Download Respiratory

Common Respiratory Problems
1
NUR 475 – Family Nurse Practitioner III
Common Respiratory Problems










Cough
Dyspnea
Hemoptysis
Asthma
Bronchitis
COPD
Pneumonia
Lung cancer
Tuberculosis
Obstructive Sleep Apnea
Lower Respiratory Infections in Older Adults (LRI)




Significant source of both morbidity and mortality in the U.S.
Include:
o Acute bronchitis
o COPD-note Gold: Global Initiative for Chronic Obstructive Lung Disease
http://www.goldcopd.com/
o Influenza
o Pneumonia
o TB
May progress from less serious airway disease to potentially fatal parenchymal
involvement before the clinician can identify and treat the original disease
LRI Statistics (2001/2003) found at http://www.cdc.gov/tb/default.htm
o COPD = 4th leading cause of death for persons age 65 years and older
o Pneumonia + influenza = 5th leading cause of death in 2002
o TB case rate for age 65+ = 6.4 per 100,000 (2008) is the highest rate of all age
groups. The number of TB cases was highest among adults ages 25 to 44 (33% of
all cases)
Keep in Mind….

More so than with many other illnesses, treatment decisions and outcomes depend
heavily on epidemiological factors such as
o Age
o Functional status
o General health-underlying co morbidities
Common Respiratory Problems
2
Cough
Most common respiratory symptom and reason patients seek an office visit



Cough duration and differential diagnosis
o Acute - < 3 weeks
 Cough due to acute respiratory tract infection resolves within 3 weeks in
the vast majority of patients (over 90%).
 Pertussis should be considered in previously immunized adults with
persistent or severe cough lasting more than 2-3 weeks.
 Common cold (viral), influenza, acute bronchitis, B pertussis infection,
exacerbations of asthma/COPD/bronchiectasis, allergic rhinitis
 Consider; pneumonia, aspiration, CHF, PE
o Subacute - 3-8 weeks
 Post-infectious cough most common, sinusitis; exacerbation of asthma,
COPD of bronchiectasis
 Consider B pertussis
o Chronic or Persistent - > 8 weeks
 Asthma, GERD, upper airway cough syndrome (previously called postnasal drip), chronic rhinosinusitis, chronic bronchitis, ACE-I induced
cough, B pertussis, bronchiectasis
Contributing factors: smoking, trauma, living environment, work environment
RED FLAG symptoms
o Copious sputum production (bronchiectasis)
o Fever, sweats, weight loss, hemoptysis (TB, lymphoma, bronchial carcinoma)
o Dyspnea with cough (COPD, HF, fibrotic lung disease)
Essential inquiries: Age, duration of cough, dyspnea (at rest or with exertion), inhalant exposure
at work or home, other symptoms, tobacco use history, vital signs-including pulse ox, chest
examination, chest x-ray if unexplained cough lasts more than 3-6 weeks.
Testing:








PPD- if at risk for TB
CBC
Sputum C&S
CXR
ECG
Stop ACE-I if taking
Spirometry
Bronchoscopy-referral
See “Evaluation of Patient with Chronic Cough” at
http://www.aafp.org/afp/2011/1015/p887.html
Common Respiratory Problems
3
Treatment





Individuals with acute cough associated with the common cold can be treated with a firstgeneration antihistamine/decongestant preparation such as Clarinex-D (desloratadine +
pseudoephedrine)
The newer generation of non-sedating antihistamines such as loratadine plays no role in
treating cough in this setting.
The use of inhaled ipratropium bromide (Atrovent) can be helpful in attenuating the post
infectious cough (Anticholinergic)
In patients with post-infectious cough, when the cough adversely affects the patient’s
quality of life and when cough persists despite use of inhaled ipratropium, consider the
use of inhaled corticosteroids with the recognition that this product will take about 1
week of use prior to providing significant symptom relief.
For severe paroxysms of post infectious cough, consider prescribing 30 to 40 mg of
prednisone per day for a short, finite period of time (5 days) when other common causes
of cough including rhinosinusitis, asthma, or GERD have been ruled out.
Central acting antitussive agents such as codeine and dextromethorphan should be
considered when other measures fail.
Dyspnea
Acute Dyspnea in the Office includes algorithms by Zoorob & Campbell retrieved from
http://www.aafp.org/afp/2003/1101/p1803.html
The Pathophysiology and Treatment of Dyspnea by James Hallenbeck, MD found at
http://69.36.35.38/accp/pccsu/pathophysiology-and-treatment-dyspnea?page=0,3
Use of the 6-Min Walk Test: A Pro and Con Review by Daniel R. Smith, MD, FCCP found at
http://69.36.35.38/accp/pccsu/use-6-min-walk-test-pro-and-con-review?page=0,3
Essential Evaluation factors: Fever, Cough, Chest pain, vital sign measurements including
pulse oximetry and temperature, Cardiac and chest examination, Chest X-ray, Arterial Blood Gas
measurement

