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Structures and Functions of
the Respiratory System
∗Ventilation
∗Diffusion (alveolar-
capillary
membrane)
∗Perfusion
∗Diffusion (capillary-
cellular level)
Gas Exchange
Ventilation
Movement of Chest Wall
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
∗ 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
inflate
- Increased compliance- destruction of
alveolar walls & loss of tissue elasticity
Diffusion
Alveolar-Capillary Membrane
Oxyhemoglobin Curve
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
Perfusion
Diffusion
Body Tissue-Blood Capillary
Progressive, irreversible airflow
limitation
Associated with abnormal
inflammatory response of lungs
to noxious particles or gases
COPD
∗Cigarette smoking
∗Occupational chemicals and dusts
∗Air pollution
∗Infection
∗Heredity- A1-antitrysin deficiency
∗Aging
COPD
EtiologyEtiology
∗ 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
Pathophysiology
∗ 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
PathophysiologyPathophysiology
∗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
PathophysiologyPathophysiology
COPD:
Chronic Bronchitis vs. Emphysema
Emphysema
Chronic Bronchitis
Blue 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
COPD
BehaviorsBehaviors
Increased A-P Diameter
Barrel-Chest
∗ PFTs ( RV, FEV1)↑ ↓
∗ CXR
∗ ABGs
∗ Sputum C&S if infection suspected
∗ EKG- RV hypertrophy
∗ 6 minute oxy-walk
COPD
DiagnosisDiagnosis
Spirometry Results
Stage I Mild 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
∗ Cor pulmonale- RV hypertrophy 2º pulmonary
hypertension (late)
∗ Exacerbations of COPD
∗ Acute respiratory failure
∗ Peptic ulcer and gastroesophageal reflux
disease
∗ Depression/anxiety
COPD
ComplicationsComplications
∗ 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
∗Ineffective Breathing Pattern
∗Impaired Gas Exchange
∗Ineffective Airway Clearance
∗Imbalanced Nutrition: Less than
Body Requirements
COPD
Nursing Diagnoses
 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
∗ 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
PathophysiologyPathophysiology
∗ 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
∗ Bronchospasm
∗ Plasma exudation
∗ Mucus secretion
∗ AHR
∗ Structural changes
Asthma Inflammation –
Effects
∗ 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 Inflammation
Clinical ManifestationsClinical Manifestations
∗ History and patterns 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
∗ 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
Therapeutic GoalsTherapeutic Goals
∗ Suppress inflammation
∗ Reverse inflammation
∗ Treat bronchoconstriction
∗ Stop exposure to risk factors that sensitized
the airway
Asthma
Collaborative ManagementCollaborative Management
 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
 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
 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
 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
Patient Teaching- MedicationsPatient Teaching- Medications
 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
Collaborative CareCollaborative Care
∗Ineffective Airway Clearance
∗Impaired Gas Exchange
∗Anxiety
∗Deficient Knowledge
Asthma
Nursing Diagnoses
∗ 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
∗ 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
PathophysiologyPathophysiology
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
∗ Usually sudden onset
∗ Fever, shaking chills, SOB, cough w/purulent sputum,
pleuritic CP
∗ Elderly/debilitated- confusion or stupor
Pneumonia
BehaviorsBehaviors
∗ Pleuritis
∗ Pleural effusion- 40% of hospitalized patients
∗ Atelectasis
∗ Bacteremia
∗ Lung abscess
∗ Empyema
∗ Pericarditis
Pneumonia- Complications
∗ CXR
∗ Sputum C&S
∗ Blood cultures
∗ ABGs
∗ Leukocytosis
Pneumonia
Diagnostic StudiesDiagnostic Studies
Pleural Effusion
Pneumonia
∗ 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
Collaborative CareCollaborative Care
∗ Fever in any hospitalized patient
∗ Pain
∗ Tachypnea
∗ Use of accessory muscles
∗ Rapid, bounding pulse
∗ Relative bradycardia
∗ Coughing
∗ Purulent sputum
Pneumonia
Nursing AssessmentNursing Assessment
∗ Consolidation
∗ Auscultation
∗ Bronchial breathing
∗ Bronchovesicular rhonchi
∗ Crackles
∗ Fremetis
∗ Egophony
∗ Whispered pectroloquy
Pneumonia
Nursing AssessmentNursing Assessment
∗ 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
Nursing DiagnosesNursing Diagnoses
∗ Hypotension and shock
∗ Respiratory failure
∗ Atelectasis
∗ Pleural effusion
∗ Delerium
∗ Superinfection
Pneumonia
Potential ProblemsPotential Problems
∗ Improving airway patency
∗ Conserving energy – rest
∗ Maintaining proper fluid balance
∗ Patient understanding of treatment and
prevention
∗ Prevention of complications
Pneumonia
Nursing GoalsNursing Goals
∗ 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 InterventionsNursing 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 InterventionsNursing 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
Nursing InterventionsNursing Interventions
∗ 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

