*NURSING > MED-SURG EXAM > Florida University: Chapter 20-31| NUR 3125 Med-Surg Exam 3,100% CORRECT (All)

Florida University: Chapter 20-31| NUR 3125 Med-Surg Exam 3,100% CORRECT

Document Content and Description Below

Florida University: Chapter 20-31| NUR 3125Med-Surg Exam 3 Chapter 20: Assessment of Respiratory Function Purpose of the respiratory system ● Deliver oxygen to the body, expels carbon dioxide... from the body ○ Works with the circulatory system ● Upper respiratory system: warms and fills air ○ Nose: serves as passageway, filters impurities, humidifies and warms air ○ Sinuses and nasal passages ■ Paranasal sinuses: lines with mucosa and ciliated pseudostratified epithelium; serve as resonating chamber in speech and are a common site for infection ● Frontal, ethmoid, sphenoid, maxillary ● Drain into the nasal cavity via ducts ○ Pharynx (throat): connects nasal and oral cavities to larynx ■ Nasopharynx: posterior to the nose and above the soft palate ■ Oropharynx: houses the tonsils ■ Laryngopharynx: extends from hyoid bone to cricoid cartilage ○ Tonsils and adenoids chain of lymph nodes: guard the body from invasion by orgasms entering the nose and throat ○ Larynx: connect pharynx and trachea, is the voice box and therefore major function is vocalization but protects lower airway from ferign substances and facilitates coughing ■ Epiglottis: covers opening to larynx during swallowing ■ Glottis: opening between vocal cords and larynx ■ Vocal cords: ligaments that produce sound, located in lumen of the larynx ■ Thyroid cartilage: largest cartilage structure, forms part of adam's apple ■ Cricoid: complete cartilaginous ring around larynx, below thyroid cartilage ■ Arytenoid cartilage: used in vocal cord movement w/ thyroid cartilage ○ Trachea: windpipe, smooth muscle with c-shaped rings of cartilage at regular intervals that give it structure and prevent collapse; passage between larynx and main stem bronchi ● Lower respiratory system: accomplishes gas exchange ○ Two lungs ■ Left: 2 lobes ■ Right: 3 lobes ○ Pleura: serous membrane that covers the lungs; visceral and parietal; permit smooth motion of the lung expansion in the thoracic cavity with lubrication ○ Mediastinum: middle of the thorax between pleural sacs; contains all the thoracic tissue outside of the lungs ○ Bronchi ■ Lobar bronchi: split into lobes of the lungs ● Segmental bronchi: facilitate postural drainage ○ Subsegmental bronchi ■ Bronchioles: no cartilage, depend on alveolar pressure and smooth muscle recoil; contain submucosal glands that cover the inside lining of the airway ■ Lined with cilia that move mucus and foriegn substances back into the larynx ○ Alveoli: where gas exchange takes place via diffusion ■ Alveolar capillary membrane ■ Alveolar cells ● Type 1: 95% of surface, barrier between air and alveolar surface ● Type 2: 5%, produce Type 1 cells and surfactant ● Alveolar macrophages: ingest foreign matter ■ Surfactant: keep surface tension low and improves lung function Function of the respiratory system ● Oxygen transport: transported by circulating blood; oxygen diffuses through capillary wall into interstitial fluid, then into cells to be used for cellular respiration ○ Perfusion: arterial venous circulation that fills pulmonary capillaries with blood ■ Influenced by alveolar pressure; pulmonary capillaries are between alveoli and when alveolar pressure is high the capillaries are squeezed, if squeezed too much it’s pulmonary hypertension ○ Oxygen diffuses from areas of high partial pressure to areas of low partial pressure ■ Transported to the cells by combining with hemoglobin proteins in RBC; process called oxyhemoglobin ● Respiration: process of gas exchange between atmosphere lungs, lungs and the blood, blood and cells/tissue ○ Pulmonary diffusion: process by which oxygen and carbon dioxide are exchanged from areas of high to low concentration at air-blood interface through alveolar membrane ■ Happens without difficulty in adults because of differences in concentration; large and thin surface area of alveolar membrane is ideal for diffusion ○ Pulmonary perfusion: actual blood flow through pulmonary vasculature ■ 2% of blood from R.V. is sent to left side of heart without participating in gas exchange ■ Low pressure system, pulmonary artery is 20-30mm sys/ 5-15 dia ■ Circulation at apex of lungs is poor when upright ○ Carbon dioxide diffuses across the alveolar-capillary membrane more easily than oxygen; is the end product of metabolic combustion ○ Oxygen in capillaries of lungs is lower than in the alveoli, which leads it to diffuse into the blood from the alveoli ● Ventilation: the movement of air in and out of the body ○ Thoracic cavity is an airtight chamber, the diaphragm is at the floor ○ Inspiration: contraction of the diaphragm and contraction of the external intercostal muscles increases space and creates negative pressure to inflate airways and expand lungs ■ ⅓ of respiratory cycle ○ Expiration: relaxation of the diaphragm and external intercostals increases pressure causing air to escape, deflation, and recoil of the lungs ■ ⅔ of respiratory cycle ○ Lung volume and capacities Table 20-1 ■ Tidal volume: volume of air inhaled and exhaled in one cycle; about 500mL ● May not vary even with severe disease ■ Inspiratory reserve: maximum volume of air that can be inhaled after normal inhalation; 3000mL ■ Expiratory reserve: maximum volume of air that can be exhaled forcibly after normal exhalation; 1100mL ● Decreased with restrictive conditions like obesity, ascites, and pregnancy ■ Residual volume: amount of air in lungs after expiratory reserve is exhaled; 1200mL ● Decreased w/ obstructive disease ■ Vital capacity: maximum volume of air exhaled from maximum inspiration; 4600mL ● VC = TV+IRV+ERV ● Can decrease in neuromuscular disease, fatigue, atelectasis, pulmonary edema, COPD, obesity ■ Inspiratory capacity: maximum inhaled after normal expiration; 3500mL ● Decrease in restrictive diseases ■ Functional residual capacity: normal volume after normal expiration; 2300mL ● FRC = ERV +RV ● Increased with COPD, decreased in ARDS and obesity ■ Total lung capacity: volume of air in lungs after maximum inspiration; 5800mL ● TLC = TV + IRV + ERV + RV ● May decrease with restrictive diseases such as atelectasis and pneumonia, increase w/ COPD ● Ventilation-perfusion ratio: adequate gas exchange depends on balanced V/Q ratio, impalances ratio results in shunting of the blood and hypoxemia ○ Supplemental oxygen may eliminate hypoxemia ○ Imbalances: chart 20-2 Inspiratory and expiratory center is in the medulla and the pons controls the rate and depth Gerontology: decline in respiratory function begins in early and middle adulthood ● Vital capacity of the lungs and strength of the respiratory muscles peak between 20 and 25 years and then decrease ● 40 years: alveolar changes begin to result in decreased surface area ● 50 years: alveoli begin to lose elasticity, walls of alveoli thicken ● Cough capability, cilia, and mucus all decrease Assessment ● Past history ○ Focus on patient’s problem and associated symptoms: Onset, location, duration, character, alleviating factors, timing, radiation, of presenting problem and any associated signs/symptoms ○ Explore health, medical conditions, injuries, hospitalizations, surgeries and medications ○ Assess for risk factors and genetic factors that may contribute to lung condition ● Normal breath sounds ○ Vesicular ○ Bronchovesicular ○ Bronchial ● Abnormal (adventitious) breath sounds - Table 20.7 ○ Crackles ○ Wheezes: high pitched musical sound on expiration (asthma) or inspiration (bronchitis) ○ Rhonchi: low pitched continuous sounds heard over lungs in partial airway obstruction ○ Stridor: inspiratory wheeze in upper airway due to blockage ○ Friction rub ● Common symptoms ○ Dyspnea: subjective feeling of difficult or labored breathing, breathlessness, and short of breath ■ Causes ● Common to cardiac and pulmonary disorders, decreased lung compliance, and increased airway resistance ● Can occur with allergic reactions, anemia, neurologic disorders, neuromuscular disorders, trauma, and disease as well as exercise ● Dyspnea on expiration with a wheeze is common with COPD ● Dyspnea with noisy breathing can come from narrowing of airway ■ Predicts adverse clinical outcomes, including increased mortality ■ Can be associated with tachycardia and hypoxemia ■ Orthopnea is dyspnea on lying flat ■ Ask: any other symptoms or cough? Was onset sudden or gradual? What time of day or night does it occur? Does it get worse when lying flat? What triggers it? 1-10 breathless scale how hard it is to breath? How severe is the SOB? ○ Cough: reflex that protects lungs from secretion accumulation and foreign bodies, results from the irritation or inflammation of the mucus membranes ■ Common causes: mucus, pus, blood, airborne irritants, asthma, GERD, infection, medications (ACEIs) ● Ask about onset and time, characteristics ■ Ask about sputum production ○ Chest pain: can occur with disease or anxiety ■ Asses quality, intensity, radiation, precipitating factors, and relationship to phases of respiration ○ Hemoptysis ■ Common causes: infection, carcinoma, abnormalities of heart or vessels, PE or infarction ○ Physical appearance/ general appearance ■ Clubbing from chronic hypoxic conditions ■ Skin color ● Cyanosis ■ Chest configuration ● Barrel chest ● Funnel chest: rickets/marfan ● Pigeon chest ● Kyphoscoliosis ■ Upper airway and lower airway exams: review ○ Abnormal breathing patterns ■ Apnea ■ Obstructive sleep apnea ○ Accessory muscle use ● Assess voice sounds ○ Bronchophony: more intense and clearer than normal when listening to lungs with stethoscope ○ Egophony: voice sounds are distorted, like A being heard instead of E ○ Whispered pectoriloquy: clearly hearing voice when listening with stethoscope to lungs despite whispering ● Assessing the critically ill ○ Be aware of ventilator associated events and risks ■ Assess for synchrony and agitation, restlessness, or other signs of distress ○ Monitor vitals and be on the lookout for hemodynamic instability and changes in mentation ○ Patient’s bed should be elevated ○ Lethargy and somnolence may be signs of increased CO2 ○ Auscultation, percussion, and palpation are essential even in critically ill patients with mechanical ventilation ○ Testing status of respiration: RR, tidal volume, minute ventilation, vital capacity, inspiratory force and compliance ○ Hypoventilation and low tidal volumes can lead to atelectasis ● ○ Assessment findings consistent with a pleural effusion include affected lung fields being dull to percussion, absence of breath sounds and a pleural friction rub may also be present ○ Pneumonia- egophony, which can be best assessed by instructing the client to repeat the letter E. The distortion produced by consolidation transforms the sound into a clearly heard A rather than E ○ Emphysema- breath sounds are faint or often completely inaudible and the expiratory phase is prolonged Diagnostic evaluations ● Pulmonary function tests: routinely used in patients with chronic respiratory disorders to aid diagnosis; performed to assess function, extent of dysfunction, response