3. Respiratory Health System

Overview

The respiratory health system is concerned with the movement and exchange of gases to meet cellular ventilatory needs. Assessment data in this area should include the respiratory structures, the process of breathing. and the effects of inadequate ventilation both at the level of the pulmonary vessels and on the level of cellular exchange.

Case studies selected for the respiratory health system presentation include common emergent problems. Problems patients with other respiratory complaints might have include foreign body aspiration, the pneumonias, epiglottitis, and near-drowning. Patients in this category frequently have alterations in other health systems including the neurological-cerebral and cardiovascular health systems.

CUE WORDS

RELATED NURSING DIAGNOSES

impaired gas exchange
ineffective airway clearance
ineffective breathing
pattern potential for suffocation
potential for aspiration

Department of Emergency Medicine Triage Protocols

Case Studies

3.1 ASTHMA: AN ELDERLY PATIENT

Kathleen J. Barnett, RN, MSN, CEN

Mrs. L. is a 65-year-old black female with a previous medical history of asthma and hypertension. Mrs. L. presents to the triage nurse with a complaint of shortness of breath of approximately 2 hr duration. The triage nurse notes the presence of supraclavicular accessory muscle use and moderate dyspnea, with audible wheezes Triage vital signs are: respirations 32, pulse 106, BP 175/110. Oral temperature is deferred because of the patient's respiratory distress and mouth breathing.

Triage Assessment, Acuity Level IV: Shortness of breath with dyspnea and tachypnea; wheezing; history of bronchial asthma.

Mrs. L. is taken immediately by wheelchair into the ED for initiation of therapy The nurse determines that Mrs. L. is on 50 mg hydrochlorothiazide daily for hypertension: and 300 mg theophylline 3 times daily and metaproterenol (Alupent) inhaler, two inhalations 4 times daily, for bronchial asthma. Mrs. L. has no known drug allergies. Mrs. L. has wheezes generalized throughout all lung fields that are graded at+2 (0= absent, +1 = mild, +2= moderate, +3= severe). Peak expiratory flow rate is measured at 90 liters/win. While initiating treatment with metaproterenol inhalant solution via nebulizer, the nurse notes that accessory muscle use is also graded at+2, and a pulsus paradoxus of12 mm Hg is present. As ordered by the physician, blood is drawn for a theophylline level and complete blood count. Intravenous access is established simultaneously with a heparin lock. An axillary temperature of 36.8° C (98.2° F) is obtained.

QUESTIONS AND ANSWERS

1. What nursing diagnoses are applicable to this patient?

   Asthma can be defined as the acute, intermittent, reversible obstruction of the airways (1). Attention to airway and breathing would be foremost on the priority list for the nurse caring for an asthmatic patient. However, the perception of breathlessness and the anxiety it generates are also significant factors for the asthmatic. Close attention to knowledge deficits or short-term memory lapses in the care of the elderly is also crucial for the patient with a chronic disease such as asthma. The following list outlines pertinent nursing diagnoses for a patient such as Mrs. L.

   Diagnosis: Ineffective breathing pattern related to bronchial obstruction or to decreased energy and fatigue
   Desired patient outcome: The patient will exhibit a respiratory rate within normal limits, diminished or absent use of accessory muscles, and diminished or absent wheezing.

   Diagnosis: Impaired gas exchange related to decreased alveolar ventilation secondary to bronchospasm and mucus plugging
   Desired patient outcome: The patient's arterial blood gas results will indicate PaCO2 < 45 mm Hg and PaO2 > 80 mm Hg (if obtained). The patient's mucosa will be pink; skin will be warm and dry.

   Diagnosis: Ineffective airway clearance related to mucus plugging and/or bronchospasm
   Desired patient outcome: The patient's wheezes will be diminished or absent. The patient will be able to expectorate and/or handle secretions effectively.

   Diagnosis: Altered cardiopulmonary tissue perfusion related hypoxemia secondary to impaired gas exchange
   Desired patient outcome: The patient will maintain a normal cardiac output as evidence by systolic BP>90mm Hg, HR<100 beats/min, and urinary output > 30 ml/hr. The patient will remain awake, alert, and oriented; skin will remain warm and dry. The patient will not experience cardiac dysrhythmias.

   Diagnosis: Anxiety related to shortness of breath or perceived breathlessness
   Desired patient outcome: Patient will state that she feels less anxious and exhibits cues of diminished anxiety and restlessness.

   Diagnosis: Activity intolerance related to fatigue and/or hypoxemia
   Desired patient outcome: Patient is able to ambulate without dyspnea.
   
   

2. What is asthma?

   Asthma is a disease characterized by airway obstruction brought on by smooth muscle spasm of the bronchioles and hypersecretion of mucous glands (1). Asthmatics demonstrate an increased tracheobronchial sensitivity to any number of factors—even laughter can induce bronchospasm (2). Infection, allergic response to inhaled antigens (animal dander, pollen, house dust, mold spores, etc.). cigarette smoking, aspirin sensitivity, exercise, cold, and stress have all been implicated as precipitating factors in asthma attacks (1).

