High-Acuity Nursing, 6th Edition

Determinants and Assessment of Pulmonary Function Objectives 1. Explain the conducting airways and the concept of ventilation. 2. Discuss external respiration and pulmonary gas diffusion. 3. Describe pulmonary perfusion and its components. 4. Differentiate between respiratory and metabolic acid-base imbalances and levels of compensation. 5. Interpret arterial blood gases, including compensatory status. 6. Conduct a focused respiratory nursing history and assessment. 7. Describe tests used to evaluate pulmonary function. 8. Discuss noninvasive and invasive methods of monitoring gas exchange and applications. I. Mechanics of Breathing—Ventilation 1. Ventilation: respiratory process has three vital components: ventilation, diffusion, and perfusion. A. The conducting airways 1. Respiratory tract can be divided into conducting and respiratory airways. 2. Conducting airways include: a) Nasal passages b) Mouth c) Pharynx d) Larynx e) Trachea f) Bronchi g) Bronchioles 3. These airways serve as an air conduit to move air to and from the atmosphere and alveoli. a) Protective functions: (1) Humidifying (2) Filtering (3) Warming air 4. Conducting airway contains a mucociliary system that removes pathogens and foreign materials. a) It captures them on the mucus layer and removes them through ciliary movement, transporting foreign particles toward the pharynx, where they can be swallowed and destroyed in the stomach. b) In high-acuity patients who require an artificial airway, the initial conducting airway is bypassed, reducing the protective functions and placing patients at increased risk of aspiration and ventilator associated pneumonia (VAP). 5. The tracheobronchial tree consists of the trachea, with right and left bronchi. a) The junction of the “Y” formed by the two primary bronchial branches is the carina, which is heavily enervated and very sensitive to stimulation. (1) When the carina is touched by a suction catheter, it can trigger bronchospasm or severe coughing. b) The right bronchus is shorter and larger in diameter and at almost a straight angle with the trachea. c) The left bronchus is longer and smaller in diameter and at a more acute angle. d) Size and positioning of the right bronchus makes it more vulnerable to pathogens and foreign particles and misplacement of endotracheal tube. 6. The trachea and bronchial walls contain a C-shaped cartilage structure present down to the bronchiole level that gives structure and protection to larger airways. 7. Toward the terminal end of the bronchial tree are the bronchioles, surrounded by smooth muscle but lacking cartilage. a) Bronchioles have the ability to regulate resistance to flow by causing constriction or dilation, controlling airflow distribution. b) Bronchioles control airflow through bronchoconstriction and bronchodilation. B. Ventilation 1. Ventilation is the first of the three components of the respiratory process. a) It is defined as the mechanical movement of airflow to and from the atmosphere and the alveoli. b) Ventilation involves the actual work of breathing, requiring nervous system control and adequate functioning of the lungs and conducting airways, thorax, and ventilatory muscles. 2. Air is able to move in and out of the lungs as a result of the changing size of the thorax caused by ventilatory muscle activity. a) When the thorax enlarges, the intrapulmonary pressure drops to below atmospheric pressure. b) Air then moves from the area of higher pressure to the area of lower pressure. c) The result is air flowing into the lungs (inspiration) until the pressure in the lungs becomes slightly higher than atmospheric pressure. d) Air then flows back out of the lungs (expiration) until pressures are again equalized. 3. Lung tissue has a constant tendency to collapse. a) The fluid lining of the alveoli has a naturally high surface tension, causing them to tend to collapse. (1) Type II cells in the alveoli secrete a lipoprotein called surfactant. (a) Surfactant has a detergent-like action that reduces the surface tension of the fluid lining the alveolar sacs, decreasing the tendency to collapse. b) Lungs are composed of elastic fibers. (1) The elastic force of these fibers seeks to return to a resting state. To maintain the lungs in an inflated state, the elastic forces must constantly be overcome by opposing forces. 4. The thorax is the primary opposing force that keeps the lungs expanded. 5. The thoracic bony structure provides a framework that maintains the lungs in a baseline inflated state, even at rest, because of the attraction between the visceral and parietal pleurae. 6. The pleura is a slick-surfaced, moist membrane. 7. The parietal pleura adheres to the thoracic walls, diaphragm, and mediastinum. 8. The visceral pleura adheres to the lung parenchyma. a) Normally, the parietal and visceral pleurae act as one membrane. 9. As the thorax increases and decreases in size, so will the lungs increase and decrease in volume. Lung Compliance 1. The ease with which the lungs can be expanded is measured in terms of lung compliance. 2. Compliance (CL) is defined in terms of lung volume (mL) and pressure (cm H2O) as CL = deltaV/deltaP, where CL is lung compliance, deltaV is change in volume (mL), and deltaP is change in pressure (cm H20). 3. Each size of alveolus has a filling capacity beyond which it becomes overexpanded and can burst. a) As the alveoli approach their filling capacity, they become less compliant. 4. Many pulmonary and extrapulmonary problems influence compliance. 5. Compliance is very sensitive to conditions that affect the lung’s tissues, particularly if the disorder causes a reduction in pulmonary surfactant, critical for maintenance of functional alveoli. a) When there is a deficiency of surfactant, compliance is decreased. b) Decreased compliance is sometimes called “stiff lungs”; it takes more force (pressure) to increase lung volume. c) Decreased compliance increases the work of breathing and causes a decreased tidal volume. d) The breathing rate increases to compensate for the decreased tidal volume. e) Pulmonary problems causing decreased compliance are called restrictive pulmonary disorders. Examples: (1) Pneumonia (2) Pulmonary edema (3) Pulmonary fibrosis (4) Pneumothorax Effects of Aging on Ventilation 1. Aging has certain effects on ventilation. 2. As a person ages, the diaphragm flattens, the chest wall becomes more rigid, the respiratory muscles weaken, and the anterior–posterior diameter of the chest increases. a) These factors contribute to decreased lung compliance, altered pulmonary mechanics, and air trapping. 3. The lung’s functional ability reduces roughly 5–20% per decade of life. 4. A person who has never smoked and has maintained normal lungs might show little, if any, clinically significant changes in ventilation through aging. 5. The aging person with a history of smoking and some degree of lung damage tends to become increasingly symptomatic with aging and is at increased risk for developing respiratory complications. PowerPoint Slides Slide 1 Mechanics of Breathing—Ventilation Slide 2 The Conducting Airways Slide 3 Ventilation Lung Compliance Effects of Aging on Ventilation II. Pulmonary Gas Exchange—Respiration and Diffusion A. Respiration is the process by which the body’s cells are supplied with oxygen and carbon dioxide is eliminated. 1. Internal and external respiration a) Internal respiration refers to movement of gases across systemic capillary-cell membrane in tissues. b) External respiration refers to movement of gases across alveolar-capillary membrane. c) Both use diffusion to exchange gases. Diffusion 1. Diffusion is the second of the three components of the respiratory process. 