Respiratory System Fall 2024 PDF

Respiratory System DR. NORRIS & DR. WILLIAMS Respiratory Structures Structural Organization of the Respiratory System Consists of the air passages and the lungs Divided into two parts by function: Conducting airways: through which air moves as it passes between the atmosphere and th...

Respiratory System DR. NORRIS & DR. WILLIAMS Respiratory Structures Structural Organization of the Respiratory System Consists of the air passages and the lungs Divided into two parts by function: Conducting airways: through which air moves as it passes between the atmosphere and the lungs Respiratory tissues of the lungs: where gas exchange takes place  Structure of the Lungs Soft, spongy, cone-shaped organs located side by side in the chest cavity ◦ Separated from each other by the mediastinum and its contents ◦ Divided into lobes (three in the right lung, two in the left) Apex: upper part of the lung; lies against the top of the thoracic cavity Base: lower part of the lung; lies against the diaphragm Protective Structures Hairs and turbinates (shell-shaped structures in nose and cilia in the upper and lower airways) trap and remove foreign particles from the air Mucosal lining (upper and lower airways) warms and humidifies air Irritant receptors trigger a sneeze or cough reflex to remove foreign particles Immune protections immune coating in the respiratory tract mucosa macrophages in the alveoli Components of the Respiratory System Ventilation The movement of air between the atmosphere and the respiratory portion of the lungs Perfusion The flow of blood through the lungs Diffusion The transfer of gases between the air-filled spaces in the lungs and the blood Ventilation Depends on the conducting airways: Nasopharynx and oropharynx Larynx Tracheobronchial tree Function: Move air out of the lungs but does not participate in gas exchange Inspiration and Expiration Inspiration Air is drawn into the lungs as the respiratory muscles expand the chest cavity. Expiration Air moves out of the lungs as the chest muscles recoil, and the chest cavity becomes smaller. Respiratory control Respiratory control centers in the brain ◦ Brainstem (neurons in Pons and Medulla): ◦ send neural impulses to the diaphragm, intercostal muscles, sternocleidomastoid muscles, and other accessory muscles, causing them to contract or relax Lung receptors ◦ Located in epithelium and smooth muscles of airways near alveolar- capillary junctions ◦ Sense irritants->cough, Prevent excessive lung inflation, Reduce capillary pressure Respiratory control Chemoreceptors ◦ Key sensors for alterations in blood chemistry (detect oxygen, carbon dioxide, and acid-base status) Two types: ◦ Central Chemoreceptors: located in the brainstem ◦ respond to pH changes in the central nervous system ◦ Peripheral Chemoreceptors: located in carotid and aortic bodies ◦ trigger an increase in ventilation in response to low oxygen levels in the blood  Tidal Volume (TV) Approx. 500 ml at rest Amount of air that moves into and out of the lungs during a normal breath Inspiratory reserve volume (IRV) App. 3000 ml at rest The amount of air that can be inhaled after a normal breath. Lung Expiratory reserve volume (ERV) App. 1100 ml at rest Capacities The amount of air that can be exhaled after a normal breath. Vital capacity (VC) Approx. 4600 ml at rest Equals the IRV plus the TV plus the ERV The maximal amount of air that can be moved in and out of the lungs with forced inhalation and exhalation.  