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NUR370 Pathophysiology and Pharmacology > Respiratory Disorders > Flashcards

Respiratory Disorders Flashcards

1
Q

S/S of Pulmonary Disease

A

a. dyspnea, altered breathing patterns
b. cough (acute, chronic)
c. hypercapnia (elevated CO2), hypoxemia (low O2)
d. hemoptysis (coughing up blood), abnormal sputum
e. cyanosis (peripheral, central)
f. chest pain
g. clubbing

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2
Q

Ventilation-Perfusion Abnormalities

VQ Ratio

A

ventilation: air getting into lungs, 4L
perfusion: blood sent to lungs, 5L

Low V/Q = impaired ventilation
i.e. bronchoconstriction
passing blood receives low oxygen levels

Shunt (very low) V/Q = blocked ventilation, collapsed alveolus
i.e. atelectasis
passing blood receives no oxygen levels

High V/Q = impaired perfusion, blocked vessel
i.e. obstructed blood flow to lung
blood is not coming by to pick up oxygen

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3
Q

Vital capacity (VC)

A

Inspiratory reserve volume (IRV): maximal amount of air drawn in after normal inspiration
+
Tidal volume (VT): amount of air from normal inhalation and exhalation
+
Expiratory reserve volume (ERV): maximal amount of air expelled after normal expiration
=
Vital capacity (VC)

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4
Q

Functional Residual Volume (FRC)

A

ERV
+
Residual Volume (RV): amount of air that remains after fully exhaling

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5
Q

Forced expiratory volume (FEV) Test

A

measures how much air a person can exhale during a forced breath

  • FEV1 first second
  • FEV2 second second
  • FEV3 third second

Forced vital capacity (FVC) total amount of air exhaled during FEV Test

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6
Q

Obstructive Pulmonary Diseases

A

airway obstruction is worse with expiration, more force and time required to expire a given volume of air
- emptying lungs is slowed

S/S: wheezing and dyspnea
manifestation: increased WOB, V/Q mismatching, decreased FEV1

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7
Q

Types of OPDs

A

a. asthma
b. chronic bronchitis
c. emphysema

chronic bronchitis + emphysema = COPD

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8
Q

Asthma

A

chronic inflammatory disorder of the bronchial mucosa

3 characteristics of asthma:

a. bronchial hyperresponsiveness
b. inflammation, constriction of airways
c. reversible airflow obstruction

*one half of all cases develop during childhood

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9
Q

Etiology of Asthma

A

a. genetic
b. allergens (pollen, dander, mold)
c. irritants (perfume, cold air, fumes)
d. viral infections
e. smoking
f. occupational toxins
g. hygiene hypothesis
lack of exposure in early development, natural development of immune system

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10
Q

Pathophysiology of Asthma

A
  1. inflammation mediated by systemic IgE production, as a result of allergen or irritant exposure
  2. IgE antibodies combine to receptors on mast cells, which signals release of histamine
  3. cellular infiltration (neutrophils, lymphocytes, eosinophils)
  4. histamine stimulates smooth muscle of airways, causing bronchoconstriction&raquo_space; reduction in airway diameter
  5. mucus accumulates in the airway, making it more difficult for air to move through
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11
Q

Clinical Manifestation of Asthma

A

a. mental status
anxious, altered LOC

b. breathing
dyspnea, purse lp breathing, diaphoresis, increased WOB (accessory muscle use), SOB, chest tightness

c. vitals
tachycardia, tachypnea, low SpO2

*asymptomatic between attacks but exacerbation can be preceded by increased symptoms over a few days

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12
Q

Symptom Severity of Asthma

A

Mild:
minimal intercostal retractions
moderate wheeze
>94% SpO2, peak flow: >80%

Moderate:
agitated, speak in phrases, substernal retraction
wheezing
91-94% SpO2, peak flow: 60-80%

Severe:
speak in words, significant respiratory distress, accessory muscles
wheezing audible w/o steth
<90%, peak flow: <60%

Impending respiratory failure:
drowsy, confused
unable to speak, marked respiratory distress
chest is silent
<90%, unable to perform
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13
Q

