Medsurg Respiratory

RESPIRATORY Chapter 27 : Assessment of the Respiratory System Role of Respiratory System: Gas exchange at level of capillaries, expel CO2, hold on to O2 and perfused to the body. Good ventilation and good perfusion! Lungs – oxygen intake Heart – oxygen delivery 1 Blood vessels/RBC – oxygen deliver 2 Ventilation: obstruction (mucus, fluid, sputum, objects) Perfusion: obstruction (PE – O2 comes in and meets resistance and prevents circulation of oxygen) Cyanosis: one of the last signs of distress – at the level of the tissue Relevant Patient History Family and personal data, smoking (pack-years), drug use, allergies, travel (high incidence of TB), geographic area of residence, nutritional status Cough, sputum production (chronic productive cough for months can indicate bronchitis), chest pain, dyspnea, paroxysmal nocturnal dyspnea (PND), orthopnea Assessment of the Lungs and Thorax Inspect thorax with patient sitting up Observe chest, compare one side with the other – look for scars Work from the apex, move downward toward base (from side to side) Rate, rhythm, depth of inspiration as well as symmetry of chest movement Examine AP diameter with lateral diameter – in barrel chest Anterior is larger Crepitus – feel any pouching of air, sound under the skin Diaphragmatic excursion: hands on both sides of the chest, both sides should expand equally Lung sounds Bronchial: harsh hollow sounds heard over the trachea and mainstem bronchi – if heard at lungs edges are abnormal Bronchovesicular: heard over the branching bronchi Vesicular: soft rustling sounds heard in lung tissue over small bronchioles. Heard over all of the lung fields, mostly posteriorly Adventitious sounds: indicate pathologic changes in the lungs Crackles/Rales: popping/velcro sound - fluid in the lungs Wheezes: squeaky, musical, continuous sounds - narrowing or spasms of bronchial structures, air trying to escape through narrow passages. Use bronchodilators to open up airway. If wheezing stops, air passage stops = BAD Rhonchi: low pitched snoring sound - congestion in upper airway Pleural friction rub: loud, rough, scratching sounds caused by inflamed surfaces of pleura rubbing together. Associated with pain on deep inspiration Other Indicators of Respiratory Inadequacy Clubbing of fingers ??Weight loss General appearance ??Activity tolerance Unevenly developed muscles – atrophy Skin and mucous membrane changes Psychosocial Assessment Stress may worsen some respiratory problems Chronic respiratory disease may cause changes in family roles, social isolation, financial problems due to unemployment or disability Discuss coping mechanisms, offer access to support systems Laboratory Tests Blood: hemoglobin, WBC, blood chemistry (tells about other organs) Standard chest x-rays, digital chest radiography, CT: fluid in lungs, consolidation Ventilation and perfusion scan Pulse oximetry (noninvasive): measures ability to inspire and expire Pulmonary Function Testing Noninvasive: test lung volumes (inspiratory, expiratory, total volume) Evaluate lung volumes and capacities, flow rates, diffusion capacity, gas exchange, airway resistance, distribution of ventilation Other Noninvasive Testing: exercise testing, skin testing (TB, cystic fibrosis) Invasive Diagnostic Tests Bronchoscopy: tube down throat into lungs – can clear airway, deep suctioning, remove air Thoracentesis – Aspiration of pleural fluid or air from pleural space Stinging sensation and feeling of pressure, correct position, motionless patient, follow-up assessment for complications Don’t pull out fluid too fast b/c pressure changes Chapter 29: Care of Patients with Noninfectious Upper Respiratory Problems Upper airway: nose, sinuses, oropharynx, larynx, and trachea Nursing priority: promote gas exchange by ensuring a patent airway Fracture of the Nose Displacement of bone or cartilage can cause airway obstruction or cosmetic deformity; potential source of infection CSF may indicate skull fracture if dripping out of nose or ears - when CSF dries on a piece of filter paper, a yellow “halo” appears. Interventions Closed reduction: putting piece of broken nose back together w/o surgery. Local or general anesthesia are used and performed within the first 24 hours. Reduction may be delayed until edema subsides. Management: pain relief and cold compresses to decrease swelling Rhinoplasty: surgical reconstruction/repair of the nose. Assess how often the patient swallows after nasal surgery is a priority because repeated swallowing may