WEEK+1+alterations+of+pulmonary+function

1. Review respiratory content from Nursing 138 (Nursing Care I).

2. Review the anatomy and physiology of the pulmonary system.

3. Review the techniques for physical assessment of the pulmonary system.

4. Review each of the following lung volumes and capacities and be able to examine the importance of evaluating each (relating to clinical scenarios): //Power points, Huether 699, 700// a. **tidal volume - TV- ** (500 ml) Volume of air inhaled and exhaled per breath. Decreases in severe resp. disease E. **Residual volume-RV;** the air that remains trapped in alveoli after max exhalation. Increases in COPD
 * b. forced vital capacity - FVC-** Max amt of air that can be exhaled as fast as possible after max. inspiration. Tells us about muscle strength and ventilatory reserve. Decreases in COPD and Restrictive diseases.
 * c. forced expiratory volume - FEV1-** Max. amt of air that can be exhaled in the 1st second of expiration. Decreases in COPD, Obesity, Ascites.
 * d. vital capacity - VC-** (4500-5000 ml, theoretical) the amount of air that can be forcibly expired after a maximal inspiration; indicates the largest amt of air that can enter and leave the lungs during respiration. Decreases in Neuromuscular Disease, Gen. fatigue, COPD, Atelectasis, Pulm. Edema
 * F. functional residual capacity - FRC-** (2300 ml norm.) Volume of air after normal exhalation. Needs to be high enough to keep alveoli open. Decreases in Atelectasis, pneumonia, Pulm. Edema, ARDS. Increases in COPD.
 * G. total lung capacity – TLC**- (5700-6200 ml) Volume of air in lungs after max. inspiration. Decreases in Atelectasis and pneumonia. Increases in COPD

5. Review serum and arterial diagnostic tests utilized in the assessment of the pulmonary system. State the normal ranges for each diagnostic test. //(Lewis 525, 527)// **Hemoglobin (Hb)**; norm man=13.5-18 g/dl (135-180 g/L); woman=12-16 g/dl (120-160 g/L). reflects amt of hemoglobin avail for combination w/ O2 **Hematocrit (Hct)**; Norm man= 40%-54%; woman= 38%-47%. Reflects ratio of RBCs to plasma. Increased Hct (polycythemia) found in chronic hypoxemia. **Arterial Blood Gases (ABGs)**; Norms; see #16. Assesses acid-base balance, ventilation status, need for O2 therapy, or change in ventilator settings. **Oximetry (SaO2); norm >95%.** Monitors the percentage of available hemoglobin that is bound to O2.

6. Examine mechanical receptors and chemoreceptors, noting the location, function, and importance of each in respiration. //Huether 712, 694 table 25-1, 699-701// **See Huether 694 table 25-1** The resp ctr in the brain stem controls respiration. The parasympathetic receptors cause lung’s sm. Musc. to constrict and sympathetic causes it to relax. Responds to… -**Neuroreceptors in the lungs** (lung receptors) monitor **mechanical** aspects of ventilation. Irritant receptors sense the need to expel unwanted substances, stretch receptors sense lung volume (lung expansion) and J-receptors sense pulmonary capillary pressure. -**Irritant receptors;** //(699)// found in epithelium of all conducting airways (nasopharynx, oropharynx, larynx, trachea, bronchi, nonrespiratory bronchioles). They are sensitive to irritants that cause them to initiate the cough and sneeze reflex to clear passages. Also cause bronchoconstriction and increased ventilatory rate. -**Stretch receptors**//; (699)// found in smooth muscles of airways. Sensitive to increases in size or volume of lungs. They decrease ventilitory rate and volume, also a mediator of cough. -**J-receptors;** //(700)// (juxtapulmonary capillary receptors) Located near capillaries in alveolar septa. Sensitive to increased pulmonary capillary pressure. Initiate rapid, shallow breathing, hypotension, and bradycardia. -**Chemoreceptors** in the circulatory system and brain stem sense the effectiveness of ventilation by monitoring the pH status of cerebrospinal fluid and the oxygen content (PaO2) of arterial blood. -**Central chemoreceptors** //(701)// monitor arterial blood indirectly by sensing changes in the pH of CSF. Located near resp. center. Sensitive to Hydrogen ion concentration in CSF. CO2 crosses blood brain barrier and combines w/ H2O to carbonic acid, which will dissociates into H+ ions that can stimulate central chemoreceptors. If PaCO2 increases, pH decreases (more H+ ions in CSF) and resp. increase in depth and rate. In COPD, inadequate ventilation is long term and receptors become insensitive to small change in PaCO2. -**Peripheral chemoreceptors;** //(702)// Located in carotid and aortic bodies. Primarily sensitive to oxygen levels in arterial blood (PaO2) and a little to pH and PaCO2. As PaO2 and pH decrease, peripheral chemoreceptors signal resp ctr to increase ventilation. These receptors don’t kick in though until PaO2 drops below 60mm Hg. In COPD, when central receptors become insensitive to high PaCO2 levels, peripheral receptors become major stimulus for breath.

