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. C.o.P.D. Kidney. Brain. . G.I.T. Aging. Sleep. Skeletal system muscle. Reproductive system. Circulatory system. BY PROF.SAMIHA MOHAMED ABOU –BAKR. PROF. OF chest diseases El-Azhar .

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Skeletal system muscle

Reproductive system

Circulatory system



PROF. OF chest diseases El-Azhar

In Egypt 14.8 % of male deaths in 1987 were smoking related, compared to 8.9 percent 1974 also WHO found that five percent of Egyptian family income is spent, in one form or another, on smoking, and six million Egyptian smokers consume a total of 42 billion cigarettes annually a figure estimated to rise to 85 billion in the next century, and 439.000 of cigarette smokers in Egypt are children 10 years old

Chronic obstructive pulmonary disease (COPD) is polygenic devastating clinical problem. Although cigarette smoking is the major risk factor, only 10-20% of smokers develop symptomatic COPD.

Alpha-1- antitrypsin (1-AT) deficiency is an important cause of lung disease, being associated with early onset adult emphysema

The genotype most often responsible for this deficiency is homozygosity of PiZ but heterozygotes may also be affected.

Several genetic loci appear to exert a strong influence on lung function, probably through an effect on lung growth and development.

Polymorphisms of the glutathione-S-transferase antioxidant genes may be associated with increased susceptibility to rapid lung function decline in smokers, according to North American researchers.

The theory of interplay . is that this inflammatory process which includes alveolar macrophages in some way releases neutrophil chemotactic factors known as (IL-8 ) causing neutrophils to emigrate from the blood space into the airspace to release elastase . In normal circumstances alpha-1-antitrypsin binds to the elastase and prevents it from binding to elastin thus destroying the structure of the lungs.

in the blood and air space release more active oxygen species in smokers, than in non smokers, these together with the 1017 oxidants in inhaled cigarette smoke inactivate the alpha-1-antitrypsin at its active site. This reduces the ability of alpha-1-antitrypsin to bind to elastase by a factor of approximately 2000 allowing active ealstase to bind to elastin and cause the enlargement of the airspace that is seen in emphysema.

P-Selectin , L-seletin adhesions are important for the transport of inflammatory cells in the systemic circulation .

Glutathione is always in balance with its oxidised form and ,intracellur, it is part of the glutathione redox system which uses the enzyme glutathione peroxidase to detoxify lipid peroxideses and hydrogen peroxide . Reduced glutathione is sacrificed for oxidised glutathione .
slide10 a mixture of 3 separate disease processes that together form the complete clinical and pathophysiological picture. These processes are chronic bronchitis, emphysema and, to a lesser extent, asthma. Each case of COPD is unique in the blend of processes; however, 2 main types of the disease are recognized.