to therapy, and are screening tests as well; measures how much air moves in and out of lungs when you breathe; can be used prior to surgery, and to test those who work in hazardous environments ○ Forced vital capacity: maximally forced expiration ○ Forced expiratory volume: volume exhaled in specific time during FVC ○ Ratio of FVC/FEV ○ Forced expiratory flow; 200-1200 ○ Forced mid expiratory flow ○ Forced end expiratory flow ○ Maximal voluntary ventilation: expired in a specified period during repetitive maximal effort; important in exercise tolerance ● Inspiratory force: inspiratory effort with one breath; measured with monometer attached to mask or ET tube ○ Normal pressure is 100cm H2O ■ <25 requires mechanical ventilation ● ABG: measures arterial O2 and CO2 levels ○ Used to assess the adequacy of alveolar ventilation and ability of lungs to provide O2 and remove CO2 ○ Also assesses acid-base balance ● Venous blood gas ● Pulse ox: noninvasive oxygen sat of the blood ○ 95-100% normal ○ Can be unreliable ● Cultures ● Sputum studies: analysis for pathogens or malignant cells ○ Can be necessary for patients on antibiotics, corticosteroids, immunosuppressants for prolonged periods (due to monitoring for opportunistic infections) ○ Ideally obtained early in the morning before the patient has had anything to eat or drink ■ Patient should clear nose and throat, rinse mouth ■ Cough deeply and expectorate sputum into container ● Imaging studies ○ X-ray ○ CT scans ○ Angiography ○ MRI ○ Fluoroscopy: live x-ray ○ Radioisotope diagnostic procedure (PETs) ○ Endoscopic procedures ■ Bronchoscopy ● Remove bodies/secretions ● Control bleeding ● Treat post-op atelectasis ● Excise lesions ● Brachytherapy ● Simple viewing ● NPO until gog returns ■ Thoracoscopy: pleural cavity examined ○ Thoracentesis: aspiration of fluid from pleural space ● Biopsy ○ Pleural ○ Lung ○ Node biopsy ○ Mediastinoscopy Chapter 21: Respiratory Care Modalities Oxygen therapy: admin of oxygen at a concentration greater than that found in the environmental atmosphere (21%) to provide adequate transport of oxygen in the blood and decrease the work of breathing, which reduces stress on the myocardium ● Indications ○ Hypoxemia: decrease in arterial oxygen tension in the blood ■ Manifested by change in mental status, impaired judgement, agistation, coma, confusion, lethargy, disorientation, dyspnea, increased BP and HR, dysrhythmias, central cyanosis (late sign), diaphoresis, and cold extremities ○ Hypoxia: decreasing in oxygen supply to tissues and cells; severe can be life threatening ■ Hypoxemic hypoxia: decreased oxygen level in blood ■ Circulatory hypoxia: inadequate capillary circulation ■ Anemic hypoxia: decreased hemoglobin concentration ■ Histotoxic hypoxia: toxic substance interferes with ability of tissue to use oxygen ● Complications ○ Oxygen toxicity: may occur when too high concentration (>50%) is administered for extended period of time ■ Caused by overproduction of free radical by-products of cellular metabolism ● Free-radicals damage the alveolar capillary membranes leading to pulmonary edema and cell death ■ Symptoms: discomfort, paresthesias, dyspnea, restlessness, fatigue, malaise, progressive respiratory difficulty, refractory hypoxemia, alveolar atelectasis, alveolar infiltrates ● Similar to ARDs ■ Prevention: use lowest effect concentration, minimize furation of high concentrations ● PEEP or CPAP can prevent or reverse atelectasis and allow lower percentages to be used ○ Absorption atelectasis: oxygen becomes absorbed too quickly and not enough of the other types of air matter (like nitrogen) is left to keep alveoli from collapsing ■ Caused by high concentration and small tidal volumes ○ Danger of fires ● Methods of administration: oxygen is dispensed from cylinders, piped-in systems, or a concentrator (most maintenance than other systems, 1-10l/min at 40% O2) ○ Low flow systems: provide partial inspired air ■ Nasal cannula: up to 6 L/min, 24-44% O2 ● >4L is drying and can lead to swallowed air ■ Nasal catheter: same as above ● Rarely used, short term therapy. Cannula needs to be changed every 8 hours ■ Simple mask: 5-8 L/min, 40-60% O2; has to be taken off to eat ■ Partial rebreather: 8-11 L/min, 50-75% O2; must be removed to eat ■ Non Rebreather: 10-15 L/min; 80-95% O2; must be removed to eat ● Has one way valve ○ High flow systems: provide all of the inspired air ■ Transtracheal cath: ⅓-4 L/min, 60-100% O2 ■ Venturi mask: 4-8 L/min, 24-40% O2; take off to eat; common in COPD patients ■ ■ Aerosol mask: 8-10 L/min, 30-100% O2 ■ Trach collar: 8-10 L/min, 30-100% O2 ■ T-piece: same as trach; heavy tubing ● Useful in weaning people off mechanical vents ■ Face tent: same as trach, bulky ○ Oxygen conserving: pulse dose 10-40 mL O2/breath ○ Hyperbaric oxygen chamber ○ Demand oxygen delivery system Incentive spirometry: a method of deep breathing that provides visual feedback to encourage the patient to inhale slowly and deeply to maximize lung inflation and prevent or reduce atelectasis ● Two sypes: volume or flow ● Used post surgery to prevent atelectasis ● Nursing care: positioning of patient, realistic goals, record outcomes, and encourage use ○ Patient education: semi fowler position or upright, use diaphragmatic breathing, inspire slowly and hold the ball in place for 3 seconds, exhale slowly ■ Cough before and after each sessions, splint incision while coughing ■ Perform 10 times in succession every hour Mini nebulizer: handheld item that dispense a moisturizing agent or medication into the lungs ● Indication: difficulty in clearing secretions, reduced vital capacity with ineffective deep breathing and coughing, and unsuccessful simpler methods, delivering aerosil, expanding the lungs ● Nursing care ○ Instruction: breath slowly through mouth with deep breaths, hold for a few seconds to increase residual capacity function; encourage coughing; monitor effectiveness ○ Diaphragmatic breathing: a helpful technique to prepare for proper use of the small-volume nebulizer Chest Physiotherapy: removes bronchial secretions, improves ventilation, and increases efficiency of respiratory muscles ● Postural drainage: allows the force of gravity to assist in the removal of bronchial secretions ○ Drained secretions are removed by cough or suction ○ Prevents or relieves obstruction caused by accumulation of secretions in bronchioles ○ Upright patients = drainage accumulates in lower part of lungs ○ ○ Nurse management: consider lobes involved, cardiac status, and structural deformities; auscultate to identify areas that need drainage and effectiveness ■ Performed 2-4x daily before meals and at bedtime, positions held for up to 10-15 minutes, changes in position requires coughing or suction; note sputum characteristics ● Chest percussion and vibration ○ Percussion: carried out by cupping the hands and lightly striking the chest wall in a rhythmic fashion over the lung segment to be drained ○ Vibration: the technique of applying manual compression and tremor to the chest wall during the exhalation phase of respiration; cough after 3-4 vibrations ○ HWFCO vest can provide chest therapy, uses air pulses to compress chest wall and dislodge secretions ○ Percussion, alternating with vibration, is performed for 3 to 5 minutes for each position, patient should use diaphragmatic breathing ○ Some mattresses can vibrate too ● Breathing retraining: exercises and breathing practices that help achieve more efficient and controlled ventilation and decrease work of breathing ○ Especially indicated in those with COPD and eczema; pursed lip breathing helps prevent airway collapse secondary to loss of lung elasticity in emphysema; encourages slow deep breathing pattern and controls breathing even during stress, improves oxygen transport ○ Promote maximal alveolar inflation and muscle relaxation; relieve anxiety; eliminate ineffective, uncoordinated patterns of respiratory muscle activity; slow the respiratory rate; and decrease the work of breathing. Can also help control anxiety with slow rhythmic breathing ○ May need low flow with exercises ○ Appropriate for all older patients whether healthy or not Home Oxygen: ● Nurse instructs the patient about oxygen: ○ Safe methods for administering in the home ○ Available in gas, liquid, concentrated ○ Portable devices ● Humidity must be provided ● See Chart 21-2 p. 516 Breathing exercises ● General instructions ○ Breath slowly and rhythmically ○ Inhale through nose to warm, filter, humidify air ○ Breath more slowly by prolonging exhalation if you feel short of breath ● Diaphragmatic: place hand on abdomen and chest ○ Breath in through nose and allow abdomen to protrude as far as possible ○ Breath out through pursed lips while contracting abdominal muscles ○ Press on abdomen while breathing out ○ Repeat for 1 minute, rest 2 minutes ● Pursed lip: increases airway pressure during expiration and reduces trapped and and airway resistance, prolongs expiration; inhale through nose 3 seconds then tighten abdominal muscle and exhale for 7 seconds through pursed lips Emergency management of upper airway obstruction ● Acute upper airway obstruction can be caused by food, vomit, clots, or anything else that can get stuck in the larynx and trachea; patients with altered LOC are at higher risk for obstruction because of loss of reflexes that protect (cough, gag, swallow) and loss of tone of muscles (tongue falls back) ● Inspect chest, consciousness, obvious signs of obstruction; palpate equal chest rise or tender areas, obvious deformities,emphysema; and auscultate for air movement and adventitious sounds; do these RAPIDLY ● Emergency measures as soon as it is identified Endotracheal intubation: provides patent airway, access for mechanical ventilation, facilitates removal of secretions ● Disadvantages: tubes cause discomfort, cough reflex is depressed because glottis closure is hindered, swallowing reflex is depressed, increased risk of aspiration and well as pneumonia, ulceration and stricture of larynx can develop ad patient loses ability to talk; cannot be used for longer than 14-21 days ● Immediately after: auscultate, check symmetry of expansion, get capnography, verify placement ○ Check cuff pressure every 8 hours. Ensure high humidity with mist in tubing ○ Use sterile suction ○ Reposition patient every 2 hours ○ Oral hygiene ● Removal: BVM ready, explain procedure ○ Suction, remove tape, deflate cuff, give 100% O2 for a few breaths ○ Suction during removal, remove at peak inhale ● Post-extubation:heated humidity and oxygen, sitting or high fowlers ○ Monitor RR and quality of chest excursions, look for changes that signify poor respiration ○ NPO for a few hours ○ Oral care ○ Educate on coughing and deep breathing Tracheostomy: opening into trachea surgically ● When a tracheostomy or endotracheal tube is in place, it is usually necessary to suction the patient’s secretions because of the decreased effectiveness of the cough mechanism ● Permits long term use of mechanical vent ● Preventing complications: used warmed, humidified air; maintain cudd pressure; suction as needed; maintain skin integrity though proper dressing change; auscultation