beyond basics resp

Orlando Regional Healthcare, Education & Development Copyright 2005 Rev. 8/15/2005

Beyond the Basics of Respiratory Care: Pulmonary Anatomy, Physiology, Evaluation and

Intervention

Self-Learning Packet

2005 This self-learning packet is approved for 4 contact hours for the following professionals:

1. Registered Nurses

2. Licensed Practical Nurses

* This packet should not be used after 8/31/2007

Respiratory Care

2005 Orlando Regional Healthcare, Education & Development 2

Purpose The purpose of this self-learning packet is to educate patient care providers on the function and care of the respiratory system in the adult patient.

This packet meets Florida State requirements for continuing education credit for nursing licensure. Orlando Regional Healthcare is an Approved Provider of continuing nursing education by Florida Board of Nursing (Provider No. FBN 2459) and the North Carolina Nurses Association, an accredited approver by the American Nurses Credentialing Center’s Commission on Accreditation (AP 085).

Objectives After completing this packet, the learner should be able to:

1. Describe the gross anatomy of the respiratory system. 2. Discuss the physiology of ventilation, gas exchange and acid-base balance. 3. Discuss the importance of the ventilation/perfusion ratio. 4. Identify respiratory medications and compare their uses. 5. Define common terms used in evaluation of the respiratory system. 6. Identify normal and abnormal pulmonary findings. 7. Compare invasive and non-invasive methods for evaluating oxygenation and ventilation. 8. Describe the methods used to monitor oxygenation and ventilation. 9. Discuss the effects of nutritional status on the respiratory system. 10. Describe nursing strategies to optimize pulmonary function and prevent complications. 11. Identify symptoms of respiratory distress and prioritize interventions. 12. Identify symptoms of respiratory decompensation and prioritize interventions.

Instructions In order to receive 4 contact hours, you must: • complete the post-test at the end of this packet • submit the post-test to Education & Development with your payment • achieve an 84% on the posttest

Be sure to complete all the information at the top of the answer sheet. You will be notified if you do not pass, and you will be asked to retake the posttest.

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Table of Contents

Introduction.......................................................................................................................................... 4

Gross Anatomy Review ....................................................................................................................... 4 Lower Airway .................................................................................................................................. 5 Thorax.............................................................................................................................................. 5 The Lungs ........................................................................................................................................ 6 Muscles of Ventilation..................................................................................................................... 7

Physiology of Breathing and Gas Exchange........................................................................................ 9 Mechanics of Breathing ................................................................................................................... 9 Mechanics of Lung Expansion ........................................................................................................ 9 Compliance and Resistance ........................................................................................................... 10 Work of Breathing ......................................................................................................................... 11 Gas Exchange ................................................................................................................................ 11 Pulmonary Vasculature.................................................................................................................. 12 Diffusion ........................................................................................................................................ 12 Lymphatic System ......................................................................................................................... 12 Regulation of Ventilation............................................................................................................... 14 Ventilation/Perfusion Relationships .............................................................................................. 14 Tissue Oxygenation ....................................................................................................................... 15

Evaluation of Pulmonary Function .................................................................................................... 17 Physical Evaluation........................................................................................................................ 17 Non-Invasive Diagnostic Monitoring ............................................................................................ 20 Invasive Diagnostic Monitoring (Arterial Blood Gases)............................................................... 26

Acute Respiratory Compromise......................................................................................................... 30 Priority Setting............................................................................................................................... 30

Interventions to Promote Respiratory Function................................................................................. 32 Therapeutic Interventions .............................................................................................................. 32

Pulmonary Pharmacology.................................................................................................................. 38

Summary ............................................................................................................................................ 43

Post-Test ............................................................................................................................................ 45

Bibliography ...................................................................................................................................... 51

Internet Resources.............................................................................................................................. 52

Glossary ............................................................................................................................................. 53

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Introduction Nurses play an integral role in promoting patients’ pulmonary health. Knowledge of the anatomy and physiology of the pulmonary system provides the foundation for treatment and evaluation of patients. This knowledge and skill base, in combination with collaboration with the multidisciplinary team, are essential to assure optimal patient outcomes.

This self-learning packet presents essential concepts of pulmonary anatomy and physiology. Also included are discussions of pulmonary evaluation and therapeutic interventions. These discussions are intended to assist in linking the physiology with common respiratory interventions. Throughout the packet there are clinical application examples. These will assist in integrating the concepts of this packet.

Gross Anatomy Review The upper airway consists of the nose, oral cavity, and pharynx. The pharynx is divided into three parts: nasopharynx, oropharynx, and laryngopharynx. The primary functions of the upper airway are to conduct, humidify and warm inspired air, prevent foreign materials from entering the lower airway, and contribute to speech, swallowing and smell.

Hyoid Bone

Soft palate Hard palate

Mandible

Tongue

Trachea

Nasopharynx

Oropharynx

Laryngopharynx

Esophagus

Larynx

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Artificial airways bypass the entire upper airway in order to better ventilate and oxygenate the patient. Because these airways also bypass the protective mechanisms provided by the upper airway, they place the patient at a higher risk of pulmonary complications.

Lower Airway The lower airway consists of the tracheobronchial tree. The primary function of the lower airway is conduction of air. It is lined with cilia that sweep mucus and debris up and out of the lungs.

Thorax The bony thorax consists of the sternum, ribs, thoracic vertebrae, clavicles, and scapulae. The bony thorax functions to protect the thoracic organs and anchor the muscles of ventilation. There are 12 pairs of ribs. Ribs 1 - 7 are directly attached to the vertebral column posteriorly and attached directly to the sternum by the costal cartilage anteriorly. Ribs 8 – 10 are known as false ribs and attach indirectly to the sternum by their costal cartilage. Ribs 11 and 12 are known as floating ribs because they do not attach anteriorly to the sternum. Between the ribs there are 11 intercostal spaces, which contain blood vessels, intercostal nerves, and the external and internal intercostal muscles.

Thyroid cartilage Cricoid cartilage

Right main stem bronchus

Left main stem bronchus

Carina

CLINICAL APPLICATION Maintenance of a patient’s airway is always a primary patient care objective. If the airway patency is lost, no other treatment modalities can prevent death.

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The Lungs The lungs are cone-shaped organs that hold between 4 – 8 liters of volume. The top portion is known as the apex, and the bottom is known as the base. The apex of each lung rises above the clavicles a few centimeters and the base rests against the diaphragm. The right lung has 3 lobes: upper, middle, and lower. The left has two lobes: upper and lower.

The mediastinum is located in the center of the thoracic cage between the right and left lungs. It contains the trachea, the heart, the great vessels, portions of the esophagus, the thymus gland, and lymph nodes. The remainder of the thorax contains the lungs, branching airways and pulmonary vasculature.

CLINICAL APPLICATION Multiple rib fractures interrupt the normal configuration of the bony thorax producing a condition called flail chest. Patients with flail chest cannot inhale and exhale normally and are at increased risk for acute ventilatory failure.

Sternal Notch

Manubrium Clavicle

Sternum

Costal cartilage

Xiphoid Process

Scapula

Left Upper Lobe

Left Lower Lobe

Right Upper Lobe

Right Middle Lobe

Right Lower Lobe

Cardiac Arch

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Muscles of Ventilation

Diaphragm

The diaphragm is the major muscle of ventilation. It is a dome-shaped musculofibrous partition located between the thoracic and abdominal cavities. It is composed of two muscles: the right and left hemidiaphragms. The diaphragm allows the esophagus, the aorta, several nerves, and the inferior vena cava to exit through it. The phrenic nerve exits the central nervous system between cervical vertebrae 3 – 5 and extends down to innervate the diaphragm assisting in controlling ventilation.

CLINICAL APPLICATION Aspiration pneumonias are often located in the right middle lobe due to the shorter, straighter right mainstem bronchus.

CLINICAL APPLICATION

Patients with cervical spine injuries of C3, C4 and C5 are often dependent on mechanical ventilation. This is due to interruption of nerve transmission to the diaphragm and other ventilatory muscles.

© Ciba Geigy

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Accessory muscles of ventilation

During vigorous exercise and the advanced stages of pulmonary disease processes (e.g. COPD) the accessory muscles of inspiration and expiration are activated to assist the diaphragm.

Muscles of Inspiration (I) Muscles of Expiration (E) Scalene muscles Rectus abdominis muscles Sternocleidomastoid muscles External abdominal obliquus muscles Pectoralis major muscles Internal abdominis obliquus muscles Trapezius muscles Transversus abdominis muscles External intercostal muscles Internal intercostal muscles

Sternocleidomastoid muscle (I) Scalene Muscle (I)

Pectoralis major muscle (I)

Rectus Abdominis (E)

External Oblique (E)

Trapezius muscle (I)

External intercostal muscle (I)

Internal intercostal muscles (E)

Lateral View Anterior

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Physiology of Breathing and Gas Exchange

Mechanics of Breathing During inspiration, the diaphragm moves downward and the lower ribs move upward and outward, increasing the size of the thorax. Changes in the thoracic size also change intrathoracic volume and pressure relative to the atmosphere. During inspiration, as the volume of the thorax increases, the pressure within the chest decreases. As a result air moves into the lungs from the atmosphere.

During expiration, the diaphragm and other respiratory muscles passively return to their normal position; thereby, decreasing the size of the thorax. As the size decreases, pressure increases and air moves out of the chest into the atmosphere. Inspiration is an active process, expiration is normally a passive process.

Mechanics of Lung Expansion The visceral pleura is a membrane that is attached to the outer surface of each lung. The parietal pleura lines the inside of the thoracic wall, diaphragm, and the lateral portion of the mediastinum. There is a potential space between the visceral and parietal pleurae known as the pleural cavity. These two membranes are moist, allowing them to glide with the movement of the lungs and ribs during ventilation.

Due to the differences in composition of the chest wall and the lung tissue, negative pressure exists between the parietal and visceral pleurae. In the intrapleural space, the pressure is less than the intra-alveolar and atmospheric pressure. This negative pressure keeps the lungs inflated.

AIR

Inspiration

Diaphragm

AIR

Expiration

Diaphragm

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Compliance and Resistance Normal lung function depends on the lung’s ability to stretch and then readily return to its normal shape. Compliance is the ability to stretch. Elasticity is the ability to return to normal shape. Abnormalities of compliance and/or elasticity result in alterations in ventilation.

Pulmonary resistance is impedance of airflow in the lung. Resistance is related to lung compliance, diameter and length of the airways, and the turbulence of airflow.

The mechanical parameters of obstruction and restriction can be determined utilizing pulmonary function tests. These determinations reflect the compliance and resistance of the pulmonary system as a whole. However, different areas of the lung normally possess different compliances. In the upright patient, gravitational effects on lung water, lung stretch, and blood flow create lower compliance in the base and higher compliance in the apices. These regional compliances change with patient position as blood and air shift within the chest cavity. Dependent areas will always have higher resistance and non-dependent areas will have increased compliance.

CLINICAL APPLICATION • Atelectasis causes collapse of the alveoli, reducing pulmonary compliance. The

subsequent increase in resistance increases the work of breathing.

• Emphysema results in a loss of elasticity, forcing exhalation to become an active process, which increases the work of breathing.

• Pneumonia increases pulmonary resistance because of decreased compliance and airways narrowed by thick secretions (consolidation), increasing the work of breathing.

CLINICAL APPLICATION The pleural space can hold a large volume of fluid or air in the presence of trauma or disease processes.

• Pneumothorax: accumulation of air in the pleural space causes collapse of lung tissue.

• Hemothorax: accumulation of blood in the pleural space which can be caused by chest trauma.

• Pleural effusion: accumulation of serous fluid in the pleural space which can be caused by the inflammatory process and some cancers.

Regardless of the source, air or fluid in the pleural space will reduce lung function.