according to gina
According to GINA
  • What is the difference between asthma and COPD (chronic obstructive lung disease)?COPD is a collective name for chronic bronchitis and emphysema, two diseases that are almost always caused by smoking. Many of the symptoms of COPD are similar to those of asthma (e.g. breathlessness, wheezing, production of too much mucus, coughing).
COPD is generally a more serious disease than asthma, because the changes in the airways are much more difficult to treat, and it usually has a worse outcome. Unfortunately, COPD can cause greater long-term disability and have a greater effect on the heart and other organ systems than asthma.
COPD is an obstructive airway disease, and in this way it is quite like asthma. In fact, early in COPD development, you may have very similar symptoms to those seen in asthma
COPD is often misdiagnosed as asthma early in its development.While the obstructive nature of asthma and COPD may be similar in some ways, they are two very different diseases
Asthma and COPD differ in many ways. COPD is usually caused by cigarette smoking while asthma is not caused by smoking, although it will be worsened by smoking. Asthma is frequently associated with allergy while COPD is not. Asthma is usually highly responsive to medications, and avoidance of symptom triggers usually results in reversibility of airway obstruction.
In contrast, the airway obstruction in COPD rarely shows much reversibility with treatment. However, the progression of COPD may be stopped or slowed down with smoking cessation. An allergist or pulmonologist can tell the difference between asthma and COPD and offer appropriate treatment.
It should be realized that asthma and COPD can coexist. If you have asthma and smoke cigarettes for years, it would not be unusual for you to develop COPD. In this case, both COPD and asthma coexist. Therefore, both diseases must be treated at the same time
Asthma and COPD have important similarities and differences . Both are chronic inflammatory diseases that involve the small airways and cause airflow limitation , both result from gene-environment interactions and both are usually characterised by mucus and bronchoconstriction.
The similarities are striking, but the differences are also striking. For example, different anatomical sites are involved COPD affects both the airways and the parenchyma, whilst asthma affects only the airways. Both asthma and COPD involve the small airways and the structural changes in the small airways are responsible for much of the physiological impairment that occurs in these diseases .
Perhaps the most important difference between asthma and COPD is the nature of inflammation, which is primarily eosinophilic and CD4-driven in asthma, and neutrophilic and CD8-driven in COPD . This is a very important distinction because the nature of the inflammation affects the response to pharmacological agents.
There is now ample evidence that inhaled corticosteroids are effective against the eosinophilic inflammation in asthma but largely ineffective against the primarily neutrophilic inflammation seen in COPD
In the definitions airway remodelling can occur in long-standing asthma, and results in partially reversible airflow obstruction. Therefore, in many (but not all) patients with long-standing asthma there is a component of chronic irreversible airflow obstruction with reduced lung function and incomplete response to a short-acting bronchodilator or to an oral or inhaled corticosteroid.
This makes the diagnosis of asthma sometimes challenging in older adults and it requires the adjustment of the goals of treatment with respect to the patient's age, as maintenance of normal lung function can no longer be a realistic goal.
It is therefore often challenging for the clinician to know which disease a patient has or what mix of diseases, since COPD is not one disease but rather a spectrum of diseases involving both the airways and parenchyma.
Because of the differences in the cells involved in asthma and COPD, and the relative lack of efficacy of pharmaceutical agents that can alter the progression of COPD (disease-modifying), the approach to the treatment of asthma and COPD is different. The essential difference is that the treatment of asthma is driven by the need to suppress the chronic inflammation, whereas in COPD, treatment is driven by the need to reduce symptoms
The treatment algorithm is based on severity for both asthma and COPD. For asthma, severity is based on symptom frequency and severity, lung function and healthcare utilisation. For COPD, the stages of severity are defined by lung function.
Chronic bronchitis
  • In this type, chronic bronchitis plays the major role. Chronic bronchitis is defined by excessive mucus production with airway obstruction and notable hyperplasia of mucus-producing glands.
Damage to the epithelium impairs the mucociliary response that clears bacteria and mucus. Inflammation and secretions provide the obstructive component of chronic bronchitis. In contrast to emphysema, chronic bronchitis is associated with a relatively undamaged pulmonary capillary bed.
Emphysema is present to a variable degree but usually is centrilobular rather than panlobular. The body responds by decreasing ventilation and increasing cardiac output. This V/Q mismatch results in rapid circulation in a poorly ventilated lung, leading to hypoxemia and polycythemia
Eventually, hypercapnia and respiratory acidosis develop, leading to pulmonary artery vasoconstriction and cor pulmonale. With the ensuing hypoxemia, polycythemia, and increased CO2 retention, these patients have signs of right heart failure and are known as "blue bloaters."
  • The second major type is that in which emphysema is the primary underlying process. Emphysema is defined by destruction of airways distal to the terminal bronchiole.
Pathology of emphysema involves
  • gradual destruction of alveolar septae
  • and of the pulmonary capillary bed,
  • leading to decreased ability to oxygenate
  • blood. The body compensates with
  • lowered cardiac output and
  • hyperventilation.
This V/Q mismatch results in relatively limited blood flow through a fairly well oxygenated lung with normal blood gases and pressures in the lung, in contrast to the situation in blue bloaters. Because of low cardiac output, however, the rest of the body suffers from tissue hypoxia and pulmonary cachexia. Eventually, these patients develop muscle wasting and weight loss and are identified as "pink puffers."
  • History: Patients with COPD present with a combination of signs and symptoms of chronic bronchitis, emphysema, and asthma. Symptoms include worsening dyspnea, progressive exercise intolerance, and alteration in mental status. In addition, some important clinical and historical differences can exist between the types of COPD
In the chronic bronchitis group, classic symptoms include the following:
    • Productive cough, with progression over time to intermittent dyspnea
