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47 Cards in this Set
- Front
- Back
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What is V/Q mismatch?
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Ventilation: alveoli, air goes in and out
Ventilatory failure is a problem in the O2 intake (ventilation) and blood delivery (perfusion) that causes a ventilation-perfusion (V/Q) mismatch in which perfusion is normal but ventilation is inadequate. It occurs when the chest pressure does not change enough to permit air movement into and out of the lungs. As a result, too little O2 reaches the alveoli and CO2 is retained. Either inadequate O2 intake or CO2 retention leads to hypoxemia. The problem is defined by a PaCO2 level above 45 mmHm in pts who have otherwise healthy lungs. Perfusion: capillary, gas exchange In oxygenation failure, chest pressure changes are normal and air moves in and out without difficulty but does not oxygenate the blood sufficiently. It occurs in the type of V/Q mismatch in which air movement and O2 intake (ventilation) are normal but lung blood flow (perfusion) is decreased. A classic cause of this V/Q mismatch is acute respiratory distress syndrome (ARDS). |
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What is normal V/Q match?
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4L/5L = 0.8
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What are causes of mismatch in the ventilation?
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pneumonia
atelectasis edema COPD: bronchitis |
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What are the causes of mismatch in the perfusion?
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pulmonary edema
shock premie COPD: emphysema ARDS |
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What is asthma "green zone?"
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-usually 80%-100% of personal best
-pt must remain on medications We're not saying they're doing well, but they're doing well with their therapy. |
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What is asthma "yellow zone?"
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-usually 50%-80% of personal best
-indicates caution -something is triggering asthma |
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What is asthma "red zone?"
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-50% or less of personal best
-indicates serious problem -definitive action must be taken with health care provider |
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What is CAL?
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Chronic airflow limitation - a group of chronic lung diseases that include:
-asthma -chronic bronchitis -pulmonary emphysema |
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What is asthma?
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A chronic condition in which reversible airflow obstruction in the airways occurs intermittently.
It can occur two ways: -inflammation that obstructs the lumen or airways -airway hyperresponsiveness and constriction of bronchial smooth muscle that cause narrowing of the airway from the outside/bronchoconstriction *inflammation can trigger hyperresponsiveness, but you might not always have hyperresponsiveness with inflammation |
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Name the various triggers that cause asthma.
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-genetics
-immune response -exercise -air pollutants -occupational factors -respiratory infection -nose and sinus problems -drugs and food additives -gastroesophageal reflux disease -psychological factors |
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Asthma and exercise
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Exercise can induce or exacerbate asthma
Pronounced with exposure to cold air Breathing through a scarf or mask may decrease the likelihood of symptoms Typically, EIA occurs after vigorous exercise, not during it (e.g., jogging, aerobics, walking briskly, climbing stairs). Airway obstruction may occur as the result of changes in the airway mucosa caused by hyperventilation that occurs during exercise with either cooling or rewarming of air and capillary leakage in the airway wall. |
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Asthma and air pollutants
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Air pollutants can trigger asthma attacks
-cigarette or wood smoke -vehicle exhaust -elevated ozone levels -sulfur dioxide |
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Asthma and occupational factors
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Most common form of occupational lung disease
Exposure to diverse agents Arrive at work well, but experience a gradual decline |
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Asthma and respiratory infection
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Respiratory infection is a major precipitating factor of an acute asthma attack
Increases inflammation hyperresponsiveness of the tracheobronchial system The respiratory syncytial virus (RSV) in children and the rhinovirus are two major factors in the development and possibly the severity of asthma. |
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Asthma and nose and sinus problems
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Allergic rhinitis and nasal polyps
Large polyps are removed Sinus problem are usually related to inflammation of the mucous membranes Kids = rhinitis salute Geriatric pts’ skin are fragile and they’ll have black eyes or around the nose. |
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Asthma and drugs and food additives
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Sensitivity to aspirin and NSAIDs
-Wheezing develops in about 2 hrs -Sensitivity to salicylates may persist -products found in many foods, beverages, and flavorings Beta-Adrenergic blockers may trigger asthma as a results of bronchospasm -oral (metoprolol) -topical eye drops (timolol) Food allergies may cause asthma symptoms -avoidance diets -rare in adults |
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Asthma and Gastroesophageal Reflux Disease (GERD)
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Reflux of acid could be aspirated into lungs, causing bronchoconstriction. Although GERD is primarily involved in nocturnal asthma, it can trigger daytime astha as well
Psychological factors can worse the disease process -Attacks can trigger panic and anxiety -Extend of effect is unknown -Emotional stress (crying, etc) can lead to hyperventilation and hypocapnia, which can cause airway narrowing -We could irritate the vagus nerve if it goes up esophagus; innervation will trigger bronchoconstriction |
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Clinical manifestations in asthma
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-dyspnea: AUDIBLE wheezes on exhalation, increased respiratory rate
-increased cough -use of accessory muscles -"barrel chest" from air trapping (AP ratio) -long breathing chest -hypoxemia (O2 sat should be above 95%) -cyanosis |
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How do you diagnose asthma?
