Structures and functions of the respiratory system
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Structures and Functions of the Respiratory System. Gas Exchange. Ventilation Diffusion (alveolar-capillary membrane) Perfusion Diffusion (capillary-cellular level). Ventilation Movement of Chest Wall. Ventilation. Depends on volume and pressure changes within thoracic cavity

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Structures and Functions of the Respiratory System

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Structures and Functions of the Respiratory System

Gas Exchange


Diffusion (alveolar-capillary membrane)


Diffusion (capillary-cellular level)

Ventilation Movement of Chest Wall


  • Depends on volume 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

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)

Factors Influencing Ventilation

  • Airway resistance- opposition to gas flow

  • Compliance- distensibility / stretchability

    - Dependent on lung elasticity & elastic recoil

    of chest wall

    - Decreased compliance- lungs difficult to


    - Increased compliance- destruction of

    alveolar walls & loss of tissue elasticity

DiffusionAlveolar-Capillary Membrane

Oxyhemoglobin Curve


  • Adequate diffusion depends 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


    - Low V/Q= blood “shunted” past area; no

    gas exchange occurs

V/Q Matching


DiffusionBody Tissue-Blood Capillary


  • Progressive, irreversible airflow limitation

  • Associated with abnormal inflammatory response of lungs to noxious particles or gases


Cigarette smoking

Occupational chemicals and dusts

Air pollution


Heredity- A1-antitrysin deficiency



Primary process is 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


Destruction of lung 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


Air goes into lungs 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:Chronic Bronchitis vs. Emphysema


Chronic BronchitisBlue Bloater versus Pink Puffer


  • Develop slowly around 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

Increased A-P DiameterBarrel-Chest


PFTs (↑ RV, ↓FEV1)



Sputum C&S if infection suspected

EKG- RV hypertrophy

6 minute oxy-walk

COPD – Classification


Cor pulmonale- RV hypertrophy 2º pulmonary hypertension (late)

Exacerbations of COPD

Acute respiratory failure

Peptic ulcer and gastroesophageal reflux disease


COPD- Collaborative Care

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

COPDNursing Diagnoses

Ineffective Breathing Pattern

Impaired Gas Exchange

Ineffective Airway Clearance

Imbalanced Nutrition: Less than Body Requirements


  • Chronic inflammatory disorder associated with airway hyperresponsiveness leading to recurrent episodes (attacks)

  • Often reversible airflow limitation

  • Prevalence increasing in many countries, especially in children


Airway hyperresponsiveness as 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

AsthmaPotential Triggers

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 Inflammation – Effects


Plasma exudation

Mucus secretion


Structural changes

Asthma InflammationClinical Manifestations


Chest tightness



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


  • History and patterns of symptoms

  • Measurements of lung function

    • PFTs- usually WNL between attacks; ↓ FVC, FEV1

    • PEFR- correlates with FEV

    • Measurement of airway responsiveness

  • CXR

  • ABGs

  • Allergy testing (skin, IgE)

AsthmaTherapeutic Goals

  • No (or minimal)* 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

AsthmaCollaborative Management

Suppress inflammation

Reverse inflammation

Treat bronchoconstriction

Stop exposure to risk factors that sensitized the airway


  • AntiinflammatoryAgents

    • 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)


  • 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


  • 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)

AsthmaPatient Teaching- Medications

  • Name/dosage/route/schedule/purpose/SE

  • Majority administered 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

AsthmaCollaborative Care

  • GINA- decrease asthma 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

AsthmaNursing Diagnoses

Ineffective Airway Clearance

Impaired Gas Exchange


Deficient Knowledge


HAP- pneumonia occurring 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


  • Congestion

    • Fluid enters 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

PneumoniaRisk 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

Pneumonia Behaviors

Usually sudden onset

Fever, shaking chills, SOB, cough w/purulent sputum, pleuritic CP

Elderly/debilitated- confusion or stupor

Pneumonia- Complications


Pleural effusion- 40% of hospitalized patients



Lung abscess



PneumoniaDiagnostic Studies


Sputum C&S

Blood cultures



Pleural Effusion


PneumoniaCollaborative Care

  • Prompt treatment with 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

PneumoniaNursing Assessment

Fever in any hospitalized patient



Use of accessory muscles

Rapid, bounding pulse

Relative bradycardia


Purulent sputum

PneumoniaNursing Assessment

  • Consolidation

    • Auscultation

      • Bronchial breathing

      • Bronchovesicular rhonchi

      • Crackles

    • Fremetis

    • Egophony

    • Whispered pectroloquy

PneumoniaNursing Diagnoses

Ineffective airway clearance 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

PneumoniaPotential Problems

Hypotension and shock

Respiratory failure


Pleural effusion



PneumoniaNursing Goals

Improving airway patency

Conserving energy – rest

Maintaining proper fluid balance

Patient understanding of treatment and prevention

Prevention of complications

PneumoniaNursing Interventions

  • Improving airway patency

    • Removing secretions – coughing vs. suctioning

    • Adequate hydration loosens secretions

    • Air humidification to loosen secretions and improve ventilation

    • Chest physiotherapy – loosens and mobilizes secretions

PneumoniaNursing Interventions

  • Promoting rest and 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

PneumoniaNursing Interventions

  • Patient education and 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- Core Measures

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

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