CLINICAL APPLICATION Frequent repositioning of patients changes the areas of lung that are dependent, facilitating an overall improvement in pulmonary function.

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Work of Breathing The energy requirement for normal breathing is up to 2% of total oxygen consumption. As the energy requirement increases with pulmonary diseases, the work of breathing increases. Normally, the work of breathing occurs during inhalation. It is the amount of work that is needed to overcome the elastic and resistive properties of the airway and lungs. Any condition that increases airway resistance, affects pulmonary elasticity, or increases the respiratory rate will increase the work of breathing.

Increases in the work of breathing place an increased demand on the ventilatory muscles. Ventilatory muscle strength is affected by age, gender, position, and underlying disease processes (including infection) that affect the cardiac and respiratory system. Electrolyte imbalances, acid-base disturbances, endocrine abnormalities (thyroid disease), and some medications (steroids and neuromuscular blocking agents) may also affect muscle strength. If the demands of breathing exceed the strength of the muscles, ventilatory failure ensues.

Gas Exchange Gas exchange is actually a combination of two separate processes: ventilation and respiration. Ventilation is the process of moving air between the atmosphere and alveoli. Respiration is the diffusion of gas across the alveolar-capillary membrane to maintain proper concentration of oxygen (O2) and carbon dioxide (CO2) in blood.

The alveoli are composed of two types of cells: Type I cells and Type II cells. Type I cells function in gas exchange. They are sensitive to injury, bacteria, and particulates. Type II cells have several functions. They can transform into Type I cells, and they can assist with the transportation of sodium and water across the endothelial membrane to prevent excessive amounts of fluid in the lung. They also produce surfactant, the loss of which can result in alveolar instability, collapse, and impairment of gas exchange.

CLINICAL APPLICATION Patients with well-compensated chronic pulmonary disease may require mechanical ventilation if a sudden increase in work of breathing, like pneumonia, causes their ventilatory muscles to tire out.

CLINICAL APPLICATION Ventilation is measured by the amount of carbon dioxide in the blood. Ventilation (or diffusion) is measured by the amount of oxygen in the blood.

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Pulmonary Vasculature The right ventricle pumps deoxygenated blood to the pulmonary arteries. The pulmonary arteries branch into the pulmonary capillaries, which surround the alveoli for gas and fluid exchange. The capillaries also aid in production and destruction of a broad range of biologically active substances. The blood leaving the capillaries enters into the pulmonary venules, carrying the blood back to the left side of the heart. Distribution of blood flow to the lungs is dependent on posture (upright, prone, or supine), gravity, and patency of the pulmonary circulation.

The bronchial circulation arises from the aorta or intercostal arteries. It provides circulation to the tracheobronchial tree downward to the terminal bronchioles.

The capillaries of the alveolar-capillary membrane form a network around each alveolus. This narrow network allows the hemoglobin to become saturated with oxygen and carbon dioxide to be eliminated.

Diffusion Diffusion is the passive movement of molecules from a region of higher concentration to one of lower concentration. It is the primary mechanism for oxygen and carbon dioxide transport in the body. There are several factors affecting diffusion: thicknesses of the capillary membrane, surface area available for diffusion, and difference in concentration of the two gases. Only the alveoli and respiratory bronchioles participate in gas exchange. The volume of conducting airways that do not participate in gas exchange is called dead space.

Lymphatic System Lymphatic vessels exist throughout the lungs so they may immediately respond to the constant exposure to the environment. They function primarily to remove foreign particles and cell debris, produce antibody and cell-mediated immune responses, remove excess fluid and protein molecules

CLINICAL APPLICATION Mobilization of a deep-vein thrombus results in a pulmonary embolus. Massive pulmonary embolism (when lodged in the respiratory system) are often fatal.

© Ciba Geigy

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that leak out of the capillaries, and keep the alveoli clear. They can clear approximately 700 cc’s of fluid per day.

CLINICAL APPLICATION When more fluid leaks out of the alveolar capillaries than the lymphatic system can clear, interstitial edema results. If enough fluid accumulates, the alveoli will become flooded, producing pulmonary edema.

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Regulation of Ventilation The central nervous system, chemoreceptors, and mechanoreceptors regulate ventilation.

Central nervous system

The muscles of ventilation are coordinated by the central nervous system. The brainstem provides automatic controls for pattern of breathing (rate and depth). The cerebral cortex allows for voluntary ventilation, such as during states of crying, laughing, singing, and talking. The spinal cord also assists by relaying the information from the brain to the muscles of ventilation.

Chemoreceptors

Chemoreceptors are located centrally, peripherally, and within the lung tissue. Central chemoreceptors are located in the brainstem and increase ventilation in response to decreases in pH. Most decreases in pH are due to elevated levels of carbon dioxide. Peripheral chemoreceptors are located in the aortic arch and carotid body. They primarily respond to arterial hypoxemia (decrease in oxygen level) by increasing the rate and depth of ventilation. They can also respond to changes in carbon dioxide levels and hydrogen ion concentration (pH) in the same manner.

Mechanoreceptors

Mechanoreceptors include stretch receptors, irritant receptors, and juxtacapillary receptors. Stretch receptors limit ventilation with increases in lung volume. Irritant receptors respond to stimulation of inhaled irritants by triggering bronchoconstriction and hyperpnea. Juxtacapillary (J) receptors are stimulated by engorgement of pulmonary capillaries and increases in interstitial fluid volume, which triggers rapid, shallow breathing.

Ventilation/Perfusion Relationships When the number of alveoli that are ventilated equals the number of alveoli that are perfused, ventilation and perfusion are equally matched. This is normal. If more alveoli are perfused than are ventilated, a ventilation-perfusion (V/Q) mismatch called shunting results. Pulmonary shunting results from problems that prevent air exchange in the alveoli (e.g. Atelectasis). If more alveoli are ventilated than are perfused, a V/Q mismatch called dead space results. Pathologic pulmonary dead space results from problems that interfere with blood flow to the alveolar capillaries (e.g. pulmonary embolism).

CLINICAL APPLICATION The normal drive for breathing is an elevated level of carbon dioxide sensed by the central chemoreceptors. Patients with chronically elevated carbon dioxide levels (e.g. COPD) lose the ability to regulate ventilation based on carbon dioxide. Instead, they depend on low levels of oxygen to stimulate breathing. This phenomenon is referred to as hypoxic drive. In patients with hypoxic drive, excessive supplemental oxygen may cause respiratory arrest.

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Ventilation/perfusion relationships vary within portions of the lung, but the normal lung has evenly matched ventilation and perfusion on average. In an upright person, ventilation exceeds perfusion in the apices, and perfusion exceeds ventilation in the bases. The middle sections of lung have even V/Q matching. These normal relationships change with changes in body position. Gravity draws blood to the dependent areas of the lung, increasing perfusion relative to ventilation. In contrast, air tends to rise causing increased ventilation relative to perfusion in non-dependent areas. Frequent position changes promote overall V/Q matching for bed-bound patients.

Tissue Oxygenation Data from many sources is required to adequately evaluate tissue oxygenation. Oxygen content, oxygen delivery, and oxygen utilization must all be considered.

The primary determinant of blood oxygen content is the hemoglobin concentration. For example, 100% oxygen saturation with a hemoglobin of 6 gm/dl delivers less oxygen to the tissues than 80% oxygen saturation with a hemoglobin of 12 gm/dl.

Oxygen delivery is dependent on cardiac output and the integrity of the vascular system. Think of the cardiac output as a locomotive that drives the train of hemoglobin boxcars around the track formed by the vascular system. Without invasive hemodynamic monitoring, adequacy of oxygen delivery is estimated by the heart rate, blood pressure, labs, and physical assessment parameters.

Signs of inadequate oxygen delivery and/or tissue oxygenation include: • altered mental status, agitation, confusion, sleepiness, or hallucinations • tachycardia, dysrhythmias, narrow pulse pressure, hypotension (a late sign) • elevated lactate or lactic acid levels • cool, clammy skin with sluggish capillary refill, pallor

Oxygen utilization is the most difficult parameter to measure. If oxygen content and supply are adequate and impaired tissue oxygenation persists, the problem is assumed to be with tissue oxygen utilization. Patients with these problems are usually cared for in a critical care unit where invasive oxygenation parameters can be monitored continuously.

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Oxyhemoglobin Dissociation Curve

The strength with which oxygen binds to the hemoglobin molecule has important clinical implications. If the oxygen binds too loosely, the hemoglobin may give up its oxygen before it reaches the tissues in need. If the oxygen binds too tightly, it may not transfer to the tissues at all. The strength of the oxygen-hemoglobin bond is graphically represented by the oxyhemoglobin dissociation curve.

Shift to the Left Shift to the Right ↑ pH ↓ pH ↓ PCO2 ↑ PCO2 ↓ Temperature ↑ Temperature ↓ DPG, HbF, COHb ↑ DPG (2,3-diphosphoglycerate)

Several variables affect the affinity of the oxygen molecule to hemoglobin. Conditions that cause enhanced release of the oxygen molecule include acidosis, fever, elevated CO2 levels, and increased 2,3-diphosphoglycerate (2,3-DPG, a by-product of glucose metabolism). This change in affinity is called a shift to the right (C waveform). Conditions that keep the oxygen molecule tightly attached to hemoglobin include hypothermia, alkalosis, low PCO2, and decrease in 2,3-DPG. This change is called a shift to the left (B waveform). A shift to the left has more negative implications for the patient than a shift to the right.

The oxyhemoglobin dissociation curve can be used to estimate the PaO2 if the oxygen saturation is known. The illustration demonstrates that if the curve is not shifted (A waveform), an oxygen saturation of 88% is equivalent to a PaO2 of about 60 mm Hg. With a left shift, the same saturation is equivalent to a much lower PaO2.

0 10 20 30 40 50 60 70 80 90 100

100 90 80 70 60 50 40 30 20 10

0

C

PaO2 (mm Hg)

% Hb Saturation

AB

Right Shift

Left Shift

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Evaluation of Pulmonary Function

Physical Evaluation Complete physical evaluation of the pulmonary system includes inspection, palpation, percussion and auscultation. A broad overview of these techniques is presented here, but an exhaustive discussion is beyond the scope of this packet.

Inspection

Inspection includes an overall evaluation of the patient’s appearance as well as a collection of specific information. Four areas to focus on for inspection are: • Tongue/lips – look for central cyanosis (blue, gray, or dark purple discoloration is a sign of

hypoxemia) • Chest wall configuration (size and shape) • Evaluation of respiratory effort (rate, rhythm, symmetry, and quality of ventilatory movement).

Abnormal ventilatory patterns are defined in the table below. • Mental status – agitation and confusion are often early signs of hypoxemia

Abnormal breathing patterns

Tachypnea Rate > 20 breaths per minute Hyperpnea • hyperventilation • Kussmaul’s respirations

Rapid, deep, and labored

Bradypnea Rate < 12 breaths per minute Dyspnea Difficult or labored breathing, shortness of breath Orthopnea Patient must sit or stand to breathe Cheyne-Stokes Episodes of slow, shallow breaths rapidly increasing in depth and rateBiot’s respiration Short burst of uniform, deep respirations, followed by periods of

apnea lasting 10 – 30 seconds indicating elevated intracranial pressures and meningitis

Palpation

Palpation is used to evaluate symmetry of chest expansion, position of anatomical structures and detect vibrations within the thorax. Three areas to focus on for palpation are: • Position of trachea (midline is normal) • Thoracic expansion • Evaluation of fremitus (vibrations felt through the chest when the patient speaks)

Percussion

Percussion is used to identify various densities under the chest wall. The two areas to focus on for percussion are evaluation of underlying lung structures and evaluation of diaphragmatic excursion.

