Respiratory Anesthesia
Lung Anatomy and Physiology
LUNG ANATOMY
1. What are the functional divisions of the airways in the lung?
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1. The three functional divisions of the airways in the lungs are the conductive airways, the transitional airways, and the respiratory airways.
Conductive airways are the airway structures from trachea to terminal bronchioles (airway generation 0 to 16). Their main function is bulk gas movement.
Transitional airways, also called the respiratory bronchioles, follow the terminal bronchioles to alveolar ducts (airway generation 16 to 20). Function of the transitional airways is not only for bulk gas movement, but also for limited gas exchange.
Respiratory airways are the alveoli and the alveolar sacs. The respiratory airways contribute to a large alveolar-capillary interface area for gas exchange (i.e., oxygen and carbon dioxide).
2. At what level is the cricoid cartilage present in adults and in neonates?
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2. The cricoid cartilage forms a complete ring around the airway. It lies at the vertebra level of C-6 in adults and C2-4 in children. It descends to C5-6 by age 5 years. This makes the neonates’ airway more anterior and the larynx more cephalic.
3. How far does an endotracheal tube (ETT) move with flexion and with extension in adults?
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3. In adults without cervical disease:
With full flexion of the cervical neck, the endotracheal tube (ETT) can move 3.8 cm, and
With full extension of the cervical neck, the ETT can be withdrawn by 6.4 cm. In infants and children, the “ETT movement” is more critical because even a 1-cm displacement can lead to extubation or carina stimulation.
4. How does cigarette smoke affect goblet cells and cilia in the lung?
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4. The histologic structures of the tracheal epithelial layer are composed of ciliated epithelium, goblet cells (mucous-producing cells), and brush cells. Cigarette smoking increases the number of goblet cells, which increases the volume of secretions. It decreases the number of ciliated cells, so it decreases the ability to clear the secretions as well.
5. Which bronchus has the greatest diameter? Which has the sharpest angle to the trachea in adults? What is the difference in the angles of the bronchi in children?
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5. Main stem bronchi are of an average diameter of 1.22 cm. The right bronchus has a greater diameter than the left bronchus. In adults, the right main stem bronchus takes off the trachea at a 25-degree angle, while the left is at a 45-degree angle. Therefore, most aspiration is directed into the right lower lobe of the lung.
In children <3 years, both bronchi take off the trachea at a 55-degree angle.
Anesthesia pearls:
Endobronchial intubation and foreign materials are more likely to occur in the right main bronchus than in the left one. The right upper lobe (RUL) is the more common lobe to be affected with foreign bodies and fluid aspiration in the supine position.
Taking off the RUL bronchus also has several anatomic variants:
In 10% of adults, the RUL bronchus departs by 2.5 cm from the carina, and
In 2% to 3% of adults, the RUL bronchus departs at the carina.
Therefore, these normal variants may make placing the right-side double-lumen ETT in the correct position difficult and unreliable.
6. What are the different types of alveolar cells?
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6. There are three different types of alveolar cells:
Type I alveolar cells cover 80% of alveolar surface, providing the area for gas exchange. They are highly mature and have low metabolic activity. During acute injury and adult respiratory distress syndrome (ARDS), these cells are injured significantly. The new type I cells will be replicated and modified from type II cells.
Type II alveolar cells are polygonal cells that have great metabolic enzymatic activities. Not only do they produce surfactants but they also modulate local electrolyte balance and endothelial and lymphatic cell function.
Type III alveolar cells are alveolar macrophages. They have migratory and phagocytic activities that are important factors in lung defense.
MUSCLES OF VENTILATION
1. Which is the primary muscle of ventilation? What are the other muscles of ventilation? What is the order of recruitment of these muscles during respiratory effort? Which phase of ventilation is active? Which is passive? Which muscles are involved in each?
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1. The primary muscle of ventilation is the diaphragm, which also has a role in coughing. The other muscles of ventilation in order of recruitment for increased respiratory effort are intercostals, abdominal, cervical strap, sternocleidomastoid, and large back/intervertebral muscles. The accessory muscles are important in that they lift the rib cage to produce negative pressure in the intrapleural space.
There are two phases in respiration: the active inspiration phase and the passive expiration phase. In general, the muscles that raise the ribs facilitate inspiration, and those that lower the ribs facilitate expiration.