   Whatever the precipitant, it induces the bronchospasm, mucus production, and edema of the mucous membranes in the bronchioles of the asthmatic. Gas exchange is impaired, and secretions are more difficult to clear. Initially, the asthmatic hyperventilates to compensate, resulting in a slightly alkalotic pH, a PaCO2 lower than normal. and a slightly lessened PaO2 (70 to 90 mm Hg). As the attack progresses, hypoxemia worsens, while the PaCO2; begins to rise due to CO2; being trapped in the distal airways. In the asthmatic. PaCO2: over 45 mm Hg and Pa02 less than 50 mm Hg is cause for alarm, as it indicates that compensatory mechanisms have been exhausted and the patient is hypoventilating.

   Generally, the smooth muscle spasm associated with asthma is reversible and is episodic in nature. However, severe, unrelenting asthma attacks that do not reverse even after 24 hr of maximum doses of traditional therapy do occur and are known as status asthmaticus.
   
   

3. If a patient is wheezing, should it be assumed that she has asthma?

   It has been estimated that over one million ED visits and 130.000 hospital admissions per year in the United States are the result of acute asthma attacks (3, 4). It has also been estimated that 4000 deaths per year are attributable to acute asthma attacks in this country (5).

   However, there are any number of conditions that may cause a person to wheeze. Bronchitis, croup, chronic obstructive pulmonary disease, acute epiglottitis. foreign body aspiration, congestive heart failure, pulmonary edema, and tracheal/laryngeal obstruction are only a few of the many causes of wheezing and should be considered in the differential diagnosis. It is helpful when a previous diagnosis of asthma has been established. However, asthma has many causes and new onset of attacks can occur throughout the life span: ED personnel should be alert to the fact that an asthmatic attack can occur in a previously undiagnosed person, and that wheezing in a known asthmatic may be caused by other disease entities. A thorough history. coupled with an accurate physical assessment, can usually discriminate between an asthma attack and other causes of wheezing.

TIP: Lack of wheezing is an ominous sign in a known asthmatic patient with significant respiratory distress and poor chest movement—this indicates minimal air exchange, severe airway obstruction, and/or fatigue, and requires immediate intervention(1).

4. Is it safe to give adrenergic agents, such as metaproterenol, if the patient is already tachycardic? When are aminophylline or corticosteroids indicated?

   The asmatic patient frequently presents with tachycardia—a manifestation of the sympathetic response to circulating catecholamines. Tachycardia can also be a compensatory response to hypoxia or anxiety.

   Adrenergic agents used for the relief of bronchospasm have varying degrees of a -,ß1 , and ß2 - receptor sympathetic stimulation. ß1-receptors stimulate the heart. ß2-receptors relax bronchial smooth muscle. and a-receptors cause peripheral vasoconstriction. Epinephrine is the prototype adrenergic bronchodilating drug—it has a marked bronchodilating effect, but also marked a-receptor activity that causes elevated BP and increased pulse rate. Modified adrenergic agents that have been developed to combat asthma have greater specificity for ß2-receptors (isoetharine. albuterol, metaproterenol, and terbutaline) and are now preferred for the treatment of bronchospasm (6). Although all sympathomimetic drugs have the potential to stimulate cardiac functioning, those delivered via nebulization and inhaled directly into the bronchial tree have several advantages: lower doses can be used. the onset of action is more rapid, and the incidence of side effects (including cardiac stimulation) is lessened (6). Since sympathomimetic drugs are recommended as initial therapy for asthma, tachycardia in and of itself is not reason to withhold adrenergic agents. If, however, the clinical picture is clouded by a low BP, altered sensorium, or significantly altered arterial blood gases, more aggressive initial therapy, including intubation, should be considered.

   Theophylline compounds, including aminophylline, reduce bronchospasm by elevating cellular levels of cyclic adenosine monophosphate (cAMP). A great number of asthmatics take theophylline preparations on a regular basis either orally or parenterally. A therapeutic level of between 10 and 20 ug/ml must be attained in order to be effective. Therapeutic and toxic levels are very close for theophylline. so the nurse should be alert to signs and symptoms of theophylline toxicity: irritability, restlessness, insomnia, agitation, headache. fever, fasciculation, vomiting, and convulsions. Ventricular fibrillation and vascular collapse can also occur. Theophylline levels are altered by age. smoking, alcohol, caffeine, and a number of drugs (6. 7).

   Corticosteroids are the most potent antiasthmatic drugs available. but have a high incidence of systemic adverse reactions, and are therefore used primarily in patients who have not responded sufficiently to other agents. Methylprednisolone sodium methyl succinate and hydrocortisone sodium succinate are the two parenteral forms most frequently administered, and prednisolone is usually the oral drug of choice.

   Atropine has been found to be effective in treating bronchoconstriction that is vagus nerve-mediated, and may be considered when other treatments have proven unsuccessful (1). When given by nebulized inhalation, side effects of tachycardia, urinary retention, and loss of visual accommodation will be lessened.
   
   

5. What are appropriate nursing interventions for the patient with asthma?

   Much of the treatment for the patient with asthma is dependent or interdependent on physician orders for pharmacological agents. However, the nursing care of the asthmatic includes far more than medications. Two key points should be remembered from the outset. First, an asthma attack is a potentially life-threatening event and should be treated immediately. A triage acuity level of IV is usually indicated, as demonstrated by this case. Interventions should be started rapidly, and some assessment information may need to wait until treatment is initiated and the patient is breathing more easily. Second, asthma attacks are anxiety-producing, and anxiety can lead to greater respiratory difficulty. The immediacy of interventions on the patient's behalf and the calm reassurance of the nurse can begin to allay the anxiety that can add to the patient's oxygen consumption.