indicate posterior nasal bleeding. Examine throat for bleeding with penlight then notify HCP. Post op care: observe for edema and bleeding, check vitals q4 hours until discharge, change drip pad PRN Instruct patient to stay in semi-Fowler’s position and move slowly. Use cool compress on nose, eyes and face to reduce swelling and bruising. Urge patient to drink at least 2500mL/day. To prevent bleeding: limit Valsalva maneuvers (forceful coughing or straining during bowel movement), not to sniff upward or blow the nose, and not to sneeze with mouth closed. Avoid aspirin and other NSAIDS because inhibits clotting (e.g., Ibuprofen). Humidifier to prevent mucosal drying. Edema lasts for weeks, final result will not be seen for 6-12 months Epistaxis: nosebleed – occurs as a result of trauma, hypertension, blood dyscrasia (e.g., leukemia), inflammation, tumor, decreased humidity, nose blowing, and chronic cocaine use. Emergency Care of a Patient with Anterior Nosebleed Maintain standard precautions Position patient upright and leaning forward to prevent blood from entering the stomach and possible aspiration Apply direct lateral pressure to the nose for 10 minutes and apply ice or cool compress To prevent re-bleeding from dislodging clots, instruct patient to not blow nose for 24 hour Cauterization (with silver nitrate) of affected capillaries may be needed; nose is packed Posterior nasal bleeding is an emergency! Emergency because cannot be easily reached and the patient may lose a lot of blood quickly Posterior packing, epistaxis catheters (nasal pressure tubes), or a gel tampon is used to stop bleeding in posterior region Observe patient for respiratory distress and for tolerance of packing or tubes. Humidification, oxygen, bedrest, antibiotics, pain medications, bacteria is drawn to glucose – monitor Interventions post tube/packing removal: petroleum jelly can be applied sparingly to nares for lubrication and comfort (excess application = increased risk of inhalation and pneumonia). Nasal saline sprays and humidification add moisture to prevent rebleeding. Avoid vigorous nose blowing, use of aspirin or other NSAIDS and strenuous activities such as heavy lifting for at least 1 month. Facial Trauma Priority action for patient with facial trauma is airway assessment for gas exchange Manifestations Stridor: partial airway obstruction and requires immediate action Shortness of breath/dyspnea Anxiety/restlessness Hypoxia and hypercarbia (elevated blood levels of CO2) Decreased oxygen saturation Cyanosis, loss of consciousness After establishing airway, assess the site of trauma for bleeding and possible fracture, check for soft-tissue edema, facial symmetry, pain or leakage of CSF from ears and nose. Check behind ears for “battle sign” (associated with skull fracture and brain trauma) Facial Trauma Interventions Priority action for patient with facial trauma is airway assessment for gas exchange Anticipate need for emergency intubation, tracheotomy (surgical incision into trachea to create airway), cricothyroidotomy (temporary airway small opening in throat between thyroid cartilage and cricoid cartilage). If shock is present – fluid resuscitation and identification of bleeding sites immediately Fixed occlusion: wiring the jaws together with the mouth in a closed position (6 – 10 weeks) Post op: oral care with irrigation device, dental liquid diet, teach how to cut wires if vomiting occurs. ** Instruct patient to keep wire cutters with him or her at all times to prevent aspiration if vomiting occurs Obstructive Sleep Apnea Breathing disruption during sleep that lasts 10 seconds and occurs a minimum of 5 times in an hour. Leads to increased levels of CO2, respiratory acidosis stimulates neural centers in the brain, waking the patient to breathe. Most common cause is upper airway obstruction by soft palate or tongue Factors: obesity, large uvula, short neck, smoking, enlarged tonsils, oropharyngeal edema Excessive daytime sleepiness, inability to concentrate, irritability Long term effects: increased risk for hypertension, stroke, neurocognitive deficits, weight gain, diabetes, and pulmonary and CVD. Epworth Sleepiness Scale – likelihood of falling asleep during eight common activities (ranked 1-3), score of 18+ are risk for severe sleep apnea Nonsurgical management: Change of sleep position, weight loss, positive-pressure ventilation (hold airway open – NPPV, BiPAP, APAP, CPAP) Modafinil (Attenace, Provigil) – helpful with narcolepsy from sleep apnea by promoting daytime