CHAPTER 4 Respiratory disorders
Respiratory assessment: general
Goal of system assessment
Evaluate for ineffective breathing patterns, impaired gas exchange, and airway obstruction.
Continuous pulse oximetry (spo2 monitoring)
• Evaluate for changes over time and/or since the last recorded reading. Results should be correlated with the arterial oxygen saturation (SaO2) readings derived from arterial blood gases.
• Pulse oximetry accuracy is dependent on the presence of an adequate pulse in the area in which the measurement probe has been applied.
• Ensure readings are done using an appropriate probe placed on the anatomical location with the best pulse and least interference. Probes are available for the finger, forehead, or ear lobe.
• Readings must be correlated with physical assessment findings and can remain normal despite signs of impending deterioration. Physical assessment findings such as use of accessory muscles or presence of tachypnea are indicative of respiratory distress but may not be reflected in a change in SpO2. If an increasing amount of oxygen (O2) is needed to maintain SpO2, this is also indicative of impending deterioration of the patient.
Observation
• Evaluate for use of accessory muscles, shortness of breath, and air hunger.
• Ensure the patient is evaluated for the presence of chronic obstructive pulmonary disease (COPD) prior to applying O2 therapy so appropriate liter flow is determined to prevent respiratory impairment.
• Evaluate facial and lip color for pallor or cyanosis indicative of hypoxemia.
Auscultation
• Listen to breath sounds to evaluate for presence of adventitious sounds that reflect factors contributing to respiratory distress, including those related to both airway obstruction and impaired gas exchange.
• Adventitious sounds: crackles (rales) indicative of fluid in alveoli, bubbles (rhonchi) indicative of secretions in bronchioles, wheezing (inflammation), inspiratory stridor (narrowing of airways due to massive inflammation or obstruction by secretions or foreign body), or pleural friction rub (inflammation)
• Lungs must be auscultated anteriorly and posteriorly in all three lobes of the right lung, the two lobes of the left lung, over the right and left main bronchi, and over the trachea.
Screening labwork
• Arterial blood gas analysis can reveal increases or decreases in pH; levels of O2, O2 saturation, CO2, and bicarbonate; base excess or base deficit indicative of impending respiratory failure; hyperpnea/tachypnea; and metabolic derangements affecting breathing patterns. Blood gas analysis may be done using either arterial blood or mixed venous blood samples. Mixed venous blood samples are available only using a pulmonary artery catheter and can be used to calculate efficacy of both O2 delivery and O2 consumption. Arterial blood gases cannot be used to calculate O2 consumption.
CARE PLANS: GENERAL APPROACHES TO RESPIRATORY DISORDERS
Impaired spontaneous ventilation with or without impaired gas exchange
Goals/outcomes
Respiratory Status: Ventilation, Vital Signs Status, Respiratory Status: Gas Exchange, Symptom Control Behavior, Comfort Level, Endurance1. Assess for patent airway; if snoring, crowing, stridor, or strained respirations are present, indicative of partial or full airway obstruction, open airway using chin lift or jaw thrust.
2. Insert an oral airway if patient becomes unconscious and cannot maintain patent airway; use a nasopharyngeal airway if patient is conscious to avoid provoking vomiting. If severely distressed, patient may require endotracheal intubation.
3. Position patient to alleviate dyspnea and insure maximal ventilation; generally, sitting in an upright position unless severe hypotension is present.
4. Monitor changes in oxygenation following position change: SpO2, SvO2, ScVO2, end-tidal CO2, A−aDO2 levels and arterial blood gases (ABGs).
5. Clear secretions from airway by having patient cough vigorously, or provide nasotracheal, oropharyngeale, or endotracheal tube suctioning, as needed.
6. Have patient breathe slowly or manually ventilate with manual resuscitator or bag-valve-mask device slowly and deeply between coughing or suctioning attempts.
7. Assist with use of incentive spirometer as appropriate.
8. Turn patient every 2 hours if immobile. Encourage patient to turn self, or get out of bed as much as tolerated if he or she is able.
9. Provide mucolytic and bronchodilating medications orally, intravenously, or by inhaler, aerosol, or nebulizer as ordered to assist with thinning secretions and relaxing muscles in lower airways.
10. Provide chest physical therapy as appropriate, if other methods of secretion removal are ineffective.
1. Ensure humidity is provided when using O2 or bilevel positive airway pressure (BiPAP) device for more than 12 hours to help thin secretions.