Status Asthmaticus

A

bronchospasm not reversed by usual measures
*life threatening

silent chest
PaCO2 greater than 70 mmHg

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14
Q

Asthma Management

A

a. administration of oxygen and inhaled beta-agonist bronchodilators (salbutamol)
b. corticosteroids (PO or IV), iptratropium bromide (bronchodilator)
c. monitoring of gas exchange and airways obstruction in response to thearpy
d. education over allergens, irritants, peak flow meters

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15
Q

Diagnostic Studies for Asthma

A

a. history, physical exam
b. pulmonary function tests
c. spirometry
- forced vital capacity
- forced expiratory volume (FEV1)
- peak expiratory flow rate (PEFR)

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16
Q

Asthma: Goals of therapy

A
  • prevent asthma-related mortality
  • prevent exacerbations
  • maintain control (activity level, symptom management, maintain expected spirometry)
  • provide optimal pharmacotherapy and avoid side effects
17
Q

Chronic Obstructive Pulmonary Disease (COPD)

A

chronic bronchitis and emphysema
characterized by progressive, irreversible airway obstructions, systemic manifestations and increasing frequency and severity of exacerbations

  • largely caused by smoking, 80-90%
  • overlap of OPDs
18
Q

Risk Factors for COPD

A

a. cigarette smoking
b. occupational dusts and chemicals
c. outdoor and indoor pollution
d. lung growth during gestation and childhood
e. genetic susceptibiliies

19
Q

Causes of COPD

A
  1. inflammation, edema and fibrosis of bronchial wall
    hypertrophy of the submucosal glands with hypersecretion of mucous
    » obstruct airflow
  2. loss of elastic lung fibers
    » impairs lung recoil and results in dynamic airway collapse
  3. loss of alveolar tissue
    » decreases the surface area for gas exchange
  4. low V/Q ratio
    » impaired ventilation
20
Q

Air trapping

A

dynamic hyperinflation: lung cannot empty fully due to narrow air passages, collapsed bronchial walls
»over time, the size of the lungs gets larger

21
Q

Chronic Bronchitis

A

hypersecretion of mucous and chronic productive cough that lasts at least 3 months of the year for at least 2 consecutive years

22
Q

Pathophysiology of chronic bronchitis

A
  1. inspired irritants increase mucous production, size and number of mucous glands, and bronchial edema; mucous is thicker than normal
  2. hypertrophied bronchial smooth muscle
  3. hypoxemia and hypercapnia
  4. airways collapse early in expiration, trapping gas in lung&raquo_space; hyperinflation of alveoli
23
Q

Progressive Injury in chronic bronchitis

A

a. increased susceptibility to infection
b. scarring and stenosis in small airways
c. large numbers of alveoli not adequately ventilated
- disrupts diffusion (gaseous exchange)
- decreased PaO2 and increased PaCO2 in pulmonary vessels
- chronic PaO2 causes reflex pulmonary vasoconstriction
d. pressure in right ventricle increases&raquo_space; Cor pulmonale&raquo_space; right side heart failure

24
Q

Clinical manifestation of Chronic Bronchitis

A

a. decreased exercise tolerance
b. wheezing
c. SOB
d. productive cough
e. polycythemia, cyanosis, clubbing
d. pulmonary hypertenion (Cor pulmonale)

Lung function tests:

  • decreased FVC, FEV1
  • increased FRC, RV
25
Q

Management of Chronic Bronchitis

A

a. smoking cessation (prevent disease progression)
b. bronchodilators
c. expectorants
d. chest physical therapy
e. antibiotics
f. steroids
g. mechanical ventilation
h. oxygen therapy

26
Q

Chronic Bronchitis: Teaching

A
  1. nutritional therapy
  2. respiratory hygiene
  3. recognition of early signs of infection
  4. breathing techniques to relieve dyspnea
27
Q

Emphysema

A

damage/destruction of alveoli, alveolar capillaries and lung tissue
(caused by changes in lung tissue, decreased elasticity)
- inner walls of the alveoli rupture, creating larger air spaced and reducing area for gas exchange
- damage alveoli cannot support bronchial tubes causing them to collapse and trap air inside&raquo_space; barrel-chest

*most people who have emphysema also have chronic bronchitis

28
Q

Structural changes from emphysema

A

a. hyperinflation of alveoli
b. destruction of alveolar walls
c. destruction of alveolar capillary walls
d. narrowed, twisted small airways
e. loss of lung elasticity