Evaluation of underlying lung structures (identifies air, liquid, or solid material) is performed by percussing over bone, muscle, fluid, or consolidated lung tissue to produce a flat or dull tone. Areas of air-filled tissue produce resonant (tympanic) tones, which are normal over healthy lung tissue. Areas of hyper-inflated tissue produce hyper-resonant tones.

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Evaluation of diaphragmatic excursion is more complex. Emphysema, pneumothorax, pleural effusion, atelectasis, consolidation, phrenic nerve injury and diaphragmatic weakness affect excursion. To evaluate, percuss the posterior chest wall at end-expiration to identify the point at which the resonant tone of the lung changes to the dull tone of the abdominal organs. The patient is then asked to inhale deeply, and the percussion is repeated. The point at which the tone of percussion changes is again noted and compared to the location noted at end-expiration. The amount of distance between the two points represents the distance the diaphragm travels downward during inspiration.

Auscultation

The three areas to focus on for auscultation are evaluation of the presence and location of normal breath sounds, abnormal breath sounds, and voice sounds. Various sounds may be heard during pulmonary evaluation. For further information on breath sounds and samples of the sounds themselves, visit one of the web sites listed in the references section of this packet.

Expiration point

Inspiration point

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Normal Breath Sounds Vesicular Heard over most of lung field; low pitch; soft and short exhalation and

long inhalation Bronchovesicular Heard over main bronchus area and over upper right posterior lung field;

medium pitch; exhalation equals inhalation Bronchial Heard only over trachea; high pitch; loud and long exhalation

Abnormal Breath Sounds Abnormal Sound Description Pathology Absent breath sounds No breath sounds in a portion of

lung (segment or entire lung) Pneumothorax Pneumonectomy Emphysematous blebs Pleural effusion Lung mass Massive atelectasis Complete airway obstruction

Diminished breath sounds Little airflow to portion of lung (segment of lung)

Emphysema Pleural effusion Pleurisy Atelectasis Pulmonary fibrosis

Displaced bronchial or bronchovesicular sounds

Bronchial or bronchovesicular sounds heard in peripheral lung fields

Atelectasis with secretions Lung mass with exudate Pneumonia Pleural effusion Pulmonary edema

Crackles (rales) Short, discrete, popping or crackling sounds

Pulmonary edema Pneumonia Pulmonary fibrosis Atelectasis Bronchiectasis

Rhonchi Coarse, rumbling, low-pitched sounds

Pneumonia Asthma Bronchitis Bronchospasm

Wheezes High-pitched, squeaking, whistling sounds

Asthma Bronchospasm Inflammation

Pleural friction rub Creaking, leathery, loud, dry, coarse sounds

Pleural effusion Pleurisy

Inspiratory stridor Crowing sound Inflammation and edema of the larynx and trachea

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Non-Invasive Diagnostic Monitoring The equipment utilized in non-invasive monitoring provides information that can validate the physical evaluation. Non-invasive monitors can either rest on the skin, or they can sample inspired or expired gases. They can monitor the patient’s status intermittently or continuously. This section will cover apnea monitoring, end-tidal carbon dioxide monitoring, and pulse oximetry.

Apnea Monitoring

Apnea monitoring produces a ventilatory waveform and respiratory rate by measuring the changes in electrical impedance between two electrodes placed on the chest wall. This technique is referred to as impedance pneumography. As air moves in and out of the chest with breathing, the impedance between the electrodes changes, producing the waveform and calculated rate. Apnea monitors detect apnea but do not provide any information on the cause. Apnea monitoring remains useful in monitoring newborns and infants; however, adult apnea monitoring has been replaced by monitoring of pulse oximetry and end-tidal CO2. The primary source of inaccuracy in apnea monitoring is patient movement, which may result in overestimation of the respiratory rate.

Capnography

Capnography (end-tidal CO2 monitoring) is a measurement of carbon dioxide in exhaled air. It may also be referred to as partial pressure end tidal carbon dioxide monitoring (PETCO2). The end-tidal CO2 (EtCO2) level is a reflection of global CO2 production in the body. Cardiac function, pulmonary function, and metabolic rate all influence the amounts of CO2 produced. The end-tidal CO2 provides information on systemic CO2 production (from exhaled alveolar gas), pathologic dead space, pulmonary blood flow, and confirmation of endotracheal tube placement. Capnography allows trending of CO2 levels using fewer arterial blood gas analyses, but does not completely replace arterial blood gas analysis. Age, smoking, general anesthesia, and systemic diseases can increase the difference between the CO2 value obtained from non-invasive monitoring and arterial blood gas monitoring. Note that capnography measures ventilation, not oxygenation.

There are three types of capnography equipment: mainstream, traditional sidestream, and Microstream. Mainstream and sidestream are utilized in mechanical ventilation and will not be discussed in this packet. Microstream is the newest capnograph equipment available. It can be used on patients without an artificial airway who are using nasal cannula-like devices.

Normal Values • ETCO2 or PETCO2 (end tidal) ~ 38

mm Hg (usually 1 – 6 mm Hg less than PaCO2)

• PaCO2 = 35 – 45 mm Hg • SPaO2 > 92% (normal 95%)

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Interpretation of End-tidal CO2 Waveforms Accurate interpretation of the end-tidal CO2 measurement depends on accurate waveform interpretation. The end-tidal CO2 (EtCO2) waveform has several components. The vertical axis represents the exhaled CO2 level. The horizontal axis represents time. The normal waveform begins at the start of exhalation as the air contained in the tracheal and large airways is exhaled. This portion of the waveform stays at the zero baseline because this volume of gas did not participate in gas exchange. As exhalation continues and alveolar air begins to mix with air from the large airways, a rapid sharp rise is noted on the waveform. The alveolar plateau then appears, which represents exhalation of mostly alveolar gas. The numeric end-tidal CO2 measurement is obtained at the end of this plateau. Inhalation then produces a rapid, sharp drop in the waveform until it returns to zero, when the cycle repeats itself.

Some physiologic abnormalities cause distinctive changes in the EtCO2 waveform. Some of the most common ones are illustrated here.

Normal Waveform A-B: A near zero baseline—Exhalation of CO2-free gas contained in dead space.

B-C: Rapid, sharp rise—Exhalation of mixed dead space and alveolar gas.

C-D: Alveolar plateau—Exhalation of mostly alveolar gas.

D: End-tidal value—Peak CO2 concentration—normally at the end of exhalation.

D-E: Rapid, sharp downstroke—Inhalation Copyright Oridion Systems Ltd.

Sustained low EtCO2 with good alveolar plateau Possible causes:

• Hyperventilation • Hypothermia • Sedation, anesthesia • Dead space ventilation

Copyright Oridion Systems Ltd.

Elevated ETCO2 with good alveolar plateau Possible causes:

• Inadequate minute ventilation/hypoventilation • Respiratory-depressant drugs • Hyperthermia, pain, shivering


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.

When deterioration from the patient’s baseline is noted, the following interventions should be performed: • check the patient for airway, breathing and circulation • stimulate the patient • consider withholding additional sedating medication • inform the physician in charge • if a procedure is in progress, stop the procedure • administer a reversal agent, if necessary

For more detailed information, please visit the following web site: www.capnography.com

Possible causes: • Cardiopulmonary arrest • Pulmonary embolism • Sudden hypotension; massive blood loss • Cardiopulmonary bypass

Exponential decrease in ETCO2


Gradually increasing ETCO2 Possible causes: • Hypoventilation • Rising body temperature/malignant hyperthermia • Increased metabolism • Partial airway obstruction • Absorption of CO2 from exogenous source Copyright Oridion Systems Ltd.

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Pulse Oximetry

Pulse oximetry (SpO2) is a measurement of the percentage of hemoglobin saturated with oxygen in the peripheral tissues. The monitor measures this percentage by passing red and infrared light from a light-emitting diode through a pulsatile tissue bed (usually a nailbed) to a sensor. It then calculates how much light is received by the sensor to determine the SpO2. The normal SpO2 is 95%. SpO2 is a different measurement than arterial oxygen saturation (SaO2). The SpO2 is typically 2 – 5% different than the SaO2. Pulse oximetry is a measure of oxygenation, but a normal SpO2 does not guarantee adequate oxygen supply to the tissues.

The infrared sensor measures the oxygen saturation of the pulsating blood (produced by heart rate) and produces the waveform. The pulse rate is measured by detecting the point at which the signal crosses a pre-determined threshold. If the waveform does not cross the threshold, a pulse rate of zero will be displayed on the monitor. The SpO2 reading itself is taken from the peak of the waveform. The SpO2 can be trended to assist with evaluation of the respiratory system, as long as there are no limiting factors affecting the value.

CLINICAL APPLICATION An anemic patient with a hemoglobin of 6 g/dL may have a low tissue oxygenation even if the pulse oximeter reads 99%.

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There are multiple sources of inaccuracy in SpO2 measurement. Inaccurate readings may result from: poor tissue perfusion, vasoconstriction, abnormal hemoglobin, pulse rate and rhythm, incorrect placement of the probe, excessive patient motion, ambient light, shivering, skin pigment, vascular dyes, thick nails (onychomycosis) or artificial nails and dark nail polish.

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As part of troubleshooting the measured value, it is important to correlate the waveform to the displayed oxygen saturation. The patient must be evaluated for effective ventilation: rate and depth. Clinical evaluation must be utilized as there may be a delay (~5 – 20 seconds) in fall of the displayed numerical value of oxygen saturation.

Examples of potential waveforms Noise Artifact: caused by ambient light, shivering

Low Perfusion: caused by hypotension, hypothermia, probe off finger, nail polish, vasoconstriction

Motion Artifact

Alarms:

DO NOT adjust an alarm setting lower just to stop its sound. It could be telling you something important. Any alarm requires a complete investigation. If the low oxygen saturation alarm sounds, check the patient’s level of consciousness (if appropriate), maintain airway appropriately, and monitor and treat breathing if necessary. If the pulse not detected alarm sounds, observe the waveform displayed and check the patient for a pulse. If no pulse, call for help and initiate BLS and ACLS when available. If there is a pulse, reposition the probe.

CLINICAL APPLICATION Patients with carbon monoxide poisoning have SpO2 readings of 100%. The carboxyhemoglobin complex reflects light in the same manner as oxyhemoglobin. Pulse oximetry cannot be used to gauge oxygenation in these patients.

For example: patients who smoke within the last four hours may not have an accurate oxygenation level.

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Comparison of Capnography and Pulse Oximetry Capnography Pulse Oximetry Measures CO2 Measures oxygen saturation Reflects ventilation Reflects oxygenation Hypoventilation / apnea detected immediately Changes lag with hypoventilation / apnea Should be used with pulse oximeter Should be used with capnography

Capnography and pulse oximetry used together with physical evaluation findings can provide an enhanced picture of the patient’s respiratory status. Other non-invasive monitoring techniques that are included in the evaluation findings are mental status, skin temperature, heart rate, and urine output. For more information on these and other monitoring techniques, consult the reference list.

Invasive Diagnostic Monitoring (Arterial Blood Gases) The primary invasive technique for monitoring respiratory function is the arterial blood gas (ABG). ABGs can identify acid-base disturbances as well as oxygen and carbon dioxide levels. It is important to relate the patient’s diagnosis, history and current clinical findings with the ABG for accurate interpretation. A complete discussion of ABG analysis is beyond the scope of this packet.

The ABG analysis includes measurement of hydrogen ion concentration (pH), partial pressure of arterial carbon dioxide (PaCO2), partial pressure of arterial oxygen (PaO2), and a calculated bicarbonate (HCO3), and base excess (BE). These measurements are used in combination to diagnose acid-base disorders and hypoxemia. The table on the following page lists common acid-base disorders with their values.