   Frequent assessment and monitoring are integral to care of the asthmatic. The nurse should be aware of these critical warning signs:

   Previous or recurrent episodes of status asthmaticus
   Previous intubations for asthma
   Peak expiratory flow rate (PEFR)<1001iters/min: forced expiratory  volume in 1 sec (FEV1) <0.5 liter
   Altered state of consciousness
   PaO2; <50 mm Hg; PaCO2; > 45 mm Hg; central cyanosis
   Pulsus paradoxus > 16 mm Hg
   Little or no response to bronchodilator therapy after 1 hr
   Moderate to severe dyspnea
   ECG abnormalities (1, 8,9)

   Frequent monitoring of vital signs is indicated, as well as monitoring of dyspnea, wheezing, accessory muscle use, and pulsus paradoxus.

TIP: The pulsus paradoxus is the difference in millimeters of mercury between the level of pressure at which the first Korotkoff's sounds are heard during expiration and the level of pressure at which one first hears Korotkoff's sounds throughout inspiration and expiration. A difference of more than 10 mm Hg is considered significant and indicates that left ventricular function is being effected by wide fluctuations in pleural pressure between inspiratory and expiratory phases. This is usually secondary to hyperinflation in the asthmatic patient.

Arterial blood gases (ABGs) are not indicated in all asthma attacks. but may be helpful in determining treatment for a moderate attack. and are critical in a severe attack. For the patient who is elderly (such as Mrs. L.), hypoxemic, or in severe distress, a cardiac monitor should be applied to assess for rhythm disturbances. The PEFR or FEV1 are significantly reduced in severe attacks of asthma: the PEFR measures the maximum flow of air at the outset of forced expiration, and FEV measures the forced expiratory volume during the first second. One of these measurements should be frequently assessed in order to trend the extent of airway obstruction.

The patient's progress toward desired outcomes should be monitored. If little or no response is seen after several inhalation treatments, another mode of therapy should be considered. The use of a theophylline compound or steroids has been described.

Concomitantly with pharmacologic therapy, oxygen should be administered. Most asthmatics are not C02 retainers, and oxygen is itself a bronchodilator (1). Therefore oxygen should not be withheld, and can be given at up to 5 liters/min without concern (1,8).

Hydration is also a key component of asthmatic therapy. Oral hydration, if tolerated, should be strongly encouraged, and intravenous hydration can be used where intravenous access is established. Keep in mind that the asthmatic may already be functioning from a fluid deficit from insensible water losses; insensible loss from the lungs will increase with hyperventilation, and diaphoresis will be greater as a result of the sympathetic response and/or fever.

TIP: The average asthmatic requires 3 to 4 liters of clear liquids per day in order to maintain adequate hydration and keep mucus secretions thin. This averages approximately 250 ml, or one 8-ounce glass, every hour while awake.

Activity should be minimized in order to decrease oxygen demand in the acutely asthmatic patient. The patient should also be placed in a sitting or high Fowler's position for maximum chest expansion and air exchange—stretchers are frequently not as appropriate for asthmatics as are chairs.

6. How might the treatment of asthma be modified for an elderly patient?

   Asthma therapy can be more complex in an older adult such as Mrs. L. because of the changes in the body with aging. The elderly patient must be assessed for preexisting cardiac conditions and renal disease that may affect breakdown and excretion of medications, leading to toxicity.

   Elderly patients have more difficulty with gastrointestinal complications of theophylline use including gastritis and reflux due to gastroesophageal incompetence. There is heightened CNS activity in the elderly contributing to insomnia, anxiety, and tremors. Steroids should be used judiciously as these may accelerate degenerative conditions that may be present (such as cataracts) or may contribute to onset of latent diabetes.

   Because of short-term memory losses or reduction in analytical abilities, treatment regimen and instruction for the elderly patient should be kept simple. Complex steroid tapers should be avoided. Extra time should be spent insuring that the patient can demonstrate proper use of an inhaler.
   
   

7. What are helpful clues to determine if hospitalization is needed?

   If after 2 to 4 hr of therapy the patient has continued dyspnea, accessory muscle use, wheezing that has not significantly improved, pulse rate > 120 beats/min, respiratory rate > 30, pulsus paradoxus > 10 mm Hg, PEFR < 200 liters/min, FEV1 < 1.5 liters, or abnormal ABGs, hospitalization is indicated.

   Other factors to consider to support admitting the patient to the hospital include a return visit to the ED within 48 hr of the last visit. symptoms that have persisted longer than 1 week, and history of prior episodes of asthma requiring hospitalization and intubation.

   Unlike the clinical picture of asthma in children or young adults, asthma in older individuals can be relatively resistant to treatment. This should be considered in patients like Mrs. L. when making the disposition. Mrs. L. is known by the ED staff to have frequent episodes of asthma, but is able to be managed with regular outpatient treatment. After receiving 5 hr of therapy that included nebulizations and a maintenance drip of aminophylline (her theophylline level was 9 mg/dl), she was discharged home. Because Mrs. L. lives at home with her daughter, a phone call was made to her daughter describing today's visit, treatment, and discharge plan.
   