Shortness of breath is a very common symptom in primary care, but diagnosing the
underlying disorder is not always easy
Complete history is key

Be sure to understand what the dyspneic patient means by “shortness of breath”
o Is it pain?
 Cardiac chest pains are often located centrally, whereas pain in pulmonary
disease may also be lateral and be aggravated by deep breathing and
coughing
 Does the effort required to breathe seem excessive?
Common Respiratory Problems



4
Does the patient have a feeling of smothering or of being unable to get a
satisfying breath?
Consider medication-induced causes:
o Beta blockers, including timolol maleate (Timoptic) eye drops used to treat
glaucoma, may aggravate CHF or induce bronchospasm in certain patients, even
those whose asthma or COPD has been subclinical. “Wheezers have more
difficulty with beta blockers.”
o Diffuse interstitial fibrosis, pleural effusion, and respiratory muscle paralysis or
weakness can all be due to medications
o Be alert for use of aminoglycosides, nitrofurantoin (Macrodantin), busulfan
(Myleran), cyclophosphamide (Cytoxan), methotrexate, and drugs thought to
induce SLE.
Obtain thorough history
o Coughing and wheezing
o Previous lung diseases (tuberculosis, pneumonia, asthma)
o Smoking habits
o Previous chest surgery
o Has the patient ever coughed blood?
 Hemoptysis associated with inflammation in 80-90% of cases, idiopathic
bronchitis being the most common cause; others are bronchiectasis,
tuberculosis, carcinoma, and aspergillosis and even less common are
pulmonary infarction from embolic disease, left heart failure, mitral
stenosis.
 Bronchiectasis: chronic dilatation of a bronchus or bronchi, with a
secondary infection that usually involves the lower portion of the
lung. Dilatation may be in an isolated segment or spread throughout the
bronchi. (Taber’s Cyclopedic Medical Dictionary, 20th ed., 2005)
Bronchiectasis is a congenital or acquired disorder of the large bronchi
characterized by permanent, abnormal dilation and destruction of
bronchial walls. May be caused by recurrent inflammation or infection of
the airways and may be localized or diffuse. Cystic fibrosis causes ½ of all
cases. Essentials of diagnosis include: chronic productive cough with
dyspnea and wheezing, recurrent pulmonary infections requiring
antibiotics, a preceding history of recurrent pulmonary infections or
inflammation, or a predisposing condition, radiographic findings of
dilated, thickened airways and scattered, irregular opacities.
o Is cough chronic? (as with asthma, emphysema, bronchitis, especially in a
smoker). Is cough productive? (amount and color of sputum)
o Environmental substances the patient may be exposed to at work and at home?
o When does the patient feel dyspneic and what circumstances and activities bring
on the sensation?
 Dyspnea at night especially paroxysmal nocturnal dyspnea (PND)
suggests left ventricular dysfunction, particularly if progressively worsens
over several months
Common Respiratory Problems




May feel well when they go to bed but wake up with a feeling of
suffocation that is relieved by sitting up or walking around (obstructive
sleep apnea)
 Patients with COPD may also become dyspneic at night, but the episode is
likely to occur after many hours in bed or in the early morning and is
relieved by bronchodilator inhalation or expectoration of significant
amounts of purulent sputum-pO2 drops at night
 Asthma patients tend to get up with dyspnea shortly after lying down
 Exertional dyspnea may reflect cardiopulmonary disease or simply poor
conditioning
 Ask how long it takes for dyspnea to be relieved after ceasing activity and
whether there is associated pain
Does dyspnea develops only while the patient is at rest?
o Uncommon and, unless the patient is very sick, may indicate psychogenic
disease, especially in a younger patient with no history of heart or lung
disease)
o Organic disease must be ruled out before diagnosing dyspnea as psychogenic.
Specific stresses or personal problems occurring?
When dyspnea is associated with specific postures, consider neuromuscular disease
o Patients with diaphragmatic paralysis have more difficulty breathing when
lying down than when sitting
o If the intercostal accessory muscles are predominantly involved in
neuromuscular deficit, the patient may be more comfortable when lying down,
with dyspnea becoming exaggerated when he is seated
Physical examination





5
Note components of breathing cycle:
o Prolonged and decreased expiration suggests airway obstruction
o Rapid and shallow breathing is more typical of CHF
o Irregular or very slow breathing may be due to neurologic disease
Mental status
Extremities:
o Edema; DVT, CHF
o Cyanosis
o Digital clubbing; right-to-left intracardiac shunt, lung cancer, interstitial
pulmonary fibrosis, chronic pulmonary disease with bronchiectasis, familial
clubbing, asbestosis, mesothelioma
Neck
o Neck vein distention (COPD, CHF, cardiac tamponade)
o Thyroid enlargement
o Trachea midline
Chest
o Inspect;
 Hyperinflation (including barrel chest) and use of accessory muscles
of breathing: substantial COPD
Common Respiratory Problems