2. Oxygenation of tissues depends on diffusion for both external and internal respiration. 3. Diffusion: the movement of gases down a pressure gradient from an area of high pressure to an area of low pressure. 4. Alveolar-capillary membrane is very thin and offers little resistance to diffusion. a) The membrane can thicken with pulmonary disease, reducing diffusion. (1) When diffusion is reduced, the carbon dioxide tension can remain normal initially because carbon dioxide diffuses 20 times faster than oxygen, but the oxygen tension decreases rapidly. 5. Factors that affect diffusion: a) Partial pressures and gradient b) Surface area c) Thickness d) Length of exposure 6. Oxyhemoglobin dissociation curve important in determining affinity of oxygen to hemoglobin, affecting diffusion. Partial Pressures of Gases 1. Atmospheric air is composed of molecules of nitrogen, oxygen, carbon dioxide, and water vapor. a) These gases combined exert about 760 mmHg of pressure at sea level. 2. The respiratory process only involves exchange of oxygen and carbon dioxide, which both exert a certain percentage of the total air pressure. a) Oxygen in alveoli exerts an average of 100 mmHg pressure; this partial pressure is called PO2 or oxygen tension. (1) When the PO2 refers to oxygen in alveoli, it is called PAO2. (2) When it refers to arterial blood, it is called PaO2. (3) When it refers to venous blood, it is called PVO2. b) Carbon dioxide in alveoli exerts an average of 40 mmHg of pressure; this partial pressure is called PCO2. c) The other abbreviations used for oxygen are also used for carbon dioxide. 3. Venous blood returning to the lungs from the tissues is oxygen-poor because the blood has dropped off its load of oxygen for the tissues’ use. 4. Venous blood is rich in carbon dioxide because of transport of carbon dioxide for removal from the lungs. 5. The differences in gas partial pressures between the alveoli and pulmonary capillary blood and the systemic capillary blood and tissues dictate which direction each gas will flow based on the law of diffusion. 6. Henry’s law: When a gas is exposed to liquid, some of it will dissolve in the liquid. The partial pressure of the gas and its solubility determine the amount that dissolves. a) Oxygen is not very soluble in plasma, and only 3% of total oxygen content dissolves in blood. 7. Difference between partial pressures is called the pressure gradient. a) In external respiration, a pressure gradient exists between the atmosphere and the alveoli and between the alveoli and the pulmonary capillaries. b) The greater the pressure difference, the more rapid the flow of gases. c) Multiple factors can increase the gradient—for example, exercise, positive pressure mechanical ventilation, and intermittent positive pressure breathing (IPPB). d) Air enters the alveoli from the atmosphere because the atmospheric air pressure is slightly higher than alveolar pressure, creating a pressure gradient. e) In external respiration, a pressure gradient exists between the alveoli and the pulmonary capillaries, causing flow of gases across the alveolar-capillary membrane. f) In internal respiration, the process is reversed. The arterial blood is rich in oxygen and poor in carbon dioxide, whereas the cells are poor in oxygen and rich in carbon dioxide. (1) The pressure differences between the PO2 and PCO2 in the blood and cells cause oxygen to move from the circulating hemoglobin into the cells. (2) The cells release carbon dioxide into the bloodstream. Lung Surface Area 1. Total surface area of the lung is very large. 2. The greater the available alveolar-capillary membrane surface area, the greater the amount of oxygen and carbon dioxide that can diffuse across it in a specific time period. 3. Emphysema is a major pulmonary disorder that destroys the alveolar-capillary membrane. a) This greatly reduces the functional surface area and consequently impairs gas exchange. 4. Many pulmonary conditions—including severe pneumonia, lung tumors, pneumothorax, and pneumonectomy—can significantly reduce functioning surface area. Alveolar-Capillary Membrane Thickness 1. Thickness of the alveolar-capillary membrane is important. 2. The thinner the membrane, the more rapid the rate of diffusion of gases. 3. Several conditions can increase membrane thickness: a) Fluid in the alveoli or interstitial spaces, or both b) An inflammatory process involving the alveoli c) Lung conditions that cause fibrosis Length of Gas Exposure 1. During rest, blood flows through the alveolar-capillary system in approximately 0.75 seconds. 2. Diffusion of oxygen and carbon dioxide requires about 0.25 seconds to reach equilibrium. 3. During periods of high cardiac output, blood flow is faster through the alveolar-capillary system. 4. Diffusion takes place during a shortened exposure time. 5. In healthy lungs, oxygen exchange is usually not impaired with high–cardiac output states. 6. Hypoxemia can result if diffusion abnormalities are present, such as pulmonary edema, alveolar consolidation, or alveolar fibrosis. Oxyhemoglobin Dissociation Curve 1. Hemoglobin is the primary carrier of oxygen in the blood. a) It has an affinity for oxygen molecules. 2. In the pulmonary capillaries, oxygen binds loosely and reversibly to hemoglobin, forming oxyhemoglobin for transport to the tissues. a) Amount of oxygen that loads onto hemoglobin is expressed as a percentage of hemoglobin saturation by oxygen (percent SaO2). 3. The affinity of hemoglobin for oxygen varies, depending on certain physiologic factors. 4. The oxyhemoglobin dissociation curve represents the relationship of the partial pressure of arterial oxygen and hemoglobin saturation. 5. The percentage saturation of hemoglobin does not maintain a direct relationship with the PaO2. 6. The top portion of the curve is flattened into a horizontal position. a) In this portion of the curve, a large alteration in PaO2 produces only small alterations in percentage of hemoglobin saturation. (1) Clinically, this means that, although administering supplemental oxygen might significantly increase the patient’s PaO2, the resulting SaO2 increase will be proportionally small. 7. The bottom portion of the curve is steep. In this portion, any alteration in PaO2 yields a large change in percentage of hemoglobin saturation. a) Clinically, this means that administration of supplemental oxygen sufficient to increase the PaO2 should yield large increases in SaO2. 8. Low PaO2 at the tissue level stimulates oxygen release from hemoglobin to tissue. 9. High PaO2 at the pulmonary capillary level stimulates hemoglobin to bind with more oxygen. 10. Slight shifts are adaptive, but severe or rapid shifts can produce life-threatening tissue hypoxia. The Effects of Aging on Diffusion 1. As a person ages, total lung surface area decreases, the alveolar-capillary membrane thickness increases, and alveoli are destroyed because of aging processes. a) These changes result in decreased diffusion across the alveolar-capillary membrane, altering the ventilation–perfusion relationship. 2. Gas exchange becomes less efficient, placing the high-acuity older patient at risk for hypoxemia and/or hypercapnia problems. 