1 What is the functional residual capacity? What factors affect it?

The functional residual capacity (FRC) is the volume in the lungs at the end of passive expiration. It is determined by opposing forces of the expanding chest wall and the elastic recoil of the lung. A normal FRC = 1.7 to 3.5 L. FRC is increased by:

Body size (FRC increases with height)

Age (FRC increases slightly with age)

Certain lung diseases, including asthma and chronic obstructive pulmonary disease (COPD).

FRC is decreased by:

Sex (woman have a 10% decrease in FRC when compared to men)

Diaphragmatic muscle tone (individuals with paralyzed diaphragms have less FRC when compared to normal individuals)

Posture (FRC greatest standing > sitting > prone > lateral > supine)

Certain lung diseases in which elastic recoil is diminished (e.g., interstitial lung disease, thoracic burns, and kyphoscoliosis)

Increased abdominal pressure (e.g., obesity, ascites)

2 What is closing capacity? What factors affect the closing capacity? What is the relationship between closing capacity and functional residual capacity?

Closing capacity is the point during expiration when small airways begin to close. In young individuals with average body mass index, closing capacity is approximately half the FRC when upright and approximately two thirds of the FRC when supine.

Closing capacity increases with age and is equal to FRC in the supine individual at approximately 44 years and in the upright individual at approximately 66 years. The FRC depends on position; the closing capacity is independent of position. Closing capacity increases with increasing intraabdominal pressure, age, decreased pulmonary blood flow, and pulmonary parenchymal disease, which decreases compliance.

3 What muscles are responsible for inspiration and expiration?

The respiratory muscles include the diaphragm, internal and external intercostals, abdominal musculature, cervical strap muscles, sternocleidomastoid muscle, and large back and intervertebral muscles of the shoulder girdle. During normal breathing inspiration requires work, whereas expiration is passive. The diaphragm, scalene muscles, and external intercostal muscles provide most of the work during normal breathing. However, as the work of breathing increases, abdominal musculature and internal intercostal muscles become active during expiration, and the scalene and sternocleidomastoid muscles become increasingly important for inspiration.

4 What is the physiologic work of breathing?

The physiologic work of breathing involves the work of overcoming the elastic recoil of the lung (compliance and tissue resistance work) and the resistance to gas flow. The elastic recoil is altered in certain pathologic states, including pulmonary edema, pulmonary fibrosis, thoracic burns, and COPD. The resistance to gas flow is increased dramatically during labored breathing. In addition to the physiologic work of breathing, a patient on a ventilator must also overcome the resistance of the endotracheal tube.

5 Discuss the factors that affect the resistance to gas flow. What is laminar and turbulent gas flow?

The resistance to flow can be separated into the properties of the tube and the properties of the gas. At low flow, or laminar flow (nonobstructed breathing), the viscosity is the major property of the gas that affects flow. Clearly the major determining factor is the radius of the tube. This can be shown by the Hagen-Poiseuille relationship:

where R is resistance, L is the length of the tube, μ is the viscosity, and r is the radius of the tube. At higher flow rate (in obstructed airways and heavy breathing), the flow is turbulent. At these flows the major determinants of resistance to flow are the density of the gas (ρ) and the radius of the tube, r.

6 Suppose a patient has an indwelling 7-mm endotracheal tube and cannot be weaned because of the increased work of breathing. What would be of greater benefit, cutting off 4 cm of endotracheal tube or replacing the tube with one of greater internal diameter?

According to the Hagen-Poiseuille relationship discussed previously, if the radius is halved, the resistance within the tube increases to sixteenfold; but if the length of the tube is doubled, the resistance is only doubled. Cutting the length of the tube minimally affects resistance, but increasing the tube diameter dramatically decreases resistance. Therefore, to reduce the work of breathing the endotracheal tube should be changed to a larger size.

7 Why might helium be of benefit to a stridorous patient?

When flow is turbulent, as is the case in a stridorous patient, driving pressure is mostly related to gas density. Use of low-density gas mixtures containing helium and oxygen lowers the driving pressure needed to move gas in and out of the area, decreasing the work of breathing.

8 Discuss dynamic and static compliance

Compliance describes the elastic properties of the lung. It is a measure of the change in volume of the lung when pressure is applied. The lung is an elastic body that exhibits elastic hysteresis. When the lung is rapidly inflated and held at a given volume, the pressure peaks and then exponentially falls to a plateau pressure. The volume change of the lung per the initial peak pressure change is the dynamic compliance. The volume change per the plateau pressure represents the static compliance of the lung.