sounds; monitor for infection; administer prescribed O2 and monitor patient O2 sat; watch for cyanosis; maintain hydration; sterile technique during care and suction ● Tracheal suctioning is performed when secretions are obviously present or adventitious sounds occur ● Semi fowler positioning should be used and patient needs effective mode of communication Mechanical Ventilation: maintains ventilation and oxygen delivery over long periods ● Indications: respiratory failure or compromised airway, surgery, shock, increased work of breathing to the point of exhaustion with other attempts at relief failing ● Classification ○ Positive pressure: mostly used today, inflates lungs and expiration occurs passively; ET ot trach tube is usually needed ■ Volume cycled: give a preset each inspiration; barotrauma can occur ■ Pressure cycled: delivers flow up to a certain pressure; volume can vary with changes in airway resistance or compliance, inconsistent TV ■ High frequency oscillatory support: low volume, high pressure; used to open airway such as atelectasis or ARDs ■ Noninvasive (no intubation): COPD, CHF, sleep-breathing disorder, respiratory failure, pulmonary edema ● CPAP: positive pressure throughout cycle ● BiPAP: independent control of inspiratory and expiratory pressures while providing pressure support ventilation ○ Patient or machine can breathe from backup breath setting ● Powerpoint: Method of positive-pressure ventilation that can be given via face masks that cover the nose and mouth, nasal masks, or other oral or nasal devices such as the nasal pillow ○ Eliminates need for endotracheal intubation or tracheostomy ○ Continuous positive airway pressure (CPAP) ○ Bilevel positive airway pressure (BiPAP) ○ Indications: respiratory arrest, serious dysrhythmias, cognitive impairment, head/facial trauma ■ Negative pressure: not used today or rarely used ● Assessment ○ Nurse evaluates physiologic status and how the patient is coping with mechanical ventilation ○ Physical assessment ■ Systematic assessment of all body systems ■ In-depth respiratory assessment including all indicators of oxygenation status ○ Respiratory assessment: vitals, rate, pattern, breath sounds, hypoxemia, evaluation of spontaneous ventilatory effort ○ Maintain bed 30 degrees or higher ○ Monitor fluid balance, edema, I&O, daily weights ○ Also assess ■ Neurologic status ■ Effective coping and emotional needs ■ Comfort level and ability to communicate needs ■ GI and nutritional needs ○ Assessment of the equipment and settings, refer to Table 21-2 - Troubleshooting Problems With Mechanical Ventilation ■ Increased peak airway pressure: caused by coughing, plugged tube from secretions, decreased lung compliance or fighting with ventilator; tube kinking, pneumothorax, atelectasis, bronchospasm ■ Decrease pressure or volume: increased compliance, leaking ventilator ■ Cardiovascular compromise: decreased venous return due to positive pressure in lungs ■ Barotrauma/pneumothorax: high pressure leads to ruptures ■ Pulmonary injection: bypassing defence mechanisms, breaks in ventilator circuit, motility and reflexes decrease ● Preventing VAP chart 21-11: sterile technique, oral care, mobility encouragement ● Patient perspective chart 21-12: ● Goals include: ○ Maintenance of patent airway: suctioning, CPT, positioning, humidity ○ Optimal gas exchange ○ Absence of trauma or infection ○ Attainment of optimal mobility ○ Adjustment to nonverbal methods of communication ○ Successful coping measures ● Collaborative problems ○ Vent problems ○ Altered cardiac function ○ Barotrauma ○ Infection and sepsis ○ Delirium ● Nursing interventions: ○ Enhance gas exchange: frequent repositioning, analgesics to relieve pain without suppressing respiration ○ Promote airway clearance: auscultate for secretions, use measures to clear secretions, ensure adequate humidification ○ Prevent trauma and infection: maintain tube patency and tube care, check cuff pressure, frequent oral hygiene, elevate head ○ Promote mobility: ROM ○ Promote communication ○ Promote coping ability: stress reduction ■ Family teaching and emotional and coping support of family as well as patient ● Weaning: withdrawal of dependence from ventilator; a collaborative process ○ 3 stages: removed from vent, then tubing, then oxygen ○ Earliest possible time consistent with patient safety, started when patient is physiologically and hemodynamically stable, has spontaneously breathing capability, has recovered from acute problems, and when the cause of respiratory failure is resolved ○ Criteria: stable and showing signs of improvement or reversal of disease cause; stable vitals and ABG important predictors of successful weaning ○ Patient prep: ■ Assess vital capacity, MIP, tidal volume, minute vent, shallow or rapid breathing, and lab values ■ Monitor activity level and dietary/nutritional status ■ Address family concerns ■ Implement method, monitor vitals, ECG, resp pattern for 30 mins and then every 5 mins after until complete ○ Methods: CPAP, SIMV, T piece trials Thoracic surgery ● Treats: lung abscesses, cancer, cysts, tumors, emphysema, and other disease ● Preop ○ Assessment and diagnosis: assessment is to ascertain functional reserve, determine whether patient will survive and recover, and ensure optimal condition for surgery ■ Assess signs and symptoms, history of smoking, cardiopulmonary tolerance, breathing pattern, how they sleep (pillow orthopnea), general physiologic status, and other medical conditions or medications ○ Improve airway clearance ○ Education ○ Relieve anxiety: listen to feeling, address fears and help them cope ● Postop ○ Monitor vitals, respiratory, and CV status ○ Improve gas exchange and breathing: keep bed elevated 30-45 degrees ○ Promote airway clearance: encourage patient to cough before performing more invasive procedures, use humidity, posturing, bronchodilators, percussion, suctioning ○ Oxygen admin ○ Positioning: promote mobility and shoulder exercises, watch pressure points, frequent positioning to allow fluids to drain ○ Pain meds: relieve pain and discomfort ○ Mechanical vent ○ Maintain fluids and nutrition ○ Watch for complications ○ Drainage: fluctuation of the water level in the water seal shows effective connection between the pleural cavity and the drainage chamber and indicates that the drainage system remains patent ● Chest drainage systems: suction source, collection chamber, valve or way to prevent air from returning to chest ○ Removes air and fluid from pleural space, re-expands the lungs ○ Wet suction/water seal: collection chamber, water seal, wet suction control ■ Requires sterile fluid in seal and suction chambers, has positive and negative pressure valves, intermittent bubbling indicates proper function, can be connected to more suctioning ○ Dry suction/water seal: collection chamber, water seal, suction regulator dial ■ Sterile fluid for water seal only, suction pressure is set with dial, positive and negative release valves, indicator to signify suction is adequate ■ Quieter than other systems ○ Dry suction/ one way valve: one way valve that only allows air out of chest ■ No fluid, easily set up in emergency ■ Works if it is knocked over, good for those ambulating ○ Management and preventing complications of drainage ■ Verify tube patency and connections, assess water seas, regulator dials ■ Look for fluctuations in water seal chamber or air leak indicators ■ Keep system below chest level ■ Assess suction control and bubbling, keep suction at prescribed level ■ Maintain fluid of wet suction systems ■ Keep air vent open if suction is off ● Prevent complications ○ Assess lung sounds, r/r/d, oxygen and pulse oc, ECG, cap refill, skin color, surgical dressing and site ○ Encourage turning, cough, deep breathing ● Patient teaching ○ Signs and symptoms to report; changes is resp status, SOB, fever, restlessness, mental changes, sputum changes; any bleeding or drainage at tube exit sites or incision; increased chest pain ○ Use of home respiratory treatment modalities ○ Importance of progressive increased activity ○ Instruction on shoulder exercises ○ Refer to Chart 21-22 for additional patient education ○ In addition, respiratory care and other treatment modalities (oxygen; incentive spirometry; CPT; and oral, inhaled, or IV medications) may be continued at home. Therefore, the nurse needs to instruct the patient and family in their correct and safe use Chapter 22: Management of Patients with Upper Respiratory Tract Disorders Upper respiratory tract disorders involve the nose, sinuses, pharynx, trachea, and bronchi; they are the most common cause for seeking healthcare ● Can be chronic, acute, severe, minor, or life threatening ● Treated in community settings: doctor offices, urgent care clinics, long term care facilities, self care at home ● Early detection of signs/symptoms and appropriate interventions is usually enough to avoid complications ● Patient teaching focuses on prevention and health promotion ● Chart 22-1 Aging adult: more serious consequences; antihistamines and decongestants should be sued cautiously due to potential interactions with other meds; more likely to have chronic pulmonary diseases; laryngitis from GERD is common; loss of muscle mass and larynx strength Upper Airway infections: most common cause of illness and absences of school and work; adults get 2-4 per year ● Rhinitis and rhinosinusitis ○ Multiple causes: odor, temp, humidity, infection, disease, allergy, age, drug induced, etc ■ Drug-induced rhinitis may occur with antihypertensive agents, such as angiotensin-converting enzyme (ACE) inhibitors and beta-blockers; “statins,” such as atorvastatin (Lipitor) and simvastatin (Zocor); antidepressants and antipsychotics such as risperidone (Risperdal); aspirin; and some anti anxiety medications ○ Signs/symptoms: rhinorrhea, congestion, discharge, sneezing, purritis, headache ○ Educate on side effects of medications and rebound congestion (rhinitis medicamentosa); avoiding triggers and common triggers, drug interactions, hand hygiene ○ Antihistamines and corticosteroids, decongestants are also used ○ Rhinosinusitis inflammation of sinuses, nasal cavity, and mucosa ■ Acute <4 weeks, subacute 4-12 weeks, ● Acute rhinosinusitis usually follows unresolved infections, or as exacerbation of allergic rhinitis ● s/s: nasal drainage, obstruction of nasal cavities, face pain, pressure or feeling of fullness, congestion, headache, stuffiness, high fever ● Complications: osteomyelitis, mucoceles, sinus thrombosis, meningitis, brain abscess, infarction of brain, orbital cellulitis, abscesses ● Treatment: bacterial- antibiotics, intranasal lavage; viral- saline lavage, decongestants (3- 4 days only), antihistamines; both- steroids if previous history of allergic rhinitis ○ Goal: shrink mucosa, relieve pain, treat infection ○ Self care: symptoms of complications, methods to promote drainage (humidity, warm compresses), avoid swimming, diving, air travel; stop smoking; trach patient about use of nasal sprays; side effects to meds and rebound congestion ■ Decongestant at first signs if recurrent ■ Complication signs: fever, severe headache, neck stiffness ■ chronic >12 weeks and 2 or