    • Frequent and recurrent pulmonary infections
    • Progressive cardiac/respiratory failure over time, with edema and weight gain
In the emphysema group, the history is somewhat different and may include the following set of classic symptoms:
    • A long history of progressive dyspnea with late onset of nonproductive cough
    • Occasional mucopurulent relapses
    • Eventual cachexia and respiratory failure
Physical: Depending on the type of COPD, physical examination may vary.
  • Chronic bronchitis (blue bloaters)
    • Patients may be obese.
    • Frequent cough and expectoration are typical.
    • Use of accessory muscles of respiration is common
Coarse rhonchi and wheezing may be heard on auscultation.
  • Patients may have signs of right heart failure (ie, cor pulmonale), such as edema and cyanosis.
  • Because they share many of the same physical signs, COPD may be difficult to distinguish from CHF. One crude bedside test for distinguishing COPD from CHF is peak expiratory flow. If patients blow 150-200 mL or less, they are probably having a COPD exacerbation; higher flows indicate a probable CHF exacerbation.
Emphysema (pink puffers)
    • Patients may be very thin with a barrel chest.
    • They typically have little or no cough or expectoration.
    • Breathing may be assisted by pursed lips and use of accessory respiratory muscles; they may adopt the tripod sitting position.
    • The chest may be hyperresonant, and wheezing may be heard; heart sounds are very distant.
    • Overall appearance is more like classic COPD exacerbation.
Causes: In general, the vast majority of COPD cases are the direct result of tobacco abuse. While other causes are known, such as alpha-1 antitrypsin deficiency, cystic fibrosis, air pollution, occupational exposure (eg, firefighters), and bronchiectasis, this is a disease process that is somewhat unique in its direct correlation to a human activity.
Lab Studies:
  • Arterial blood gas
    • Arterial blood gas (ABG) analysis provides the best clues as to acuteness and severity.
    • In general, renal compensation occurs even in chronic CO2 retainers (ie, bronchitics); thus, pH usually is near normal.
    • Generally, consider any pH below 7.3 a sign of acute respiratory compromise
Serum chemistry
    • These patients tend to retain sodium.
    • Diuretics, beta-adrenergic agonists, and theophylline act to lower potassium levels; thus, serum potassium should be monitored carefully.
    • Beta-adrenergic agonists also increase renal excretion of serum calcium and magnesium, which may be important in the presence of hypokalemia.
  • CBC - Polycythemia
Imaging Studies:
  • Chest x-ray
    • Chronic bronchitis is associated with increased bronchovascular markings and cardiomegaly.
    • Emphysema is associated with a small heart, hyperinflation, flat hemidiaphragms, and possible bullous changes.
Other Tests:
  • Pulse oximetry
    • Pulse oximetry does not offer as much information as ABG.
    • When combined with clinical observation, this test can be a powerful tool for instant feedback on the patient's status.
    • The presence of underlying cardiac disease is highly likely.
    • Establish that hypoxia is not resulting in ischemia.
    • Establish that the underlying cause of respiratory difficulty is not cardiac in nature.
Pulmonary function tests
    • Decreased forced expiratory volume in 1 second (FEV1) with concomitant reduction in FEV1/forced vital capacity (FVC) ratio
    • Poor/absent reversibility with bronchodilators
    • FVC normal or reduced
    • Normal or increased total lung capacity (TLC)Increased residual volume (RV)
    • Normal or reduced diffusing capacity
The stages of COPD are defined primarily by lung function . This emphasises the important clinical message that the diagnosis of COPD requires the measurement of lung function. The stages of COPD suggested in the GOLD Guidelines are as follows. Stage 0: At risk, cough or sputum present but lung function normal.
Stage 1: Mild COPD, FEV1/forced vital capacity (FVC) <70%, with an FEV1 80% predicted, with or without chronic symptoms. Stage 2: Moderate COPD, FEV1/FVC <70% and FEV1 % pred>30% and <80%. Stage 2 is split at an FEV1 of 50% pred since the existing data support the value of inhaled corticosteroids below an FEV1 of 50% pred but not above. Stage 3: Severe COPD, FEV1 <30% pred and FEV1/FVC <70%.
In the GOLD guidelines, Stage 0 is a newly defined stage that was included to give a strong public health message that symptoms of chronic cough and sputum production should alert the clinician to the presence ofan ongoing pathophysiological process even when lung function is normal.
This may progress to clinically significant COPD in a proportion of those exposed (in particular to tobacco smoke) . The analogy that is perhaps most relevant is that mild hypertension in some but not all (or indeed the majority), with mild elevation of blood pressure will progress to clinically significant hypertension.
The treatment goals for COPD are as follows: 1) the prevention of disease progression; 2) the relief of symptoms; 3) improvement in exercise tolerance; 3) improvement in health status; 4) the prevention and treatment of exacerbations; 5) the prevention and treatment of complications; 5) a reduction in mortality; and 6) minimisation of side-effects from treatment
As already emphasised, the approach to the management of COPD is driven by the need to control symptoms . At all stages, every attempt should be made to reduce exposure to risk factors,
including the following. 1) Avoiding noxious agents, including tobacco smoke, indoor air pollution and occupational exposures. The key strategy here is to encourage smoking cessation. 2) Reducing the impact of asthma exacerbations. The most effective preventive approach is to ensure annual influenza vaccination.
The use of antibiotics is still controversial. These patients are almost uniformly heavily colonized with Haemophilus influenzae, streptococcal pneumonia, and others; however, researchers have not proven these organisms to be the cause of the exacerbation. In fact, viruses are thought to be the instigating factor in as many as half of the cases. In addition, the particular antibiotic chosen seems to have much less effect on outcome than the particular host factors of the patient.
Although some analyses have suggested statistically significant improvement in outcome in those patients who receive empiric antibiotic coverage, the lack of quality studies and power leaves the subject open for debate. If antibiotics are given, the choice should provide coverage against pneumococcus, H influenzae, Legionella species, and gram-negative enterics.
Drug Category: Bronchodilators -- These agents act to decrease muscle tone in both small and large airways in the lungs, thus increasing ventilation. Category includes subcutaneous medications, beta-adrenergic agonists, methylxanthines, and anticholinergics. Note that only 10-15% of all patients with COPD have a true reversible (ie, bronchospastic) component; however, because predicting response is impossible on presentation, all patients should be treated with aggressive bronchodilator therapy.