29
Q

Clinical Manifestations of emphysema

A
  • dyspnea on exertion
  • tachypnea
  • wheezing, prolonged expiration
  • a/p chest diameter increased (barrel chest)
  • hyperresonance
  • tripod position
  • weight loss
  • cor pulmonale (late symptom)

Lung function tests:

  • decreased V, FVC, FEV
  • increased FRC, RV, TLC
  • no significant improvement with bronchodilators
30
Q

Management of emphysema

A

a. oxygen and supportive ventilation
b. inhaled bronchodilators (over time)
c. inhaled anticholinergic agents and beta agonist
d. inhaled corticosteriods can be added
e. smoking cessation
f. pulmonary rehabilitation
- nutritional support
- exercise training
- breaking exercise and retraining

31
Q

COPD and depression of ventilation

A

= those with COPD have chronically high levels of CO2 and become desensitized
some may rely on *Hypoxia drive to breath

supplemental oxygen MAY knock out stimulus to breath because their lungs want to hold on to CO2..but this does not mean O2 should be withheld!! this is still an important intervention!

32
Q

Respiratory Defense Mechanism

A

a. naso-pharyngeal: surface lysosome and immunoglobulin (IgA) removes particles from air
- impaired by common cold, trauma to nose

b. glottic and cough reflex protect against aspiration
- impaired by stroke, sedation

c. mucociliary blanket: trap and remove particles from respiratory tract
- impaired by smoking, virus, irritating gas

d. sinus: humidifies air and collects bacteria or pollutant to be swallowed and destroyed by stomach acid

e. pulmonary macrophages: remove micro-organisms from lungs
- impaired by cold, smoking, alcohol intoxication

33
Q

Pneumonia

pneumonitis

A

acute inflammation of the lower respiratory tract that involves the lung parenchyma, including the alveoli and the bronchioles

  • usually marked increase in interstitial and alveolar fluid
  • antibiotics reduce morality
  • mortality rate highest in children and elderly
  • 1/2 of deaths are caused by streptococcus pneumoniae, vaccine preventable
34
Q

Etiology of pneumonia

A
  • Infectious causes
  • invasion by microorganisms: bacteria, viruses, fungi, parasites
  • aspiration of food, fluids or vomitus
  • inhalation of toxic or caustic chemicals, smoke, dusts, gases
35
Q

Risk factors for pneumonia

A
  • age
  • smoking
  • URI
  • tracheal intubation
  • prolonged immobility
  • immunosuppressive therapy
  • non-functional immune system
  • malnutrition, dehydration
  • chronic disease states
  • exposure to air pollution
  • altered consciousness (sedation, seizure, anesthesia, intoxication)
36
Q

Pathophysiology of pneumonia

A

microorganisms commonly enter lower airways but extensive defense mechanisms prevent infection
»
when defenses are compromised, organisms penetrate sterile lower respiratory tract = inflammatory pulmonary response
»
inflammation + exudate = fluid filled alveolar sac that cannot exchange O2 and CO2 effectively
»
alveolar exudates consolidate and are difficult to expectorate

37
Q

Clinical manifestations of pneumonia

A
  • fever, chills, sweats, malaise
  • pleuritic chest pain, cough, purulent sputum, hemoptysis
  • dyspnea, tachypnea, headache and fatigue
  • altered mental state

Chest auscultation
a. bronchial breath sounds over area of consolidation
b. crackles may be heard over affected area
Tactile fremitus increased over affected area

38
Q

Pneumonia Assessment

A

a. history of recent travel
b. risk factors: smoking, exposure to smoking, comorbidities

c. symptoms
- sputum (c&s)

d. physical findings
- general appearance, respiratory distress, LOC
- crackles, wheezed
- dullness to percussion, fremitus, whispered pectoriloquy

e. vitals
- tachypnea, tachycardia, fever, decreased SpO2

f. imaging
- CT

g. blood cultures, serum hematology (WBC), urinalysis, rule our influenza

39
Q

Management of pneumonia

A

a. antibiotic therapy (specific to bacterial agent)
* most cases of viral pneumonia are treated symptomatically

b. respiratory support
- O2 therapy
- chest physiotherapy
- postural drainage
- tracheal suctioning
c. nutritional support and fluid intake to keep secretions thin and body hydrated
d. prevention strategies - vaccination

NUR370 Pathophysiology and Pharmacology (20 decks)

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