more of these: mucopurulent drainage, facial pain, hyposmia, nasal obstruction ● Manifestation: impaired mucociliary clearance and ventilation, cough, hoarseness, headaches, periorbital edema, pain in face, mouth breathing, sore throat, adenoidal hypertrophy; fatigue and congestion are common, decreased taste/smell and fullness of ears ○ Worse in morning ● Assessment: abnormalities of the mucous membranes, oropharynx drainage, palpation ● Complications: orbital cellulitis, subperiosteal abscess, sinus thrombosis, meningitis, encephalitis, ischemic infarction; brain abscess, subdural empyema, meningitis, epidural abscess ● Management: hydration, OTC sprays, NSAIDs, deconfestions, elevation of bed, avoid smoke or fumes, antibiotics are common and can last 2-4 weeks to eradicate maybe as long as 12 months; corticosteroids, mast cell stabilizers, and leukotriene inhibitors ● Education: prescribed regimen should be followed, blow nose gently to avoid further irritation, apply heat, elevate HOB, increase flids ■ Bacterial or viral ■ Recurrent: 4+ per year ● Viral rhinitis: most frequent viral infection; aka common cold ○ s/s: low grade fever, nasal congestion, rhinorrhea and discharge, halitosis, sneezing, watery eyes, sore/scratchy throat, malaise, chills, headache, muscle ache ■ Last 1-2 weeks ■ ○ Management: fluids, rest, expectorants, NSAIDs, antihistamines, salt water gargles ○ ● Pharyngitis: painful inflammation of pharynx aka SORE THROAT ○ Most commonly caused by group A-B streptococcus (strep throat) ■ Strep warrants antibiotic treatment ■ Bacterial infections can become severe and life threatening ● Warrant penicillin usually ■ GAS strep can exhibit scarlet fever, vomiting, and anorexia; usually malaise, fever, headache, myalgia, nausea, and swollen passages ○ Symptoms: pain, fever, vasodilation, edema, tissue damage, exudate on tonsils ○ Viral infections usually subside within 3-10 days ○ Signs: fiery red pharyngeal membrane and tonsils, lymphoid follicles that are swollen and flecked with exudate, enlarged and tender cervical lymph nodes, and NO cough; fever, malaise are also sometimes present ○ Chronic ■ Hypertrophic: thickening and congestion of pharyngeal membrane ■ Atrophic: late stage of hypertrophic, membrane is thin, whitish, glistening, and wrinkled ■ Chronic granular: numerous swollen lymph follicles on pharyngeal wall ● Irritation, fullness of throat, mucus, post nasal drip, ● Sore throat that is worse on swallowing but does not have pharyngitis suggests thyroiditis ■ Management: correct conditions that cause cough, avoid irritants, congestive relief, gargles and lozenges ● Tonsillectomy may help ● Tonsillitis: symptoms include include sore throat, fever, snoring, and difficulty swallowing ● Adenoiditis; tonsillitis ○ May cause mouth breathing, earache, draining ears, frequent head colds, bronchitis, foul-smelling breath, voice impairment, and noisy respiration ○ Complications: Infection can cause middle ear infections, can cause deafness; can cause sleep apnea; acute mastoiditis ○ Enlarged adenoids can block nose ○ Care: fluids increase, analgesics, salt water, rest, antibiotics if bacterial ■ Tonsillectomy if chronic or complications persist ● Peritonsillar abscess: ○ S/s: acute illness with severe sore throat, fever, tismus, drooling, inflammation, spasm, severe pain, raspy voice, dysphagia, otalgia, odynophagia; tender and enlarged cervical nodes, erythema of oropharynx, purulent tonsil ○ Management medical.surgical: antibiotics, aspiration, drainage, airway mgmt ○ Nursing management: encourage use of prescriptions including topical anesthetics, mouthwashes, gargles, irrigations ■ Gargle gently ever 1-2 hours for 24-36 hours post procedure ● Laryngitis: voice abuse, exposure to pollutants, or part of URI; can occur with GERD, may be isolated infection only involving vocal cords ○ Aphonia or hoarseness is the obvious signs, dry cough and dry, sore throat that gets worse in the evening, pain that's worse in the morning and improves in warm climate; tickle feeling ○ Rest voice, avoid irritants, antibacterials and aerosols, avoid irritants; sometime corticosteroids and PPIs are used ○ Nursing: rest voice, maintain well-humidity environments, encourage fluids ■ Note that symptoms can extend as long as 10 days after antibiotic therapy ■ Report loss of voice with sore throat that makes swallowing difficult, hemoptysis, and noisy respirations ■ Continued hoarseness after 5 days rest should be reported for possible malignancy ● General planning ○ Airway management and aspiration risk ○ Pain management ○ Communication strategy ○ Increase hydration ○ Patient teaching ■ Prevention of upper airway infections-clients with nasotracheal and nasogastric tubes in place are at risk for development of sinus infections ■ Hand washing ■ When to contact health provider ■ Need to complete antibiotics ■ Flu vaccine ○ Home care ● Interventions: elevate head, analgesics, gargles, liquids, soft/bland diet, rest, head elevation; heat or ice Obstruction and trauma of the upper airway ● Obstructive sleep apnea ○ S/S: Chart 22-4; snoring, sleepiness, and significant other report; chronic fatigue, nighttime awakenings, insomnia, early morning awakenings, hypersomnolence, weight gain, increased aging, snoring, morning headaches, pulmonary hypertension, dysrhythmias, irritability ○ Diagnosis: sleep study ○ Treatment: CPAP, BiPAP, oxygen therapy, surgery, weight loss, avoiding alcohol, positional sterapy, oral appliances; some medication ● Epistaxis: nasal hemorrhage ○ Anterior septum is the most common site ○ Can result in airway compromise or significant blood loss ○ Risk Chart 22-5: local infections, systemic infections, dry membranes, corticosteroids or illicit drugs, trauma, arteriosclerosis, HTN, tumor, aspirin, liver disease, thrombocytopenia, ROWS ○ Treatment ■ Pinch nose 5-10 mins and lean forward ■ Decongestants as vasoconstrictors ● Phenylephrine spray ■ Cauterization w/ silver nitrate or electrocautery ■ Gauze packing or balloon cath for 3-4 days ■ Antibiotics for risk of rhinosinusitis and sepsis ○ Management: Airway, breathing, circulation; control bleeding, provide emesis basin ■ Vital signs, possible cardiac monitoring and pulse oximetry ■ Reduce anxiety ■ Patient teaching: ● Avoid nasal trauma, nose picking, forceful blowing, spicy foods, tobacco, exercise; avoid high altitudes, nasal trauma ● Adequate humidification to prevent dryness ● Pinch nose to stop bleeding; if bleeding does not stop in 15 minutes, seek medical attention ● Nasal obstruction ○ Possible causes: deviated septum, turbinate hypertrophy, polyps, congestion ○ S/S: mouth breathing, dry mouth/lips, sleep deprivation, infections ○ Management: remove obstruction or cause; corticosteroids, leukotriene inhibitors, and antibiotics ■ Surgery ○ Elevate HOB, oral hygiene; teach patient not to blow nose and signs of bleeding ● Fractures of the nose ○ S/S: bleeding, deformity, pain, swelling, obstruction of nasal passages ■ Look for cerebral fluid! ○ Complications: hematoma, infection, abscess, necrosis; not common ○ Management: cold compresses, packing bleed, surgery; examine chance of spinal fracture; maintain airway ○ Nursing: head elevation, cie packs, packing for bleeding, mouth rinses and oral care, analgesics ■ Patient should avoid sports for 6 weeks ○ Treatment: reduction of fracture, control epistaxis and edema ● Laryngeal obstruction ○ Causes: anaphylaxis, foreign body, tumor, angioedema, infection, subglottic stenosis ○ S/S: edema, lowered O2 sat, use of accessory muscles, choking ○ Treatment: subcutaneous epinephrine, tracheostomy, corticosteroid, oxygen, ice to reduce edema ○ Laryngeal cancer: half of all head and neck cancers, 13k cases annually and 3.6k deaths ■ Most common in those over 65, 4x more common in men; 55% lymph node involvement 16% bilaterally ■ Risk Chart 22-6 ● Carcinogens: tobacco, alcohol, asbestos, paint fumes, food and cement duse, chemicals, tar, mustard gas, leathers, metals ● Other factors: nutritional deficiency, history of alcohol abuse, genetic predisposition, gender, race (AA/white more common), weak immune system, age (>65) ■ S/S ● Early: Hoarseness of more than 2 weeks, Persistent cough, Sore throat or pain burning in throat; Raspy voice, lower pitch; Lump in neck ● Late: Dysphagia, dyspnea, Nasal obstruction, Persistent hoarseness, Persistent ulceration, Foul breath, General debilitation ■ Diagnosis: History and physical; Laryngoscopy; FNA biopsy; Barium swallow study; Endoscopy, CT, MRI, PET scan; Tumors grade and stage by TNM system ■ Treatment ● Stages 1 and 2: radiation, cordectomy, endoscopic laser excision, partial laryngectomy ● Stages 3 and 4: radiation, chemo, total laryngectomy ● Goals: cure, preservation of safe and effective swallowing, preservation of useful voice, avoiding permanent tracheostomy ● Surgical management ○ Vocal cord stripping: removal of mucosa to treat dysplasia, hyperkeratosis, leukoplakia; can cure lesions ○ Cordectomy ○ Laser surgery ○ Partial or complete laryngectomy ● Speech therapy: helps with loss or alteration of speech ■ Assessment: Health history; Physical, psychosocial, and spiritual assessment;Nutrition, BMI, albumin, glucose, electrolytes ● Literacy, hearing, and vision; may impact communication after surgery ● Coping skills and available support systems for patient and family after surgery ■ Postop: reduce anxiety, maintain airway, control secretions, support communication and nutrition/hydration, promote positive body image, self-care management ■ Complications: resp distress, hemorrhage, infection, wound breakdown, aspiration, tracheostomal stenosis Chapter 23: Chest and Lower Respiratory Disorder Management Atelectasis: closure or collapse of the alveoli; one of the most common abnormalities seen on a chest x-ray ● Acute: occurs most often in postop setting or in people who are immobilized and have a shallow, monotonous breathing pattern, are splinting, and have impaired cough ● Excess secretions or mucus plugs can also cause obstruction of airglow and result in atelectasis in an area of the lung, or any reduced ventilation or blockage ○ Atelectasis can be observed in patients with a chronic airway obstruction that impedes or blocks flow of air, this is more insidious and slower in onset ● Causes: foreign body, tumors, altered breathing, retained secretions, pain, alterations in small airway functions, prolonged supine positioning, increased abdominal pressure, reduced lung volumes from neuro or muscular disorders, defects, and surgical procedures ● Chronic: pulmonary infection may be present ● Symptoms: increasing dyspnea, cough, and sputum production ○ Central cyanosis (late), tachypnea, resp distress, plural pain, axiety ● Assessment and diagnosis: decreased breath sounds and crackles over affected area ○ X-ray may suggest diagnosis before symptoms appear ○ Pulse ox can drop below 90 ○ Effectiveness of oxygen therapy is assessed by ABG or pulse ox ● Prevention ○ Frequent turning ○ Early mobilization ○ Strategies to expand lungs and manage secretions ■ Frequent turning, early ambulation, lung-volume expansion maneuvers (deep-breathing exercises, incentive spirometry), and coughing, serve