Drug NameTerbutaline (Brethaire, Bricanyl) -- Acts directly on beta2-receptors to relax bronchial smooth muscle, relieving bronchospasm and reducing airway resistance. Adult Dose0.25 mg (0.25 mL of 1 mg/mL concentration) SC; not to exceed 0.5 mg SC q4h ContraindicationsDocumented hypersensitivity; tachycardia resulting from cardiac arrhythmias
  • Interactions Beta-blockers may inhibit bronchodilating, cardiac, and vasodilating effects; concomitant MAOIs may result in a hypertensive crisis; concomitant
Pregnancy- Usually safe but benefits must outweigh the risks. PrecautionsCaution in coronary disease; through intracellular shunting, may decrease serum potassium levels, which can produce adverse cardiovascular effects (decrease usually transient and may not require supplementation
Drug NameTheophylline) -- Acts to increase collateral ventilation, respiratory muscle function, mucociliary clearance, and central respiratory drive. Acts partly by inhibiting phosphodiesterase, elevating cellular cyclic AMP levels, or antagonizing adenosine receptors in bronchi, resulting in relaxation of smooth muscle.
However, clinical efficacy is controversial, especially in acute setting. Author advocates this medicine only if patient was taking medicine already and had subtherapeutic level. Do not give IV form (aminophylline) because it can precipitate arrhythmias, especially in patients such as these who are already in an excess catecholamine state. Measure serum level to adjust dose.Note that most recent meta-analyses and other literature have failed to show a benefit from the use of methylxanthines in acute exacerbations
Adult DoseTarget concentration: 10 mcg/mLDosing = (target concentration - current level) x 0.5 (ideal body weight)
ContraindicationsDocumented hypersensitivity; uncontrolled arrhythmias; hyperthyroidism
  • Interactions barbiturates, carbamazepine,
  • ketoconazole, loop diuretics, charcoal, hydantoins,
  • phenobarbital, phenytoin, rifampin, isoniazid, and
  • sympathomimetics may decrease effects; effects may increase with allopurinol, beta-blockers, ciprofloxacin, corticosteroids, disulfiram, quinolones, thyroid hormones, ephedrine, carbamazepine, cimetidine, erythromycin, macrolides, propranolol, and interferon
Pregnancy - Safety for use during pregnancy has not been established. PrecautionsCaution in peptic ulcer, hypertension, tachyarrhythmias, hyperthyroidism, or compromised cardiac function; do not inject IV solution faster than 25 mg/min; patients diagnosed with pulmonary edema or liver dysfunction are at greater risk of toxicity because of reduced drug clearanceAgain, author recommends not giving the IV form at all
Drug NameIpratropium bromide (Atrovent) -- Anticholinergic medication that appears to inhibit vagally mediated reflexes by antagonizing action of acetylcholine specifically with muscarinic receptor on bronchial smooth muscle. Vagal tone can be increased by as much as 50% in patients with COPD, so this can have a profound effect.
Dose can (and should) be mixed with first beta-agonist nebulizer because it can take up to 20 min to begin having effect. Admitted controversy exists regarding efficacy of ipratropium, but it still should be part of total treatment picture.
  • Adult Dose0.5 mg/nebulizer treatment; can be mixed with albuterol and used as part of first nebulized treatment on presentation to hospital
ContraindicationsDocumented hypersensitivity
  • InteractionsDrugs with anticholinergic properties, such as dronabinol, may increase toxicity; albuterol increases effects Pregnancy - Usually safe but benefits must outweigh the risks
  • PrecautionsNot indicated for acute episodes of bronchospasm; caution in narrow-angle glaucoma, prostatic hypertrophy, and bladder neck obstruction
Drug NameIpratropium and albuterol (Combivent)
  • -- Ipratropium is chemically related to atropine.
  • It has anti-secretory properties and, when
  • applied locally, inhibits secretions from serous
  • and seromucous glands lining the nasal mucosa.
Drug NameTiotropium (Spiriva) -- A quaternary ammonium compound. Elicits anticholinergic/antimuscarinic effects with inhibitory effects on M3 receptors on airway smooth muscles, leading to bronchodilation. Available as a capsule dosage form containing a dry powder for oral inhalation via the HandiHaler inhalation device. Helps COPD patients by dilating narrowed airways and keeping them open for 24 h. Adult DoseInhale contents of 1 cap (18 mcg) via HandiHaler device qd
ContraindicationsDocumented hypersensitivity InteractionsCoadministration with other anticholinergic containing drugs (eg, ipratropium) may increase toxicity risk Pregnancy - Safety for use during pregnancy has not been established.
PrecautionsFor maintenance treatment only; not effective for acute (rescue) therapy of bronchospasm; discontinue use and consider other treatments if immediate hypersensitivity reactions (including angioedema) or paradoxical bronchospasm occur; caution with narrow-angle glaucoma, prostatic hyperplasia, or bladder neck obstruction;; may also cause constipation, increased heart rate, blurred vision, glaucoma, and urinary difficulty or retention; monitor patients with moderate-to-severe renal impairment
Drug Category: Corticosteroids -- These agents have been shown to be effective in accelerating recovery from acute COPD exacerbations. Although they may not make a clinical difference in the ED, they have some effect by 6-8 h into therapy; therefore, early dosing is critical.
  • Some newer studies are suggesting that inhaled corticosteroids (eg, nebulized budesonide) may be equally effective as IV or PO steroids in the mild-to-moderate exacerbation; however, further studies are needed.
Drug NameMethylprednisolone
  • -- Usually given in IV form in ED for initiation of corticosteroid therapy, although PO form theoretically equally efficacious.
  • Two forms equal in potency, time of onset, and adverse effects. Inhaled corticosteroids probably equally efficacious and have fewer adverse effects for patients discharged from ED.
  • Adult Dose125 mg IV q6h recommended dose, but true optimal dose not knownAlternative: 1-2 mg/kg IV q6h; not to exceed 125 mg; this dose often used in children
Contraindications :Documentedhypersensitivity; viral, fungal, or tubercular skin infections InteractionsCoadministration with digoxin may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels; phenobarbital, phenytoin, and rifampin may decrease levels (adjust dose); monitor patients for hypokalemia when taking concurrent diuretics
Pregnancy - Safety for use during pregnancy has not been established.
  • PrecautionsHyperglycemia, edema, osteonecrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections are possible complications
Drug Category: Electrolyte supplements –
