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13 Cards in this Set

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Work of breathing depend on
_Compliance
+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:
+Epineprine:
+Stimulate sympathetic nerves make airway dilate
Gas exchange

Neurochemical control resp.center 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:
+Strutural
+Funtional
+Defense mechanism
+Strutural:
_Elasticity
*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

+Funtional:
*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)
+Define
+Asthma attack
+S/s
+Attack triggers
+Self care requisites
+REVERSIBLE obstruction of bronchioles & intermediate-sized airways.Airway inflammation.Hyperreactive airways
_ Attack:
Wheezing
Dyspnea
Chest tightness
Cough
Reduction in peak expiratory flow rate, forced expiratory volumes
Prolonged expiratory phase
_S/S:
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
_triggers:
Allergens
Exercise
Respiratory infections
Nose & sinus problems
Drugs & food additives
GERD
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
Meds
Emphysema:
+Define:
+patho:
+significances
_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:
+Define:
+significances:
_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
Smoking
Chemical, pollutant exposure
Genetic predisposition - alpha1 antitrypsin deficiency increases susceptibility to environmental factors [emphysema]
COPD clinical manifestation
Cough*
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
_Bronchodilators:
+Inhaled
*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

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

+Systemic
*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

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