7. Explain the properties of compliance and elastic recoil as they relate to the normal function of the lung in ventilation. **//(//**//p. point, Huether 703,704, 712)// **Compliance;** //(704, p.p.)//; is the measure of lung and chest wall distensibility. It is the opposite of elasticity, compliance is increased in normal aging and in emphysema and decreased in ARDS, pneumonia, pulmonary edema and fibrosis.

**Elastic Recoil;** //(703, p.p)//; is the tendency of the lungs to return to the resting state after inspiration, normal recoil permits passive expiration. Accessory muscles are used to compensate for poor elastic recoil as in //**emphysema**//. Muscular effort is needed to overcome the resistance of the lungs to expansion. During expiration, the muscles relax and the elastic recoil of the lungs causes the thorax to decrease in volume until, once again, balance between the chest wall and lung recoil forces is reached

8. Describe the mechanics of breathing. //(Huether 702, 712)// The interaction of forces and counterforces involving the muscles of inspiration and expiration, alveolar surface tension, elastic properties of the lungs and chest wall, and resistance to airflow. Alterations in any of these increase the work of breathing or metabolic energy needed for adequate ventilation and oxygenation of blood. **Muscles of inspiration;** //(702)// diaphragm, external intercostal muscles, and accessory muscles. When Diaphragm contracts or flattens, it increases volume of thoracic cavity. Contraction of intercostal muscles elevate ant. Portion of ribs, increasing volume of cavity. Accessory muscles of inspiration are sternocleidomastoid and scalene muscles. These help when exercising. **Muscles of expiration;** there are none b/c relaxed expiration is passive. With cough or airway obstruction, the abdomen and internal intercostal muscles assist. When abd muscles contract diaphragm is pushed up and volume of thorax is decreased. The internal intercostal muscles pull down the anterior ribs decreasing thorax diameter. **Surface Tension;** //(702)// Occurs at alveolus and tends to make expansion difficult. Surfactant lowers surface tension by coating the alveolar side of the alveolarcapillary membrane and making the radius of it’s surface smaller. Makes alveoli much easier to inflate at low lung volumes (after expiration) than at high lung volumes (after inspiration). If surfactant not adequate, surface tension causes alveolar collapse, decreased lung expansion, more work breathing and gas-exchange abnormalities. Less surface tension also keeps fluid out of alveoli. **Elastic Properties of lungs and Chest Wall;** //(703)// permit expansion during inspiration and return to resting volume during expiration. Caused by elastin fibers in alveolar walls and surface tension. Lung compliance decreases w/ PULMONARY EDEMA. Chest wall expansion due to configuration of bones and muscles. Chest wall compliance seen w/ SPINAL DEFORMITY or OBESITY See #7 for elastic recoil and compliance. **Airway resistance;** //(704)// determined by diameter areas of the airways and density, viscosity, and velocity of the gas. Airway resistance is normally very low. Greater resistance during expiration. Usually occurs in nose. Also in oropharynx and larynx. Occurs w/ bronchoconstriction, and edema of bronchial mucosa and airway obstructions such as mucus plugging, bronchospasms, tumors, and foreign bodies. Seen with ASTHMA and CHRONIC BRONCHITIS

