Only $2.99/month

Terms in this set (13)

-Dyspnea: is defined as "a subjective experience of breathing discomfort that is comprised of qualitatively distinct sensations that vary in intensity. Its often described as breathlessness, air hunger, shortness of breath, labored breathing, and preoccupation with breathing.
-Orthopnea: is dyspnea that occurs when an individual lies flat and is common in individuals with heart failure. The recumbent position redistributes body water, causes the abdominal contents to exert pressure on the diaphragm, and decreases the efficiency of the respiratory muscles.
-Cough: is a protective reflex that helps clear the airways by an explosive expiration. Inhaled particles, accumulated mucous, inflammation, or the presence of a foreign body initiates the cough reflex by stimulating the irritant receptors it the airway.
-Abnormal sputum: Changes in the amount, color, and consistency of sputum provides information about progression of disease and effectiveness of therapy. The gross and microscopic appearances of sputum enable the clinician to identify cellular debris or microorganisms, which aids in diagnosis and choice of therapy.
-Hemoptysis: is the expectoration of blood or bloody secretions. This is sometimes confused with hematemesis, which is the vomiting of blood. Blood produced with coughing is usually bright red, and has an alkaline pH, and is mixed with frothy sputum. Blood that is vomited is dark, has an acidic pH, and is mixed with food particles.
-Kussmaul respiration (hyperpnea): is characterized by a slightly increased ventilatory rate, very large tidal volumes (Tidal volume is the lung volume representing the normal volume of air displaced between normal inhalation and exhalation when extra effort is not applied), and no expiratory pause. Labored breathing occurs whenever there is increased work or breathing, especially if the airways are obstructed. Strenuous exercise or metabolic acidosis induces hypernea.
-Cheyne-stokes respirations: characterized by alternating periods of deep and shallow breathing. Apnea lasting from 15 to 60 seconds is followed by ventilations that increase in volume until a peak is reached; the ventilation (tidal volume) decreases again to apnea. Cheyne-stokes respirations result from any condition that reduces blood flow to the brain stem.
-Cyanosis: is a bluish discoloration of the skin and mucous membranes caused by increased amounts of desaturated or reduced hemoglobin (which is bluish) in the blood. It generally develops when 5 g of hemoglobin is desaturated, regardless of hemoglobin concentration.
-Clubbing: is the selective bulbous enlargement of the end (distal segment) of a digit (finger or toe) (Fig 26-1); its severity can be graded from 1 to 5 based on the extent of nail bed hypertrophy and the amount of changes in the nails themselves or as early, moderate, or severe.
-Pain: Pain caused by pulmonary disorders originates in the pleurae, airways, or chest wall. Infection and inflammation of the parietal pleura cause sharp or stabbing pain when the pleura stretches during inspiration. The pain is usually localized to a portion of the chest wall, where a unique breath sound called a pleural friction rub may be heard over the painful area. Laughing or coughing makes pleural pain worse. Pleural pain is common with pulmonary infarction (tissue death) caused by pulmonary embolism and emanates from the area around the infarction.
-Hypoventilation is inadequate ventilation in relation to metabolic demands. Hypoventilation occurs when minute volume (tidal volume times respiratory rate) is reduced. It is caused by alterations in pulmonary mechanics or in the neurological control of breathing. When alveolar ventilation is normal, carbon dioxide (CO2) is removed from the lungs at the same rate it is produced by cellular metabolism; therefore arterial and alveolar Pco2 values remain at normal levels (40 mm Hg). With hypoventilation,CO2 removal is slower than CO2 production and the level of CO2 in the arterial blood (Paco2) increases, causing hypercapnia (Paco2 greater than 44mm Hg). This results in respiratory acidosis that can affect the function of many tissues throughout the body. Hypoventilation is often overlooked until it is severe because breathing pattern and ventilatory rate may appear to be normal and changes in tidal volume can be difficult to detect clinically. Blood gas analysis (i.e. measurement of the Paco2 of arterial blood) reveals the hypoventilation. Pronounced hypoventilation can cause somnolence or disorientation.
-Hyperventilation is alveolar ventilation exceeding metabolic demands. The lungs remove CO2 faster than it is produced by cellular metabolism, resulting in decreased Paco2, or hypocapnia (Paco2 less than 36 mm Hg). Hypocapnia results in a respiratory alkalosis that can also interfere with tissue function. Like hypoventilation, hyperventilation can be determined by arterial blood gas analysis. Increased respiratory rate or tidal volume can occur with severe anxiety, acute head injury, pain, and in response to conditions that cause insufficient oxygenation of the blood.
