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| The exchange of gases between blood and cells is called? |
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| The following belong to the conducting portion of the respiratory system |
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| Nasal passages, mouth and pharynx, larynx, trachea, bronchi and bronchioles. |
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| The structure which closes off the larynx is the |
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| The correct order of structures in the respiratory passageways |
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| Pharynx, larynx, trachea, bronchi, bronchioles |
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| The exchange of gases occurs in the |
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| The volume of air that can be exhaled after normal exhalation is the |
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| Expiratory reserve volume |
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| The volume of air in a normal breath is called |
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| Gas exchange in the lungs happens by the process of |
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| Most oxygen in the blood is transported as |
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| The primary chemical stimulus for breathing is the concentration of |
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| Carbon Dioxide in the blood |
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| Inflammation of the bronchi in the lower respiratory tract. S/S: Persistent cough; Clear, mucoid sputum; Fever; HA; Malaise; SOB on exertion; Rhonchi or expiratory wheezing; No consolidation or infiltrates on CXR. Causes: Usually Viral-rhinovirus, influenza; Bacterial- smokers (strep pneumoniae, haemophilus influenzae), nonsmokers (mycoplasma pneumoniae, chlamydia pneumoniae). Risk factors: Cigarette smoke, exposure to irritants, low resistance that may result from a cold. |
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| Terminal air spaces in the respiratory tract and the actual sites of gas exchamge between the air and the blood. |
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| Extend from the trachea and branch off to the left and right. Airway lined with a mucosal surface and supported by cartilaginous rings. Accompanied by the pulmonary arteries, veins, and lymph vessels, enter the lungs through a slit called the hilum. Conducts air into the lungs. No gas exchange here. |
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| Connects the oropharynx with the trachea. Walls are supported by firm cartilaginous structures that prevent collapse during inspiration. Functions: speech and protecting the lungs from substances other than air. "Watchdog of the lungs". Two pairs of folds: upper pair- vestibular folds, protective function; lower pair- vocal folds, produces the vibrations required for making vocal sounds. The vocal folds and the elongated opening between them are called the glottis. Epiglottis, located above the larynx, leaf-shaped piece of cartilage, moves downward to cover the larynx when swallowing. |
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| In constant motion, move the mucociliary blanket (protects the respiratory system by entrapping dust, bacteria, and other foreign particles), with its entrapped particles in an escalator-like fashion toward the oropharynx, from which it is expectorated or swallowed. The function in clearing the lower airways is optimal at normal oxygen levels and is impaired when oxygen levels are higher or lower than normal. Impaired by drying conditions, such as breathing heated but unhumidified indoor air during winter. Cigarette smoking slows down or paralyzes the motility. This slowing allows the residue to accumulate in the lungs, decreasing the efficiency of this pulmonary defense system. |
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| Divided into three sections: nasopharynx, oropharynx and laryngopharynx. Nasopharynx: air passess through the nasal passages, it is filtered, warmed and humidified. Outer nasal passages are lined with course hairs, which filter and trap dust. upper portion of nasla cavity is lined with a mucous membrane that contains small blood vessels, supplying warmth and moisture to the air we breath. Oropharynx: extends posteriorly from the soft palate to the epiglottis. Only opening between the nose, mouth and lungs. Obstruction leads to immediate cessation of ventilation. Laryngopharynx: part of the throat that connects to the esophagus. Air enters larynx anteriorly. |