2. Administer supplemental O2 using liter flow and device as ordered.
3. Restrict patient and visitors from smoking while O2 is in use.
4. Document pulse oximetry with O2 liter flow in place at time of reading as ordered. Oxygen is a drug; the dose of the drug must be associated with the O2 saturation or the reading is meaningless.
5. Obtain arterial blood gases if patient experiences behavioral changes or respiratory distress to check for hypoxia or hypercapnia.
6. Monitor for hypoventilation, especially in patients with COPD.
7. Monitor for changes indicative of O2 toxicity in patients receiving higher concentrations of O2 (more than FIO2 45%) for longer than 24 hours. Changes will be apparent in chest radiograph and breath sounds. Absorption atelectasis may be present. The higher the O2 concentration, the greater is the chance of toxicity.
8. Monitor for skin breakdown where O2 devices are in contact with the skin, such as nares, around the ears, and around edges of mask devices.
9. Provide O2 therapy during transportation and when patient gets out of bed.
10. If patient is unable to maintain SpO2 reading of more than 88% off O2, consult with the respiratory care practitioner/therapist and the physician about the need for home O2 therapy.
1. Monitor rate, rhythm, and depth of respirations.
2. Note chest movement for symmetry of chest expansion and signs of increased work of breathing such as use of accessory muscles or retraction of intercostal or supraclavicular muscles. Consider use of noninvasive positive pressure ventilation for impending respiratory failure.
3. Monitor for snoring, coughing, and possibly choking-type respirations when patients have a decreased level of consciousness to assess if airway is obstructed by tongue.
4. Monitor for new breathing patterns that impair ventilation, which may need aggressive management in a specialized, highly skilled setting.
5. Note that trachea remains midline, as deviation may indicate patient has a tension pneumothorax.
6. Auscultate breath sounds before and after administration of respiratory medications to assess for improvement.
7. Evaluate changes in O2 saturation (SaO2), pulse oximetry (SpO2), end-tidal CO2 (ETCO2), ScVO2, and ABGs as appropriate.
8. Monitor for dyspnea and note causative activities/events.
9. If increased restlessness or unusual somnolence occur, evaluate patient for hypoxemia and hypercapnia as appropriate.
10. Monitor chest radiograph reports as new images become available.
Cough Enhancement, Acid-Base Management, Mechanical Ventilation, Artificial Airway Management, Oral Health MaintenanceAcute asthma exacerbation
Pathophysiology
Life-threatening asthma exacerbation results from bronchial smooth muscle contraction (bronchospasm), bronchial inflammation leading to airway edema, and mucus plugging. When an episode of bronchospasm (critical airway narrowing) is not reversed after 24 hours of maximal doses of traditional inhaled short-acting beta2-adrenergic agonists (SABAs) such as albuterol or levalbuterol, injected systemic beta2-agonists such as epinephrine, inhaled anticholinergics such as ipratropium, and systemic steroid therapy with prednisone, prednisolone, or methylprednisolone, the refractory patient may be diagnosed with status asthmaticus (SA). Common triggers for asthma exacerbations include respiratory tract infections, allergens (airborne or ingested), air pollutants, smoke, and physical irritants (e.g., cold air, exercise). Anxiety or “panic” attacks and use of beta-adrenergic blocking agents and nonsteroidal anti-inflammatory drugs (NSAIDs) may predispose patients to development or exacerbation of severe asthma.
Assessment
Goal of system assessment
• Evaluate for ineffective breathing patterns, impaired gas exchange, and airway obstruction.
• Determine patient’s prior treatment regimen; classify which “step” of treatment has been needed to control symptoms; patient may need to move to the next step of treatment to maintain control.
• Classify severity of exacerbation: should be determined following initial assessment and diagnostic testing.
History and risk factors
• Asthma symptoms: Cough (especially if worse at night), wheezing, recurrent difficulty breathing, recurrent chest tightness
• Family history: Patients with either family history or atopic disease are at higher risk of asthma.
• Common triggers: Symptoms worsen with viral respiratory infections, environmental airborne allergens, irritants in the home (mold, mildew, wood-burning stove, cockroaches, dust mites, animal dander, carpeting laid over concrete), recent emotional upset, aggressive exercise, fear, frustration, food, new medications, changes in weather (especially exposure to cold air), occupational chemicals or allergens, and hormonal changes (menstrual cycle).