3. Over time, the airways become larger, increasing dead space ventilation, and terminal airways lose supportive structures, which can result in air trapping. a) Both the gas exchange and airway changes can lead to carbon dioxide retention. PowerPoint Slides Slide 1 Pulmonary Gas Exchange—Respiration and Diffusion Slide 2 Respiration Slide 3 Diffusion Partial pressures of gases Pressure gradient Lung surface area Alveolar-capillary membrane thickness Length of gas exposure Slide 4 Oxyhemoglobin Dissociation Curve Slide 5 The Effects of Aging on Diffusion III. Pulmonary Gas Exchange—Perfusion A. Perfusion is the third component of the respiratory process. 1. Perfusion refers to the pumping or flow of blood into tissues and organs. 2. Perfusion can be divided into two circulatory systems: a) Systemic system (1) Vast, running from aorta through right atrium of heart b) Pulmonary system (1) Much smaller than systemic system, beginning with pulmonary artery in right ventricle, running through the lungs and back into left ventricle (2) Depends on adequate perfusion in the systemic system (3) Adequate perfusion in both systems needed for oxygenation of tissues in entire body (4) Both perfusion systems composed of a complex network of blood vessels of varying sizes and functions (5) Pulmonary perfusion depends on three factors: (a) Cardiac output (CO) (b) Gravity (c) Pulmonary vascular resistance (PVR) Cardiac Output 1. A function of stroke volume (SV) and heart rate (HR): CO = SV × HR. 2. Normal cardiac output is between 4 and 8 liters per minute. 3. Stroke volume is a function of ventricular preload, afterload, and contractility. 4. Common measurement is mean arterial pressure (MAP). a) Can be approximated using the equation MAP = [2(Pdias) + Psys]/3. b) A MAP of <60 mmHg is inadequate for perfusing major organs, such as the brain, heart, and kidneys. c) Clinical goal is to maintain MAP at 70 or above to prevent hypoperfusion, which can lead to organ ischemia and multiple organ dysfunction syndrome (MODS). Gravity 1. Effects of gravity on blood are important for pulmonary gas exchange. 2. Blood has weight and, therefore, is gravity dependent. a) It naturally flows toward dependent areas of the body. 3. Gravity has a major influence on the relationship between ventilation and pulmonary perfusion. Ventilation–Perfusion Relationship 1. Normal diffusion of gases requires a certain balance of alveolar ventilation and pulmonary perfusion. 2. Should a significant imbalance in this relationship develop, normal gas exchange cannot take place in affected areas. 3. Relationship of ventilation (V) to perfusion (Q) is expressed as a ratio of alveolar ventilation to pulmonary capillary perfusion (V/Q ratio). 4. For approximately every 4 liters of air flowing into alveoli, about 5 liters of blood flows past, for an average of 4:5, or 0.8. 5. Balance of ventilation to perfusion is greatly affected by the PAO2 and PACO2. 6. This balance depends on adequate diffusion of oxygen and carbon dioxide across the alveolar-capillary membrane and movement of oxygen into and carbon dioxide out of the alveoli. 7. When breathing spontaneously, airflow naturally moves toward the diaphragm, which results in more air movement into the bases and peripheral lung during inspiration. 8. Pulmonary capillary perfusion is gravity dependent, making perfusion greatest in the dependent areas of the lungs. 9. Because ventilation and perfusion are both greatest in the bases of the lungs, the greatest amount of gas exchange occurs in this portion of the lung fields. 10. In upper lungs, moderate alveolar ventilation and significantly reduced perfusion result in a “high” V/Q ratio. 11. In lower lungs, there is a moderate increase in ventilation with a significant increase in perfusion, resulting in a “low” V/Q ratio. 12. The clinical significance of ventilation–perfusion balance becomes apparent when considering high-acuity patients needing prolonged bed rest. 13. Because blood is gravity dependent, it will shift from the lung bases to whichever lung area is in the dependent position while air continues to be drawn toward the diaphragm. Pulmonary Shunt 1. Pulmonary shunt refers to the percentage of cardiac output that flows from the right heart and back into the left heart without undergoing pulmonary gas exchange (true shunt or physiologic shunt). 2. Pulmonary shunting is a major cause of hypoxemia in high-acuity patients. 3. Helps explain how problems in ventilation and perfusion originate. 4. Two types of true shunts: anatomic and capillary Anatomic Shunt 1. Anatomic shunt: not all blood that flows through the lungs participates in gas exchange. 2. Anatomic shunt refers to blood that moves from right heart and back into left heart without contact with alveoli, approximately 2–5% of blood flow. 3. Normal anatomic shunting occurs as a result of emptying of the bronchial and several other veins into the lung’s own venous system. 4. Abnormal anatomic shunting can occur because of heart or lung problems. Capillary Shunt 1. Capillary shunt is the normal flow of blood past completely unventilated alveoli. 2. Blood flowing by the affected units will not take part in diffusion. 3. Capillary shunt results from consolidation or collapse of alveoli, atelectasis, or fluid in the alveoli. Absolute Shunt 1. The combined amount of anatomic shunt and capillary shunt is called absolute shunt. a) The total percentage of cardiac output involved in absolute shunt has important clinical implications. b) Lung tissue affected by absolute shunt is unaffected by oxygen therapy because it involves nonfunctioning alveoli. c) Shunting of >15% of cardiac output can result in severe respiratory failure. d) Patients with acute respiratory distress syndrome (ARDS) generally have an absolute shunt of >20% of cardiac output. e) A hallmark of ARDS is refractory hypoxemia consistent with absolute shunt. Shuntlike Effect 1. Shuntlike effect is not a true shunt because the shunting is not complete. 2. Shuntlike effect exists when there is an excess of perfusion in relation to alveolar ventilation; that is, alveolar ventilation is reduced but not totally absent. 3. Common causes: a) Bronchospasm b) Hyperventilation c) Pooling of secretions 4. Hypoxemia secondary to shuntlike effect is very responsive to oxygen therapy. Venous Admixture 1. Venous admixture refers to the effect that pulmonary shunt has on the contents of the blood as it drains into the left heart and out into the system as arterial blood. 2. Beyond the shunted areas, the fully reoxygenated blood mixes with the completely or relatively unoxygenated blood. 3. The oxygen molecules remix in the combined blood to establish a new balance, resulting in a PaO2 that is higher than that which existed in blood affected by shunt but lower than it would be with normal alveoli. Estimating Intrapulmonary Shunt 1. The simplest way to estimate intrapulmonary shunt is by calculating the P/F ratio (PaO2/FIO2). 2. It is best used when the patient’s PaCO2 is stable, because it is not sensitive to changes in that value. Pulmonary Vascular Resistance (PVR) 1. PVR measures the resistance to blood flow in the pulmonary vascular system, a low-resistance system. 