Lung volumes

The tidal volume (V_T) represents the amount of air moved into or out of the lungs during a normal ventilatory excursion. Monitoring of this lung volume is important when the patient is receiving ventilatory support. Because the V_T measurement is highly variable, it is not an extremely helpful parameter in pulmonary function tests. Clinically, the V_T can be estimated at 7 mL/kg. For example, a man who weighs 70 kg has a V_T of approximately 490 mL (7 × 70 = 490).

The expiratory reserve volume (ERV) is the maximal amount of air that can be expired from the resting position after a normal spontaneous expiration. The ERV reflects muscle strength, thoracic mobility, and a balance of forces that determine the resting position of the lungs and chest wall after a normal expiration. This lung volume is usually decreased in patients who are morbidly obese (see Chapter 45). This lung volume also is decreased in the immediate postoperative period in patients who have undergone an upper abdominal or thoracic operation.^5,9,10

The residual volume (RV) is the volume of air that remains in the lungs at the end of a maximal expiration. This lung volume represents the balance of forces of the lung elastic forces and thoracic muscle strength. Patients with skeletal muscle relaxant that was not adequately reversed at the end of the anesthetic period may have an elevated RV because enough muscle strength cannot be generated to force all the air out of the lungs. As the RV increases, more air remains in the lungs so that the air does not participate adequately in gas exchange and becomes dead-space air. As the dead-space volume of air increases, it can impinge on the V_T and hypoxemia can ensue. The importance of the RV is that it allows for continuous gas exchange throughout the entire breathing cycle by providing air to most of the alveoli and it aerates the blood between breaths. Consequently, the RV prevents wide fluctuations in oxygen and carbon dioxide concentrations during inspiration and expiration.⁴

The inspiratory reserve volume (IRV) reflects a balance of the lung elastic forces, muscle strength, and thoracic mobility. The IRV is the maximal volume of air that can be inspired at the end of a normal spontaneous inspiration. Physiologically, the IRV is available to meet increased metabolic demand at a time of excess physical exertion. It assists in moving a larger volume of air into the alveoli through each ventilatory cycle to increase the overall performance and efficiency of the respiratory system.

Lung capacities

The inspiratory capacity (IC) is the maximal volume of air that can be inspired from the resting expiratory position. The IC is the sum of the V_T and the IRV.

The functional residual capacity (FRC) represents the previously mentioned resting position. The FRC is the volume of air that remains in the lungs at the end of a normal expiration when no respiratory muscle forces are applied. At FRC, the mechanical forces of the lung and thorax are at rest and no air flow is present. Because the FRC is usually reduced in patients who are recovering from anesthesia, this particular lung capacity is of great importance to the perianesthesia nurse when intensive nursing care is rendered. For this reason, breathing maneuvers, such as the sustained maximal inspiration (SMI), are instituted in the PACU to raise the FRC (see the next section on lung mechanics). The FRC represents the sum of the ERV and the RV. A severe increase in the FRC is often associated with pulmonary distention, which is technically a state of hyperinflation of the lung. This state of hyperinflation can be caused by two abnormal conditions: airway obstruction and loss of elasticity. Airway obstruction is exemplified by an episode of acute bronchial asthma; a loss of lung elasticity is usually associated with emphysema. A severe decrease in FRC is associated with pulmonary fibrosis and can be the sequela of postoperative atelectasis.

The vital capacity (VC) is the amount of air that can be expired after the deepest possible inspiration. The VC is the sum of the V_T, the ERV, and the IRV. The VC measures many factors that simultaneously affect ventilation, including activity of respiratory centers, motor nerves, and respiratory muscles, and thoracic maximum, airway and tissue resistance, and lung volume.

The total lung capacity (TLC) is the total amount of air in the lung at a maximal inspiration. The TLC is the sum of the VC and the RV.

Clinical measurements of the TLC, FRC, and RV are difficult because these values include a gas volume that cannot be exhaled; therefore the measurements require sophisticated pulmonary function testing equipment with gas dilution techniques or plethysmography. Measurements of lung volumes and capacities are useful in the evaluation of lung function.⁵

Mechanical features of the lungs

Mechanical forces of the respiratory system actually determine the lung volumes and capacities. For an understanding of how these lung volumes and capacities are determined and how they are affected by anesthesia and surgery, the perianesthesia nurse should become familiar with the balance-of-forces concept of the respiratory system (see the section on combined mechanical properties of the lungs and chest wall). The PACU stir-up regimen is designed to increase the postoperative patient’s lung volumes and capacities with enhancement of the mechanical forces of the respiratory system.

The lungs and chest wall are viscoelastic structures, one within the other. Because they are elastic, the lungs always want to collapse or recoil to a smaller position. Therefore, as can be seen in the pressure-volume (P-V) curve of the lungs alone (Fig. 12-8), at less than RV the lungs are collapsed and no pressure is transmitted across the lungs (i.e., no transpulmonary pressure). When the lungs are inflated to a volume halfway between RV and TLC, the lungs seek to recoil or collapse back to the resting position equal to or less than RV, which is reflected by an increase in transpulmonary pressure. When the lungs are fully inflated at TLC, a maximal transpulmonary pressure is also exhibited. By analogy, when a balloon is completely deflated, the pressure measured at the mouth of the balloon is zero. When the balloon is partially inflated, the pressure increases as the elastic forces of the balloon try to make the balloon recoil to its resting position. If the balloon is maximally inflated, the elastic recoil of the balloon is greater, as is the pressure measured at the mouth of the balloon.

FIG. 12-8 Static deflation pressure-volume curve for lung. Positive pressures represent pressures that tend to decrease lung volume. TLC, Total lung capacity; RV, residual volume.

(From Drain C: Physiology of the respiratory system related to anesthesia, CRNA 7: 163–180, 1996.)

Pulmonary hysteresis

Inflation and deflation paths of the P-V curve of the lung are not aligned on top of each other (Fig. 12-9). The path of deformation (inspiration) to TLC is different from the path followed when the force is withdrawn (expiration) from TLC to RV. This phenomenon is known as pulmonary hysteresis. The following factors contribute to pulmonary hysteresis: properties of the tissue elements (a minor factor), recruitment of lung units, and the surface tension phenomenon (surfactant).¹

FIG. 12-9 Inflation and deflation paths of pressure-volume curve of lungs.

(From Koeppen BM, Stanton BA: Berne and Levy’s physiology, ed 6 [updated edition], St. Louis, 2010, Mosby.)

Recruitment of lung units

Recruitment of lung units has an important part in pulmonary hysteresis. For an understanding of recruitment of lung units, the nurse must be familiar with the concept of airway closure. An apex-to-base gradient of alveolar size exists in the lung (Fig. 12-10). This gradient occurs because of the weight of the lung, which tends to pull the lung toward its base. As a result, the pleural pressure is more negative at the apex than at the base of the lung. Ultimately, at low lung volumes, the alveoli at the apex are inflated more than the alveoli at the base. At the base of the lungs, some alveoli are closed to ventilation because the weight of the lungs in that area causes the pleural pressure to become positive. Airways open only when the critical opening pressure is achieved during inflation and the lung units peripheral to them are recruited to participate in volume exchange. This process is called radial traction or a tethering effect on airways. An analogy of a nylon stocking can aid in the explanation of this concept. When no traction is applied to the nylon stocking, the holes in the stocking are small. As traction is applied to the stocking from all sides, each nylon filament pulls on the others, which spreads apart all the other filaments; and the holes in the stocking enlarge. Similarly, as one airway opens, it produces radial traction on the next airway and pulls the next airway open; in other words, it recruits airways to open. The volume of air in the alveoli behind the closed airways is termed the closing volume (CV). The CV plus the RV is termed the closing capacity (CC). The CC normally occurs at less than the FRC.⁵

FIG. 12-10 Alveolar size from apex to base of lungs, as subject inhales from residual volume (A) to total lung capacity (B).

During the early emergence phase of anesthesia, patients usually have low lung volumes, which can lead to airway closure. Consequently, a postoperative breathing maneuver that has a maximal alveolar inflating pressure, a long alveolar inflating time, and high alveolar inflating volume, such as the SMI or yawn maneuver, should be used to facilitate the maximal recruitment of lung units. With the recruitment of lung units, the FRC could be raised out of the closing volume range and ultimately hypoxemia could be reduced.