   

8. What discharge instructions should be given to the asthmatic patient who is successfully treated in the ED?

   The asthmatic patient being discharged from the ED must be made aware that improvement in respiratory status to the extent that a patient can be discharged does not indicate that lung function has returned to normal. In fact, lung function may remain compromised for a week or more following an asthma attack (9). The patient may respond partially to therapy, but residual airway obstruction may put her at high risk for relapse. The patient should be told that her lung function is abnormal, and that compliance with medications, hydration, and avoidance of precipitating factors is critical to her continued improvement.

   Medication regimens should be reviewed thoroughly with the patient. If the patient is taking a theophylline preparation, she should be instructed that alcohol, smoking, and caffeine can alter the theophylline level, and therefore should be avoided. (Smoking is an airway irritant that should be avoided anyway.) Theophylline should be taken with meals to avoid gastric upset. If the patient is to take a steroid taper, the taper schedule should be clearly defined and reviewed. If inhalers are used at home, be sure the patient is instructed in their proper use. The patient should be able to return demonstrate, particularly the firing of the inhaler at midinspiration. Adequate hydration and asthma triggers for the patient should be reviewed.

REFERENCES

1. Downie RL: Obstructive airway disease. Top Emerg Med 8(4): 13-31, 1987.
   
   
2. Korenblat PE: Asthma: diagnosis. Mod Med 57:70-83, 1989.
   
   
3. Rosen P, Baker FJ, Braen OR, et al.: Emergency medicine: concepts and clinical practice. St. Louis: C.V. Mosby, 1983.
   
   
4. Tintinalli JE, Rothstein RJ, Krome RL, et al.: Emergency medicine: a comprehensive guide. New York: McGraw-Hill, 1985.
   
   
5. Eisenberg MS, Copass MK: Emergency medical therapy. Philadelphia: W.B. Saunders, 1982.
   
   
6. AMA Drug Evaluations, 5th ed. American Medical Association, Chicago, Illinois, 1983.
   
   
7. Gahart BL: Intravenous medications. St. Louis: C.V. Mosby, 1985.
   
   
8. Mowad L, Ruhle DC: Handbook of emergency nursing: the nursing process approach. East Norwalk, CT: Appleton &Lange, 1988.
   
   
9. Fischi MA, Pitchenik A, Gardner LB: An index predicting relapse and need for hospitalization in patients with acute bronchial asthma. N Engl J Med 305(14): 783- 88,1981.

3.2 SHORTNESS OF BREATH:  SPONTANEOUS PNEUMOTHORAX

Barbara Van de Castle, RN, MSN

Nancy is a 25-year-old white female who, at the triage area of the ED, is complaining of shortness of breath and chest pain. Nancy states these symptoms began suddenly, a day and a half ago. while she was sitting down after dancing. She was fine while dancing, but the pain came on at rest. The pain is only on the left side of her chest, and the pain gets worse with each breath. On a scale of 1 to 10 the pain is a 7. Nancy is anxious and is slightly diaphoretic. Nancy states she smokes one pack of cigarettes a day and has no significant medical history. Her vital signs are respirations 34, pulse 124 and regular, BP 144/90, oral temperature 99.4° F.

Triage Assessment, Acuity Level III: sudden onset of pain and shortness of breath. moderate respiratory distress, respiratory rate 30 to 40.

An x-ray is ordered at the triage area and completed for PA and LAT chest. In the treatment area Nancy's physical assessment is completed by the treatment nurse. Nancy's breath sounds are faint, but heard bilaterally. She is obviously tachypneic. No cyanosis is present. ABG results on room air are PaO2 of 67 mm Hg, PaCO2 of 30 mm Hg, pH of 7.50, and a HCO3 of 18, showing a respiratory alkalosis and mild hypoxia. The physician reports that the chest x-ray shows a 15% left upper pneumo-thorax. The diagnosis of spontaneous pneumothorax is made.

QUESTIONS AND ANSWERS

1. What is a spontaneous pneumothorax, and how does one occur?

   Spontaneous pneumothorax is a term used to describe a sudden, unexpected collapse or partial collapse of a lung. Spontaneous pneumothorax can occur in a person who may or may not have any underlying pulmonary disease. Apparently healthy young people, usually between the ages of 20 and 40 years, often experience these events. The usual cause is rupture of either a subpleural bleb at the surface of the lung, a sub clinical localized bullous disease, or an erosion through the pulmonary pleura. A bleb is a large, flaccid vesicle that when ruptured allows air to leak from the pulmonary alveoli. The causes of blebs or bullae in otherwise healthy persons is not known, but a familial predisposition has been reported. Risk factors for a spontaneous pneumothorax include emphysema and chronic obstructive pulmonary disease (COPD), blunt chest trauma, lung surgery, some forms of cancer, and smoking. Smoking increases the risk of first spontaneous pneumothorax 9-fold in females and 22-fold in males, as compared to nonsmokers. Men are 3 times as likely to develop a spontaneous pneumothorax as women. Pneumothoraces of this nature can occur during inactivity or low-activity periods and are not related to physical activity or sudden movements.
   