wakefulness – does not treat sleep apnea Surgical management: Adenoidectomy, uvulectomy, or uvulopalatopharyngoplasty Disorders of the Larynx Vocal cord paralysis May result from injury, trauma, diseases that affect the larynx, laryngeal nerves, or vagus nerve. Prolonged intubation with endotracheal tube may cause temporary or permanent paralysis. May affect both cords or only one One cord: airway remains patent but the voice is affected Open bilateral vocal cord paralysis: hoarseness; a breathy weak voice, aspiration of food At increased risk of aspiration because the airway is open during swallowing Injecting polytef (Teflon) into affected cord to enlarge toward unaffected cord. This improves closure during speaking and eating Bilateral closed vocal cord paralysis causes airway obstruction and is an emergency if the manifestations are severe and the patient cannot compensate – Stridor is the major manifestation. Interventions: securing airway, place patient in high-Fowlers position to aid in breathing. Teach patient to hold breath during swallowing, tuck chin down and tilt the forehead forward during swallowing, Upper Airway Obstruction Interruption in airflow through nose, mouth, pharynx, or larynx Life-threatening emergency Early recognition essential in preventing further complications, including respiratory arrest Causes: tongue edema, laryngeal edema, thick secretions, head and neck cancer, stroke, facial/tracheal/laryngeal trauma, burns, anaphylaxis Interventions for Upper Airway Obstruction Assess cause of obstruction When obstruction is due to tongue falling back or excessive secretions, slightly extend the patients head and neck and insert a nasal or oral airway, suction to remove obstructing secretions Maintenance of patent airway and ventilation Cricothyroidotomy: emergency procedure and is only done when it is the only way to secure airway. This is a temporary airway (example: anaphylactic reaction when airway is swelled shut) Endotracheal intubation (nasotracheal or orotracheal): inserting a tube into trachea via nose or mouth Tracheotomy: for patient who cannot easily be intubated with an endotracheal tube. Chapter 30: Care of Patients with Noninfectious Lower Respiratory Problems Chronic Airflow Limitation: Asthma, Pulmonary Emphysema, and Chronic Bronchitis Asthma Chronic condition in which reversible airflow obstruction in the airways occurs sporadically Intermittent and reversible airflow obstruction affecting airways only, not alveoli More common in adult women than men Slightly more prevalent among African-Americans than Caucasians With bronchial asthma, the bronchiole is obstructed on expiration, particularly by muscle spasm, edema of the mucosa, and thick secretions. Occurs in two ways: Inflammation – obstructs the airway lumens (insides). Inflammation of the mucous membranes lining the airways is a key event in triggering an asthma attack It occurs in response to the presence of specific allergens; general irritants such as cold air, dry air, or airborne particles, aspirin and other NSAIDS (lead to wheezing and asthma like symptoms caused by increased production of leukotriene) Airway hyperresponsiveness can trigger bronchoconstriction – airways close or collapse No gas exchange occurs with constriction of the airway Can occur with exercise and upper respiratory illness Collaborative Management Assessment History: triggers, allergist, last rxn, medications, family hx, better/worse, occupation Physical assessment/clinical manifestations During an acute episode: audible wheeze (louder on exhalation) and increased respiratory rate Increased cough with inflammation Use of accessory muscles: observe for muscle retraction at the sternum and suprasternal notch and between ribs. “Barrel chest” from air trapping – anterior posterior diameter increases with air trapping Long breathing cycle: patient may not be able to speak more than a few words in between breaths. Cyanosis (late stage): oral mucosa and nail bed color, changes in level of cognition, consciousness and tachycardia Hypoxemia: poor blood oxygen levels Laboratory Assessment ABGs – acidotic, alkolotic, CO2 retaining – show the effectiveness of gas exchange Arterial O2 may decrease in acute asthma attack – difficult time inhaling oxygen Arterial CO2 may decrease early in attack and increase later (indicating CO2 retention ) Allergic asthma with elevated serum eosinophil count, immunoglobulin E levels Sputum with eosinophils, mucous plugs, with shed epithelial cells **Pulmonary