Equal pressure point

The equal pressure point (EPP) has many clinical implications to perianesthesia practice. More specifically, intraoperative and postoperative mechanical ventilations, along with pursed lips and abdominal breathing of the patient with compliant airways, are based on this concept.

The alveoli and airways can be imagined as a balloon in a box (Fig. 12-11). Flow out of the balloon is facilitated by the recoil of the balloon, which forces the air out of the balloon through the neck and out into the atmosphere. The addition of pressure all over the box forces the air out of the balloon at a higher rate of flow. Physiologically, the balloon recoil is analogous to the alveolar recoil pressure. The pressure pushing down on the balloon and its neck corresponds to a positive pleural pressure that is generated on a forced expiratory maneuver. For the air to move out of the alveoli, the alveolar pressure must exceed the pressure at the mouth. The pressure inside the neck of the balloon corresponds to the intraluminal airway pressure. Consequently, the alveolar pressure comprises the recoil pressure of the alveoli and the plural pressure. Also, the pressure to generate air flow decreases down the airway to the mouth (see Fig. 12-11). During a forced expiratory maneuver, the plural pressure pushes down on the alveoli and the airways. If the alveolar recoil pressure is 30 and the plural pressure is 20, the alveolar pressure is 50. The pressure inside the airway (intraluminal pressure) decreases progressively downstream toward the mouth. The EPP occurs when the intraluminal pressure is equal to the plural pressure (20 = 20); from that point, the plural pressure exceeds the intraluminal pressure and dynamic compression of the airway occurs. Total collapse of the airways from the EPP and the mouth does not normally occur because of the compliance of the airways. Physiologically, the dynamic compression reduces the airways radius and thus results in an increase in flow rates in the compressed area that aids physiologic mechanisms, such as the cough maneuver, to sheer and expel secretions and mucus out of the airways.⁵

FIG. 12-11 Pressure changes in the chest and lung during inspiration and forced expiration. The pleural pressure around the airways is usually negative (less than atmospheric). During inspiration, the chest wall expands and there is a greater negative pleural pressure, drawing air into the airways. At forced expiration, the pleural pressure may become positive, forcing air out. The equal pressure point (EPP) is where airway pressure equals pleural pressure.

(From Naish J: Medical sciences, St. Louis, 2009, Saunders.)

In the patient with highly compliant airways (i.e., with chronic obstructive pulmonary disease), the dynamic compression can completely close the airways. The air that is trapped increases the FRC and becomes dead space. The harder the patient tries to expel air, the greater the plural pressure becomes and more dynamic compression occurs; thus a vicious cycle ensues. Interventions to help these patients move air out of the lungs are focused on a reduction of the amount of dynamic compression on the airways. The interventions are to increase the expiratory time and provide physiologic positive end-expiratory pressure (PEEP). Lengthening of the expiratory time aids in reduction of the amount of positive plural pressure on the airways, and physiologic PEEP enhances the airway’s intraluminal pressure in the highly compliant airways. In the awake patient with highly compliant airways, abdominal breathing prolongs the expiratory time and pursed-lip breathing provides physiologic PEEP. In the patient who is anesthetized, prolonging the expiratory time (i.e., inspiration:expiration ratio of 1:3) on the ventilator and use of physiologic PEEP (i.e., 5 cm/H₂O) aids in moving air out of the airways.

Pulmonary time constant

The pulmonary time constant is similar to the half-life used in assessment of the pharmacokinetic activity of drugs. A time constant represents the amount of time necessary for flow to decrease by a rate equal to half the initial flow. A time constant equals the resistance multiplied by the compliance. Therefore the time necessary to reach each time constant depends on the individual values of resistance and compliance. In normal conditions, the decrease in flow at the first time constant is approximately 37% of the initial flow, or approximately 63% of the total volume added or removed from the lungs. The first time constant represents the time necessary for removing or adding 63% of the total volume of air in the lungs. The decrease in flow rate at the second time constant is approximately 14%, and the percent volume of air added or removed from the lungs is 86%. The decrease in flow at the third time constant is 5%, with a corresponding 95% volume added or removed; therefore the higher the time constant, the more air removed or added to the lungs.⁴

The clinical implications of time constants are extremely important in the perianesthesia care of patients who have received an inhalation anesthetic. Patients who have increased airway resistance or increased C_L, or both, have a prolonged time necessary for filling and emptying of the lungs. The lung units in this situation are referred to as slow lung units. The patient with slow lung units usually has chronic obstructive pulmonary disease. Patients with a significant amount of increased secretions also have some slow lung units. Consequently, patients with slow lung units usually have a slow emergence from inhalation anesthesia. Patients with a low C_L, such as patients with pulmonary fibrosis, have fast lung units. As a result, these patients can fill or empty the lungs rather rapidly and have a rapid emergence from inhalation anesthesia.

Mechanical features of the chest wall

Because of its elastic properties, the chest wall always springs out or recoils outward, seeking a larger resting volume. The resting volume of the lungs alone is less than the RV, and the resting volume of the chest wall is approximately 60% of the VC.

The action of the chest wall can be illustrated with the analogy of a wire screen attached around a balloon. The wire screen tends to spring outward so that the screen pulls the balloon open at lower balloon volumes. A measure of the pressure at the mouth of the balloon reflects a negative number. At approximately 60% of the total capacity of the balloon, the screen no longer tends to spring outward. At that point, the addition of air causes the screen to push down on the balloon—a reflection of a positive pressure at the mouth of the balloon. The screen around the balloon can be likened to the chest wall. As shown in Fig. 12-12, at lower lung volumes, the chest wall clearly is inclined to recoil outward, thus creating a negative pressure. At approximately 60% of the VC, the chest wall starts to push down on the lungs, thus creating a positive pressure. The result of the interplay between the chest wall’s strong tendency to spring outward and the lung’s strong tendency to recoil inward is the subatmospheric pleural pressure.⁵

FIG. 12-12 Pressure-volume curve of chest wall during deflation going from TLC to RV. Positive pressures of the chest wall represent pressures that tend to decrease lung size, and negative pressures represent pressures that tend to increase lung volume because of outward recoil tendency of chest wall at approximately 60% of vital capacity or less. TLC, Total lung capacity; RV, residual volume.

(From Drain C: Physiology of the respiratory system related to anesthesia. CRNA 7:163–180, 1996.)

Pleural pressure can become positive during a cough or other forced expiratory maneuvers. Pneumothorax can occur when the chest wall is opened or when air is injected into the pleural cavity. With this occurrence, the lungs collapse because they naturally recoil to a smaller position; the ribs flare outward because of their natural inclination to recoil outward. Clinically, inspection of a patient with a pneumothorax may reveal protruding ribs on the affected side.

The two types of pneumothorax are open (simple) and closed (tension). Simple pneumothorax occurs when air flow into the pleural space results in a positive pleural pressure. The lungs collapse because the recoil pressure is not counterbalanced with the negative pleural pressure. Treatment for a pneumothorax can be conservative or more aggressive, depending on the type and amount of pneumothorax. Aggressive treatment consists of the insertion of chest tubes into the pleural space to recreate the negative pleural pressure. This maneuver reestablishes normal ventilatory excursions. In most instances, the air leak between the lung and the pleural space seals after the chest tubes have been removed. If air continues to flow into the intrapleural space but cannot escape, the intrapleural pressure continually increases with each succeeding inspiration. Like a one-way valve, pressure increases and a tension pneumothorax develops. In a brief period, as the intrapleural pressure increases, the affected lung is compressed and puts a great amount of pressure on the mediastinum. Hypoxemia and reduction in cardiac output result, and if treatment is not instituted immediately, the patient may die. Treatment consists of immediate evacuation of the excess air from the intrapleural space with either chest tubes or a large-bore needle. A tension pneumothorax is truly a medical emergency.²

Combined mechanical properties of the lungs and chest wall

The combined P-V characteristics of the lungs and the chest wall have many implications for the perianesthesia nurse. The combined P-V curve is the algebraic sum of the individual P-V curves of the lungs and chest wall. When no muscle forces are applied to the respiratory system, the FRC is determined by a balance of elastic forces between the lungs and the chest wall (Fig. 12-13). Any pathophysiologic or pharmacologic process that affects the elasticity of either the lungs or the chest wall affects the FRC.