Normal values for arterial and venous samples:

pH PaCO2 PaO2 HCO3

(calculated) Base Excess

(calculated)

02 Sat

Arterial 7.35 – 7.45 35-45 80 – 100 22 – 26 -2 TO +2 mEq/Liter

95%

Venous 7.31 – 7.41 44 – 55 35 – 40 22 – 26 70 – 75%

Hypoxemia

The following table reviews alterations in arterial blood gases. Note that the PaO2 is not used in determining the acid-base disorders present on an ABG. The PaO2 measurement is used solely to determine the partial pressure of oxygen in the patient’s blood – the level of hypoxemia. Remember that the PaO2 measures gas exchange or diffusion. The normal PaO2 is greater than 80 mm Hg. Hypoxemia is defined as a PaO2 of < 80 mm Hg. If the patient is not ventilating appropriately, hypoxemia can often be corrected with administration of supplemental oxygen. If hypoxemia persists despite supplemental oxygen and adequate ventilation, a problem at the level of the alveolar-capillary membrane is most likely the cause. In such an instance, the hypoxemia will not resolve until the underlying pathology has been corrected.

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Alterations in Arterial Blood Gasses

pH PaCO2 PaO2 HCO3 Base Excess

02 Sat

Respiratory Acidosis ↓ ↑ Normal

Respiratory Alkalosis ↑ ↓ Normal

Metabolic Acidosis ↓ Normal ↓ Negative

Metabolic Alkalosis ↑ Normal ↑ Positive

Compensated Respiratory Acidosis

7.35 - 7.40 ↑ ↑

Compensated Respiratory Alkalosis

7.40 - 7.45 ↓ ↓

Compensated Metabolic Acidosis

7.35 - 7.40 ↓ ↓

Compensated Metabolic Alkalosis

7.40 - 7.45 ↑ ↑

Respiratory Acidosis

Respiratory acidosis is defined as a pH less than 7.35 with a PaCO2 greater than 45 mm Hg. Acidosis is caused by an accumulation of CO2 which combines with water in the body to produce carbonic acid; thus, lowering the pH of the blood. Any condition that results in hypoventilation can cause respiratory acidosis. These conditions include: • Central nervous system depression related to head injury • Central nervous system depression related to medications such as narcotics, sedatives, or

anesthesia • Impaired respiratory muscle function related to spinal cord injury, neuromuscular diseases, or

neuromuscular blocking drugs • Pulmonary disorders such as atelectasis, pneumonia, pneumothorax, pulmonary edema, or

bronchial obstruction • Massive pulmonary embolus • Hypoventilation due to pain, chest wall injury/deformity, or abdominal distension

The signs and symptoms of respiratory acidosis are centered within the pulmonary, nervous, and cardiovascular symptoms. Pulmonary symptoms include dyspnea and respiratory distress. Nervous system manifestations include headache, restlessness, and confusion. If CO2 levels become extremely high, drowsiness and unresponsiveness may be noted. Cardiovascular symptoms include tachycardia and dysrhythmias.

Increasing ventilation will correct respiratory acidosis. The method for achieving this will vary with the cause of hypoventilation. If the patient is unstable, manual ventilation with a bag-valve-

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mask (BVM) is indicated until the underlying problem can be addressed. After stabilization, rapidly resolvable causes are addressed immediately. Causes that can be treated rapidly include pneumothorax, pain, and CNS depression related to medications. If the cause cannot be readily resolved, the patient may require mechanical ventilation while treatment is rendered. Although patients with hypoventilation often require supplemental oxygen, it is important to remember that oxygen alone will not correct the problem.

Respiratory Alkalosis

Respiratory alkalosis is defined as a pH greater than 7.45 with a PaCO2 less than 35 mm Hg. Any condition that causes hyperventilation can result in respiratory alkalosis. These conditions include: • Hypoxemia (i.e. early stages of pneumonia) • Psychologically mediated responses, such as anxiety or fear • Pain • Increased metabolic demands, such as fever, sepsis, pregnancy, or thyrotoxicosis • Medications, such as salicylates • Central nervous system lesions

Signs and symptoms of respiratory alkalosis are largely associated with the nervous and cardiovascular systems. Nervous system alterations include light-headedness, paresthesias, confusion, inability to concentrate, and blurred vision. Cardiac symptoms include dysrhythmias and palpitations. Additionally, the patient may experience dry mouth, diaphoresis, and tetanic spasms of the arms and legs. Treatment of respiratory alkalosis centers on resolving the underlying problem. Patients presenting with respiratory alkalosis have dramatically increased work of breathing and must be monitored closely for respiratory muscle fatigue. When the respiratory muscles become exhausted, acute ventilatory failure may ensue.

Metabolic Acidosis

Metabolic acidosis is defined as a bicarbonate of less than 22 mEq/L with a pH of less than 7.35. Metabolic acidosis is caused by either a deficit of base in the bloodstream or an excess of acids, other than CO2.. Decreased levels of base are caused by diarrhea and intestinal fistulas. Causes of increased acids include: • Renal failure • Diabetic ketoacidosis • Anaerobic metabolism (lactic acidosis) • Starvation • Salicylate intoxication

Symptoms of metabolic acidosis center around the central nervous system, cardiovascular, respiratory, and the GI system. Nervous system manifestations include headache, confusion, and restlessness progressing to lethargy, then stupor or coma. Cardiac dysrhythmias are common and Kussmaul respirations occur in an effort to compensate for the pH by blowing off more CO2. Warm, flushed skin, nausea, and vomiting are also commonly noted.

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As with most acid-base imbalances, the treatment of metabolic acidosis is dependent upon the cause. The presence of metabolic acidosis should spur a search for hypoxic tissue somewhere in the body. Hypoxemia can lead to anaerobic metabolism system-wide, but hypoxia of any tissue bed will produce metabolic acids as a result of anaerobic metabolism even if the PaO2 is normal. The only appropriate way to treat this source of acidosis is to restore tissue perfusion to the hypoxic tissues. Other causes of metabolic acidosis should be considered after the possibility of tissue hypoxia has been addressed.

Current research has shown that the use of sodium bicarbonate is indicated only for known bicarbonate-responsive acidosis, such as that seen with renal failure. Routine use of sodium bicarbonate to treat metabolic acidosis results in subsequent metabolic alkalosis with hypernatremia and should be avoided.

Metabolic Alkalosis

Metabolic alkalosis is defined as a bicarbonate level greater than 26 mEq per liter with a pH greater than 7.45. Metabolic alkalosis can be caused by either an excess of base or a loss of acid within the body. Excess base occurs from ingestion of antacids, excess use of bicarbonate, or use of lactate in dialysis. Loss of acids can occur secondary to protracted vomiting, gastric suction, hypochloremia, excess administration of diuretics, or high levels of aldosterone.

Symptoms of metabolic alkalosis are mainly neurological and musculoskeletal. Neurologic symptoms include dizziness, lethargy, disorientation, seizures and coma. Musculoskeletal symptoms include weakness, muscle twitching, muscle cramps and tetany. The patient may also experience nausea, vomiting, and respiratory depression.

Metabolic alkalosis is one of the most difficult acid-base imbalances to treat. Bicarbonate secretion through the kidneys can be stimulated with Diamox but resolution of the imbalance will be slow. In severe cases, IV administration of acids may be used. It is significant to note that metabolic alkalosis in hospitalized patients is usually iatrogenic in nature.

CLINICAL APPLICATION Acute respiratory Distress Syndrome (ARDS) is a condition in which the alveolar capillary membrane becomes leaky and the alveoli fill with fluid. Patients with ARDS initially present with respiratory alkalosis and hypoxemia that is refractory to 100% oxygen. The respiratory alkalosis results from compensatory tachypnea caused by the hypoxemia. ARDS patients often require invasive mechanical ventilation until the underlying capillary abnormality has resolved.

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Acute Respiratory Compromise It is essential to recognize the signs of respiratory compromise. The three sources of respiratory decompensation are inadequate airway, inadequate ventilation, and inadequate gas exchange. It is important to understand that these often overlap. An inadequate airway, for example, will produce inadequate ventilation and gas exchange as well if not resolved rapidly. If symptoms of respiratory distress and decompensation are not promptly addressed, acute respiratory failure and death can follow.

Priority Setting The first priority is always the establishment and maintenance of a patent airway. Second, ventilation (breathing) must be established or optimized. After these two interventions are carried out, primary problems with gas exchange can be diagnosed and treated. All other respiratory interventions are secondary to these three.

Inadequate Airway

An inadequate airway can be fatal if not treated promptly. Opening the airway is the number one patient care priority for patients who cannot maintain an open airway independently. Without a patent airway, the patient will die regardless of any other therapeutic measures.

Interventions to maintain an open airway include: • Positioning – head-tilt, chin-lift or jaw-thrust maneuvers (for patients with suspected cervical

injury) • Artificial airways – oropharyngeal and nasopharyngeal airways, endotracheal and tracheostomy

tubes, esophageal obturators, and laryngeal mask airways

Airway maintenance techniques are taught in basic and advanced life support courses. Refer to your hospital’s policies for the use of these techniques and devices.

Signs and Symptoms of Inadequate Airway: • Stridor • Noisy respirations • Supraclavilcular and intercostal retractions • Flaring of nares • Labored breathing with use of accessory

muscles

CLINICAL APPLICATION The most common source of airway obstruction in unconscious adults is the tongue. Correct positioning of the head and/or use of an oropharyngeal or nasopharyngeal airway are effective interventions.

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Signs and Symptoms of Inadequate Gas Exchange: • Tachypnea • Decreased PaO2 • Increased dead space • Central cyanosis • Chest infiltrates on X-ray evaluation • Decreased SpO2

Inadequate Ventilation

Inadequate ventilation may exist even when the airway is patent. Remember that ventilation is the movement of air in and out of the lungs. Inadequate ventilation is not the same as absence of breathing. Respiratory rates less than ten or greater than thirty are frequently associated with inadequate ventilation. Interventions to restore adequate ventilation depend on the cause. Supplemental oxygen alone will not help a patient with inadequate ventilation. If the patient is acutely decompensating, the bag-valve-mask (BVM) can be used to augment ventilation until definitive treatment can begin. The BVM is a complex device to learn. Use of the BVM is taught in basic and advanced life support courses.

Potential causes of inadequate ventilation include: • Inadequate airway • Problems with nerve transmission and/or muscle strength causing inadequate ventilation due to

spinal cord injury, neuromuscular diseases, respiratory muscle fatigue, or neuromuscular blocking medications

• Increased pulmonary resistance causing inadequate ventilation due to bronchospasm, pain, decreased pulmonary compliance, and restricted chest wall movement

• Depressed respiratory drive causing inadequate ventilation due to central nervous system dysfunction, overdoses of sedatives or narcotics, and elimination of hypoxic drive.

Inadequate Gas Exchange

Inadequate gas exchange will result from airway and ventilation problems, but may exist independently. Any process that interferes with the function of the alveolar-capillary membrane will impair gas exchange. Examples of such pathologies include acute respiratory distress syndrome (ARDS), pneumonia, pulmonary edema, and pulmonary fibrosis.

Patients with inadequate gas exchange will remain hypoxic despite an adequate airway and optimized ventilation. Hypoxemia due to poor gas exchange will be refractory to supplemental oxygen until the underlying cause is resolved. Treatment of patients with inadequate gas exchange is directed toward correction of the underlying cause.

Signs and Symptoms of Inadequate Ventilation: • Absence of air exchange at nose and mouth • Minimal/absent chest wall motion • Manifestations of obstructed airway • Central cyanosis • Decreased or absent breath sounds (bilateral,

unilateral) • Restlessness, anxiety, confusion • Paradoxical motion involving a significant

portion of chest wall • Decreased PaO2, increased PaCO2, decreased pH

CLINICAL APPLICATION Cardiogenic pulmonary edema fills the alveoli with fluid, limiting gas exchange. Although supplemental oxygen is given, the definitive treatment is to increase fluid excretion and improve cardiac function.