6
o Palpate;
 Subcutaneous emphysema or crepitus
 Tactile and vocal fremitus - diminished in COPD, normal or enhanced
in CHF, absent with significant pleural effusion or a pneumothorax
o Percuss;
 Dullness – consolidations or effusions
 Hyper-resonance – pneumothorax or bullous emphysema
o Auscultate;
 Absent – pneumothorax, pleural effusion, airway obstruction
 Stridor - upper airway obstruction, epiglotitis (stridor, drooling, fever),
croup
 Wheezing – asthma, COPD, pulmonary edema, pulmonary emboli
 Decreased - airway obstruction
 Inspiratory and expiratory crackles (rales) - left CHF, pulmonary
edema and pneumonia
 Coarse crackles - interstitial pulmonary fibrosis or significant left
ventricular failure
 In patients with COPD - scattered fine basilar crackles can be present
from retained secretions (often heard at very end of expiration)
Heart auscultation;
o Dysrhythmia
o S3 gallop: left ventricular dysfunction (would also have jugular venous
distension, liver enlargement, peripheral edema)
o Increased second pulmonic sound (especially when associated with a pleural
rub) may mean pulmonary infarction, pulmonary HTN or cor pulmonale
o Distant heart sounds; COPD, obese persons, those with pericardial disease and
cardiac tamponade
o Check for scars on the chest that may indicate prior thoracic or cardiac
surgery
Abdominal - hepatojugular reflex, hepatomegaly, ascites (CHF)
Differential Diagnosis

Cardiopulmonary causes
o Heart diseases; CHF, CAD, dysrhythmias, pericarditis, MI
o Pulmonary; COPD, new-onset asthma or exacerbation, pneumonia,
pneumothorax, PE, pulmonary edema, restrictive lung disorders, respiratory
muscle dysfunction . . .
 Subtle interstitial disease-encompasses 180 disease entities with many not
having a specific cause: pulmonary fibrosis from Amiodarone,
antineoplastic agents, environmental, infections, systemic disorderssarcoidosis, Wegener’s granulomatosis, See Table 9-19, p. 292-Lange
2013
 Pleural effusion-a volume of fluid greater than 7-14 mL in this space is
abnormal. Many mechanisms come into play: increased hydrostatic
pressures in the microvascular circulation, decreased oncotic pressures in
Common Respiratory Problems



7
the microvascular circulation, lung collapse which decreases pleural space
pressure, increased permeability of the microvascular circulation,
obstruction of lymphatic drainage (neoplasm or sarcoidosis). A common
presentation of many pulmonary and systemic diseases. Many are
asymptomatic. Most common symptoms are dyspnea, nonproductive
cough, and pleuritic chest pain.
 Primary or secondary hypertension (including that following silent
pulmonary embolism)
Upper airway obstruction; epiglottitis, croup, foreign body
Systemic causes; anemia, hyperthyroidism, obesity, ascites, pregnancy
o May be a consequence of poor conditioning (a normally sedentary person who
suddenly undertakes strenuous activity)
Psychogenic; panic attacks, hyperventilation, pain, anxiety
Diagnostic testing





CBC, complete metabolic profile
Chest x-ray-What is a quality chest film? Use the RIPE mnemonic.
o Rotation. To determine the degree of rotation in a radiograph, measure the
distance between the medial heads of the clavicles and the adjacent spinous
processes in the upper thorax. In a truly straight film, the distances should be the
same.
o Inspiration. To check for an adequate degree of inspiration, count the anterior
ribs on the right. In a good radiograph, 6 anterior ribs should be visible above the
right hemidiaphragm.
o Position. Identification of a gas-fluid level (often in the gastric fundus), alignment
of the scapulae with the lungs, and a posteroanterior (PA) label all help establish
the patient was upright.
o Exposure. A good film must have both adequate penetration of the patient and
sufficient contrast to distinguish between adjacent structures of different densities.
If the intervetebral disks of the lower thoracic spine are visible through the heart
and the pulmonary vessels posterior to the heart on the left can be identified, the
exposure is probably adequate.
Resting ECG
Basic spirometry (the FEV1/FVC ratio of predicted/referenced value is the critical
measurement). Interpretation of spirometry discussed in
http://www.aafp.org/afp/2004/0301/p1107.pdf
o < 30% = very severe obstructive pulmonary disease
o 30-49% = severe obstructive pulmonary disease
o 50-79% = moderate obstructive pulmonary disease
o > 80% = mild obstructive pulmonary disease or may not have pulmonary disease
May need ventilation-perfusion scan, stress testing or cardiac catheterization
Common Respiratory Problems
Hemoptysis