FIG. 12-13 Combined P-V curves of lungs and chest wall. Individual P-V curves of lungs and chest wall are represented with dashed lines. They are transposed from static deflation P-V curves of lungs (see Fig. 12-8) and chest wall (see Fig. 12-12). The combined P-V curve is the algebraic sum of deflation curves of the lungs and chest wall. In a combined P-V curve, FRC can be seen to be determined by balance of elastic forces of the lungs and chest wall when no respiratory muscles are applied. P-V, Pressure-volume; TLC, total lung capacity; RV, residual volume; FRC, functional residual capacity.

(From Koeppen BM, Stanton BA: Berne and Levy’s physiology, ed 6 [updated edition], St. Louis, 2010, Mosby.)

Alterations in the balance of pulmonary forces in the perianesthesia patient

During the induction of anesthesia, the shape of the P-V curve of the chest wall is altered. This agent-independent phenomenon is probably the result of loss of chest wall elasticity. Thus the P-V curve of the chest wall of a patient with normal lung function is shifted to the right, the balance of forces occurs sooner, and the FRC decreases (Fig. 12-14). This shift to the right affects the P-V curve of the lung; it also shifts to the right, and secondary changes occur in the lung. More specifically, the changes consist of an increase in lung recoil (↑Pst_L) and a decrease in C_L (↓C_L). Ultimately, the lung becomes stiffer, and the FRC decreases and may drop into the closing capacity range. Therefore, during tidal ventilation, some airways are closed to ventilation and ventilation-perfusion mismatching occurs (↓ alveolar ventilation/perfusion [↓V_A/Q_C]), which ultimately leads to hypoxemia. Research indicates that this phenomenon, coupled with sighless breathing patterns in the PACU, can cause patients to have hypoxemia in the recovery phase of the anesthetic (see the section on postoperative lung volumes).⁹

FIG. 12-14 P-V curve representing the lung mechanics of a patient in the immediate postoperative period who has undergone upper abdominal or thoracic surgical procedure. This patient has a loss of chest wall elastic recoil that causes lungs to become less compliant. Consequently, the combined P-V curve shifts to the right, leading to a decline in the FRC because balance of forces occurs at lower lung volumes. P-V, Pressure-volume; FRC, functional residual capacity; TLC, total lung capacity; RV, residual volume.

(From Drain C: Pathophysiology of the respiratory system related to anesthesia. CRNA 7:181–192, 1996.)

Gas exchange

The major aspects of gas exchange are discussed in the section on blood gas transport. Because of the implications for perianesthesia nursing care, the concepts of transit time and pulmonary vascular resistance are presented here.

Of the 5 L of blood that flows through the lungs every minute, only 70 to 200 mL are active in gas exchange at any one time. The time a red blood cell (RBC) takes to cross the pulmonary capillary bed is 0.75 seconds, but the RBC takes only 0.25 seconds to become saturated with oxygen—that is, until all the oxygen-bonding sites on the hemoglobin molecule are occupied. Because the transit time is 0.75 seconds and the saturation time is only 0.25 seconds, the body has a tremendous backup of 0.5 seconds for hemoglobin saturation with oxygen.⁵ If the RBCs move across the pulmonary capillary bed at an accelerated pace (decreased transit time), the amount of time available for oxygen to saturate the RBCs is decreased. During stress or exercise, however, the complete saturation of the hemoglobin can still be accomplished because the transit time of a RBC rarely decreases at less than 0.25 seconds.⁵

However, this process is not true for patients with interstitial fibrosis who have a thickened respiratory exchange membrane. These patients may have a normal PaO₂ at rest, but exercise or exertion of surgery increases the cardiac output and decreases the RBC transit time; therefore the hemoglobin does not become completely saturated during its passage through the pulmonary capillary bed. This phenomenon occurs because more time is needed for oxygen to pass through the diseased membrane. For these patients, the lower limit for complete saturation may be 0.5 seconds, not 0.25 seconds. As a result, patients with disorders of the respiratory exchange membrane can have a lower oxygen saturation (SaO₂) on the pulse oximeter with any exertion that could decrease RBC transit time. Clinically, this phenomenon is sometimes called desaturation on exercise. Patients in the PACU who are suspected of having this problem should be given low-flow oxygen and be closely monitored for desaturation via a pulse oximeter. Because of the possibility of desaturation, the low-flow oxygen administration should not be discontinued until the patient’s condition stabilizes, which could indicate continued administration after the patient is discharged from the PACU. Measures should be started to reduce the extrinsic factors, such as stress, elevated body temperature, and anxiety, which increase the cardiac output.

The pulmonary and systemic circulations have the same pump—the heart. The pulmonary system receives the same cardiac output as the systemic circulation, approximately 5 L/min. The pulmonary circulation, in comparison with the systemic circulation, is a low-pressure system with low resistance to flow, distensible vessels with extremely thin walls, and a small amount of smooth muscle. Many stimuli affect pulmonary vascular resistance. Probably the most potent vasoconstrictor of the lung is alveolar hypoxia. Research indicates that neuroendothelial bodies, which respond to a low PaO₂, may exist close to the pulmonary vascular bed. In addition, the neuroendothelial bodies can liberate prostaglandins or histamine, or both, when alveolar hypoxia is present. Pulmonary vascular resistance does not seem to be affected by the volatile anesthetics such as enflurane and isoflurane. However, nitrous oxide can increase pulmonary vascular resistance, especially in patients with preexisting pulmonary hypertension. Neonates who may or may not have preexisting pulmonary hypertension are prone to developing increased pulmonary vascular resistance when nitrous oxide is administered. If a patient in the PACU is prone to developing increased pulmonary vascular resistance, the effect of nitrous oxide on pulmonary vascular resistance is almost dissipated as a result of the rapid excretion from the lungs of nitrous oxide because of its low blood-gas coefficient.⁸

In the postoperative period, if a patient has atelectasis in some portion of the lungs, the PaO₂ in that particular area of the lungs is reduced. As a result, the neuroendothelial bodies are stimulated to produce increased pulmonary vascular resistance in that area of the lungs. Eventually, the blood is redirected or shunted to areas of the lungs that are adequately ventilated. As a result, the SaO₂ in a patient with atelectasis may indicate hypoxemia (<90%). After 5 to 12 minutes, the SaO₂ may be slightly improved because of the increased pulmonary vascular resistance in the area of atelectasis. Therefore the perianesthesia nurse should continue to use an aggressive stir-up regimen on a patient with atelectasis, even though the patient’s SaO₂ values indicate a slight improvement.

Reservoir for the left ventricle

In regard to functioning as a reservoir for the left ventricle, the pulmonary veins are considered extensions of the left ventricle.

Nutrition

The pulmonary circulation can be divided into the bronchial circulation and the actual pulmonary circulation. The bronchial circulation carries nutrients and oxygen down to the respiratory bronchioles in the lungs. The bronchial circulation empties its deoxygenated blood via the pulmonary veins to the left heart. The pulmonary circulation carries nutrients to the respiratory bronchioles and the alveoli.¹

Protection

The role of the lungs in protection is vital for the preservation of the human organism. For example, on the surface of the pulmonary epithelium are invaginations called caveolae. Bradykinin and angiotensin I are enzymatically converted on the surface of the caveoli. Ninety percent of the bradykinin is deactivated in the caveoli during each pass through the lungs, and angiotensin I is converted to angiotensin II with angiotensin-converting enzyme in the lungs. In the presence of hypoxia, the conversion of angiotensin I to angiotensin II is inhibited. Also, in the hypoxemic state, less than 12% of the bradykinin is deactivated by the lungs, and in the hypoxemic state the liberated bradykinin then become prostaglandins. Interestingly, the inappropriate levels of prostaglandins as a result of hypoxemia in the chronic state are thought to produce the clubbing of the fingers in patients with long standing chronic hypoxemia. Finally, the pulmonary epithelium also deactivates norepinephrine and serotonin. Serotonin plays an important part in platelet aggregation. Increased levels of serotonin from decreased lung function caused by hypoxia or lung disease lead to a high risk for venous thrombus. The implications for PACU care are that patients who are immobile and hypoxemic (SaO₂ < 90%) should be monitored for pulmonary and systemic thromboemboli.¹

Factors that affect oxygen transport

The association portion of the oxygen-hemoglobin dissociation curve is not necessarily a fixed line determined solely by the PaO₂. The height and the slope of the curve are dependent on many factors, including pH and temperature. Generally, a decrease in pH (an increase in hydrogen ions) or an increase in body temperature causes a shift of the curve to the right, which leads to a decrease in the height and slope of the curve. Ultimately, less saturation (loading) of the hemoglobin is found for a given PaO₂. As a result, patients who have a low pH or high temperature, or both, probably benefit from a higher fraction of inspired oxygen (FiO₂) than normal for facilitation of an appropriate level of saturation of hemoglobin. However, arterial blood gas determinations should be analyzed before changes in the FiO₂ are made.