9. Discuss the clinical significance of decreased lung compliance.//(heuther 704,711)// A decrease indicates that the lung or chest wall is abnormally stiff or difficult to inflate. Clients would have a harder time taking deep breaths which could lead to hypoxemia, respiratory distress, pneumonia, decreased LOC Aging & The Pulmonary SystemElasticity/Chest Wall
 * Chest wall compliance decreases because ribs become ossified and joints grow stiffer, which results in increased work of breathing.
 * Kyphoscoliosis may curve the vertebral column.
 * Respiratory muscle strength decreases.
 * Elastic recoil diminishes, possibly the result of loss of elastic fibers.
 * //Result//: Lung compliance increases and ventilatory capacity (VC) declines, residual volume (RV) increases, total lung capacity (TLC) is unchanged, ventilatory reserves decline, ventilation-perfusion ratios fall.

10. Discuss the clinical significance of increased airway resistance.//(Huether 704)// Airway resistance is determined by the length and radius of the airways. Normally it is very low, 1/2 of total resistance is in the nose next highest is in the pharynx. Very little resistance in the conducting airways of the lungs because of their large cross-sectional area. Airway resistance increases when the diameter of the airways decreases. Bronchoconstriction, which increases airway resistance, can be caused by stimulation of parasympathetic receptors in the bronchial smooth muscle and by numerous irritants and inflammatory mediators.[|2] Bronchodilation, which decreases resistance to airflow, is caused by β2-adrenergic receptor stimulation. Airway resistance can also be increased by edema of the bronchial mucosa and by airway obstructions such as mucus, tumors, or foreign bodies. More muscular effort is required when lung compliance decreases (e.g., in pulmonary edema), chest wall compliance decreases (e.g., in spinal deformity or obesity), or airways are obstructed by bronchospasm or mucous plugging (e.g., in asthma or bronchitis).[|6] An increase in the work of breathing can result in a marked increase in oxygen consumption and an inability to maintain adequate ventilation.

11. Analyze the four components of normal respiratory function: //(p.point,// //Huether 699, 705-707, 712)// **a) Ventilation;** //(699);// Usually involuntary movement of air into and out of lungs. Inspiration of O2 (needed for cellular metabolism) and expiration of CO2 (produced by cellular metabolism). Necessary to maintain normal PaCO2 and pH. -Rate and volume regulated by resp. ctr in Medulla and Pons (brainstem)  *Neurons lead to resp. muscles  *ANS innervates lungs; Sympathetic-dilation of bronchi, Parasymp-constriction ; respond to receptors in lungs and chemoreceptors  *Normal breathing prompted by increased CO2.  **b) Alveolar-capillary diffusion;** //(705);// O2 from alveoli to capillary blood * O2 and CO2 diffuses from high concentration to lower concentration *O2 is at higher concentration in alveoli than in capillaries * CO2 diffuses 20 times faster than O2 *Factors that affect diffusion of gases; -increased distance between alveoli and capillaries, b/c of fluid. Eg; Pulm Edema -decreased surface area of membrane; Eg; if portion of lung is removed, or Emphysema **c) Perfusion;** blood flow to and from lungs. Depends on; *Alveoli-capillary blood flow  *Cardiac output and Hemoglobin (O2 carrying capacity)  **d) Capillary-tissue diffusion;**

__//**1**////**2. Examine the oxyhemoglobin dissociation curve and relate significant clinical conditions.**//__ A shift to the right depicts hemoglobin's decreased affinity for oxygen or an increase in the ease with which oxyhemoglobin dissociates and oxygen moves into the cells. A shift to the left depicts hemoglobin's increased affinity for oxygen, which promotes association in the lungs and inhibits dissociation in the tissues. The oxyhemoglobin dissociation curve is shifted to the right by acidosis (low pH) and hypercapnia (increased PaCO2). In the tissues, the increased levels of carbon dioxide and hydrogen ions produced by metabolic activity decrease the affinity of hemoglobin for oxygen. The curve is shifted to the left by alkalosis (high pH) and hypocapnia (decreased PaCO2). In the lungs, as carbon dioxide diffuses from the blood into the alveoli, the blood carbon dioxide level is reduced and the affinity of hemoglobin for oxygen is increased. The shift in the oxyhemoglobin dissociation curve caused by changes in carbon dioxide and hydrogen ion concentrations in the blood is called the **Bohr effect**. The oxyhemoglobin curve is also shifted by changes in body temperature and increased or decreased levels of 2,3-diphosphoglycerate (2,3-DPG), a substance normally present in erythrocytes. Hyperthermia and increased 2,3-DPG levels shift the curve to the right. Hypothermia and decreased 2,3-DPG levels shift the curve to the left. 2,3-DP**G**
 * R**ise
 * I**n
 * H**+(acidosis)
 * T**EMP

