




• 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


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)

• 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

Alveolar-Capillary Membrane

• 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

Body Tissue-Blood Capillary

COPD
 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- A
1
-antitrysin deficiency

Aging

COPD

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

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

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
 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

PFTs ( ↑ RV, ↓ FEV1)

CXR

ABGs

Sputum C&S if infection suspected

EKG- RV hypertrophy

6 minute oxy-walk

Stage I
Stage II Moderate
Stage III Severe
Stage IV
Mild
Very
Severe
Spirometry Results
FEV
1
/FVC < 0.70
FEV
1
≥ 80% predicted
FEV
1
/FVC < 0.70
50% ≤ FEV
1
< 80% predicted
FEV
1
/FVC < 0.70
30% ≤ FEV
1
< 50% predicted
FEV
1
FEV
1
/FVC < 0.70
< 30% predicted
OR
FEV
1
< 50% predicted PLUS chronic respiratory failure

COPD

Cor pulmonale- RV hypertrophy 2º pulmonary hypertension (late)

Exacerbations of COPD

Acute respiratory failure

Peptic ulcer and gastroesophageal reflux disease

Depression/anxiety


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

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

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


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


Bronchospasm

Plasma exudation

Mucus secretion

AHR

Structural changes


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

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
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


Suppress inflammation

Reverse inflammation

Treat bronchoconstriction

Stop exposure to risk factors that sensitized the airway

Asthma
 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)

 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
 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
 Name/dosage/route/schedule/purpose/SE
 Majority administered by inhalation (MDI, DPI, nebulizers)
 Spacer + MDI- for poor coordination
 Care of MDI- rinse with warm H
2
O 2x/week
 Potential for overuse
 Poor adherence with asthma therapy is challenge for LT management
 Avoid OTC medications

Asthma
 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 O
2
Sat>90%, ABGs,
MDI B-agonist; if severe- anticholinergic nebulized w/B agonist, systemic corticosteroids

Nursing Diagnoses

Ineffective Airway Clearance

Impaired Gas Exchange

Anxiety

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


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


Pleuritis

Pleural effusion- 40% of hospitalized patients

Atelectasis

Bacteremia

Lung abscess

Empyema

Pericarditis


CXR

Sputum C&S

Blood cultures

ABGs

Leukocytosis


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

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


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


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