At the dissociation portion of the oxygen-hemoglobin dissociation curve, the same is true. This portion is not a fixed line because it also changes position in response to physiologic processes. At the tissue level, metabolically active tissues produce more carbon dioxide and more acid (↓ pH) and have an elevated temperature. These products of metabolism shift the curve to the right. The curve shifts far more in response to physiologic processes in the dissociation portion than in the association part. Metabolically active tissues produce more carbon dioxide and need more oxygen. The effect of carbon dioxide on the curve is closely related to the fact that deoxyhemoglobin binds hydrogen ions more actively than does oxyhemoglobin. As a result, at the tissue level, increased carbon dioxide decreases the affinity of hemoglobin for oxygen. The dissociation portion of the curve is shifted to the right and more oxygen is given to the tissue. This effect of carbon dioxide on oxygen transport is called the Bohr effect.

2,3-Diphosphoglycerate (2,3-DPG) regulates the release of oxygen to the tissue; it is a glycolytic intermediary metabolite that is more concentrated in the RBCs than anywhere else in the body. High concentrations of 2,3-DPG shift the oxyhemoglobin dissociation curve to the right, which makes oxygen more available to the tissues. Lower concentrations of 2,3-DPG cause a shift of the curve to the left, which ultimately leads to the release of less oxygen to the tissues. The clinical implications of these observations involve the administration of outdated whole blood. Whole blood stored longer than 21 days has low levels of 2,3-DPG. As a result, if outdated blood is administered to a patient, the tissues do not receive an appropriate amount of oxygen because of the shift to the left of the oxygen-hemoglobin dissociation curve.³

Pulse oximetry and the oxygen dissociation curve

Oxygen delivered to the tissues is determined by the cardiac output and the CaO₂. Most of the oxygen is bound to the hemoglobin, and the percentage of the oxygen bound to the hemoglobin is expressed as the SaO₂. The amount of oxygen that is dissolved in simple solution in the arterial blood is the PaO₂. A gradient is set from the lung to the tissues in regard to oxygen delivery and is represented by the oxygen dissociation curve. A normal curve, without any shifts left or right, is determined by the PaCO₂, pH, body temperature, and hemoglobin and 2,3-DPG levels. A normal curve is therefore set at values of PaCO₂ of 40 torr, pH of 7.4, temperature of 37° C, and hemoglobin of 15 g/dL. With the oxygen dissociation curve (see Fig. 12-16), the PaO₂ can be determined with the SaO₂ reading on the pulse oximeter. For example, an SaO₂ of 90% corresponds to a PaO₂ of 60 torr. With the curve, at an SaO₂ less than 90%, the PaO₂ drops rapidly (the dissociation portion of the curve). Clinically, an SaO₂ of 90% can be considered hypoxemia, and severe hypoxemia occurs when the PaO₂ is less than 40 torr or the SaO₂ is 75%.¹⁰

Carbon dioxide in simple solution

Approximately 12% of the total amount of carbon dioxide transported in the body is physically dissolved in solution.

Carbaminohemoglobin

Approximately 30% of carbon dioxide is transported as carbaminohemoglobin, a chemical combination of carbon dioxide, and hemoglobin that is reversible because the binding point on the hemoglobin is on the amino groups and is a loose bond. This chemical bonding of carbon dioxide with hemoglobin can be graphically described with the use of the carbon dioxide dissociation curve. Two differences are found between the carbon dioxide dissociation curve (Fig. 12-17) and the oxygen-hemoglobin dissociation curve. First, over the normal operating range of blood the partial pressure of carbon dioxide (PCO₂) from 47 torr (venous or PvCO₂) to 40 torr (arterial or PaCO₂), the slope of the carbon dioxide dissociation curve is nearly linear and not sigmoid like the oxygen-hemoglobin dissociation curve. Second, the total carbon dioxide content is approximately twofold the total oxygen content. Oxygen has a definite effect on carbon dioxide transport. On the upper curve, or venous portion of the carbon dioxide curve, note that the point for the PvCO₂ is 47 and the PvO₂ is 40. On the lower curve, or arterial carbon dioxide curve, observe the points for the PaCO₂ of 40 torr and the PaO₂ of 100 torr. Notice how the venous carbon dioxide curve is shifted to the left and is above the arterial curve. This description is the effect of oxygen on carbon dioxide transport, or the Haldane effect. In terms of physiologic significance, the Haldane effect plays a more important role in gas transport than does the Bohr effect. Specifically in the lungs, the binding of oxygen with hemoglobin tends to displace carbon dioxide from the hemoglobin (oxyhemoglobin is more acidic than deoxyhemoglobin). At the tissue level, oxygen is removed from the hemoglobin (as the result of a pressure gradient), which reduces the acidity of the hemoglobin and enables it to bind more carbon dioxide. In fact, because the hemoglobin is in the reduced state (deoxygenated), the hemoglobin can carry 6 volumes percent more carbon dioxide than the amount of carbon dioxide that could be carried by oxyhemoglobin.⁴

FIG. 12-17 Carbon dioxide dissociation curves for whole blood at 37° C at different oxyhemoglobin saturations. a, Arterial point (code: am); v-, mixed venous point.

(From Levitzky M: Pulmonary physiology, ed 5, New York, 1999, McGraw-Hill.)

Bicarbonate

Sixty-five percent of carbon dioxide is transported as bicarbonate, which is the product of the reaction of carbon dioxide with water. When the carbon dioxide and water join, they form carbonic acid. Almost all the carbonic acid dissociates to bicarbonate and hydrogen ions, as seen in the following equation:

This reaction occurs mostly within the RBCs because carbonic anhydrase accelerates the hydration of carbon dioxide to carbonic acid 220 to 300 times faster than if carbon dioxide and water were joined without this enzymatic catalyst.⁴

When the bicarbonate produced in this reaction in the RBCs exceeds the bicarbonate ion level in the plasma, it diffuses out of the cell. The positively charged hydrogen ion tends to remain within the RBC and is buffered by hemoglobin. Chloride, a negatively charged ion that is abundant in the plasma, diffuses into the RBC to maintain electric balance because of ionic imbalance. This movement is called the chloride shift. Because of the increase in osmotically active particles within the cell, water from the plasma diffuses into the RBCs. This process explains why the RBCs in the venous side of the circulation are slightly larger than the arterial RBCs (Fig. 12-18).

FIG. 12-18 Transport of carbon dioxide in blood.

(From Hall JE: Guyton and Hall Textbook of medical physiology, ed 12, Philadelphia, 2011, Saunders.)

As the venous blood enters the pulmonary capillaries, the carbon dioxide in simple solution freely diffuses to the alveoli. The carbaminohemoglobin reverses to free the carbon dioxide, which diffuses across the alveoli and is then expired. The hydrogen and the bicarbonate combine to form carbonic acid, which is rapidly broken down by carbonic anhydrase to form carbon dioxide and water. The carbon dioxide then diffuses through the alveoli and is expired.

Not all carbon dioxide is eliminated with pulmonary ventilation. Other buffer systems that remove excess carbon dioxide are acid-base buffers and urinary excretion by the kidneys. The respiratory system can adjust to rapid fluctuations in carbon dioxide, whereas the kidneys may need hours for restoration of a normal carbon dioxide tension.