Respiratory failure is defined as inadequate gas exchange such that PaO2<or= 50 mm Hg or Paco2 >or= 50 mm Hg with pH <or=7.25. Respiratory failure can result from direct injury of the lungs, airways, or chest wall or indirectly because of injury to another body system, such as the brain or spinal cord. It can occur in individuals who have an otherwise normal respiratory system or in those with underlying chronic pulmonary disease. Most pulmonary diseases can cause episodes of acute respiratory failure. If the respiratory failure is primarily hypercapnic, it is the result of inadequate alveolar ventilation and the individual must receive ventilatory support, such as with a big-valve mask or mechanical ventilator. If the respiratory failure is primarily hypoxemic, it is the result of inadequate exchange of oxygen between the alveoli and the capillaries and the individual must receive supplemental oxygen therapy. Many people will have combined hypercapnic and hypoxemic respiratory failure and will require both kinds of support. Respiratory failure is an important potential complication of any major surgical procedure, especially those that involve the central nervous system, thorax, or upper abdomen. The most common postoperative pulmonary problems are atelectasis, pneumonia, pulmonary edema, and pulmonary emboli. People who smoke are at risk, particularly if they have preexisting lung disease. Limited cardiac reserve, chronic renal failure, chronic hepatic disease, and infection also increase the tendency to develop postoperative respiratory failure. Prevention of postoperative respiratory failure includes frequent position changes, deep-breathing exercises, and early ambulation to prevent atelectasis and accumulation of secretions. Humidification of inspired air can help loosen secretions. Incentive spirometry gives individuals immediate feedback about tidal volumes, which encourages them to breathe deeply. Supplemental oxygen is given for hypoxemia, and antibiotics are given as appropriate to treat infection. If respiratory failure develops, the individual may require mechanical ventilation from time to time.
Atelectasis is the collapse of lung tissue. There are three types of atelectasis:
1. Compression atelectasis-is caused by external pressure exerted by tumor, fluid, or air in pleural space or by abdominal distention pressing on a portion of lung, causing alveoli collapse.
2. Absorption atelectasis- results from removal of air from obstructed or hypoventilated alveoli or from inhalation of concentrated oxygen or anesthetic agents
3. Surfactant impairment-results from decreased production or inactivation of surfactant, which is necessary to reduce surface tension in the alveoli and thus prevent lung collapse during expiration. Surfactant impairment can occur because of premature birth, acute respiratory distress syndrome, anesthesia induction, or mechanical ventilation.
Atelectasis tends to develop after surgery and is estimated to occur in more that 90% of individuals administered a general anesthetic. Postoperative persons are often in pain, breathe shallowly, are reluctant to change position, and produce viscous secretions that tend to pool in dependent portions of the lung. Clinical manifestations of atelectasis are similar to those of pulmonary infection including dyspnea, cough, fever, and leukocytosis. Prevention and treatment of postoperative atelectasis usually include deep-breathing exercises, frequent position changes, and early ambulation. Deep breathing and the use of an incentive spirometer help open connections between patent and collapsed alveoli, called pores of Kohn (fig 26-5). This allows air to flow into the collapsed alveoli (collateral ventilation) and aids in the expulsion of intrabronchial obstructions.
-Exposure to toxic gases: Inhalation of gaseous irritants can cause significant respiratory dysfunction. Commonly encountered toxic gases include smoke, ammonia, hydrogen chloride, sulfur dioxide, chlorine, phosgene, and nitrogen dioxide. Inhalation injuries in burns can include toxic gasses from household or industrial combustants, heat, and smoke particles. Inhaled toxic particles cause damage to the airway epithelium, mucus secretion, inflammation, mucosal edema, ciliary damage, pulmonary edema, and surfactant inactivation. Acute toxic inhalation is frequently complicated by acute respiratory distress syndrome (ARDS) and pneumonia. Initial symptoms include burning of the eyes, nose, and throat; coughing; chest tightness; and dyspnea. Hypoxia is common. Treatment includes mechanical ventilation with PEEP, and support of the cardiovascular system. Steroids are sometimes used, although their effectiveness has not been well documented. Most individuals recover quickly. Some, however, may improve initially and then deteriorate as a result of bronchiectasis or bronchiolitis (inflammation of the bronchioles).