  • Magnesium is used to replenish stores that become depleted in periods of adrenergic excess such as asthma attacks, COPD exacerbations, and diuretic use.
  • Drug NameMagnesium sulfate -- Thought to produce bronchodilation through counteraction of calcium-mediated smooth muscle constriction. Again, for every study showing positive finding, probably another shows no benefit, but given properly, magnesium is safe and may have some benefit.
  • Adult Dose1.2-2 g IV over 15 min; not to exceed 150 mg/min
ContraindicationsDocumented hypersensitivity;
  • heart block; Addison disease; myocardial damage
  • ; severe hepatitis InteractionsConcurrent nifedipine may cause hypotension and
  • neuromuscular blockade; may increase
  • neuromuscular blockade seen with
  • aminoglycosides and potentiate neuromuscular
  • blockade produced by tubocurarine, vecuronium,
  • or succinylcholine; may increase CNS effects and
  • toxicity of CNS depressants and betamethasone;
  • may increase cardiotoxicity of ritodrine
Pregnancy - Safe in pregnancy
  • PrecautionsMay alter cardiac conduction, leading to heart block in digitalized patients;
  • respiratory rate, deep tendon reflexes, and renal function should be monitored when administered parenterally;
caution when administering magnesium dose, since may produce significant hypertension or asystole; in overdose, calcium gluconate, 10-20 mL IV of 10% solution, can be given as antidote for clinically significant hypermagnesemia
In cases in extremis, CPAP or BiPAP may be attempted prior to intubation. This can be started in the ED and continued for several hours in the hospital.
inspiratory positive airway pressure (IPAP) of 10 cm H2O and an expiratory positive airway pressure (EPAP) of 2 cm H2O, with further adjustments based on the individual. This is contingent on the patient's ability to withstand the mask. This treatment is not a substitute for intubation; rather, it is a mean of trying to avoid intubation.
Inhaled nitric oxide has been suggested, but at this point does not seem to have a role in acute treatment.
  • Lung volume reduction surgery has also been touted as effective, but most recent studies demonstrate varying levels of success.
Surgical Care: Over the past 50-75 years, researchers have described a variety of surgical approaches to improve symptoms and restore function in patients who have emphysema. Only giant bullectomy and, possibly, the lung volume reduction surgery (LVRS) are useful.
    • Removal of giant bullae has been a standard approach in selected patients for many years.
    • The bullae in patients with emphysema generally range in size from 1-4 cm in diameter; however, on occasion, bullae can occupy more than 33% of the hemithorax (eg, giant bullae).
    • Giant bullae may compress adjacent lung tissue, thereby reducing the blood flow and ventilation to the healthy tissue. Removal of these bullae may result in the expansion of compressed lungs and improved function.
Patients who are symptomatic and have an FEV1 of less than 50% of the predicted value have a better outcome after bullectomy. This surgery is performed through midline sternotomy, a lateral incision, or by video-assisted thoracoscopy. Postoperative bronchopleural air leak is the major potential complication.
Giant bullectomy can produce subjective and objective improvement in selected patients—in those who have bullae that occupy at least 30%, and preferably 50%, of the hemithorax and compress adjacent lung, who have FEV1 of less than 50% of the predicted value, and who otherwise have relatively preserved lung function.
Lung volume reduction surgery
    • Nearly 40 years ago, Brantigan et al first reported resectional surgery for diffuse emphysema in 33 patients. They resected 20-30% of each lung that appeared most diseased. Brantigan hypothesized that removal of a portion of the emphysematous lung increased the radial traction on the airways in the remaining lung, improving expiratory airflow and mechanical function of the respiratory system, thereby reducing symptoms.
Recently, the LVRS gained considerable momentum after researchers documented a marked improvement in the FEV1 (ie, +82%), the FVC (ie, +27%), and the 6-minute walk distance and quality of life indices. Currently, large prospective studies are underway in the United States and Canada to evaluate the effectiveness and the long-term outcome and benefits of LVRS.
The indications and patient selection criteria for LVRS are not rigorously defined. Generally, the candidates for LVRS have symptoms secondary to severe emphysema, marked hyperinflation (ie, elevated residual volume [RV]/total lung capacity [TLC] ratio), and CT scan evidence of heterogeneous emphysema. The study excluded patients who are hypercapnic or have pulmonary hypertension or other cardiac risk factors.
The surgical approach uses a midline sternotomy with stapling of the lung margins. Surgeons generally resect 20-30% of each lung from the upper zones. The LVRS procedure has a mortality rate of 0-18%. Several complications, including pneumonia and prolonged air leaks, have been observed.
Lung transplantation
    • Lung transplantation is a relatively new therapy for advanced lung disease. Patients with COPD are the largest single category of patients who undergo the process. The timing of transplant is difficult, but patients selected to receive a transplant should have a life expectancy of 2 years or less due to COPD.
    • With lung transplantation, the profound dyspnea and limited lifestyle is exchanged for an improved quality of life but at the risk of worsening survival.
Patients who state that they "feel back to normal" and have no overt reason for admission can reasonably be discharged home with follow-up arrangements. The corollary to this is that patients who state they "do not feel comfortable," regardless of the numbers, are the best predictors of outcome and probably should be admitted. Data on risk factors for relapse and need for admission are limited at present.
When their condition is stable, patients may be seen biannually.
  • Check theophylline level with each dose adjustment, then every 6-12 months.
  • For patients on home oxygen, check ABGs yearly or with any change in condition. Monitor oxygen saturation more frequently than ABGs.
Acute exacerbation of COPD
    • Acute exacerbation of COPD is one of the major reasons for hospital admission in the United States.
    • Because of the lack of clinical studies, the general consensus supports the need for hospitalization of patients who develop severe respiratory dysfunction, disease progression, and other comorbid conditions (eg, pneumonia, poor response to outpatient management).
    • The purpose of hospitalization is to manage the patient's acute decompensation and to prevent further deterioration.
Pharmacotherapy of COPD exacerbations