• Comorbid conditions: Sinusitis, rhinitis, gastroesophageal reflux disease (GERD), obstructive sleep apnea (OSA), allergic bronchopulmonary aspergillosis (ABPA)
1. Classify asthma severity: Intermittent (step 1 treatment) or persistent: mild, moderate, severe (steps 2, 3, 4, 5, and 6 treatments); steps differ for children under age 5, children between 5 and 12 years old, and adults.
2. Classify severity of exacerbation: Mild to severe or life threatening
3. Assess control: Determine if pattern of previous exacerbations is inherent to the current episode.
4. Compliance/ability to control: Assess the patient’s knowledge and skills for self-management.
5. Identify precipitating factors: Situation: exposure at home, work, daycare, or school to inhalant allergens or irritants; time of day, season or time of year, relationship of symptoms to meals, deterioration in other health conditions or menses
6. Identify comorbid conditions that may impair asthma management (e.g., sinusitis, rhinitis, GERD, OSA, obesity, stress, or depression).
7. Surgery: Asthmatic patients are at high risk for exacerbations following endotracheal intubation, general anesthesia, and ventilation provided during surgical or other invasive procedures. Impaired cough, hypoxemia, and hypercapnia may trigger exacerbation.
Spirometry or peak expiratory flow
• Peak expiratory flow (PEF): Measurement of rate or force of exhalation; those with easier breathing will have higher values than those in distress. A peak flowmeter is used by patients at home to assess asthma control. Those with more severe asthma may have difficulty discerning worsening of symptoms and may use PEF several times daily to assess for declining rate of exhalation.
• Assesses degree of obstruction and reversibility in patients older than 5 years
• Spirometry is essential for establishing the diagnosis of asthma. Patients’ perceptions of airflow obstruction are highly variable. Spirometry or PEF provides an objective measurement to help classify severity of exacerbation.
• Decreased to less than 40% of predicted value indicates severe exacerbation; less than 25% of predicted value for life threatening
Vital signs (severe to life-threatening asthma exacerbation)
• Presence of fever: Temperature elevation helps discern whether patient’s condition is related to a microbe (fever) versus an allergen (afebrile).
• Pulse oximetry: Oxygen saturation is decreased from patient’s baseline value.
• Tachycardia (HR greater than 140 bpm) and tachypnea (RR greater than 40 breaths/min)
• Hypotension may be present; hypotension is exacerbated by underlying dehydration often present with patients with severe asthma.
Observation
• Severe attacks render patients unable to speak due to breathlessness.
• Use of accessory muscles; fatigued, with or without diaphoresis
• Ashen, pale, or gray/blue facial color, lip color, or nail beds
• Chest expansion may be decreased or restricted.
• Altered level of consciousness (confusion, disorientation, agitation)
• Agitation is more commonly associated with hypoxemia while somnolence is associated with hypercapnia (elevated CO2 level).
• Increased nasal secretions, mucosal swelling, nasal polyps
Screening labwork
• Complete blood count (CBC with WBC differential): Evaluates for elevated white blood cells indicative of chronic inflammation due to allergic response and infection including presence of eosinophils, neutrophils, and mononuclear cells
4-1 RESEARCH BRIEF
From Etminan M, Sadatsafavi M, Jafari S, et al: Acetaminophen use and the risk of asthma in children and adults. Chest 136(5):1316–1323, 2009.