Essential Inquiries: Smoking history, Fever, Cough, and other symptoms of lower
respiratory tract infection, Nasopharyngeal or gastrointestinal bleeding, Chest x-ray and
complete blood count
 Definitions
o Scant hemoptysis: blood-tinged sputum
o Frank hemoptysis: < 600 ml of blood in 24 hour
o Massive hemoptysis: > 600 ml of blood in 24 hours
 History
o Cough
o Sputum production
o Fever, chills, night sweats, weight loss
o Chest pain
o Gurgling, wheezing
o URI symptoms
o Smoking
o Travel to Africa, Asia, South America
 Clinical Findings
o Vital Signs; elevated temperature, heart & respiratory rates, hypotension
o General; Anxiety, pallor
o HEENT; chest nares and oropharynx, URI signs
o Neck; Supraclavicular adenopathy-helps diagnosis of lung cancer
o Chest
o Extremities: cyanosis, clubbing, edema
 Differential Diagnosis
o Scant or frank:
 Bronchitis
 Bronchiectasis
 Lung cancer
 Active TB
 Chronic necrotizing pneumonia
 PE with infarction
 HF
o Massive:
 TB
 Bronchiectasis
 Necrotizing pneumonia
 Lung abscess
 Fungal lung infection
 Bronchogenic cancer
 Diagnostic testing
o CXR
o CBC with diff
o T &C
o Coagulation profile
8
Common Respiratory Problems

o Chemistry profile
o ABGs
o UA (hematuria-vasculitis)
o Sputum analysis
o Echo (if diastolic murmur-all diastolic murmurs are pathological)
o Bronchoscopy
o PPD
o CT scan and/or angiography
Management
o Scant or frank bleeding
 Antibiotic trial if infection present
 Antitussive (nonsedating dose)
 Treat underlying condition
 Oxygen prn
o Massive:
 Assess ABCs
 Oxygen (mask)
 Volume resuscitation
 Foley catheter
 Positioning
 Bronchoscopy
 Mild sedation (anxiety)
***Case study group #1
Asthma
Expert Panel Report 3: Guidelines for Diagnosis and Management of Asthma
http://www.nhlbi.nih.gov/guidelines/asthma/asthsumm.htm
Asthma Care Quick Reference:
http://www.nhlbi.nih.gov/guidelines/asthma/asthma_quickref.htm
See Lange (2013) page 243-259
Essentials of diagnosis: Episodic or chronic symptoms of airflow obstruction: breathlessness,
chest tightness, wheezing and cough; Complete or partial reversibility of airflow obstruction,
either spontaneously or following bronchodilation therapy; Symptoms frequently worse at night
or in the early morning; Prolonged expiration and diffuse wheezes on physical examination;
Limitation of airflow on pulmonary function testing or positive bronchoprovocation challenge.
Note Stepwise Approach for Managing Asthma in Adults and Children > 5 Years of Age and;
Quick relief for asthma in readings.
Morbidity and Mortality
32.6 million people had had an asthma diagnosis in their lifetime
22.2 million people are currently diagnosed with asthma
9
Common Respiratory Problems
10
12.2 million people suffer from asthma attacks annually
Approximately 4000 asthma-related deaths occur annually
Approximately 11 people die from asthma each day
What is asthma? “A common chronic disorder of the airways that is complex and characterized
by variable and recurring symptoms, airflow obstruction, bronchial hyperresponsiveness, and
underlying inflammation. “ NHLBI, 2007
Making the diagnosis….Is it asthma?
History of
Recurrent wheezing
Recurrent chest tightness
Recurrent cough
Recurrent difficulty breathing
Troublesome cough at night
Cough or wheezes after exercise
Symptoms worse after exposure to airborne allergens, viral infections, smoke, pollutants
or other irritants
Symptoms influenced by menstrual cycle, strong emotions such as laughing or crying
Per EPR-3: Consider the diagnosis of asthma and perform spirometry if any of these indicators
are present. These indicators are not diagnostic by themselves but the presence of multiple key
indicators increases the probability of the diagnosis of asthma. Spirometry is needed to make the
diagnosis of asthma.
Goal of asthma therapy: Achieve control
Reduce impairment
Prevent chronic and troublesome symptoms
Require infrequent use of inhaled short-acting beta2 agonist (≤ 2 days/week)
Maintain (near) “normal” pulmonary function
Maintain normal activity levels
Meet patients’ expectations of and satisfaction with asthma care
Reduce risk
Prevent recurrent exacerbations
Minimize need for emergency department visits or hospitalizations
Prevent progressive loss of lung function
Provide optimal pharmacotherapy with minimal or no adverse effects
Examples of Controller Drugs to Prevent Inflammation-Mainstay of asthma care
Inhaled Corticosteroids
Leukotriene receptor
Mast cell stabilizers-good for
antagonists, leukotriene
kids as kids have mast cell
modifiers
release
Mometasone (Asmanex)
Montelukast (Singulair)
Cromolyn (Intal)
Fluticasone (Flovent)
Zafirlukast (Accolate)
Nedocromil (Tilade)
Budenoside (Pulmocort)
Zileuton (Zyflo)
Beclomethasone (QVAR)
Triamcinolone (Azmacort)
Common Respiratory Problems
11
Medications to Treat or Prevent Bronchospasm
Rescue drugs for bronchospasm-takes one
To prevent bronchospasm-these are not
minute to start working
rescue drugs, takes one hour to work
Short acting beta 2 agonists such as
Long-acting beta2-agonists such as
Albuterol (Proventil), pirbuterol (Maxair),
salmeterol (Serevent)
levabuterol (Xopenex-pronounced Zopenex)
Acute asthma flare management-Aggressive treatment of inflammation with corticosteroid,
i.e., Prednisone 40-60 mg qd X 3-10 days (average 5-7 days).This takes six hours to start
working and will see a change in 24 hours.
PEF-peak expiratory flow meters-handheld device, home monitoring tool PEF should be
measure in the morning before administration of a bronchodilator and in the afternoon after
taking a bronchodilator. A 20% change in PEF values from morning to afternoon or from day
to day suggests inadequately controlled asthma. PEF values less than 200L/min indicate
severe airflow obstruction.
Routine chest x-ray usually shows only hyperinflation.
Acute Bronchitis
Definition: inflammation of the tracheobronchial tree typically resulting from viral infection
with adenovirus or influenza. Most are 90% viral and 10% bacterial. The most common bacterial
pathogens are atypical pathogens: M. pneumonia, C. pneumoniae (not revealed by gram stain)