9 How does surface tension affect the forces in the small airways and alveoli?

Laplace’s law describes the relationship between pressure (P), tension (T), and the radius (R) of a bubble and can be applied to the alveoli.

As the radius decreases, the pressure increases. In a lung without surfactant present, as the alveoli decrease in size, the pressure is higher in small alveoli, causing gas to move from the small to larger airways, collapsing in the process. Surfactant, a phospholipid substance produced in the lung by type II alveolar epithelium, reduces the surface tension of the small airways, thus decreasing the pressure as the airways decrease in size. This important substance helps keep the small airways open during expiration.

10 Review the different zones (of West) in the lung with regard to perfusion and ventilation

West described three areas of perfusion in an upright lung, and a fourth was later added. Beginning at the apices, they are:

Zone 1: Alveolar pressure (P_Alv) exceeds pulmonary artery pressure (P_pa) and pulmonary venous pressure (P_pv), leading to ventilation without perfusion (alveolar dead space) (P_Alv > P_pa > P_pv).

Zone 2: Pulmonary arterial pressure exceeds alveolar pressure, but alveolar pressure still exceeds venous pressure (P_pa > P_Alv > P_pv). Blood flow in zone 2 is determined by arterial-alveolar pressure difference.

Zone 3: Pulmonary venous pressure exceeds alveolar pressure, and flow is determined by the arterial-venous pressure difference (P_pa > P_pv >P_Alv).

Zone 4: Interstitial pressure (P_interstitium) is greater than venous and alveolar pressures; thus flow is determined by the arterial-interstitial pressure difference (P_pa > P_interstitium > P_pv > P_Alv). Zone 4 should be minimal in a healthy patient.

A change from upright to supine position increases pulmonary blood volume by 25% to 30%, thus increasing the size of larger-numbered West zones.

11 What are the alveolar gas equation and the normal alveolar pressure at sea level on room air?

The alveolar gas equation is used to calculate the alveolar oxygen partial pressure:

where P_AO₂ is the alveolar oxygen partial pressure, FiO₂ is the fraction of inspired oxygen, P_b is the barometric pressure, P_H2O is the partial pressure of water (47 mm Hg), P_aCO₂ is the partial pressure of carbon dioxide, and RQ is the respiratory quotient, dependent on metabolic activity and diet and is considered to be about 0.825. At sea level the alveolar partial pressure (P_AO₂) is:

Knowing the P_aO₂ allows us to calculate the alveolar-arterial O₂ gradient (A-a gradient). Furthermore, by understanding the alveolar gas equation we can see how hypoventilation (resulting in hypercapnia) lowers P_aO₂, and therefore P_aO₂.

12 What is the A-a gradient and what is a normal value for this gradient?

The alveolar-arterial O₂ gradient is known as the A-a gradient. It is the difference in partial pressure of O₂ in the alveolus (P_aO₂), calculated by the alveolar gas equation, and the partial pressure of O₂ measured in the blood (P_aO₂):

A normal A-a gradient is estimated as follows:

13 What is the practical significance of estimating A-a gradient?

The A-a gradient, together with the P_aO₂ and P_aCO₂, allows systematic evaluation of hypoxemia, leading to a concise differential diagnosis. As previously stated, the ABG provides an initial assessment of oxygenation by measuring the P_aO₂. The A-a gradient is an extension of this, for by calculating the difference between the P_aO₂ and the P_aO₂ we are assessing the efficiency of gas exchange at the alveolar-capillary membrane.

14 What are the causes of hypoxemia?

Low inspired oxygen concentration (FiO₂): To prevent delivery of hypoxic gas mixtures during an anesthetic, oxygen alarms are present on the anesthesia machine.

Hypoventilation: Patients under general anesthesia may be incapable of maintaining an adequate minute ventilation because of muscle relaxants or the ventilatory depressant effects of anesthetic agents. Hypoventilation is a common problem after surgery.

Shunt: Sepsis, liver failure, arteriovenous malformations, pulmonary emboli, and right-to-left cardiac shunts may create sufficient shunting to result in hypoxemia. Since shunted blood is not exposed to alveoli, hypoxemia caused by a shunt cannot be overcome by increasing FiO₂.