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-pulmonary function tests:
FVC: forced vital capacity (volume of air exhaled from full inhalation to full exhalation) FEV: forced expiratory volume (volume of air blown out as hard and fast as possible during the first second of the most forceful exhalation after the greatest inhalation) PEF: peak expiratory flow (fastest airflow rate reached at any time during exhalation) -chest x-ray -arterial blood gases -oximetry -allergy testing -blood levels of eosninophils -sputum culture and sensitivity |
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What are some management intervention for asthmatics?
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-avoid triggers of acute attacks
-pre-medicate before exercising (pt take bronchodilator 15-30 min before exercise) |
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Differentiate between control and reliever asthmatic drugs.
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Control: used everyday to reduce responsiveness
Reliever: used to stop attack -bronchodilators: SABA, LABA -anti-inflammatory: corticosteroids, leukotriene modifiers, monoclonal antibody to IgE |
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What are the first line drugs for asthma?
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Bronchodilators: SABA and LABA
Anti-inflammatory agents: corticosteroids |
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What are the different types of bronchodilators are there for asthma?
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short-acting beta 2 agonist (SABA)
long-acting beta 2 agonist (LABA) cholinergic antagonist methylxanthines |
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What are the different types of anti-inflammatory agents are there for asthma?
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corticosteroids
NSAIDs leukotriene antagonist immunomodulators |
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What are the different types of inhaler devices?
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MDI - metered dose inhaler
DPI - dry powder inhaler nebulizer |
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How can you tell when an MDI is full, half full, or empty?
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Med/Surg Pg. 609
DPIs indicate the amount of remaining drug; however MDIs do not. Demonstrate how to check approximate aerosol inhaler drug levels by placing the inhaler in water. Full inhalers sink to the bottom. An empty inhaler floats on its side. This technique is controversial because it is only a general approximation. The more recommended technique is for the pt to count the number of doses as they are used; however many pts have difficulty keeping the dose count accurate. |
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Describe SABAs (bronchodilators)
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Beta 2 adrenergic agonist (albuterol, metaproterenol)
-effective for relieving acute bronchospasm -onset of action in minutes and duration of 4-8 hr (check pt at 4 hr mark) -Prevent release of inflammatory mediators (histamine) from mast cells -Not for long-term use Side effects: tremors, anxiety, tachycardia (may lead to fib), palpitations, nausea |
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Describe LABAs (bronchodilators)
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Beta 2 adrenergic agonist (Serevent Diskus)
-contraindicated as lone drug -not first choice for long term control -fixed schedule, not PRN -you should be concern if pt is using this; it has no rescue component Side effects: severe asthma and death if used alone or incorrectly |
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Describe anticholinergic drugs/cholinergic antagonist (bronchodilator)
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ipratropium (Atrovent)
-blocks action of acetylcholine -used when pt cannot tolerate bronchodilator, SABA -onset is slower than beta 2 adrenergic agonist, peaking 30 min - 1 hr and lasting up to 4-6 hr -most common SE is dry mouth Side Effects: drug alert of peanut allergy (soya lecithin as a carrier) |
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Describe methylxanthines (bronchodilators)
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theophylline