   

2. What is the medical management of a spontaneous pneumothorax?

   A first-time spontaneous pneumothorax is treated conservatively if the size of the collapse is under 20% of the lung field. No chest tube needs to be placed, but the patient should be asked to cough and deep breathe at regular intervals to enhance the reexpansic of the lung. A chest x-ray should be repeated at 4 to 6 hr to observe for increasing or decreasing percentage of the lung collapse. Of course, if the signs and symptoms become worse, the frequency of the chest x-rays should increase. A baseline room air ABG should be performed and oxygen administered as needed. If the patient's signs and symptoms improve. the patient will probably be able to be discharged from the ED with close and frequent follow-up with a private physician or at a clinic. If the signs and symptoms do not improve or the chest x-ray shows an increasing percentage of pneumothorax (> 20%), the patient will be admitted to the hospital and a chest tube may be placed.
   
   

3. What nursing care problems are present with a patient that has a spontaneous pneumothorax?

   Although medical interventions are conservative and limited at this time, the nursing care needs of this patient are significant. Nancy is at risk for further respiratory compromise and should be assessed frequently. The feeling of breathlessness that occurs with a partial pneumothorax can induce anxiety and enhance hyperventilation that could exacerbate the already present respiratory alkalosis.

   Diagnosis: Impaired gas exchange related to decreased functional lung tissue with secondary tachypnea
   Desired patient outcome: The patient will have a regular rate of respiration between 18 to 22 and an ABG of PaO2; of 80 to 100 mm Hg, PaCO2 of 35 to 45 mm Hg, pH of 7.35 to 7.45. and an HCO3 of 21 to 28 mEq/L; the patient's breath sounds will be heard in both lung fields and are clear and equal.

   Diagnosis: Ineffective breathing pattern related to decreased functional lung tissue, feelings of breathlessness, and anxiety resulting in tachypnea
   Desired patient outcome: The patient will have a regular respiratory pattern with equal chest expansion and a rate of 18 to 22; the patient will state her breathing is easier and that her feelings of breathlessness are diminished.

   Diagnosis: Pain related to altered pulmonary tissue integrity and pleura! irritation
   Desired patient outcome: The patient will state that the pain is absent or decreased to a tolerable level: the patient will not exhibit nonverbal cues of pain.

   Diagnosis: Anxiety related to the unknown cause of her feelings of breathlessness and chest pain
   Desired patient outcome: The patient will describe her feelings of anxiety and use effective coping mechanisms to manage her feelings: the patient will describe an increase in psychological and physiological comfort.

   Diagnosis: Knowledge deficit related to etiology and signs and symptoms of a spontaneous pneumothorax
   Desired patient outcome: The patient will describe what a pneumothorax is, how it occurs, and her risk factors: the patient will state actions that she will take to reduce her risk: the patient will state signs and symptoms of a spontaneous pneumothorax and the actions she will take if the symptoms recur.
   
   

4. What nursing actions should be taken to support this patient?

   Nancy should receive continuous monitoring other vital signs and respiratory function, at least every 1/2 to 1 hr. The nurse should assess Nancy for decreased breath sounds, increased respiratory distress. tachycardia, tachypnea, use of accessory muscles, and cyanosis. Any deterioration in the patient's condition should be reported to the physician immediately. The nurse can provide comfort measures for the patient by applying ordered oxygen and positioning the patient in an upright position to reduce the effort required to breathe. Talking with the patient at frequent intervals and perhaps having a family member stay with her should make her feel less anxious. Verbal reassurances can be made by the nurse in conjunction with various nursing activities, such as during vital-sign checks, hourly rechecks of ABGs. and auscultating breath sounds.

   Concurrent documentation should be completed to obtain a total picture of the patient's progress. Current ABG results should be compared with the patient's signs of improvement. The nurse can make recommendations to the medical plan of care for the patient from her nursing assessment and knowledge of normal progression for this type of problem.
   
   

5. What information will Nancy need prior to discharge?

   When Nancy is discharged from the ED, she must be aware that she could develop another spontaneous pneumothorax. If she becomes aware of recurrent signs and symptoms of a spontaneous pneumothorax, she must call her physician or go to an emergency room for a diagnostic chest x-ray and treatment. Nancy should inform her family that she has this problem and how they can help recognize the symptoms. Nancy should be told to reduce or stop her cigarette smoking. She is referred to her private doctor to help her in this process as well as to check her lung condition. Nancy can be told she will not need to limit her exercise as studies show there is no correlation between physical activity and increased incidences of spontaneous pneumothorax.

SUGGESTED READINGS

Bensc L. Gunnar E, Odont D. Wiman LG: Smoking and the increased risk of contracting spontaneous pneumothorax Chest 96(6):1009-1012. 1987.

Bense L. Wiman LG. Hedensticrna G: Onset of symptoms in spontaneous  pneumothorax thorax: correlations to physical activity. J Resp Dis 71:181-186,1987.

Price SA. Wilson LM: Pathophysiology: Clinical concepts of disease processes. 3rd ed. New York: McGraw-Hill. 1986.