-Allergic alveolitis: Inhalation of organic dusts can result in an allergic inflammatory response called extrinsic allergic alveolitis, or hypersensitivity pneumonitis. Many allergens can cause this disorder, including grains, silage, bird droppings or feathers, wood dust (particularly redwood and maple), cork dust, animal pelts, coffee beans, fish meal, mushroom compost, and molds that grow on sugarcane, barley, and straw. The lung inflammation, or pneumonitis, occurs after repeated, prolonged exposure to the allergen. Lymphocytes and inflammatory cells infiltrate the interstitial lung tissue, releasing a variety of autoimmune and inflammatory cytokines. Recent studies suggest an important role for interleukin-17, which promotes epithelial cell injury. Allergic alveolitis can be acute, subacute, or chronic. The acute form causes fever, cough, and chills a few hours after exposure. In the subacute form, coughing and dyspnea are common and sometime necessitate hospital care. Diagnosis is made by history of exposure, chest x-ray, and serologic testing. Treatment consists of removal of the offending agent and administration of corticosteroids. Recovery is complete if the offending agent can be avoided in the future. With continued exposure, the disease becomes chronic and pulmonary fibrosis develops.
Pulmonary edema is excess water in the lung. The normal lung is kept dry by lymphatic draining and a balance among capillary hydrostatic pressure, capillary oncotic pressure, and capillary permeability. In addition, surfactant lining the alveoli repels water, keeping fluid from entering the alveoli. Predisposing factors for pulmonary edema include include heart disease, acute respiratory distress syndrome, and inhalation of toxic gasses. The pathogenesis is shown in Fig 26-6. The most common cause of pulmonary edema is left-sided heart disease. When the left ventricle fails, filling pressures on the left side of the heart increase. Vascular volume redistributes into the lungs, causing an increase in pulmonary capillary hydrostatic pressure. When the hydrostatic pressure exceeds oncotic pressure (which holds fluid in the capillary), fluid moves out into the interstitial space (the space within the alveolar septum between alveolus and capillary). When the flow of fluid out of the capillaries exceeds the lymphatic system's ability to remove it, pulmonary edema develops. Another cause of pulmonary edema is capillary injury that increases capillary permeability, as in cases of acute respiratory distress syndrome or inhalation of toxic gases, such as ammonia. Capillary injury and inflammation causes water and plasma proteins to leak out of the capillary and move into interstitial space, increasing the interstitial oncotic pressure (which is usually very low). As the interstitial oncotic pressure begins to exceed capillary oncotic pressure, water moves out of the capillary and into the lungs. Pulmonary edema also can result from obstruction of the lymphatic system. Drainage can be blocked by compression of lymphatic vessels by edema, tumors, and fibrotic tissue and by increased systemic venous pressure.
Similarities: The Obstructive lung disease(s) are characterized by airway obstruction that is worse with expiration. More force (i.e., use of accessory muscles of expiration) is required to expire a given volume of air and emptying of the lungs is slowed. In adults the major obstructive lung diseases are asthma, chronic bronchitis, and emphysema. Asthma is one of the most common lung disorders in the US. Because many individuals have both chronic bronchitis and emphysema, these disorders together are often called chronic obstructive pulmonary disease (COPD). Asthma is more acute and intermittent than COPD, even though it can be chronic (fig 26-8). The unifying symptom of obstructive lung diseases is dyspnea, and the unifying sign is wheezing. Individuals have an increased work of breathing, ventilation-perfusion mismatching, and a decreased forced expiratory volume in 1 second.

Clinical manifestations:
-Asthma: Between attacks, individuals are asymptomatic and pulmonary funtction tests are normal. At the beginning of an attack, the individual experiences chest constriction, expiratory wheezing, dyspnea, nonproductive coughing, prolonged expiration, tachycardia, and tachypnea. Severe attacks involve the accessory muscles of respiration and wheezing is heard during both inspiration and expiration. A pulsus paradoxus (decrease in systolic blood pressure during inspiration of more than 10 mm Hg) may be noted. Peak flow measurements should be obtained. Because the severity of blood gas alterations is difficult to evaluate by clinical signs alone, arterial blood gas tensions should be measured if oxygen saturation falls below 90%. Usual finding are hypoxemia with an associated respiratory alkalosis. In late asthma response, symptoms can be even more severe than the initial attack.
-Chronic Bronchitis: See table 26-2
-Emphysema: See table 26-2
-COPD: See bottom of fig 26-10

READ 689-694