.
At the tissue level, oxygen is exchanged for carbon dioxide.
Cellular or tissue respiration can be divided into aerobic,
which generates 32 ATPs, and anaerobic, which generates two ATPs.

''What are the major muscles of respiration?''

The muscles of breathing are the inspiratory muscles and the expiratory muscles.
The major inspiratory muscle during normal breathing is the diaphragm.
Its contraction is responsible for 75 percent of the changes in intrathoracic volume during quiet inspiration.
This causes the base of the thoracic cavity to descend by about 1.5 to 7 centimeters.
The inspiratory muscles are the diaphragm and the external intercostal muscles during quiet or normal breathing.
During forced inspiration, accessory muscles like the sternocleidomastoid,
the strap muscles of the neck, the scalene muscles, and the pectoralis major muscles are involved.
Expiration during normal breathing is a passive process due to the elastic recoil of the lung.
During forced expiration, accessory muscles including the abdominal muscles are called into play.

''What determines the impedance of the respiratory system?''

The movement of air in and out of the lungs is determined by the impedance of the respiratory system,
or the resistance to the flow of gases and the alveoli filling up with gas.
This can be divided into elastic resistance and non-elastic resistance to the gas flow.
Elastic resistance depends on the lung tissue itself, including the alveoli,
the interstitial tissue, and the degree of elasticity or the elastin present.
It also determines how easily the alveoli expand during inspiration and come back to their basal state.
The lung is also a gas-liquid interface.
Inside the alveoli, there is liquid surfactant, and outside the lungs,
around the lungs and the pleura, there is negative pressure in the pleural space with some pleural liquid.

''Why is surfactant important for alveolar stability?''

Surface tension forces tend to collapse the lung or the alveoli.
When the alveoli become small at the end of expiration,
the surface tension forces reduce the area of interface, favoring alveolar collapse according to Laplace's law.
Surfactant acts like a splint; it reduces the surface tension of the alveoli, especially at the end of exhalation.
It is a lecithin, a form of protein secreted by the type 2 alveolar pneumocyte.
Its ability to lower surface tension is directly proportional to its concentration within the alveolus.
In smaller alveoli, surfactant becomes more concentrated around the membrane, reducing surface tension and preventing collapse.
In larger alveoli, surfactant is spread out thinner and less concentrated,
so there is a relative increase in surface tension which prevents overdistension at the end of inspiration.

''What is lung compliance and what are its determinants?''

Compliance is delta V by delta P, or the change in lung volume based on the change in transpulmonary pressure.
Normal lung compliance is about 0.2 to 0.3 liters per centimeter of water.
The transpulmonary pressure is the transpleural pressure (Ppl minus alveolar pressure, Pal).
The pleural pressure is lower in the upper regions and higher in the lower regions,
creating a transpulmonary pressure drop from apex to base.
This means lower lung regions expand more easily for a given increase in transpulmonary pressure.
A rightward shift of the pressure-volume curve indicates it is more difficult to expand the lung,
as seen in fibrotic lung diseases like idiopathic fibrosis, sarcoidosis, and interstitial edema.
A left shift is seen in conditions with loss of elasticity like emphysema or chronic bronchitis.

''What are the different lung volumes and capacities?''

Tidal volume is the volume of air exchanged during a normal breath.
Inspiratory reserve volume is the maximum additional volume that can be inspired above the tidal volume.
Expiratory reserve volume is the maximum volume that can be expired below the tidal volume.
Residual volume is the volume remaining after maximal expiration.
Inspiratory capacity is the tidal volume plus the inspiratory reserve volume.
Functional residual capacity is the expiratory reserve volume plus the residual volume.
Vital capacity is the maximum volume expelled after a maximum inspiration.
Total lung capacity is the sum of all volumes and capacities.

''What is the Functional Residual Capacity and why is it important in anesthesia?''

The functional residual capacity (FRC) is the sum total of the expiratory reserve volume and the residual volume.
It is determined by the balance between the inward elastic recoil of the lungs and the outward recoil of the thoracic cage at the end of expiration.
For an anesthesiologist, the FRC is important because it is the degree of latitude we have with the patient's oxygenation.
It also directly determines the amount of time we have for airway management and airway control.
The FRC decreases with paralysis and with anesthesia.
It is also affected by body size, gender, and posture, decreasing by 0.5 to 1 liter when moving from erect to supine.