    • Physicians recommend a stepwise approach to drug therapy that takes into consideration the causes and complications related to the exacerbation, the degree of reversible bronchospasm, recent drug use, and contraindications to treatment. Sedation and pain management must be provided, despite a potential for respiratory depression, to ensure patient comfort and safety
Patients with exacerbations respond to inhaled beta2 agonists and anticholinergic aerosols. Treatment is initiated with an inhaled beta2 agonist delivered via a spacer or nebulizer; inhaled ipratropium bromide usually is added. The combination therapy may act synergistically and may allow using lower dosages of beta agonists. The efficacy of theophylline or intravenous aminophylline is not definitely established, and theophylline and intravenous aminophylline may cause toxicity.
Corticosteroids generally are recommended and may be used intravenously for a short period. When response occurs, lower the dosage. Careful observation and spirometric evaluation are needed to prove the continuing benefit of steroids after a course of 1-2 weeks.
Antibiotic therapy
    • When the patient has 2 or more Winnipeg criteria, prescribe an antibiotic.
    • The risk stratification scheme for antibiotic selection is recommended as follows: treat low-risk patients with amoxicillin, trimethoprim/sulfamethoxazole, or doxycycline. Treat high-risk patients, those who had multiple exacerbations in the past, and/or those with underlying cardiopulmonary dysfunction with a new generation macrolide, a second-generation cephalosporin, or a fluoroquinolone.
Intensive care admission: Indications for intensive care admission are confusion, lethargy, respiratory muscle fatigue, worsening hypoxemia, respiratory acidosis (ie, pH <7.30), or when a patient requires invasive or noninvasive mechanical ventilation.
Assisted ventilation
    • Progressive airflow obstruction may impair oxygenation and/or ventilation to the degree that the patient requires assisted ventilation.
The general guidelines for determining the ideal time to initiate ventilatory support are (1) patients who have experienced progressive worsening of respiratory acidosis and/or altered mental status and (2) clinically significant hypoxemia despite supplemental oxygen.
  • Patients may be treated with noninvasive mask ventilation or translaryngeal
Patients may be treated with noninvasive mask ventilation or translaryngeal intubation and mechanical ventilation. Following noninvasive ventilation, provide adequate patient supervision and ensure patient's mental alertness and tolerance of appliances. Hemodynamic instability, difficulty with clearing of secretions, and copious secretions are contraindications to noninvasive assisted ventilation.
The main goal of assisted positive pressure ventilation in acute respiratory failure complicating COPD is to rest the ventilatory muscles and restore gas exchange. Major risks are ventilator-associated pneumonia, barotrauma, and laryngotracheal complications associated with intubation.
  • These devices help to decrease the work of breathing and maintain positive end-expiratory pressure (PEEP).
  • Patient must be alert with no excess secretions.
Heliox usually is a 60:40 mixture of helium and oxygen.
  • Helium is a smaller particle than oxygen and in small airways promotes laminar flow and facilitates both oxygen transport and carbon dioxide diffusion.
  • Many patients who seem to breathe better on Heliox return to a worsened respiratory state when removed from Heliox.
  • For the vast majority of patients, cessation of smoking is the only true means of prevention
Smoking cessation, physical intervention
  • The transition from smoking to not smoking occurs in 5 stages: precontemplation, contemplation, preparation, action, and maintenance. Smoking intervention programs include self-help, group, physician-delivered, workplace, and community programs.
Setting a quit date may be helpful. Physicians and other healthcare providers should participate in setting the target date and follow-up with respect to maintenance.
  • Successful cessation programs usually employ the following resources and tools: patient education, a quit date, follow-up support, relapse prevention, advice for healthy lifestyle changes, social support systems, and adjuncts to treatment (eg, pharmacological agents).
smoking cessation pharmacologic intervention
Smoking cessation, pharmacologic intervention
  • Supervised use of pharmacologic agents is an important adjunct to self-help and group smoking cessation programs.
  • Nicotine is the ingredient in cigarettes primarily responsible for the addiction. Withdrawal from nicotine may cause unpleasant adverse effects, including anxiety, irritability, difficulty concentrating, anger, fatigue, drowsiness, depression, and sleep disruption. These effects usually occur during the first several weeks.
Nicotine replacement therapies after smoking cessation reduce withdrawal symptoms. If a smoker requires his or her first cigarette within 30 minutes of waking up, they most likely are highly addicted and would benefit from nicotine replacement therapy.
Several nicotine replacement therapies are available. Nicotine polacrilex is a chewing gum and has better quit rates than counseling alone. Nicotine replacement therapy chewing pieces are marketed in 2 strengths (ie, 2 mg, 4 mg). An individual who smokes 1 pack per day should use 4-mg pieces. The 2-mg pieces are to be used by individuals who smoke less than 1 pack per day. Instruct the patient to chew hourly and also to chew when needed for their initial cravings for 2 weeks. Gradually reduce the amount chewed over the next 3 months.
Transdermal nicotine patches are available readily for replacement therapy. Long-term success rates are 22-42%, compared with 2-25% with a placebo. These agents are well tolerated, and the adverse effects are limited to localized skin reaction. Nicotine replacement therapy patches are sold under the following trade names: Nicoderm, Nicotrol, and Habitrol. Each of these products is dosed with a scheduled graduated decrease in nicotine over 6-10 weeks.
The use of the antidepressant is also effective for smoking cessation. This nonnicotine aid to smoking cessation enhances central nervous nonadrenergic function. A recent study demonstrated that 23% of patients sustained cessation at 1 year, compared with 12% who sustained cessation with the placebo. Bupropion may also be effective in patients who not been able to quit smoking with nicotine replacement therapy.
The most recent drug to receive approval for smoking cessation is varenicline . It is a partial agonist selective for alpha4, beta2 nicotinic acetylcholine receptors. Action is thought to result from activity at a nicotinic receptor subtype, where its binding produces agonist activity while simultaneously preventing nicotine binding. Agonistic activity is significantly lower than nicotine
  • Some complications that must be anticipated in COPD treatment include the following:
    • Incidence of pneumothorax due to bleb formation is relatively high; consider pneumothorax in all patients with COPD who have increased shortness of breath.