as the first-line measures to minimize or treat atelectasis by improving ventilation ■ Incentive spirometer use ■ Voluntary deep breathing, coughing ○ Pressurized metered-dose inhaler ○ Suctioning ● Medical and Nursing management ○ Improve ventilation and remove secretions ○ Turning, ambulation, expansion of lungs and coughing ○ PEEP, CPAP, bronchoscopyy BPT ○ ET intubation and mechanical ventilate ○ Thoracentesis ○ ICOUGH chart 23-2 ■ IS, cough/deep breathing, oral care, understanding, getting up 3x/day, HOB elevation Pulmonary infections ● SARS ● Lung abscess: most are complications of bacterial pneumonia ○ Symptoms: mild cough to acute illness, pleural friction rub, fever, foul smelling and bloody sputum, leukocytosis, pleurisy, dyspnea, weakness, anorexia, weight loss are all common ■ Crackles and friction rub, decreased breath sounds ○ Drainage through posturing and CPT ○ IV antibiotics 3+ weeks, oral antibiotics after 4-12 weeks ○ Nursing: administer meds, CPT, encourage deep breathing and cough exercise, diet high in protein and calories, provide emotional support ■ Oral hygiene, and antimicrobial therapy for pneumonia as preventative ● TB: infection of mycobacterium tuberculosis ○ <10k cases/yr in the US; most are from immigrant reactivations and originate outside of the US ■ Risk: close contact, immunocompromisation, substance abuse, those who have inadequate care, pre existing conditions, immigration or travel to countries with high incidence, overcrowded housing ■ Preventing transmission: ○ S/S: low grade fever, cough, hemoptysis, night sweats, fatigue, weight loss; purulent sputum, hemoptysis ■ Older adults may present with altered mental status, fever, anorexia, and weight loss ○ Assessment: history and physical ■ TB skin test: mantoux ■ Chest X ray ■ Sputum test + culture ■ Drug susceptibility test ○ Treatment: medications, table 23-4 ■ Isoniazid (can be used as preventative), rifampin, rifabutin, rifapentine, pyrazinamide, ethambutol ○ Nursing: promote airway clearance, activity, and nutrition; prevent transmission ■ Advocating adherence to treatment is key to treating and controlling spread; treatment can last two years. ■ Empty stomach or 1 hours before meals ■ ING should avoid tyramine and histamine (aged foods) ■ Rifampin alters coags, digoxin, OC, theophylline, and verapamil ■ Rifampin changes fluid colors ■ Monitor for hepatitis, neurologic changes, and rash ● Tracheobronchitis: inflammation of the trachea and bronchial tree; prevention by treatment of URIs ○ Mucopurulent sputum ○ Rx: antibiotics, suctioning, intubation, humidification, vapor therapy, steam, heat to chest, fluid intake increased; no antihistamines because they dry ○ Nursing: encourage bronchial hygiene such as coughing and fluids, precautions against overexertion ● Pneumonia: Inflammation of the lung parenchyma caused by various microorganisms, including bacteria, mycobacteria, fungi, and viruses ○ Classification ■ Community acquired (CAP): in community or within 48 hours of admission ■ Healthcare associated (HCAP): nonhospitalized patients but in acute ot LTC, receiving therapy that depresses immune response, wound care within 30 days, hemodialysis, infusion, or family member with MDRB ■ Hospital acquired (HAP): after 48 hours from admission ■ Ventilator associated (VAP): 48 hours after intubation ■ Aspiration pneumonia ■ Charts 23-3 and 23-4 ○ Risks Table 23-2 ■ Underlying disorders and diseases such as HF, DM, alcoholism, COPD, AIDS, and flu infection, CF; B-lactam therapy in the past 3 months, recent antibiotic therapy, corticosteroid use, lung disease, malnutrition ○ Manifestations: varies on type, organism, underlying disease ■ Streptococcal: Sudden onset of chills, rapidly rising fever, pleuritic chest pain, tachypnea, and respiratory distress ■ Viral, mycoplasma, or Legionella: relative bradycardia ■ Other: Respiratory tract infection, headache, low-grade fever, pleuritic pain, myalgia, rash, and pharyngitis ■ Orthopnea, crackles, increased tactile fremitus, purulent sputum ○ Assessment and diagnosis: ■ History, physical, X-ray, blood and sputum cultures, bronchoscopy ○ Med management: antibiotics, fluids, oxygen, antipyretics, antitussives, decongestants, and antihistamines ■ Other: hydration, antipyretics, antitussives, warm moist air, antihistamines, decongestant, rest, oxygen ■ Table 23-3 ○ Nursing: vitals, secretion characteristics, cough characteristics ■ Monitor for tachypnea and shortness of breath, new lung sounds, changes in mental status, fatigue, edema, dehydration, and heart failure ■ Gerontology: the diagnosis of pneumonia may be missed because the classic symptoms of cough, chest pain, sputum production, and fever may be absent or masked in older adult patients. In addition, the presence of some signs may be misleading ■ Plan for improves airway patency, increased activity, proper fluids and nutrition ■ Interventions: IS, nutrition, hydration, rest, activity, teaching, self-care, oxygen w/ humidity, coughing techniques, CPT, positioning ○ Vaccination: reduces incidence, hospitalizations for cardiac conditions, and death in older populations ■ Recommended for all adults >65 and adults >19 who have impaired immune system ■ Other preventative measures: Table 23-2 ○ Complications: shock, hypovolemia, pleural effusion, empyema, delirium ● Aspiration: inhalation of foriegn material into the lungs, can lead to pneumonia ○ s/s: tachycardia, dyspnea, central cyanosis, hypertension, hypotension, and potential death ○ Risk Chart 23-5: seizures, brain injury, decreased LOC, flat position, stroke, swallowing disorders, cardiac arrest ○ Interventions: elevate HOB, don't stimulate gag reflex, check tube patency, thick fluids for those who have dysphagia ○ Prevention: compensate for absent reflexes through thick liquids, positioning, oral care; low use of sedatives; check for residuals ● Pleural conditions: involve membrane of lungs and chest wall, pleural space; sharp knifelike pain ○ Pleurisy: inflammation of the pleurae ■ Pain related to respiratory movement: taking deep breath, coughing, and sneezing worsens pain; pain is usually only on one side and may become minimal or absent when breath is held ● Pain may disappear or decrease as pleural fluid develops ■ Friction rub can be heard with stethoscope early on but may disappear ■ Diagnosis: X-ray, sputum analysis, thoracentesis ■ Treatment: underlying cause, provide analgesia, teaching to splint ribs when coughing with hands or pillow, comfort turning ○ Pleural effusion: fluid collection in pleural space usually secondary to heart failure, TB, pneumonia, pulmonary infections ■ S/S: Fever, chills, pleuritic pain, dyspnea; dyspnea, coughing, difficulty lying flat ● Decreased or absent breath sounds; decreased fremitus; and a dull, flat sound on percussion ● May have tracheal deviation away from affected side ■ Transudative effusion is most commonly from HF ■ Exudative effusion is commonly from inflammation related to infection or tumors ■ Diagnosis: Chest x-ray, chest CT, and thoracentesis ■ Treat underlying cause: thoracentesis, relieving dyspnea and discomfort, prevention of reaccumulation of the fluid, pleurectomy, chemical pleurodesis ■ Nursing: record thoracentesis fluid, send for labs, if chest tube is used monitor ○ Empyema: Accumulation of thick, purulent fluid in pleural space; complication of bacterial pneumonia or lung abscess ■ Acutely ill and has signs and symptoms similar to those of an acute respiratory infection or pneumonia; can also result from chest trauma, hematogenous infection of pleural space, nonbacterial infection, and iatrogenic causes ■ Chest auscultation demonstrates decreased or absent breath sounds over the affected area, decreased fremitus ■ Diagnosis: Chest CT and a diagnostic thoracentesis ■ Treatment: Drain fluid and administer antibiotics for 4 to 6 weeks Pulmonary edema: defined as abnormal accumulation of fluid in the lung tissue, the alveolar space, or both. It is a severe, life-threatening condition. ● Classified as cardiogenic or noncardiogenic ● Noncardiogenic pulmonary edema: occurs due to damage of the pulmonary capillary lining. It may be due to direct injury to the lung (e.g., chest trauma, aspiration, and smoke inhalation), hematogenous injury to the lung (e.g., sepsis, pancreatitis, multiple transfusions, and cardiopulmonary bypass), or injury plus elevated hydrostatic pressures ● Management of noncardiogenic pulmonary edema mirrors that of cardiogenic pulmonary edema; hypoxemia may persist despite oxygen due to intrapulmonary shunting of the blood ARDS: Characterized by sudden, progressive pulmonary edema, increasing bilateral lung infiltrates visible on chest x-ray, absence of an elevated left atrial pressure, rapid onset of severe dyspnea, hypoxemia that does not respond to supplemental oxygen therapy; reduced lung compliance is common ● Risk factors Chart 23-9 ○ Aspiration, drug ingestion or overdose, hematologic disorders, prolonged inhalation of high concentrations of oxygen, smoke, corrosive substances , local infection, metabolic disorders, shock, trauma, surgery, fat or air emboli, sepsis ■ 26-58% mortality caused by MODS ● Patho: severe mismatch of ventilation-perfusion, alveolar collapse, lung compliance decreases, hypoxemia results; pulmonary vasoconstriction, microemboli, and pulmonary hypotension lead to dead space ● Medical management: treatment of underlying disease ○ Intubation and ventilation with PEEP ○ Hypovolemic treatment ○ Prone positioning for oxygenation, reposition often ○ Nutritional support, enteral feedings ○ Reduce anxiety ● Nursing: close monitoring in ICY, positioning, reduce anxiety, vent care Pulmonary hypertension: elevation of pulmonary arterial pressure and secondary right heart ventricular failure ● Classification ○ Group 1: Pulmonary Arterial Hypertension (PAH) ■ Sporadic idiopathic PAH ■ Heritable idiopathic PAH ■ Drug and toxin-induced PAH ■ PAH due to diseases such as connective tissues disorders, HIV infection, portal hypertension, congenital heart disease ○ Group 2: PH due to left heart disease ■ Systolic dysfunction ■ Diastolic dysfunction ■ Valvular heart disease ○ Group 3: PH due to chronic lung diseases and/or hypoxemia ■ Chronic obstructive pulmonary disease ■ Interstitial lung disease ■ Mixed restrictive and obstructive lung disease ■ Sleep disordered breathing ○ Group 4: Chronic thromboembolic pulmonary hypertension (CTEPH) ■ Due to thromboembolic occlusion of the proximal or distal pulmonary vasculature ○ Group 5: PH with unclear multifactorial mechanisms ■ Hematologic disorders ■ Systemic disorders (e.g., sarcoidosis) ■ Metabolic disorders ● S/S: dyspnea, substernal chest pain, weakness, fatigue, syncope, hemoptysis, RHF symptoms, anorexia and abd pain in RUQ ● Assessment and diagnosis: hx, physical, X-ray, pulmonary function studies, ECG, echocardiogram ○ Right heart cath to assess hemodynamic abnormalities (pressure >25mm) ○ ECG reveals right ventricular hypertrophy, right axis deviation, and tall peaked P waves in inferior leads; tall anterior R waves; and ST-segment depression, T-wave inversion, or both anteriorly ● Management: CCBs, prostanoise, endothelin antagonists, phosphodiesterase 