''What is closing volume and closing capacity?''

The volume above the residual volume during expiration at which the terminal airways begin to close is called the closing volume.
The sum of the residual volume and the closing volume is termed the closing capacity.
This airway closure in the terminal and small alveoli at the lung bases is a normal physiological phenomenon.
It is accelerated or extenuated by anesthesia and by increasing pleural pressure during expiration.
When pleural pressure becomes positive and exceeds the pressure inside the airways, it may lead to airway collapse or closure.
In supine position, FRC is reduced while closing capacity is not affected, so closure may occur above FRC even in young subjects.

''What is airway resistance and where is it highest?''

The opposite of compliance (delta P by delta V) is resistance, which can be elastic or non-elastic.
Normal total airway resistance is about 0.5 to 2 centimeters of water.
This is mainly contributed by the medium-size bronchi.
Resistance in larger airways is low because of the large diameter, making flow easier.
Resistance in smaller airways is lower because of the large total cross-sectional area.
Important causes of increased airway resistance include bronchospasm, secretions, mucosal edema,
and volume-related and flow-related airway collapse.

''What is the Equal Pressure Point?''

The equal pressure point (EPP) is the point in the airway where dynamic compression occurs.
At this point, the transpulmonary pressure becomes equal to the intra-alveolar pressure.
Flow would not occur beyond the EPP.
In a normal young adult breathing spontaneously, this point is usually at the larger airways which have a cartilaginous component.
In disease conditions like emphysema and asthma, the EPP moves towards the smaller airways because the elastic tissues that normally support them are destroyed.
Anesthesia can also cause the same effect, and as lung volume decreases, ventilation is affected and alveoli collapse.

''How is the work of breathing divided?''

The work of breathing during quiet inspiration can be divided into elastic work and non-elastic work.
Non-elastic work includes basic airway resistance, which contributes to about 25-28% of total resistance,
and viscous resistance (about 7%), which is the viscosity of the lung tissue itself and of the gas used for ventilation.
Elastic work constitutes about 65% of the work of breathing.
Elastic work involves factors that increase it and thus affect the total work of breathing.

''What is dead space and what are its components?''

Dead space refers to the inspiratory gas that remains in the airway at the end of exhalation and does not take part in alveolar gas exchange.
It can be apparatus dead space, which is added by masks and airway equipment.
It can also be anatomical dead space and physiological or alveolar dead space.
Anatomical dead space is the volume of the conducting passages up to the middle and terminal bronchioles.
Alveolar dead space consists of alveoli that are well ventilated but poorly perfused, representing wasted ventilation.
Total physiological dead space is the sum of anatomical and alveolar dead space.
In an upright, spontaneously breathing patient, this is normally about 150 ml for an adult, or about 2 ml per kg, approximately 30% of tidal volume.

''What factors affect dead space?''

Patient-based factors and our manipulations affect dead space.
Upright posture increases dead space as the lungs expand.
Supine position decreases anatomical dead space.
Neck extension increases anatomical dead space while flexion reduces it.
Age increases the total physiological dead space.
Artificial airways decrease dead space by moving the start of ventilation closer to the gas exchange units.
Positive pressure ventilation can increase dead space, as can bronchodilators which relax the bronchi.
Pulmonary embolism and hypotension increase dead space due to lack of perfusion to ventilated alveoli.
Diseases like emphysema increase dead space because many alveoli are splintered open.

''What is the oxyhemoglobin dissociation curve?''

The oxyhemoglobin dissociation curve shows the total oxygen carried in the blood.
In ideal conditions at the alveoli, hemoglobin is 100% saturated with oxygen.
At the tissue level, hemoglobin gives up oxygen to the cells and takes up carbon dioxide.
A shift to the right of the curve means hemoglobin gives up oxygen more readily, which happens with increased CO2, increased temperature, increased 2,3-DPG, or acidosis.
A shift to the left means hemoglobin does not release oxygen easily, causing tissue hypoxia, which happens with fetal hemoglobin, alkalosis, decreased temperature, and decreased 2,3-DPG.