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Structure and function of Respiratory System

  • 1. Structures and Functions of the Respiratory System
  • 4. 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
  • 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 • 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
  • 9. 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
  • 13. Progressive, irreversible airflow limitation Associated with abnormal inflammatory response of lungs to noxious particles or gases COPD
  • 14. ∗Cigarette smoking ∗Occupational chemicals and dusts ∗Air pollution ∗Infection ∗Heredity- A1-antitrysin deficiency ∗Aging COPD EtiologyEtiology
  • 15. ∗ 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 Pathophysiology
  • 16. ∗ 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 PathophysiologyPathophysiology
  • 17. ∗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 PathophysiologyPathophysiology
  • 18.
  • 21. Chronic Bronchitis Blue Bloater versus Pink Puffer
  • 22.  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 COPD BehaviorsBehaviors
  • 24. ∗ PFTs ( RV, FEV1)↑ ↓ ∗ CXR ∗ ABGs ∗ Sputum C&S if infection suspected ∗ EKG- RV hypertrophy ∗ 6 minute oxy-walk COPD DiagnosisDiagnosis
  • 25.
  • 26. Spirometry Results Stage I Mild 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 ∗Impaired Gas Exchange ∗Ineffective Airway Clearance ∗Imbalanced Nutrition: Less than Body Requirements COPD Nursing Diagnoses
  • 30.  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
  • 31. ∗ 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 PathophysiologyPathophysiology
  • 32.
  • 33.
  • 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 ∗ Plasma exudation ∗ Mucus secretion ∗ AHR ∗ Structural changes Asthma Inflammation – Effects
  • 36. ∗ 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 Inflammation Clinical ManifestationsClinical Manifestations
  • 37. ∗ History and patterns 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 (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 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  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 Patient Teaching- MedicationsPatient Teaching- Medications
  • 44.  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 Collaborative CareCollaborative Care
  • 45. ∗Ineffective Airway Clearance ∗Impaired Gas Exchange ∗Anxiety ∗Deficient Knowledge Asthma Nursing Diagnoses
  • 46. ∗ 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
  • 47. ∗ 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 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 sudden onset ∗ Fever, shaking chills, SOB, cough w/purulent sputum, pleuritic CP ∗ Elderly/debilitated- confusion or stupor Pneumonia BehaviorsBehaviors
  • 50. ∗ Pleuritis ∗ Pleural effusion- 40% of hospitalized patients ∗ Atelectasis ∗ Bacteremia ∗ Lung abscess ∗ Empyema ∗ Pericarditis Pneumonia- Complications
  • 51. ∗ CXR ∗ Sputum C&S ∗ Blood cultures ∗ ABGs ∗ Leukocytosis Pneumonia Diagnostic StudiesDiagnostic Studies
  • 54. ∗ 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 Collaborative CareCollaborative Care
  • 55. ∗ Fever in any 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 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 Nursing DiagnosesNursing Diagnoses
  • 58. ∗ Hypotension and shock ∗ Respiratory failure ∗ Atelectasis ∗ Pleural effusion ∗ Delerium ∗ Superinfection Pneumonia Potential ProblemsPotential Problems
  • 59. ∗ Improving airway patency ∗ Conserving energy – rest ∗ Maintaining proper fluid balance ∗ Patient understanding of treatment and prevention ∗ Prevention of complications Pneumonia Nursing GoalsNursing Goals
  • 60. ∗ 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 InterventionsNursing Interventions
  • 61. ∗ 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 InterventionsNursing Interventions
  • 62. ∗ 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 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

  1. 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 &amp; 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.
  2. 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
  3. Oxygen &amp; carbon dioxide move back &amp; forth across alveolar-capillary membrane Diffusion occurs from higher to lower concentrations Ability of lungs to oxygenate arterial blood adequately is determined by PaO2 &amp; O2 saturation
  4. 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)
  5. EBP: Global Initiative for Chronic Obstructive Lung Disease (GOLD) Surgery- LVRS, bullectomy, lung transplant
  6. 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