ANATOMY AND PHYSIOLOGY: The respiratory system consists of all the organs involved in breathing.

These include the nose, pharynx, larynx, trachea, bronchi and lungs. The respiratory system does two very important things: it brings oxygen into our bodies, which we need for our cells to live and function properly; and it helps us get rid of carbon dioxide, which is a waste product of cellular function. The nose, pharynx, larynx, trachea and bronchi all work like a system of pipes through which the air is funneled down into our lungs. There, in very small air sacs called alveoli, oxygen is brought into the bloodstream and carbon dioxide is pushed from the blood out into the air. When something goes wrong with part of the respiratory system, such as an infection like pneumonia, chronic obstructive pulmonary diseases, it makes it harder for us to get the oxygen we need and to get rid of the waste product carbon dioxide. Common respiratory symptoms include breathlessness, cough, and chest pain.

along with the heart. cone-shaped organs which take up most of the space in our chests. Each segment receives its own blood supply and air supply. The Lungs Structure The lungs are paired. . called µbronchopulmonary segments¶. All these structures act to funnel fresh air down from the outside world into your body. There are about 10 of them in each lung. The right lung has three lobes but the left lung has only two. it travels down your throat through the larynx (or voicebox) and into the trachea (or windpipe) before entering your lungs. Their role is to take oxygen into the body. From there. or big sections of tissue separated by µfissures¶ or dividers. The upper airway is important because it must always stay open for you to be able to breathe. It also helps to moisten and warm the air before it reaches your lungs. These are divided up into µlobes¶. These are pyramidal-shaped areas which are also separated from each other by membranes. which we need for our cells to live and function properly. and to help us get rid of carbon dioxide. which is a waste product. a left lung and a right lung.The Upper Airway and Trachea When you breathe in. because the heart takes up some of the space in the left side of our chest. We each have two lungs. air enters your body through your nose or mouth. The lungs can also be divided up into even smaller portions.

so that oxygen and carbon dioxide can move (or diffuse) between them. This fresh air has lots of oxygen in it. It is important that the air in the alveoli and the blood in the capillaries are very close together. . known as the alveoli. Traveling in the opposite direction is carbon dioxide. and get rid of the waste product carbon dioxide. you bring in to your body the oxygen that you need to live. and some of this oxygen will travel across the walls of the alveoli into your bloodstream.COPD VERSUS HEALTHY LUNG How they work Air enters your lungs through a system of pipes called the bronchi. In this way. until they eventually form little thin-walled air sacs or bubbles. which are very small branches of the pulmonary arteries. which crosses from the blood in the capillaries into the air in the alveoli and is then breathed out. The alveoli are where the important work of gas exchange takes place between the air and your blood. So. Covering each alveolus is a whole network of little blood vessel called capillaries. These pipes start from the bottom of the trachea as the left and right bronchi and branch many times throughout the lungs. air comes down the trachea and through the bronchi into the alveoli. when you breathe in.

meaning they receive a very large blood supply. your muscles need to work to fill your lungs with air. From there. The Work of Breathing The Pleurae The lungs are covered by smooth membranes that we call pleurae. Breathing out (expiration) does not normally require your muscles to work. without any friction. The pleurae are important because they help you breathe in and out smoothly. When you breathe in. come directly from the right side of your heart. At rest. a µvisceral¶ layer which sticks closely to the outside surface of your lungs. and more oxygen can be absorbed into the bloodstream. The Diaphragm and Intercostal Muscles When you breathe in (inspiration). This is because your lungs are very elastic. which supply the lungs. and when your . the diaphragm contracts and flattens out. and a µparietal¶ layer which lines the inside of your chest wall (ribcage). They also make sure that when your ribcage expands on breathing in. your lungs expand as well to fill the extra space. a large. This is because the pulmonary arteries. sheet-like muscle which stretches across your chest under the ribcage. it is shaped like a dome curving up into your chest. it is pumped all around your body to supply oxygen to cells and organs. The newly oxygen-rich blood then travels back through the paired pulmonary veins into the left side of your heart. They carry blood which is low in oxygen and high in carbon dioxide into your lungs so that the carbon dioxide can be blown off. does much of this work. expanding the space in your chest and drawing air into your lungs. The diaphragm. Other muscles. including the muscles between your ribs (the intercostal muscles) also help by moving your ribcage in and out. The pleurae have two layers.Blood Supply The lungs are very vascular organs.