''How is carbon dioxide transported in the blood?''

Carbon dioxide is carried mainly in three forms in the blood.
It is carried as dissolved carbon dioxide in plasma.
It is carried as bicarbonate in the buffer system.
The major form, about 75 to 80 percent, is as carbamino compounds,
especially as carbamino hemoglobin in combination with the hemoglobin.

''How does anesthesia affect lung volumes?''

Changing a patient from an upright position to supine reduces the FRC by 0.8 to 1 liter in a young adult.
Once anesthesia is induced, there is another 0.4 to 0.5 liter decrease in the FRC.
The end-expiratory lung volume is thus reduced from approximately 3.5 liters to 2 liters under anesthesia.
Anesthesia per se causes a fall in the functional residual capacity despite maintenance of spontaneous breathing.
The resistance of the total respiratory system and the lungs during anesthesia increases in both spontaneous breathing and mechanical ventilation.

''What causes atelectasis during anesthesia?''

General anesthesia causes accelerated atelectasis, especially at the basal part of the lung.
This happens in approximately 90 percent of all patients who are anesthetized.
It can be seen during spontaneous breathing and after muscle paralysis,
and whether an IV anesthetic or an inhaled anesthetic is given.
During an uneventful anesthetic, about 15 to 20 percent of the lung is regularly collapsed at the lung bases.
This atelectasis is independent of age, so children can have as much as the elderly.
Patients with COPD might have less atelectasis for the first 45 minutes due to autopEEP splinting alveoli.

''Can we prevent atelectasis during anesthesia?''

Interventions like the application of 10 cm water of positive end-expiratory pressure (PEEP) can be used to splint the alveolus open.
Recruitment maneuvers, like a sigh or a double tidal volume, can reopen collapsed lung tissue.
For complete reopening, an inflation pressure of about 40 cm of water may be needed, corresponding to a vital capacity maneuver.
Minimizing gas resorption by giving a maximum of about 40 percent oxygen, even at the end of the procedure, can help.
Preoxygenation with a CPAP of 6 cm of water can compensate for anesthesia-induced FRC reduction.
Using anesthetics that do not paralyze muscles, like ketamine, can prevent atelectasis from forming.

''What is the problem with using 100% oxygen for preoxygenation or at the end of anesthesia?''

100% ventilation with 100% oxygen can cause collapse of the terminal affected alveoli (absorption atelectasis).
If we avoid this or use normal atmospheric ventilation (20-25% oxygen) or 30-50% oxygen for pre-oxygenation in normal subjects,
it can eliminate atelectasis formation during induction and reduce it at recovery.
At the end of anesthesia, giving 100% oxygen can cause alveoli that are ventilated but not perfused to have all oxygen absorbed, leading to collapse.
This can be prevented by giving a maximum of about 40 percent oxygen for ventilation, even at the end of the anesthetic procedure.

''How does the three-compartment lung model explain impaired oxygenation during anesthesia?''

In the upper part of the lung, alveoli are always open and easy to ventilate (Zone 1).
In the middle and lower parts, during expiration, the EPP can move into the terminal alveoli, causing no ventilation beyond that point (Zone 2).
At the bottom of the lung, there is maximum perfusion, but alveoli can be collapsed with no ventilation, creating a physiological shunt (Zone 3).
Under anesthesia, ventilation is distributed mainly to the upper lung regions, decreasing to the lower parts.
PEEP can increase ventilation in the dependent lung and create a more even distribution.

''How do anesthetic drugs affect respiratory drive?''

Spontaneous breathing is frequently reduced during anesthesia.
Inhaled anesthetics as well as intravenous anesthetics reduce sensitivity to carbon dioxide or reduce the respiratory drive.
Anesthesia also reduces the physiological response to hypoxia and attenuates the hypoxic response.
This may be due to an effect on the carotid body chemoreceptors.

Mechanical Ventilation in Anesthesia

''What is the role of mechanical ventilation under anesthesia?''

Under anesthesia, brainstem respiratory centers are depressed, and respiratory mechanics are altered.
Gas exchange is affected.
Ventilators create the best possible environment for respiration to happen.
They keep the lung units open and minimize ventilation-perfusion mismatch.
By instituting mechanical ventilation and optimizing conditions, we can prevent postoperative pulmonary complications.

