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ALTERATIONS OF PULMONARY FUNCTION
respiration consists of two processes - ANS - - alveolar ventilation: movement of air into the lungs (external respiration), distribution of oxygen and removal of CO
- perfusion: pulmonary circulation, distribution of blood flow (movement of O2 and CO between the lungs and tissues) internal respirations - ANS - oxygen utilization is the use of O2 by cells to release energy factors affecting lung performance - ANS - gas exchange, work of breathing surfactant - ANS - decreases alveoli surface tension loss of surfactant - ANS - causes alveoli collapse, called atelectasis airway resistance - ANS - relationship pressure and airflow higher airway resistance with - ANS - smaller airway diameter small changes in pediatric airways cause - ANS - large incremental increases in airway resistance lung compliance - ANS - ability to stretch relationship between lung volume and pressure
compliance = - ANS - change in volume / change in pressure forced vital capacity (FVC) - ANS - measurement of the amount of air that can be forcefully exhaled from the lungs after the deepest inhalation forced expiratory volume in 1 second (FEV1) - ANS - amount of air expelled from lungs in 1 sec after a maximal inspiration diagnostic criteria for asthma FEV1/FVC ratio - ANS - low = obstructive disease normal = restrictive disease dyspnea - ANS - subjective sensation of uncomfortable breathing orthopnea - ANS - difficulty breathing when lying down paroxysmal nocturnal dyspnea (PND) - ANS - shortness of breath at night cough - ANS - protective reflex that helps clear the airway acute cough - ANS - resolves in 2-3 weeks chronic cough - ANS - lasts longer than 3 weeks abnormal sputum - ANS - changes in amount, consistency, color, and odor
acute respiratory failure - ANS - gas exchange is inadequate (hypoxemia) Pao2 is ≤50 mmHg hypercapnia occurs, during which partial pressure of carbon dioxide (PaCO2) is ≥50 mmHg pH is ≤7. requires ventilatory support, oxygen, or both chest wall restriction - ANS - chest wall is deformed, traumatized, immobilized, or made heavy by fat; work of breathing is increases, and ventilation may be compromised because of a decrease in tidal volume impaired respiratory muscle function is caused by - ANS - neuromuscular disease flail chest - ANS - the instability of a portion of the chest wall from rib or sternal fractures causes paradoxical movement of the chest with breathing pneumothorax - ANS - presence of air or gas in the pleural space primary (spontaneous) pneumothorax - ANS - occurs unexpectedly in healthy individuals secondary pneumothorax - ANS - is caused by chest trauma, rupture of bleb/bulla, or mechanical ventilation
iatrogenic pneumothorax - ANS - is caused by medical treatments, especially transthoracic needle aspiration open pneumothorax - ANS - air pressure in the pleural space equals barometric pressure, because air that is drawn into the pleural space during inspiration is forced back out during expiration tension pneumothorax - ANS - site of pleural rupture acts as a one-way valve, permitting air to enter on inspiration but preventing its escape by closing up during expiration is life threatening pneumothorax clinical manifestations - ANS - sudden pleural pain, tachypnea, and dyspnea tension severe hypoxemia, tracheal deviation away from the affected lung, and hypotension pneumothorax treatment - ANS - chest tube if persistent air leak: surgery, pleurodesis, or thoracoscopic surgical techniques pleurodesis - ANS - instillation of a caustic substance, such as talc, into the pleural space pleural effusion - ANS - presence of fluid in the pleural space
severe cases: ultrasound-guided pleural drainage, instillation of fibrinolytic agents, or deoxyribonuclease (DNase) injected into the pleural space surgical debridement restrictive lung disease: aspiration - ANS - passage of fluid and solid particles into the lungs, the right lower lobe is the most frequent site for this aspiration clinical manifestations - ANS - both choking and intractable cough have a sudden onset aspiration treatment - ANS - supplemental oxygen; may require mechanical ventilation restrict fluids to decrease blood volume and minimize pulmonary edema administer steroids during the first 72 hours after aspiration may need broad-spectrum antibiotics restrictive lung disease: atelectasis - ANS - collapse of lung tissue compression atelectasis - ANS - external compression on the lung absorption atelectasis - ANS - gradual absorption of air from obstructed or hypoventilated alveoli surfactant impairment - ANS - decreased production or inactivation of surfactant