Abdominal muscles: assist depression of the ribs and increase intra-abdominal pressure to facilitate passive exhalation.
Cervical strap muscles: elevate the sternum and the upper portions of the chest.
Sternocleidomastoid muscles: elevate the sternum and increase the anterior-posterior diameter of the chest wall.
Large back muscles and paravertebral muscles of the shoulder girdle: augment inspiration by enlarging the rib cage during maximum and high levels of ventilatory effort and activity.
2. What is the difference between slow- and fast-twitch muscle fibers?
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2. There are two types of ventilatory muscle fibers defined by their response time to electrical stimulation. Slow-twitch muscle fibers are fatigue-resistant for endurance. The diaphragm is composed of at least 50% of these fibers that have high oxidative capacity. Fast-twitch fibers are for strength, and respond rapidly to electrical stimulation but fatigue quickly. They allow the muscle to produce greater force over a short time, and support the maximal ventilation effort.
3. Why is the sternocleidomastoid muscle important to respiratory function?
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3. The sternocleidomastoid muscle is important to respiratory function because it elevates the sternum, thereby increasing the anteroposterior (AP) diameter of the chest wall.
VENTILATION CONTROL
1. Where are the inspiratory centers of respiration?
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1. Ventilation is controlled by the central and the peripheral nervous system. The mechanisms in controlling the central ventilation are very complex. It is located in the brain stem at the medulla and the pons. The inspiratory and the expiratory centers of respiration are at the medulla.
The inspiratory center of respiration is located in the dorsal respiratory group (DRG) of the medulla oblongata. The DRG has rhythmic activity and functions as a pacemaker for the respiratory system. It persists even when all nerves are blocked or sectioned → ataxic and gasping ventilation (apneustic breathing).
The expiratory coordinating center is located in the ventral respiratory group (VRG) in the medulla oblongata. The VRG functions as an inhibitor; it prohibits further use of the inspiratory muscles and allows passive expiration to finish the respiratory cycle. The inspiratory and expiratory neurons function through negative feedback so as not to antagonize one another.
2. Where is the apneustic center? What is its purpose?
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2. The apneustic center is located in the middle/lower pons. Although it does not directly control ventilation, it processes information in the medulla. With activation, its stimulation of the DRG results in sustained inspiration.
3. Where is the pneumotaxic center? What is its purpose?
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3. The pneumotaxic center is in the rostral pons. Its function is to limit the depth of inspiration. It has no intrinsic rhythmic activity, but when maximally activated it will increase respiratory frequency secondarily. Injury to the pneumotaxic center produces a decrease in ventilation rate and an increase in tidal volume (TV).
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4. How do central chemoreceptors affect ventilation?
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4. There are two chemoreceptor centers in ventilation: the central chemoreceptors and the peripheral chemoreceptors.
The central chemoreceptors respond primarily to changes in carbon dioxide (CO2) pressure, pH, and acid-base disturbances. The ventilation response to an elevated PaCO2 is rapid (within 1 to 2 minutes) by increasing TV and respiratory rates.
Peripheral chemoreceptors primarily respond to hypoxia. They are composed of the carotid and aortic bodies (at the aortic arch and its branches). When stimulated, these cause increased ventilatory rate and TV. The carotid bodies have predominantly ventilatory effects, while the aortic bodies have primarily circulatory effects. The hypoxic ventilatory drive is stimulated when PaO2 falls below 65 mm Hg.
COMPLIANCE
1. Define lung compliance.
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1. Compliance is defined as the change in volume per change in pressure. Compliance may also be measured as the lung compliance, the chest compliance, or both.
Clung = change in lung volume/change in transpulmonary pressure = 150 to 200 mL/chH2O
Cchest = change in chest volume/change in transthoracic pressure = 200 mL/chH2O
1/Ctotal = 1/Cchest wall + 1/Clung
In the supine position, the chest wall compliance is decreased because of the increasing abdominal contents pushing against the diaphragm. Increases in lung volume, pulmonary blood volume, and extravascular lung water (i.e., inflammation, edema, and fibrosis) increase the lung compliance. Normal (lung and chest together) compliance is 100 mL/cm H2O.