In patients who require long-term steroid use, the possibility of adrenal crisis is very real; at a minimum, patients with steroid-dependent COPD should receive stress dosing in the event of an exacerbation or any other stressor.
Infection (common)
  • Cor pulmonale
  • Secondary polycythemia
  • Bullous lung disease
  • Acute or chronic respiratory failure
  • Pulmonary hypertension
  • Malnutrition
  • Patient's age and postbronchodilator FEV1 are the most important predictors of prognosis.
  • Young age and FEV1 greater than 50% of predicted are associated with a good prognosis. Older patients and those with more severe lung disease do worse.
Supplemental oxygen (when indicated) has been shown to increase survival rates.
  • Smoking cessation improves prognosis.
  • Cor pulmonale, hypercapnia, tachycardia, and malnutrition indicate a poor prognosis
Oxygen delivery systems
    • The continuous flow nasal cannula is the standard means of oxygen delivery for the stable hypoxemic patient. It is simple, reliable, and generally well tolerated. Each liter of oxygen flow adds 3-4% to the fraction of inspired oxygen (FiO2). Nasal oxygen delivery also is beneficial for most mouth-breathing patients. Humidification generally is not beneficial when the patient receives oxygen by nasal cannula at flows of less than 5 L/min.
Oxygen conserving devices function by delivering all of the supplemental oxygen during early inhalation. These devices improve the portability of oxygen therapy and may reduce overall costs. Three distinct oxygen-conserving devices exist—reservoir cannulas, demand pulse delivery devices, and transtracheal oxygen delivery.
Transtracheal oxygen delivery involves the insertion of a catheter percutaneously between the second and third tracheal interspace. Transtracheal oxygen delivery is invasive and requires special training by the physician, the patient, and the caregiver. The procedure has risks as well as medical benefits but has limited application.
Pharmacologic treatment of COPD is targeted to
  • symptom reduction. With the exception of
  • smoking cessation and continuous long-term
  • oxygen treatment, drug therapy does not modify
  • the natural history of COPD. Recent long-term
  • pharmacologic studies in COPD have evaluated
  • prevention of exacerbations and/or
  • hospitalization as the primary outcome.
Tiotropium, a long-acting anticholinergic agent, reduces the frequency of exacerbations and the use of health care resources in patients with moderate-to-severe COPD. Inhaled steroids may also reduce the frequency and severity of exacerbations in patients with severe COPD. Whether the combination of inhaled steroids and long-acting bronchodilators has additive effects on lung function and/or exacerbations is still unclear.
pulmonary rehabilitation
Pulmonary rehabilitation
  • Many patients with COPD are unable to enjoy life to the fullest because of shortness of breath, physical limitations, and inactivity.
  • Pulmonary rehabilitation encompasses an array of therapeutic modalities designed to improve the patient's quality of life by decreasing airflow limitation, preventing secondary medical complications, and alleviating respiratory symptoms.
The 3 major goals of the comprehensive management of COPD are the following:
  • Lessen airflow limitation
  • Prevent and treat secondary medical complications (eg, hypoxemia, infection)
  • Decrease respiratory symptoms and improve quality of life
Pulmonary rehabilitation, a multidisciplinary team approach
    • Successful implementation of a pulmonary rehabilitation program usually requires a team approach, with individual components provided by health care professionals who have experience in managing COPD (eg, physician, dietitian, nurse, respiratory therapist, exercise physiologist, physical therapist, occupational therapist, recreational therapist, cardiorespiratory technician, pharmacist, psychosocial professionals).
This multidisciplinary approach emphasizes patient and family education, smoking cessation, medical management (eg, oxygen, immunization), respiratory and chest physiotherapy, physical therapy with bronchopulmonary hygiene, exercise, vocational rehabilitation, and psychosocial support.
Benefits of pulmonary rehabilitation: As a result of rehabilitation, improvements occur in the objective measures of quality of life, well being, and health status, including a reduction in respiratory symptoms and an increase in exercise tolerance and functional activities (eg, walking, less anxiety and depression, increased feelings of control, self-esteem). Pulmonary rehabilitation also results in substantial savings in healthcare costs by reducing use of hospital and medical resources
Components of pulmonary rehabilitation
    • Pulmonary rehabilitation programs usually are conducted in an outpatient setting. A rehabilitation program may include a number of components and should be tailored to the needs of the individual patient. Provide all patients who complete the program with guidelines for continuing at home.
Education is key to comprehensive pulmonary rehabilitation. The educational component prepares the patient and families to be actively involved in providing care. This reliance on patients to assume charge of their care is known as collaborative self-management
Exercise training is a mandatory component of pulmonary rehabilitation. Patients with COPD should perform aerobic lower extremity endurance exercises regularly to enhance performance of daily activities and reduce dyspnea. Upper extremity exercise training improves dyspnea and allows increased activities of daily living requiring the use of upper extremities
Breathing retraining techniques (eg, diaphragmatic, pursed lip breathing) may improve the ventilatory pattern and prevent dynamic airway compression
Patient Education:
  • The best education comes in 2 forms.
    • Educate patients to the dangers of smoking and the improvement in quality of life attainable with smoking cessation.
    • Instruct patients with COPD to present early during an exacerbation and not wait until they are in distress.
Be wary of discharging patients with exacerbations when they do not feel comfortable with their breathing, regardless of their oxygen saturation, ABG, or other test results.
  • Always look for underlying cardiac ischemia with acute exacerbations. With hypoxia and distress, many of these patients can have unrecognized underlying ischemia
Administer as much oxygen as necessary to avoid hypoxia. If the patient retains excessive carbon dioxide, intubate.
  • A common mistake is utilizing a high respiratory rate after intubation. The patient most likely is acidotic and has marginally normal or low potassium due to diuretic and bronchodilator therapy. With a too rapid respiratory rate, the patient will become alkalotic, causing an intracellular shift in potassium with potentially dangerous hypokalemia as a result.
g i t