5 inhibitors ○ Surgery: lung transplant, heart-lung transplants ● Nursing: identify those at risk such as COPD, PE, congenital heart disease, and mitral valve disease patients ○ Oxygen teaching and admin ● Cor pulmonale: RSHF/ hypertrophy of the heart Pulmonary Embolism: Obstruction of the pulmonary artery or one of its branches by a thrombus (or thrombi) that originates somewhere in the venous system or in the right side of the heart; best defined by degree of hemodynamic instability ● Inflammatory process obstructs area, results in diminished or absent blood flow ○ Bronchioles constrict, further increasing pulmonary vascular resistance, pulmonary arterial pressure, and right ventricular workload ● Ventilation–perfusion imbalance, right ventricular failure, shock occurs ● Risk factors: trauma, surgery, pregnancy, heart failure, hypercoagulability, immobility, venous stasis ● S/S: dyspnea most common symptom, tachypnea most common sign for possible pulmonary embolism, chest pain, anxiety, fever, apprehension, cough, diaphoresis, hemoptysis, and syncope ● Assessment and diagnostic: ECG (ST-T wave abnormalities), x-ray, pulse ox, ABG; V/Q scan ○ D-dimer assay, pulmonary arteriogram ● Prevention: exercise to avoid venous stasis, early ambulation, stockings ● Treatment: Measures to improve respiratory and vascular status; Anticoagulation and thrombolytic therapy; Surgical interventions; oxygen, anticoag therapy; thrombolytic therapy Sarcoidosis: interstitial lung disease that includes granulomatous disease of unknown etiology ● Noninfectious organized collection of macrophages appear as nodules ● Low compliance, inpaired diffusion, reduced lung volume ● S/S: dyspnea, hemoptysis, congestion, fatigue, anorexia, weight loss, uveitis, joint pain, fever, anorexia, fatigue, weight loss ○ Lesions can also appear on skin, liver, spleen, kidney, and in CNS ● Assessment and diagnosis: biopsy, X-ray, XT, pulmonary function tests, ABGs ● Medical management: corticosteroids Pneumoconiosis: occupational lung diseases; nonneoplastic alteration of lung resulting from inhalation of mineral or inorganic dust; best define ● Silicosis; Coal worker’s pneumoconiosis; Asbestos ● Preventable, not treatable ○ Reduce exposure and use protective gear and devices ● Find out: exposure agent, length of time, symptoms, lack of other explanations for symptoms ● Nursing: advocate for education and preventative measures ● Table 23-5 Lung Cancer ● Leading cause of death in the United States; 1.4 cancer deaths ○ >85% caused by cigarette smoke ● Classification: 15% SCLC and 85% NSCLC tumors ○ NSCLC: ■ Squamous cell cancer: usually more centrally located and arises more commonly in the segmental and subsegmental bronchi ■ Adenocarcinoma is the most prevalent carcinoma; occurs peripherally as peripheral masses or nodules and often metastasizes ■ Large cell carcinoma (also called undifferentiated carcinoma): fast-growing tumor that tends to arise peripherally ■ Bronchoalveolar cell cancer: found in the terminal bronchi and alveoli and is usually slower growing compared with other bronchogenic carcinomas ● S/S: chronic cough, dyspnea, hemoptysis, pain, recurring fever, chest pain and tightness, hoarseness, dysphagia, head and neck edema ● Assessment and diagnosis: x-ray, CT, sputum cytology (rare), bronchoscopy, fine-needle aspiration, any number of scans ● Treatment: ○ Surgery (Chart 23-13: types of lung resection: lobectomy, bilobectomy, sleeve resection, pneumonectomy, segmentectomy, wedge resection, chest wall resection); Radiation and Chemotherapy ○ Palliative care ● Nursing care ○ Airway clearance, relieve dyspnea, reduce fatigue, pain management, psychological support ● Tumors of mediastinum have similar treatments, symptoms, management Chest trauma ● Blunt trauma: often results in hypoxemia, hypovolemia, cardiac failure from tamponade, contusion, or increased intrathoracic pressure ● Sternal, rib fractures: pain, crepitus, tenderness, ecchymosis, swelling, and deformity ○ Splint chest by breathing in shallow manner and avoiding moving leads to diminishes ventilation, atelectasis, pneumonitis, hypoxemia ○ Management: surgical fixation is rarely necessary ■ Small segments: clear airway measures, pain relief ■ Mild-moderate: fluid replacement and monitor intake, physiotherapy ■ Severe flail chest: ET intubation, ventilation, stabilize chest ● 2 or more ribs factures at 2 or more sites: BIND ● Pulmonary contusion: common injury associated with flail chest; damage to lung tissues resulting in hemorrhage and edema; results in fluid in interstitial and alveolar spaces ● Penetrating trauma ● Pneumothorax: can be spontaneous or traumatic ○ Traumatic: laceration in lung allows air to escape ■ Open pneumo: wound open on chest wall ○ Tension pneumo: air drawn in from lacerated lung or small opening in chest wall ○ Simple pneumo: air enters pleural space through breach of pleura ■ Associated with emphysema and diffuse interstitial lung disease ■ sudden onset of chest pain is an initial characteristic symptom ○ Pleuritic pain that is usually sudden, can have minimal distress, dyspnea, use of accessory muscles, diminished breath sounds, deviation of trachea, hypotension, tachycardia, and diaphoresis Chapter 24: Management of Patients with Chronic Pulmonary Disease COPD: a slowly progressive respiratory disease of airflow obstruction; preventable and treatable but not curable or reversible; involves the airways and pulmonary parenchyma ● Pathophysiology: scar tissue in airways results in narrowing, scar tissue in parenchyma decreased elastic recoil (compliance); scar tissue in the pulmonary vasculature causes thickened vessel lining and hypertrophy of the smooth muscle (pulmonary hypertension) ● Emphysema: abnormal distension of air spaced beyond the terminal bronchioles with destruction of the walls of the alveoli ○ Decreased alveolar surface area increases “dead space”, impairs oxygen diffusion ■ Hypoxemia and hypercapnia result ○ Increased pulmonary artery pressure may cause right sided heart failure (cor pulmonale) ○ S/S: Wheezing ● Chronic Bronchitis: cough and sputum production for at least 3 months in two consecutive years; irritation causes the mucus glands and goblet cells to increase in number ○ Ciliary function reduced, bronchial walls thicken and airways narrow, mucous may plug airways ○ Alveoli become damaged, fibrosed, and alveolar macrophage function diminishes ○ Increased risk for respiratory infection ○ S/S: Excess sputum and productive cough ● Chronic cough, sputum, and dyspnea; weight loss, barrel chest, clubbing of the fingers ● Tripod positioning ● Assessment ○ Health history (Chart 24-2) ○ Pulmonary function tests ○ Spirometry ○ ABG ○ X-ray ○ Alpha1 antitrypsin screening for genetic mutation in patients under 45 or family history - EMPHYSEMA ● Complications: Pneumonia, atelectasis, pneumothorax, cor pulmonale, respiratory insufficiency and failure ● Management: promote smoking cessation, manage exacerbations, supplemental oxygen, flu and pneumonia vaccines, pulmonary rehab ○ Chart 24 -1 Reducing Risk Factors; environmental risk factors include prolonged and intense exposure to occupational dusts and chemicals, indoor air pollution, outdoor air pollution ○ Surgery: lung volume reduction, transplant (COPD), bullectomy ○ Meds: ■ bronchodilators, MDIs ● Beta-adrenergic agonists ● Muscarinic antagonists (anticholinergics) ● Combinations ■ Corticosteroids: short term in COPD only ■ Antibiotics ■ Mucolytics ■ Antitussives ● Nursing: review diagnostic tests, improve breathing pattern and activity tolerance, medication education, care plan ○ Achieving airway clearance-changes in the airway require that the nurse monitor the patient for dyspnea and hypoxemia ○ Resping PaO2 60mm or higher, Sat 90% ○ Chart 24-4: how to use an inhaler Cystic Fibrosis: most common autosomal recessive disease in causations; the mutation changes chloride transport which leads to thick secretions in the lungs, pancreas, liver, intestines, and reproductive tract ● Genetic screening and counseling for couples at risk and to detect carriers ● Respiratory infections are the leading cause of morbidity and mortality ● S/S: productive cough, wheezing, hyperinflation of lungs, obstructive disease results in pulmoary function tests ● Medical Management ○ Chronic: control infections, antibiotics ○ Acute: aggressive therapy involves airway clearance and antibiotics based on results of sputum cultures ○ Anti-inflammatory agents; corticosteroids (inhaled, oral, IV during exacerbations); Inhaled bronchodilators ○ Oral pancreatic enzyme supplementation with meals ○ Cystic fibrosis transmembrane conductance regulator (CFTR) modulators are a new class of drugs and help to improve function of the defective CFTR protein ● Nursing ○ Strategies that promote removal of pulmonary secretions ○ CPT and breathing exercises ○ Remind patient to reduce risk factors for resp infection ○ Adequate fluid and electrolyte intake ○ Palliative care ○ Discuss end-of-life issues and concerns Bronchiectasis: chronic irreversible dilation of the bronchi and bronchioles from destruction of muscles and connective tissue ● Causes: obstruction, pulmonary infections, diffuse airway injury, genetic disorders, abnormal host defenses, and idiopathic ○ S/S: prolonged history of chronic cough with sputum, purulent sputum in copious amounts, clubbing of the fingers ○ Dx: CT ○ Management: postural drainage, CPT, smoking cessation, antimicrobial therapy, bronchodilators and mucolytics ■ Focus on alleviating symptoms and clearing secretions ■ Teaching: smoking cessations, early signs/symptoms of respiratory infections, and conserving energy ● Postural drainage: patients and families are taught to perform postural drainage and to avoid exposure to people with upper respiratory or other infections Asthma: chronic inflammatory disease of the airways that causes hyperresponsiveness, mucosal edema, and mucus production ● Inflammation leads to cough, chest tightness, wheezing, and dyspnea ● Reversible spontaneously or with treatment ● Allergy is the strongest predisposing factor ● S/S: cough, dyspnea, wheezing ○ Exacerbations: cough, wheezing, chest tightness, dyspnea, diaphoresis, tachycardia, hypoxia, central cyanosis ● Medications ○ Quick relief: Beta 2 Adrenergic agonists, anticholinergics ○ Long acting: corticosteroids, long acting B2 adrenergic antagonists, leukotriene modifiers ● Patient teaching: ○ Proper inhalation techniques ○ Implementing an action plan ○ When and how to seek assistance ○ How to perform peak flow monitoring: measure highest airflow during a forced expiration with peak flow meter ○ Identification, recognising, and avoiding triggers ● Status asthmaticus: magnesium sulfate as bronchodilator and smooth muscle relax only for short term use ● Bronchial Thermoplasty for uncontrolled asthma ● Nursing: Assessing airway, skin turgor, administration of fluids Chapter 25: Assessment of Cardiovascular Function Review of Anatomy and Physiology ● Three layers of the heart ○ Endocardium: inner layer of endothelial tissue that lines heart and valves ○ Myocardium: muscular middle layer made of myocytes ○ Epicardium: outer layer ○ Pericardium ● Four chambers ○ Right Atrium: deoxygenated blood from the body ○ Right Ventricle: deoxygenated blood to the lungs ○ Left Atrium: oxygenated blood from the lungs ○ Left Ventricle: oxygenated blood to the body ■ 2-3x more muscular than the right ventricle ○ Atria are thinner than ventricles ● Valves ○ Atrioventricular: separate the atria and ventricles; open during diastole, close during systole ■ Tricuspid: right side; three leaflets ■ Bicuspid (mitral): left side; two leaflets ○ Semilunar: close during diastole, open during systole; 3 leaflets ■ Pulmonic: right to lungs ■ Aortic: left to body ○ Papillary muscles and chordae tendineae help open and close ● Coronary Arteries: supply the heart with needed oxygen and nutrients ○ Heart uses 70-80% of delivered oxygen ○ Perfuse during diastole, increased HR decreases perfusion time and increases risk for MI ○ Left coronary artery ■ Three branches ● Main ● Left anterior descending ● Circumflex: circles around to the lateral left wall of the heart ○ Right coronary artery ■ Main artery travels down to and supplies blood to the inferior wall ■ Posterior descending artery: supplies blood to the posterior ○ Blood returned through coronary sinus veins into RA ● Cardiac Conduction: begins at SA node, moves to AV node, bundle of His, bundle branches, purkinje fibers left and right ○ Depolarization: electrical activation of the cell caused by influx of sodium and outflux of potassium ○ Repolarization: return of cell to resting phase while potassium re-enters and sodium exits ○ Refractory times ■ Effective refractory period: phase in which cells are incapable of depolarizing ● Time in phase 0 to 3 ■ Relative refractory period: phase in which cells require stronger than normal stimulus to depolarize ● Short time in phase 3 ○ ● Hemodynamics: blood flows from regions of higher pressure to lower pressure, pressure are generated during diastole and systo ● Cardiac cycle: events that occur from the beginning of one heartbeat to the next ○ Diastole: all four chambers relax simultaneously, allowing the ventricles to fill ○ Atrial Systole: contraction of the atria ○ Ventricular Systole: contraction of the ventricles ● Cardiac output: amount of blood pumped by ventricle in liters per minute ○ CO = SV x HR ○ Stroke volume: amount of blood ejected with each heartbeat ■ Dependent upon ● Preload: degree of stretch of cardiac muscle fibers at end of diastole; LV end-diastolic pressure ○ Frank-starling law: muscle fibers stretch as volume increases, resulting in stronger contraction and greater SV, maintained until physiologic limit of muscle is reached ■ Greater length of stretch means greater degree of shortening ○ Decreased by reduction in blood volume returning to ventricles (hypovolemia) ● Afterload: resistance to ejection of blood from ventricle ○ Affected by systemic vascular resistance and pulmonary vascular resistance, vasodilation, etc ○ Inverse relationship with preload ● Contractility: ability of cardiac muscle to shorten in response to electrical impulse, force generated by contracting myocardium ○ Increased by catecholamines, SNS, medications ○ Increased contractility results in increased stroke volume ○ Decreased by hypoxemia, acidosis, medications ○ Ejection fraction: percent of end diastolic volume ejected from the LV after each beat; 55-65% normal ■ <40% indicates decreased LV function, HF ○ Influencing factors ■ Autonomic nervous system ■ Baroreceptors Assessment ● Health history ○ Common symptoms of CV disease ■ Chest pain or discomfort ● Location ● Severity ● Duration ■ Pain/discomfort in other areas of the upper body ■ SOB/dyspnea ■ Peripheral edema ■ Weight gain ■ Abd distention ■ Palpitations ■ Fatigue ■ Dizziness, syncope ■ Changes in LOC ○ Other changes ■ Changes within the last few years ■ Any checkups/testing done ○ Medications ○ Nutrition ■ BMI ■ Self-monitoring ■ Labs ■ Eating habits ○ Sleep/rest ■ Orthopnea ■ Paroxysmal nocturnal dyspnea ■ Sleep disorders and breathing ○ Self-perception/ self-concept ■ Effects on life ■ Perception of condition ■ Perception of influence ■ Feelings ○ Elimination ■ Nocturia is common with HF ○ Changes in activity/exercise symptoms ○ Home environment: things like stairs ● Demographics ● Family/genetic history ● Cultural/social factors ○ Roles and relationships ○ Coping and stress: stress tolerance, anxiety, depression ○ Sexual dysfunction from medication, fatigue, etc ● Risk factors ○ Modifiable ■ Nutrition ■ Activity/exercise ■ Sleep/rest ■ Smoking ○ Non-modifiable ● Physical assessment ○ General appearance ○ Skin and extremities ■ Peripheral pulses ■ Edema ■ Signs of obstruction ● Pain, pallor, pulselessness, paresthesia, poikilothermia ■ Cap refill ■ Clubbing of nails ■ Hair loss, skin color changes, dry or scaly skin, ulcerations ○ Pulse pressure: difference between systolic and diastolic ■ <30mm signifies significant reduction in cardiac output ○ BP ■ Orthostatic changes ○ Arterial pulses ■ Rate, rhythm, force, symmetry, contour (carotid) of wave ○ JVD, JV pulses: estimate right sided heart function ○ Heart: inspection, palpation, auscultation of the Z ■ Sounds: S1 heart best at apex, AV close; S2 heart at base/pulmonic area, semilunar close ● Murmurs, rubs, extra sounds S3 and S4, gallops ○ Brief assessment of other symptoms ■ Lung sounds ■ Abd distension ■ Hepatojugular reflux ■ Bladder distension ● Gerontological considerations ○ Decreased elasticity of arteries, loss of connective tissue = more palpable peripheral pulses ○ COPD deformities, kyphonsis - may affect impulse palpation in chest ○ Hypertension common ■ Associated S4 is common, S2 split can be heard ○ Orthostatic hypotension ● Lab tests Table 25-4 ○ Cardiac biomarkers ■ CK, Ck-MB ■ Myoglobin ■ Troponin T ■ Troponin I ○ Blood chem, hematology, coagulation ■ BUN, calcium, creatinin, magnesium, potassium sodium ■ PTT 60-70s, aPTT 20-39s ■ PT: 9.5-12s ■ INR: 1 ■ CBC, platelets, WBC, HCT, HGB ○ Lipids ○ BNP: regulates P and fluids ○ C-reactive proteins: responsive to systemic inflammation, predicts CVD risk ○ Homocysteine: amino acid linked with atherosclerosis because it damages endothelial lining and promotes thrombus ■ Elevation means high risk for CAD, stroke, PVD but is not independent predictor of CAD ■ Genetic factors and diet low in folate, B6, B12 are associated with elevated levels ■ 12 hour fast before measurement ■ <12 mcmol/L optimal, 12-15 borderline, >15 high risk ● Electrocardiography ○ 12 lead: diagnose dysrhythmias, conduction abnormalities, and chamber enlargement, as well as myocardial ischemia, injury, or infarction. It can also suggest cardiac effects of electrolyte disturbance and antiarrhythmic meds ○ Continuous monitoring: ■ Hardwired: EDs, critical care, progressive care ● Monitor multiple leads simultaneously, monitor ST ● Provided graded visual and audible alarms ● Interpret and store alarms ● Trend data over time ● Print copies ■ Telemetry: nursing care, outpatient programs ● Wireless system, allows patient to ambulate while one or 2 leads are monitored ● Leads 2 and V1 are most commonly monitored ■ Lead systems:3 ,4, 5 lead systems ■ Ambulatory monitoring: continuous or intermittent home monitoring, can evaluate pacemaker functioning, identify etiology of syncope or palpitations, evaluate treatment effectiveness ○ Nursing interventions: reduce alarm fatigue, ensure safety, ensure free from artifacts, assess for skin changes near electrodes ■ Respond to and correct all alarms immediately ● Stress testing: determines presence of CAD, cause of chest pain, functional capacity, effectiveness of meds, occurrence of dysrhythmias and evaluates goals ○ Patient walks on treadmill with intensity progressing according to protocols ○ ECG, vitals, symptoms monitored: 2 or more leads ○ Terminated when target HR is achieved ■ If chest pain develops before target, stop exam and monitor patient ○ Contraindications: unstable angina, MI within 48 hours, uncontrolled dysrhythmias with hemodynamic compromise, aortic stenosis, myocarditis, pericarditis, decompensated HF ○ Nursing: fast for 3 hours before, exercise clothes and method review, monitor until stable after test ● Pharmacologic stress test: vasodilators given to mimic exercise ○ Adenosine, dobutamine, dipyridamole, regadenoson ○ Aminophylline reversal ○ Nursing: no caffeine 24 hours, no food 3 hears before ● Diagnostic testing ○ CXR: size, positioning, contour of heart; calcifications and physiological alterations ○ Radionuclide imaging ■ Myocardial perfusion imaging: determines if perfusion is compromised, evaluates damage after Mi ● Positron emission tomography (PET scan) ○ Lower radiation doses, faster, better pictures, but limited amounts of facilities able to do it ○ One tracer for flow and one for metabolic function ○ Glucose needs to be in normal range ○ No alcohol or caffeine 24 hours ○ Baseline scan ○ Glucose monitoring ● Single photon emission computed tomography (SPECT): more widely available and easier to perform; diagnostic and prognostic value better established ○ Painless, noninvasive ○ Arms over heads, injection of tracer, 30 mins of scanning ● Reversible vs fixed defects ○ Taken at rest and during stress ● Pregnant or nursing women should not undergo ● Tests of ventricular function and wall motion ○ ERNA/MUGA scanning: records heart during heartbeats to evaluate function, wall motion, ejection fraction ○ Computer Tomography (CT): Cross sectional X-rays ■ Ct angio: enhances visualization, used with caution in kidney insufficiency ● Evaluates arteries for stenosis, aorta for aneurysm or dissection, graft patency after CABG, veins in those with afib, and abnormalities in structure ● EBCT: calculated calcium store, useful for those with low risk for CAD events ● Nursing: expect lushing, metallic taste, nausea, bradycardia with contrast; be prepared to hold breath ○ Magnetic resonance angiography: physiologic and anatomic; valuable in diagnosing diseases of the aorta, heart muscle, and pericardium, as well as congenital heart lesions. The application of this technique to the evaluation of coronary artery anatomy is limited because the quality of the images are distorted by respirations, the beating heart, and certain implanted devices ■ Cannot visualize small distal coronary arteries ■ No patients with metal or pacemakers, jewelry must be removed ■ Patient must be motionless ○ Echocardiography ■ Noninvasive ultrasound that measures ● Ejection fraction ● Size, shape of cardiac structures ● Motion of cardiac structures ■ Transthoracic: poor quality images ■ Transesophageal: better images, sedation and anesthetic (topical) needed ● Important first line eval for CVD, HR, valve disease, dysrhythmia ● Nursing: NPO 6 hours prior, consents, IV lines, vitals, LOC monitoring, ECG and O2 ○ Bed rest 45 degrees after ■ Nursing: patient may be asked to turn onto left side and hold their breath ○ Cardiac catheterization: diagnoses structural and functional diseases of the heart and great vessels ■ Involves radiopaque catheter insertion, fluoroscopy ■ Right heart cath: pulmonary artery pressure and oxygen sat may be obtained; biopsy of myocardial tissue may be obtained; RV and valve functions ■ Left heart