atelectasis clinical manifestations - ANS - dyspnea, cough, fever, leukocytosis atelectasis treatment - ANS - main goal is prevention deep breathing, position changes, ambulation, pain management restrictive lung disease: bronchiectasis - ANS - persistent abnormal dilation of the bronchi cylindrical, saccular, and varicose bronchiectasis clinical manifestations - ANS - chronic productive cough: longer than 3 weeks, coughing stuff up bronchiectasis treatment - ANS - sputum culture antibiotics, bronchodilators: anti-inflammatory drugs, chest physiotherapy, supplemental oxygen, surgery restrictive lung disease: bronchiolitis - ANS - diffuse inflammation of small airways or bronchioles most common in children occurs in adults with chronic bronchitis or those with a viral infection or who have inhaled toxic gases bronchiolitis clinical manifestations - ANS - rapid ventilatory rate; significant use of accessory muscles; low-grade fever; dry, non-productive cough; hyperinflated chest
pulmonary edema treatment for increased capillary permeability resulting from injury - ANS - remove offending agent and supportive therapy to maintain adequate oxygenation, ventilation, and circulation POPE treatment - ANS - provide PEEP ventilation treatment for any type of pulmonary edema - ANS - provide supplemental oxygen and/or mechanical ventilation obstructive lung diseases - ANS - airway obstruction that is worse with expiration; more force or more time is required to expire a given volume of air; emptying the lungs is slowed obstructive lung disease common signs and symptoms - ANS - dyspnea and wheezing obstructive lung diseases clinical manifestations - ANS - increased work of breathing, ventilation- perfusion mismatching, decreased force expiratory volume in one second (FEV1) common obstructive disorders - ANS - asthma, COPD, emphysema, chronic bronchitis obstructive lung disease: asthma - ANS - chronic inflammatory disorder of the bronchial mucosa causes bronchial hyperresponsiveness, constriction of the airways, and variable airflow obstruction that is reversible asthma characteristic signs and symptoms - ANS - sense of breathlessness, tightening of the chest, wheezing, dyspnea, cough
asthma cause - ANS - immune-mediated airway inflammation asthma pathophysiology - ANS - symptoms of asthma result from a combination of inflammation and bronchoconstriction, so treatment must address both components obstructive lung disease: chronic obstructive pulmonary (COPD) - ANS - chronic, progressive, largely irreversible disorder characterized by airflow restrictions and inflammation COPD signs and symptoms - ANS - chronic cough, excessive sputum production COPD risk factors - ANS - smoking cigarettes, occupational dusts and chemicals, indoor air pollution from biomass fuel used for cooking/heating, outdoor air pollution, any factor that affects lung growth during gestation and childhood (kids with allergies while young, NICU babies, secondhand smoke) symptoms of COPD result largely from two pathologic processes - ANS - chronic bronchitis and emphysema both chronic bronchitis and emphysema are caused by an exaggerated inflammatory reaction to
- ANS - cigarette smoke chronic bronchitis - ANS - defined by a chronic cough and excessive sputum production results from hypertrophy of mucus-secreting glands in the epithelium of the larger airways emphysema - ANS - enlargement of the air space within the bronchioles and alveoli brought on by deterioration of the walls of these air spaces; loss of elastic recoil
asthma treatment goals - ANS - - reduce the impairment (frequency of attacks)
- reduce risk of reoccurrence peak flow meter - ANS - a handheld device often used to test those with asthma to measure how quickly the patient can expel air peak flow green zone - ANS - 80 to 100 % of your usual or "normal" peal flow rate signals all clear asthma is in good control keep using medicines as directed peak flow yellow zone - ANS - 50 to 80 % of your usual or "normal" peak flow rate signals caution airways are narrowing, and you need to take action take additional medicines listed in the yellow zone of asthma action plan call doctor and let them know peak flow red zone - ANS - less than 50 % of your usual or "normal" peak flow rate signals medical alert severe airway narrowing
take quick-relief medicine right away contact provider right away if symptoms do not improve, call 911 or go to the nearest emergency room drugs fo asthma: two main pharmacologic classes - ANS - - anti-inflammatory agents: glucocorticoids such as Prednisone
- bronchodilators: beta 2 agonists such as Albuterol asthma inhalation drug therapy advantages - ANS - - therapeutic effects are enhanced
- systematic effects are minimized
- relief of acute attacks is rapid asthma inhalation drug therapy four types - ANS - - metered dose inhalers (MDIs)
