Which would the nurse include when teaching a client about the use of an incentive spirometer quizlet?

An incentive spirometer (spy-rom-uh-ter) is a simple, plastic medical device that exercises your lungs. Your healthcare provider may recommend that you use an incentive spirometer after an illness, surgery or an injury to your chest or abdomen.

An incentive spirometer helps prevent lung infections by expanding your lungs, strengthening your lungs, keeping your lungs inflated and clearing mucus and other secretions from your chest and lungs. You may have low oxygen levels after surgery or a serious illness, and an incentive spirometer helps you achieve a normal oxygen level.

How big is an incentive spirometer?

An incentive spirometer is small. It’s about the size of a small bottle, and you can hold it in one hand.

What does an incentive spirometer do for your lungs?

With regular use, an incentive spirometer helps your lungs expand so you can take deep, full breaths instead of short, shallow breaths.

What is the benefit of an incentive spirometer?

An incentive spirometer is like an exercise machine for your lungs. It helps you maintain your lung strength, or it helps your lungs get stronger after an injury or illness.

After surgery, an incentive spirometer can:

• Improve lung ventilation. Ventilation is how much air enters your lungs when you breathe in and how much air leaves your lungs when you breathe out.
• Recover from anesthesia quickly. An incentive spirometer helps clear anesthesia from your lungs.
• Loosen mucus from your lungs. Deep exhalations help prevent mucus and fluids from building up in your lungs.
• Help prevent lung complications. Slow, deep breaths fully inflate your lungs, which help clear any fluids that may cause lung conditions, such as pneumonia.

What are the two types of incentive spirometers?

There are two types of incentive spirometer:

• Flow-oriented incentive spirometer (FIS). An FIS device makes you work harder to breathe. It helps increase the muscles in your upper chest.
• Volume-oriented incentive spirometer (VIS). A VIS device doesn’t make you work as hard as an FIS device to breathe. It helps improve activity and movement in your diaphragm.

Who should use an incentive spirometer?

Your healthcare provider may give you an incentive spirometer in the following situations:

• Ribcage injuries. Rib fractures are common injuries. Your ribs may be sore to the touch, and it may hurt to breathe or cough. Everyday activities such as walking, running or going upstairs may also be painful or uncomfortable.
• Bed rest. Bed rest means you should rest in bed or on a comfortable couch at home and restrict your movements and activities. Your healthcare provider may recommend bed rest after surgery or an injury.
• Asthma. Asthma causes your airways to become inflamed, tighten and produce mucus.
• Pneumonia. Pneumonia causes air sacs in your lungs to fill with mucus and other fluids. An incentive spirometer helps loosen mucus and fluids from your lungs.
• Chronic obstructive pulmonary disease (COPD). COPD is a group of diseases that causes permanent lung damage. You can’t reverse COPD damage to your lungs, but an incentive spirometer can help alleviate your symptoms.
• Cystic fibrosis. Cystic fibrosis causes mucus to build up in your organs, including your lungs.
• Sickle cell anemia. Sickle cell anemia is an inherited blood disorder. It can cause cells to clump together and can clog blood vessels in your lungs, which may cause chest pain, a cough and trouble breathing.
• Atelectasis. Atelectasis prevents your lungs from properly inflating.

How do I use an incentive spirometer?

To properly use an incentive spirometer, you should:

1. Sit on the edge of your bed if possible. If you can’t, sit up as far as you can in bed.
2. Hold the incentive spirometer in an upright position.
3. Place the mouthpiece in your mouth and tightly seal your lips around it.
4. Breathe in as slowly and deeply as possible. You’ll notice a yellow piston rising toward the top of the column. The yellow piston should reach the blue outlined area.
5. Hold your breath for as long as possible, or at least five seconds. Exhale slowly and allow the piston to fall to the bottom of the column.
6. Rest for a few seconds, and then repeat the first five steps at least 10 times every hour you’re awake.
7. Place the yellow indicator on the side of your incentive spirometer to show your best breath. Use the indicator as a goal to work toward during each slow, deep breath.
8. After each set of 10 deep breaths, cough deeply to clear your lungs. If you have an incision from surgery, firmly press a pillow or rolled-up towel against your incision when coughing to provide support.
9. Once you can get out of bed safely, take frequent short walks and practice coughing. You can usually stop using the incentive spirometer once you can walk around, unless otherwise instructed by your healthcare provider.

