Downloaded 28 times
More Related Content
Similar to Structure and function of Respiratory System
Structure and function of Respiratory System
- 1. Structures and Functionsof the Respiratory System
- 2.
- 3.
- 4. Ventilation • Depends onvolume and pressure changes within thoracic cavity • Diaphragm is major muscle of inspiration; also external intercostal muscles. Contraction increases diameter of thoracic cavity intrathoracic pressure→ ↓ air flows into respiratory system→ • Expiration is passive process d/t lung elasticity. ↑ intrathoracic pressure air flows out of lungs→ • Accessory muscles
- 5. Control of Ventilation ∗Neural control- respiratory center in medulla & pons ∗ Central chemoreceptors – sensitive to pH ∗ Peripheral chemoreceptors- sensitive to paO2 ∗ Patients with COPD- hypoxic drive ∗ WOB- amount of effort required for the maintenance of a given level of ventilation (as WOB s, more↑ energy is expended for adequate ventilation)
- 6. Factors Influencing Ventilation • Airwayresistance- opposition to gas flow • Compliance- distensibility / stretchability - Dependent on lung elasticity & elastic recoil of chest wall - Decreased compliance- lungs difficult to inflate - Increased compliance- destruction of alveolar walls & loss of tissue elasticity
- 7.
- 8.
- 9. Ventilation-Perfusion • Adequate diffusiondepends on balanced ventilation- perfusion (V/Q) ratio • Normal lung: V=4L/min; Q= 5L/min (0.8) • If imbalanced: gas exchange interrupted - High V/Q= “wasted” or dead-space ventilation - Low V/Q= blood “shunted” past area; no gas exchange occurs
- 10.
- 11.
- 12.
- 13. Progressive, irreversible airflow limitation Associatedwith abnormal inflammatory response of lungs to noxious particles or gases COPD
- 14. ∗Cigarette smoking ∗Occupational chemicalsand dusts ∗Air pollution ∗Infection ∗Heredity- A1-antitrysin deficiency ∗Aging COPD EtiologyEtiology
- 15. ∗ Primary processis inflammation ∗ Inhalation of noxious particles→ inflammatory cells release mediators (leukotrienes, interleukins, TNF) airways→ become inflammed with increased goblet cells excess mucus production (bronchitis)→ & structural remodeling to peripheral airways with d collagen & scar tissue↑ COPD Pathophysiology
- 16. ∗ Destruction oflung tissue caused by imbalance of proteinases/antiproteinases results in emphysema with loss of attachments & peripheral airway collapse (Centrilobar- affects respiratory bronchioles/upper lobes/mild disease; panlobar- alveolar ducts, sacs, respiratory bronchioles- lower lobes/AAT deficiency COPD PathophysiologyPathophysiology
- 17. ∗Air goes intolungs easily but unable to come out; air trapped in distal alveoli, causing hyperinflation & overdistension ∗PV thickens with surface area for↓ gas exchange- V/Q mismatch COPD PathophysiologyPathophysiology
- 19. COPD: Chronic Bronchitis vs.Emphysema
- 20.
- 21. Chronic Bronchitis Blue Bloaterversus Pink Puffer
- 22. Develop slowlyaround 50 years of age after history of smoking Cough, sputum production, dyspnea In late stages, dyspnea at rest Wheezing/chest tightness- may vary Prolonged I:E, BS, tripod position, pursed-lip breathing,↓ edema ↑ A-P diameter of chest Advanced- weight loss, anorexia (hypermetabolic state) Hypoxemia, possible hypercapnia Bluish-red color from polycythemia, cyanosis COPD BehaviorsBehaviors
- 23.