bacteria. cigar. diminished lung capacity. When smoking damages this cleansing mechanism. The most important risk factor for COPD is cigarette smoking. and other types of tobacco smoking. meaning that there is less area for gases to be exchanged across. Smoking depresses the activity of scavenger cells and affects the respiratory tract¶s ciliary cleansing mechanism. than a younger person would. causing an increased . The air spaces get bigger and lose their elasticity. These include: y y y Enlargement of the alveoli. pushing the air out as they go. which keeps breathing passages free of inhaled irritants. This change is sometimes referred to as ¶senile emphysema¶. In addition.muscles relax at the end of inspiration your lungs simply recoil back into their resting position. The strength of the respiratory muscles (the diaphragm and intercostal muscles) decreases. The alveoli greatly distend. This change is closely connected to the general health of the person. All of these changes mean that an older person might have more difficulty coping with increased stress on their respiratory system. Smoking also irritates the goblet cells and mucus glands. so that it takes more effort to breathe in and out. passive smoking contributes to respiratory symptoms and COPD. and other foreign matter. PREDISPOSING FACTORS Risk factors for COPD include environmental exposures and host factors. The compliance (or springiness) of the chest wall decreases. Other risk factors are pipe. The Respiratory System and Ageing The normal process of ageing is associated with a number of changes in both the structure and function of the respiratory system. such as with an infection like pneumonia. airflow is obstructed and air becomes trapped behind the obstruction.

the inflammatory response causes pulmonary vasculature changes that are characterized by thickening of the vessel wall. and pulmonary vasculature. The parenchymal changes may occur as a consequence of inflammation or environmental or genetic factors (eg. carbon monoxide (a by product of smoking) combines with hemoglobin to form carboxyhemoglobin. When activated by chronic inflammation. As a result.accumulation of mucus. parenchyma. contributing to narrowing of the airways and causing a cough with sputum. Early in the course of COPD. Smoking. Airflow obstruction may also be caused by parenchymal destruction. In the airways of the lung. Alpha1-antitrypsin deficiency). In addition to inflammation. Genetically susceptible people are sensitive to environmental factors (eg. the hallmark of chronic bronchitris is an increased number (hyperplasia) and increased size (hypertrophy) of the goblet cells and mucous glands of the airway. Chronic bronchitis is defined in clinical terms as a cough with sputum production on most days for 3 months of a year. air pollution. allergens) and eventually developed chronic obstructive symptoms. Hemoglobin that is bound by carboxyhemoglobin cannot carry oxygen efficiently. which in turn produces more irritation. A host risk factor for COPD is a deficiency of alpha antitrypsin. use of tobacco products. and the release of inflammatory medicators. even if they do not smoke. a disease of the alveoli or gas exchange units. PATHOPHYSIOLOGY In COPD. an enzyme inhibitor that protects the lung parenchyma from injury. This deficiency predisposes young people to rapid development of lobular emphysema. . as is seen with emphysema. proteiness and other substances may be released. there is more mucus than usual in the airways. Carriers of this genetic defect must be identified so that they can modify environmental risk factors to delay or prevent overt symptoms of disease. the airflow limitation is both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases. Over time. infection. this injury-and-repair process causes scar tissue formation and narrowing of the airway lumen. The inflammatory response occurs throughout the airways. infectious agents. These changes may result from exposure to cigarette smoke. processes related to imbalances of proteinases and antiproteinases in the lung may be responsible for airflow limitation. Because of the chronic inflammation and the body¶s attempts to repair it. CHRONIC BRONCHITIS Lung damage and inflammation in the large airways results in chronic bronchitis. damaging the parenchyma of the lung. for 2 consecutive years. narrowing occurs in the small peripheral airways. and damage to the lung. In addition.