2. Three main factors determine the amount of pulmonary resistance: a) The length of the vessels b) The radius of the vessels c) The viscosity of the blood (1) Of these factors, the major determinant of pulmonary vascular resistance is vessel radius (caliber), which is altered by: (a) The volume of blood in the pulmonary vascular system (b) The amount of vasoconstriction (c) The degree of lung inflation 3. Factors related to the volume of blood in the pulmonary vascular system include capillary recruitment and distention. a) Recruitment is most influential. (1) The small pulmonary capillaries open up (are recruited) in response to an increase in blood flow. (2) When pulmonary blood flow is low (e.g., shock), the smaller capillaries can receive so little blood that they collapse. b) Distention occurs in response to increased cardiac output or increased intravascular fluid volume. (1) By distending, the capillaries can accommodate the increased flow. (2) Distention of capillaries decreases PVR. 4. Pulmonary vasoconstriction occurs in response to hypoxia, hypercapnia, and acidosis. a) Vasoconstriction is a major cause of increased PVR in the high-acuity patient. b) Hypoxia is the strongest stimulant for pulmonary vasoconstriction. c) When an area of the lung becomes hypoxic, vasoconstriction is triggered. This response diverts blood flow to more functional areas of the lungs and results in reduction in impact of shunt. 5. Degree of lung inflation has impact on diameter of pulmonary capillaries; as lung inflates, capillaries become stretched. a) In states of high lung inflation, capillaries become compressed, which decreases their diameter and increases PVR. b) Lower lung volumes are associated with decreased PVR. 6. Calculating pulmonary vascular resistance requires a flow-directed pulmonary artery catheter. a) The calculation measures resistance, which is a function of pressure and flow. b) Pressure is determined by mean pulmonary artery pressure and pulmonary capillary wedge pressure. c) Flow is measured as cardiac output. Cor Pulmonale 1. Refers to right ventricular hypertrophy and dilation secondary to pulmonary disease. 2. A complication of both restrictive and obstructive pulmonary diseases. 3. It can cause right heart failure and is a major cause of death in chronic obstructive pulmonary disease (COPD). 4. Cor pulmonale results from a sequence of events precipitated by pulmonary hypertension. PowerPoint Slides Slide 1 Pulmonary Gas Exchange—Perfusion Perfusion Cardiac output Slide 2 Gravity Ventilation–perfusion relationship Slide 3 Pulmonary Shunt Anatomic shunt Capillary shunt Absolute shunt Shuntlike effect Venous admixture Slide 4 Estimating Intrapulmonary Shunt Slide 5 Pulmonary Vascular Resistance (PVR) Cor Pulmonale IV. Acid–Base Physiology and Disturbances 1. Acid-base status is another determinant of gas exchange because lungs play critical role in homeostasis 2. Also source of severe acid-base imbalances in presence of certain pulmonary disease states A. Acid-base physiology 1. Acid–base balance is crucial to the effective functioning of body systems. 2. Severe imbalances can be lethal. 3. Acids are substances that dissociate or lose ions. 4. Bases are substances capable of accepting ions. 5. A buffer is a substance that reacts with acids and bases to maintain a neutral environment of stable pH. 6. pH represents free hydrogen ion (H+) concentration. a) An increase in H+ concentration lowers pH and increases acidity. b) A decrease in H+ concentration increases pH and increases alkalinity. 7. Body’s acids include volatile acids and nonvolatile acids. a) Volatile acids can convert to a gas for excretion. (1) Carbonic acid rapidly converts to carbon dioxide for excretion from the lungs. b) Nonvolatile (metabolic) acids cannot be converted to gas, so they must be excreted through the kidneys. (1) The kidneys are capable of excreting only a small amount of acid each day, and they respond slowly to changes. (2) Hydrogen ions are excreted in the proximal and distal tubules of the kidneys in exchange for sodium. Maintaining Acid–Base Balance: Buffer Systems and Compensation 1. Buffer systems a) Buffering mechanisms represent chemical reactions between acids and bases to maintain a neutral environment. b) Bases react with excess hydrogen ions (H+), and acids react with excess HCO3 to prevent shifts in pH. c) The buffering mechanisms are triggered quickly in response to any change in pH. 2. Compensation a) The process whereby an abnormal pH is returned to within normal limits through counterbalancing acid–base activities. b) Compensation occurs over time; it is referred to in terms of the degree or level to which the body has achieved compensation. c) Four levels of compensation (1) Uncompensated (acute) (a) The pH is abnormal because other buffer and regulatory mechanisms have not begun to correct the balance. (2) Partially compensated (a) The pH is abnormal, but body buffers and regulatory mechanisms have begun to respond. (3) Compensated (chronic) (a) The pH has returned to within normal limits. (4) Corrected (a) All acid–base parameters have returned to normal ranges. Metabolic (Renal) Compensation Mechanism 1. Bicarbonate buffer system is the major buffering system in the body. 2. Its components are regulated by the lungs (CO2) and kidneys (HCO3). 3. Additional nonbicarbonate buffers include hemoglobin, serum proteins, and the phosphate system. 4. The bicarbonate system is a relatively slowly responding system, taking hours to days. 5. The metabolic compensation mechanism controls the rate of elimination or reabsorption of hydrogen and bicarbonate ions in the kidney. 6. With increased acid loads, H+ elimination and bicarbonate reabsorption are increased. 7. In alkalosis, H+ is reabsorbed, and HCO3 is excreted. 8. Metabolic compensation is slow, beginning in hours but taking days to reach maximum compensation. a) This delayed compensatory mechanism helps explain why so many respiratory problems initially cause acute (uncompensated) acid–base disturbances. Respiratory (Pulmonary) Compensation Mechanism 1. The respiratory buffer system is a rapid-response compensatory mechanism for metabolic acid–base disturbances; it responds within minutes. 2. The lungs have two ways to compensate: a) Alveolar hypoventilation in response to metabolic alkalosis (1) Hypoventilation retains CO2. b) Alveolar hyperventilation in response to metabolic acidosis (1) Hyperventilation blows off CO2. Respiratory Acid-Base Disturbances 1. Primary respiratory disturbances are reflected in changes in the PaCO2. a) Normal as in respiratory acidosis b) Below normal as in respiratory alkalosis Respiratory Acidosis 1. Occurs when the PaCO2 moves above 45 mmHg and the pH drops below 7.35. 2. Hypercapnia, elevated CO2, indicates alveolar hypoventilation. a) The lungs are not blowing off enough carbon dioxide, causing a carbonic acid excess. b) Carbon dioxide is considered an acid because it combines with water to form carbonic acid. c) Essential to determine cause of hypoventilation and correct it when possible. 3. A “chronic” abnormal acid–base state means that a state of compensation exists. 4. Chronic respiratory acidosis usually is associated with a chronic obstructive pulmonary disease. 5. Elevation of carbon dioxide occurs gradually over many years; the body can compensate to maintain a normal pH by elevating the bicarbonate. 6. Additional stressors can cause decompensation, producing respiratory failure. Respiratory Alkalosis 1. This occurs when PaCO2 falls below 35 mmHg, with a corresponding rise in pH to greater than 7.45. 2. Decreased carbon dioxide indicates alveolar hyperventilation. a) Lungs are eliminating too much carbon dioxide, creating a carbonic acid deficit. 3. In respiratory alkalosis, there is insufficient carbon dioxide available to combine with water to form carbonic acid. 4. Effective treatment involves determining the cause of the hyperventilation and providing the necessary intervention. 