13. Explain the changes that occur in the pulmonary system across the life span. //(older adults Huether 711, Lewis 517; children;Pilli 1226.)// **Older adults;** Decreased lung capacity, tidal volume, and expiratory reserve volume; increased residual volume; breathe less deeply, exhale less forcibly leading to lung stasis and greater chance of pneumonia. *Decreased chest wall compliance (ossification of ribs, stiffening of joints, kyphosis) *Decreased Elastic recoil (loss of elastic fibers) *Alterations in gas exchange *Increases in airflow resistance *Decreased exercise resistance **Children;** Newborns produce little respiratory mucus, which makes them more susceptible to respiratory infections than older children. Excessive production of mucus in children up to 2 yrs can actually lead to obstruction because their bronchial lumens are so small. After 2 the RT bronchus is shorter, wider and more vertical the the LFT. This is why foreign body's most often lodge in the RT brochus. Infants use their abdominals to breath until 2 or 3 when they change to thoracic breathing. In infants the walls of the airway have less cartilage and are more likley to collapse after expiration. This means the infant is less likley to develope bronchospasms as readily as an older child. Therefore wheezing may not be a prominant finding in infants even when the lumen is severely compromised.

14. Identify the clinical indicators of pulmonary disease. //(p.point, Huether 714-716)// *dyspnea; can’t get enough air. Seen in nasal flaring, use of accessory musclesand retractions, also associated w/ anxiety -orthopnea; difficulty breathing in supine position; need fowler’s, semi-fowler’s -paroxymal nocturnal dyspnea; wake up gasping for air & have to sit up/stand to relieve dyspnea *Abnormal breathing patterns; affect rate, depth, regularity, and effort -Kussmaul respirations (hyperpnea); slightly increased rate, very large tidal volumes, and no expiratory pause. Causes; exercise, metabolic acidosis -Cheyne-Stokes respirations: alternating periods of deep and shallow breathing. Periods of apnea followed by increasing volume breathing until peak is reached, then decreasing volume to apnea. Causes; conditions that slow blood flow to brainstem. -Hyper, hypoventilation; see # 15 *Cough, abnormal sputum, hemoptysis; coughing up blood or bloody secretions-usually a sign of infection of bronchi (bronchitis), lung tissue (TB, lung abscess), or cancer, pulmonary infarction * Use of accessory muscles * Barrel chest * Pain; usually localized and may hear sound of //pleural friction rub// over site * Clubbing (sign of chronic hypoxemia) * Circumoral cyanosis; blue lips, Cyanosis of skin and mucosa; caused by desaturated or reduced hemoglobin in blood; low PaO2, pulm or cardiac shunts. Low cardiac output, cold environment, anxiety In adults, not evident until severe hypoxemia present LATE sign

15. Describe hyperventilation and hypoventilation. //(acid-base handout, Huether 715)// **Both are determined by ABGs** **a) hyperventilation;** PaCO2 < 35 mmHg,; excessive alveolar ventilation in relation to metabolic demands. most common cause is from anxiety, also; head injury, pain, insufficient O2 to blood. *Too much CO2 removal; increased resp. rate or tidal volume  *Results in Respiratory alkalosis  **b) hypoventilation;** PaCO2 >45 mmHg, decreased resp rate, shallow breathing; inadequate alveolar ventilation in relation to metabolic demands; may result from diseases affecting lungs, diseases of nerves & musc of chest, impairment of mech of breathing, drugs that slow pt’s breathing, or in neurologic control of breathing., *CO2 removal inadequate causing high PaCO2 levels * Results in resp. acidosis that can affect fx of many tissues