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| Recurring paroxysms of diffuse wheezing, dyspnea, and cough resulting from inflammation and spasmodic contractions of the bronchi. Chronic disorder of the airways that causes episodes of airway obstruction, bronchial hyperresponsiveness, airway inflammation, mucosal edema, increased viscid secretions, and smooth muscle contraction that are usually reversible. Exaggerated hypersensitivity response to a variety of of stimuli. S/S: episodic wheezing and feelings of chest tightness to an acute, immobilizing attack. Coughing, SOB. Causes: respiratory infections, emotional stress, or weather changes. Often worse at night. Risk factors: Family history, smoker, overweight, low birth weight. |
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| Incomplete expansion of a lung or portion of lung. Caused by airway obstruction, lung compression such as pneumothorax or pleural effusion, or increased recoil of the lung due to loss of pulmonary surfactant. May be present at birth or develop during the neonatal period or later in life. S/S: tachypnea, tachycardia, dyspnea, cyanosis, signs of hypoxemia, diminished chest expansion, absence of breath sounds, and intercostal retractions. |
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| Smallest of the conducting airways. No cartilage present and their walls are composed mainly of smooth muscle and elastic fibers. Bronchospasm of these muscles can impair air flow. The elastic fibers, which radiate from teh outer layer of the bronchial wall and connect with elastic fibers arising from other parts of the bronchial tree, exert tension on the bronchial walls; by pulling uniformly in all directions, they help maintain airway patency. |
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| Airway obstruction of the major and small airways. Common in middle-aged men and associated with chronic irritation from smoking and recurrent infections. History of chronic productive cough for at least 3 consecutive months in at least 2 consecutive years. Early feature: hypersecretion of mucus in the large airways, associated with hypertrophy of the submucosal glands in the trachea and bronchi. Viral and bacterial infections are a common result. Labeled "blue bloaters", cyanosis and fluid retention associated with right sided heart failure. |
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| Chronic Obstructive Pulmonary Disease (COPD) |
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| Chronic and recurrent obstruction of airflow in the pulmonary airways. Airflow obstruction is usually progressive and is accompanied by inflammatory responses to noxious particles or gases. Leading cause of morbidity and mortality. Risk factors: host and environmental. Causes: smoking, hereditary deficiency in alphaone-antitrypsin, asthma and airway hyperresponsiveness. Inflammation and fibrosis of the bronchial wall, along with excess mucus secretion, obstruct airflow and mismatching of ventilation and perfusion. S/S: fatigue, exercise intolerance, cough-usually in am, sputum production, SOB. Late stages: recurrent respiratory infections and chronic respiratory failure. Encompass two types of obstructive airway disease: emphysema and chronic bronchitis. |
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| Loss of lung elasticity and abnormal enlargement of the airspaces distal to the terminal bronchioles, with destruction of the alveolar walls and capillary beds. Leads to hyperinflation of the lungs and produces an increase in total lung capacity (TLC). Causes: smoking (incites lung injury), inherited deficiency of alphaone-antitrypsin (antiprotease enzyme that protects the lung from injury). Results from the breakdown of elastin and other alveolar wall components by enzymes, called proteases, that digest proteins. Two types: centriacinar or centrilobular and panacinar. Centriacinar affects the bronchioles in the central part of the respiratory lobule, initial preservation of the alveolar ducts and sacs, most common and seen more in males. Panacinar produces intial involvement of the peripheral alveoli and later extends to the more central bronchioles, common in alphaone-antitrypsin deficiency. "Pink puffer", lack of cyanosis, use of accessory muscles and pursed lip breathing, barrel chest- decrease in breath sounds. |