- 24. ∗ PFTs (RV, FEV1)↑ ↓ ∗ CXR ∗ ABGs ∗ Sputum C&S if infection suspected ∗ EKG- RV hypertrophy ∗ 6 minute oxy-walk COPD DiagnosisDiagnosis
- 26. Spirometry Results Stage IMild FEV1/FVC < 0.70 FEV1 ≥ 80% predicted Stage II Moderate FEV1/FVC < 0.70 50% ≤ FEV1 < 80% predicted Stage III Severe FEV1/FVC < 0.70 30% ≤ FEV1 < 50% predicted Stage IV Very Severe FEV1/FVC < 0.70 FEV1 < 30% predicted OR FEV1 < 50% predicted PLUS chronic respiratory failure COPD – Classification
- 27. ∗ Cor pulmonale-RV hypertrophy 2º pulmonary hypertension (late) ∗ Exacerbations of COPD ∗ Acute respiratory failure ∗ Peptic ulcer and gastroesophageal reflux disease ∗ Depression/anxiety COPD ComplicationsComplications
- 28. ∗ Smoking cessation ∗Medications- bronchodilators (inhaled & step-wise), Spriva (LA anticholinergic), ICS ∗ Oxygen therapy ∗ RT- PLB, diphragmatic, cough, CPT, nebulization therapy ∗ Nutrition- Avoid over/underweight, rest 30” before eating, 6 small meals, avoid foods that need a great deal of chewing, avoid exercise 1 hr before meal, take fluids between meals to avoid stomach distension COPD- Collaborative Care
- 29. ∗Ineffective Breathing Pattern ∗ImpairedGas Exchange ∗Ineffective Airway Clearance ∗Imbalanced Nutrition: Less than Body Requirements COPD Nursing Diagnoses
- 30. Chronic inflammatorydisorder associated with airway hyperresponsiveness leading to recurrent episodes (attacks) Often reversible airflow limitation Prevalence increasing in many countries, especially in children Asthma
- 31. ∗ Airway hyperresponsivenessas a result of inflammatory process ∗ Airflow limitation leads to hyperventilation ∗ Decreased perfusion & ventilation of alveoli leads to V/Q mismatch ∗ Untreated inflammation can lead to LT damage that is irreversible ∗ Chronic inflammation results in airway remodeling Asthma PathophysiologyPathophysiology
- 34. ∗ Allergens –40% ∗ Exercise (EIA) ∗ Air pollutants ∗ Occupational factors ∗ Respiratory infections – viral ∗ Chronic sinus and nose problems ∗ Drugs and food additives – ASA, NSAIDs, ß-blockers, ACEi, dye, sulfiting agents ∗ Gastroesophageal reflux disease (GERD) ∗ Psychological factors- stress Asthma Potential TriggersPotential Triggers
- 35. ∗ Bronchospasm ∗ Plasmaexudation ∗ Mucus secretion ∗ AHR ∗ Structural changes Asthma Inflammation – Effects
- 36. ∗ Cough ∗ Chesttightness ∗ Wheeze ∗ Dyspnea ∗ Expiration prolonged -1:3 or 1:4, due to bronchospasm, edema, and mucus ∗ Feeling of suffocation- upright or slightly bent forward using accessory muscles ∗ Behaviors of hypoxemia- restlessness, anxiety, HR & BP, PP↑ Asthma Inflammation Clinical ManifestationsClinical Manifestations
- 37. ∗ History andpatterns of symptoms ∗ Measurements of lung function ∗ PFTs- usually WNL between attacks; FVC, FEV↓ 1 ∗ PEFR- correlates with FEV ∗ Measurement of airway responsiveness ∗ CXR ∗ ABGs ∗ Allergy testing (skin, IgE) Asthma DiagnosisDiagnosis
- 38. ∗ No (orminimal)* daytime symptoms ∗ No limitations of activity ∗ No nocturnal symptoms ∗ No (or minimal) need for rescue medication ∗ Avoid adverse effects from asthma medications ∗ Normal lung function ∗ No exacerbation ∗ Prevent asthma mortality ∗ * Minimal = twice or less per week Asthma Therapeutic GoalsTherapeutic Goals
- 39. ∗ Suppress inflammation ∗Reverse inflammation ∗ Treat bronchoconstriction ∗ Stop exposure to risk factors that sensitized the airway Asthma Collaborative ManagementCollaborative Management