Forced vital capacity (FVC) The maximal amount of air that is exhaled from the lungs during a forced exhalation Forced expiratory volume in 1 second (FEV1) Lung Maximal amount of air that can be expired from the lungs in 1 second. Capacities Residual Volume (RV) The air that remains in the lungs after forced respiration Total lung capacity (TLC) Total amount of air in the lungs when they are maximally expanded and is the sum of the VC and RV. Diffusion Oxygen and carbon dioxide are exchanged at alveolar capillary junctions Two major process occur: ◦ Oxygen is trying to get to all the cells. ◦ Carbon dioxide is trying to escape through the lungs. Effectiveness depends on: ◦ Partial pressure and solubility of gas ◦ Thickness, surface areas of membranes Partial Pressure The collision of oxygen and carbon dioxide creates pressure Partial pressure of oxygen in the arterial blood: PaO2 Partial pressure of carbon dioxide in the arterial blood: PaCO2 Measured in mm Hg Gas Exchange  Oxygen and Carbon Dioxide Transport PaO2 of arterial blood normally is above 80 mm Hg. PaO2 is a major factor in determining the percentage of hemoglobin in the blood that's bound to oxygen, known as the oxygen saturation (SaO2). Carbon Dioxide Diffusion and Transport Carbon dioxide: a cellular waste product ◦ Released by cells into bloodstream ◦ Dissolved in the plasma ◦ Bound to hemoglobin ◦ Diffused into red blood cells as bicarbonate ◦ Diffuses through alveolar capillary junction ◦ Exhaled through lungs Functions of Bronchial Smooth Muscle The tone of the bronchial smooth muscles surrounding the airways determines airway radius. The presence or absence of airway secretions influences airway patency. Bronchial smooth muscle is innervated by the autonomic nervous system. ◦ Parasympathetic: vagal control ◦ Bronchoconstrictor ◦ Sympathetic: β2-adrenergic receptors ◦ Bronchodilator Impaired Ventilation A problem of blocking airflow in and out of the lungs Two major mechanisms implicated: ◦ Compression or narrowing of the airways ◦ Disruption of the neuronal transmissions needed to stimulate the mechanics of breathing Impaired Diffusion Restricted transfer of oxygen or carbon dioxide across the alveolar capillary junction Depends on: ◦ Solubility and partial pressure of the gas ◦ Surface area and thickness of the membrane Impaired Ventilation–Perfusion (V/Q) Matching Causes of increased V/Q Causes of decreased V/Q ratio (lung is ventilated, ratio (lung is perfused, but but not perfused): not ventilated): Emphysema (type of Chronic bronchitis (type COPD) of COPD) Heart disease Asthma Pulmonary Edema Pulmonary Hypertension Airway obstruction Liver disease Pneumonia Altered Ventilation and Diffusion General Manifestations of Impaired Ventilation and Diffusion Cough, mucus, hemoptysis Dyspnea, orthopnea Adventitious lung sounds Use of accessory muscles Chest pain Barrel chest The Effects of Impaired Ventilation and Diffusion Hypoxemia ◦ Decreased oxygen in the arterial blood ◦ Leads to a decrease in PaO2 Hypoxia ◦ Oxygen deprivation in the cells Hypercapnia ◦ Increased carbon dioxide in the blood Hypoxemia (low levels of O2 in blood) Results from: ◦ Inadequate O2 in the air ◦ Disease of the respiratory system ◦ Dysfunction of the neurological system ◦ Alterations in circulatory function Mechanisms ◦ Hypoventilation ◦ Impaired diffusion of gases ◦ Inadequate circulation of blood through the pulmonary capillaries ◦ Mismatching of ventilation and perfusion Hypercapnia (Increased arterial PCO 2) Too much carbon dioxide in the blood Caused by hypoventilation or mismatching of ventilation and perfusion Common causes: COPD, sleep apnea Symptoms of respiratory distress and hypoxia EARLY SYMPTOMS LATE SYMPTOMS Restlessness Extreme restlessness to stupor Tachycardia Severe dyspnea Tachypnea, exertional dyspnea Slowing of respiratory rate Orthopnea, tripod positioning Bradycardia Anxiety, difficulty speaking Cyanosis (peripheral or central) Poor judgment, confusion Intercostal retractions Disorientation Cyanosis ◦ Cyanosis ◦ Oxygen saturation 90 Beta-2 agonists ◦ Albuterol, salmeterol, levalbuterol, formoterol Anticholinergics ◦ Ipratropium, tiotropium Anti-inflammatory drugs ◦ Glucocorticoids ◦ Beclomethasone, prednisone (oral), fluticasone, budesonide ◦ Mast cell stabilizer ◦ Cromolyn Leukotriene modifiers ◦ Montelukast Beta-2 agonists Drugs: Albuterol, salmeterol, levalbuterol, formoterol Mechanism of action: selectively activate beta-2 receptors of lungs which results in bronchodilation (AKA bronchodilators) Administration: ◦ Oral beta 2 agonists ◦ All are long acting (oral is not used as much as the inhalers) ◦ Inhaled beta 2 agonists ◦ Short acting (albuterol); onset is fast- minutes, thus used as rescue inhaler ◦ Long acting (salmeterol, formoterol); can have a slower onset 10-30 min, however, it has been found that formoterol may have a faster onset; maintenance therapies Adverse reactions: ◦ Tachycardia, tremor, angina Beta 2 Agonists Drug and Food Interactions: oBeta blockers, especially non-selective agents, may diminish or block the effects of B2 agonists. oMonoamine oxidase inhibitors (MAOI) Nursing Evaluations and Interventions oMonitor heart rate, report it >20 bpm. oAlso monitor for angina symptoms- chest pain, arm pain and/or palpitations oSuggest avoiding products with caffeine Short acting versus long acting beta 2 agonists SHORT ACTING LONG ACTING Examples: Salmeterol and formoterol Examples: albuterol Characteristics of action times: Characteristics of action times: ◦ Onset of action for salmeterol: slow (10-30 min) oOnset is fast- minutes, thus used as ◦ Onset of action for formoterol: 1-3 minutes rescue inhaler ◦ Duration of action for both drugs: 12 hours oDuration of action for inhalers 3-6 hours Uses and typical dosing schedule: Uses and typical dosing schedules: ◦ Long-term maintenance/prophylaxis: 1-2 puffs BID ◦ Acute bronchospasm: q 4-6 hours PRN ◦ Formoterol can be used for exercise prophylaxis ◦ Exercise-induced bronchospasm: prior to ◦ Neither should be used for acute attacks exercise ◦ Should not be used alone. Use with an inhaled glucocorticoid if the glucocorticoid ineffective Inhaled Glucocorticoids Drugs: beclomethasone, fluticasone, budesonide ◦ Glucocorticoids are the drugs of choice for maintaining asthma control Mechanism of action: ◦ Primarily suppress inflammation ◦ May increase the number of beta 2 receptors, increase response to beta 2 agonists, decrease mucus production Uses: ◦ Maintenance/prophylaxis of asthma (must be used on a fixed schedule, not PRN) ◦ Acute exacerbations Administration: inhaled, oral, parenteral Inhaled Glucocorticoids Adverse Reactions: oHoarseness oOropharyngeal candidiasis (“thrush”): ◦ preventions: gargle to rinse and spit after each use ◦ May use a spacer to help prevent thrush Drug and Food Interactions: None major with inhalers Nursing Evaluations and Interventions oMonitor for oral candidiasis. Advise client to rinse and spit after each use of inhaler and to report white patches in the mouth. Glucocorticoids for acute exacerbations Prednisone, methylprednisolone Administration is mainly oral, although methylprednisolone may be given oral or IV Acute exacerbation requires high dose oral or IV glucocorticoids ◦ Short course at high dose (5-7 days) ◦ Unlike the beta 2 agonists that work immediately to reverse bronchoconstriction, glucocorticoids take several hours for effects on inflammation to begin ◦ Again, glucocorticoids are used to reduce inflammation but will not work for acute bronchospasm Adverse Reactions with oral/IV agents and nursing interventions ◦ Adrenal suppression with long term use, taper dose and do not stop abruptly ◦ Osteoporosis /bone loss with chronic use; avise to take calcium + vitamin D ◦ Hyperglycemia, especially in clients with diabetes; monitor glucose ◦ GI upset and peptic ulcer disease, clients may take with food and avoid NSAIDs ◦ Monitor for symptoms of infections Order of inhaler use If client has multiple inhalers: When using a beta 2 agonist inhaler and glucocorticoid