5. Chronic respiratory alkalosis is uncommon. The same factors causing acute respiratory alkalosis could cause a chronic state if the problem remained uncorrected. Base Excess Deficit (BE) 1. A measure of the amount of buffer required to return the blood to a normal pH state. 2. A base excess is present if the BE is greater than +2 mEq/L. a) Signals the presence of a metabolic alkalosis state 3. A base deficit is present if BE is less than –2 mEq/L. a) Signals the presence of a metabolic acidosis state Metabolic Acidosis 1. Defined clinically as HCO3 < 22 mEq/L, pH < 7.35, with a base deficit (less than –2). 2. Metabolic acidosis can be caused by an increase in metabolic acids or excessive loss of base. 3. Examples of conditions that can cause an increase in H+ concentration. 4. Examples of conditions that precipitate a decrease in bicarbonate (HCO3) levels. Lactic Acidosis 1. Acid metabolites, such as lactic acid (lactate), result from cellular breakdown and anaerobic metabolism. 2. The normal range for serum lactate is 0.5–2.0 mEq/L. 3. High-acuity patients are at risk for developing elevated levels of lactate because lactic acidosis is closely associated with shock and other severe physiologic insults. 4. During shock, cellular hypoxia drives serum lactate up rapidly, usually >5 mEq/L. a) This rise often precedes decompensatory signs and can be an indicator of impending shock. 5. Other conditions that can cause lactic acidosis include severe dehydration, severe infection, severe trauma, diabetic ketoacidosis, and hepatic failure. Metabolic Alkalosis 1. Clinically defined as bicarbonate (HCO3) level > 26 mEq/L, pH > 7.45, and a base excess (greater than +2). 2. Metabolic alkalosis occurs when amount of alkali increases or excessive loss of acid occurs. a) A common cause of increased alkali is ingestion of alkaline drugs due to overuse of antacids or over-administration of sodium bicarbonate during a cardiac arrest emergency. b) Decreased acid conditions: (1) Loss of gastric fluids (2) Treatment with steroids (3) Diuretic therapy causing loss of potassium (4) Binge–purge syndrome PowerPoint Slides Slide 1 Acid–Base Physiology and Disturbances Acid-base physiology Slide 2 Maintaining Acid–Base Balance: Buffer Systems and Compensation Metabolic (Renal) Compensation Mechanism Respiratory (Pulmonary) Compensation Mechanism Slide 3 Respiratory Acid–Base Disturbances Slide 4 Respiratory Acidosis Respiratory Alkalosis Base Excess Deficit (BE) Slide 5 Metabolic Acidosis Lactic Acidosis Metabolic Alkalosis V. Arterial Blood Gases (ABGs) 1. Interpretation of ABGs provides valuable information on patient’s acid-base and oxygenation status. 2. The following section focuses on the determinants of oxygenation status and interpretation of the entire ABG. A. Determinants of oxygenation status 1. There are three major determinants of oxygenation status: a) PaO2 b) SaO2 or (SpO2) c) hemoglobin PaO2 1. This represents the partial pressure of the oxygen dissolved in arterial blood (3% of total oxygen) (normal value 80–100 mmHg), not the total amount of oxygen available. 2. It is an important indicator of oxygenation because PaO2 and oxygen saturation (SaO2) maintain a relationship. a) This relationship is reflected in the oxyhemoglobin dissociation curve. SaO2 and SpO2 1. Oxygen saturation (SaO2) is the measure of the percentage of oxygen combined with hemoglobin compared with the total amount it could carry (normal value > 95%). 2. The degree of saturation is important in determining the amount of oxygen available for delivery to the tissues. Hemoglobin 1. Hgb or Hb is the major component of red blood cells (normal values 12–15 g/dL in women, 13.5–17 g/dL in men). 2. It is composed of protein and heme, which contains iron. 3. Oxygen binds to the iron atoms on the four heme groups of each hemoglobin molecule. 4. Hemoglobin is the major carrier of oxygen in the blood and is an important factor in tissue oxygenation. Arterial Blood Gas 1. ABG normal values typically are reported as normal-at-sea-level (760 mmHg) partial pressures, room air (21% oxygen), and a blood temperature of 37°C (98.6°F). 2. Age also affects normal ABG values. 3. Newborns have a lower PaO2, as do elderly people, whose PaO2 decreases approximately 25–30% (in the 30- to 80-year range). 4. Normal ABG values are ranges for normal, healthy adults. Arterial Blood Gas Interpretation 1. A single ABG measurement represents only a single point in time. 2. Arterial blood gases are most valuable when trends are evaluated over time, correlated with other values, and incorporated into the overall clinical picture. 3. Interpretation of ABGs includes determination of acid–base state, level of compensation, and oxygenation status. 4. The severity of hypoxemia is frequently referred to in terms of being mild, moderate, or severe, but the exact associated PaO2 levels are somewhat arbitrary. a) Mild hypoxemia: PaO2 60–75 mmHg b) Moderate hypoxemia: PaO2 45–59 mmHg c) Severe hypoxemia: PaO2 < 45 mmHg 5. Although acid-base balance determination is presented first, oxygenation status is often analyzed first, based on patient’s need and person performing analysis PowerPoint Slides Slide 1 Arterial Blood Gases (ABGs) Slide 2 Determinants of Oxygenation Status PaO2 SaO2 and SpO2 Slide 3 Hemoglobin Slide 4 Arterial Blood Gas Arterial Blood Gas Interpretation VI. Focused Respiratory Nursing History and Assessment 1. Many high-acuity patients are at increased risk for being admitted with pulmonary diseases or developing respiratory complications Nursing History 1. When a patient is admitted to the hospital in acute distress, the nurse initially assesses airway, breathing, and circulation, and the nurse immediately takes appropriate action based on those assessments. 2. As soon as feasible, information regarding the immediate events leading to admission should be obtained. a) A recent history gives important clues as to etiology and chain of events related to the current problem. 3. The presence of severe respiratory distress limits the amount of health history information a patient can relate. a) Minimize questions directed to the patient to reduce stress on breathing. b) State inquiries in a way that requires very brief answers. Social History 1. Assess tobacco and alcohol use. a) Assess number of cigarettes smoked per day and number of years patient has smoked. b) Alcohol use in association with prescribed drug therapy can adversely affect patient’s respiratory condition. c) Problems with alcohol withdrawal can complicate cardiopulmonary status should delirium tremens develop. Nutritional History 1. Nutritional state is crucial to assess because malnutrition can contribute to developing respiratory failure. 2. Many patients with chronic pulmonary disorders are admitted to hospital in a malnourished state, which negatively affects patient outcomes. a) Protein–calorie deficit weakens muscles, including respiratory muscles. b) Malnutrition is associated with weakened immune system, increasing susceptibility to infection, making it harder to fight against existing infections. c) Increased stress associated with acute infection can precipitate acute respiratory failure. d) High-carbohydrate diet increases carbon dioxide load in body, which can lead to ventilatory complications. Cardiopulmonary History 1. Often difficult to differentiate between problems of pulmonary and cardiovascular etiology. 2. Of particular importance are data concerning pre-existing cardiovascular conditions such as history of hypertension, coronary artery disease, or previous myocardial infarction. 