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| Most important causes of acute upper respiratory tract infections. Virus belongs to the Orthomyxoviridae family. Three types: A, B, and C. A: ability to infect multiple species, including avian and mammalian. Contagious. Transmission occurs by inhalation of droplet nuclei. Incubation period is 1-4 days, can be infectious starting one day before initial symptoms. Can cause three types of infections: uncomplicated URI (rhinotracheitis), viral pneumonia and a respiratory viral infection followed by a bacterial infection. S/S: fever, chills, malaise, muscle aching, HA, profuse, watery nasal discharge, nonproductive cough and sore throat. Viral pneumonia: occurs as a complication and characterized by rapid production of fever, tachypnea, tachycardia, cyanosis, and hypotension. Secondary complications: sinusitis, otitis media, bronchitis, and bacterial pneumonia. |
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| Abnormal collection of fluid or exudate in the pleural cavity. Occurs when the rate of fluid formation exceeds the rate of its removal. Fluid may be transudate (clear fluid- hydrothorax- CHF; LDH) or exudate (specific gravity greater than 1.020; LDH), purulent (pus), chyle (milky) sanguineous (bloody). Empyema: infection in the pleural cavity that results in exudate containing glucose, proteins, leukocytes and debris from dead cells and tissue. Chylothorax: effusion of lymph in the thoracic cavity; results from trauma, inflammation, or malignant infiltration; most common in neonates. S/S: fever, increased WBC, other signs of inflammation, decreases lung expansion, dullness or flatness with percussion, diminshed breath sounds, hypoxemia-decreased surface area, corrected with oxygen; dyspnea-most common symptom-fluid compresses lung. |
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| Also called pleuritis. Inflammation of the pleura. Common in infectious processes such as respiratory infections that extend to involve the pleura. Pain is a fequent symptom, unilateral and abrupt onset. When the central part of the diaphragm is irritated, the pain may be referred to the shoulder. Deep breathing is painful, tidal volumes small, breathing more rapid. Reflex splinting of chest. Musculoskeletal pain: result of frequent, forceful coughing, bilateral, inferior portion of rib cage. Myocardial pain: substernal area not affected by respiratory movements. Treatment: analgesics and nsaid's. |
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| Occurs due to the rupture of an air-filled bleb, or blister, on the surface of the lung. Rupture allows atmospheric air from the airways to enter the pleural cavity. Air flows from the alveoli into the pleural space, causing the involved portion of the lung to collpase as a result of its own recoil. Primary: healthy person; blebs usually located at top of lungs; often in tall boys and young men; smoking; talc lung. Secondary: underlying lung disease (asthma, TB, cystic fibrosis, sarcoidosis, bronchogenic carcinoma and metastatic pleural disease); most common-emphysema; life-threatening. Catamenial: relation to the menstrual cycle and usually recurrent; women 30-40 and history of endometriosis; right lung; develops within 72 hours of menses; cause unknown. |
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| Presence of air in the pleural space. Partial or complete collapse of the affected lung. Can occur without an obvious injury (spontaneous) or as a result of direct injury to the chest or major airways (thraumatic). Tension pneumothorax: life threatening condition in which increased pressure within the pleural cavity impairs both respiratory and cardiac function. |
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| Penetrating or nonpenetrating injuries. Fractured or dislocated ribs most common cause from nonpenetrating injury. Hemothorax may accompany. Some causes: Transthoracic needle aspirations, central line insertion, intubation, and positive pressure ventilation. Also can occur as a complication of CPR. |
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| Special surface tension-lowering molecules that line the inner surface of the alveoli. Without surfactant, lung inflation would be extremely difficult. It helps to keep the alveoli dry and prevent pulmonary edema. Also provides for stability and more even inflation of the alveoli. |
