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13 Cards in this Set

  • Front
  • Back
Work of breathing depend on
+Lung & chest wall stretchability
+Alveolar surface tension
_Airway resistance
Normally low - small differences in pressure produce large volumes of air flow
Airway constricted by:
Airway dilated by:
_Costricted by:
+Histamine: allergy, asthma
+Stimulate parasympathetic nerves make the airway constrict.
_Dilated by:
+Stimulate sympathetic nerves make airway dilate
Gas exchange

Neurochemical control in brain stem
1/passive diffusion thru alveolar-cappilary membrane
2/fr. greater gas P to lesser
3/Hemoglobin molecules:
+give up CO2
+load up O2

Neuro control(response to stimulies:
+PaCO2:_Inc=>inc ventilation
_Decr=> decr ventila.
+Aterial PaCO2.
CO2 retainers
_People who chronically hypoventilate have increased arterial CO2 levels
_CNS inspiratory center stops responding to this stimulus
_Hypoxemia becomes stimulus for breathing
_Raising arterial oxygen pressure to “normal” levels eliminates “hypoxemic drive”
Pt may stop breathing
_Administer oxygen cautiously
For most, O2 sat of ≤ 90% is safe [also provides adequate tissue oxygenation]
_Not everyone w/ diagnosis COPD is a CO2 retainer
_Arterial blood gas [ABG] analysis needed to determine who is/isn’t
_If you don’t have that info, be cautious
_Think of O2 as a medication & administer as ordered
Arterial oxygen content
Equilibrium between oxygen
Dissolved in plasma = PaO2
Chemically bound to hemoglobin
Degree of binding = “O2 saturation”
Most of the oxygen is bound to Hgb
Conditions in alveoli favor binding
Conditions in capillary bed favor unbinding -> tissue oxygenation
Adequate tissue oxygenation depends on adequate Hgb.
COPD:airflow limitation
Varying combination of 3 disease?
_Asthma: better over time
_Emphysema & chronic bronchitis: progressive, get worse over time
Respiration changes in aging:
+Defense mechanism
*Loss of elastin -> alveolar dilation, lung hyperinflation, inadequate deflation
*Inc’d # of collagen cross-links -> ’d rigidity
_Chest wall:
*Joints between ribs & sternum / spinal column become sclerosed -> ’d chest wall compliance
*Osteoporotic kyphosis may further limit expansion
*requires increased muscular work
_Respiratory muscles
*Atrophy w age
*Being physically active increases muscle strength, endurance

*Dec’d vital capacity, FEV1
*Inc’d residual volume, functional residual capacity, total lung volume
*Inc’d ventilation/perfusion mismatch
*Dec’d gas diffusion
*Lower arterial oxygen pressure

+Defense mechanism:
*Decr’d mucociliary activity
*Decr’d cough reflex
*Decr’d alveolar macrophage function
Asthma(get better over time)
+Asthma attack
+Attack triggers
+Self care requisites
+REVERSIBLE obstruction of bronchioles & intermediate-sized airways.Airway inflammation.Hyperreactive airways
_ Attack:
Chest tightness
Reduction in peak expiratory flow rate, forced expiratory volumes
Prolonged expiratory phase
May or may not wheeze
If very severe,marked decrease in volume of breath sounds
Feels like he’s suffocating
Sits up, leans forward
Uses accessory muscles
Respiratory infections
Nose & sinus problems
Drugs & food additives
Emotional stress
_Self care:
Avoid triggers
Prophylactic inhaler use
Peak expiratory flow self-monitoring [routinely & during attacks]
Seeking medical care when flows < 50% of personal best
_Abnormal, permanent enlargement of air spaces distal to terminal bronchioles. Destruction of alveolar & alveolar capillary walls
Hyperinflation of alveoli
Small airway narrowing
Loss of lung elasticity
CO2 retention in later stages
_Decreased gas exchange [hypoxemia & CO2 retention]
PFTs: Inc total lung capacity, decreased forced expiratory volume
Reduced size of pulm. capillary bed -> inc. flow through remaining vessels -> pulm HTN -> right ventricular failure [cor pulmonale]
Chronic bronchitis:
_Excessive MUCUS production in bronchi Pathologic changes causing this include hyperplasia of mucous-secreting glands, increase in goblet cells
Chronic inflammation / COUGH
Small airway narrowing
Recurrent infection chronic changes include destruction of cilia & altered function of alveolar macrophages
COPD 's risk factors
Chemical, pollutant exposure
Genetic predisposition - alpha1 antitrypsin deficiency increases susceptibility to environmental factors [emphysema]
COPD clinical manifestation
Sputum production*
Dyspnea on exertion*
Activity limitation
Weight loss common
COPD 's med:
+Bronchodilators:inhaled & systemic
+Anti-inflamatory: corticosteroid, mast cell stabiliers and leukotriene modifiers
*Beta-adrenergic agonists
Short-acting, e.g., albuterol
Longer-acting, e.g., salmeterol [Serevent]:Block bronchial smooth muscle constriction
Beta 2 Agonists
Rapid-acting - 1st drug to use in attack [lasts 3-4 hrs.]
Longer-acting - b.i.d. dosage
May be sole agent in mild asthma of adults

E.g., ipratropium [Atrovent]:Anticholinergic, e.g. Atrovent
Beta 2 / Anticholinergic combo, e.g. Duoneb

*Xanthines - e.g., theophylline [Theo-Dur]
Cardiostimulatory:Xanthines, e.g., theophylline [Theo-dur]
More adverse effects
CNS & cardiovascular stimulation
Anorexia, nausea
Blood level monitoring required

+Leukotriene modifiers
E.g. zafirlukast [Accolate] & montelukast [Singulair]
+Mast cell stabilizers
Moderate to severe asthma
Rinsing after use & spacer help prevent yeast infection
Highly effective
Serious adverse effects w/ long-term therapy