CNS stimulant -less effective long-term bronchodilator -alleviates early phase of attacks but has little effect on bronchial hyper responsiveness -narrow margin of safety; obtain blood levels Side effects related to toxicity: severe dysrhythmias (v-fib) and convulsions; monitor ECG waves and patterns -- Cox has given this drug 5 times in 41 yrs; not your go-to drug for asthma; use only if pt isn't responding to beta 2 adrenergic If pt has severe dysrhythmia, administer lidocaine (also used for anesthesia and v-fib) Onset of convulsions include: feel weird, smell weird things, see lights If pt has convulsions, administer diazepam |
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Describe corticosteroids (anti-inflammatory agents)
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fluticasone (Flovent), budesonide (Pulmicort)
Glucocorticoids -first-line therapy for pts with persistent asthma -suppress inflammatory response -inhaled form is used in long-term control -systemic form to control exacerbations and manage persistent asthma -reduce bronchial hyperresponsiveness -decrease mucous production Usually ICSs must be administered for 1-2 wk before maximum therapeutic effects can be seen |
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What are the side effects of corticosteroids (anti-inflammatory agent)
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-oropharyngeal candidiasis and dysphonia
-can be reduced using a spacer or by gargling after each use -prolonged therapy risks of adrenal suppression and in children growth retardation (Addison's; we're suppressing the epi/norepi, lethargy, HR down); must slowly wean pt off corticosteroids -pre-menopausal women should take adequate amount of calcium and vitamin D and should participate in regular weight-bearing exercise |
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Describe leukotriene modifiers (anti-inflammatory agents)
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zafirlukast, montelukast, zileuton
-Blocks action of leukotrienes - potent bronchoconstrictors Leukotriene modifiers or inhibitors: -have both bronchodilator and anti-inflammatory effects -not indicated for acute attacks -used for prophylactic and maintenance therapy Side effects: depression, withdrawal, loss of appetite and energy, suicidal thinking and behavior Leukotriene modifiers can be used as add-on therapy (not substitute for) the doses of ICS. It is given PO. |
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Describe monoclonal antibody to IgE (anti-inflammatory agent)
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omalizumab (Xolair)
Monoclonal antibody -decreases circulating free IgE levels -prevents IgE from attaching to mast cells, preventing release of chemical mediators (histamine) -subcut administration q 2-4 wk Side effects: injection site, viral, respiratory infections, anaphylaxis Watch pt for 5 minutes after drug administration; adverse effects are immediate |
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Name some other management interventions for asthmatics.
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-Inhalation of drugs is preferable to avoid systemic side effects.
-Using a MDI with a spacer is easier and improves inhalation of the drug. -DPI requires less manual dexterity and coordination (geri pts with arthralgia and poor coordination). |
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What is status asthmaticus?
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A severe, life-threatening, acute episode of airway obstruction that intensifies once it begins and often does not respond to common therapy.
Observe for use of accessory muscles for breathing and distention of neck veins. If condition is not reversed, patient can develop pneumothorax (stress on lungs is so great to pull out air that it develops a weakspot and pops a lung; we worry about mediastinal shift) and cardiac/respiratory arrest. Treatment: -IV fluids with large bore needle to deliver meds right away -potent systemic bronchodilator (theophylline) -steroids -epinephrine -oxgen We know therapy is working when pt starts to move air and pulse O2/ABGs are better; CO2 starts to move out and be removed like supposed to |
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What are the risk factors/etiology for COPD?