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Interventions to Promote Respiratory Function Many therapeutic techniques exist to maintain and improve pulmonary function. Several of these techniques are detailed below. The choice of intervention will be made through collaboration among the nurse, respiratory therapist, and physician. No matter which interventions are chosen, the nurse and/or respiratory therapist will be responsible for evaluating and documenting the patient’s response during and after treatment.

Therapeutic Interventions

Pursed-lip breathing

Pursed-lip breathing is used to facilitate complete exhalation in patients with obstructive pulmonary diseases like COPD or emphysema. This technique can be used to reduce air-trapping and dyspnea during periods of stress.

Teach the patient to assume a position of comfort before beginning. Instruct the patient to inhale and pause, then exhale slowly through pursed lips, as if blowing. Pursed-lip breathing is a slow, controlled technique and will be ineffective if performed rapidly. Document the patient’s understanding and ability to perform the technique.

Deep breathing and coughing

Deep breathing and coughing are used to facilitate re-expansion of collapsed alveoli (atelectatic lungs) following surgery or injury. It is an essential component of pulmonary toilet for any patient at risk for atelectasis and subsequent pneumonia. Deep breathing and coughing exercises are most effective when timed to follow peak effectiveness of pain medications. Patients with thoracic or abdominal incisions will be able to cough more strongly and with less pain if they hold a pillow or towel snugly against their incision before they begin the cough.

To teach deep breathing and coughing, instruct the patient to assume a position of comfort. An upright position will enhance full expansion of the lung bases. Instruct the patient to take several deep breaths, holding each one to a slow count of five at peak inspiration. If a spontaneous cough has not occurred following these breaths, instruct the patient to cough deeply from the diaphragm. Tell the patient that it is not always necessary to clear sputum with coughing; pulmonary benefit is achieved whether the cough is productive or not. Document the quantity, color, odor, and consistency of any sputum produced and the strength of the patient’s cough effort.

Incentive Spirometry

Incentive spirometry is used as an adjunct to deep breathing and coughing. Use of the incentive spirometer gives patients and clinicians visual feedback on the volume of air inspired and the quality of the patient’s technique.

Proper use of the incentive spirometer begins with the patient assuming a position of comfort. An upright posture will facilitate complete lung expansion. Instruct the patient to form a seal around the mouthpiece with the lips and to inhale slowly through the mouth. If the patient has difficulty isolating inhalation to the mouth, a nose clip may be used.

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The goal of incentive spirometry is for the patient to achieve a volume of approximately 10 ml/kg if there is no underlying pulmonary disease. This volume target may need to be decreased for patients with pulmonary dysfunction. A properly drawn breath will be slow and steady; most incentive spirometers have an indicator to gauge proper speed. Instruct the patient to rest briefly between every third breath to avoid fatigue and hyperventilation. Generally, incentive spirometry should be performed with a frequency of ten breaths every two hours while awake. Hourly incentive spirometry exercises may be indicated for postoperative patients, those with diagnosed significant atelectasis, or deterioration of pulmonary evaluation findings. Each time incentive spirometry is performed, document the volume achieved by the patient, the number of repetitions performed, and the patient’s tolerance of the procedure.

Peak Expiratory Flow Monitoring

Peak expiratory flow (PEF) monitoring is a technique used to provide objective data on airway obstruction for patients with asthma. Baseline expiratory flow readings are taken during periods of optimal symptom management to define a “personal best” PEF. The personal best readings are then compared against those taken during exacerbations of disease to establish relative severity and the effectiveness of therapeutic interventions.

To perform a PEF measurement, the patient should be instructed to use her own PEF monitor. Readings taken on different devices cannot be accurately compared. Three measurements are taken and the best of the three is recorded. Accuracy of a PEF measurement is dependent on technique. If the patient is unable to inhale fully and exhale forcefully into the device, the result will be inaccurate. Due to this diminished reliability, PEF measurements are not generally used during severe exacerbations of pulmonary disease.

Abdominal/Diaphragmatic Breathing

Abdominal and diaphragmatic breathing is utilized for patients with chronic and acute obstructive ventilatory disorders, as well as patients with spinal cord injury. It is a combination of deep breathing and pursed-lip exhalation with the use of a pillow to facilitate full exhalation.

To instruct the patient in this technique, first have him assume a position of comfort. An upright position will facilitate lung expansion. The patient holds a pillow over the abdomen and is instructed to inhale slowly, pushing the diaphragm down. When performed correctly, the breath will result in the relaxed abdominal muscles bulging outward; the patient should feel a displacement of the pillow. The patient should pause after inhalation, then exhale using the pursed lip technique previously described while hugging the pillow firmly against the abdomen.

Postural Drainage, Percussion, and Vibration

Postural drainage, percussion, and vibration are techniques used to aid in clearance of pulmonary secretions when patients cannot clear them independently. These techniques are most commonly used for chronic management of cystic fibrosis, bronchiectasis, and severe atelectasis. Percussion and vibration are contraindicated in the presence of hemoptysis, bleeding disorders, rib fractures or a predisposition to pathologic fractures, and in patients who do not tolerate the head-down position. Some patients respond to this technique with increased dyspnea and wheezing; in this event, the treatment should be stopped, and the physician notified.

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To perform postural drainage, the patient will be positioned to facilitate drainage from the target area of lung. An exhaustive discussion of all positions is beyond the scope of this packet. Refer to your hospital’s policies or one of the references at the end of this packet for further information. Once the desired position is achieved, it is held for five minutes, and the patient is instructed to cough. If clearance of secretions is not achieved, percussion and vibration may be added. Percussion and vibration should be done only over the ribs. Avoid the sternum, vertebral processes, and tissues below the ribs to prevent patient injury. To perform percussion, the hands are held in a cupped position and clapped quickly and firmly against the patient’s ribs over the area to be drained for a period of one to three minutes. Vibration follows percussion using the flattened hands in the same manner over the same area for a period of two to three breaths. Document the positions used, length of treatment, patient’s tolerance of treatment, and the character and quantity of any sputum produced.

High-Frequency Chest Oscillation

This technique replaces postural drainage with percussion and vibration in appropriate patients. High-frequency chest oscillation utilizes a special vest attached to a mechanical device that produces high-frequency vibration applied to the chest wall.

To use the device, place the patient in a sitting position and apply the vest. Cycle through all the ordered frequencies. To aid in clearing secretions, ask the patient to cough after each change in frequency. The entire treatment requires about fifteen minutes to complete.

Flutter Valve

The flutter valve is a small hand-held device used to loosen and mobilize secretions in patients with cystic fibrosis and bronchiectasis.

To use the flutter valve, the patient is instructed to assume an upright position and inhale deeply. After inhalation, the breath is held briefly, and the patient then exhales through the flutter valve. When performed correctly, exhaling through the valve will produce a feeling of vibration in the patient’s chest. This vibration should stimulate a spontaneous cough.

Acapella ™

The Acapella ™ positive expiratory therapy system is similar to a flutter valve. The basic instructions for use are the same, except that the patient using the Acapella ™ can be in any position. Additional advantages of the Acapella ™ are adjustable resistance, couplers for use with a mask, capability to use the device while an aerosol treatment is in progress, and two sizes for varying clinical needs.

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The blue Acapella ™ is used for children and patients with COPD. The green Acapella ™ is used for all other clinical needs. Set the dial to the lowest resistance for the first use. This is accomplished by turning the dial on the blunt end fully counter-clockwise. The patient should be able to exhale for 3 – 4 seconds through the device. If the patient cannot manage this, turn the dial clockwise to increase the resistance. Increased resistance allows the patient to exhale at a slower pace.

Orotracheal & Nasotracheal Suctioning (Refer to your hospital’s Patient Care Policy)

Suctioning is indicated for signs of respiratory distress with noisy wet breathing, rhonchi ,and ineffective cough effort. Suctioning is contraindicated if the patient has bronchospasm or croup associated with wheezing.

To perform suctioning, familiarize yourself with your hospital’s policies and procedures. Suctioning produces intense discomfort and anxiety for the patient. Explain that being suctioned “takes your breath away” momentarily. Reassure the patient that you will be monitoring their oxygenation status closely during the procedure and explain the precautions taken to assure their safety. Document the instruction provided.

Although policies may vary, the following are some general principles for suctioning. Place the patient in semi-Fowler’s position. Prepare a sterile field for your equipment, and maintain sterile technique during the procedure. If the patient is uncooperative, it may be helpful to have a second clinician in the room during suctioning. Select an appropriate catheter. Hyperoxygenate the patient before suctioning by applying supplemental oxygen and ask the patient to take several slow, deep breaths. Keep the oxygen mask or cannula in place throughout the procedure. Don sterile gloves. Lubricate the catheter liberally with sterile water-soluble lubricant jelly, and advance it to the trachea via either the mouth or nose. DO NOT apply suction during insertion of the catheter. Ask the patient to cough when the tip of the catheter reaches the epiglottic area to facilitate passage of the catheter into the trachea. Pass the catheter into the trachea, but avoid passing the catheter until resistance is felt, as this causes injury to the trachea. Apply suction for 5-10 second intervals while simultaneously rotating and withdrawing the catheter. Monitor oxygen saturation and heart rate during each pass and maintain SpO2 > 90% or at baseline. Document the characteristics of any sputum obtained and the patient’s tolerance of the procedure.

Oxygen

All tissues in the body require oxygen and will suffer damage if deprived for more than a few minutes. Though oxygen is in the air around us, supplemental oxygen is classified as a medication. Like any other medication, it has specific indications, precautions, and side effects associated with its use.

Indications for supplemental oxygen include cardiac or respiratory arrest, chest pain, and diagnosed or suspected hypoxemia. The threshold for hypoxemia in most patients is a PaO2 < 55 mm Hg or an SaO2 < 90%. If pulmonary hypertension, cor pulmonale, or mental status changes are present or if the patient has heart disease, oxygen should be administered when the PaO2 is less than 60 mm Hg.

If the ambient air is low in oxygen, then provision of oxygen is a corrective intervention. In all other cases, oxygen administration is a supportive therapy; it either buys time for the patient until the primary pathologic process can be resolved, or it aids in symptom management for chronic disease. Any patient in respiratory or cardiac arrest must receive 100% oxygen via a bag-valve-mask (BVM) device. For all other patients, the lowest effective concentration of oxygen will be administered.

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A complete discussion of all methods of oxygen administration is beyond the scope of this packet. In general, oxygen is non-invasively administered using either low-flow or high-flow delivery systems. Low-flow systems include nasal cannulas, simple face masks, partial rebreathing masks, and non-rebreathing masks. High-flow systems are capable of more precise control of the percentage of oxygen delivered to the patient. They include Venturi and aerosol face masks. For either high or low flow systems to be effective, the patient must be capable of moving sufficient volume in and out of the lungs with each breath. If the patient cannot do this, mechanical ventilation is required.

Oxygen toxicity is a very real threat to patients receiving greater than 50% oxygen for periods longer than 24 hours. Oxygen toxicity can cause cellular damage to the lung tissue that leads to pulmonary fibrosis. Other negative effects of oxygen include: • Accidental fires and burns • Dryness of the mucous membranes • Blindness (in premature infants) • Atelectasis

Oral Care

Oral care is a key component of nursing care. It is a primary intervention for patient comfort and the removal of dental plaque. Dental plaque is a reservoir for pathogens in the oropharynx. The most common bacteria colonized related to respiratory infections are methicillin-resistant Staphylococcus and Pseudomonas species. The toothbrush is the most effective way to remove plaque. All patients require frequent routine toothbrushing to reduce oropharyngeal pathogens and stimulate the gums.