Patients with severe wheezing who have not been diagnosed with asthma should be evaluated for other causes of upper airway obstruction and “cardiac asthma.” Patients with left ventricular failure may wheeze if interstitial fluid increases to the point where bronchioles are compressed or if the pulmonary interstitial edema is severe enough to cause bronchospasm. Asymmetric breath sounds or chest pain may signal that the patient has a pneumothorax. Stridor may indicate the patient has an impending respiratory emergency, versus wheezing that may be present regardless of situation in poorly controlled asthmatics. Stridor is commonly seen with acute airway narrowing related to acute allergic reaction or anaphylaxis.| Test | Purpose | Abnormal Findings |
|---|---|---|
| Arterial blood gas analysis (ABG) | Assess for abnormal gas exchange or compensation for metabolic derangements. Initially PaO2 is normal and then decreases as the ventilation-perfusion mismatch becomes more severe. A normal PCO2 in a distressed asthma patient receiving aggressive treatment may indicate respiratory fatigue, which causes a progressively ineffective breathing pattern, which can also lead to respiratory arrest. Oxygenation assessment differs from acid base balance assessment, wherein the PCO2 value is used as the hallmark sign for respiratory failure induced acidosis. | pH changes: Acidosis may reflect respiratory failure; alkalosis may reflect tachypnea. Carbon dioxide: Elevated CO2 reflects respiratory failure; decreased CO2 reflects tachypnea; rising PCO2 is an ominous, since it signals severe hypoventilation, which can lead to respiratory arrest. Hypoxemia: PaO2 less than 80 mm Hg) Oxygen saturation: SaO2 less than 92% Bicarbonate: HCO3 less than 22 meq/L Base Deficit: less than -2 |
| Complete blood count (CBC) with WBC differential | WBC differential evaluates the strength of the immune system’s response to the trigger of exacerbation and for presence of infection. | Eosinophils: increased in patients not receiving corticosteroids; indicative of magnitude of inflammatory response. Increased WBC count: More than 11,000/mm3 is seen with bacterial pneumonias. WBCs may be increased by asthma in the absence of infection. The Hematocrit (Hct): may be increased from hypovolemia and hemoconcentration. |
| Pulmonary function tests (PFTs)/spirometry | The hallmark sign of asthma is a decreased FEV1 (forced expiratory volume in the first second)/FVC (forced vital capacity.) If PEF rate does not improve with initial aggressive inhaled bronchodilator treatments, morbidity increases. | Forced expiratory volume (FEV): decreased during acute episodes; if less than 0.7, narrowed airways prevent forceful exhalation of inspired volume (Table 4-1). Peak expiratory flow rate (PEF): less than 100–125 L/min in a normal-sized adult indicates severe obstruction to air flow. |
| Pulse oximetry (SpO2) | Noninvasive technology that measures the oxygen saturation of arterial blood intermittently or continuously using a probe placed on the patient’s finger or ear. When using pulse oximetry, it is helpful to obtain ABG values to compare the oxygen saturation and evaluate the PaO2, PaCO2, and pH. | Normal Spo2: more than 95%. Correlation of SpO2 with SaO2 (arterial saturation) is within 2% when SaO2 is more than 50%. Temperature, pH, PaCO2, anemia, and hemodynamic status may reduce the accuracy of pulse oximetry measurements. Presence of other forms of Hgb in the blood (carboxyhemoglobin or methemoglobin) can produce falsely high readings. |
| Serologic studies | Acute and convalescent titers are drawn to diagnose a viral infection. | Increased antibody titers: a positive sign for viral infection. |
| Chest radiograph | Evaluates the severity of air trapping; also useful in ruling out other causes of respiratory failure (e.g., foreign body aspiration, pulmonary edema, pulmonary embolism, pneumonia). | The x-ray usually shows lung hyperinflation caused by air trapping and a flat diaphragm related to increased intrathoracic volume. |
| 12-Lead ECG (electrocardiogram) | Evaluates for dysrhythmias associated with stress response and asthma medications. | Sinus tachycardia: important baseline indicator; use of some bronchodilators (e.g., metaproterenol) may produce cardiac stimulant effects and dysrhythmias. |
| Sputum gram stain, culture and sensitivity | Culture and sensitivity may show microorganisms if infection is the precipitating event. The most reliable specimens are obtained via bronchoalveolar lavage (BAL) during bronchoscopy, or using a protected telescoping catheter (mini or using BAL) to decrease risk of contamination from oral flora. |
Gross examination may show increased viscosity or actual mucous plugs. Gram stain positive: Indicates organism is present. Culture: Identifies organism. Sensitivity: Reflects effectiveness of drugs on identified organism. |
| Diagnostic fiberoptic bronchoscopy using PSB (protected specimen brush) and BAL | Obtains specimens during simple bronchoscopy without contaminating the aspirate; modified technique (mini-BAL) is also effective without the need of full bronchoscopy. | Gram stain positive: Indicates organism is present. Culture: Identifies organism. Sensitivity: Reflects effectiveness of drugs on identified organism. |
| Serum theophylline level | Important baseline indicator for patients who take theophylline regularly; therapeutic level is close to the toxic level. If additional theophylline is given, serial levels should be measured within the first 12–24 hr of treatment and daily thereafter. Patients are monitored for side effects (e.g., nausea, nervousness, dysrhythmias). | Acceptable therapeutic range is 10–20 mcg/ml. There is little evidence to support clinical benefit for adding theophylline to inhaled β-adrenergic blocking agents and steroids for patients with acute, severe asthma who were not already using theophylline regularly. |
Collaborative management
Care priorities
The goal of asthma management is to control the disease using a stepped approach to therapies. Ideal control is attained when patients are free of daytime symptoms, do not awaken breathless or coughing at night, have few or no limitations on activities, do not regularly use rescue medications, have no exacerbations, and maintain a forced expiratory volume in 1 second (FEV1) and/or peak expiratory flow rate (PEFR) greater than 80% of the predicted value. When prevention fails, the potential for life-threatening respiratory failure is high during exacerbations unresponsive to treatment within the first hour. Management is directed toward decreasing bronchospasm and increasing ventilation. Other interventions are directed toward treatment of complications (Table 4-1).