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| Infectious disease caused by the mycobacterium, M. More resistant to destruction. Organism can persist in old necrotic and calcified lesions and remain capable of reinitiating growth. Acid-fast bacilli. Can infect any organ, but more commonly the lungs. Thrive in oxygen rich environment. Cause disease in the upper lobe or upper parts of the lower lobe of the lungs, where ventilation and oxygen are greatest. Two forms: M. tuberculosis hominis-humans and M. tuberculosis bovis- bovine. bovine is aquired by drinking milk from infected cows, affect GI tract. Hominis is airborne spread by minute, invisible particles called droplet nuceli that are harbored in the respiratory secretions of persons with active TB. Coughing, sneezing, and talking create droplets; droplets evaporate leaving the organism, which remain suspended in the air and are ciculated by air currents. Living under crowded and confined spaces increase the risk for spread. Primary TB: previously unexposed; abrupt high fever, pleuritis, and lymphadenitis. Secondary TB: reinfection; low-grade fever, night sweats, easy fatigued, anorexia, weight loss; cough usually dry, but later becomes productive with purulent and sometimes blood-tinged sputum. Dyspnea and orthopnea develop as the disease progresses. |
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| Inflammation of parynchymal structures of the lung, such as the alveoli and the bronchioles. Inhalation of irritating fumes or aspiration of gastric contents can result in severe pneumonia, much less common than infectious agents. Classified according to type of agent (typical or atypical) causing the infection, distribution of the infection (lobar or broncho), and setting (community or hospital) in which it occurs. Community aquired: bacterial or viral; most common cause S. pneumoniae; viral causes- influenza, respiratory syncytial virus (RSV), adenovirus, parainfluenza virus. Hospital aquired: mostly bacterial. |
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| Loss of cough reflex, damage to ciliated endothelium that lines the respiratory tract, or impaired immune defenses predispose to colinization and infection of the lower respiratory system. Rsik factors: antibiotic therapy that alters the normal bacterial flora, diabetes, smoking, chronic bronchitis, and viral infection. Two types: pneumococcal and Legionnaire. Pneumococcal: most common cause; S. pneumoniae; edema, red hepatization, gray hepatization and resolution. S/S: onset sudden; maliase, severe shaking, chills and fever. Legionnaire: form of bronchopneumonia caused by Legionella pneumophila; environment aquired; infection occurs when water that contains the pathogen is aerosolized into droplets and inhaled or aspirated by a host. S/S: 2-10 days after infection; onset abrupt; malaise, weakness, lethargy, fever and dry cough; CNS disturbances, GI tract, arthralgia, elevation in body temp, diarrhea, hyponatremia and confusion. Consolidation of lung tissues and impairs gas exchange. |
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| Caused by a variety of agents, most common is Mycoplasma pneumoniae. Common with children and young adults. Other etiologic agents include: influenza, RSV, adenovirus, rhinovirus, rubella and varicella, and Chlamydia pneumoniae. Some cases, cause is unknown. Patchy involvement of the lung, largely confined to the alveolar septum and and pulmonary interstitium. S/S: fever, HA, muscle aches and pains; cough when present is dry, hacking and nonproductive. |
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| Principle muscle of inspiration. When contracts, abdominal contents are forced downward and chest expands from top to bottom. Inspiration: size of the chest wall increases, intrathoracic pressure becomes more negative, and air is drawn into the lungs; aided by the external intercostal muscles; accessory muscles- scalene (elevate first two ribs) and sternocleidomastoid (raise sternum) muscles; other muscles- alae nasi, produce flaring of the nostrils during obstructed breathing. Paralysis of one side causes the chest to move up on that side rather than down during inspiration because of the negative pressure, this is called paradoxical movement. Expiration: elastic components of the chest wall and lung structures that were stretched during inspiration recoil, causing the size of the chest caivty to decrease and the pressure in the chest cavity to increase; passive; abdominal and internal intercostal muscles can be used to increase effort. |
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Primarily affected by the partial pressures exerted by the different gases in the alveoli - the basic functional unit of the lungs. Is always linked with the function of the circulatory system. You breathe in oxygen - which in turn increases the PaO2 in the alveoli causing it to diffuse in the alveolar membrane into the capillaries surrounding it. Waste products coming from the different cells of the body (in this case carbon dioxide) is transported until it reaches the alveolar capillaries. The blood is oxygen depleted that is carbon dioxide rich which makes the partial pressure exerted by Carbon dioxide is greater than that of oxygen as a result, Carbon dioxide diffuses from the capillaries into the alveoli and is exhaled.