16. Define, discuss the significance of the following terms and identify the normal value for: //(acid-base handout)// **a) pH; Norm; 7.35-7.45;** reflects overall H+ concentration in body fluids, the balance of acid and bases. The higher H+ in blood, the lower the pH; the lower the H+, the higher the pH. pH is necessary for normal enzyme, cell function, and metabolism. *If blood is acidic, (high H+ ions, pH is low) the force of cardiac contraction diminishes.  *If blood is alkaline, (low H+ ions, pH is high) neuromuscular function becomes impaired.  *A pH below/above 6.8-7.8 usually fatal.  **b) PaCO2; Norm; 35-45 mmHg;** reflects the level of CO2 in blood **c) PaO2; Norm; 80-100 mmHg:** **d) HCO3; Norm; 22-26 mEq/L;** Bicarbonate; increase causes metabolic alkalosis. Decrease causes metabolic acidosis **e) Base excess;** too much HCO3 ???? **f) Anion gap;** //(Huether 117 Box 4-1, table 4-12 p.116)// Useful in determining different types of metabolic acidosis. Represents the difference between the sum of Na+ and K+ and the sum of HCO3 and Cl-. *In metabolic acidosis a normal anion gap= conditions r/t bicarbonate loss w/ retention of chloride to maintain an ionic balance. Called //hyper chloremic metabolic acidosis.// Seen in Diarrhea, renal HCO3 loss, decreased renal H+ secretion //*//An elevated anion gap = acidosis assoc. w/ accumulation of anions other than chloride (eg. Lactate, ketoacidate). Seen in increased H+load: Ketoacidosis( eg; diabetes, starvation) Lactic acidosis (shock, hypoxemia), Ingestion or decreased H+ excretion (proximal and distal renal tubule acidosis)

17. Explain the influence of the hydrogen ion concentration on body fluids.(Huether 113, handout) Hydrogen ion is needed to maintain membrane integrity and the speed of metabolic enzyme reactions. The lower the [H+], the more basic the solution and the higher the pH. In biologic fluids, a pH of less than 7.4 is defined as acidic and a pH greater than 7.4 is defined as basic or alkaline. Acid-base imbalances are caused by changes in the concentration of hydrogen in the blood; an increase causes acidosis, and a decrease causes alkalosis. An acid is a substance that can donate H+ to a base. PH reflects the overall H+ concentration in the body fluids.

18. Discuss the regulatory mechanisms of the body to reconstitute an acid-base balance and maintain homeostasis. //(acid-base handout)// **a) chemical buffers;** Act immediately, most efficient pH-balancing force. EG; Bicarbonate, phosphate, protein. Combine with excess acids or bases. Found in blood, ECF, ICF. **b) respiratory system;** Responds in minutes, but is temporary**.** Regulate CO2 in blood, which combines w/ H2O to form H2CO3 (carbonic acid). Regulate rate and depth of resp in response to chemoreceptors detection of pH in CSF. *Faster, deeper breath=less CO2 in lungs and <H2CO3, so pH increases. *Slower, shallower breath = more CO2 in lungs and decreased pH. **c) renal system;** Long-term response, may take 24 hrs. Absorb or excrete acids and bases. Kidneys can also produce bicarbonate. *When blood is acidic, kidneys reabsorb HCO3 and excrete H+.  *When blood is alkaline, the kidneys excrete HCO3 and retain H+

19. Identify the values of each of the terms in objective #16 as they relate to the following acid- base imbalances: //(acid-base handout, huether 115-118)// **a) Respiratory acidosis;** pH <7.35, PaCO2 <45 mmHg, HCO3-(bicarb) 22-26mEq/L (normal). **Caused by** hypoventilation. When the lungs don’t eliminate enough CO2. **b) Respiratory alkalosis;** pH >7.45, PaCO2 >45 mmHg, HCO3(bicarb) 22-26mEq/L (normal). **Caused by** hyperventilation. When the lungs eliminate too much CO2. **c) Metabolic acidosis;** pH <7.35, HCO3 <22 mEq/L, PaCO2 is normal. **Caused by** ; * ingestion of an acidic substance or one that can be metabolized to an acid  * production of excess acid  * kidneys unable to excrete norm amts of acid  * a loss of base  **d) Metabolic alkalosis;** pH >7.45, HCO3 > 26 mEq/L, PaCO2 is normal. **Caused by;** * loss of stomach acid *an excess loss of sodium (norm 135-145 mEq/L) or potassium (3.5-5.0 mEq/L) * a renal loss of H+ * a gain of base