Cough is usually present, and mucoid sputum is produced in 1/2 of cases.
Acute Bronchitis in the Older Adult
•
Most common early symptoms
– anorexia
– malaise
– headache
•
Chest pain and fever can be present in severe infection
•
Lung findings often unremarkable; rhonchi and wheezing may occur (esp. in COPD)
Diagnosis
•
Secondary bacterial infection is common following influenza and in those with COPD or
immunocompromising illnesses.
•
Most common causative bacteria are Haemophilus influenzae and Streptococcus
pneumoniae. In COPD pts, Moraxella catarrhalis.
•
CXR should be performed in patients who appear ill or do not respond to initial treatment.
Treatment
•
General supportive therapy:
– rest
– fluids
– antipyretic-analgesic agents
– cough suppressants, if appropriate
Common Respiratory Problems
12
•
Antibiotic selection per sputum Gram stain and culture (ideally)
Empirical Treatment
•
Most common causative organisms can usually be treated with:
– amoxicillin
– second-generation cephalosporins
– erythromycin
– tetracyclines
– trimethoprim-sulfamethoxazole
Prophylaxis
•
For patients with severe chronic bronchitis, prophylaxis with low-dose tetracycline or TMPSMZ may be prescribed during winter months or when an exacerbation would be lifethreatening.
•
Use of the influenza and pneumonia vaccines is highly recommended for age 65+,
especially those with chronic disease.
***Case study group #2
Chronic Obstructive Pulmonary Disease (COPD)
Asthma is no longer part of diagnosis
Essentials of Diagnosis: History of cigarette smoking; Chronic cough, dyspnea (in emphysema),
and sputum production (in chronic bronchitis); Rhonchi, decreased intensity of breath sounds,
and prolonged expiration on physical examination; Airflow limitation on pulmonary function
testing that is not fully reversible and most often progressive.
From Prescribers Letter, September 3, 2009:
RUMOR: You can’t abruptly stop Advair or Symbicort.
TRUTH:
This is only partly true.
Some patients want to stop these combo inhalers...due to warnings
about an increased risk of death with long-acting beta-agonists.
Tell patients they DON’T need to taper long-acting beta-agonists
(salmeterol, formoterol).
Instead, recommend switching to just an inhaled steroid.
If asthma symptoms worsen, suggest increasing the steroid dose. If
this isn’t enough, suggest adding an oral leukotriene modifier like
montelukast (Singulair) for asthma or an inhaled anticholinergic like
ipratropium or tiotropium for COPD.
On the other hand, it can be important to taper inhaled steroids...to
prevent severe asthma exacerbations.
Recommend tapering an inhaled steroid over 2 to 4 weeks before
stopping...not because of adrenal risks but to lessen the risk of asthma
exacerbations.
Keep in mind that salmeterol and formoterol should NOT be used
alone for asthma. Explain that unless they are being used
prophylactically to prevent exercise-induced bronchospasm, they
need to be used with an inhaled steroid to reduce the potential risk of
Common Respiratory Problems
13
death.
If COPD symptoms worsen on a beta-agonist alone, suggest
adding an inhaled anticholinergic.
Watch for patients who may be abruptly stopping an inhaled
steroid because they can’t afford their meds. Emphasize the
importance of taking their inhaled steroid regularly. If they can’t, try
to recommend alternatives or suggest a patient assistance program
Pathogenesis-the inflammation of COPD differs from asthma so the use of anti-inflammatory
medications and the response to those medications are different. The inflammation of asthma is
mediated through eosinophils and mast cells. The inflammation of COPD includes neutrophils,
macrophages, and CD8 T lymphocytes (Chisholm-Burns, p. 232).
•
“COPD” generally includes:
– chronic bronchitis
– emphysema
•
Normal aging--> panlobular emphysema (a decrease in supporting elastic lung structure
with resultant loss of alveoli)
•
In the absence of lung disease, normal respiratory reserves are more than adequate to cope
with the changes due to aging.
•
Symptomatic disease results from centrilobular emphysematous damage to alveoli,
generally due to:
– smoking
– occupational exposures
•
Chronic bronchitis: excessive bronchial mucus production and a chronic cough that persists
for at least 2 successive years in the absence of any specific disease
•
Mucus hypersecretion and inflammation of the bronchial mucosa --> nonuniform airway