The consequence of these changes is a limitation of airflow. and dyspnea. or ³I can not get enough air in´. there is squamous metaplasia (an abnormal change in the tissue lining the inside of the airway) and fibrosis (further thickening and scarring of the airway wall). Common signs are: y y y y y y tachypnea. seen as swelling of the ankles. barrel chest).e. The hypoxia and fluid retention leads to them being called ³Blue Bloaters. sputum or mucus production. As chronic bronchitis progresses. Patients with advanced COPD that have primarily chronic bronchitis rather than emphysema were commonly referred to as ³blue bloaters´ because of the bluish color of the skin and lips (cyanosis) seen in them. and tiredness. A complication of advanced COPD is cor pulmonale. In the advanced stages of COPD.Microscopically there is infiltration of the airway walls with inflammatory cells. dyspnea tends to get gradually worse so that it can occur during milder. When this happens. cyanosis. An excess of carbon dioxide in the blood can cause headaches. Other symptoms of COPD are a persistent cough. Over the years. a rapid breathing rate wheezing sounds or crackles in the lungs heard through a stethoscope breathing out taking a longer time than breathing in enlargement of the chest. can occur. chest tightness. ³I feel out of breath´. EMPHYSEMA . Symptoms of cor pulmonale are peripheral edema. a bluish discoloration of the lips caused by a lack of oxygen in the blood. dyspnea can become so bad that it occurs during rest and is constantly present. Some people have COPD and have none of these signs. everyday activities such as housework. There are a few signs of COPD that a healthcare worker may detect although they can be seen in other diseases. drowsiness or twitching (asterixis).´ ACUTE BRONCHITIS PHYSICAL MANIFESTATIONS One of the most common symptoms of COPD is shortness of breath (dyspnea). People with COPD typically first notice dyspnea during vigorous exercise when the demands on the lungs are greatest. Inflammation is followed by scarring and remodeling that thickens the walls and also results in narrowing of the airways. People with COPD commonly describe this as: ³My breathing requires effort´. a strain on the heart due to the extra work required by the heart to pump blood through the affected lungs. particularly the front-to-back distance (hyperinflation) active use of muscles in the neck to help with breathing breathing through pursed lips increased anteroposterior to lateral ratio of the chest (i. People with advanced (very severe) COPD sometimes develop respiratory failure. wheezing.

possibly increased TLC. pH. Chest X-ray ± in late stages. In susceptible individuals. 3) vaccinating against flu influenza and pneumonia and 4) regular oxygen supplementation and 5) pulmonary rehabilitation. and increased CO2. As a result. FEV1 to FVC ration. It is often caused by exposure to toxic chemicals. and treatment is available.Emphysema is a chronic obstructive pulmonary disease (COPD. 2. decreased vascular markings. In advanced disease. there are signs of fluid overload such as pitting peripheral edema. TREATMENT The goals of COPD treatment are 1) to prevent further deterioration in lung function. as alveolar collapsibility has decreased. central cyanosis and finger clubbing. Emphysema is characterized by loss of elasticity (increased pulmonary compliance) of the lung tissue caused by destruction of structures feeding the alveoli. owing to the action of alpha 1 antitrypsin deficiency. 3. Alpa1-antitrypsin assay useful in identifying genetically determined deficiency in emphysema. It is important to note that when one stops smoking the decline in lung function eventually reverts to that of a non-smoker. increased rettrosternal space. and a difficult to palpate apex beat. airflow is impeded and air becomes trapped in the lungs. . 2) to alleviate symptoms. 4. PFTs demonstrative airflow obstruction ± reduced forced vital capacity (FVC). FEV1. Patients who continue to smoke have a more rapid deterioration in lung function when compared to others who quit. flattened diaphragm. This causes the small airways to collapse during forced exhalation. both due to hyperinflation. There may be decreased breath sounds and audible expiratory wheeze. including long-term exposure to tobacco smoke. 2) taking medications to dilate airways (bronchodilators) and decrease airway inflammation. The chest has hyper resonant percussion notes. Quitting cigarette smoking The most important treatment for COPD is quitting cigarette smoking. cigarette smoking can result in a much more dramatic loss of lung function. formerly termed a chronic obstructive lung disease). Symptoms include shortness of breath on exertion. hyperinflation. The face has a ruddy complexion if there is a secondary polycythemia. Sufferers who retain carbon dioxide have asterixis (metabolic flap) at the wrist. ABG levels.decreased PaO2. as it is otherwise known. increased residual volume to total lung capacity (TLC) ratio. 3) to improve performance of daily activities and quality of life. PHYSICAL MANIFESTATIONS Signs of emphysema include pursed-lipped breathing. the constriction of air passages isn¶t always immediately deadly. possible bullae. DIAGNOSTIC EVALUATION 1. and an expanded chest. However. particularly just above the liver. Aging itself can cause a very slow decline in lung function. in the same way as other obstructive lung diseases. The treatment strategies include 1) quitting cigarette smoking.