1. Determine severity of asthma exacerbation:
a. Acute severe: PEFR is less than 40% of predicted or personal best in a patient who is unable to speak a complete sentence in one breath, with RR greater than 25 breaths/min and HR greater than 110 bpm.
b. Life threatening: In a patient with severe asthma, the PEFR is less than 25% of predicted or personal best, SpO2 less than 92%, PaO2 less than 80 mm Hg; PCO2 35 to 35 mm Hg, silent chest, weak respiratory effort, exhaustion, cyanosis, bradycardia, hypotension, dysrhythmias, confusion, coma.
c. Near fatal: PCO2 greater than 45 mm Hg and/or requiring mechanical ventilation using increased positive pressure to overcome inspiratory pressures; patient also has other findings of life-threatening exacerbation.
Patients have profound hypoxia and can tolerate high doses of O2 (FIO2) unless they retain CO2 and breathe by hypoxic drive. Most asthmatics are able to tolerate high flow O2, versus those with other obstructive lung disease who cannot. Oxygen dosage must be limited in nonintubated, mechanically ventilated patients who breathe via hypoxic drive to avoid hypoventilation and respiratory arrest. Humidified O2 therapy is begun immediately to correct hypoxemia and thin secretions. PaO2 is kept slightly above normal unless the patient retains CO2, to compensate for the increased O2 demands imposed by the increased work of breathing. The degree of hypoxemia and patient response determine the method of O2 delivery. A high-flow device (e.g., 100% nonrebreather mask) delivers more precise and higher FIO2. Management of anxiety must be considered, especially if the patient will not wear a mask because of feelings of suffocation.
5. Pharmacotherapy to manage acute asthma exacerbation:
Vigorous therapy is initiated to decrease bronchospasms, help reduce airway inflammation, and help remove secretions. Treatment is continued until wheezing is eliminated and pulmonary function tests return to baseline (Table 4-1).
• Bronchodilators: Dilate smooth muscles of the airways to help relieve bronchospasms, resulting in increased diameter of functional airways. SABAs are the mainstay of asthma exacerbation management, while long-acting beta-adrenergic agonists (LABAs) are used for long-term control of asthma. Theophylline and aminophylline are no longer recommended for management of acute bronchospasms.
• Corticosteroids: Given intravenously during the acute phase of the exacerbation to decrease the inflammatory response, which causes edema in upper airways. Administration should decrease reactivity and swelling of the airways. Dosage varies according to severity of episode and whether patient currently is taking steroids. The patient may be converted to inhaled corticosteroids once the acute phase has been resolved. Acute adrenal insufficiency can develop in patients who take steroids routinely at home, if these drugs are not given to the patient during hospitalization.
• Anticholinergics: Inhaled medications used to reduce vagal tone of the airways, thus helping to reduce bronchospasms. Ipratropium (Atrovent) is used in combination with inhaled SABAs for severe, acute asthma.
• Magnesium sulfate: American Thoracic Society asthma management guidelines (2008) recommend consideration of a single dose of magnesium sulfate 1.2 to 2 g over 20 minutes for patients with severe, life-threatening, or fatal exacerbation who have an inadequate or ineffective response to inhaled bronchodilators.
• Sedatives and analgesics: Used in more limited doses in patients who are not intubated or mechanically ventilated, unless the person is extremely agitated and unable to cooperate with therapy. These agents depress the central nervous system (CNS) response to hypoxia and hypercapnia. Once mechanical ventilation is in place, the dosage is titrated until the patient is comfortable and/or hypoxemia or hypercapnia begins to resolve.
• Buffers: Sodium bicarbonate may be given to correct severe acidosis not corrected by intubation and mechanical ventilation. Generally, this is only a temporizing measure to help relieve lactic acidosis. The physiologic response to bronchodilators improves with correction of metabolic acidosis.
• Antibiotics: Given if a respiratory infection is suspected, as evidenced by fever, purulent sputum, or leukocytosis.