- respimats
- dry-powder inhalers (DPIs)
- nebulizers anti-inflammatory drugs for asthma - ANS - foundation of asthma therapy taken daily for long-term control principal anti-inflammatory drugs are the glucocorticoids (like Budesonide, Fluticasone)
oral use of glucocorticoids - ANS - - for patients with moderate to severe persistent asthma or for management of acute exacerbations of asthma or COPD
- potential for toxicity; should be used only when symptoms cannot be controlled with safer medications (inhaled glucocorticoids, inhaled beta 2 agonists)
- treatment should be as brief as possible adverse effects of oral glucocorticoids - ANS - - short-term therapy adverse effects are rare
- long term therapy adverse effects include: adrenal suppression, osteoporosis, hyperglycemia, peptic ulcer disease, and in young patients growth suppression initially but does not impact final adult height glucocorticoids and adrenal suppression - ANS - - prolonged glucocorticoid use can decrease the ability of the adrenal cortex to produce glucocorticoids of its own
- life-threatening at times of severe physiologic stress (like surgery, trauma, or systemic infection)
- high levels of glucocorticoids are required to survive severe stress
- adrenal suppression prevents production of endogenous glucocorticoids
- patients must be given increased doses of oral or IV glucocorticoids at times of stress
- failure to do so can be fatal glucocorticoids and discontinuation - ANS - - must be done slowly
- recovery of adrenocortical function takes several months
- dosage of exogenous sources must be reduced gradually
- during this time, patients-including those switched to inhaled glucocorticoids-must be given supplemental oral or IV glucocorticoids at times of severe stress
anti-inflammatory drugs: leukotriene receptor antagonists - ANS - suppress effects of leukotrienes in patients with asthma, leukotriene modifiers can reduce bronchoconstriction and inflammatory responses such as edema and mucus secretion leukotrienes - ANS - promote smooth muscle constriction, blood vessel permeability, and inflammatory responses through direct action and recruitment of eosinophils and other inflammatory cells leukotriene receptor antagonists - ANS - second-line agents dosed orally leukotriene receptor antagonists adverse effects - ANS - generally well tolerate but can cause adverse neuropsychiatric effects such as:
- depression
- suicidal thinking
- suicidal behavior available leukotriene receptor antagonists - ANS - - Zileuton (Zyflo)
- Zafirlukast (Accolate)
- Montelukast (Singulair) montelukast (singulair) - ANS - leukotriene receptor antagonist uses include prophylaxis and treatment of asthma, prevention of exercise induced bronchospasm, and relief of allergic rhinitis
omalizumab adverse effects - ANS - - injection-site reactions
- viral infection
- upper respiratory infection
- sinusitis
- headache
- pharyngitis
- cardiovascular events
- malignancy
- life-threatening anaphylaxis interleukin-5 receptor antagonists - ANS - Benralizumab Mepolizamub Reslizumab interleukin-5 receptor antagonists contraindications - ANS - hypersensitivty interleukin-4 receptor alpha antagonists - ANS - Dupilumab interleukin-4 receptor alpha antagonists contraindications - ANS - hypersensitivity bronchodilators - ANS - - provide symptomatic relief but do not alter the underlying disease process (inflammation)
- in almost all cases, patients taking a bronchodilator should also be taking a glucocorticoid for long-term suppression of inflammation
- principal bronchodilators are the beta 2 adrenergic agonists
bronchodilators (beta2 adrenergic agonists) mechanism of action - ANS - - through activation of beta2 receptors in the smooth muscle of the lung, these drugs promote bronchodilation, relieving bronchospasm
- beta2 agonists have a limited role in suppressing histamine release in the lung and increasing ciliary motility bronchodilators use in asthma and COPD - ANS - inhaled short-acting beta2 agonists (SABAs)
- taken PRN to abort an ongoing attack
- EIB: taken before exercise to prevent an attack
- hospitalized patients undergoing a severe acute attack: nebulized SABA is the traditional treatment of choice
- delivery with an MDI in the outpatient setting may be equally effective bronchodilator examples - ANS - Albuterol (ProAir, Proventil) Lebalbuterol (Xopenex) bronchodilators: inhaled long-acting beta2 agonists (LABAs) - ANS - - long-term control in patients who experience frequent attacks
- dosing is on a fixed schedule, not PRN
- effective in treating stable COPD
- when used to treat asthma, must always be combined with a glucocorticoid
- use alone in asthma is contraindicated LABA inhaled examples - ANS - - Salmeterol (Servent Diskus)
- Formoterol