If you feel dizzy or lightheaded at any point while using an incentive spirometer, immediately stop using the device and alert your healthcare provider.

How often should I use an incentive spirometer?

When you’re awake, you should use your incentive spirometer at least 10 times every hour.

Are there any risks to using an incentive spirometer?

Yes, there are some risks associated with using an incentive spirometer.

If you don’t properly clean and disinfect your incentive spirometer, it’s possible for you to spread bacteria. Clean your incentive spirometer’s tubing, breathing valve and mouthpiece before someone else uses it.

An incentive spirometer also requires you to exhale deeply, which may spread airborne microbes such as influenza and COVID-19. It’s a good idea to avoid using an incentive spirometer around other people, especially if you’re not feeling well.

If you have cystic fibrosis, you’re also at a higher risk of upper respiratory tract infections when you use an incentive spirometer or other lung function testing equipment.

How do I clean my incentive spirometer?

If you have an incentive spirometer for home use, it’s a good idea to clean it daily.

Detach the mouthpiece from the base of the device and clean it with clean running water and antibacterial soap for about 20 seconds. Then wash the rest of the spirometer with water and soap.

You can also put on protective gloves and soak the separate pieces in a 5% bleach and water solution for about five to 10 minutes. Periodically swish the pieces in the solution to help clean the device. Thoroughly rinse the pieces in clean running water after five to 10 minutes.

Make sure the incentive spirometer is dry before your next use.

Is an incentive spirometer good for my heart?

An incentive spirometer isn’t specifically good for your heart. However, it’s helpful as you recover from many types of surgery, including open heart surgery.

During many open heart surgery procedures, your healthcare provider will hook you up to a heart-lung bypass machine. A heart-lung bypass machine connects to your heart. It temporarily takes over for your heart and lungs, so blood still circulates around your body, but it moves away from your heart. It also deflates your lungs.

When there is no air in your lungs, they may create mucus. An incentive spirometer helps remove the mucus and other fluids from your lungs as you recover from the procedure.

A note from Cleveland Clinic

An incentive spirometer is a medical device that helps your lungs recover after surgery or a lung illness. You may find it challenging to use the device at first, but keep it up! The more you use an incentive spirometer, the stronger your lungs will get. Don’t forget to use the indicator on the side of the device to help you track your progress and achieve your goals.

Your healthcare provider can answer any questions you have about how to use the device.

Learning Outcome

• Identify risk factors for atelectasis

• Compare and contrast obstructive versus non-obstructive atelectasis

• Describe expected assessment and diagnostic findings in a patient experiencing atelectasis

• Select appropriate nursing interventions to support a patient experiencing atelectasis.

• Describe medical interventions that may be used for atelectasis

• Identify key patient education interventions

The word "atelectasis" is Greek in origin; It is a combination of the Greek words atelez (ateles) and ektasiz (ektasis) meaning "imperfect" and "expansion". It results from the partial or complete, reversible collapse of the small airways leading to an impaired exchange of CO2 and O2. The incidence of atelectasis in patients undergoing general anesthesia is 90%.[1]

Nursing Diagnosis

• Impaired Gas Exchange and appropriate NANDA nursing diagnosis for atelectasis.

Atelectasis is one of three types: compressive,  due to lung tissue compression,  resorptive, caused by absorption of alveolar air, or related to an impairment of pulmonary surfactant production or function.[2]] It is categorized as either obstructive, non-obstructive, postoperative, and rounded atelectasis. 

