Anti cholinergics
Studies suggest that these
agents may be more effective in COPD than are beta agonists and they have fewer
side effects. The most common error is to use at too low a dose. They can be
given 4-6 puffs tid-qid. Onset of action slower than beta agonists.
3. Theophylline
This drug probably has utility
in patients with significant side effects from high dose beta agonists (allowing
the use of two drugs below their toxic levels) as well as in patients with
nocturnal symptoms. It enhances muscle function and may have some
anti-inflammatory effect.
4. Steroids
20-30% of patients with COPD
will improve lung function if given a trial of steroids. A simple pre-and
post-bronchodilator spirometry is not sufficiently sensitive to predict who will
or will not respond to steroids. One approach is to give 40 mg of Prednisone
orally qd for 2 weeks as a trial to determine if the airway’s obstruction is
reversible. Since many patients get a non-specific euphoria and increase in
energy, it is important to document pulmonary function before and during
administration of steroids to convince yourself that there is objective evidence
that they have made a difference. If patients have an increase in FEV1, the oral
steroid should be tapered and an inhaled steroid initiated in an effort to
sustain the benefit. Consider a steroid trial in patients who have moderate to
severe functional limitation.
D. Oxygen therapy
Long-term oxygen therapy
improves survival in hypoxemic patients with COPD. Improved pulmonary
hemodynamics plays a role. Oxygen administration reverses hypoxic pulmonary
vasoconstriction, reduces pulmonary artery pressure and right ventricular work,
and improves cardiac output and oxygen delivery to the tissues. Assessment of
need for oxygen therapy can be accomplished with an arterial blood gas or pulse
oximeter. Patients must demonstrate pAO2 < 55 or oxygen saturation < 88% (or
PAO2 of 55-60, 02 sat of 89% with signs of tissue hypoxia such as cor pulmonale,
polycythemia, right ventricular failure, or impaired mental status). In patients
with marginal values at rest or patients with polycythemia, one should also
assess oximetry during exercise and consider nocturnal testing (especially if
polycythemia or right ventricular failure is present). Oxygen supplementation
during exercise reduces dyspnea, pulmonary hemodynamics are improved, and
exercise capability increases. While nasal prongs are most common way to deliver
supplemental oxygen, one should consider a transtracheal catheter in young
individuals who are concerned about the cosmetic impact of nasal prongs, and in
patients who wish their portable 02 containers to last for longer periods before
being refilled (one can achieve the same results using lower flow rates with
transtracheal as compared to nasal prong oxygen). Patients must be cautioned not
to smoke when using supplemental oxygen.
E. Exercise/pulmonary
rehabilitation
1. Deconditioning: Many
patients with COPD and exertional dyspnea fall into a cycle of reduced activity,
deconditioning, more dyspnea, further reductions in activity, more severe
deconditioning, etc. This usually occurs slowly over months to years. Studies
have demonstrated that many of these patients have greatly reduced aerobic
capacity, low anaerobic threshold, and peripheral muscle and cardiovascular
deconditioning. These factors can be improved with an exercise program. It is
important to ask the patient whether he, at the time exercise must be stopped,
is limited by "fatigue," "leg discomfort," or "shortness of breath." If dyspnea
is the culprit, one should then inquire about the quality of the sensation.
Patients limited by deconditioning respond to exercise programs (minimum of 3-4
times/week) with improved functional capability. Both lower extremity and upper
extremity exercise have shown to be beneficial. Exercise training may have
additional benefit of enhancing clearance of lung secretions.
2. Inspiratory Muscle
Training: Experimental studies have demonstrated that dyspnea correlates with
the ratio of inspiratory pressure achieved on each breath to the maximal
inspiratory pressure possible for that patient. Thus, increasing the maximal
inspiratory pressure (MIP) by strengthening ventilatory muscles would alleviate
dyspnea. Clinical studies have been equivocal. Training is recommended for
patients with clearly reduced MIP, i.e., <50 cmH20
utilizing a training device that insures a minimal inspiratory effort on each
breath (threshold trainer) since one study has demonstrated that without such a
device, patients will prefer to hypoventilate rather than work hard to breathe
in.
3. Desensitization to Dyspnea:
Much of what is accomplished in rehabilitation programs results from
desensitization to the discomfort associated with obstructive airways disease.
Patients given education and social support learn to tolerate the symptom. They feel more "in control
functional status that
accompanies not only the breathlessness but the anxiety that often results. Much
of the breathing retraining techniques that are taught (e.g., pursed lips
breathing, diaphragmatic breathing) may work in part by giving the patient
coping strategies for dealing with his discomfort.
F. Volume reduction surgery
1. Two basic physiologic
principles behind the surgery:
(A) the chest is hyperinflated
which places the muscles of inspiration at a mechanical disadvantage;
(B) large bullae compress
relatively normal areas of lung. Removal of region of lung that consists
primarily of large bullae will reduce the size of the thorax, lengthen the
diaphragm, and allow greater ventilation of relatively normal lung.