3. Previous pulmonary problems, as well as prehospital activity tolerance, can also help differentiate pulmonary from cardiac problems. Sleep–Rest History 1. Pulmonary problems frequently interfere with sleep and rest. 2. If the respiratory problem is severe enough to cause hypoxia, the patient often exhibits restlessness associated with inadequate oxygenation of the brain. 3. Pulmonary disorders can increase the work of breathing, which can interfere with sleep and rest. 4. Patients in respiratory distress might sleep poorly because they fear they will cease to breathe when they are unaware. 5. Others cannot sleep because of their level of general discomfort. 6. Dyspnea and air hunger are anxiety-producing and threatening experiences for pulmonary patients. Common Complaints Associated with Pulmonary Disorders 1. If a respiratory problem is suspected, nurse should obtain information about the most common respiratory complaints: dyspnea, chest pain, cough, sputum, and hemoptysis. 2. Interview the patient or family (subjective data), and perform a nursing assessment (objective data). 3. Regular assessment of common respiratory symptoms is also important. Dyspnea 1. A subjective symptom 2. Two major categories: a) Orthopnea b) Paroxysmal nocturnal dyspnea Subjective Data 1. Dyspnea is the feeling of having difficulty breathing or shortness of breath. 2. It is associated with increased work of breathing and supply-and-demand imbalance. a) The body’s ability to respond. 3. Progressive dyspnea is noted in both restrictive and obstructive pulmonary disorders. Orthopnea 1. A type of dyspnea associated with cardiac problems or severe pulmonary disease. 2. It refers to a state in which the patient assumes a head-up position to relieve dyspnea. 3. Orthopnea can be mild or severe. 4. Ask how many pillows are needed for breathing comfortably while at rest. 5. A state where additional pillows are needed for breathing comfortably while lying down is sometimes called “pillow orthopnea.” 6. Paroxysmal nocturnal dyspnea (PND) is associated with left heart failure. 7. Patient reports waking at night after being asleep several hours with a sudden onset of severe orthopnea. 8. Upon sitting up or getting out of bed, the dyspnea is relieved, and the patient can resume sleep. 9. It is a form of transient mild pulmonary edema. 10. Fluids that have been congested in the lower extremities during the day shift to the heart and lungs, causing a fluid volume overload when the person becomes horizontal for several hours. Objective Data 1. Nurse may note tachypnea, nasal flaring, use of accessory muscles, or abnormal arterial blood gases. 2. Patient may voluntarily assume a high-Fowler sitting position secondary to orthopnea. 3. Severe tachypnea, a respiratory rate of >30 breaths per minute, significantly increases the work of breathing. 4. If allowed to continue, respiratory muscle fatigue can occur, which could cause acute respiratory failure. Chest Pain 1. Critical to differentiate pain caused by pulmonary disease or pain caused by cardiac disease. Subjective Data 1. When assessing chest pain, note how long the pain has been present, whether it radiates, and the triggering and alleviating factors. 2. Can be helpful in differentiating cardiogenic pain from pleuritic pain. a) Cardiogenic pain (1) Generally described as dull, pressure-like discomfort often radiating to jaw, back, or left arm (2) Unaffected by breathing b) Pleuritic pain (1) Described as sharp and knifelike (2) When patient is between breaths or the breath is held, pain decreases or stops (3) Pain increases with deep breathing but doesn’t radiate (4) Pleural friction rub sometimes can be auscultated at the focal pain point 3. Most pulmonary disorders affect only lung parenchyma, which is insensitive to pain. 4. The attached visceral pleurais insensitive as well. 5. The parietal pleura is well innervated, and when inflammation occurs, it can trigger sharp pain. Objective Data 1. Note splinting, shallow respirations, tachypnea, facial changes associated with pain, and increased blood pressure and pulse. Cough Subjective data 1. Assess frequency, character (dry, productive, congested), duration, triggers and pattern of occurrence, and alleviating factors. Objective data 1. Observe strength, character, and frequency of cough. Sputum 1. Characteristics of, or changes in, provide important information about a pulmonary disease. Subjective data 1. Obtain description of sputum production. 2. If patient has a disease associated with chronic production of sputum, ask for description of usual quantity, characteristics, and color, as well as any changes in sputum associated with current problem. Objective data 1. Monitor sputum regularly for quantity and characteristics. 2. Sputum changes should be noted and documented. 3. Normal secretions are thin and clear. Hemoptysis 1. Refers to expectoration of bloody secretions. 2. Determine source of bleeding: upper or lower airway. Subjective Data 1. Can be of cardiovascular or pulmonary origin. 2. Common causes: pulmonary embolism and cardiogenic pulmonary edema secondary to left heart failure. 3. Most common source is lung disease. 4. Information to obtain includes color, consistency and quantity, and frequency and duration. Objective data 1. Assess for color, consistency, quantity, frequency, and duration. Focused Respiratory Assessment 1. The onset of acute respiratory distress can be rapid and severe. 2. The nurse should be alert to changes from previously assessed baseline data and data trends. 3. When such changes are noted, a rapid focused respiratory assessment should be immediately conducted, focusing on key data that strongly suggest an acute alteration in respiratory function. Inspection 1. Inspect skin color for cyanosis: observe lips, earlobes, and beneath tongue for central cyanosis. 2. In patients with dark skin color, cyanosis can be observed on lips and tongue. 3. Cyanosis is not a reliable indicator of hypoxia, because it depends on amount of reduced hemoglobin present. 4. When present, cyanosis is a late sign of respiratory distress. 5. Inspect shape of chest, and observe chest movement for symmetry and rate, depth, and pattern of breathing. 6. Chest may be palpated for tactile fremitus and chest expansion. 7. Chest percussion can help detect presence of air, fluid, or consolidation. Auscultation 1. Auscultation is important. 2. Diaphragm of stethoscope is best for hearing most breath sounds and comparing one lung with the other. Normal Breath Sounds 1. There are three types of normal breath sounds: a) Vesicular, bronchial (tubular), and bronchovesicular. Abnormal Breath Sounds 1. Auscultate chest for diminished or absent sounds; presence of abnormal breath sounds associated with change in lung status. 2. Adventitious breath sounds are heard on top of other breath sounds and are never normal. 3. When abnormal breath sounds are present, nurse should assess and document location and when in respiratory cycle they are heard. 