There are four types of nonobstructive atelectasis: compression, adhesive, cicatrization, relaxation, and replacement atelectasis.  Compression atelectasis happens when there is increased pressure exerted on the lung which causes a  transmural pressure difference between the extra and intra-alveolar space that results in alveolar collapse. During anesthesia, diaphragmatic relaxation occurs inhibiting the natural lowering of the diaphragm that occurs during spontaneous breathing.     Lying in the supine position further displaces the diaphragm toward the head resulting in additional inhibition of gas exchange due to the further impairment of the transmural pressure gradient resulting in an increased risk of atelectasis.     Adhesive atelectasis occurs due to either a surfactant deficiency or dysfunction.  This type is commonly seen in patients with  Adult Respiratory Distress Syndrome (ARDS) or among premature infants with Respiratory Distress Syndrome (RDS). Surfactant prevents alveolar collapse by decreasing alveolar surface tension.  Alterations to surfactant production and function tend to increase the surface tension within the alveoli lead creating instability resulting in collapse.  Cicatrization atelectasis results in the contraction of the lung tissue to the development of parenchymal scar tissue.  Cicatrization atelectasis is often seen in tuberculosis, fibrosis, and other chronic destructive lung diseases. Relaxation atelectasis occurs when there is a loss of contact between the parietal and visceral tissue.  This happens with pneumothoraces and pleural effusions. Replacement atelectasis occurs when a tumor replaces the alveoli of an entire lobe of the lung, seen with bronchioalveolar carcinoma, resulting in the complete collapse of the lung.

In obstructive atelectasis, the air in the alveoli is absorbed distal to the point of obstruction.  This is why it is referred to as resorptive atelectasis.  In this instance, there is a mismatch between ventilation due to complete or partial obstruction of the alveoli and the uninterrupted perfusion of the alveoli.   The presence of the ongoing ventilation-perfusion mismatch due to the obstruction results in the absorption of the gas in the alveoli precipitating the collapse.  Obstructive atelectasis may be caused by intrathoracic tumors, mucous plugs, and foreign bodies. Children are at risk for resorption atelectasis due to aspiration foreign bodies because there are less developed collateral pathways for ventilation.

Adults with COPD are less likely to develop resorptive atelectasis related to an obstructive lesion due to better-developed collateral ventilation secondary to airway destruction. General anesthesia contributes to the development of absorptive atelectasis through the use of high inspiratory concentrations of oxygen ( FiO2).  The risk for atelectasis due to the use of high FIO2 during anesthesia is related to the rates at which oxygen and nitrogen are absorbed into the bloodstream.   Oxygen is rapidly absorbed, whereas nitrogen is not.  Increasing the amount of oxygen inspired decreases the amount of nitrogen available to hold the alveoli open.

Postoperative atelectasis is normally seen within typically 72 hours of surgery using general anesthesia. Atelectasis is a known complication of general anesthesia.

Rounded atelectasis is rare.  It is most often associated with asbestosis.  It occurs because the lung tissue folds to the pleura.

 Any of these mechanisms of atelectasis may contribute to perioperative atelectasis.  Most frequently seen are the absorptive and compression variety.[3]

Middle lobe syndrome is the result of either an extraluminal or intraluminal obstruction of the bronchi which results in either a recurrent or fixed atelectasis of the lingula and right middle lobe of the lung. Inflammation, alterations in bronchial anatomy, and the presence of collateral ventilation are nonobstructive causes.   Middle lobe syndrome is treated via bronchoscopy and bronchoalveolar lavage.  Bronchiectasis may result from chronic atelectasis. Middle lobe syndrome has been associated with Sjorgen syndrome and treatment with steroids has shown promise.

The incidence of atelectasis does not demonstrate gender differences. COPD, asthma, and increased age do not impact incidence either.[4] Atelectasis is more common in those who have recently had surgery using general anesthesia.  Incidence has been reported as high as 90% in this group.[1] Research has demonstrated that the dependent portions of the lungs show indications of atelectasis within five minutes of beginning general anesthesia. [5]  Atelectasis is more common following cardiac surgery with cardio-pulmonary bypass than any other surgery, including thoracotomy; however, the risk of atelectasis is higher in patients undergoing abdominal or thoracic surgery.[3] Obesity and pregnancy increase the risk for atelectasis due to upward displacement of the diaphragm (see the section on epidemiology).  

Typically, atelectasis is asymptomatic. However, a patient might also present with decreased or absent breath sounds, crackles, cough, sputum production, dyspnea, tachypnea, and/or diminished chest expansion.

Atelectasis is usually clinically diagnosed in a patient with known risk factors. If an X-ray is warranted, a chest film, chest CAT scan (CT), and/or thoracic ultrasound may be useful to diagnose atelectasis. A chest x-ray will show platelike, horizontal lines in the area of atelectasis. Atelectasis is not usually seen on convention chest X-rays until it is significant. 