The oesophageal dismotility occurs regardlees the presence or absence of hypoxemia or hypercapnea.

Routine motility studies can be added to a chest list used for follow up of COPD patient, for detection of gastro oesophageal reflux.

A clear evidence for the relationship between weight loss and plasma tumour necrosis factor production, acute phase protein, has been shown .

The proposed cytokine – leptin link in pulmonary cachexia may explain the poor response to nutritional support in some of the cachectic patients with C.O.P.D (Cachexcia is defined as accelerated loss of skeletal muscle in the context of chronic inflammatory response

The mid thigh muscle cross-sectional area as measured by CT scan predicts mortality .


Regulation of (H+) is of crucial importance for maintenance of normal cellular functions. It is largely regulated by the ratio of the concentrations of carbon dioxide and bicarbonate which is an interplay between the renal and respiratory response.

COPD patients have impairment in their renovascular heamodynamics in response to hypoxaemia in the form of impaired renal function reserve especially during an acute exacerbation.

It seems likely that the development of oedema in COPD may, at least in part, be due to non-cardiac factors.

Regulation of (H+) is of crucial importance for maintenance of normal cellular functions. It is largely regulated by the ratio of the concentrations of carbon dioxide and bicarbonate which is an interplay between the renal and respiratory response.

COPD patients have impairment in their renovascular heamodynamics in response to hypoxaemia in the form of impaired renal function reserve especially during an acute exacerbation.

It seems likely that the development of oedema in COPD may, at least in part, be due to non-cardiac factors.


Sleep related hypoxaemia and hypercapnia occur in COPD particularly during rapid eye movement sleep.

Sleep studies are not routinely indicated for patients with COPD associated with respiratory insufficiency but only where there is clinical suspicion of a problem.