2. How does lung compliance relate to lung elasticity?
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2. Elastic recoil is usually measured as compliance. Both the lungs and the chest have elastic properties. Elastic forces of the chest wall and the lung pleura are opposed. The natural elastic recoil forces of the lung attempt to collapse the lung, while the natural elastic recoil forces of the chest try to expand the chest wall, creating a small negative interpleural pressure. In open pneumothorax, the chest wall is fully expanded and the lung is fully collapsed.
3. What are the determinants of resistance to laminar gas flow and to turbulent flow? What is the kind of flow in an ETT?
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3. Laminar flow and turbulent flow exist together within the respiratory tract in mixed patterns. Laminar flow generally occurs in the distal to the small bronchioles (<1 mm) and can be calculated by
Resistance = 8 × length × viscosity/3.14 × (radius)4.
Turbulent flow generally occurs in the large airways, including the ETT. It occurs at high gas flow rate and is usually audible. When flow is turbulent, the driving pressure is mostly related to the gas density. Therefore, low density gases (i.e., helium) may be added to lower the driving pressure needed to move gas in and out of an area with large airway obstruction.
The most important factor in determining airway resistance is the radius of the airway. Therefore, changing the ETT diameter dramatically changes the resistance of the tube, when compared with changing the length. Airway resistance can also be increased by bronchospasm, secretions, mucosal edema, reduced lung volumes (increased small airway resistance) and high gas flow. Four conditions will change laminar flow to turbulent flow: high gas flow, sharp angle flow, tube branching, and changing the tube diameter.
The Reynold’s number shows that the transition from laminar flow to turbulent flow in a tube is determined by several parameters:
Reynold’s number = Linear Velocity × Diameter × Gas Density/Gas Viscosity
Reynold’s number <1000 is associated with laminar flow
Reynold’s number between 1500 and 2000 is associated with turbulent flow
CHEMICAL CONTROL OF BREATHING
1. What is apneic threshold? What is the relationship between PaCO2 and ventilation?
How does general anesthesia affect the carbon dioxide (CO2) ventilatory response curve?
How do opioids, surgical stimulation or hypoxia affect the same?
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1. The apneic threshold is the maximal PaCO2 that does not initiate spontaneous ventilation. It is approximately 5 mm Hg below resting PaCO2 regardless of its baseline level. Apnea results in an increase of PaCO2 regardless of its baseline level. Apnea results in an increase of PaCO2 of 3 mm Hg/minute at normal metabolic rate.
In the awake patient, the ventilation response to an increase in inspired CO2 is in the range of 20 to 80 mm Hg. For each mm Hg increase in PaCO2, minute ventilation increases by 2 L/minute. The slope of the CO2 response curve is considered to represent PaCO2 sensitivity.
 ▪ FIGURE A-6. Partial arterial pressure of CO2 (Paco2) ventilatory response curve. GA, general anesthesia; NMB, neuromuscular blockade. |
General anesthesia, inhaled anesthetics, barbiturates, opioids, and other IV sedatives will decrease the slope and shift the CO2 ventilatory response curve to the right. General anesthetics impact breathing and promote hypoventilation by depressing the central chemoreceptors and the external intercostal muscle activity, and increasing the apneic threshold. However, surgical stimulation will reverse this change to varying and unpredictable degrees.
Ventilatory responses to O2 have wide ranges. With anesthetics, peripheral response to hypoxemia (PaO2) is more sensitive than PaCO2. Therefore, quantitative hypoxemia sensitivity is not clinically useful. The CO2 response curve can be left-shifted and steepened with true hyperventilation. In these situations, increases in minute ventilation and decreases in PaCO2 both create respiratory alkalemia, including the following:
Arterial hypoxemia
Metabolic academia
Central etiologies (intracranial hypertension, hepatic cirrhosis, anxiety, fear, and drugs such as aminophylline, salicylates)
2. What are the factors that will shift the curve to the left or to the right?
GAS MOVEMENT AND EXCHANGE
1. What is gas convection? What is gas diffusion? Where in the respiratory tree does each occur?
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1. Gas convection is the movement of all the gas molecules in the same direction. It is the primary mechanism responsible for gas flow in large and most small airways (up to 15th generation bronchioles).
Gas diffusion is the random molecular motion that results in the complete mixing of all gases. It is the primary mechanism responsible for gas flow in terminal bronchioles (16th generation) to alveoli. Diffusion refers to the passive movement of molecules across a membrane that is governed by a concentration gradient.