Respiratory acid-base imbalances

Respiratory acidosis is characterized by a PaCO₂ above the normal range of 36 to 44 torr. All other primary processes that tend to cause acidosis are metabolic. Some common causes of carbon dioxide retention and respiratory acidosis are summarized in Box 12-1.

Respiratory alkalosis is characterized by a reduced PaCO₂. Hyperventilation frequently causes this disorder. Common causes of excessive carbon dioxide elimination and respiratory alkalosis are summarized in Box 12-2.

In respiratory alkalosis or acidosis, a linear exchange takes place between the carbon dioxide and bicarbonate concentrations, which is summarized as follows:

Another rule for determining whether the acid-base disorder is entirely respiratory in origin is that an acute increase in PaCO₂ by 12 torr produces a corresponding decrease in pH by 0.07 pH units. In chronic hypercapnia, each increase in PaCO₂ by 12 torr results in a corresponding decrease in pH by 0.03 pH units. PaCO₂ and pH changes that deviate significantly from these standards suggest that the acid-base disorder is not completely respiratory in origin. For example, if a patient who is recovering from a spinal anesthetic in the PACU has blood gases (room air) of PaO₂ of 92 torr, PaCO₂ of 30 torr, and pH of 7.47 compared with preoperative arterial blood gas values (room air) of PaO₂ of 80 torr, PaCO₂ of 40 torr, and pH of 7.40, then the rule can be applied. Because the PaCO₂ decreased by 12 torr and the pH increased by 0.07 pH units, the patient clearly has respiratory alkalosis and not a metabolic disorder. Moreover, by applying the 12-12 concept, it is likely that this patient probably has acute hyperventilation because the PaCO₂ decreased by 12 and thus the PaO₂ should increase by 12, or from 80 to 92 torr.

Metabolic acid–base imbalances

Metabolic acidosis usually results with an increase in nonvolatile acids or a loss of bases from the body. The usual result is a deficit in buffer, base excess, and bicarbonate. Because acidosis stimulates respiration, the PaCO₂ usually decreases. The magnitude of the ventilatory response usually differentiates between acute and chronic metabolic acidosis. Some of the common causes of metabolic acidosis are summarized in Box 12-3.

Metabolic alkalosis is produced by an excessive elimination of nonvolatile acids (such as in vomiting, gastric aspiration, and hypokalemic alkalosis) or by an increase in bases (such as in alkali administration or hypochloremic alkalosis caused by some diuretics). A summary of blood gas discrepancies in each condition is provided in Table 12-3.

Distribution of ventilation

A gravity dependent gradient of pleural pressure in the upright lung exists at resting lung volumes. The weight of the lung tends to pull the lung tissue toward the base of the lung. As a result, the intrapleural pressure is more negative at the apex of the lung in comparison with the intrapleural pressure at the base and over the V_T range (the alveoli at the apex being more fully inflated compared with the alveoli at the base). Consequently, the alveoli at the base have a greater capacity for volume change during inspiration, whereas the alveoli at the apex are already “stretched,” or distended. In a healthy subject who breathes out to RV and then inspires in small steps, the initial inspired air (a small portion) goes to the apex and the base remains completely underventilated. After a certain lung volume is attained, the base of the lung receives almost all the air because of the capacity of the alveoli at the base of the lung for volume change. Therefore, because of the mechanical properties of the lung, the greatest volume change during inspiration from RV to TLC occurs near the base of the lungs.⁵

Distribution of perfusion

A gravity-dependent gradient for perfusion in the lungs exists; approximately 80% to 90% of blood flow occurs from the middle portion to an area near the base of the lungs. Therefore the blood flow per unit of lung volume increases down the lung from the apex to the base.

Matching

Matching of alveolar ventilation (V._A) to perfusion (Q._C) is defined in terms of a certain volume of alveolar gas that is necessary for arterialization of a given volume of mixed venous blood. The normal alveolar ventilation ratio is:

If blood and gas were matched equally throughout the lung, the V. _A/Q. _C would be 1. However, in the healthy lung, the matching of ventilation to perfusion is not proportional, which results in varying V. _A/Q. _C throughout the lung. More specifically, ventilation at the apex is high as opposed to perfusion, and perfusion is higher than ventilation at the base of the lung. Finally, if all the V. _A/Q. _C relationships were added together, the mean ratio would be 0.8.⁵

Hypoventilation

The PaO₂ and PaCO₂ are determined with the balance between the addition of oxygen and the removal of carbon dioxide by the alveolar ventilation and the removal of oxygen and the addition of carbon dioxide by the pulmonary capillary blood flow. If the alveolar ventilation is decreased (with no other lung pathologic changes present), the PaO₂ decreases and the PaCO₂ increases. In fact, the PaO₂ decreases almost proportionally to the increase in the PaCO₂. Recall the calculations made in the 12-12 concept. At any specific inspired oxygen tension, a 12-torr increase in the PaCO₂ causes an approximate 12-torr decrease in the arterial oxygen tension. For example, if the normal PaCO₂ is equal to 40 torr and the PaO₂ is equal to 95 torr and the patient’s alveolar ventilation decreases because of opioids given in the PACU, the PaCO₂ increases to 60 torr. The new PaO₂ should be 71 torr (change of 20 torr in the PaCO₂, so 12 + 12 = 24 – 95 = 71). Therefore, with assessment of blood gas data and with the 12-10 relationship determined to be present, hypoventilation should be suspected. Note that the 12-10 relationship does not have to be exact, but if the numbers are close to the 12-10 relationship, hypoventilation is the probable cause. An increased FiO₂ value affects the 12-10 relationship. However, most patients in the PACU undergo low-flow oxygen therapy; therefore the FiO₂ is usually between 25% and 50%. Consequently, if the values seem to change proportionally, hypoventilation can still be suspected. Hypoventilation is the most common cause of hypoxemia in the PACU. Nursing interventions should include administration of a higher FiO₂ via low-flow oxygen therapy, stimulation of the patient, use of an aggressive stir-up regimen, and possible pharmacologic reversal of opioids or muscle relaxants.⁹

Ventilation or perfusion mismatching

If the 12-10 relationship is not present during the analysis of the arterial blood gases, V. _A/Q. _C mismatching is probably the cause. However, it is difficult to determine whether the mismatching problem is the result of increased or decreased V. _A/Q. _C. As seen in Fig. 12-19 normal V. _A/Q. _C exists when appropriate matching of ventilation to perfusion occurs. Decreased V. _A/Q. _C occurs when the matching ventilation is reduced in comparison with perfusion of the alveoli, and increased V. _A/Q. _C is caused by increased ventilation as compared with perfusion.

FIG. 12-19 Graphic representation of normal and abnormal matching of ventilation (V˙_A) to perfusion (Q˙_C).

(From Heuther SE, McCance KL: Understanding pathophysiology, ed 3, St. Louis, 2004, Mosby.)

Decreased ventilation to perfusion

Reduced ventilation, in comparison with perfusion, ((V. _A/Q. _C) can be caused by excessive secretions or partial bronchospasm. Intrapulmonary shunting results when atelectasis or airway closure occurs. In these situations, oxygen cannot diffuse properly across to the pulmonary capillary blood. In decreased V. _A/Q. _C, some oxygen diffuses across from the alveoli to the pulmonary capillary blood. Thus, the alveolar-arterial oxygen difference (PAO₂ – PaO₂) is slightly reduced. If a large gradient exists in the PAO₂ – PaO₂ value, intrapulmonary shunting is probably present. For a patient who is breathing room air, the normal PAO₂ – PaO₂ value is between 5 and 15 torr. When a patient is breathing oxygen at a FiO₂ of 0.5 (50%), the PAO₂ – PaO₂ value should be approximately 50 torr. A gradient greatly in excess of 50 torr suggests V. _A/Q. _C mismatching. The focus of the nursing interventions for improvement of decreased V. _A/Q. _C is on airway clearance, reinflation of alveoli, and enhanced patency of the airways. The newly advocated stir-up regimen of turn, cascade cough, and SMI should improve the decreased V. _A/Q. _C. Percussion or vibration, or both, may also need to be instituted to facilitate secretion clearance. In addition, if partial bronchospasm (expiratory wheeze) is suspected, the attending physician should be consulted about instituting appropriate bronchodilator therapy.