Oral hygiene products, other than the toothbrush, are not effective at removing plaque and may cause complications. Hydrogen peroxide solutions remove debris but concentrated solutions can cause superficial burns. Lemon and glycerin swabs are acidic and cause irritation and decalcification of the teeth. Foam swabs stimulate the mucosal tissues, but do not remove plaque.

Oxygen can cause respiratory depression in patients with chronically elevated blood levels of carbon dioxide. This depression of the hypoxic drive to breathe can result in ventilatory failure. Administration of oxygen to these patients must be undertaken with extreme care.

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Nutrition

Adequate nutrition is essential for patients with pulmonary compromise. Mechanisms of malnutrition include insufficient intake, improper absorption and distribution, or accelerated consumption of nutrients. Patients with pulmonary disease also may have difficulty eating due to shortness of breath and activity intolerance.

Protein-calorie malnutrition is commonly found in hospitalized patients. Insufficient protein intake results in muscle wasting and ventilatory muscle weakness. Excessive intake of carbohydrates produces an excess of carbon dioxide that increases demands on the respiratory system.

Nutritional evaluation is based on four categories: anthropometric measurements (body mass index), laboratory data, physical exam, and diet and health history.

Body mass index evaluates weight in relation to height. It is measured by dividing the weight in pounds by the height in inches squared. It can also be measured by dividing the weight in kilograms by the height in meters squared.

The general guidelines for BMI are as follows: BMI < 18.5 = underweight BMI range 18.5 – 24.9 = desirable BMI range 25 – 29.9 = overweight BMI > 30 = obese

The use of the BMI as a nutritional indicator can cause problems. Overweight and obese patients require just as much nutrition during periods of illness as patients with normal body weight. Therefore, do not withhold nutrition based on a high BMI.

Laboratory values used to evaluate nutrition include serum albumin or prealbumin, serum creatine, complete blood count, triglycerides, calcium, phosphorus, magnesium, and urine –24-hr BUN.

Anemia: Normocytic ( MCV, MCHC) Common with protein deficiency

Anemia: Microcytic (↓ MCV, MCH, MCHC) Indicative of iron deficiency or blood loss

Anemia: Macrocytic (↑ MCV) Common in folate and vitamin B12 deficiency

Lymphocytopenia Common in protein deficiency

Enteral nutrition should be initiated within 24 hours if the patient is unable to adequately meet the nutritional requirements. If enteral feeding is contraindicated, parenteral feeding may be chosen. Refer to your hospital’s guidelines for further information.

Inadequate intake can be caused by alcohol abuse, anorexia, prolonged nausea, vomiting, confusion, coma, poor dentition, and poverty.

Inadequate digestion or absorption can be caused by previous GI surgeries, medications such as antacids, H2 receptor antagonists, cholestyramine, and anticonvulsants.

Increased nutrient loss can be caused by blood loss, severe diarrhea, fistulas, draining abscesses, wounds, decubitus ulcers, peritoneal dialysis or hemodialysis, and corticosteroid therapy.

Increased nutrient requirements can be caused by fever, surgery, trauma, burns, infection, some types of cancer, and physiologic demands, such as pregnancy, lactation, or growth.

BMI = weightheight x height

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Pulmonary Pharmacology Many drugs produce physiologic changes in the lungs. Bronchodilators, mucolytics, and anti-inflammatories will be discussed here; for information on other types of respiratory medications, refer to the reference list at the end of this packet.

Each of the medications works in a different way. Bronchodilators increase the diameter of the conducting airways by reducing bronchial smooth muscle tone. Mucolytics alter the quantity and character of bronchial secretions. Anti-inflammatories reduce airway inflammation, secondarily increasing airway diameter and decreasing secretions. Dosages and frequencies of all these drugs depend on the patient's age, disease being treated, severity of pulmonary compromise, and presence of underlying disease processes. For information on dosing any of the drugs discussed in this packet, refer to a current drug handbook or your clinical pharmacist.

Most respiratory drugs are delivered via the inhaled or oral routes. A few drugs may be administered as IV infusions, but these are less common. Inhaled drugs have several unique advantages for patients with respiratory disease. Inhaled drugs allow high concentrations of medications to be delivered directly to the lung and airway tissues with minimal systemic side effects. Because the drugs are delivered directly to the affected tissue, time of onset for inhaled drugs is much faster than that for drugs delivered via the oral or intravenous routes.

The effectiveness of inhaled medications is dependent upon proper administration technique. The most common delivery device for inhaled medication is the metered dose inhaler (MDI). If an MDI is utilized, a spacer should be used to reduce the amount of medication deposited on the oral mucosa and oropharynx. Use of an MDI requires that the patient be able to coordinate inhalation and breath-holding with delivery of the medication. If the patient is unable to coordinate breathing to this degree, a nebulizer may be a better choice.

Patients are not the only people who have difficulty properly administering an MDI; the process also frequently challenges medical professionals. Here are the correct steps for administration of medication via an MDI with a spacer.

Instruct and/or assist the patient to: 1. Shake the inhaler and remove the cap 2. Assemble the inhaler and the spacer according

to the directions supplied with the spacer 3. Fully exhale 4. Inhale deeply and slowly through the spacer

as the canister is pressed 5. Hold the full inhalation for 10 to 15 seconds 6. Exhale back into the spacer, then inhale again

without pressing the canister 7. Exhale into room air 8. Wait 30 – 60 seconds and repeat the process for each puff prescribed 9. If the inhaler contains a steroid, rinse mouth with water. Do not swallow the water. This will

help prevent oral thrush. 10. Thoroughly rinse and dry equipment after each use.

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Bronchodilators

There are three major classes of bronchodilators: beta-adrenergic agonists, anticholinergics, and methylxanthines. The most common and effective bronchodilator medications are inhaled beta-adrenergic agonists. Stimulation of the beta-2 adrenergic receptor stimulates relaxation of bronchial smooth muscle and subsequent increases in airway diameter. Anticholinergic bronchodilators work by blocking the bronchoconstrictive effects of acetylcholine. They are the preferred first-line bronchodilators for COPD. Methylxanthines, like Theophylline, are also effective as bronchodilators, although their mechanism of action is not clearly understood. Short and long acting preparations of all three classes are available, though long-acting anticholinergics are still being investigated. The most commonly used route for administration of beta-agonists and anticholinergics is inhalation, but some bronchodilators are also available as oral preparations. Methylxanthines are available only in oral and intravenous forms.

The most common side effects of bronchodilators are tachydysrhythmias and nervousness. Patients have likened the sensation of these side effects to the feeling one gets upon seeing that a police officer is about to pull you over. The patient’s heart rate and neurologic status must be monitored during therapy, as well as their symptom severity and breath sounds before and after treatments. In assition, methylxanthines require monitoring of drug levels to avoid toxic side effects such as tachydysrhythmias and seizures, especially among the elderly.

Common Bronchodilator Medications:

Anticholinergics: Atropine Sulfate (nebulized), Ipratropium Bromide

Beta-Adrenergic agonists • Non-selective: Epinephrine, Ephedrine and Isoproterenol • Short-acting Beta selective: Albuterol, Bitolterol, Metaproterenol, Pirbuterol and Terbutaline• Long-acting Beta selective: Salmeterol

Methylxanthines: Theophylline, Dyphylline and Aminophylline

Contraindications to and Common Side Effects of Bronchodilators:

Anticholinergics • Contraindications: hypersensitivity to drug, peanuts, or soya lecithin • Side Effects: Cough, dry mouth, nervousness, agitation, dizziness, palpitations, urinary

retention, constipation, worsening narrow angle glaucoma

Beta-Adrenergic agonists • Contraindications: hypersensitivity to beta adrenergic agents, cardiac dysrhythmias, narrow

angle glaucoma • Side Effects: palpitations, tachycardia, anxiety, irritability, tremor, GI upset, dry mouth,

cough, hoarseness, headache, flushing

Methylxanthines: • Contraindications: hypersensitivity, peptic ulcer disease, seizure disorder • Side Effects: GI irritation, diarrhea, increased gastroesophageal reflux, palpitations,

tachycardia, potentiation of diuresis, arrhythmias, convulsions, death

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Racemic Epinephrine

Racemic epinephrine has a unique role in urgent treatment of acute laryngedema. Inhaled epinephrine is an adrenergic agonist and causes rapid reduction in the size of blood vessels in the laryngeal area. Racemic epinephrine is indicated for acute laryngedema such as that seen after the removal of endotracheal tubes. The primary symptom of acute laryngedema is inspiratory stridor accompanied by respiratory distress.

While waiting for a racemic epinephrine treatment to be ordered and prepared, position the patient’s head to maintain a patent airway using the jaw-thrust maneuver and be prepared to administer positive pressure ventilations using a BVM device and supplemental oxygen. Also make sure emergency resuscitation equipment is close at hand in case the patient’s status deteriorates and notify a respiratory therapist or physician that emergency intubation may be required.

Mucolytics

The mucolytics function to liquefy pulmonary secretions. Mucolytics are indicated when secretions remain thick and tenacious despite adequate hydration of the patient. The three most commonly used mucolytics are Acetylcysteine, Dornase Alfa, and Guaifenesin. Be prepared to suction the patient receiving mucolytics if they do not have an effective cough.

Acetylcysteine is a liquid medication that can be nebulized or taken orally. The patient should be instructed to rinse the mouth after administration of either form. If the medication is nebulized, provide for face washing, as the mist makes the skin sticky. Acetylcysteine is contraindicated in hypersensitivity. Common side effects include increased secretions, bronchoconstriction, tracheal irritation, nausea, vomiting, and stomatitis. Acetylcysteine is not compatible with antibiotics and must not be administered at the same time.

Guaifenesin is a commonly prescribed mucolytic that is effective in managing short-term thickened secretions. It is contraindicated for patients under 12 or those with chronic cough due to asthma or emphysema. Its effectiveness in treatment of COPD remains to be proven. The most common side effects of Guaifenesin are nausea, vomiting, rash, urticaria, and inhibition of platelet adhesion.

Dornase Alfa is the mucolytic of choice for patients with cystic fibrosis (CF). It reduces the viscosity of secretions by dissolving the high concentrations of DNA present in the sputum of CF patients. Dornase Alfa is a recombinant human protein produced by ovary cells of Chinese hamsters and is contraindicated in known hypersensitivity to either the drug itself or Chinese hamster ovarian cells. The most common side effects of Dornase Alfa are pharyngitis and laryngitis. Apnea, though infrequent, can be a fatal complication. The patient’s respiratory status and pharyngeal tissues should be monitored during administration. Patients should be instructed to rinse the administration equipment and their mouths after each dose. For full benefit, Dornase Alfa must be taken daily and does not substitute for other treatment strategies for CF.

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Steroids: Systemic: Prednisone, Prednisolone, Methylprednisolone, Cortisone, Hydrocortisone and Dexamethasone Inhaled: Budesonide, Fluticasone, Triamcinolone, Beclomethasone, and Flunisolide

NSAIDS: Cromones: Cromolyn sodium and Nedocromil sodium Leukotriene receptor blockers: Zileuton Leukotrine inhibitors: Montelukast and Zafirlukast

Antiinflammatory Drugs

Antiinflammatory medications are used in the chronic treatment of asthma and COPD to reduce inflammation of the airways. Reduction of inflammation provides two primary benefits: it increases airway diameter by decreasing tissue swelling, and it decreases the amount of bronchial secretions produced. Although these drugs are essential components of long-term care for patients with pulmonary disease, they are not rapid in onset and are ineffective as solo therapy for acute exacerbations of disease.

There are two main categories of antiinflammatories used for pulmonary dysfunction: steroids and non-steroidal antiinflammatories (NSAIDS). The steroids may be taken systemically (taken PO or IV) or inhaled. The NSAIDS used for pulmonary disease are all inhaled.