**20. Compare and contrast acute and chronic respiratory acidosis in relation to etiology, physiology and clinical manifestations**. (M/S 335,6) **Etiology-** COPD, barbituate or sedative overdose, chest wall abnormality (eg. Obesity), severe pneumonia, atelectasis, respiratory muscle weakness( eg. Guillain-Barre syndrome), mechanical hypoventilation **Physiology-** CO2 retention from hypoventilation, compensatory response to HCO3 retention by kidney **Clinical Manifestations-** **Neurologic:** drowsiness, disorientation, dizziness, headache, coma **Cardiovascular**: decreased BP, ventricular fibrillation(related to hyperkalemia from compensation, warm flushed skin(rt peripheral vasodialtion) **Neuromuscular:** seizures  **Respiatory:** hypoventilation with hypoxia( lungs unable to commpensate when there is a resp. prob.)

**21. Differentiate among ischemia, hypoxia, and hypoxemia**. **Hypoxemia,** or reduced oxygenation of arterial blood (reduced PaO2), is caused by respiratory alterations, whereas **hypoxia,** or reduced oxygenation of cells in tissues, may be caused by alterations of other systems as well. Although hypoxemia can lead to tissue hypoxia, tissue hypoxia can result from other abnormalities unrelated to alterations of pulmonary function, such as low cardiac output or cyanide poisoning. Hypoxemia results from problems with one or more of the major mechanisms of oxygenation: 1 Oxygen delivery to the alveoli a Oxygen content of the i nspired air (FiO2) b Ventilation of the alveoli 2 Diffusion of oxygen from the alveoli into the blood a Balance between alveolar ventilation and perfusion ( v/q match) b Diffusion of oxygen across the alveolar capillary barrier 3 Perfusion of pulmonary capillaries. > **(Patho 717)** **Hypoxia,** or lack of sufficient oxygen, is the single most common cause of cellular injury (  __Figure 3-6__ ). Hypoxia can result from a decreased amount of oxygen in the air, loss of hemoglobin or hemoglobin function, decreased production of red blood cells, diseases of the respiratory and cardiovascular systems, and poisoning of the oxidative enzymes (cytochromes) within the cells. The most common cause of hypoxia is **ischemia** (a local state in which the cells are deprived of blood supply). **(patho 66)** **(PP p10)** **Hypoxia-**decreased tissue oxygenation determined by: cardiac index, Hgb, SaO2, vessel patency, cellular demand -not directly measured, anaerobic metabolism **Hypoxemia-** insufficient oxygenation; low levels of O2 blood; measured in ABG- Mild <80, moderate <60, severe <40 ; manifested by changes in mental status; can lead to hypoxia Hypoxemia can be caused by inadequate ventilation of well-perfused areas of the lung (low v/q). Mismatching of this type, called **shunting,** occurs in atelectasis, in asthma as a result of bronchoconstriction, and in pulmonary edema and pneumonia when alveoli are filled with fluid. When blood passes through portions of the pulmonary capillary bed that receive no ventilation, right-to-left shunt occurs, resulting in decreased systemic PaO2 and hypoxemia. Hypoxemia also can be caused by poor perfusion of well-ventilated portions of the lung (high v/q), resulting in wasted ventilation. The most common cause of high v/q is a pulmonary embolus that impairs blood flow to a segment of the lung. An area where alveoli are ventilated but not perfused is termed **alveolar dead space** (can be caused by pulmonary emboli and decreased CO2). **23. Explain the physiological criteria and related etiology for respiratory failure. (Patho p.718, PP 12-14, and M/S ch.68)** Acute respiratory failure Respiratory failure is defined as inadequate gas exchange such that PaO2 # _50mm Hg or PaCO2 $ _50mm Hg with pH # _7.25. Respiratory failure can result from direct injury to 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 bag-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. Smokers 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 turning, deep breathing, 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 for a time. **24. Analyze the mechanisms that would create a potential complication of respiratory failure for various clinical scenarios and include interventions for its prevention**. See #23 from patho p.718 **25. Examine the etiology, pathophysiology, clinical manifestations, and collaborative management of the client with acute respiratory distress syndrome (ARDS), to include the newborn to an elderly client. (Patho p.724-726, MS ch 68, PP p 15, Pilli p.777)** **Etiology-** **Infant-**deficient of sufactant, deficient alveolar suface area, meconium aspiration, **Adult-** Shock, inhalation injuries, drug OD, Trauma, Pneumonia, embolism, DIC(disseminated intravascular coagulation), pancreatitis, cardiopulmonary bypass **Pathophysiology-** **Infant** see Pilli p.777 **Adult-** Systemic Inflammatory response(SIR), Inflammatory cellular responses and mediators and cytokines released from neutraphils and macrophages fighting something else causes lung damage, occurs within 90 min. of SIR and within 24 hrs. of the initial insult, result is massive inflammatory response by lungs **Clinical Manifestations-** **Infant-**low body tenp., nasal flaring, sternal and subcostal retractions, tachypnea, cyanotic mucous membranes, seesaw resp. (on inspiration the anterior chest wall retracts and the abdomen protrudes, on expiration the sternum rises), heart failure AEB decreased urine output and edema of the extremities, pale gray skin, periods of apnea, bradycardia, pneumothorax **Adult-** classic signs and symptoms of ARDS are marked dyspnea; rapid, shallow breathing; inspiratory crackles; respiratory alkalosis; decreased lung compliance; hypoxemia unresponsive to oxygen therapy (refractory hypoxemia); and diffuse alveolar infiltrates seen on chest radiographs, without evidence of cardiac disease. **Collaborative management-** **Infant-(pilli 778)** surfactant replacement, O2 administration, ventilation, muscle relaxants, liquid ventilation, nitric oxide **Adult-**Early detection, supportive therapy, prevention of complications, O2, ventilation, prevention of infections, surfactant replacement
 * 22. Compare and contrast between the concepts of deadspace and shunting, and discuss the clinical significance of both. (Patho 718, PP 11,12)**