''What factors lead to perioperative hypoxemia?''

Factors can be patient-related or procedure-related.
Patient-related factors include age group or category, such as infants, the morbidly obese, and pregnancy, who have a classically reduced FRC.
In COPD, smokers, and the elderly, the closing volume is increased.
Procedure-related factors include patient positioning, which can reduce FRC (e.g., Trendelenburg, lithotomy).
Use of high inspired oxygen without PEEP can lead to absorption atelectasis.
When the duration of the procedure is long, there is a possibility of progressive lung de-recruitment.

''What is Volume Control Ventilation?''

In Volume Control Ventilation (VCV), we set a tidal volume and a respiratory rate.
We can manipulate the I:E ratio, add PEEP, and adjust the FiO2.
We are controlling the volume; pressure is a dependent variable.
If the patient develops bronchospasm, the set volume will still be delivered, but the peak pressure will go up.
Minute ventilation is guaranteed independent of changes in airway compliance and resistance.
VCV is useful during surgical procedures that affect respiratory system compliance, such as changes in patient position or peritoneal CO2 insufflation.

''What are peak pressure and plateau pressure?''

Peak pressure (Ppeak or PIP) is the maximum pressure achieved during inspiration.
Plateau pressure (Pplat) is obtained by setting an inspiratory pause.
The pressure then comes down to a plateau, which is the pressure reflected at the lung units.
When discussing lung injury and barotrauma, we are mostly worried about plateau pressure.
The difference between peak pressure and plateau pressure indicates the resistive pressure, or the work done to overcome airway resistance.
The plateau pressure itself indicates the elastic pressure, or the work done against lung compliance.

''What is Pressure Control Ventilation?''

In Pressure Control Ventilation (PCV), we set an inspiratory pressure.
Here, the tidal volume delivered becomes a dependent variable.
We set the inspiratory pressure, respiratory rate, I:E ratio, and PEEP.
The inspiratory flow has a decelerating flow pattern, not a square wave.
The breath cycle attains the set pressure limit, maintains it until cycling, then goes to exhalation.
When a compliance or resistance issue arises, the set pressure is kept constant, but the volume will be lower.
PCV is well-tolerated for ventilating children using supraglottic devices as it helps reduce air leak and gastric insufflation.

''What is Pressure Control Ventilation - Volume Guaranteed?''

In PCV-VG mode, you set a tidal volume.
The machine first switches to volume control mode to see how much pressure is required to deliver that tidal volume.
Once that pressure value is known, it switches over to pressure control mode ventilation with that pressure as the inspiratory pressure.
This results in a decelerating flow pattern, which has the advantages of PCV, such as better distribution of lung volumes.
Additionally, the tidal volume is guaranteed.
If compliance changes, the machine will reset or change the pressure control value to ensure the set tidal volume is delivered.

''How should tidal volume be set during anesthesia?''

Conventional belief is 10 ml per kg, but this should be avoided.
Growing evidence suggests that large tidal volume ventilation without PEEP increases alveolar inflammation.
Large tidal volume has more adverse hemodynamic consequences, as cardiac output is reduced proportionally to the tidal volume.
A reduction to 6-8 ml per kg is advised for patients susceptible to lung injury.
The body weight used for this calculation is the predicted body weight, not actual body weight, as lung size is related to height.

''What is the role of Positive End-Expiratory Pressure?''

PEEP keeps the airways open at the end of expiration.
It compensates for anesthesia-induced reduction in FRC.
It prevents end-expiratory lung volume from dropping below the closing capacity, thus preventing small airways from collapsing.
PEEP prevents repeated opening and closure of small airways and progressive lung de-recruitment.
It should be used with caution in hypovolemia and right ventricular dysfunction, and avoided when intracranial hypertension is a concern.
Most anesthetized patients can benefit from a small level of PEEP, but it is best used as a rescue strategy rather than a routine practice.

''What is Driving Pressure?''