obstruction --> hypoxemia --> retention of CO2 --> cause or exacerbate pulmonary hypertension
--> elevated right-sided heart pressures
Diagnosis (-the dyspnea panel may be helpful here.)
•
One of the most common complications of an acute exacerbation of chronic bronchitis is
dyspnea secondary to Heart Failure.
•
Left-sided heart failure can be triggered by the additional hypoxemia of an acute infection
•
Since rhonchi and adventitious sounds are frequently present with COPD, lung auscultation
is typically not diagnostic
•
A 4th heart sound (S4) and pedal edema may be helpful diagnostic signs. Signs of cor
pulmonale include increased pulmonic component of the second heart sound, jugular venous
distension, hepatomegaly.
•
CXR only minimally useful (pulmonary edema may be masked)
• Spirometry is required to confirm the diagnosis. The presence of a postbronchodilator
FEV1/FVC ratio less than 70% confirms the presence of airflow limitation that is not fully
reversible. You don’t need full pulmonary function tests with lung volumes and diffusion
capacity to establish the diagnosis . (Tierney)
Note article differentiating asthma from COPD. Other differential diagnoses include: Asthma,
HF, Bronchiectasis, TB, Obliterative Bronchiolitis, Diffuse Panbronchiolitis (GOLD document)
Common Respiratory Problems
14
Treatment: Long-term therapy for elderly with COPD
•
Controlling symptoms
Medications
1. Short-acting bronchodilators, both beta agonists and anticholinergics, are the mainstay of
therapy for COPD.
2. Long-acting bronchodilators are indicated for moderate to severe COPD. Currently two
beta agonists (formoterol, salmeterol) and long-acting anticholinergic (tiotropium-Spirva)
are available.
3. Inhaled corticosteroids are recommended for patients with moderate to severe COPD
with frequent exacerbations (incidents which worsen symptoms).
4. Systemic corticosteroids (IV or pills) are beneficial for treatment of severe exacerbations.
5. Antibiotics may be beneficial for treatment of exacerbations. (Lange 2013, p 263)
Respiratory Bacteria
Gram positive
S. pneumonia
Pathogens Associated with COPD Exacerbation
Viral (20-50%)
Less common resp. bacteria
(usually in advanced disease
or repeat exacerbations)
Rhinovirus
Enterobacteriaceae spp.
Influenza virus
Pseudomonas spp. - inpatient
Gram negative
H. influenza
M. catarrhalis
Atypical pathogens
M. pneumonia
C. pneumonia
Legionella spp.
6. Theophylline in low doses may reduce frequency of exacerbations in patients who
tolerate it (it has many side effects).
•
•
Maximizing independent self-care
Reducing frequency of hospitalization
Acute Exacerbations
•
Anticholinergic drugs, beta-adrenergic drugs, bronchodilators, corticosteroids (If baseline
FEV1 < 50% of predicted, add a corticosteroid such as prednisone 40 mg qd for 10 days.
Consider using an inhaled corticosteroid such as nebulized budesonide (Pulmicort) during nonacidotic exacerbations), and oxygen should be progressively employed in a stepwise fashion.
Antimicrobial therapy is likely indicated when symptoms of breathlessness and cough are
accompanied by altered sputum characteristics that are indicative of bacterial infection such as
increased purulence and /or change in volume. Consider chest x-ray with fever and/or low SaO2.
•
Verify compliance with existing therapy
•
Monitor the adequacy of existing therapy (e.g., with a theophylline level-a lower dose of
Theo helps improve the action of the steroid)
Common Respiratory Problems
15
•
Escalate existing therapy to maximal dosages
•
Add new therapeutic agents directed at the presenting symptoms or apparent precipitating
event
•
Change mode of therapy delivery (po→IV)
When to Hospitalize?
•
If new oxygen therapy is prescribed or escalation of oxygen supplementation to levels that
must be closely monitored
•
Questionable compliance
•
Intravenous therapy
•
Use of nebulizer treatments more often than every 4 hours
Prevention
•
Smoking cessation
•
Proper nutrition and hydration
•
Exercise-pulmonary rehab
•
Use of continuous oxygen therapy
•
Prevention of pneumonia through use of flu and pneumococcal vaccine
***Case study group #3
Pneumonia
http://www.idsociety.org/uploadedFiles/IDSA/GuidelinesPatient_Care/PDF_Library/CAP%20in%20Adults.pdf
Essentials of Diagnosis/Community-Acquired Pneumonia Symptoms and signs of acute lung
infection: fever or hypothermia, cough with or without sputum, dyspnea, chest discomfort,