3.3 PULMONARY EMBOLISM

Barbara Van de Castle, RN, MSN

George, a 52-vear-old black male. appears at the triage desk complaining of chest pain over his right chest that goes from front to back. The pain is described as sharp and stabbing and has lasted for 3 hr. The pain occurred suddenly while George was lying in bed this morning. The pain intensifies with deep breathing, coughing, and movement. George appears anxious, dyspneic. and has rates over his right upper and lower lobes. His respirations are 42. pulse 118 and regular, BP 150/99. temperature 10l.O°F. George has a medical history of COPD and is on many medication' He has no known drug allergies. George states that his problem today does not feel like his usual exacerbation of COPD and that he has been taking his medications including aminophylline regularly. There is no swelling or redness in George’s extremities.

Triage Assessment, Acuity Level IV: Severe respiratory distress. RR > 40, accessory muscle use and pulmonary congestion.

QUESTIONS AND ANSWERS

1. What are the likely medical diagnoses for this patient and how are they differentiated?

   Since George has a history of COPD, problems such as pleural effusion, pulmonary edema, pulmonary embolism (PE), or exacerbation of his COPD should be considered. Also, a MI or angina should be evaluated as possible etiologies for his symptoms. A chest x-ray. 12-lead ECG. and a room air ABG will be ordered initially to aid in the medical diagnosis by the physician. George's chest x-ray showed normal changes associated with COPD. Pleural effusion, pulmonary edema. and other pathologies were not evident. A 12-lead ECG helps to identify ischemic cardiac changes as well as changes that occur with pulmonary hypertension or pulmonary embolus. George's ECG showed changes indicating a pulmonary embolism. These changes include tall peaked P waves in leads II and III, right atrial and ventricular strain pattern, right QRS axis shift, right bundle branch block (RBBB) pattern, and ST segment and T wave changes. A room air ABG is ordered to assess the patient's oxygenation and ventilation status. Since a pulmonary embolus is suspected at this point. George's ABGs were evaluated with this etiology in mind. Unfortunately, the PaO2 has poor predictive value in excluding a pulmonary embolus. However, a decreased PaC02 in the presence of a normal PaO2 can increase the suspicion for a PE. George's COPD can complicate the interpretation of the ABGs. However, his reported hypoxia continues to support the potential diagnosis of PE.

TIP: ABGs can be used to evaluate oxygenation and ventilation mismatching (shunting) by evaluating the alveolar-arterial oxygen gradient [P(A-a)02]. An increased P(A-a)O2 gradient is an expected consequence of acute PE.

Because George's room air ABG, chest x-ray, and ECG strongly suggest a pulmonary embolus, he was sent to nuclear radiology for a ventilation-perfusion (VQ) scan where a positive diagnosis for a PE was made. Had this test been undiagnostic, a pulmonary angiogram may have been indicated.

2. What is a PE and who is at risk for developing one?

   A PE occurs when material, such as a blood clot, breaks free from its attachment and circulates through the blood vessels to the right side of the heart. The clot is then lodged in the main pulmonary artery or one of its branches. Ninety per cent of pulmonary emboli come from thrombi in the lower extremities. Another source is the right side of the heart in the presence of atrial fibrillation or valvular disease. Emboli can also occur from air. vegetations, or other foreign matter. Predisposing factors to venous thrombosis and PE are venous stasis, increased blood coagulability, use of contraceptive medication, immobilization, postoperative conditions, complications of trauma. and some malignancies.

   The signs and symptoms of PE are extremely variable, depending on the size of the material or clot. These signs and symptoms range from none to sudden death caused by a massive embolus at the bifurcation of the main pulmonary artery. The classic signs of a moderately sized pulmonary embolus include unexplained dyspnea, tachypnea, tachycardia, and restlessness. Pleuritic pain, friction rub, hemoptysis, and fever are not usually present unless pulmonary infarction has occurred.
   
   

3. What is the medical management that the nurse can anticipate for a PE?

   Treatment of PE is directed toward stabilizing the patient and preventing recurrent emboli. Prophylactic low-dose heparin is frequently ordered to begin anticoagulation. In some instances thrombolytic agents that lyse clots such as streptokinase, urokinase, or t- PA may be indicated. Thrombolytic therapy is associated with considerable risk, including untoward bleeding, and is reserved for patients with massive PEs and shock. Oxygen is given as needed to treat hypoxemia and narcotic analgesics may be given for pain relief.

   Supportive measures to monitor cardiopulmonary function may be required during the acute phase of the PE, such as arterial pressure monitoring lines, cardiac monitor, Foley catheter to monitor urinary output, and a pulse oximeter to monitor capillary 02 saturation.
   
   

4. What nursing care problems are present for a patient with a PE?

   Even though the diagnosis of a PE can be difficult, the patient care team must act quickly to prevent more thrombi and prevent shock. George is quite anxious and is having difficulty breathing.

   Diagnosis: Activity intolerance related to imbalance of oxygen supply and demand, pulmonary shunting, shortness of breath, and pain
   Desired patient outcome: The patient will have a regular rate of respiration between 18 and 22; the patient will describe understanding of his allowed activity and will state his mobility limits: the patient will verbalize an understanding of the need for supplemental oxygen and medications that may increase his tolerance for activities; the patient verbalizes increased comfort and ability to perform activities.