- 40. Antiinflammatory Agents Corticosteroids- suppress inflammatory response. Reduce bronchial hyperresponsiveness & mucus production, B2 receptors↑ ∗ Inhaled – preferred route to minimize systemic side effects ∗ Teaching ∗ Monitor for oral candidiasis ∗ Systemic – many systemic effects – monitor blood glucose ∗ Mast cell stabilizers- NSAID ; inhibit release of mediators from mast cells & suppress other inflammatory cells (Intal, Tilade) Asthma MedicationsMedications
- 41. Antiinflammatory Agents Leukotriene modifiers Block action of leukotrienes Accolate, Singulair, Zyflo) Not for acute asthma attacks Monclonal Ab to IgE ↓ circulating IgE Prevents IgE from attaching to mast cells, thus preventing the release of chemical mediators For asthma not controlled by corticosteroids Xolair SQ Asthma MedicationsMedications
- 42. Bronchodilators B-agonists-SA for acute bronchospasm & to prevent exercised induced asthma (EIA) (Proventil, Alupent); LA for LT control Combination ICS + LA B-agonist (Advair) Methylxanthines- Theophylline: alternative bronchodilator if other agents ineffective. Narrow margin of safety & high incidence of interaction with other medications Anticholinergics- block bronchoconstriction . Additive effect with B-agonists (Atrovent) Asthma MedicationsMedications
- 43. Name/dosage/route/schedule/purpose/SE Majorityadministered by inhalation (MDI, DPI, nebulizers) Spacer + MDI- for poor coordination Care of MDI- rinse with warm H2O 2x/week Potential for overuse Poor adherence with asthma therapy is challenge for LT management Avoid OTC medications Asthma Patient Teaching- MedicationsPatient Teaching- Medications
- 44. GINA- decreaseasthma morbidity/mortality & improve the management of asthma worldwide Education is cornerstone Mild Intermittent/Persistent: avoid triggers, premedicate before exercise, SA or LA Beta agonists, ICS, leukotriene blockers Acute episode: Oxygen to keep O2Sat>90%, ABGs, MDI B-agonist; if severe- anticholinergic nebulized w/B agonist, systemic corticosteroids Asthma Collaborative CareCollaborative Care
- 45. ∗Ineffective Airway Clearance ∗ImpairedGas Exchange ∗Anxiety ∗Deficient Knowledge Asthma Nursing Diagnoses
- 46. ∗ HAP- pneumoniaoccurring 48 hours or longer after admission ∗ VAP- pneumonia occurring 48-72 hours after ET intubation ∗ HCAP- hospitalized for 2 or more days within 90 days of infection; resided in LTC facility; received IV therapy or wound care within past 30 days of current infection; attended a hospital or dialysis clinic ∗ Aspiration pneumonia- abnormal entry of secretions into lower airway Pneumonia
- 47. ∗ Congestion ∗ Fluidenters alveoli; organisms multiply & infection spreads ∗ Red hapatization ∗ Massive capillary vasodilation; alveoli filled with organisms, neutrophils, RBCs, & fibrin ∗ Gray hepatization ∗ Blood flow decreases & leukocytes & fibrin consolidate in affected part ∗ Resolution ∗ Resolution & healing; exudate processed by macrophages Pneumonia PathophysiologyPathophysiology
- 48. Pneumonia Risk FactorsRisk Factors ∗Aging ∗ Air pollution ∗ Altered LOC ∗ Altered oral normal flora secondary to antibiotics ∗ Prolonged immobility ∗ Chronic diseases ∗ Debilitating illness ∗ Immunocompromised state ∗ Inhalation or aspiration of noxious substances ∗ NG tube feedings ∗ Malnutrition ∗ Resident of Long-term care ∗ Smoking ∗ Tracheal intubation ∗ Upper respiratory tract infection
- 49. ∗ Usually suddenonset ∗ Fever, shaking chills, SOB, cough w/purulent sputum, pleuritic CP ∗ Elderly/debilitated- confusion or stupor Pneumonia BehaviorsBehaviors
- 50. ∗ Pleuritis ∗ Pleuraleffusion- 40% of hospitalized patients ∗ Atelectasis ∗ Bacteremia ∗ Lung abscess ∗ Empyema ∗ Pericarditis Pneumonia- Complications
- 51. ∗ CXR ∗ SputumC&S ∗ Blood cultures ∗ ABGs ∗ Leukocytosis Pneumonia Diagnostic StudiesDiagnostic Studies
- 52.
- 53.