An MDI is a pressurized canister containing a medication that is released when the canister is compressed. Bronchodilators can be inhaled. if the overinflated portions of lung are removed surgically. As compared with bronchodilators given orally.Nicotine in cigarettes is addictive. and intense craving for cigarettes. the compressed lung may expand and . need to smoke shortly after waking up in the morning. pursed lip breathing). Proper use of spacer devices can greatly increase the proportion of medication reaching the airways. To maximize the delivery of the medications to the airways. and. Incorrect use of the MDI can lead to deposition of much of the medication on the tongue and the back of the throat instead of on the airways. Lung volume reduction surgery (LVRS) has received much fanfare in the lay press. therefore. less medication reaches the rest of the body. cessation of smoking can cause symptoms of nicotine withdrawal including anxiety. Spacer devices can hold the released medications long enough for patients to inhale them slowly and deeply into the lungs. taken orally or administered intravenously. Patients likely to develop withdrawal symptoms typically smoke more than 20 cigarettes a day. and have difficulty refraining from smoking in non-smoking areas. proper breathing techniques (diaphragmatic breathing. therefore. depression. some 25% of smokers can stop smoking without developing these symptoms. and. LVRS is a surgical procedure used to treat some patients with COPD. poorly-functioning upper parts of the lung compress and impair function of the better-functioning lung elsewhere. irritability. Even in those smokers who develop symptoms of withdrawal. However. A standard amount of medication is released with each compression of the MDI. The premise behind this surgery is that the over-inflated. anger. Metered dose inhalers (MDIs) are used to deliver bronchodilators. difficulty concentrating or sleeping. An essential ingredient in this program is the use of increasing physical exercise to overcome the reduced physical capacity that usually has developed over time. and proper use of respiratory equipment and medications. In addition. the patient has to learn to coordinate inhalation with each compression. fatigue. Bronchodilators Treating airway obstruction in COPD with bronchodilators is similar but not identical to treating bronchospasm in asthma. Oxygen Therapy Other treatments y y Pulmonary rehabilitation has become a cornerstone in the management of moderate to severe COPD. there are fewer side effects. Spacers are tube-like chambers attached to the outlet of the MDI canister. Pulmonary rehabilitation is a program of education regarding lung function and dysfunction. spacers can be helpful. To decrease the deposition of medications on the throat and increase the amount reaching the airways. occupational and physical therapy are used to teach optimal and efficient body mechanics. Inhaled bronchodilators are popular because they go directly to the airways where they work. Bronchodilators are medications that relax the muscles surrounding the small airways thereby opening the airways. Thus. the symptoms will decrease after several weeks of abstinence.

Ipratropium bromide (Atrovent) usually is administered via a MDI. They are called ³agonists´ because they activate the beta-2 receptor on the muscles surrounding the airways. Beta-2 agonists can be administered by MDI inhalers or orally. The action of beta-2 agonists starts within minutes after inhalation and lasts for about 4 hours. even among those without demonstrable reversibility in airway obstruction. o In contrast. A national study was completed in 2003. Patients primarily with emphysema at the top of their lungs. Anti-cholinergic drugs such as ipratropium bromide (Atrovent) dilate airways by blocking the receptors for acetylcholine on the muscles of the airways and preventing them from narrowing. metaproterenol (Alupent). these are often referred to as maintenance inhalers. whose exercise tolerance was low even after pulmonary rehabilitation. On average. Activation of beta-2 receptors relaxes the muscles surrounding the airways and opens the airways. tremor. PHARMACOLOGIC INTERVENTIONS y y Beta-agonists o Beta-2 agonists have the bronchodilating effects of adrenaline without many of its unwanted side effects. beta-2 agonists are especially helpful for patients who are acutely short of breath. In patients with COPD. palpitations or fast heart rate. Proventil). seemed to do the best with this procedure. but after two years returned to about the same levels as before the procedure. Because of their short duration of action. Levalbuterol (Xopenex) is a recently approved Beta-2 agonist. terbutaline (Brethaire). Beta-2 agonists with a slower onset of action but a longer period of activity. the diaphragm and the chest cavity achieve more optimal positioning following the surgery.function better. pirbuterol (Maxair). and low blood potassium. their effectiveness is diminished. o Side effects of beta-2 agonists include anxiety. Anti-cholinergic Agents o Acetylcholine is a chemical released by nerves that attaches to receptors on the muscles surrounding the airway causing the muscles to contract and the airways to narrow. Examples of beta-2 agonists include albuterol (Ventolin. Along with some of these inhalers to be mentioned. Because of their quick onset of action. These drugs last twelve hours and should be taken twice daily and no more. Evidence suggests that when these drugs are used routinely. such as salmeterol xinafoate (Serevent) and formoterol fumarate (Foradil) may be used routinely as maintenance medications. Patients with forced expiratory volume in FEVI of less than 20% of predicted and either diffuse disease on the CAT scan or lower than 20% diffusing capacity or elevated carbon dioxide levels had higher mortality. ipratropium has been shown to . The role of LVRS is at present is very limited. and isoetharine (Bronkosol). In addition. and this improves breathing further. these medications should be used for symptoms as they develop rather than as maintenance. The best criteria for choosing patients for LVRS are still uncertain. These are referred to as rescue inhalers. Dilating airways helps to relieve the symptoms of dyspnea (shortness of breath). Beta-2 agonists have been shown to relieve dyspnea in many COPD patients. lung function and exercise capacity among surviving surgical patients improved significantly following LVRS.