inhaler, the beta 2 agonist is used first, then the glucocorticoid inhaler When using 3 inhalers, the short-acting beta-2 agonist is always first, the glucocorticoid last Separate the administration of different medications by 5 minutes Theophylline Mechanism of action: relaxes the smooth muscle of bronchi causing bronchodilation Uses: Still used for some with chronic asthma, but less effective than beta 2 agonists, but longer duration of action; may be a good choice for nocturnal symptoms Administration: ◦ PO: doses must be individualized ◦ IV: for emergencies in the form of aminophylline Adverse reactions ◦ GI effects, increase heart rate, insomnia Drug and Food Interactions ◦ Ciprofloxacin (fluoroquinolones) and cimetidine increase theophylline levels ◦ Inducers such as rifampin, phenytoin decrease theophylline levels; this includes cigarette smoking ◦ Caffeine increases theophylline levels and CNS/cardiac symptoms Theophylline Nursing Evaluation and Intervention oMost products are sustained released and should not be crushed oAdvise clients to avoid caffeine and not to smoke cigarettes oNurse to monitor drug levels and educate clients about symptoms of toxicity oToxicity: narrow therapeutic range, toxicity directly related to blood levels (must check regularly) ◦ Therapeutic range 5-15 mcg/ml ◦ At mildly elevated blood levels: GI effects, insomnia and restlessness ◦ At higher blood levels: Cardiac dysrhythmias, seizures; death due to cardiovascular collapse Inhaled Anticholinergic Drugs Drugs: Ipratropium (short acting) and tiotropium and aclidinium (long acting) Mechanism: Improves lung function by blocking muscarinic receptors in the bronchi, thereby reducing bronchoconstriction Administration and use for asthma and COPD ◦ By inhalation to relieve bronchospasm; advise clients not to swallow tiotropium capule Adverse reactions- include anticholinergic side effects ◦ Headache ◦ Dry mouth and irritation of the pharynx; fluids and sucking on hard candy may help with dry mouth ◦ Glaucoma –may increase intraocular pressure ◦ ATI notes a contraindication to ipratropium if allergic to peanuts due to the product containing soy lecithin. However, the newer products do not contain soy lecithin and are safe if patients have peanut allergy. https://www.aaaai.org/tools-for-the- public/conditions-library/asthma/peanut-allergic-and-soy-allergic-patients-can-safe 107 COPYRIGHT © 2019 BY ELSEVIER, INC. ALL RIGHTS RESERVED. Leukotriene modifiers Montelukast Mechanism of action: block leukotriene receptors and/or synthesis which results in ◦ Bronchodilation, decreased airway inflammation, edema, and decreased mucus plugging of airway Uses: ◦ Maintenance/prophylaxis of asthma in adults and children (above 6 months of age) ◦ Seasonal allergies and perennial allergies; Not for acute asthma attacks Administration: orally at bedtime due to when the drug level peaks to match evening asthma symptoms Adverse reactions: Black Box warning for neuropsychiatric disorders- suicide ideation/depression, aggressive behavior Nursing evaluation and intervention : Monitor behavioral changes and advise client to report suicide ideations Drugs for Upper Respiratory Disorders Antihistamines Mechanism of action: inhibit H1 receptors in various sites (blood vessels of skin and mucus membranes; nerves) to block effects of histamine Main effects: decrease edema, redness, itching, pain, mucus production First generation: dipenhydramine, chlorpheniramine ◦ Sedating; anticholinergic side effects; may cause confusion, incoordination, and dizziness (esp. elderly) Second generation: cetirizine, fexofenadine, loratadine, azelastine (nasal spray) ◦ Little to no sedation, dizziness, or anticholinergic effects ◦ More expensive Drugs for Upper Respiratory Disorders Sympathomimetic (Decongestants) Pseudoephedrine, phenylephrine, oyxmetazoline (Afrin nasal drops) Mechanism of action: ostimulate alpha-1 receptors of blood vessels → vasoconstriction → decreased edema Uses: reduce nasal congestion of allergies and “colds” Administration routes and effects: ◦Intranasal: onset of action is rapid, effects intense ◦Oral: onset delayed, effects moderate but more prolonged Drugs for Upper Respiratory Disorders Sympathomimetic (Decongestants) Adverse Reactions ◦Intranasal: rebound congestion if used > 3-5 days ◦Oral: CNS stimulation (nervous/agitation, insomnia), cardiac- increased BP and HR, abuse potential Nursing Evaluation and Intervention ◦ Intranasal: advise client to avoid using more than 3-5 days; taper to discontinue ◦ Oral: avoid use in clients with cardiovascular conditions as these drugs cause vasoconstriction and may worsen these disorders Drugs for Upper Respiratory Disorders Intranasal glucocorticoids A first-line therapy for chronic allergy symptoms ◦ Mometasone, Budesonide, fluticasone Mechanism of action: ◦ Block inflammatory response to allergens. Relieves symptoms of allergic rhinitis. Dosage and administration: ◦ Works best when used regularly on daily basis and before symptoms begin ◦ Use lowest effective dose ◦ May take > 1 week to see results Adverse reactions ◦ Dry nasal mucosa (bleeding); burning & itching of nasal mucosa ◦ Systemic effects: adrenal suppression (rare at recommended doses) Drugs for Upper Respiratory Disorders- Non-opioid cough suppressants (antitussives) Dextromethorphan: most effective non-opioid antitussive ◦ Non-opioid but derived from opioids ◦ Abuse potential with high doses due to euphoria with high doses ◦ No dependence ◦ No respiratory depression (except with OD) Adverse Reaction: Dextromethorphan may interact with monoamine oxidase inhibitors (MAOI) Benzonatate: similar in structure to tetracaine, a local anesthetic. Decreases sensitivity of respiratory tract ◦ Should not be chewed (can numb mouth/pharynx); caution with hot items or chewing gum Drugs for Upper Respiratory Disorders- Opioid Cough Suppressants Drugs: Codeine/guaifenesin combination, hydrocodone/chlorpheniramine combination Mechanism of action: suppress cough reflex by directly affecting cough center Adverse Reactions: oGI- nausea, constipation oCNS- dizziness, sedation, respiratory depression Drug and Food Interactions: oCNS depressants, including alcohol may worsen adverse reactions Nursing Evaluations and Interventions oAdvise client to take with food if nausea occurs. Constipation may require laxative. oAdvise caution if driving or using dangerous equipment oAbuse and addiction potential Drugs for Upper Respiratory Disorders- Expectorant-Guaifenesin Drug- Guaifenesin (Robitussin and Mucinex brands) Mechanism of action: “expectorant”; renders cough more productive by stimulating flow of respiratory secretions. This drug is found in many OTC cough/cold products and in prescription products. Adverse Reactions: oGI upset- take with food oDizziness or drowsiness- avoid driving or operating hazardous equipment Drug and Food Interactions: None major Nursing Evaluation and Intervention: oEducate clients to drink plenty of fluids oAdvise clients of caution when driving or using dangerous equipment until s/he knows how the drug will affect them oDo not crush sustained released formulations Drugs for Upper Respiratory Disorders- Mucolytics Drug: Acetylcysteine and hypertonic saline Mechanism of Action: decreases viscosity of mucus to enhance flow Administration: Via inhalation as a mucolytic; oral/IV for acetaminophen overdose Adverse Reaction- May cause bronchospasms, a potential concern in clients with asthma Nursing Evaluation and Intervention oEducate clients that the drug smells like rotten eggs oMonitor for aspiration and the need for suctioning due to increased flow of secretions oMonitor clients with asthma for bronchospasms