   Diagnosis: Impaired gas exchange related to bronchoconstriction and decreased alveolar ventilation and accumulation of pulmonary interstitial fluid
   Desired patient outcome: The patient will have a regular rate of respiration between 18 and 22; Pa02 and PaCO2; will return to baseline for this patient. The patient will have a decrease in the amount of rales heard in the right lobes of the lung: the patient's mucous membranes will be pink.

   Diagnosis: Pain related to pleural ischemia and irritation of lung tissue
   Desired patient outcome: The patient will state that the pain is relieved or decreased to a tolerable level; the patient will not exhibit nonverbal cues of pain.

   Diagnosis: Anxiety related to sudden onset of chest pain and shortness of breath
   Desired patient outcome: The patient will describe his feelings of anxiety; the patient will state an understanding of his situation and demonstrate ability to focus on new knowledge and skills; the patient will describe feeling less anxious.
   
   

5. What nursing action should be taken to support this patient?

   The nurse will continue to monitor vital signs and ABG results frequently, as ordered. Medications will be administered, and the patient will be monitored for untoward effects. The patient will need a nurse at his bedside continually, at least during the most acute stage. While there, the nurse can talk to the patient, encourage relaxation. and explain procedures and equipment. Comfort measures can be used including positioning, maintaining a comfortable room temperature. providing a damp cool cloth, and, if ordered, a few ice chips for his dry mouth. Reassurance can be a key intervention for the patient as breathlessness and pain can generate fear.
   
   

6. What information will George need to know to prevent future pulmonary emboli?

   Prevention of venous stasis will be important for George because of his activity intolerance. A balance must be maintained so that George stays active but is not overcome with shortness of breath. Ted hose or other antithrombolytic stockings will be fitted for George even while he is in the hospital, and these will be important to maintain while at home. When George is ready to be discharged from the hospital, the nurse will need to help him identify activities that he can perform that minimize fatigue. Moderate activity combined with short rest periods will be helpful. A fluid intake up to 3000 ml/day should be encouraged.

   George will need instruction on the use and complications of anti-coagulant medications including the possibility of increased bleeding. George should also be instructed on the signs and symptoms of thrombophlebitis and recurrence of pulmonary emboli and actions that should be taken. The ED nursing report to the inpatient unit should include patient status and progress for each of the identified nursing diagnoses.

SUGGESTED READINGS

Bohachick P, Eldridge R: Chest pain after cardiac surgery. Crit Care Nurse 8(1):16-23, 1988.

Cvitanic 0, Marino P: Improved use of arterial blood gas analysis in suspected pulmonary embolism. Chest 95:48-51, 1989.

Johnson BC, Dungca CU, Hoffmeisier D, Wells SJ: Standards for critical care. St. . Louis: C.V. Mosby, 1985.

Price SA, Wilson LM: Pathophysiology : Clinical concepts of disease processes. 3rd ed. New York: McGraw-Hill. 1986.

3.4 SMOKE INHALATION AND CYANIDE POISONING

Cathy Robey-Williams, RN, MS, CCRN

At 3:15 AM fire department crews were dispatched to a dwelling fire. A brick row home was found fully engulfed in flames. A second alarm was sounded. Neighbors believed that George Johnson was at home when the fire started. At 3:40 A M the rescue crew exited the home with a middle-aged black male. unconscious with ago-nal respirations. The parademic crew that had been standing by began treating the patient by ventilating him with positive pressure oxygen. George had a pulse and had no apparent bleeding, so the crew quickly moved him into the ambulance to complete the secondary survey.

George was unresponsive to deep pain: his pupils were dilated and reacted sluggishly to light. His mustache and nasal hair were singed. His entire body was covered with soot. and his sputum was carbonaceous. George's skin was warm and dry. his capillary refill time delayed, color dusky, and mucous membranes gray.

The rescue officer reported that George was found in a third-floor smoke-filled bedroom with no open fire near him. It appeared that the source of the fire was the living room couch on the first floor.

As the paramedic attempted intubation, George gagged on the tube and aroused slightly. Therefore oxygen was applied at 15 liters/min via a non-rebreather mask. George's vital signs at this time were BP 160/100. pulse 110. and respirations 28. Breath sounds were heard bilaterally. with coarse rhonchi throughout all lung fields. The ECG showed that George was in a sinus tachycardia with occasional unifocal PVCs. An intravenous line was established with an 18 gauge catheter and D-, W solution infused slowly. En route to the hospital the paramedic notified the ED of George's condition, field assessment, treatment, and estimated time of arrival. The paramedic also requested and was granted an i)rder from the ED physician for 2 mg intravenous Narcan and 25 g intravenous D50 W, to be administered en route.

Triage Assessment, Acuity Level IV: Inhalation injury, hair singed: color pale. dusky: severe pulmonary congestion.

Based on the field report, the paramedics bypassed the triage area and immediately brought George to the resuscitation area. Upon arrival George is noted to be approximately 60 years old, weighing 80 kg. George is somewhat combative, pulling at his oxygen mask and attempting to sit up on the stretcher. He is not comprehending instructions given by the resuscitation team, and he is nonverbal. George appears healthy and is ventilating spontaneously, though mildly tachypneic. George's physical exam remains the same as that reported by the paramedics, and all other systems are clear of injury.