Read more: http://wiki.answers.com/Q/Explain_the_gas_exchange_that_takes_place_within_the_lungs#ixzz1lXnRCpmS
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| Pathological condition wherby the whole body or region of the body is deprived of an adequate oxygen supply. When alveolar oxygen levels drop below 60mm Hg, marked vasoconstriction may occur, and at very low oxygen levels, the local flow may be almost abolished. Occurs at high altitudes and in persons with chronic hypoxia due to lung disease, causes vasoconstriction thoughout the lung. Prolonged hypoxia can lead to pulmonary hypertension and increased workload on the right heart. S/S: tachypnea, SOB, dizziness, lack of coordination, muscle fatigue, visual impairment, seizures and coma are late findings. |
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| Reduction in blood oxygen levels (PO2). Can result from an inadequate amount of O2 in the air, disease of the respiratory system, dysfunction of the neurologic system, or alterations in circulatory function. Mechanisms leading to a reduction in PO2: hypoventilaton, impaired diffusionof gases, inadequate circulation of blood through the pulmonary capillaries and mismatching of ventilation and perfusion. If the PO2 of the tissues fall below a critical level, aerobic metabolism ceases and anaerobic metabolism takes over, with formation and release of lactic acid. Mild S/S: increased HR, peripheral vasoconstriction, diaphoresis, and mild increase in BP, slight impairment of mental performance, visual acuity and hyperventilation. More pronounced: personality changes, restlessness, agitated or combative, uncoordinated muscle movements, euphoria, impaired judgement, delirium, eventually stupor and coma. Chronic S/S: increased ventilation, pulmonary vasoconstriction, increased production of RBC. |
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| Deep or rapid breathing that leaves the feeling of breathlessness. Mechanism of action: alveolar ventilation that exceeds metabolic demands. Lungs remove CO2 ata a faster rate than it is produced by cellular metabolism, resulting in a low PaCO2 <35 mmHg (normal 35-45 mmHg). Causes: stress, anxiety, lung disorders, head injuries, stroke, aspirin overdose. S/S: breathlessness, chest pain, lightheadedness, numbness in hand/feet/face/lips, slurred speech. |
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| Slow, shallow respirations which do not meet the body's needs. Mechanism of action: ventilation is inadequate to perform normal gas exchange. Results in increased PaCO2 levels in the body >45 mmHg and low PO2 levels in the blood <95%. Causes: stroke, drug overdose, obesity, Guillian Barre, Myasthenia Gravis, obstructive sleep apnea. S/S: HA, confusion, drwosiness, increased BP, increased HR, unconsciousness. |
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| Subjective sensation or a person's perception of difficulty in breathing that includes the perception of labored breathing and the reaction to that sensation. Also called SOB. Observed in: pneumonia, asthma, and emphysema. Cause unknown. Mechanisms: increased sensitivity to changes in ventilation perceived through CNS mechanisms; reduced ventilatory capacity or breathing reserve; stimulation of neural receptors in the muscle fibers of the intercostals and diaphragm and of receptors in the skeletal joints. |
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| Uncommon type of COPD characterized by a permanent dilation of the bronchi and bronchioles caused by destruction of the muscle and elastic supporting tissue as the result of a vicious cycle of infection and inflammation. Localized: tumors, foreign bodies, mucus plugs. Generalized: bilateral, affects lower lobes. S/S: atelectasis, obstruction of the smaller airways, and diffuse bronchitis. Recurrent bronchopulmonary infection, coughing, production of copious amounts of foul smelling purulent sputum, hemoptysis, weight loss, anemia, clubbing of fingers (mod-advanced). |
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| Specific type of pleural effusion in which there is blood in the pleural cavity. Bleeding may be the result of a chest injury, complication of chest surgery, malignancies, or rupture of great vessel such as aortic aneurysm. Minimal: 300-500ml in pleural space; usually clears in 10-14 days. Moderate: 500-1000ml fills 1/3 pleural space and may produce signs of lung compressionand loss of intravascular volume; requires immediate drainage and replacement of intravascular fluids. Large: fills 1/2 or more of one side of the chest; 1000ml or more, usually caused by bleeding from high-pressure vessel such as an intercostal or mammary artery; immediate drainage or surgery to control bleeding. S/S: alterations in oxygenation, ventilation, respiratory effort, and breath sounds, blood loss, increased HR (sudden and distressing). |