At this point, a clarification of terms used to describe decreased V. _A/Q. _C and shunt is in order. Basically, intrapulmonary shunts result in the mixing of venous blood that has not been properly oxygenated into the arterial blood (pulmonary vein). Anatomic shunts, which occur normally, are attributed to the 2% or 3% of the cardiac output that bypasses the lungs. The shunted unoxygenated venous blood comes mainly from the bronchial circulation, which empties into the pulmonary veins, and from the thebesian vessels that drain the myocardium into the left heart. Intrapulmonary shunts occur when mixed venous blood does not become oxygenated when it passes by underventilated, unventilated, or collapsed alveoli. Absolute intrapulmonary shunts, sometimes called true shunts, are associated with totally unventilated or collapsed alveoli. Shuntlike intrapulmonary shunts are the areas of low V. _A/Q. _C in which blood draining the partially obstructed alveoli has a lower arterial oxygen content than the alveolar capillary units that are well matched. As a result, the presence of anatomic shunts is normal. Abnormal shunts can be classified as physiologic shunts. Physiologic shunts are composed of the anatomic shunts plus intrapulmonary shunts (absolute and shuntlike intrapulmonary shunts).

Increased ventilation to perfusion

According to Fig. 12-20, compromise of the circulation to the individual alveolocapillary unit creates an excess of ventilation in comparison with perfusion. If the flow of blood in the pulmonary capillary is partially obstructed, increased V. _A/Q. _C results. If the flow of blood is completely obstructed, such as with a pulmonary embolus, only ventilation continues and produces wasted or dead space. Wasted ventilation is the total amount of inspired gas that does not contribute to carbon dioxide removal; it is also known as physiologic dead space (V_Dphysio). V_Dphysio is that volume of each breath that is inhaled but does not reach functioning terminal respiratory units. V_Dphysio has two components: alveolar and anatomic dead space. Alveolar dead space (V_Dalv), as depicted in Fig. 12-20, is that volume of air contributed by all those terminal respiratory units that are overventilated relative to their perfusion. Anatomic dead space (V_Danat) consists of the volume of air in the conducting airways that does not participate in gas exchange. This category includes all air down to the respiratory bronchioles. The following formula depicts V_Dphysio:

FIG. 12-20 The shunt-dead-space continuum.

(From Beachey W: Respiratory care anatomy and physiology, ed 2, St. Louis, 2007, Mosby.)

Normally, V_Dphysio consists mainly of V_Danat, with the V_Dalv component being minute, which explains why the normal V_Dphysio volume in milliliters is approximately equal to the weight of a person in pounds. For example, a person who weighs 150 lb has a V_Dphysio of 150 mL. When alveoli become overventilated in comparison with perfused, the V_Dalv increases, which in turn increases the V_Dphysio.

The amount of V_Dphysio can be determined with the Bohr equation. Clinically, the Bohr equation is commonly referred to as the V_D/V_T. The ratio of dead space (V_D) to V_T can be used to determine whether the obstruction to pulmonary capillary blood flow is partial (V. _A/Q. _C) or complete (wasted ventilation). The V_D/V_T can be derived from the following equation:

in which the PaCO₂ is the arterial carbon dioxide partial pressure and the PECO₂ is the partial pressure of the expired carbon dioxide.

The V_D/V_T ratio is normally 0.3. If the V_D/V_T increases to 0.6, more than half of the V_T is dead space. The minute ventilation (V_E) can double in most patients, but beyond that amount, the effort is too exhausting and a V_D/V_T ratio of more than 0.6 usually mandates that the patient’s ventilation be assisted mechanically.

Peripheral chemoreceptors

The carotid and aortic bodies are the peripheral chemoreceptors and are located at the bifurcation of the common carotid arteries and at the arch of the aorta, respectively. The carotid and aortic bodies are responsible for the immediate increase in ventilation as a result of lack of oxygen. These peripheral chemoreceptors are composed of highly vascular tissue and glomus cells. The carotid and aortic bodies monitor only the PaO₂, not the CaO₂ of the hemoglobin; therefore the receptors are not stimulated in conditions such as anemia and carbon monoxide and cyanide poisoning.

The carotid bodies are much more important physiologically than are the aortic bodies. The carotid bodies respond, in order of degree of response, to low PaO₂, high PaCO₂, and low pH. The carotid bodies respond to a low PaO₂, and the response is augmented by a high PaCO₂, a low pH, or both. The physiologic responses to the stimulation of the carotid sinus are hyperpnea, bradycardia, and hypotension. The aortic bodies, however, respond to a low PaO₂ and to a high PaCO₂, but not to pH. The results of stimulation of the aortic bodies are hyperpnea, tachycardia, and hypertension.

The carotid and aortic bodies mainly respond to a low PaO₂. This response is commonly called the hypoxic or secondary drive. The impulse activity in these chemoreceptors begins at a PaO₂ of approximately 500 torr. A rapid increase in impulses occurs at a PaO₂ lower than 100 torr. The impulses are greatly increased as the PaO₂ falls to a value less than 60 torr. At less than 30 torr, the impulse activity from the chemoreceptors decreases because of the direct oxygen deficit in the glomus cells. In addition, these peripheral arterial chemoreceptors are stimulated by low arterial blood pressure and increased sympathetic activity.⁵

Central chemoreceptors

The central chemoreceptors lie near the ventral surface of the medulla. Specifically, these chemosensitive areas are near the choroid plexus (venous blood) and next to the cerebrospinal fluid (CSF). The central chemoreceptors respond indirectly to carbon dioxide because the blood-brain barrier allows lipid-soluble substances (e.g., carbon dioxide, oxygen, water) to cross the barrier, whereas water-soluble substances (e.g., sodium, potassium, hydrogen ion, bicarbonate) pass through the membrane at extremely slow rates. Bicarbonate requires active transport to cross the barrier; therefore carbon dioxide enters the CSF and is hydrated to form carbonic acid. The carbonic acid rapidly dissociates to form hydrogen ion and bicarbonate. The hydrogen ion concentration in the CSF parallels the arterial PCO₂. Actually, the hydrogen ion concentration stimulates ventilation via hydrogen receptors located in the central chemoreceptor area. In summary, carbon dioxide has little direct effect on the stimulation of the receptors in the central chemoreceptor area, but does have a potent indirect effect. This indirect effect is the result of the inability of hydrogen ions to easily cross the blood-brain barrier. For this reason, changes in hydrogen ion concentration in the blood have considerably less effect in stimulating the chemoreceptor area than do changes in carbon dioxide. Consequently, the central chemoreceptor area precisely controls ventilation and therefore the PaCO₂. For that reason, the index to the adequacy of ventilation is the PaCO₂.

Bicarbonate is the only major buffer in the CSF. The pH of the CSF is a result of the ratio between bicarbonate and carbon dioxide in the CSF. Carbon dioxide is freely diffusible in and out of the CSF via the blood-brain barrier. However, bicarbonate is not freely diffusible and requires active or passive transport to enter or leave the CSF. When an acute increase in the PaCO₂ occurs, carbon dioxide enters the CSF and is hydrated, and hydrogen ions and bicarbonate are formed. The hydrogen ion stimulates the chemoreceptors, and the bicarbonate decreases the pH of the CSF. The resultant hyperpnea lowers the blood PaCO₂ and thus creates a gradient that favors the diffusion of carbon dioxide out of the CSF. The blood PaCO₂ and pH are corrected immediately, but the pH in the CSF requires some time to reestablish a normal carbon dioxide–bicarbonate level because bicarbonate is poorly diffusible. This process is usually not a problem with normal respiratory function. However, for the patient with chronic carbon dioxide retention (chronic hypercapnia) who has hyperventilation to a normal PaCO₂ of 40 torr, serious deleterious effects can occur. Patients with a chronically elevated PaCO₂ have a higher amount of carbon dioxide and bicarbonate in the CSF, but the ratio is maintained in a chronic situation. In this instance, the patient is breathing at a higher set point. That is, instead of maintenance at 40 torr, the normal PaCO₂ for this patient might be maintained at 46 torr and near-normal sensitivity to changes in the PaCO₂ may be present. If this patient underwent aggressive ventilation in the PACU with the goal of lowering the PaCO₂ to 40 torr, significant negative repercussions could occur. With a lower PaCO₂, the carbon dioxide in the CSF diffuses out and the bicarbonate remains because of its inability to diffuse out of the CSF. Thus, an excess of bicarbonate compared with carbon dioxide (↑ bicarbonate pool) exists in the CSF and causes the primary stimulus to ventilation to cease. Because the patient’s condition is hyperventilation, the PaCO₂ decreases and the PAO₂ increases (because of the 12-10 concept). Therefore the secondary (hypoxic) drive may also become extinguished, and this patient may have no effective drive for ventilation. If patients with chronic hypercapnia are acutely hyperventilated, they must be monitored for apnea once the accelerated ventilation is discontinued. A more appropriate technique is the maintenance of the PaCO₂ at the level that is normal for that patient to avoid an apneic situation.⁴ Thus, for the patient with chronic carbon dioxide retention who is emerging from anesthesia, an overaggressive stir-up regimen (hyperventilation) should be avoided. The patient should perform the SMI at normal intervals, and the arterial blood gas values should be closely monitored.