On chest X-ray, the displacement of interlobar fissures, pulmonary opacification, and/or tracheal shift toward the affected side is seen with atelectasis.[6]

Chest CT  shows densities in the dependent lung and decreased volume in the affected side.   

Fiberoptic bronchoscopy may allow direct visualization of atelectasis.  It can be both diagnostic and therapeutic, as it may reveal the cause of an obstruction causing the atelectasis (i.e., tumor, mucous plug, or foreign body).

Arterial blood gas may demonstrate arterial hypoxemia and respiratory alkalosis with normal PaCO2. PaCO2 may be lower due to increased minute ventilation often seen in atelectasis. 

 A transient lung dysfunction leading to atelectasis caused by general anesthesia generally resolves itself within 24 hours. Unfortunately, some patients may develop significant respiratory complications resulting in increased morbidity and mortality without treatment.  Prevention of atelectasis is achieved through the avoidance of general anesthesia, early mobility, adequate pain treatment including minimization of parenteral opioid use.  When general anesthesia is required, steps should be taken to prevent the development of atelectasis such as: using continuous positive airway pressure (CPAP),  using the lowest possible FiO2 during anesthesia administration, use of PEEP (positive end-expiratory pressure), engaging in lung recruitment maneuvers, and using low tidal volumes.[7] One study demonstrated engaging in intraoperative alveolar recruitment followed by PEEP effectively prevented lung atelectasis in obese patients resulting in better oxygenation, shorter recovery room time, and fewer pulmonary complications postoperatively.[8]

Sitting upright increases functional residual capacity (FRC)  decreasing atelectasis.[9]  Other interventions that have been used to decrease atelectasis include deep breathing; early ambulation; proper use of an incentive spirometer or acapella device; chest physiotherapy; tracheal suctioning if intubated; and use of positive pressure ventilation.  Each of these interventions temporarily increases the transmural pressure gradient resulting in the re-expansion of collapsed areas of the lung. Preoperatively patients should be taught atelectasis prevention measures, such as incentive spirometry. In the case of incentive spirometry, it is believed that this intervention should begin preoperatively and then continue postoperatively with hourly use encouraged to achieve maximal benefit.

 Mucolytic agents (acetylcysteine) and recombinant human DNase (dornase alpha) are pharmacologic agents which may be of some benefit in patients with cystic fibrosis, as mucous plugs are often seen in this patient population.

Bronchoscopy may be used to manage atelectasis. In one study, bronchoscopy resulted in improved lung function reversing atelectasis 76% of the time.  Bronchoscopy should be used when mechanical obstruction of the bronchus is suspected and coughing or suctioning has not been successful. Bronchoscopy should also be considered when early ambulation, incentive spirometry, bronchodilators, and humidity,  have not been successful after 24 hours of use. 

Engaging in preventative strategies early and promptly recognizing atelectasis will improve patient outcomes and significantly decrease cost.[10]

Patients enter the hospital environment with a variety of risk factors that place them at risk for the development of atelectasis.  Among these risk factors is a history of cardiovascular disease, pulmonary disease, particularly chronic obstructive pulmonary disease, neuromuscular disease, kidney failure, cancer, and autoimmune disorders.  In addition, tobacco use, obesity, traumatic injury, advanced age, and recent respiratory illness are also risks.[10] Careful assessment of the patient's respiratory status is required throughout the hospitalization.    Particular attention should be given to lung sounds for diminishment and /or crackles. Complaints of dyspnea should be reported.  The presence of cough should be further assessed for sputum production.  Characteristics of sputum should be reported to the physician. Vital signs should be monitored for tachypnea.  Fever may occur, but this is not necessarily attributable to atelectasis.[10]

Incentive spirometry has been a mainstay of nursing postoperative atelectasis prevention.  Recent studies have indicated that incentive spirometry alone may not be sufficient to prevent untoward outcomes in postoperative patients.  Evidence indicates that the use of deep breathing, adequate pain relief, directed cough, and early patient mobilization are also necessary to increase lung volumes [11].