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| Inflammation or painful reaction to allergy or cell-lining damage. A stimulus or agent which induces the state of irritation is an irritant. Irritants are typically thought of as chemical agents (for example phenol and capsaicin) but mechanical, thermal (heat), and radiative stimuli (for example ultraviolet light or ionising radiations) can also be irritants. Irritation also has non-clinical usages referring to bothersome physical or psychological pain or discomfort. |
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| Develops when a blood-borne substance lodges in a branch of the pulmonary artery and obstructs blood flow. May consist of a thrombus, air that has accidentally been injected during IV infusion, fat that has been mobilized from the bone marrow after a fracture or from a traumatized fat depot, or amniotic fluid that has entered the maternal circulation after rupture of the membranes at the time of delivery. Arise from deep vein thrombosis in the lower extremeties. Mechanical obstruction of the pulmonary circulation and neurhumoral reflexes causing vasoconstriction. Obstruction of pulmoary blood flow causes reflex bronchoconstriction in the affected area of the lung, wasted ventilation and impaired gas exchange, and loss of alveolar surfactant. Pulmonary HTN and right heart failure may develop. Risk factors: venous stasis, venous endothelial injury, and hypercoagulability, oral contraceptives, women who smoke. S/S: depend on size and location; chest pain, dyspnea, increased RR, moderate hypoxemia. Small emboli: pulmonary HTN. Moderate: breathlessness, pleuritic pain, apprehension, slight fever, cough productive of blood-streaked sputum, tachycardia. Massive: sudden collapse, crushing substernal chest pain, shock, LOC, pulse rapid and weak, low BP, JVD, skin cyanotic and diaphoretic; often fatal. |
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| Granulomas found in the lung |
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| Inhalation of inorganic dust or particulate matter |
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| Enlargement of air spaces and destruction of lung tissue |
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| Excessive concentration of hemoglobin |
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Definition
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| Incomplete expansion of the lung or a portion of the lung |
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| Right Sided Heart Failure |
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Definition
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| Increased mucus production and destruction of small airways |
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Definition
| Chronic Obstructive Bronchitis |
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| Movement of gas in and out of lung |
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| Increased carbon dioxide in arterial blood |
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| Release of inflammatory chemicals from mast cells in the airways. Makes up 1/3 to 1/2 of all cases of asthma. Commonly affects children and young adults. Also called allergic asthma because attacks are IgE-mediated responses to specific antigens. |
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| Release of inflammatory chemicals from mast cells inthe airways. Develops in middle age and has less favorable prognosis. Respiratory infections may be causative. No allergen can be identified, and it is not IgE mediated. |
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| Acute respiratory infection caused by a coronavirus. The pneumonia is severe and has a mortality rate of 10%. |
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| Diffuse Interstitial Pulmonary Fibrosis |
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Definition
| Restrictive disorder characterized by thickening of the alveolar interstitium. The disorder is an immune-mediated disorder that follows an initial lung injury. Lung tissues are characteristically infiltrated by immune cells (macrophages and lymphocytes). Excess fibrin deposition results in stiff, noncompliant lungs. Vital capacity, tidal volume, FRC, and diffusion capacity are generally reduced. Respiratory rate increases to compensate for the small tidal volume. S/S: dyspnea, fever, enlarged lymph nodes-pulmonary and generalized symptoms of inflammation. |
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| Abnormal protein deposits (granulomas) in the lung. Granulomas are fibrotic and are associated with immune cells (histiocytes). Cause unknown. S/S: dyspnea, fever, enlarged lymph nodes-pulmonary and generalized symptoms of inflammation. |
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Definition
Central: sensing changes in the PCO2 of the blood, located in the medulla; surrounded by brain extracellular fluid and respond to changes in its hydrogen ion concentration.
Peripheral: located in the carotid and aortic bodies; monitor arterial blood oxygen levels, also monitor carbon dioxide. |
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