In some patients with chronic carbon dioxide retention (chronic hypercapnia), the sensitivity to hydrogen ions via the carbon dioxide may be effectively decreased to the point at which the primary stimulus to ventilation becomes the low PaO₂ at the carotid and aortic bodies. The low PaO₂ becomes an effective stimulus to ventilation, especially when the PaCO₂ is elevated. The high PaCO₂ augments the response to the low PaO₂ with the peripheral chemoreceptors. For this reason, the patient breathes via the hypoxic drive. Because the carotid bodies are the major peripheral chemoreceptors, patients who use the hypoxic drive may also have bradycardia and hypotension. For that reason, patients with abnormally high preoperative PaCO₂ values who have bradycardia and hypotension should be suspected of using the hypoxic drive as the primary drive to ventilation. In the PACU, patients suspected of primary use of this drive should be monitored closely and given oxygen to attain adequate oxygen content (a hemoglobin saturation of between 80% and 90%). The primary goal is to keep the patient oxygenated without extinguishing the main control of ventilation. High-flow techniques that use a Venturi mask that works on the Venturi principle to ensure precise FiO₂ values (i.e., 24% to 50%) can be used with these patients.

Response to carbon dioxide

Carbon dioxide is the primary stimulus to ventilation. The carbon dioxide response test is used for assessment of the ventilatory response to carbon dioxide. In this test, the subject inhales carbon dioxide mixtures (with the PaO₂ held constant) so that the inspired PaCO₂ gradually increases. Normally the V_E increases linearly as the PaCO₂ increases (Fig. 12-21). Some disease states and drugs cause the carbon dioxide response curve to shift to the left or the right. If the curve shifts to the left, the subject is more responsive to carbon dioxide. Factors such as thyroid toxicosis, aggressive personality, salicylates, and ketosis shift the curve to the left. A decreased ventilatory response to carbon dioxide occurs when the curve is shifted to the right and is called a blunted response. Patients who have a blunted response to carbon dioxide need intensive perianesthesia nursing care. The ventilatory response to an increased concentration of inspired carbon dioxide is blunted by hypothyroidism, mental depression, aging, general anesthetics, barbiturates, and narcotics. Many patients in the PACU either have these conditions or have received these drugs during surgery. This blunted response to carbon dioxide is one of the main justifications for supplemental oxygen administration to all patients who are emerging from anesthesia in the PACU. This response is also the rationale behind the need for critical perianesthesia nursing care that includes frequent assessment and interventions such as the stir-up regimen for prevention of respiratory depression.¹

FIG. 12-21 Carbon dioxide response curve.

(From Traver G: Respiratory nursing: the science and the art, New York, 1982, John Wiley and Sons.)

Upper airways receptors

Receptors that are sensitive to mechanical stimulation and chemical agents and have afferent pathways via the trigeminal and olfactory nerves are located in the nose. Activation of these receptors can cause apnea, bradycardia, and sneezing. When a patient is to undergo nasal intubation, the perianesthesia nurse should monitor for bradycardia and apnea and be prepared for necessary interventions. Atropine or glycopyrrolate (Robinul) may be necessary for the vagolytic effect; succinylcholine may facilitate the intubation. Finally, to provide positive-pressure ventilation, a bag-valve-mask system should be immediately available in case apnea occurs.

Receptors located in the epipharynx are sensitive to mechanical stimulation. Their activation is associated with the sniff or aspiration reflex. Mechanical stimulation of these receptors causes deep inspiration, bronchodilatation, and hypertension. This reflex is a protective reflex that allows material in the epipharynx to be brought down to the pharynx, clearing the nasal airways. In the larynx are irritant receptors that respond to both mechanical and chemical stimulation. Afferent pathways from these receptors travel along the internal branch of the superior laryngeal nerve. Stimulation invokes many responses, including coughing, slow deep breathing, apnea, bronchoconstriction, and hypertension. In addition, the trachea possesses irritant receptors. Stimulation of these receptors can cause responses such as coughing, bronchoconstriction, and hypertension.

During any procedure that involves the intubation of the trachea, the perianesthesia nurse should be prepared to assess the appropriate cardiorespiratory parameters and implement nursing care as necessary.

Lung receptors

Pulmonary stretch receptors (PSRs) lie within the smooth muscle of the small airways. These receptors are activated by marked distention or deflation (atelectasis) of the lungs. On marked inflation of the lungs, the activation of the PSR leads to a slowing of inspiratory frequency because of an increase in expiratory time. Bronchodilatation and tachycardia also can result from activation of these receptors. The PSRs are thought to be part of the Hering-Breuer reflex. The low threshold for the PSR is present for approximately the first 3 months of life; afterward, the threshold is high throughout adulthood. For the adult, the Hering-Breuer reflex is not important in the control of ventilation except in the anesthetized state. When an adult is administered general anesthesia and ventilation with prolonged maximal lung inflations, a prolonged expiratory time can result because of activation of the PSR.³

Of great interest in regard to the pathogenesis of asthma are the irritant receptors that lie between the airway epithelial cells. These receptors respond to chemical irritants (e.g., histamine) and mechanical irritants (e.g., small particles and aerosols) that irritate the pulmonary epithelium. The irritant receptors are mediated by vagal afferent fibers, and on receptor stimulation, bronchoconstriction and hyperpnea occur. The pathogenesis of asthma is suggested to revolve around the sequence of histamine release, which stimulates the irritant receptors and ultimately leads to bronchoconstriction mediated via the vagus nerve.

The J-receptors, or juxtapulmonary capillary–receptors, are located in the wall of the pulmonary capillaries. Like the irritant receptors, the afferent impulses of J-receptors are transmitted to the central nervous system by the vagus nerve. Normal stimuli of the J-receptors include pneumonia, pulmonary congestion, and increased interstitial fluid pressure. Stimulation of these receptors by interstitial or pulmonary edema results in tachypnea, bradycardia, and hypotension.⁹ Therefore the nurse should always evaluate the rate of ventilation in the assessment of patients who are at risk for development of pulmonary edema. With the knowledge that interstitial edema usually precedes pulmonary edema and that increased interstitial congestion stimulates the J-receptors, the nurse should consider a rapid shallow breathing pattern to be a danger signal and report it to the attending physician.

Located in the walls of the large systemic arteries, especially in the aortic and carotid sinuses, are stretch receptors called baroreceptors. These receptors help to control the systemic blood pressure; they also affect ventilation. When the systemic blood pressure increases, a reflex hypoventilation occurs because of stimulation of the baroreceptors; however, a low systemic blood pressure causes the baroreceptors to produce a reflex hyperventilation. As a result, if a patient in the PACU has a significant amount of hypertension or hypotension, a reflex ventilatory response usually occurs because of the stimulation of the baroreceptors in the large systemic arteries.

The brainstem

Located bilaterally in the upper pons is the pneumotaxic center. This center functions to fine-tune the respiratory pattern with modulating the activity of the apneustic center and regulating the respiratory system’s response to stimuli such as hypercarbia, hypoxia, and lung inflation. Near the pontomedullary border is the apneustic center. This center is probably the site of the inspiratory cutoff switch that terminates inspiration. In fact, apneusis, which consists of prolonged inspirations with occasional expirations, results when the apneustic center has been deactivated. Consequently, the apneustic center is also a fine-tuner of the rhythm of breathing.