Generally contraindicated in acute phases of exacerbation because of acute respiratory decompensation and hyperreactive airways. Once the crisis is over, the patient may benefit from percussion and postural drainage every 2 to 4 hours to help mobilize secretions.
CARE PLANS: ACUTE ASTHMA EXACERBATION
related to ineffective breathing patterns secondary to narrowed airways
1. 
Monitor for signs of increasing hypoxia at frequent intervals: Restlessness, agitation, and personality changes are indicative of severe exacerbation. Cyanosis of the lips (central) and of the nail beds (peripheral) are late indicators of hypoxia.
2. Monitor for signs of hypercapnia at frequent intervals: Confusion, listlessness, and somnolence are indicative of respiratory failure and near-fatal asthma exacerbation.
3. Monitor ABGs when continuous pulse oximetry values or patient assessment reflects progressive hypoxemia or development of hypercapnia. Be alert to decreasing PaO2 and increasing PaCO2 or decreasing O2 saturation levels, indicative of impending respiratory failure.
4. Monitor for decreased breath sounds or changes in wheezing at frequent intervals. Absent breath sounds in a distressed asthma patient may indicate impending respiratory arrest.
5. Position patient for comfort and to promote optimal gas exchange. High-Fowler’s position, with the patient leaning forward and elbows propped on the over-the-bed table to promote maximal chest excursion, may reduce use of accessory muscles and diaphoresis due to work of breathing.
6. Monitor FIO2 to ensure that O2 is within prescribed concentrations. If patient does not retain CO2, 100% nonrebreather mask may be used to provide maximal O2 support. If the patient retains CO2 and is unrelieved by positioning, lower-dose O2, bronchodilators, and steroids, intubation and mechanical ventilation may be necessary sooner than in patients who are able to receive higher doses of O2 by mask.
1. Monitor intubated and mechanically ventilated patients for increased intrathoracic pressure (auto-PEEP) due to “breath stacking,” wherein the next breath is delivered prior to complete emptying of the first breath. Each subsequent breath failing to completely empty increases lung volume and predisposes the patient to volutrauma, pneumothorax, and decreased cardiac output (CO) resulting from the hyperinflated lungs causing pressure increases inside the thorax which impede venous return to the heart.
2. Monitor for hypotension. Decreased venous return can lead to hypotension. Auto-PEEP should be suspected in an intubated asthmatic patient who is hypotensive following intubation and initiation of mechanical ventilation, when there is no other obvious cause (e.g., tension pneumothorax). If auto-PEEP is suspected, consult with the respiratory therapist and the physician to modify ventilator settings.
Respiratory Status: Airway Patency
1. Monitor patient’s ability to clear tracheobronchial secretions frequently. Set up suction equipment at the bedside.
2. Encourage oral fluid intake or administer intravenous (IV) fluids within patient’s prescribed limits to help decrease viscosity of the secretions.
3. Encourage coughing to clear secretions and deep breathing unless patient is already coughing uncontrollably or going into respiratory failure. If the patient can manage to take deep breaths, respiratory failure is manageable.
4. Provide humidified O2 to help liquefy tracheobronchial secretions.
5. Evaluate whether patient may benefit from chest physiotherapy, after crisis phase of exacerbation has been resolved. Discuss with physician. If appropriate, teach significant others to perform chest physiotherapy.
6. Teach patient proper coughing technique for effective management of secretions.
7. Instruct patient to take several deep breaths. Instruct significant others in coaching this technique.
8. After the last inhalation, teach patient to perform a succession of coughs (usually three or four) on the same exhalation until most of the air has been expelled.
9. Explain that patient may need to repeat this technique several times before the cough becomes productive.
1. Determine patient’s previous asthma control status, including which “step” of therapy was implemented (Table 4-3).
2. Compare current status to past exacerbation responses to determine respiratory status.
3. Ensure spirometry measurements (FEV1, FVC, FEV1/FVC ratio) or PEFR readings are obtained before and after use of a short-acting bronchodilator.
4. Educate patient about use of a PEFR meter at home.
5. Determine patient’s compliance with treatments.
6. Note onset, frequency, and duration of coughing and advise patient to avoid triggers of coughing if identified.
7. Coach in breathing or relaxation exercises.
8. Encourage patient to breathe slowly and deeply. Teach pursed-lip breathing technique to assist patient with controlling respirations as appropriate:
9. Teach patient and family how to decrease metabolic demands for O2 by limiting or pacing patient’s activities and procedures.
10. Schedule rest times after meals