2. Preliminary data indicate a
positive response to surgery with improved gas exchange, lung function, and
exercise capacity. The procedure is palliative - the underlying lung disease
continues to progress and, in some cases, the surgery may hasten deterioration.
Patients with heterogeneous disease (i.e., some regions of lung with severe
emphysema, other areas with relatively normal lung) do better than those with
homogeneous disease.
G. Lung transplantation:
Single-lung transplants have
proven successful. Procedure remains limited by lack of donor organs, cost, and
complications associated with immunosuppressive therapy. Survival for single
lung transplants: 67% at 1 year, 57% at 2 years, and 47% at 4 years. Results
somewhat better in recent years.
V. Acute Respiratory
Insufficiency - identify the cause. COPD "exacerbation" is an overused term that
conveys little information about the acute problem.
A. Risk factors
1. Airway reactivity: Patients
with significant airways reactivity are at risk for developing acute on chronic
respiratory insufficiency when exposed to stimuli that trigger bronchospasm (eg,
allergens, heat and humidity, cold air, pollutants, cigarette smoke, etc).
2. Infections: Patients with
COPD, particularly if history of chronic bronchitis, have impaired airway
clearance. COPD increases the incidence of acute respiratory infections,
including acute bronchitis and pneumonia.
3. Congestive heart failure:
Frequent comorbid condition in patients with COPD. Failure may be difficult to
diagnose in acutely ill individual - classical rales may not be present, CXR may
not demonstrate vascular redistribution and interstitial edema. CHF must always
be considered in patient with acute or subacute deterioration in symptoms.
B. Management
1. Antibiotics: Several
studies have shown the benefit of using antibiotics in patients with COPD,
especially if a history of chronic bronchitis or a change in the quality or
quantity of sputum. If no evidence of pneumonia and patient does not appear
"toxic," oral antibiotics are adequate.
2. Bronchodilators: Most
physicians start with beta agonists which can be given every 30-60 minutes if
patient is in moderate to severe respiratory distress. The drug can be given by
metered dose inhaler with spacer or by nebulization. There is some evidence that
addition of ipratropium gives greater bronchodilation than beta agonist alone
without increased side effects.
3. Theophylline: Generally
reserved for the most severe cases unresponsive to inhalational therapy and
steroids. Potential toxicity is equivalent to the potential gain.
4. Corticosteroids: Used in
patients with evidence of airways reactivity and previous bronchodilator
response. If patient's history not well documented, steroids are generally used
in cases of moderate to severe respiratory insufficiency.
5. Oxygen therapy: Therapy is
guided by oxygen saturation. Oxygen saturation should be assessed with exercise
prior to discharge. The patient may not return to baseline level of gas exchange
for 4-6 weeks after acute decompensation, especially if an infection was
present. While administration of supplemental oxygen to patient with COPD and
chronic hypercapnia may cause an increase in PaCO2,
evidence now repudiates the classical teaching that such patients will "stop
breathing." Respiratory drive in these patients is supranormal due to
combination of factors including dyspnea, stimulation of pulmonary and chest
wall receptors, as well as deranged gas exchange. While administration of oxygen
reduces the hypoxic drive to breathe, overall ventilatory drive remains above
normal. Increased hypercapnia appears to be due to combination of (a) reduced
ventilation, (b) change in V/Q mismatch, and (c) the Haldane effect, i.e., the
shift in the carbon dioxide/Hgb dissociation curve to the right. Remember -
hypoxia kills! Give adequate supplemental oxygen to get 02
saturation to 90%. If this causes severe respiratory acidosis and
acidemia, then the patient should be intubated and mechanically ventilated.
Venturi masks allow greater control of inspired concentration of oxygen than
nasal prongs and other masks.
6. Noninvasive ventilatory
support: Several studies suggest that use of BIPAP in patient with acute
respiratory insufficiency due to COPD and superimposed process may obviate the
need for intubation and mechanical ventilation. Noninvasive ventilation cannot
be used in patients with depressed mental status, excessive secretions,
inability to protect their airway, apneas, or inability to cooperate with
therapists. CPAP in the chronic state may reduce chronic hypercapnia in some
patients with COPD as well as alleviate exertional dyspnea. Many patients with
COPD tolerate nasal masks poorly. It is still an experimental intervention. CPAP
has also been shown to benefit patients with congestive heart failure, probably
in part by reducing afterload on the left ventricle. Data is less convincing for
patients with pneumonia or asthma.
VI. Special Considerations
A. Acute respiratory failure
and mechanical ventilation
1. Role of respiratory muscle
fatigue: In the presence of paradoxical motion of the abdomen and increasing
respiratory frequency with decreasing tidal volumes, muscle fatigue is probably
contributing to the patient's decline. Institution of ventilatory support under
these circumstances has been shown to "instantly" eliminate the EMG activity in
the diaphragm. This finding is only demonstrated when the muscle is fatigued.
