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

Structures and Functions of the Respiratory System


Gas exchange

Gas Exchange

Ventilation

Diffusion (alveolar-capillary membrane)

Perfusion

Diffusion (capillary-cellular level)


Ventilation movement of chest wall

Ventilation Movement of Chest Wall


Ventilation

Ventilation

  • 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

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

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

    inflate

    - Increased compliance- destruction of

    alveolar walls & loss of tissue elasticity


Diffusion alveolar capillary membrane

DiffusionAlveolar-Capillary Membrane


Oxyhemoglobin curve

Oxyhemoglobin Curve


Ventilation perfusion

Ventilation-Perfusion

  • 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

    ventilation

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

    gas exchange occurs


V q matching

V/Q Matching


Perfusion

Perfusion


Diffusion body tissue blood capillary

DiffusionBody Tissue-Blood Capillary


Structures and functions of the respiratory system

COPD

  • Progressive, irreversible airflow limitation

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


Copd etiology

COPDEtiology

Cigarette smoking

Occupational chemicals and dusts

Air pollution

Infection

Heredity- A1-antitrysin deficiency

Aging


Copd pathophysiology

COPDPathophysiology

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


Copd pathophysiology1

COPDPathophysiology

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


Copd pathophysiology2

COPDPathophysiology

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

COPD:Chronic Bronchitis vs. Emphysema


Emphysema

Emphysema


Chronic bronchitis blue bloater versus pink puffer

Chronic BronchitisBlue Bloater versus Pink Puffer


Copd behaviors

COPDBehaviors

  • 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 diameter barrel chest

Increased A-P DiameterBarrel-Chest


Copd diagnosis

COPDDiagnosis

PFTs (↑ RV, ↓FEV1)

CXR

ABGs

Sputum C&S if infection suspected

EKG- RV hypertrophy

6 minute oxy-walk


Copd classification

COPD – Classification


Copd complications

COPDComplications

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

Exacerbations of COPD

Acute respiratory failure

Peptic ulcer and gastroesophageal reflux disease

Depression/anxiety


Copd collaborative care

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


Copd nursing diagnoses

COPDNursing Diagnoses

Ineffective Breathing Pattern

Impaired Gas Exchange

Ineffective Airway Clearance

Imbalanced Nutrition: Less than Body Requirements


Asthma

Asthma

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

  • Often reversible airflow limitation

  • Prevalence increasing in many countries, especially in children


Asthma pathophysiology

AsthmaPathophysiology

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


Asthma potential triggers

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

Asthma Inflammation – Effects

Bronchospasm

Plasma exudation

Mucus secretion

AHR

Structural changes


Asthma inflammation clinical manifestations

Asthma InflammationClinical Manifestations

Cough

Chest tightness

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 diagnosis

AsthmaDiagnosis

  • 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)


Asthma therapeutic goals

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


Asthma collaborative management

AsthmaCollaborative Management

Suppress inflammation

Reverse inflammation

Treat bronchoconstriction

Stop exposure to risk factors that sensitized the airway


Asthma medications

AsthmaMedications

  • 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)


Asthma medications1

AsthmaMedications

  • 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 medications2

AsthmaMedications

  • 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 patient teaching medications

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


Asthma collaborative care

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


Asthma nursing diagnoses

AsthmaNursing Diagnoses

Ineffective Airway Clearance

Impaired Gas Exchange

Anxiety

Deficient Knowledge


Pneumonia

Pneumonia

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


Pneumonia pathophysiology

PneumoniaPathophysiology

  • 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


Pneumonia risk factors

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

Pneumonia Behaviors

Usually sudden onset

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

Elderly/debilitated- confusion or stupor


Pneumonia complications

Pneumonia- Complications

Pleuritis

Pleural effusion- 40% of hospitalized patients

Atelectasis

Bacteremia

Lung abscess

Empyema

Pericarditis


Pneumonia diagnostic studies

PneumoniaDiagnostic Studies

CXR

Sputum C&S

Blood cultures

ABGs

Leukocytosis


Pleural effusion

Pleural Effusion


Pneumonia1

Pneumonia


Pneumonia collaborative care

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


Pneumonia nursing assessment

PneumoniaNursing Assessment

Fever in any hospitalized patient

Pain

Tachypnea

Use of accessory muscles

Rapid, bounding pulse

Relative bradycardia

Coughing

Purulent sputum


Pneumonia nursing assessment1

PneumoniaNursing Assessment

  • Consolidation

    • Auscultation

      • Bronchial breathing

      • Bronchovesicular rhonchi

      • Crackles

    • Fremetis

    • Egophony

    • Whispered pectroloquy


Pneumonia nursing diagnoses

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


Pneumonia potential problems

PneumoniaPotential Problems

Hypotension and shock

Respiratory failure

Atelectasis

Pleural effusion

Delerium

Superinfection


Pneumonia nursing goals

PneumoniaNursing Goals

Improving airway patency

Conserving energy – rest

Maintaining proper fluid balance

Patient understanding of treatment and prevention

Prevention of complications


Pneumonia nursing interventions

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


Pneumonia nursing interventions1

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


Pneumonia nursing interventions2

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

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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