Driving pressure is the pressure difference between plateau pressure and PEEP.
It is what drives the gas mixture into the lung.
The higher the driving pressure, the more severe the postoperative lung outcomes.
In mechanical ventilation, we always try to reduce the driving pressure, preferably to less than 15 cm of water.
Driving pressure is the result of interaction between the ventilator and the respiratory system.
An intraoperative increase in driving pressure at a given tidal volume reflects a lower respiratory system compliance.

''How are recruitment maneuvers performed?''

Recruitment maneuvers are often performed by switching the ventilator to manual mode,
changing the setting to maximum pressure with the APL valve, and squeezing the bag for some time, then releasing.
Another option is to stepwise increase the tidal volume or PIP.
Recruitment maneuvers have undoubted efficacy as rescue interventions to revert desaturation due to lung collapse.
There is little evidence to recommend their use on a routine preventive basis.

''How should respiratory rate and FiO2 be set?''

Respiratory rate is set to target a desired PaCO2 or EtCO2, generally aiming for 35-40 mmHg.
A higher respiratory rate reduces expiratory time, which can potentially induce intrinsic PEEP (auto-PEEP) in patients like those with COPD.
Optimal PaCO2 depends on the type of surgery and patient's pre-existing conditions.
FiO2 is intended to compensate for anesthesia-induced gas exchange impairment.
Oxygen is toxic to the tracheobronchial tree and lung; high FiO2 favors absorption atelectasis.
Use of high FiO2 may increase the incidence of wound infections, but evidence is not strong enough for a generalized recommendation.

''What is Pressure Support Ventilation?''

PSV is used to reduce the work of breathing related to airway device resistance.
It helps counteract the respiratory depressant effects of anesthetic medications.
It supports ventilation during emergence from anesthesia in line with the patient's efforts.
It is often used with supraglottic airway devices, with peak pressures kept between 15-20 cm H2O to avoid leakage and gastric insufflation.
With most anesthesia machines, a minimum respiratory rate can be set as a backup in case the patient becomes hypopneic or apneic.

''How do you choose a mode of ventilation?''

The choice depends on patient factors, surgical procedures, and the available technology.
Pressure Control Ventilation or PCV-VG may be preferred when a supraglottic airway is in place, or in patients where high inspiratory pressures may be dangerous (e.g., emphysema, neonates).
Volume-guaranteed modes may be preferred to maintain minute ventilation in patients with high or changing intra-abdominal pressures, such as in morbid obesity, laparoscopic surgeries, or pregnancy.
No single mode is superior; it is dictated by patient and surgery characteristics, and must be complemented with monitoring.

''What is lung protective ventilation during anesthesia?''

It aims to reduce the stress and strain on the lungs during mechanical ventilation.
This involves using low tidal volumes or driving pressures.
PEEP can keep the lung open.
Recruitment maneuvers, when required, can reopen collapsed alveoli.
It aims to reduce alveolar overdistension and prevent cyclic atelectasis (atelectotrauma).
These strategies are beneficial not only for patients with lung injury but for all patients to avoid doing harm.

''What is the role of non-invasive respiratory support post-operatively?''

Non-invasive ventilation (NIV) can be in the form of CPAP or BiPAP.
It can rapidly relieve dyspnea, reduce the work of breathing, and help avoid reintubation.
NIV can re-expand collapsed areas of the lung.
It has a role as a preventive measure in at-risk patients or in those developing mild pulmonary complications.
CPAP or BiPAP should always be considered to avoid reintubation in patients developing hypoxic respiratory failure after surgery.
When hypercapnia is predominant or coexists with hypoxemia, BiPAP should be preferred.

''What is High Flow Nasal Oxygen?''

HFNC devices deliver high flow, humidified oxygen heated to body temperature.
They are usually well tolerated.
Clinical indications include improving pre-oxygenation.
They can provide ongoing oxygenation and CO2 removal during intubation, especially during a prolonged attempt or awake fiberoptic intubation.
They provide oxygenation, reduce work of breathing, and facilitate CO2 elimination during surgical procedures like bronchoscopy.
They can also provide respiratory support after extubation in the post-anesthesia care unit.

''How can peak and plateau pressure be used to differentiate lung pathologies?''