Long acting theophylline preparations can be given orally once or twice a day. Tiotropium (SPIRIVA) is a long acting and more powerful version of Ipratropium and has been shown to be more effective. heart rhythm problems. Thus. Theolair. In patients who respond poorly to either beta-2 agonists or ipratropium alone. o In comparing ipratropium with beta-2 agonists in the treatment of patients with COPD. many doctors use oral corticosteroids as the treatment of last resort. Excessively high levels in the blood can lead to nausea. dosages of methylxanthines are lowered to avoid high blood levels. Theophylline. Ipratropium is especially suitable for use by elderly patients who may have difficulty with fast heart rate and tremor from the beta-2 agonists.y y alleviate dyspnea. Corticosteroids o When airway inflammation (which causes swelling) contributes to airflow obstruction. studies suggest that ipratropium may be more effective in dilating airways and improving symptoms with fewer side effects. Patients who have difficulty using inhaled bronchodilators but no difficulty taking oral medications find theophylline particularly useful. high doses of oral corticosteroids over prolonged periods can have serious side effects. relaxes the muscles surrounding the airways but also prevents mast cells around the airways from releasing bronchoconstricting chemicals such as histamine. Uniphyl. Slo-Bid. In patients with heart failure or cirrhosis. Unfortunately. vomiting. and weight gain. o The disadvantage of methylxanthines is their side effects. Methylxanthines are administered orally or intravenously. diabetes mellitus. bone fractures. such as cimetidine (Tagamet). Ipratropium usually is well tolerated with minimal side effects even when used in higher doses. theophylline can help patients with COPD who have heart failure and pulmonary hypertension. anti-inflammatory medications (more specifically. Interactions with other medications. Twenty to thirty percent of patients with COPD show improvement in lung function when given corticosteroids by mouth. Dosage and blood levels of theophylline or aminophylline have to be closely monitored. improve exercise tolerance and improve FEV1. Therefore. When it is . thinning of the skin and easy bruising. Theophylline also may increase the force of contraction of the heart and lower pressure in the pulmonary arteries. they are prescribed at the lowest possible doses for the shortest period of time to minimize side effects. Examples of corticosteroids include Prednisone and Prednisolone. insomnia. calcium channel blockers (Procardia). like a beta agonist. and even seizures. including osteoporosis. Ipratropium has a slower onset of action but longer duration of action than the shorter-acting beta2 agonists. Theophylline also can act as a mild diuretic and increase urination. When oral corticosteroids are used. quinolones (Cipro). Theo-24) and aminophylline are examples of methylxanthines. corticosteroids) may be beneficial. a combination of the two drugs sometimes results in a better response than to either drug alone without additional side effects. high blood pressure. emotional changes. and allopurinol (Zyloprim) also can alter blood levels of methylxanthines. Methylxanthines o Theophylline (Theo-Dur.