2. Ventilator settings: Most
patients with COPD who develop respiratory failure are easily ventilated
following intubation. Usually, the FIO2 can be kept < 0.5. Patients usually do
not fight the ventilator (in keeping with the thought that muscle fatigue is
contributing to the respiratory failure), and peak pressures are not
particularly high (reflecting the increased compliance of the lungs in
emphysema). Assist control or IMV modes of ventilation are equally acceptable.
Tidal volumes and frequency settings on the ventilator are determined primarily
by the patient's size, the desired PaCO2, and the presence of autoPEEP. a.
AutoPEEP: autoPEEP or intrinsic PEEP occurs when the patient has inadequate time
to exhale; i.e., the next inspiration occurs while exhalation is in progress and
there is positive pressure in the airway at the moment of initiation of
inspiration. If the ventilator frequency is too high, one may create autoPEEP by
not allowing sufficient time for exhalation.
b. Post-hypercapnic metabolic
alkalosis: Patients with acute respirator failure may have an acute on chronic
respiratory acidosis. When placing such a patient on the ventilator, one should
aim for a PaCO2 that approximates the patient's baseline state. If the
ventilator is set with too high a minute ventilation, one will produce an
alkalosis because the patient's kidneys have retained bicarbonate to compensate
for the chronic hypercapnia. If this is not recognized quickly, the kidney will
excrete bicarbonate and you may have difficulty weaning the patient from the
ventilator.
3. Weaning: Assuming the
patient has had an acute, reversible problem that has precipitated respiratory
failure, one is almost always able to wean the patient from the ventilator.
Attention must be paid to the patient's volume status (occult CHF is often a
factor in preventing weaning), nutrition, judicious use of anxiolytics, and
airways secretions. Among a number of criteria for successful weaning, the
respiratory frequency to tidal volume is now felt to be most predictive, f/Vt <
100 predicts successful spontaneous ventilation (note: tidal volume expressed in
liters).
B. Surgery
1. Preoperative evaluation
a. Non-thoracic surgery: No
level of lung function is an absolute contraindication to non-thoracic surgery.
However, severe airways obstruction is associated with a higher rate of
complications. The farther the procedure from the diaphragm, the lower the
risk. In upper abdominal surgery, the mortality rate may be as high as 3-5% with
morbid events occurring in as many as 80% of patients. If the procedure is
elective, discontinuation of smoking for several weeks prior to surgery may
result in diminution of secretions and improved gas exchange (ideally, stop
cigarettes for 8 weeks prior to surgery). Baseline blood gases and spirometry
should be obtained.
b. Thoracic surgery: If
contemplating removal of lung tissue in a patient with limited pulmonary
reserve, it is important to not cause the patient to become a "respiratory
cripple" or an individual who cannot be weaned from mechanical ventilation.
Factors to consider include (a) the predicted postoperative FEV1, which should
be > 0.8 L, (b) diffusing capacity > 40% predicted, and (c) PaCO2 < 45 mm Hg.
For patients facing a pneumonectomy, contraindications include an FEV 1 < 2 L
and a diffusing capacity < 60% of predicted. Quantitative ventilation and
perfusion scans may be helpful in predicting the impact of pulmonary resections
on postoperative function. In addition to measures of lung function as outlined
above, there is evidence that a patient's functional status may also be a useful
predictor of postoperative morbidity and mortality. Patients with a maximal
oxygen consumption during an exercise test that is greater than 15 mL/kg/min
have better outcomes.
2. Management: Maximize lung
function preoperatively with bronchodilators (consider short course of
steroids), good bronchopulmonary hygiene should be assured if excessive
secretions, and exercise program should be initiated. Use of epidural anesthesia
postoperatively has greatly facilitated airways clearance and early mobilization
of patients, preventing additional complications.
C. Screening for lung cancer
1. Routine: Several large
studies have demonstrated no survival benefit associated with routine radiologic
screening for patients with COPD (PA and lateral CXR). Routine screening of
sputum cytology is also not beneficial.
2. Hemoptysis: Hemoptysis in
the presence of a normal CXR is associated with 5-10% incidence of malignancy on
bronchoscopy. Risk increases with (a) age > 40; (b) history of cigarette
smoking; and (c) duration of hemoptysis greater than 10 days. One or two
episodes of hemoptysis in setting of acute respiratory infection and normal CXR
generally does not warrant bronchoscopy. Hemoptysis in a smoker that occurs
without evidence of infection and is repeated at a prolonged interval (i.e.,
more than 10 days) raises more suspicion.
D. Sleep Disorders
1. Patients with COPD have a
higher prevalence of insomnia, excessive daytime sleepiness, and nightmares than
the general population.
2. Many patients desaturate
during REM sleep, and may be related to hypoventilation during sleep. Suspect in
patients with borderline oxygen saturation at rest, polycythemia, and evidence
of right ventricular failure. It is not yet clear whether treating isolated
nocturnal desaturation has an impact on mortality.
3. Obstructive sleep apnea may
coexist with COPD and some studies suggest the incidence of OSA in these
patients is greater than would be expected based on the relative frequencies of
the two conditions.
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