Systemic steroids The goal of systemic steroid therapy is to achieve symptom control with the lowest dose and shortest treatment time possible. Systemic steroids are indicated for treatment of severe exacerbations of inflammatory pulmonary diseases such as asthma and the bronchitis component of COPD. They are contraindicated in patients with hypersensitivity or systemic fungal infections.

Long-term use of systemic steroids inhibits endogenous steroid production, placing the patient at risk for acute adrenal insufficiency if the medication is abruptly withdrawn. Adrenal insufficiency may also result if the patient is exposed to a significant stress such as infection or illness during or after steroid therapy. Though acute adrenal insufficiency is a rare complication of steroid therapy, it can be fatal and is often not diagnosed. Here’s how to recognize it:

• Risk factors: current or past corticosteroid use of 20 mg of hydrocortisone (or equivalent) for longer than 7 – 10 days. Suppression of the hypothalamic-pituitary-adrenal axis may continue for 2 – 12 months after steroid therapy has been withdrawn.

• Examination findings: confusion and altered mental status, vomiting, petechiae, signs of dehydration, tachycardia, severe hypotension and cardiovascular collapse

• Lab findings: hyponatremia, hyperkalemia, hypoglycemia, azotemia, hypercalcemia • Diagnostics: ACTH stimulation test confirms diagnosis

Immediate care of the patient with acute adrenal insufficiency and cardiovascular collapse is focused on supportive measures to restore intravascular fluid volume and tissue perfusion. Prepare to rapidly administer IV fluids and monitor the patient’s blood pressure and heart rate. The second priority is to administer glucocorticoid replacement per physician prescription. Then prepare to transfer the patient to a critical care unit for hemodynamic monitoring and stabilization. Monitor fluid balance, vital signs, and body weight to gauge the patient’s response to therapy.

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Patients with peptic ulcer disease, heart failure, hypertension, seizure disorders, diabetes, myasthenia gravis, hypothyroidism, and cirrhosis are at a higher risk of complications from systemic steroid therapy. Patients who are taking systemic steroids must be educated about the risks of abruptly stopping their medications. They need to know that they must follow administration instructions carefully and report their current and past steroid use to all health care providers. The patient also needs to be aware of the more common side effects of systemic steroid use. These are: • Insomnia • Increased appetite • Indigestion or peptic ulcer • Erythema, itching, skin dryness, acne • Impaired wound healing • Hyperglycemia • Sodium and water retention

Instruct the patient to take their medication with food if GI upset occurs. Children receiving long-term systemic steroid therapy require close assessment due to the medications affecting the process of growth and development. Patients on systemic steroids should be monitored for infection using a CBC. Steroids may mask the normal signs and reduce the patient’s immune response. Also, monitor fluid balance, electrolyte balance, blood sugar, weight, and blood pressure.

Inhaled Steroids Inhaled steroids produce effective reduction in inflammatory response with minimal systemic side effects. They are used for control of chronic airway inflammation in patients with asthma, bronchitis, and COPD. The most common side effects of inhaled steroid therapy are related to deposition of the drug on the oral mucosa. These side effects include: • Sore throat, hoarseness, dry mouth • Cough • Oral thrush The oral side effects can be reduced significantly by utilization of a spacer with the inhaler and rinsing the mouth after use. Make every effort to prevent the patient from developing thrush. When oral thrush appears in patients on oral steroids, it responds to treatment slowly and can predispose the patient to more serious infections.

Systemic side effects of inhaled steroids have been reported. They usually occur when high doses are given for a prolonged period of time. The main systemic side effect is mild adrenal insufficiency with suppression of the hypothalamic-pituitary-adrenal axis. Acute adrenal insufficiency with hypotension has not been associated with use of inhaled steroids. Inhaled steroids are preferred over oral steroids because of the decreased likelihood of systemic side effects.

Teach the patient receiving inhaled steroids that these drugs are used to prevent symptoms. Inhaled steroids have no effect when taken for acute symptoms. The patient may not see any improvement of symptoms until the medication has been used consistently for 1-2 weeks. To limit side effects, review the importance of spacer use and proper oral care with the patient. Monitor breath sounds and PEF measurements along with the patient’s subjective reports to gauge effectiveness of therapy.

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NSAIDS Two types of non-steroidal antiinflammatory medications are commonly used to control asthma: cromones and leukotriene modifiers. Cromones inhibit degranulation of sensitized mast cells, thereby decreasing airway inflammation. The leukotriene modifiers work by blocking effects or inhibiting production of substances that produce long term inflammation. These drugs are used to control the symptoms of mild to moderate persistent asthma. They are contraindicated for treatment of acute bronchoconstriction or status asthmaticus. Patient on NSAID therapy should have their PEF monitored as well as subjective reports of symptom control.

Cromones can be administered via several routes: oral, dry-powdered inhaler (DPI), aerosol, or nebulized. The maximum effectiveness of cromones is not achieved until they have been consistently taken for 4 – 6 weeks. Instruct patients to continue taking their medication regularly, even when they are symptom free. Patients must also understand that cromones are not effective treatment for acute bronchoconstriction. Side effects of inhaled cromones include bronchospasm, laryngeal edema, wheezing, cough, and pharyngeal irritation. Side effects of orally administered cromones include dizziness, drowsiness, headache, nausea, urinary frequency, joint swelling / pain, and lacrimation.

Leukotriene modifiers produce their effects on symptom management faster than inhaled steroids but are less effective than steroids in the long run. They are orally administered, making them a good choice for patients who cannot coordinate MDI administration. As with any medication whose function is to control symptoms, these medications must be taken daily whether symptoms are present or not. They are ineffective when used to treat acute bronchospasm. The most common side effects are headache, nausea, vomiting, diarrhea, and abdominal pain.

Summary This completes the content of the packet. You should now be sufficiently familiar with the concepts presented to do the following:

• Describe the gross anatomy of the lungs, thorax, and pharynx.

• Compare the roles of the ventilatory muscles.

• Define terms commonly used in evaluation of the respiratory system and identify normal and abnormal breath sounds.

• Describe methods used to invasively and non-invasively evaluate pulmonary function.

• Discuss the effects of nutrition, positioning, and oral care on the pulmonary system.

• Identify common respiratory medications.

• State the signs of respiratory compromise and prioritize interventions.

If you would like to research any of these topics in greater depth, please refer to the list of references. Many of them are available in medical libraries. Remember that policies and procedures vary among institutions. If you have any questions regarding appropriate procedures for respiratory care, refer to your hospital’s procedure manual.

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• Submit the answer sheet and payment ($10.00 for Orlando Regional Healthcare team members / $20.00 for non-team members) to: Orlando Regional Healthcare Education & Development, MP 14 1414 Kuhl Ave. Orlando, FL 32806

Achieve an 84% on the posttest. (You will be notified if you do not pass and will be asked to retake the posttest.)

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Post-Test Directions: Complete this test using the bubble sheet provided on the previous page.

For each muscle listed (Questions 1-5), indicate if it is used mainly during inspiration or expiration. If used for inspiration, mark A; if used for expiration, mark B. 1. Diaphragm

2. External abdominal muscle

3. External intercostal muscle

4. Transversus abdominis muscle

5. Sternocleidomastoid muscle

6. The diaphragm is innervated by the: A. Phrenic nerve B. Spinal accessory nerve C. Intercostal nerve D. Brachial plexus nerve

7. The muscles of ventilation are coordinated by the central nervous system to control:

A. Arterial oxygen content B. Pulmonary compliance C. Respiratory rate and depth D. Bronchoconstriction / bronchodilation

8. Effectiveness of ventilation is measured using blood levels of:

A. Oxygen B. Carbon Dioxide C. Hemoglobin D. Electrolytes

9. The work of breathing is NOT affected by:

A. Pulmonary resistance B. Pulmonary compliance C. Tachypnea D. Passive exhalation

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10. A patient with a disease process that diminishes gas exchange at the alveolar-capillary membrane would have: A. A slow respiratory rate B. Noisy respirations C. Absent chest wall movement D. Tachypnea

11. Diffusion is a process of:

A. Movement of molecules from higher concentration to lower concentration B. Movement of molecules from lower concentration to higher concentration C. Movement of molecules in any direction D. Active transport of molecules

12. At the peak of inspiration, the diaphragm is normally:

A. Dome-shaped B. Flattened C. Relaxed D. Semi-flattened

13. Select the correct statement about ventilation/perfusion relationships in the normal lung. A. Ventilation is greater than perfusion at the base B. Ventilation equals perfusion at the apex C. Ventilation and perfusion are unaffected by position D. Perfusion exceeds ventilation in dependent areas

Match the following descriptions to the correct abnormal breathing patterns: 14. Rapid, deep and labored breathing

15. Slow breathing pattern, less than 12 breaths per minute

16. Irregular pattern with period of apnea

17. Fast breathing pattern, greater than 20 breaths per minute

18. Labored breathing

A. Dyspnea

B. Tachypnea

C. Hyperpnea

D. Biot’s

E. Bradypnea

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Match the description to the correct breath sound: 19. Barely audible sounds

20. Fine popping sounds

21. Musical sounds

22. Soft breezy sounds

23. Hypoventilation is best detected by a(n): A. Pulse oximetry monitor B. Apnea monitor C. End-tidal carbon dioxide monitor D. Peak expiratory flow monitoring

24. The shift in the oxyhemoglobin dissociation curve that has the most negative clinical

implications is a shift to the: A. Top B. Bottom C. Left D. Right

25. Pulse oximetry cannot be used to monitor oxygenation when the patient has:

A. Respiratory Acidosis B. Metabolic Alkalosis C. Carbon monoxide poisoning D. Acute respiratory distress

26. Identify the most likely cause for the following SpO2 waveform:

A. Hypertension B. Low perfusion C. Motion artifact D. Normal function

A. Diminished breath sounds

B. Vesicular breath sounds

C. Crackles

D. Wheezes

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27. Capnography is used to measure A. Respiratory rate B. Respiratory pattern C. Oxygenation D. Ventilation

28. Mark the letter that corresponds to the portion of the EtCO2 waveform which represents end-

expiration:

29. The most common invasive test for measurement of oxygenation and ventilation is:

A. Pulse oximetry B. Arterial blood gas C. End-tidal CO2 D. Apnea monitoring

30. Respiratory alkalosis is most commonly associated with: A. Slow, shallow breathing B. Deep, rapid breathing C. Hypoxemia D. Apnea

31. The best way to correct respiratory acidosis is: A. Increase ventilation B. Increase oxygenation C. Administer sodium bicarbonate D. Decrease oxygenation

32. Oxygen is indicated for: A. Tachypnea B. Elevated CO2 levels C. Hypoxemia D. Airway obstruction

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33. Supplemental oxygen can cause respiratory depression in patients who have: A. Hypoxic drive to breathe B. Bronchospasm C. Hypercapnea D. Tachypnea

34. The most important intervention for a patient experiencing respiratory compromise is:

A. Check the respiratory rate B. Apply supplemental oxygen C. Assure a patent airway D. Apply a pulse oximeter

35. Select the therapeutic technique that decreases atelectasis in the postop patient: A. Coughing and deep breathing B. Peak expiratory flow measurement C. Percussion and vibration D. Nasotracheal suction

36. To prevent the spread of bacteria to the respiratory tract, the best nursing intervention is to

provide oral care with a: A. Swab B. Toothette C. Toothbrush D. Peroxide mixture

37. Nutritional support for patients with respiratory compromise and inadequate oral intake

should begin within: A. One hour B. 24 hours C. 72 hours D. One week

38. Inhaled medications are frequently used to treat pulmonary disease because they:

A. Deliver less drug to the affected tissue B. Increase systemic side effects C. Decrease systemic side effects D. Have a longer time of onset

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39. The class of drugs that is most effective for acute bronchospasm is: A. Short-acting beta adrenergic agonists B. Long-acting beta-adrenergic agonists C. Inhaled corticosteroids D. Leukotriene inhibitors

40. The most serious side effect of systemic corticosteroid therapy is:

A. Peptic ulcer disease B. Hyperglycemia C. Tachycardia D. Acute adrenal insufficiency

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Bibliography AACN News (2002). Vol . 20 No. 2. AACN, Aliso Viejo California. Ahya, S.N., Flood K., Paranjothi, S. (2001). The Washington Manual of Medical Therapeutics 30th

Ed. Lippincott Williams & Wilkins. Philadelphia, Pennsylvania. Branson, R.D., Hess, D.R., Chatburn, R.L. (1999). Respiratory Care Equipment 2nd Ed. Lippincott

Williams & Wilkins: Philadelphia, Pennsylvania. Carroll, P. "Procedureal Sedation Capnography's Heightened Role" (October 2002). RN, Vol 65 No.