4. Adventitious sounds are classified as: a) Crackles b) Rhonchi c) Wheeze d) Plural rub e) Diminished or absent lung sounds Crackles 1. Relatively discrete, delicate popping sounds of short duration associated with either fluid or secretions in small airways or alveoli, or opening of alveoli from a collapsed state. a) Most commonly heard during inspiration b) Described as either fine or coarse (1) Fine crackles (a) Delicate, high-pitched, short duration (b) Sound of rubbing hair between one’s fingers (c) Conditions include: atelectasis and pneumonia (2) Coarse or loud crackles (a) Louder, high-pitched, longer duration (b) Sound of Velcro separating (c) Conditions include: bronchitis and pulmonary edema Rhonchi 1. Heard as coarse, “bubbly” sounds a) Most common during expiration and are auscultated over larger airways b) Associated with accumulation of fluid or secretions in larger airways Wheeze 1. Caused by air passing through constricted airways. a) Wheeze has a musical quality: can be high- or low-pitched. b) Heard on inspiration or expiration and is of long duration. Stridor 1. A type of wheeze caused by upper airway obstruction from inflamed tissue or foreign body. a) Described as a high-pitched, inspiratory wheeze heard louder over neck than over chest wall b) Can develop from airway edema, resulting from problems such as thermal burn inhalation injury or airway trauma during extubation Pleural Rub 1. Caused by inflammation of pleural linings. a) When inflammation occurs, linings become resistant to free movement. b) Characteristic sound is heard during breathing and ceases between breaths or with breath holding. c) Also referred to as pleural friction rub Decreased or Absent Breath Sounds 1. Caused by diminished or absent air flow to an area of the lungs. a) When assessed, nurse should document the location. b) In patients with lung hyperinflation disorders such as chronic obstructive pulmonary disease (COPD) and acute asthma, generalized loss of breath sounds can indicate a potentially life-threatening hypoventilation situation. Vital Signs and Hemodynamic Values 1. These give crucial baseline data and are important indicators of changing patient status over time. 2. Vital signs include arterial blood pressure, pulse rate and rhythm, respiratory rate and rhythm, and temperature. 3. Pulse oximeter reading should be obtained. 4. If a pulmonary artery catheter is in place, important monitoring assessments include central venous pressure (CVP), pulmonary artery pressure, pulmonary artery wedge pressure, mean arterial pressure, and cardiac output. 5. Hemodynamic monitoring generally is initiated when cardiac involvement is suspected or fluid status is questioned. 6. The presence of pulmonary hypertension can alter hemodynamic measurements. PowerPoint Slides Slide 1 Focused Respiratory Nursing History and Assessment Slide 2 Nursing History Social History Nutritional History Cardiopulmonary History Sleep–Rest History Slide 3 Common Complaints Associated with Pulmonary Disorders Dyspnea Subjective data Slide 4 Orthopnea Objective data Slide 5 Chest Pain Subjective Data Objective Data Slide 6 Cough Subjective data Objective data Slide 7 Sputum Subjective data Objective data Slide 8 Hemoptysis Subjective data Objective data Slide 9 Focused Respiratory Assessment Inspection Auscultation Slide 10 Normal Breath Sounds Slide 11 Abnormal Breath Sounds Crackles Rhonchi Wheeze Stridor Pleural rub Decreased or absent breath sounds Slide 12 Vital Signs and Hemodynamic Values VII. Pulmonary Function Evaluation 1. Provider or medical team initiates orders for pulmonary function testing a) Assists to diagnose or update or evaluate pulmonary status 2. Implementation and interpretation of tests becomes interdisciplinary approach Pulmonary Function Tests (PFTs) 1. Ventilation is measured using pulmonary function tests. 2. These tests provide baseline data and a means to monitor progress of functional impairments. 3. They help differentiate a restrictive pulmonary problem from an obstructive problem. 4. PFTs are useful for monitoring effectiveness of therapeutic interventions. 5. Diagnostic PFT is usually conducted in a pulmonary laboratory using special computerized equipment that accurately measures pulmonary volumes, capacities, and air flow. 6. Simpler measures of pulmonary function can be taken at bedside easily, using a spirometer. Bedside Pulmonary Function Measurements 1. High-acuity patients are at risk of developing pulmonary complications associated with immobility and respiratory muscle fatigue. 2. Pulmonary function may be monitored in patients at particular risk for ventilatory decompensation. 3. Of interest are tidal volume, vital capacity, and minute ventilation. a) Tidal volume and vital capacity help monitor respiratory muscle strength. (1) Both of these PFTs can be easily measured using a respiratory spirometer and frequently are part of weaning criteria during mechanical ventilation. Tidal Volume (VT or TV) 1. Amount of air that moves in and out of lungs with each normal breath. 2. When TV drops below 4 mL/kg, a state of alveolar hypoventilation develops. 3. Acute respiratory failure results when hypoventilation becomes severe and results in hypercapnia. Vital Capacity (VC) 1. VC is the maximum amount of air expired after a maximal inspiration. 2. Normal vital capacity differs with gender, height, weight, and age. 3. It decreases with age and in the presence of acute or chronic restrictive pulmonary diseases. Minute Ventilation (VE) 1. The total amount of expired air in 1 minute. 2. Used as a rapid method of measuring total lung ventilation changes. 3. Not considered an accurate measure of alveolar ventilation. 4. Normal minute ventilation is 5–10 L/minute. 5. When it increases to >10 L/minute, the work of breathing is significantly increased. 6. Minute ventilation <5 L/minute indicates patient at risk for problems associated with hypoventilation. Forced Expiratory Volumes (FEVs) 1. FEVs are important diagnostic measurements that help differentiate restrictive pulmonary problems from obstructive problems and measure airway resistance. 2. They are also important in determining severity of obstructive diseases. 3. FEVs measure how rapidly a person can forcefully exhale air after a maximal inhalation, measuring volume (in liters) over time (in seconds). 4. Patients with a restrictive airway problem are able to push air forcefully out of their lungs at a normal rate. 5. Persons with an obstructive disorder have a delayed emptying rate. 6. FEV testing generally is not conducted at the bedside. PowerPoint Slides Slide 1 Pulmonary Function Evaluation Slide 2 Pulmonary Function Tests (PFTs) Bedside Pulmonary Function Measurements Tidal Volume (VT or TV) Vital Capacity (VC) Minute Ventilation (VE) Forced Expiratory Volumes (FEVs) VIII. Noninvasive and Invasive Monitoring of Gas Exchange 1. High-acuity patients frequently require monitoring of their oxygenation or ventilation status. When possible, noninvasive technologies such as pulse oximetry and capnography are used. 2. When hemodynamic monitoring is also needed, an invasive arterial line is inserted because it can continuously monitor hemodynamics, measure arterial oxygen saturation, and provide ready access to arterial blood for ABG sampling. Pulse Oximetry 1. A noninvasive technique for monitoring arterial capillary hemoglobin saturation (SpO2) and pulse rate. 2. It uses light wavelengths to determine oxyhemoglobin saturation. 3. It also detects pulsatile flow to differentiate between venous and arterial blood. 4. A sensor is placed on a finger, nose, or ear, and an oximeter provides a constant assessment of arterial oxygen saturation. 5. Fingers are most commonly used for sensor placement, but adequacy of peripheral circulation must be considered when choosing the best sensor location. 6. Pulse oximetry is best used as an adjunct to other assessment modalities in providing continuous information for evaluation of oxygenation status. 7. Ideally, the continuous arterial oxygen readings reflect the patient’s oxygenation status and alert the clinician to subtle or sudden changes. 