2. Where is the greatest resistance to airflow in the lungs? What type of flow is found in the convective airways?
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2. During normal ventilation, gas flow with convective airways (smaller airways) is laminar (which reduces resistance of gas flow). In the lungs, the greatest resistance to airflow occurs in the large airways where the velocity of gases is the greatest (which becomes a turbulent flow).
3. Can a diffusion defect cause hypercarbia?
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3. CO2 is 20 times more diffusible across human membranes than O2. In other words, because CO2 crosses membranes easily, clinical hypercarbia is never the result of defective diffusion. It is, however, the result of the imbalance between alveolar ventilation and CO2 production. In the lungs, diffusion is the primary mode of gas transportation. Diffusion begins in the terminal bronchioles (16th airway generation), mainly in the alveolar sacs and alveoli. 4. Diffusion capacity is measured by pulmonary function tests (PFTs). Decreasing the surface area available for diffusion leads to a mismatch of ventilation and perfusion, thereby decreasing diffusion capacity.
4. What causes decreased diffusing capacity?
DISTRIBUTION OF BLOOD FLOW AND VENTILATION
1. Define the blood flow in the three zones of West.
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1. Pulmonary blood flow is uniformly distributed by gravity. The lower portion of the lung receives greater blood flow than the upper areas. On the basis of the gravity-dependent blood flow distribution in the lungs, each lung has been divided into three zones by West. Blood flow is dependent on the relationship between the pulmonary artery pressure (Pa), the alveolar pressure (PA), and the pulmonary venous pressure (PV).
Zone I: PA > Pa > PV
Zone I receives ventilation in the absence of perfusion, which creates alveolar dead space ventilation. In hypovolemic shock, decreased pulmonary artery pressure results in enlarged Zone I.
Zone II: Pa > PV > PA
Zone II best matches ventilation with perfusion.
Zone III: Pa > PA > PV
Zone III is the most gravity-dependent area of the lung with capillary perfusion in excess of ventilation, creating a physiologic shunt.
2. Which alveoli are the most distended at rest: those at the top of the lung or the ones at the bottom?
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2. Alveolar pressure is the same throughout the lungs; the pleural pressure (Ppl) gradient creates the difference in transpulmonary pressure (PA – Ppl). At rest, the apex of the lungs has more negative intrapleural pressure. The alveoli are less or not compressed, with relatively large alveolar volume. Therefore, the distending pressure of this area is greater. However, at the base of the lungs where the negative intrapleural pressure is less, the alveoli are more compressed and the distending pressure is lower. During inspiration, intrapleural pressure is decreased at the base of the lungs and is greater than at the apex because of diaphragmatic activity. Therefore, more ventilation occurs in the dependent areas of the lungs.
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3. (a) Where does optimal ventilation-perfusion ([V with dot above]/[Q with dot above]) matching occur?
(b) Which part of the lung has an increased [V with dot above]/[Q with dot above] ratio?
(c) Which part of the lung has a decreased [V with dot above]/[Q with dot above] ratio?
VENTILATION-PERFUSION RATIO: DEAD SPACE
1. Define dead space.
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1. Dead space (VDS) is alveolar ventilation without perfusion, or TV that does not participate in gas exchange.
Physiologic dead space = anatomic dead space + alveolar dead space
Anatomic dead space is in the conducting airways, and alveolar dead space is in the volume of the gas in alveoli that do not participate in gas exchange because the alveoli are underperfused (i.e., West Zone I).
2. What would the [V with dot above]/[Q with dot above] ratio be for an absolute dead space?
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2. The value of absolute dead space is when [V with dot above]/[Q with dot above] = infinity.
3. In normal patients, is most of the physiologic dead space anatomic or alveolar?
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3. In normal patients, most dead space is anatomic dead space, extending from the oropharynx to terminal bronchioles, in which no gas exchange occurs. It is 2 mL/kg of ideal body weight.
4. List some of the causes of alveolar dead space.
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4. Physiologic dead space is mainly affected by changes in alveolar dead space. Alveolar dead space may be caused by the following:
Decreased pulmonary blood flow,
Decreased cardiac output,
Pulmonary embolism (fat, thrombus, air, or amniotic fluid),
Chronic obstructive pulmonary disease (COPD),
Positive end-expiratory pressure (PEEP),
Intense pulmonary vasoconstriction, and
ARDS (intense pulmonary vasoconstriction, lung contusion, or pulmonary edema).