10. Montvale, New Jersey. Coen, M. “Pulse Oximetry: User Beware!” Advance for Nurses. Florida. April 4, 2005. Des Jardins, T., (2002). Cardiopulmonary Anatomy & Physiology 4th Ed. Delmar Thomson

Learning, Inc.: Albany New York. Frakes, M.A. (2001). “Measuring End-tidal Carbon Dioxide: Clinical Applications and Usefulness.”

Critical Care Nurse Vol 21, No. 5, October 2001. AACN, Aliso Viejo California. Grap, M.J., et.al. (2003). “Oral Care Interventions in Critical Care: Frequency and

Documentation”. American Journal of Critical Care, Volume 12 No. 2. The Inno Vision Group: Aliso Viejo, California.

Hess, D.R, MacIntyre, N.R., Mishoe, S.C., Galvin, W.F., Adams, A.B., Saposnick, A.B. (2002). Repsiratory Care Principles and Practice. W.B. Saunders Company: Philadelphia, Pennsylvania.

Jubran, A. “Pulse Oximetry”. (1999). Critical Care, Vol 3 No 2. Lanken, P. N., (2001). The Intensive Care Unit Manual. W.B. Saunders Company: Philadelphia,

Pennsylvania. MacIntyre, N.R., Branson, R.D. (2001). Mechanical Ventilation. W.B. Saunders Company:

Philadelphia, Pennsylvania. Netter, F.H. (1989). Atlas of Human Anatomy. Ciba-Geigy Corporation: Summit, New Jersey. O’Donnell, J.M., Bragg, K., Sell, S. (2003). “Procedural Sedation Safely navigating the twilight

zone” Nursing 2003, Vol 33, No. 4. Lippincott Williams & Wilkins Springhouse, Pennsylvania.

Rau, Jr., J.L. (2002). Respiratory Care Pharmaclogy 6th Ed. Mosby, St. Louis Missouri. Richard, J.C., et.al. (2003). “Respective effects of end-expiratory and end-inspiratory pressures on

alveolar recruitment in acute lung injury”. Critical Care Medicine Vol. 31, No. 1. St. John, E. “Protocols for Practice Airway Management” Critical Care Nurse Vol 24, No.2. April

2004. AACN, Aliso Viejo, California. Thompson, J.M., McFarland, G.K., Hirsch, J.E., Tucker, S.M. (2002). Mosby’s Clinical Nursing 5th

Edition. Mosby: St. Louis, Missouri. Tobin, M.J. (1994). Principles and Practice of Mechanical Ventilation. McGraw-Hill, Inc. New

York, New York. Urden, L.D., Stacy, K.M., Lough M.E. (2002). Thelan’s Critical Care Nursing Diagnosis and

Management. Mosby: St. Louis Missouri. Youngkin, E.Q., Sawin K.J., Kissinger J.F., Israel, D.S. (1999). Pharmacotherapeutics a primary

care clinical guide. Appleton & Lange. Stamford, Connecticut.

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Zampella, M. A. (2003). “COPD: Managing flare-ups”. RN Magazine Travel Nursing Today. January. Montvale, New Jersey.

Internet Resources American Association of Respiratory Care – Clinical Practice Guidelines

www.aarc.org

Virtual Hospital lung sounds http://www.vh.org/adult/provider/internalmedicine/LungSounds/LungSounds.html

Virtual Stethoscope http://sprojects.mmip.mcgill.ca/MVS/MVSTETH.HTM

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Glossary ABG: Arterial blood gas. A test which analyses arterial blood for oxygen, carbon dioxide and bicarbonate content in addition to blood pH. Used to test the effectiveness of respiration/ventilation.

Acidosis: A pathologic state characterized by an increase in the concentration of hydrogen ions in the arterial blood above the normal level. May be caused by an accumulation of carbon dioxide or acidic products of metabolism or a by a decrease in the concentration of alkaline compounds.

Adrenergic: Relating to drugs that mimic the actions of the sympathetic nervous system

Alkalosis: A state characterized by a decrease in the hydrogen ion concentration of arterial blood below normal level. The condition may be caused by an increase in the concentration of alkaline compounds, or by decrease in the concentration of acidic compounds or carbon dioxide.

Alveoli: Plural of Alveolus. Terminal air spaces that contain numerous capillaries in their speta, which serves as sites for gas exchange.

Alveolus: A small cell, cavity or socket.

Agonist: A drug capable of combining with receptors to initiate drug actions; it possesses affinity and intrinsic activity.

Anticholinergic: Antagonistic to the action of parasympathetic or other cholinergic nerve fibers.

Apnea: cessation of breathing.

Asthma: A disease process that is characterized by paradoxical narrowing of the bronchi (lung passageways) making breathing difficult.

Bronchodilator: A medication that acts to dilate the lumen of the airway to allow the unrestricted passage of air. These medications are commonly given to asthma patients who manifest wheezing.

Bronchospasm: An abnormal constriction of the smooth muscle of the bronchi resulting in an acute narrowing and obstruction of the respiratory airway. A cough with generalized wheezing usually indicates this condition. The most common cause of bronchospasm is asthma.

Capnogram: a continuous record of the carbon dioxide content of expired air.

Capnography: continuous measurement and graphical display of the carbon dioxide (CO2) level of a patient’s exhaled breath.

Capnometry: Measurement of CO2 in proximal airway during inspiration and expiration.

Chemoreceptor: any cell that is activated by a change in its chemical milieu and results in a nerve impulse.

Chronic obstruction pulmonary disease (COPD): a disease process involving chronic inflammation of the airways, including chronic bronchitis (disease in the large airways) and emphysema (disease located in smaller airways and alveolar regions). The obstruction is generally permanent and progressive over time.

Compliance: a measure of distensibility of a chamber expressed as a change in volume per unit change in pressure.

Corticosteroids: any of various adrenal-cortex steroids (such as corticosterone, cortisone, and aldosterone) used especially as anti-inflammatory agents.

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Cyanosis: a dark bluish or purplish discoloration of the skin and mucous membrane due to deficient oxygenation of the blood.

Dead space: area in which there is no gas exchange.

Diaphragm: the musculomembranous partition between the abdominal and thoracic cavities.

Diffusion: the random movement of molecules or ions or small particles in solution or suspension under the influence of thermal motion toward a uniform distribution throughout the available volume.

Hypercapnemia: an excess of carbon dioxide in the blood

Hypocapnemia: a deficiency of carbon dioxide in the blood

Hypoxemia: below-normal oxygen content in arterial blood due to deficient oxygenation of the blood and resulting in hypoxia.

Hypoxia: reduction of oxygen supply to tissue below physiological levels despite adequate perfusion of the tissue by blood.

Hypoperfusion: decreased blood flow through an organ.

Hyperventilation: a state in which there is an increased amount of air entering the pulmonary alveoli (increased alveolar ventilation), resulting in reduction of carbon dioxide tension and eventually leading to alkalosis.

Hypoventilation: a state in which there is a reduced amount of air entering the pulmonary alveoli.

Lactate: a salt or ester of lactic acid. Lactic acid is a byproduct of oxidation, metabolism of sugar.

Leukotriene: product of eicosanoid metabolism with postulated physiologic activity such as mediators of inflammation and roles in allergic reactions.

Mechanoreceptor: a receptor which responds to mechanical pressure or distortion.

Mucolytic: capable of dissolving, digesting or liquefaction of mucous.

Noninvasive: descriptive of diagnostic procedures which do not involve the insertion of needles, cannulas, or other devices that require penetration of the skin.

Oxygenation: the process of supplying, treating or mixing with oxygen.

Oxygen delivery system: a device used to deliver oxygen concentrations above ambient air to the lungs through the upper airway.

Oxyhemoglobin: hemoglobin in combination with oxygen.

Peak Expiratory Flow Rate (PEFR): measurement of the maximum rate of airflow attained during a forced vital capacity determination.

Perfusion: the passage of fluid (usually blood) through out the body (organs and tissues).

Pneumothorax: an abnormal state characterized by the presence of gas (as air) in the plueral cavity.

Pulmonary Artery: the short wide vessel arising from the conus arteriosus of the right ventricle and conveying unaerated blood to the lungs.

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Pulmonary Embolism: the lodgment of a blood clot in the lumen of a pulmonary artery, causing a severe dysfunction in respiratory function.

Pulse Oximetry: determination of arterial saturation of hemoglobin: the absorption of light by blood is measured spectrophotometrically.

Resistance: impedance to flow in a tube or conduit; quantified as a ration of the difference in pressure between the two points along a tube length divided by the volumetric flow of the fluid per unit time.

Respiration: breathing; gas exchange, specifically the exchange by a living organism of carbon dioxide (CO2), a waste product formed during the oxidation of food molecules, for oxygen (02), which the organism needs to continue oxidizing its food.

Respiratory insufficiency: the inability of the body to provide adequate arterial oxygenation.

Spacer: a device used to improve aerosol delivery by stabilizing particle size and reducing the need for breath/actuation coordination.

Spectrometry Equipment: devices that measure emission or absorption of light as a function of wavelength.

Surfactant: lung lining fluid that reduces surface tensions

Tachypnea: an abnormally rapid (usually shallow) respiratory rate. The normal resting adult respiratory rate is 12 – 20 breaths/minute.

Ventilation: movement of gas(es) into and out of the lungs

Volume: space occupied by matter measured in milliliters or liters

V/Q ratio: the ratio of ventilation (V) to perfusion (Q).

V/Q Mismatch: Ventilation/Perfusion mismatch – an imbalance between ventilation compared to perfusion. Extremes are shunt perfusion and dead space ventilation.

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Self-Learning Packet Evaluation Name of Packet: Date:

Employee Non-Employee

Your position? RN LPN Respiratory Radiology Lab Social Work Rehab Clin Tech

Other: If RN/LPN, which specialty area?

Med/Surg Adult Critical Care OR/Surgery ED Peds Peds Critical Care OB/GYN L&D

Neonatal Behavioral Health Cardiology Oncology Other:

Please take a few moments to answer the following questions by marking the appropriate boxes.

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Disagree

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1) The content provided was beneficial. 2) The packet met its stated objectives. 3) The packet was easy to read. 4) The posttest reflected the content of the packet. 5) The course was: Mandatory Optional Please answer the following questions: How long did this packet take you to complete? ___________________________________________ What have you learned that you will apply in your work? ____________________________________ What was the best part of the packet? ____________________________________________________ What would you suggest be done differently? _____________________________________________ __________________________________________________________________________________ Additional Comments: ______________________________________________________________________________________________________________ _______________________________________________________ Thank you for your input.

Please return this evaluation to Education & Development, either in person or by mail: Mailpoint #14, 1414 Kuhl Avenue, Orlando, FL 32806

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