Function Tests Most accurate with use of spirometry – baseline PFTs are obtained for all patients diagnosed with asthma Forced vital capacity (FVC): volume of air that can be forcibly exhaled after full inspiration Forced expiratory volume in first second (FEV1): test how much/speed someone can breathe out in one second Peak expiratory flow rate (PEFR): 80-100% (green zone) of expired volume (800 is highest). Maximal speed of air being exhaled Example: baseflow is 800, patient presents with 400 – 50% of normal baseflow) 15% - 20% decrease below expected value for age, gender, and size is common for the patient with asthma 80% of personal best (green zone) – no increases in drug therapy are needed 50% - 80%: (yellow zone) – patient needs to use prescribed reliever drug Frequent readings in the yellow zone or increasing use of reliever drugs indicates the need to reassess the asthma plan for the need to change controller drugs. <50% (red zone) – serious respiratory obstruction – use reliever drugs and seek emergency help, need IV therapy to correct Airway responsiveness is tested by measuring PEF and FEV1 before and after the patient inhales the drug methacholine, which induces bronchospasm in susceptible people Interventions Teaching for self-management: knowing their triggers Teach patient to assess asthma severity at least daily with peak flow meter (assess 2-3x a day for 2 weeks while asthma is under control to get a baseline) Avoid potential environmental triggers, such as smoke, fire-places, dust, mold, and weather changes of warm to cold Avoid food that has been prepared with monosodium glutamate or metabisulfite (fast food, Chinese food, dried fruits, lime/lemon juices, grape juices, wine) Use bronchodilator 30 minutes before physical activity with exercise-induced asthma Personal medication therapy plan: need to know all of their meds and ADE Drug Therapy Based on step category for severity and treatment Control therapy/Preventive therapy (controller drugs) Change airway responsiveness to prevent asthma attacks (ex: wear a scarf covering mouth when going out into the cold, scarf warms air) Used every day, regardless of symptoms Singulair (daily med to prevent attack/triggers) Rescue/Reliever drugs Used to actually stop attack once it has started – not used everyday Teach patient with asthma to always carry the rescue inhaler with them **Bronchodilators Cause bronchiolar smooth muscle relaxation, no effect on inflammation – use immediately If patient has airflow obstruction by both bronchospasm and inflammation, at least two types of drug therapy are needed. Beta2 agonists bind to the beta2- adrenergic receptors and cause an increase in smooth muscle relaxation Short-acting beta2 agonists provide rapid but short-term relief. These inhaled drugs are most useful when an attack begins or as a premedication when the patient is about to begin an activity that is likely to induce an attack (albuterol, bitolterol, levalbuterol, pirbuterol, terbuterol – dilators) Long-acting beta2 agonists are delivered by inhaler directly to the bronchioles. Drug needs time to build up an effect but the effects are longer lasting. Useful in preventing an asthma attack, but have no value during an acute attack (Foradil, Serevent). These drugs should never be prescribed as the only drug therapy for asthma. ADE: anxiety, increased HR, n/v, urinary retention Nursing Implications: Check HR, monitor for urinary retention, proper use of inhaler, use bronchodilator before steroid inhaler, may cause sleep disturbance Cholinergic antagonists/anticholinergic drugs: block the parasympathetic NS, resulting in bronchodilation and drying up of pulmonary secretions. Atrovent – used as in inhalant, short acting used several times a day. Spiriva – long acting and once daily use ADE: Dry mouth, blurred vision, cough Do not exceed 12 doses in 24 hours of Atrovent Methylxanthines (deriphyllin): used when other types of management are ineffective. Dosage needed for effectiveness produces serious side effects – monitor blood levels. ADE: GI distress, sleepiness, cardiac dysrhythmias, hyperactivity, tachycardia Administer oral forms with food, avoid caffeine, check HR, crosses placenta **Anti-inflammatory agents Corticosteroids: Short term basis for moderate asthma because of serious side effects. Both inhaled corticosteroids and those taken orally are controlled drugs. They are not effective in reversing symptoms during an asthma attack and should not be used as reliever drugs. Teach patients to take