Two groups of neurons are located in the medullary center, above the spinal cord: the dorsal respiratory group (DRG) and the ventral respiratory group (VRG). The DRG is composed of inspiratory neurons and is the initial intracranial processing site for many reflexes that affect breathing. It is probably the site of origin of the rhythmic respiratory drive. The DRG sends motor fibers via the phrenic nerve to the diaphragm; it sends inspiratory fibers to the VRG, which is also part of the medullary center. However, the VRG does not send fibers to the DRG; therefore the reciprocal inhibition theory of the regulation of breathing seems unlikely. The VRG is composed of both inspiratory and expiratory cells. The VRG neurons are driven by the cells of the DRG; therefore respiratory rhythmicity and the processing of sensory inputs do not occur initially within the VRG. The major function of the VRG is to project impulses to distant sites and to drive either the spinal respiratory motor neurons (primary intercostal and abdominal) or the auxiliary muscles of breathing innervated by the vagus nerve.

The DRG receives information from almost all the chemoreceptors, the baroreceptors, and the other sensors in the lung. In turn, the DRG generates a breathing rhythm that is fine-tuned by the apneustic center (inspiratory cutoff switch) and the pneumotaxic center. The inspiratory motor impulses are sent to the diaphragm and to the VRG. The VRG then drives spinal respiratory neurons (innervating the intercostal and abdominal muscles) or the auxiliary muscles of respiration innervated by the vagus nerve. Again, the cerebral cortex can override these centers if voluntary control of breathing is desired. In addition, the vagus nerve has a profound effect on many aspects of the control of breathing because the afferent pathways of the vagus nerve from the stretch receptors, J-receptors, and irritant receptors serve to modulate the rhythm of breathing. Therefore any dysfunction that includes transection of the vagi results in irregular breathing patterns, depending on the level of dysfunction (pons or medulla).

Preexisting pulmonary disease

Patients with preexisting pulmonary disease can have clinical or subclinical manifestations of the disease state. Consequently, preoperative pulmonary function tests are valuable when assessing the presence or absence of pulmonary pathophysiology and determining operative risk. Obstructive lung disease (i.e., asthma, emphysema, and chronic bronchitis), the most common category of lung disease, can be assessed with flow-volume measurements. Most pulmonary researchers suggest that a maximal voluntary ventilation that is less than 50% of what is predicted, a maximal expiratory flow rate less than 220 L/min, or a forced expiratory volume in 1 second less than 1.5 L indicates an increased operative risk for pulmonary complications. These flow-volume measurements are valuable predictors of the patient’s ability to generate an adequate cough, which is a pulmonary defense mechanism rendered ineffective in the immediate postoperative period by anesthesia and surgery.⁹ Consequently, these patients need vigorous informed nursing care in the immediate postoperative period. Priorities of nursing care should include frequent use of the stir-up regimen of turn, cascade cough, and SMI, along with the use of appropriate nursing interventions designed to enhance secretion clearance, which ensures airway patency.

Patients with restrictive lung disease (i.e., pulmonary fibrosis and morbid obesity) represent a significant risk for postoperative pulmonary complications when pulmonary function test results reveal a VC or a diffusion capacity of less than 50% of predicted values or exercise arterial blood gas values that show slight hypoxemia on exertion. In the PACU, these patients need a vigorous stir-up regimen with attention to tissue oxygenation via monitoring for hypoxemia. This regimen is needed because, during the surgical experience and in the PACU, physiologic stress can occur. One of the major products of physiologic stress is an increase in cardiovascular parameters, which reduces the transit time of the RBCs across the respiratory gas exchange membrane. Because of the pathologic changes in the respiratory membrane, patients with restrictive lung disease can have desaturation on exertion, such as in the stress reaction.¹¹

Cigarette smoking

Chronic cigarette smoking has been shown to increase the incidence rate of postoperative pulmonary complications. Patients who smoke only 12 cigarettes per day have a sixfold increase in pulmonary morbidity rates in the postoperative period. The incidence rate of pulmonary embolism is higher in the smoker because of increased coagulability produced by chronic cigarette smoking. The ciliated epithelium of the lungs is damaged by chronic cigarette smoking. This damage can cause some blockage of the mucociliary transport system, which finally results in bronchiolar obstruction, infection, and atelectasis. Patients who smoke should be encouraged to stop smoking for at least 2 weeks before surgery to allow the mucociliary transport system to return to a nearly normal level of function. The focus of nursing care for the active chronic cigarette smoker should be similar to the interventions discussed for the patient with obstructive lung disease as the major clinical issue is a thickened pulmonary membrane that inhibits the transport of oxygen to the blood and carbon dioxide crossing over from the blood to the air. This also plays a part in the emergence from anesthesia because patients who are chronic cigarette smokers will have a slow emergence, especially when the anesthesia time exceeds 2 hours.⁴

Obesity

The patient who is markedly overweight has a significant chance of developing postoperative pulmonary complications caused by the altered lung volumes and capacities from the excess adipose tissue. Expansion of the lungs is hindered by an enlarged abdomen, which elevates the diaphragm and adds weight on the chest wall, thereby hindering the outward recoil of the chest wall. This hindrance leads to decreased thoracic wall compliance and ultimately to a reduced FRC. Finally, these complications result in hypoxemia from increased airway closure and V. _A/Q. _C abnormalities (see Chapter 45). The goal of nursing interventions in the PACU is the prevention of further airway closure; therefore a vigorous stir-up regimen, including early ambulation, should help prevention of further reduction in the FRC. That measure reduces the amount of airway closure, alleviates the hypoxemia, and ultimately improves the outcome of the patient.^3,15

Advanced age

Patients of advanced age (older than 70 years) have a slightly higher risk of developing postoperative pulmonary complications. A greater decrease in the FRC after surgery in patients of advanced age has been shown. Because the closing volume increases with age, significant airway closure can occur after surgery during tidal ventilation. Although advanced age is not associated with the same degree of risk as the factors previously discussed, it can increase the danger of the other risk factors. However, patients of advanced age should receive a vigorous stir-up regimen in the PACU, if only because of the alterations in lung mechanics.⁹

Eyes

Premature infants who have a high PaO₂ for longer than 24 hours are at risk for development of retrolental fibroplasia, which is caused by vasoconstriction of the blood vessels of the retina as a result of high oxygen concentrations in the blood. Retrolental fibroplasia presents in an acute form as vascular retinopathy at the developing edge of blood vessels in the premature infant’s eye. This presentation is followed by perivascular exudation, tissue hyperplasia, and scar tissue that exerts traction on the retina and leads to retinal detachment and destruction of the infant’s vision. Research indicates that the incidence rate of acute retrolental fibroplasia is inversely proportional to birth weight. Most of the clinical research indicates that, to minimize the risk of development of retrolental fibroplasia, the infant’s PaO₂ should be maintained between 60 and 90 torr. Perianesthesia nurses should use their best-informed judgment when caring for these infants. As with the adult, the infant who needs a high-inspired oxygen concentration to provide adequate oxygenation should not be denied oxygen because of fear of complications.⁶

Lungs

Concentrations of oxygen greater than 60% damage the lungs within 3 or 4 days. A 120% oxygen concentration administered for 24 to 48 hours also causes pulmonary damage, the signs of which are manifested by type II cell dysfunction in the lung. The type II cells secrete surfactant, and the lack of surfactant in the alveoli leads to alveolar collapse. The hyperoxic environment also stops the ciliary action in the lungs. The early symptoms of this disorder include cough, nasal congestion, sore throat, reduced VC, tracheobronchitis, and substernal discomfort. The early signs of airway irritation may appear when a patient has received 80% to 120% oxygen continuously for 8 hours or longer. The lung appears to indefinitely tolerate oxygen concentrations lower than 40%.¹

Central nervous system

Headache is an early indicator of oxygen toxicity. As oxygen toxicity continues to develop, the patient exhibits some confusion. When a patient is receiving a high concentration of oxygen and has these signs and symptoms, the attending physician should be notified. Convulsions usually are not seen in the PACU but can occur when oxygen is delivered in above-normal atmospheric pressure, such as in hyperbaric oxygen chambers.