Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
13 Cards in this Set
- Front
- Back
|
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 |