sweatrs or rigors; Bronchial breath sounds or rales are frequent auscultatory findings;
Parenchymal infiltrate on chest radiograph; Occurs outside of the hospital or less than 48 hours
after admission in a patient who is not hospitalized or residing in a long-term care facility for
more than 14 days before the onset of symptoms.
Essentials of Diagnosis/Hospital Acquired Pneumonia Occurs more than 48 hours after
admission to the hospital and excludes any infection present at the time of admission; At least
two of the following: fever, cough, leukocytosis, purulent sputum; New or progressive
parenchymal infiltrate on chest x-ray; Especially common in patients requiring intensive care or
mechanical ventilation
Pathogenesis
•
Mortality in older persons: 15-70%, depending on etiology and population at risk
•
Incidence: 25-44/1000 in the community; 68-114/1000 in chronic care facilities
•
High co-morbidity: 80-90% of elderly pneumonia patients have one+ concomitant illnesses
(DM, CV, COPD, chronic CHF, alcoholism)
•
Aspiration is believed to be the most common route of infection in elderly patients
•
Usual mechanism: unapparent introduction of oropharyngeal secretions into the lung while
swallowing, lying supine, or sleeping
Common Respiratory Problems
16
Most common organisms
•
In the community:
– S. pneumonia-“Strep will kill you.” Most common cause of fatal community-acquired
pneumonia.
– H. influenzae
– Atypicals: M. pneumoniae, Chlamydia pneumoniae, Legionella species
•
In hospital-acquired bacterial pneumonia:
– Klebsiella pneumonia-likes alcoholics
– H. flu
– S. pneumoniae,
– Staph. Aureus
Most Common Pathogens Encountered in Respiratory Tract Infections
CAP Sinusitis
ABECB
Pharyngitis
Streptococcus pneumonia
√
√
√
Hemophilus influenza*
√
√
√
Moraxella catarrhalis*
√
√
Atypicals
√
√
Mycoplasma pneumoniae
Chlamydia pneumoniae
Legionella Sp.
Streptococcus pyogenes
√
Viruses
√
√
√
√
*Can produce Beta-lactamase
ABECB=acute bacterial exacerbation of chronic bronchitis
From: Slain, D. (2009). Infectious Disease Therapeutics: What you Must Know about
Antimicrobial Therapy in the Era of Resistance.
Physical Findings
•
Presentation of pneumonia in the elderly is frequently nonspecific.
•
Poor appetite and weakness
•
Slower, insidious onset
•
A respiratory rate > 28 is often earliest clue.
•
Fever may be blunted or absent
•
Suspect pneumonia when has significant dyspnea or functional impairment
Diagnosis
•
Confirming diagnosis usually depends on the CXR, although an infiltrate may be obscured
by pulmonary edema or not apparent until 24-48 hours after rehydration.
•
Normal or mildly elevated total WBC count accompanied by a left shift in the differential is
characteristic but nonspecific.
•
ABGs, sputum specimen analysis
Treatment
See Lange (2013) page 267 for treatment of common organisms
•
RTO
Common Respiratory Problems
•
17
CXR 6 weeks after ABT done
Caution with...
•
Aminoglycosides: nephrotoxic, ototoxic
•
Erythromycin: multiple drug interactions and GI intolerance
•
Ciprofloxacin: inadequate coverage of S. pneumoniae; high incidence of delirium
Prevention
•
May be achieved in part by vaccination against influenza and pneumococcus
Lung Cancer
http://www.cancer.gov/types/lung
Essentials of Diagnosis: New cough, or change in chronic cough; Dyspnea, hemoptysis,
anorexia, weight loss; Enlarging nodule or mass, persistent opacity, atelectasis, or pleural
effusion on chest x-ray or CT; cytologic or histologic findings of lung cancer in sputum, pleural
fluid or biopsy specimen.
Review of content discussed in Pathophysiology regarding pathogenesis, symptoms
Diagnosis and Treatment-Lange, pp. 1595-1603. May develop pleural effusion. Can be sent
home with portable chest tube.
***Case study group #4
Tuberculosis
http://www.cdc.gov/tb/
http://www.who.int/mediacentre/factsheets/fs104/en/
Essentials of Diagnosis:
Fatigue, weight loss, fever, night sweats, and cough
Pulmonary infiltrates on chest x-ray, most often apical-p. 246, Imaging
+ TB skin test
Acid-fast bacilli on smear of sputum and sputum culture positive for M. tuberculosis
Characteristics of antituberculous drugs-Lange, 2013, p. 284 (dosages)
***Case study group #5
Obstructive Sleep Apnea (OSA)
Essential Evaluation: Excessive sleepiness or fatigue, snoring, witnessed apnea, crowded
airway, high-risk conditions (see below), polysomnogram test
Prevalence