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-cigarette smoking
-occupational chemicals and dust -air pollution -infection -heredity (alpha-antitrypsin [ATT] deficiency; genetic risk factor for COPD; accounts for 3% of COPD) -aging (some degree of emphysema is common because of physiologic changes of aging lung tissue) Important to ask pt if a family member has this disease in assessment. The pathology occurs over years (chronic) unlike asthma. |
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Name the defining features of COPD.
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-Irreversible airflow limitations during forced exhalation due to loss of elastic recoil (loss of elastic recoil means lots of exchange component)
-airflow obstruction due to mucous hypersecretion, mucosal edema, and bronchospasm (mucous on alveoli leads to poor gas exchange) Primary process is inflammation. -inhalation of noxious particles (trigger) -mediators released cause damage to lung tissue (leukotrienes, COX lead to bronchospasm) -airways inflamed -parenchyma destroyed Supporting structures of lungs are destroyed. -air goes in easily, but remains in lungs -bronchioles tend to collapse (if alveoli are inflamed, inflammation travels up to bronchioles; bronchioles are damaged quicker because they don't have elastic recoil) -cause barrel-chest look (doesn't not increase surface area because alveoli are destroyed and no exchange) Pulmonary vascular changes -blood vessels thicken -surface area for diffusion of O2 decreases |
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What are common characteristics of COPD?
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-mucous hypersecretion
-dysfunction of cilia -hyperinflation of lungs -gas exchange abnormalities If you can't get mucous out, then patient has pneumonia and need culture sputum and ABX. |
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What are the two conditions of COPD?
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Emphysema and chronic bronchitis
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What are the distinguishing symptoms of emphysema?
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-loss of elasticity
-hyperinflation of lungs -dyspnea related to air trapping caused by loss of elastic recoil in alveolar walls, overstretching and enlargement of alveoli into bullae, collapse of small airway (bronchiole) -CO2 retention: produced faster than eliminated *Bullae: not an area for gas exchange |
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What are the distinguishing symptoms of chronic bronchitis?
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-inflammation
-vasodilation -mucosal edema -congestion -bronchospasm -affects the airways, not alveoli -production of large amounts of thick mucus |
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What are the complications of COPD?
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COPD affects all tissues, leads to anoxia and death.
-hypoxemia (metabolic needs are not met, can lead to death) -respiratory infections -HF related to cor pulmonale (high pulmonary resistance) & dysrhythmia (insufficient O2, leads to dysrhythmia and a-fib; assess for JVD) -exacerbations of COPD -peptic ulcer disease -depression/anxiety |
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What is cor pulmonale?
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Hypertrophy of right side of heart
-result of pulmonary hypertension -late manifestation of chronic pulmonary heart disease -eventually causes right-sided heart failure -dyspnea -distended neck veins -hepatomegaly with upper quadrant tenderness -peripheral edema -weight gain Management includes continuous low flow of O2. |
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What is the general assessment to observe for in COPD?
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-characteristically underweight with adequate caloric intake
-chronic fatigue -dyspnea (orthopneic, tripod positioning) -causes chest breathing (use of accessory and intercostal muscles; rapid shallow 40-50 bpm; silent chest indicates serious airflow obstruction) -prolonged expiratory phase -wheezes -decreased breath sounds (pt may need to breath louder than normal for auscultated breath sounds to be heard) -increased AP diameter 'barrel chest' -bluish-red color of skin Polycythemia develops as a result of increased production of red blood cells as the body attempts to compensate for chronic hypoxemia. |
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Lab findings with COPD
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ABG typical findings: respiratory acidosis
-pH is low (acidic) -PaCO2 is increased (makes pH acidic) -PaO2 is low -Bicarbonate: increased advanced emphysema Dx confirmed by pulmonary function tests, chest x-ray, spirometry Spirometry typical findings: -reduced FEV/FVC ratio < 70% -increased residual volume O2 Sat often < 90% ECG can show signs of right ventricular failure Sputum cultures WBC elevation indicates infection |
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Drug therapy for COPD
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slide 49
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