Transcript Alterations in Respiratory Function

Structures and Functions of
the Respiratory System
Gas Exchange
Ventilation
Diffusion (alveolarcapillary
membrane)
Perfusion
Diffusion (capillarycellular level)
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 ventilationperfusion (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
COPD
Progressive, irreversible airflow
limitation
Associated with abnormal
inflammatory response of lungs
to noxious particles or gases
COPD
Etiology
Cigarette smoking
Occupational chemicals and dusts
Air pollution
Infection
Heredity- A1-antitrysin deficiency
Aging
COPD
Pathophysiology
 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 (Centrilobaraffects respiratory bronchioles/upper
lobes/mild disease; panlobar- alveolar ducts,
sacs, respiratory bronchioles- lower lobes/AAT
deficiency
COPD
Pathophysiology
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
Emphysema
Chronic Bronchitis
Blue Bloater versus Pink Puffer
COPD
Behaviors
 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
COPD
Diagnosis
 PFTs (↑ RV, ↓FEV1)
 CXR
 ABGs
 Sputum C&S if infection suspected
 EKG- RV hypertrophy
 6 minute oxy-walk
COPD – Classification
Spirometry Results
Stage I
Mild
Stage II
Moderate
Stage III
Severe
Stage IV
Very
Severe
FEV1/FVC < 0.70
FEV1 ≥ 80% predicted
FEV1/FVC < 0.70
50% ≤ FEV1 < 80% predicted
FEV1/FVC < 0.70
30% ≤ FEV1 < 50% predicted
FEV1/FVC < 0.70
FEV1 < 30% predicted
OR
FEV1 < 50% predicted PLUS
chronic respiratory failure
COPD
Complications
 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
 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
Ineffective Breathing Pattern
Impaired Gas Exchange
Ineffective Airway Clearance
Imbalanced Nutrition: Less than
Body Requirements
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
 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
 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
 Bronchospasm
 Plasma exudation
 Mucus secretion
 AHR
 Structural changes
Asthma Inflammation
Clinical 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
 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
 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
 Suppress inflammation
 Reverse inflammation
 Treat bronchoconstriction
 Stop exposure to risk factors that sensitized
the airway
Asthma
Medications
 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
Medications
 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
Medications
 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
 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
 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
Ineffective Airway Clearance
Impaired Gas Exchange
Anxiety
Deficient Knowledge
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
 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
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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
 Pleuritis
 Pleural effusion- 40% of hospitalized patients
 Atelectasis
 Bacteremia
 Lung abscess
 Empyema
 Pericarditis
Pneumonia
Diagnostic Studies
 CXR
 Sputum C&S
 Blood cultures
 ABGs
 Leukocytosis
Pleural Effusion
Pneumonia
Pneumonia
Collaborative 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
 Fever in any hospitalized patient
 Pain
 Tachypnea
 Use of accessory muscles
 Rapid, bounding pulse
 Relative bradycardia
 Coughing
 Purulent sputum
Pneumonia
Nursing Assessment
 Consolidation
 Auscultation
 Bronchial breathing
 Bronchovesicular rhonchi
 Crackles
 Fremetis
 Egophony
 Whispered pectroloquy
Pneumonia
Nursing 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
 Hypotension and shock
 Respiratory failure
 Atelectasis
 Pleural effusion
 Delerium
 Superinfection
Pneumonia
Nursing Goals
 Improving airway patency
 Conserving energy – rest
 Maintaining proper fluid balance
 Patient understanding of treatment and
prevention
 Prevention of complications
Pneumonia
Nursing 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 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 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