The most common cause of increased physiologic dead space ventilation in the operating room (OR) and intensive care unit (ICU) is decreased cardiac output and pulmonary blood flow. Normally during mechanical ventilation, the dead space: alveolar ventilation ratio is 1:1. However, during spontaneous ventilation, the ratio is 1:2.
5. Define VDS/VT. What is the normal value? Can the end-tidal CO2 value from the mass spectrometer be used in the formula for VDS/VT?
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5. VDS/VT is the measure of physiologic dead space divided by the mixture of all expired gases (TV):
VDS/VT = Alveolar PCO2 − Expired PCO2/Alveolar PCO2
Expired PCO2 (PECO2) is the average PCO2 from the mixture of all expired gas samples over a period of time, not the end-tidal PCO2. The alveolar PCO2 is determined by alveolar ventilation and CO2 production. The normal value is approximately 0.2 to 0.4, but during positive-pressure ventilation (PPV) it is 0.33 to 0.5.
The mass spectrometer end-tidal CO2 value is not accurate because it includes the gas in the anatomic dead space as well as the gas left in the circuit.
VENTILATION-PERFUSION RATIO SHUNT
1. Define shunt. What would the [V with dot above]/[Q with dot above] ratio be for an absolute shunt?
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1. Shunt is lung that is perfused but poorly ventilated. The absolute shunt effect is a result of venous admixture and may occur in acute lobar atelectasis, advanced pulmonary edema, postoperative atelectasis, or consolidated pneumonia.
2. What is the difference between a physiologic shunt and an anatomic shunt?
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2. Physiologic shunt is estimated as 2% to 5% of cardiac output. It is that portion of total cardiac output that returns to the left heart and systemic circulation without receiving O2 in the lung (also called post pulmonary shunt). It includes the thesbian veins, bronchial veins, mediastinal veins, and pleural veins. Anatomic shunt is associated with pathophysiologic changes such as congenital heart disease (patent ductus arteriosus, ventricular septal defect, and atrial septal defect), right to left intrapulmonary anatomic shunts, or atrioventricular (AV) malformation in hepatic failure.
3. Define Qshunt/Qtotal.
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3. The fraction of cardiac output that passes through a shunt can be calculated by
QS/QT = CcO2 − CaO2/CcO2 − CvO2
CcO2 = oxygen content of end pulmonary capillary blood
CaO2 = arterial oxygen contents
CvO2 = mixed venous oxygen content
(a) Blood oxygen content
Oxygen content | = Bound oxygen + dissolved oxygen |
= 1.34 × Hb × SaO2 + PaO2 × 0.003 |
(b) Oxygen consumption
Vo2 = Cardiac output(L/mL) × (CaO2 − CvO2)
(c) Arterial oxygenation
A-a gradient = PAO2 − PaO2
PAO2 = FiO2(PB − PH2O)PAO2/0.8
PaO2 = 102 − age in years/3
(d) Hemoglobin dissociation curve
PULMONARY FUNCTION TESTS
1. Match the following on a pulmonary function tests (PFT) graph:
_______Tidal volume,
_______Residual volume,
_______Inspiratory reserve volume,
_______Expiratory reserve volume,
_______Vital capacity,
_______Inspiratory capacity,
_______Functional residual capacity (FRC),
_______Total lung capacity,
_______Closing volume,
_______Airways begin to close,
_______Closing capacity.
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View Answer
1. The PFTs are the measurement of a patient’s airflow (spirometry), lung volume, and diffusing capacity for inspired carbon monoxide (DLCO). The results, based on age and height of the patient, are calculated and reported as a percentage of a predicted normal value and classified into obstructive, restrictive, or mixed respiratory disease.
 ▪ FIGURE A-9. TLC, Total lung capacity; IC, inspiratory capacity; FRC, functional residual capacity; VC, vital capacity; RV, residual volume; IRV, inspiratory reserve volume; TV, tidal volume; ERV, expiratory reserve volume. |
TV 500 mL (6 to 8 mL/kg)
Residual Volume (RV) 1200 mL
Expiratory Reserve Volume (ERV) 1100 mLRelated posts:
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