8. In some patients, use of oximetry can decrease frequency of invasive ABG measurements if acid–base and ventilation are not problems. Causes of Inaccurate Readings 1. Many factors can alter the accuracy of pulse oximetry in high-acuity patients. 2. Technical problems a) Motion artifact: a major cause of false alarms and inaccurate readings b) External light sources: can compete with the pulse light source c) Improper sensor placement: might not be able to register arterial pulsations because of lack of sufficient arterial flow 3. Physiologic factors a) Hemoglobin level affects oxygen content of blood. b) Acid–base imbalance: Acidosis can cause a lower saturation reading, and alkalosis can cause a higher reading because of shifts in the oxyhemoglobin dissociation curve. c) Vasoconstrictive situations: Sensor might read more accurately if removed from distal sites and attached to a more central location. d) Cardiac dysrhythmias. Capnography 1. Capnometry is the numeric measurement of CO2 2. Capnography is the noninvasive measurement of carbon dioxide concentration in expired gas. 3. It results in a single value measurement called the PETCO2 (partial pressure of end-tidal CO2). 4. Continuous bedside monitoring of CO2 is accomplished using infrared light absorption or mass spectrometry. 5. Infrared analyzers measure carbon dioxide based on its strong absorption band at a distinctive wavelength. 6. A capnogram displays the capnometry measurements as a continuous waveform that can be read, breath by breath, throughout the breathing cycle. 7. CO2 can be sampled using either sidestream or mainstream techniques. Capnography Applications 1. Capnography is commonly used to monitor the adequacy of ventilation in surgical and procedural anesthesia, postoperative recovery, critical care units, and emergency departments (EDs). 2. New ACLS guidelines for CPR and emergency care call for the use of capnography to confirm endotracheal tube placement and monitor the adequacy of ventilation 3. The Agency for Healthcare Research and Quality (AHRQ) recommends monitoring oxygenation (using pulse oximetry and respiratory rate) and ventilation (using capnography) for postoperative patients receiving patient-controlled analgesia (PCA) to reduce the risk of potentially life-threatening respiratory depression. 4. Other applications include the detection of mechanical ventilator problems and confirmation of enteric feeding tube placement. 5. End-tidal carbon dioxide monitoring may be used to assess ventilatory status and provide an early warning of changes in ventilation. a) An abnormally low etco2 (less than 30 mm Hg) is most commonly associated with hyperventilation, hypothermia, pulmonary embolism, or decreased cardiac output. b) Increased etco2 (greater than 44 mm Hg) is associated with increased production of carbon dioxide (e.g., fever or increased cardiac output) or hypoventilation (e.g., respiratory center depression or neuromuscular diseases). 6. The usefulness of bedside capnography is not without limitations. a) In patients with morbid obesity, severe pulmonary edema, or ventilation–perfusion abnormalities, the etco2 may not accurately reflect Paco2 . b) May still be helpful if a correlation between Paco2 and etco2 can be established and used for trending. c) Unfortunately, many high-acuity patients develop ventilation–perfusion abnormalities, which may limit the usefulness of etco2 monitoring. Types of Capnography 1. CO2 is sampled for capnography in three ways. a) Infrared analyzers are applied either sidestream or mainstream b) Colorimetric capnography uses pH-sensitive paper to estimate ETCO2 ranges. Sidestream 1. When a sidestream analyzer is used, a small volume of exhaled gas is diverted from the main airway circuit through a small tube and is analyzed in a special chamber apart from the airway circuit. a) Major disadvantage: values are indirect estimated measurements b) Major disadvantage: can be used with patients that are not intubated. Mainstream 1. Mainstream analyzers are placed in-line as part of the airway circuit, and continuous ETCO2 directly in real time. a) Major disadvantage: requires the patient to be intubated. Colorimetric Capnography 1. Uses pH-sensitive paper that changes color based on the patient’s exhaled pH to represent a range of etco2 2. Most commonly used in the ED to assess for proper endotracheal tube (ETT) placement a) Also used in the field by emergency squads and in ICU settings. 3. A CO2 detector device is attached to the ET tube following tube insertion, the patient is given six breaths, and the device is read at full-end expiration. 4. The device rapidly responds to the patient’s exhaled CO2 with three color ranges: a) For example, with a Nellcor EASYCAP II (Nellcor, Boulder, CO), the detector device has a color range of purple to yellow with interpretation as follows: (1) Color range A (purple): 0.03% to less than 0.5% etco2 (less than 4 mmHg CO2); interpretation: ET tube is not in the trachea (2) Color range B (brown): 0.5% to less than 2% etco2 (4 to less than 15 mmHg CO2); interpretation: ET tube may be in the esophagus, and patient may have hypocarbia or low pulmonary blood flow (3) Color range C (yellow): 2% to 5% etco2 (15 to 38 mmHg CO2); interpretation: ET tube is properly located in the trachea 5. While colorimetric capnography is adequate for assessing proper ETT placement, it does not provide precise etco2 data and therefore has limited applications The Capnogram 1. The pattern that is visible on the capnography screen. 2. A normal capnogram shows an etco2 within several mm Hg of arterial Paco2 at the end of the plateau phase (the end-tidal CO2). 3. In a normal capnogram, the carbon dioxide concentration is zero at the beginning of expiration, gradually rising until it reaches a plateau. 4. The end-tidal carbon dioxide is the highest concentration at the end of exhalation. 5. etco2 monitoring is used in the clinical setting as a noninvasive indirect method of measuring Paco2. 6. In a normal person, etco2 is 30–43 mm Hg, typically 4 to 6 mm Hg below Paco2. Invasive Blood Gas Monitoring 1. The arterial catheter is an invasive means to monitor hemodynamic status as well as pulmonary gas exchange status. 2. Arterial catheters are most commonly inserted into a radial artery but also can be inserted into a femoral or other artery. 3. A major advantage of drawing blood, including arterial blood gases from the arterial line, is that frequent samples can be obtained without causing additional trauma and pain to the patient from repeated needle sticks. PowerPoint Slides Slide 1 Pulse Oximetry Slide 2 Causes of Inaccurate Readings Slide 3 Capnography Capnography Applications Slide 4 Types of Capnography Sidestream Mainstream Colorimetric Capnography Slide 5 The Capnogram Slide 6 Invasive Blood Gas Monitoring IX. Chapter Summary X. Clinical Reasoning Checkpoint XI. Post-Test XII. References Suggestions for Classroom Activities Discuss the different mechanisms the body uses to compensate for acid–base imbalances. Discuss the impact on the respiratory system when patients are placed on extended bedrest. What nursing interventions can be implemented to reduce the risk factors for pulmonary complications? Suggestions for Clinical Activities Discuss clinical conditions that can arise from acid–base imbalances. Compare and contrast the oxygenation levels of a young adult of 25, a middle-aged adult of 40, and an older adult of 75. Are there any gender differences? What factors will change the findings between the generations? Wagner et al., Instructor’s Resource Manual for High-Acuity Nursing, 6th Edition ©2014 by Education, Inc.