Dyspnea, tachypnea, and increased work of breathing as exhibited by the use of accessory muscles during respirations should be reported to the physician. Changes in the character of lung sounds, cough, and sputum production should also be reported.[10]

Preventing atelectasis is vital to improving the outcomes of the postoperative patient. Unfortunately, atelectasis may not always be prevented.  Therefore, early recognition and treatment are also important, as this can decrease the length of hospitalization, cost, and improve patient outcomes.

Prevention and treatment of atelectasis require an interprofessional team effort. Physicians, particularly surgeons and anesthesiologists, must consider the role of anesthesia in atelectasis. Nursing needs to monitor the patient pre and post-procedure. Pharmacists can provide regarding the use of opioids and mucolytics. The nurses administering these medications should report on the efficacy of therapy as well as any adverse events, resulting in dose or medication changes, or other interventions. Nursing should help to educate the patient and family regarding interventions to minimize the risk of atelectasis, such as incentive spirometry. incentive spirometry. In summary, atelectasis management takes a collaborative interprofessional team to optimize patient outcomes. [Level V]

Atelectasis is a partial collapse of the lung which causes shortness of breath. It may be the result of several different processes, most often associated with poor inspiratory effort, airway obstruction blocking air movement into the lung, additional pressure placed on the outside of the lung, or alterations in the production or function of a protein called surfactant in the lung. Treatment addresses underlying causes of the condition but consists most often of supportive measures, such as deep breathing, incentive spirometry, and providing supplemental O2. 

In the past, it was believed that postoperative fever was caused by atelectasis.  There is no evidence to support this belief.[12]

Review Questions

post op atelectasis chest x-ray. Image courtesy S Bhimji MD

Post surgical atelectasis. Image courtesy Dr Chaigasame

Chest computed tomography showing extensive emphysema in the right middle lobe and compressive atelectasis of the right upper lobe. Courtesy: Humberto C. Sasieta , Francis C. Nichols , Ronald S. Kuzo , Jennifer M. Boland , and James P. Utz .

1.

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Peroni DG, Boner AL. Atelectasis: mechanisms, diagnosis and management. Paediatr Respir Rev. 2000 Sep;1(3):274-8. [PubMed: 12531090]

Magnusson L, Spahn DR. New concepts of atelectasis during general anaesthesia. Br J Anaesth. 2003 Jul;91(1):61-72. [PubMed: 12821566]

Gunnarsson L, Tokics L, Gustavsson H, Hedenstierna G. Influence of age on atelectasis formation and gas exchange impairment during general anaesthesia. Br J Anaesth. 1991 Apr;66(4):423-32. [PubMed: 2025468]

Brismar B, Hedenstierna G, Lundquist H, Strandberg A, Svensson L, Tokics L. Pulmonary densities during anesthesia with muscular relaxation--a proposal of atelectasis. Anesthesiology. 1985 Apr;62(4):422-8. [PubMed: 3885791]

Tokics L, Hedenstierna G, Strandberg A, Brismar B, Lundquist H. Lung collapse and gas exchange during general anesthesia: effects of spontaneous breathing, muscle paralysis, and positive end-expiratory pressure. Anesthesiology. 1987 Feb;66(2):157-67. [PubMed: 3813078]

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Talab HF, Zabani IA, Abdelrahman HS, Bukhari WL, Mamoun I, Ashour MA, Sadeq BB, El Sayed SI. Intraoperative ventilatory strategies for prevention of pulmonary atelectasis in obese patients undergoing laparoscopic bariatric surgery. Anesth Analg. 2009 Nov;109(5):1511-6. [PubMed: 19843790]

Craig DB, Wahba WM, Don HF, Couture JG, Becklake MR. "Closing volume" and its relationship to gas exchange in seated and supine positions. J Appl Physiol. 1971 Nov;31(5):717-21. [PubMed: 5117187]

Restrepo RD, Braverman J. Current challenges in the recognition, prevention and treatment of perioperative pulmonary atelectasis. Expert Rev Respir Med. 2015 Feb;9(1):97-107. [PubMed: 25541220]

Mavros MN, Velmahos GC, Falagas ME. Atelectasis as a cause of postoperative fever: where is the clinical evidence? Chest. 2011 Aug;140(2):418-424. [PubMed: 21527508]