o Corticosteroids also can be inhaled. and oral yeast infections. Nevertheless. it is not clear whether inhaled corticosteroid have the same benefit as oral corticosteroids. Vancenase. . Replacement of the missing or inactive AAT by injection can help prevent progression of the associated emphysema.y necessary to use long term oral steroids. Monitor serum theophylline level. mometasone furoate (Asmanex) and flunisolide (Aerobid). Inhaled corticosteroids have been useful in treating patients with asthma. 2. hypertension. Supportive Care 1. overwhelming respiratory infection Right-sided heart failure. Rinsing out the mouth after use of a steroid inhaler also can decrease these side effects. reduced adventitious sounds. Treatment of Alpha-1 antitrypsin deficiency o Emphysema can develop at a very young age in some patients with severe alpha-1 antitrypsin deficiency (AAT). dysrhythmias Depression Skeletal muscle dysfunction NURSING INTERVENTIONS Monitoring 1. Keep the patient¶s room as dust-free as possible. Beconase. A spacing device placed between the mouth and the MDI can improve medication delivery and reduce the side effects on the mouth and throat. fluticasone (Flovent). doctors are less concerned about using inhaled corticosteroids because of their safety. cardiac arrhythmias. Inhaled corticosteroids have many fewer side effects than long term oral corticosteroids. triamcinolone acetonide (Azmacort). Eliminate all pulmonary irritants. 5. loss of voice. but in patients with COPD. to ensure therapeutic level and prevent toxicity. and cough. COMPLICATIONS 1. central nervous system stimulation. tachycardia. Monitor oxygen saturation at rest and with activity. 4. budesonide (Pulmicort). Monitor condition after administration of aerosol bronchodilators to assess for improved aeration. as ordered. and Vanceril). medications are often prescribed to help reduce the development of the above side effects. particularly cigarette smoke. The side effects of inhaled corticosteroids include hoarseness. Examples of inhaled corticosteroids include beclomethasone dipropionate (Beclovent. 3. Monitor for adverse effects of bronchodilators ± tremulousness. reduced dyspnea. Smoking cessation usually reduces pulmonary irritation. This therapy is of no benefit in other types of COPD. 3. sputum production. Respiratory failure Pneumonia. 2. 4.

Warn patient to stay out of extremely hot or cold weather and to avoid aggravating bronchial obstruction and sputum obstruction. Maintain the patient¶s nutritional status. Review with the patient the objectives of treatment and nursing management. color and consistency). 11. Use pursed lip breathing at intervals and during periods of dyspnea to control rate and depth of respiration and improve respiratory muscle coordination. 6. 12. changes in character of sputum (amount. 4. 10. increasing difficulty in raising sputum. 3. depression and acceptance. Avoid dairy products if these increases sputum production. 5. 7. increasing of shortness of breath. Instruct and supervise patient¶s breathing retraining exercises. Education and health maintenance 1. and to avoid crowds and areas with poor ventilation. Train the patient in energy conservation technique. Add moisture (humidifier. increasing coughing and wheezing. Discuss and demonstrate relaxation exercises to reduce stress. Warn patient to avoid persons with respiratory infections. Teach the patient how to recognize and report evidence of respiratory infection promptly such as chest pain. and anxiety.5 liters daily) within level of cardiac reserve. 8.2. 2 to 2. 3. 4. 9. Encourage high level of fluid intake ( 8 to 10 glasses. Give inhalations of nebulized saline to humidify bronchial tree and liquefy sputum. tension. 15. Advise the patient to avoid respiratory irritants. vaporizer) to indoor air. Assess the patient for reactive-behaviors such as anger. 14. . Suggest that high efficiency particulate air filter may have some benefit. 2. Encourage use of portable oxygen system for ambulation for patients with hypoxemia and marked disability. Reemphasize the importance of graded exercise and physical conditioning programs. Encourage the patient to assume comfortable position to decrease dyspnea. 13. Use postural drainage positions to help clear secretions responsible for airway obstructions. 5. Teach controlled coughing.


cardiac output and events of early primary hypertension disruption of sodium-potassium pump net increase of intracellular sodium & calcium Prolongs vasoconstriction Stimulates smooth muscle hypertrophy & hyperplasia Decreases arterial lumen size Inflammation Release of histamine.cellular retention of sodium water retention. water. leukotrienes. proteins. with increased ECF volume increased blood volume. calcium. prostaglandins Increase vascular permeability Increase sodium. humoral substances Increase vessel thickening Calcium increases smooth muscle contraction Increase vasoconstriction Increase peripheral resistance Blood pressure elevation .

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