corticosteroids on scheduled basis, even when no manifestations are present (Prednisone, Asmanex, Flovent, Pulmicort) Teach patient to use good mouth care and to check mouth daily for lesions or drainage NSAIDs: anti-inflammatory/ pain Cromone: purpose is to prevent asthma attack triggered by inflammation or allergens Leukotriene antagonists (Singulair) – do not reverse symptoms during an asthma attack Immunomodulators (Xolair) ADE: Cardiac dysrhythmias Encourage oral care after use Other Treatments for Asthma Exercise and activity to promote ventilation and perfusion Oxygen therapy via mask or nasal cannula (acute asthma attack) – dilate airway first Status Asthmaticus – Emergency, severe, life-threatening, acute episode of airway obstruction Intensifies once it begins, often does not respond to common therapy Patient presents with extremely labored breathing and wheezing, accessory muscles and distention of neck veins. Patient can develop pneumothorax and cardiac/respiratory arrest Treatment – IV fluids (insensible fluid loss – sweating), potent systemic bronchodilator, steroids, epinephrine (correct breathing), oxygen (ventilator) Prepare for emergency intubation. Sudden absence of wheezing indicates complete airway obstruction and requires a tracheotomy Patient may be intubated/mechanically ventilated Magnesium relaxes smooth muscles in the bronchioles – given IV Chronic Obstructive Pulmonary Disease Includes: Emphysema & Chronic bronchitis Characterized by bronchospasm and dyspnea COPD tissue damage not reversible; increases in severity, eventually leads to respiratory failure Emphysema Loss of alveoli elasticity and hyperinflation of lung – no gas exchange is occurring Dyspnea; need for increased respiratory rate Increased amount of air is trapped in the lungs due to loss of elastic recoil in alveolar walls, overstretching and enlargement of alveoli into bullae (air filled spaces), collapse of small airways (bronchioles) Once loss of alveoli, they cannot grow back Carbon dioxide is produced faster than it can be eliminated, resulting in carbon dioxide retention and respiratory acidosis Interaction of Chronic Bronchitis and Emphysema in COPD: Chronic bronchitis airway problem COPD Mucus blocking airway Pulmonary emphysema alveolar problem COPD Alveoli are damaged, congestion in lungs Chronic Bronchitis Inflammation of bronchi and bronchioles caused by chronic exposure to irritants, especially cigarette smoke Irritant triggers inflammation, vasodilation, congestion, mucosal edema, bronchospasm Affects only airways, not alveoli – congestion in bronchioles, prevents ventilation, need shunt Production of large amounts of thick mucus Complications of COPD Hypoxemia/tissue anoxia and acidosis from build up of CO2: occurs due to decreased gas exchange Respiratory infections: increased mucus and poor oxygenation. Bacteria cant be expelled (pneumonia) Cardiac failure, especially cor pulmonale (right sided heart failure caused by pulomonary disease), chamber around heart collects fluid Hypoxia/hypoxemia ? Increasing dyspnea Fatigue ? Visible pulsations below sternum Cyanotic lips ? Distended neck veins Warm, cyanotic hands and feet with bounding pulses Cardiac dysrhythmias: result from hypoxemia, drug effects, acidosis Physical Assessment & Clinical Manifestations History: risk factors such as age, gender (see more in older men), and occupational history. Smoking history, describe breathing problems, difficulty sleeping/eating General appearance: clubbing, accessory muscle use, tripod, barrel chest, AP diameter Respiratory changes: fast RR, productive cough, wheezing, asymmetric chest expansion Cardiac changes: palpitations, edema of feet and ankles, nail beds, oral mucosa Late stage emphysema patient may have pallor or cyanosis and is usually underweight Dyspnea Assessment Tool: indicate the amount of SOB you are having at this time by marking on the line: no shortness of breath |-----------| shortness of breath as bad as can be Laboratory Assessment ABG values for abnormal oxygenation, ventilation, acid-base status. As COPD worsens, the amount of oxygen in the blood decreases and amount of carbon dioxide increases. Chronic respiratory acidosis (increased arterial CO2) – problem in advanced emphysema Metabolic alkalosis – retention of bicarb Sputum samples: test for bacterial cause, blood in sputum CBC: inflammatory response – eosinophils present Hemoglobin and hematocrit to determine polycythemia (compensatory increase in RBCs) Serum electrolytes: low