1 in 20 adults have OSA with daytime impairment
Common Respiratory Problems







18
As common as adult asthma
26% of adult clinical population at-risk
32% of primary care adult patients at high-risk
30% of cardiology clinic population
Mortality rate similar to breast and colon cancer, significantly lower testing rate
80-90% undiagnosed and untreated; especially women with lower BMI
“Typical” OSA patient model (snoring, obese, sleepy, middle-aged male) misses up to
30% of cases
Pathogenisis




Crowded or narrow oropharynx relaxes in sleep and partially (hypopnea) or fully (apnea)
obstructs airway
Airway collapse alerts carbon dioxide and oxygen levels, then stimulates the brain to
cause a partial arousal
Leads to frequent arousals, sleep loss and in some cases hypoxemia
Familial trend likely due to anatomical characteristics
Symptoms


Daytime; excessive sleepiness, fatigue, unrefreshing sleep, morning/nocturnal headache,
decreased memory/concentration/attention/judgment, personality changes (irritable,
aggressive, anxious, depressed), weight gain, sexual dysfunction
Nighttime; snoring, gasps or pauses in breathing, nocturnal choking of dyspnea, restless
sleep, frequent awakenings, insomnia (W>M), mouth breathing, nocturia, nocturnal
gastroesophageal reflux, nocturnal diaphoresis
Signs














Overweight/obese; BMI > 25 kg/m3 (93% sensitive, 74% specific)
Large neck size; > 16 inches (61% sensitive, 93% specific)
Crowded oropharynx; large uvula, long soft palate, lateral crowding, macroglossia,
narrow or high arched hard palate, retrognathia, micrognathia, mid-facial hypoplasia
High-risk for OSA
HTN; 30%, particularly newly diagnoses and drug-resistant
Atrial fibrillation; 50% new onset and recurrent
CHF; 26-50%
CAD; 2-fold greater occurrence
Nocturnal dysrhythmias; frequent
Stroke/TIA;72% and increased with recurrent stroke
Obesity; 40%
T2DM; 23-40% and poor glycemic control
Pre-operative; >70% of bariatric patients, 66% with difficult intubation
Driving occupations; 3-fold increase of motor vehicle crashes
Common Respiratory Problems
19
Differential diagnosis


Nighttime symptoms;
o Primary snoring
o Panic attacks
o Larygospasm (GERD)
o Dsypnea due to pulmonary edema
o Central sleep apnea
o Nonobstructive alveolar hypoventilation
Daytime symptoms;
o Insufficient sleep syndrome
o Narcolepsy or idiopathic hypersomnia
o Periodic limb movement disorder
o Hypothyroidism
o T2DM
o Depression
Key health consequences of untreated OSA



Function related; excessive sleepiness, motor vehicle crashes (3.71 relative risk,
estimated 980 deaths/year), neurocognitive deficits
Disease related; HTN (OSA is an independent risk factor, JNC 7) , MI, cardiac
dysrhythmias (atrial fibrillation-49%, 40% reduction in recurrence with CPAP), CHF
(30-70%, 26-43% improvement in LVEF with CPAP), Stroke/TIA (57% initial, 74%
recurrent), impaired glucose metabolism, obesity, depression, erectile dysfunction
20.3 deaths: 1,000 person-years
Screening




Recommend screening all adults with high-risk conditions
Incorporate sleep questions into ROS (amount of sleep, snoring, unusual breathing in
sleep, excessive sleepiness and fatigue, insomnia, unusual behaviors in sleep, drowsy
driving)
Berlin Questionnaire – validated in primary care populations
STOP-Bang screening tool – validated in surgical populations
Diagnostic testing



Polysomnogram
CPAP titration
TSH, CBC, CMP, ferritin in selected cases
Treatment



CPAP (continuous positive airway pressure); most effective, average compliance 40-60%
Weight loss; 10% reduction in BMI reduces rate of apnea
Oral appliances; 30-60% effective overall, more effective in mild OSA, retrognathia,
lower BMI
Common Respiratory Problems

20
Surgical-multiple procedures; least effective overall
Additional information




Read overview of OSA at: http://emedicine.medscape.com/article/302773-overview
Dodson, K.J. (2008). Cardiovascular Effects of Sleep Apnea. The Journal for Nurse
Practitioners, 33 (6), 439-444.
http://www.webmd.com/sleep-disorders/understanding-obstructive-sleep-apneasyndrome
American Academy of Sleep Medicine website:
http://www.aasmnet.org/AboutAASM.aspx
Chronic Insomnia
First line treatment: Cognitive behavioral therapy, which includes:
 Stimulus control: aims to establish consistency in sleep patterns and maintain an
association of sleep with the bed and bedroom (e.g., only go to sleep when tired)
 Sleep restriction: limits time in bed to sleep time, gradually increasing the time spent in
bed as sleep efficiency improves
 Relaxation training: training to reduce somatic tension and control bedtime thought
patterns that impair sleep
Insufficient evidence on effectiveness of benzodiazepine hypnotics, melatonin, or trazodone.
See: “Management of Chronic Insomnia Disorder in Adults: A Clinical Practice Guideline
From the American College of Physicians” at http://annals.org/article.aspx?articleid=2518955