**26. Compare and contrast between the following major obstructive lung diseases; asthma, chronic bronchitis, and emphysema and examine the pathophysiology, clinical manifestations and collaborative management of each.** **27. Describe how an allergic response can trigger childhood asthma attacks.** Inflammation resulting in hyperresponsiveness of the airways is the major pathologic feature of asthma. It is initiated by a Type I hypersensitivity reaction (see  __Chapter 7__ ). Exposure to allergens (with subsequent immunologic activation in the atopic individual with production IL-4 and IgE) or irritants results in a cascade of events beginning with mast cell degranulation and the release of multiple inflammatory mediators (  __Figure 26-9__ ). Some of the most important mediators that are released during an asthma attack are histamine, interleukins, prostaglandins, leukotrienes, and nitric oxide. Vasoactive effects of these cytokines include vasodilation and increased capillary permeability. Chemotactic factors are produced that result in bronchial infiltration by neutrophils, eosinophils, and lymphocytes. Eosinophils release a variety of toxic chemicals that contribute to inflammation and tissue damage. The resulting inflammatory process produces bronchial smooth muscle spasm, vascular congestion, edema formation, production of thick mucus, impaired mucociliary function (see  __Figure 26-8__ ), thickening of airway walls, and increased bronchial hyperresponsiveness. In addition, the autonomic control of bronchial smooth muscle is dysregulated because of production of toxic neuropeptides leading to acetylcholine-mediated bronchospasm. **28. Interpret a set of blood gases obtained during an acute asthma attack. (MS table 29-3 p 614)** **pH-** first increases, then normalizes, then decreases **PaCO2-** first decreases, then normalizes, then increases **PaO2-** continuously decreases

**29. Examine the following respiratory tract infections; pneumonia (bacterial, viral, atypical, aspiration), and tuberculosis relative to their pathophysiology, clinical manifestations and collaborative management.**