Ventilation-perfusion (V/Q) mismatch: Ventilation and perfusion of the alveoli in the lung ideally have close to a one-to-one relationship, promoting efficient oxygen exchange between alveoli and blood. When alveolar ventilation and perfusion to the lungs are unequal (V/Q mismatching), hypoxemia results. Causes of V/Q mismatching include atelectasis, lateral decubitus positioning, bronchial intubation, bronchospasm, pneumonia, mucous plugging, pulmonary contusion, and adult respiratory distress syndrome. Hypoxemia caused by V/Q mismatching can usually be overcome by increasing FiO₂.

Diffusion defects: Efficient O₂ exchange depends on a healthy interface between the alveoli and the bloodstream. Advanced pulmonary disease and pulmonary edema may have associated diffusion impairment.

15 What are the A-a gradients for the different causes of hypoxemia:

Low fractional concentration of inspired O₂: normal A-a gradient

Alveolar hypoventilation: normal A-a gradient

Right-to-left shunting: elevated A-a gradient

Ventilation/perfusion mismatch: elevated A-a gradient

Diffusion abnormality: elevated A-a gradient

16 Discuss V/Q mismatch. How can general anesthesia worsen V/Q mismatch?

V/Q mismatch ranges from shunt at one end of the spectrum to dead space at the other end. In the normal individual alveolar ventilation (V) and perfusion (Q) vary throughout the lung anatomy. In the ideal situation V and Q are equal, and V/Q = 1. In shunted lung the perfusion is greater than the ventilation, creating areas of lung where blood flow is high but little gas exchange occurs. In dead-space lung, ventilation is far greater than perfusion, creating areas of lung where gas is delivered but little blood flow and gas exchange occur. Both situations can cause hypoxemia. In the case of dead space, increasing the FiO₂ will potentially increase the hemoglobin oxygen saturation, whereas in cases of shunt it will not. In many pathologic situations both extremes coexist within the lung.

Under general anesthesia FRC is reduced by approximately 400 ml in an adult. The supine position decreases FRC another 800 ml. A large enough decrease in FRC may bring end-expiratory volumes or even the entire tidal volume to levels below the closing volume (the volume at which small airways close). When small airways begin to close, atelectasis and low V/Q areas develop.

17 Define anatomic, alveolar, and physiologic dead space

Physiologic dead space (V_D) is the sum of anatomic and alveolar dead space. Anatomic dead space is the volume of lung that does not exchange gas. This includes the nose, pharynx, trachea, and bronchi. This is about 2 ml/kg in the spontaneously breathing individual and is the majority of physiologic dead space. Endotracheal intubation will decrease the total anatomic dead space. Alveolar dead space is the volume of gas that reaches the alveoli but does not take part in gas exchange because the alveoli are not perfused. In healthy patients alveolar dead space is negligible.

18 How is V_d/V_t calculated?

V_d/V_t is the ratio of the physiologic dead space to the tidal volume (V_t), is usually about 33%, and is determined by the following formula:

Alveolar PCO₂ is calculated using the alveolar gas equation, and expired PCO₂ is the average PCO₂ in an expired gas sample (not the same as end-tidal PCO₂).

19 Define absolute shunt. How is the shunt fraction calculated?

Absolute shunt is defined as blood that reaches the arterial system without passing through ventilated regions of the lung. The fraction of cardiac output that passes through a shunt is determined by the following equation:

where Qs is the physiologic shunt blood flow per minute, Qt is the cardiac output per minute, Ci_O2 is the ideal arterial oxygen concentration when V/Q = 1, CaO₂ is arterial oxygen content, and Cv_O2 is mixed venous oxygen content. It is estimated that 2% to 5% of cardiac output is normally shunted through postpulmonary shunts, thus accounting for the normal alveolar-arterial oxygen gradient (A-a gradient). Postpulmonary shunts include the thebesian, bronchial, mediastinal, and pleural veins.

20 What is hypoxic pulmonary vasoconstriction?

Hypoxic pulmonary vasoconstriction (HPV) is a local response of pulmonary arterial smooth muscle that decreases blood flow in the presence of low alveolar oxygen pressure, helping to maintain normal V/Q relationships by diverting blood from under ventilated areas. HPV is inhibited by volatile anesthetics and vasodilators but is not affected by intravenous anesthesia.

21 Calculate arterial and venous oxygen content (CaO₂ and CvO₂)

Oxygen content (milliliters of O₂/dl) is calculated by summing the oxygen bound to hemoglobin (Hgb) and the dissolved oxygen of blood:

where 1.34 is the O₂ content per gram hemoglobin, SaO₂ is the hemoglobin saturation, [Hgb] is the hemoglobin concentration, and PaO₂ is the arterial oxygen concentration.