Among the initial treatments/or George in the ED are intubation, mechanical ventilation with oxygen at 100%, positive end expiratory pressure (PEEP) 5 c.m. and a second intravenous line. Blood samples are drawn for routine analysis. The ABG sample as well as the venous sample drawn at the scene are both sent to the lab for carboxyhemoglobin levels for comparison. A Foley catheter is inserted.

Alupent nebulization is initiated. The team leader then uses a fiber-optic bronchoscope to visualize the damage to the lower airway. Bronchial inflammation and mucosal ulceration are noted.

George's updated ABG results are Pa02 62, PaCO2 56, and pH 7.28. The field COHb is 36% and ED COHb is 24%. Three-hundred milligrams of sodium nitrate is administered intravenously followed by 12.5 g of sodium thiosulfate intravenously.

Throughout the resuscitation George's vital signs remained stable. Hyperbaric oxygenation therapy is considered and transportation arrangements are made for u helicopter to fly George to the closest chamber, located at a naval hospital 100 mile-away.

QUESTIONS AND ANSWERS

1. What is the etiology and complications of smoke inhalation?

   Inhalation injury is associated with very high mortality. Smoke inhalation is the leading cause of death within the first 24 hr following exposure to fire (1).

   Inhalation injury is most often present when there is a closed-space accident, with presence of heavy smoke, and the patient is unconscious. Smoke inhalation produces injury through direct heat. irritant gases, and contaminated particles that are aerosolized (2). Direct thermal damage to the lower airway is rare except in the case of victims exposed to super-heated steam. Steam has 4000 times greater heat-carrying capacity than air. Mechanisms that help protect against thermal injury include reflex laryngospasm and the efficient cooling system of the respiratory labyrinth apparatus (2, 3). Irritant gases and aerosolized contaminated particles produce the more frequent sequelae seen in the ED. Toxic gases occur from combustion (burning) and thermal degradation (melting) of synthetic materials (3). Inhalation of these toxic gases can cause damage to pulmonary tissues and alter respiratory function (3).

   There are many gases that are produced in any house fire. Carbon monoxide (CO) and cyanide are highly correlated and are the most lethal. Both gases act on the systemic functions of metabolism and respiration (4).

   Hydrocyanic acid is the gas form of cyanide which can be inhaled or absorbed through the skin. Hydrocyanic acid is formed through the burning of materials containing polyurethane. Polyurethane and polyvinylchloride are found in many home furnishings. Cyanide is normally present in humans in small amounts. Cigarette smoking or diet (lima beans) can increase levels slightly. Cyanide is detoxified in the liver by conversion to thiocyanate which is readily excreted by the kidneys (5). Cyanide in free form rapidly combines with ferric ion. interfering with mitochondrial oxidation. The result is a block in cellular respiration producing hypoxia at the tissue and cell level (5).

   Other gases formed from the burning of polyurethane include hydrogen chloride, chlorine, and phosgene. Other irritant gases formed in the burning of other household materials such as wood. cotton, and paper are the aldehydes. Ammonia is formed by the burning of nylon. All can cause mucosal irritation and damage.

   CO is the most immediate cause of death from fire and smoke (6). It has an affinity for hemoglobin 210 times stronger than oxygen (7). Inhalation of 0.1 % CO in room air decreases the oxygen-carrying capacity of hemoglobin by 50%. This reduction in the oxygen saturation of hemoglobin shifts the oxyhemoglobin dissociation curve to the left. CO also binds with myoglobin thus decreasing the oxygen-carrying capability to the muscle. Loss of tissue oxygen leads to ischemia, especially dangerous to the myocardium (6).

   The long-term results of CO poisoning at the cellular and tissue level are most pronounced on the CNS. CO acts on the brain to increase cerebral perfusion and increase cerebral capillary permeability, resulting in cerebral edema, increased intracranial pressure, and brain hypoxia (2, 3. 6). It is thought that the permanent neurological changes seen after CO intoxication may be due to degeneration of the brain caused by inhibition of aerobic metabolism at the cellular level. which may continue for up to 4 hr postinjury. See Table 3.4.1 for a list of CO levels and associated symptoms. (8).

   Smoke inhalation in general produces a range of upper and lower airway injury from minor edema to necrosis of the respiratory epithelium. Bronchospasm may occur as a direct result of airway irritation (2, 6). Inhaled particles, if small enough, gain entry into the lower airway and effect immediate changes on respiratory structures. Cilia cease functioning. Histamine, serotonin, and kallikreins are released. Surfactant activity is decreased, and mucosal edema. bronchorrhea and sloughed mucosa cause increased airway resistance and airway obstruction (2, 4, 6).

   The increase in capillary permeability that is seen after an inhalation injury lasts up to 36 hr after exposure and is caused by a release of vasoactive substances such as prostaglandins, histamine, and leukotrienes. Protein movement out of the vascular compartment changes oncotic pressure which exacerbates the fluid shift (9). To compound the problem, inhalation injury increases formation of lymph as well as increases bronchial blood flow tenfold (6). The net effect of these changes is interstitial edema, shunting, and decreased lung compliance.

   The clinical course of smoke inhalation begins with acute pulmonary insufficiency which is seen immediately postburn and progresses to pulmonary edema 6 to 72 hr after injury. Bronchopneumonia develops 3 to 10 days after injury and usually coincides with expectoration of epithelial casts (6, 10).