phosphate, potassium, calcium, and magnesium reduce muscle strength Chest x-ray: with advanced emphysema shows hyperinflation and a flattened diaphragm Pulmonary function test: peak expiratory volume Interventions Improve oxygenation and reduce carbon dioxide retention Hydration: thin secretions, encourage 2-3L/day Prevent weight loss: patient with COPD often has food intolerance, nausea, early satiety (feeling too “full” to eat), and poor appetite. Malnourished patients lose muscle mass and strength, lung elasticity, and alveolar-capillary surface area. Dyspnea management: SOB interferes with eating. Four to six meals per day may be preferred. Use pursed lip and abdominal breathing and use prescribed bronchodilator 30 minutes before meal Food selection: easy to chew, non-gas forming. Avoid dry foods that stimulate coughing and caffeine-containing drinks that increase urine output and may lead to dehydration Urge patient to eat high-calorie, high-protein foods. Minimize anxiety: anxiety can increase dyspnea. Use of pursed-lip and diaphragmatic breathing techniques during periods of anxiety and panic. Improve activity tolerance – not during episode. Take time with ADLs Energy conservation: planning and pacing of activities for best tolerance and minimal discomfort Prevent respiratory infection: Teach to avoid crowds, pneumonia vaccinateion, suction, mucolytics, chest PT Community – Based Care Home care management Long-term use of oxygen Pulmonary rehabilitation program Teaching for self-management Drug therapy Manifestations of infection Breathing techniques Relaxation therapy Pulmonary Arterial Hypertension Occurs in the absence of other lung disorders, and its cause is unknown Blood vessel constriction with increasing vascular resistance in the lung Eventually the right side of the heart fails (cor pulmonale) from the continuous workload of pumping against the high pulmonary pressures Without treatment, death within 2 years of diagnosis 50% of patients have genetic mutation in the BMP2 gene Early manifestations are dyspnea and fatigue Pharmacologic Interventions Warfarin therapy: taken daily to achieve INR of 1.5 – 2.0 Calcium channel blockers: used to dilate blood vessels Endothelin-receptor antagonists (Tracleer): induce blood vessel relaxation and decrease pulmonary arterial pressure. Cause general vessel dilation and some degree of hypotension. macitentan (Opsumit): approved for adults with PAH. Oral drug taken once daily – teach patients to take drug with a glass of water and not to break/chew/crush tablet. Contraindicated in women who are pregnant or breast feeding (can cause birth defects) Digoxin, diuretics, and oxygen therapy Chest Tube Placement Chest tube used to remove excess air, fluid, blood, bacteria between pleural space Chamber 1 – drainage collection container - collects fluid draining from patient (2500 mL) Chamber 2 – Water seal prevents air from re-entering patient’s pleural space – prevents what comes out from going back in (one way valve). Should always contain 2cm of water to prevent air from returning to the patient. Bubbling in this chamber indicates air drainage from the patient. Seen when intrathoracic pressure is greater than atmospheric pressure (pneumothorax, exhales, couch, sneeze) Chamber 3 – suction regulator Air leak meter – pneumothorax ??Pneumothorax – air in chamber Hemothorax – blood in lung ??Pleural effusion – fluid in lung Empyema – pus/mucus in lung Management of Chest Tube Drainage Systems Patient: Ensure dressing around tube is tight and intact Assess for difficulty breathing/pulse ox Check tube insertion site for condition of skin, redness, purulent drainage or excess bleeding Reposition patient who reports a “burning” pain in the chest Drainage System: Keep drainage system lower than the level of the patients chest Avoid kinks and loops in tubing Assess bubbling in the water seal chamber – should only appear during exhalation, forceful cough, sneeze or position change Immediately Notify HCP or Rapid: Drainage greater than 70 mL/hour Chest tube falls out of patients chest (cover the area with sterile gauze) Drainage tube stops within 24 hours Water seal: should only see bubbling with pneumothorax or pneumo/hemo thorax (due to trauma) If you see bubbling with hemothorax/pleural effusion/empyema – indicates air leakage – check patient! Tension pneumothorax: build up of pressure causes tracheal deviation (ex: if RIGHT sided tension pneumo – trachea deviates to the LEFT side) Tidaling is good (fluid moving in wave like motion)