- 54. ∗ Prompt treatmentwith antibiotics ∗ Oxygen, analgesics, antipyretics ∗ Influenza vaccine ∗ Pneumococcal vaccine ∗ Nutrition ∗ PSI – Pneumonia Patient Outcomes Research Team Severity Index ∗ Determine whether to treat at home or in hospital Pneumonia Collaborative CareCollaborative Care
- 55. ∗ Fever inany hospitalized patient ∗ Pain ∗ Tachypnea ∗ Use of accessory muscles ∗ Rapid, bounding pulse ∗ Relative bradycardia ∗ Coughing ∗ Purulent sputum Pneumonia Nursing AssessmentNursing Assessment
- 56. ∗ Consolidation ∗ Auscultation ∗Bronchial breathing ∗ Bronchovesicular rhonchi ∗ Crackles ∗ Fremetis ∗ Egophony ∗ Whispered pectroloquy Pneumonia Nursing AssessmentNursing Assessment
- 57. ∗ Ineffective airwayclearance RT copious tracheobronchial secretions ∗ Activity intolerance RT altered respiratory function ∗ Risk for fluid volume deficit RT fever and dyspnea ∗ Knowledge deficit about the treatment regimen and preventive health measures Pneumonia Nursing DiagnosesNursing Diagnoses
- 58. ∗ Hypotension andshock ∗ Respiratory failure ∗ Atelectasis ∗ Pleural effusion ∗ Delerium ∗ Superinfection Pneumonia Potential ProblemsPotential Problems
- 59. ∗ Improving airwaypatency ∗ Conserving energy – rest ∗ Maintaining proper fluid balance ∗ Patient understanding of treatment and prevention ∗ Prevention of complications Pneumonia Nursing GoalsNursing Goals
- 60. ∗ Improving airwaypatency ∗ Removing secretions – coughing vs. suctioning ∗ Adequate hydration loosens secretions ∗ Air humidification to loosen secretions and improve ventilation ∗ Chest physiotherapy – loosens and mobilizes secretions Pneumonia Nursing InterventionsNursing Interventions
- 61. ∗ Promoting restand conserving energy ∗ Bedrest with frequent changes of position ∗ Energy conservation ∗ Sedatives to decrease work of breathing and energy expenditure unless contraindicated ∗ Promoting fluid intake ∗ Dehydration is possible RT insensible fluid losses through respiratory tract ∗ If not contraindicated, increase fluid intake to 2 liters/day Pneumonia Nursing InterventionsNursing Interventions
- 62. ∗ Patient educationand home care considerations ∗ Increase activities as tolerated – fatigue and weakness may be prolonged ∗ Breathing exercises to clear the lungs should be taught ∗ Smoking cessation if indicated – smoking destroys tracheobronchial ciliary action, which is the first line of defense for the lungs. Smoking also irritates the mucus cells of the bronchi and inhibits the function of alvolar macrophages ∗ Patient is encouraged to get influenza vaccine because influenza increases risk for secondary bacterial infections ∗ Staphylococcus ∗ H. influenzae ∗ S. pneumonae ∗ Encouraged to get Pneumovax against S. pneumonae Pneumonia Nursing InterventionsNursing Interventions
- 63. ∗ Oxygenation assessment(ABGs, oximetry) ∗ Pneumococcal vaccine (>65yo; prior to DC) ∗ BC performed within 24h prior to after hospital arrival ∗ BC before first antibiotic ∗ Adult smoking cessation advice ∗ Antibiotic timing- within 4 hours of arriving to hospital ∗ Influenza vaccine Pneumonia- Core Measures
Editor's Notes
- #2 Upper respiratory tract Lower respiratory tract Surfactant Blood supply Chest wall Lungs Extend from clavicles (apex) to diaphragm (base) Left lung- 2 lobes; right lung- 3 lobes & larger Each lobe consists of segments (lobules) Respiratory System- Defense Mechanisms Filtration of air Mucociliary clearance Cough Reflex bronchoconstriction Alveolar macrophages Blood Supply Pulmonary circulation- provides lungs with blood for gas exchange via pulmonary artery. Oxygen-carbon dioxide exchange occurs. Bronchial circulation- bronchial arteries arise off thoracic aorta. Provides oxygen to bronchi and other pulmonary tissues.
- #4 Chest wall Thoracic cage- ribs (24) and sternum; protect lungs and heart Parietal pleural Visceral pleura Intrapleural space- contains pleural fluid Normal pressure in pleural space is negative Diaprhagm is major muscle or respiration- innervated by phrenic nerve (C3-C5) est Wall
- #8 Oxygen & carbon dioxide move back & forth across alveolar-capillary membrane Diffusion occurs from higher to lower concentrations Ability of lungs to oxygenate arterial blood adequately is determined by PaO2 & O2 saturation
- #15 80%-90% of COPD deaths are related to smoking Air pollution- harmful to those with existing lung disease A1-antitrysin deficiency (1%-2% of cases)
- #29 EBP: Global Initiative for Chronic Obstructive Lung Disease (GOLD) Surgery- LVRS, bullectomy, lung transplant
- #35 Asthma Inflammation: Cells and Mediators Inflammatory cells Mast cells Eosinophils Th2 cells Basophils Neutrophils Platelets Structural cells Epithelial cells Smooth muscle cells Endothelial cells Fibroblast Nerves Mediators Histamine Leukotrienes Prostanoids PAF Kinins Adenosine Nitric oxide Cytokines Chemokines Growth factors