If [Hgb] = 15 g/dl, arterial saturation = 96%, and PaO₂ = 90 mm Hg, mixed venous saturation = 75%, and PvO₂ = 40 mm Hg, then:

and

22 How is CO₂ transported in the blood?

CO₂ exists in three forms in blood: dissolved CO₂ (7%), bicarbonate ions () (70%), and combined with hemoglobin (23%).

23 How is PCO₂ related to alveolar ventilation?

The partial pressure of CO₂ (PCO₂) is inversely related to the alveolar ventilation and is described by the equation:

where V_CO2 is total CO₂ production and V_alveolar is the alveolar ventilation (minute ventilation less the dead space ventilation). In general, minute ventilation and PCO₂ are inversely related.

24 What factors alter oxygen consumption?

Factors increasing oxygen consumption include hyperthermia (including malignant hyperthermia), hypothermia with shivering, hyperthyroidism, pregnancy, sepsis, burns, pain, and pheochromocytoma. Factors decreasing oxygen consumption include hypothermia without shivering, hypothyroidism, neuromuscular blockade, and general anesthesia.

25 Where is the respiration center located in the brain?

The respiratory center is located bilaterally in the medulla and pons. Three major centers contribute to respiratory regulation. The dorsal respiratory center is mainly responsible for inspiration, the ventral respiratory center is responsible for both expiration and inspiration, and the pneumotaxic center helps control the breathing rate and pattern. The dorsal respiratory center is the most important. It is located within the nucleus solitarius where vagal and glossopharyngeal nerve fibers terminate and carry signals from peripheral chemoreceptors and baroreceptors (including the carotid and aortic bodies) and several lung receptors. A chemosensitive area also exists in the brainstem just beneath the ventral respiratory center. This area responds to changes in cerebrospinal fluid (CSF) pH, sending corresponding signals to the respiratory centers. Anesthetics cause repression of the respiratory centers of the brainstem.

26 How do carbon dioxide and oxygen act to stimulate and repress breathing?

Carbon dioxide (indirectly) or hydrogen ions (directly) work on the chemosensitive area in the brainstem. Oxygen interacts with the peripheral chemoreceptors located in the carotid and aortic bodies. During hypercapnic and hypoxic states the brainstem is stimulated to increase minute ventilation, whereas the opposite is true for hypocapnia and normoxia. Carbon dioxide is by far more influential in regulating respiration than is oxygen.

27 What are the causes of hypercarbia?

Hypoventilation: Decreasing the minute ventilation ultimately decreases alveolar ventilation, increasing PCO₂. Some common causes of hypoventilation include muscle paralysis, inadequate mechanical ventilation, inhalational anesthetics, and opiates.

Increased CO₂ production: Although CO₂ production is assumed to be constant, there are certain situations in which metabolism and CO₂ production are increased. Malignant hyperthermia, fever, thyrotoxicosis, and other hypercatabolic states are some examples.

Iatrogenic: The anesthesiologist can administer certain drugs to increase CO₂. The most common is sodium bicarbonate, which is metabolized by the enzyme carbonic anhydrase to form CO₂. CO₂ is absorbed into the bloodstream during laparoscopic procedures. Rarely CO₂-enriched gases can be administered. Carbon dioxide insufflation for laparoscopy is a cause. Exhaustion of the CO₂ absorbent in the anesthesia breathing circuit can result in rebreathing of exhaled gases and may also result in hypercarbia.

28 What are the signs and symptoms of hypercarbia?

Hypercarbia acts as a direct vasodilator in the systemic circulation and as a direct vasoconstrictor in the pulmonary circulation. It is also a direct cardiac depressant. Cerebral blood flow increases in proportion to arterial CO₂. An increase in catecholamines is responsible for most of the clinical signs and symptoms of hypercarbia. Hypercarbia causes an increase in heart rate, myocardial contractility, and respiratory rate along with a decrease in systemic vascular resistance. Higher systolic blood pressure, wider pulse pressure, tachycardia, greater cardiac output, higher pulmonary pressures, and tachypnea are common clinical findings. In awake patients symptoms include headache, anxiety/restlessness, and even hallucinations. Extreme hypercapnia produces hypoxemia as CO₂ displaces O₂ in alveoli.