The difference between peak pressure and plateau pressure reflects airway resistance.
In an airway resistance issue like bronchospasm, this difference goes up (high peak pressure, normal plateau pressure).
If it is a lung stiffening issue like ARDS, pneumonia, or a sudden pneumothorax, the plateau pressure goes up.
If plateau pressure rises, the tidal volume must be reduced and the cause investigated.
If only peak pressure is rising with an acceptable plateau pressure, the issue is in the airway (e.g., bronchospasm, circuit kinking).

Q&A Session and Audience Interaction

''What is the answer to the poll question: Increased lung compliance is associated with?''

The correct answer is increasing age.
In conditions like emphysema, there is a loss of elastic tissue which increases lung compliance.
Increasing pulmonary venous pressure would reduce volume.
High expanding volumes would increase resistance, the opposite of compliance.
Interstitial fibrosis decreases compliance.
Low lung volumes associated with hypoventilation are not a direct cause of increased compliance.

''What is the answer to the poll question on pulmonary function?''

The correct answer is that vital capacity is equivalent to the inspiratory reserve volume, tidal volume, and expiratory reserve volume.
Tidal volume is the volume of quiet breathing, not maximal inspiration.
Residual volume is the volume remaining after forced expiration, not passive expiration.
Residual volume cannot be measured directly; it is calculated.
Tidal volume is not measured by the single-breath nitrogen technique; that measures FRC.

''What are the true statements regarding ventilation modes?''

In volume control mode ventilation, gas distribution may be uneven, particularly in patients with lung disease. (True)
During pressure control mode ventilation, tidal volume varies with changes in lung compliance. (True)
Pressure support ventilation mode helps to reduce the work of breathing and support ventilation during emergence. (True)
Driving pressure is defined as the difference between peak pressure and PEEP. (False; it is the difference between plateau pressure and PEEP).

''What are the true statements on lung protective ventilation?''

It aims to reduce alveolar overdistension. (True)
It helps to prevent cyclic atelectasis or prevent atelectotrauma. (True)
Low tidal volumes and reduced plateau and driving pressures are used. (True)
Use of PEEP or recruitment maneuvers. (True)
It is not beneficial for patients without lung injury. (False; it should be a routine habit for all patients to do no harm).

''Is preoxygenation with 100% or 30% oxygen better?''

Conventional teaching and practice involve preoxygenation with 100% oxygen for a higher margin of safety and more apnea time.
However, CT studies have shown that 100% oxygen in a normal patient can cause absorption atelectasis.
If a difficult airway is not anticipated, preoxygenation with an FiO2 of 30-50% is beneficial in preventing atelectasis intraoperatively.
Giving 100% oxygen is more harmful at the time of extubation than at intubation, as it can cause postoperative atelectasis.

''What is the role of artificial surfactant in ARDS due to COVID?''

COVID is a case of severe ARDS with membrane disruption and endothelial injury, affecting gas exchange and transport.
As it is a severe ARDS, people have tried artificial surfactant for ventilation.
Starting surfactant therapy early might help in severe ARDS.
There is a KL4 surfactant that has been newly manufactured and is being tried for patients with COVID-19-related ventilation.

''Please explain hypoxic pulmonary vasoconstriction.''

HPV is a protective physiological mechanism in cases of regional hypoxia and hypoventilation.
When some alveoli are collapsed or not ventilated, perfusion is directed away from that affected lung towards the normal lung.
This helps to increase the ventilation-perfusion ratio back towards normal.
HPV is a protective mechanism in regional hypoxia and hypoventilation, but not in global hypoxia or severe ARDS.

''Is it necessary to keep the patient in a head-up position after extubation?''

Yes, it is desirable to have at least a 10-15 degree head-up tilt.
This removes a little of the thoracic splinting, making respiratory excursions easier.
It opens up the airway and decreases the chance of secretions getting into the lungs.

''How much trigger should be kept in volume control for adult patients?''

It is a general habit to increase the trigger to suppress breaths, which is not good.
The generally accepted trigger setting is either 1 to 2 cm of water.
You cannot kill a patient's efforts by raising the trigger to 5 or more.
If you want to suppress breaths during weaning, you should add an opioid or sedative, and if the patient is tachypneic, they may not be ready for weaning.