cath: ● Involves use of contrast to visualize patency of arteries and LV function ● Premedicate with antihistamines and steroids if previous reaction to contrast ○ Sodium bicarb and acetylcysteine can protect renal tubules from acidic environment ● Eval aortic arch, branches, coronary artery patency, LV function, valves function ● Angiography performed ■ Labs needed: metabolic, renal, coag studies, CBC ■ Risk for contrast nephropathy: increased baseline serum creatinine by 25% or more or absolute increase by .5mg/dL within 48-72 hours ■ Interventions - Nursing ● Patient needs to fast for 8-12 hours before ● Observe site for bleeding, hematoma ● Assess peripheral pulses ● Evaluate temp, color, and cap refill of affected extremity ● Screen for dysrhythmias ● Maintain bed rest 2 to 6 hours ● Instruct patient to report chest pain, bleeding ● Monitor for contrast-induced nephropathy ● Ensure patient safety ○ Electrophysiology testing: distinguish atrial vs ventricular tachy when 12 lead can’t; evaluate how life threatening dysrhythmias are induced; evaluate AV node function and med effeciveness ○ Hemodynamic monitoring ■ Central venous pressure: measure pressure in vena cava or right atrium (2-6mmHg normal) ● >6 increased preload of RV ● <3 reduced RV preload ● Most valuable when monitored over time and correlated with patient status ● Rises with hypervolemia ■ Pulmonary artery pressure: assess LV function, diagnosing etiology of shock, eval response to medical interventions, administer meds, monitor RA pressure with proximal lumen ● Fluoroscopy may be used ● Right subclavian vein commonly used ■ Intra-arterial BP monitoring: critically ill hypertension and hypotension monitoring ● Allen’s test before using radial artery ■ Minimally invasive cardiac output monitoring devices ● Check transducer, flush system and pressure bag, ● Pressure system should be free of bubbles, check stopcock of transducer is level with atrium using phlebostatic axis ● Establish zero reference point by placing on axis, opening transducer to air, activation zero function key ■ Arterial catheters introduced into vessels/chambers, connected to pressure system that includes ● Disposable flush (saline/heparin) ● Pressure bag around flush that in maintained at 300mm Hg, delivers 3-5ml/hour ● Transducer to convert pressure into electrical signal ● Amplifier that increases signal for display on oscilloscope ■ Complications: pneumothorax, infection, air embolism, infection ■ Nursing: monitor for ischemia (distal) and obstruction, hemorrhage, ecchymosis, dissection, air embolism, pain, arteriospasm, blood loss, infection ○ Minimally invasive: several types Chapter 26: Management of Patients with Dysrhythmias and Conduction Problems Dysrhythmias: disorders of formation or conduction (or both) of the electrical impulses within the heart ● Cause disturbances of ○ Rate ○ Rhythm ○ Blood flow ○ Hemodynamics ● Diagnosis ○ Analysis of electrographic waveform ● Normal electrical conduction ○ SA node -> AV node ○ AV node -> Bundle of his ○ Bundle -> right and left bundle branches ○ Branches -> Purkinje fibers ○ Depolarization: systole, contraction ○ Repolarization: diastole, relaxation ● Types ○ Atrial ■ Premature atrial complex ■ Atrial flutter ■ Atrial fibrillation ○ Ventricular ■ Premature ventricular complex ■ Ventricular tachycardia ■ Ventricular fibrillation ■ Ventricular asystole ● Conduction abnormalities ○ First degree AV block: the PR is constant but greater than 0.20 seconds ■ Atrial impulses conducted slower than normal ○ Second degree AV block, Tpe 1 (wenckebach): progressively longer PR durations until there is a nonconducted P wave ■ Repeating pattern in which all but one of the atrial impulses conducted through AV node (⅘ conducted); each impulse takes longer than the one before ■ QRS normal but can be abnormal ■ PR becomes longer and longer until there is a P wave without QRS ■ P:QRs 3:2, 4:3, 5:4, so on ○ Second degree AV block, Type 2: constant PR interval and presence of more P than QRS ■ Only some atrial impulses conducted ■ P:QRS 2:1, 3:1, so on ■ QRS usually abnormal but can be normal ○ Third degree AV block: irregular PR intervals ■ No atrial impulse conducted through AV into ventricles ■ One impulse stims ventricles and another strims atria ● AV dissociation (can occur during VT) ■ ECG ● Ventricular rate is lower than atrial rate ● PP regular, RR regular, neither are equal to each other ● QRS normal with junctional rhythm, QRS abnormal with idioventricular rhythm ● PR very irregular ● More P than QRS ○ Medical management: treat cause, increase HR to maintain output ● Causes ○ Contributing factors: ■ Manipulation of the autonomic nervous system ● SNS increases HR (+ chronotropy), increases conduction through AV (+ dromotropy), increases force of myocardial contraction (+ inotropy) ○ Also constricts peripheral vessels, increasing BP ● PSNS: reduces HR, conduction, and force ○ Dilates arteries, lowering BP ECG ● Obtaining ■ Medications ■ Serum imbalances ○ Electrodes reduce skin’s electrical impedance, adhere to skin ○ Do not clean with alcohol ○ Gently abrade with gauze to expose inner conductive layer ○ Clip chest hair ● Electrode placement ○ ○ Artifact results from poor adhesion ● Types ○ Continuous: typically uses 2-5 electrodes ○ 12 lead: reflects electrical activity primarily in the LV ■ Attached to ECG machine at bedside for intermediate recording ○ Cardiac monitor at bedside for continuous: hardware monitoring, ICU typically ○ Small box that patient carries and continuously transmits by radio waves: telemetry ○ Small lightweight tape recorder-like machine that patient wears and records that is later viewed with scanner: ambulatory or holter monitor ● Interpretation ○ P wave: normal <.11s ■ Represents atrial depolarization, SA -> AV conduction ○ QRS complex: normally .04-.12s, represents ventricular depolarization ■ Q <.04s <25% R wave amplitude ○ T wave: represents ventricular repolarization where cells regain negative charge or resting state ○ U wave: rarely seen but sometimes seen in patients with hypokalemia, hypertension, or heart disease ■ Thought to represent repolarization of purkinje fibers ○ PR interval: normal .12-.2 seconds ■ Represents SA stimulation, atrial depolarization, conduction through AV before ventricular depolarization ■ Beginning of P to beginning of QRS complex ○ ST segment: early ventricular repolarization ■ Lasts from end of QRS to beginning of T ■ Normally isoelectric but depression and elevation can occur with STEMI, cardiac damage, sign of ischemia ○ QT interval: total time for ventricular depolarization and repolarization ■ Beginning of QRS to end of T ■ Usually .32-.4s if HR is 65-95 bpm ○ TP interval: isoelectric normally ■ End of T to beginning of P ○ PP interval: Beginning of P to P ■ Measures atrial rate and rhythm ○ RR interval: QRS to QRS ■ Measures ventricular rate and rhythm. ○ waves <5mm lowercase, >5mm uppercase ● Normal sinus rhythm: impulse originates in SA node and occurs at a rate of 60-100 bpm ○ Conduction: travel of electrical impulse ○ AV node slows impulse to allow atria to fill ventricles (atrial kick); accounts for ⅓ of ventricular volume ejected ○ When analyzing consider ■ Ventricular and atrial rate ■ Ventricular and atrial rhythm ■ QRS shape and duration ■ P waves and P:QRS ratio ■ PR interval ■ QRS interval ● Sinus dysrhythmias: originate in SA node ○ Bradycardia: slower than normal rate ■ Causes ● Lower metabolic needs: sleep, athletic training, hypothyroidism ● Vagal response: vomiting, suctioning, severe pain, bearing down to pass stool, etc ● Medications: CCBs, BBs, amiodarone ● SA node dysfunction (sick sinus syndrome) ● Increased ICP ● CAD; MI of the inferior wall, Decompensated HF ● Hypoxemia ■ Treated if presents with symptoms: SOB, angina, altered mental status, hypotension, ST changes, PVCs ● Medication: .5mg atropine every 3-5min via IV bolus for max of 3mg ● Transcutaneous pacing ● Catecholamines ■ Characteristic normal, just reduced rate ○ Tachycardia: faster than normal rate, other things normal ■ Causes ● Physiologic of psychological stress: blood loss, anemia, shock, hypovolemia, hypervolemia, HF, pain, hypermetabolic states, fever, exercise anxiety ● Medications, stimulants, illicit drugs ● Enhanced SA automaticity, sympathetic response, reduced parasympathetic tone that doesn't match demands: inappropriate sinus tachycardia ● ANS dysfunction ○ POTS: increase in HR by 30bpm or more when moving from sitting to standing ■ Treatment: determined by severity of symptoms, cause ● Usually treated if persistent and causing hemodynamic instability ○ Synchronised cardioversion ● Vagal maneuvers: carotid sinus massage, gagging, bearing down, forceful and sustained coughing, cold stimulus on face ● Adenosine: only if QRS is monomorphic ● BBs, CCBs rarely used ● Catheter ablation of SA node ● Sinus arrhythmias: SA node impulse is irregular in rhythm ○ Rate increases with inspiration and decreases with expiration ○ Not normally treated because does not cause significant hemodynamic effect ● Atrial dysrhythmias: originate in foci within atria and not SA node ○ Premature atrial complex: impulse starts in atrium before sinus node ■ Causes: caffeine, alcohol, nicotine, stretched atrial myocardium (hypervolemia), anxiety, hypokalemia, hypermetabolic states (pregnancy), atrial ischemia, injury, infarction ■ Often seen with sinus tachy ■ ECG: ● Early P waves, short PP interval sometimes followed by long PP interval (noncompensatory pause) ● QRS abnormal = aberrantly conducted PAC ● Absent QRS = blocked PAC ● PR interval normal ● Can be common in normal hearts ● Pulse deficit may exist ■ Management: not commonly treated, if >6 per minute it may indicate worsening disease or other serious dysrhythmias ● Treat cause ○ Atrial flutter: conduction defect in the atrium and causes a rapid, regular atrial impulse at a rate between 250 and 400 bpm ■ Atrial rate faster than AV node can conduct, not all impulses conducted into ventricle ● Therapeutic AV node block ■ ECG ● Atrial rates 250-400 bpm, ventricular 75-150 bpm ● Rhythms usually regular but v-rhythm may be irregular ● QRS usually normal but may be abnormal or absent ● P wave: saw-tooth pattern (F waves) ● P:QRS ratio 2-4:1 ■ Treatment: vagal maneuvers, adenosine, antithrombotic therapy, electrical cardioversion ○ Atrial fibrillation: most common sustained dysrhythmia, results from abnormal impulse formation from structural or electrophysiological abnormalities cause rapid, disorganized, and uncoordinated twitching of atria ■ Causes electrophysiologic changes (remodeling of atrial circuit) and structural remodeling (fibrosis) which leads to continued dysrhythmias ■ Both extrinsic and intrinsic cardiac autonomic nervous system thought to pay roles (includes brain and spinal cord) ● CANS: highly interconnected network of autonomic ganglia and nerve cell bodies embedded within the epicardium, largely within the atrial myocardium and great vessels (pulmonary veins) ● Hyperactive autonomic ganglia in the CANS are thought to play a critical role in atrial fibrillation, resulting in impulses that are initiated from the pulmonary veins and conducted through to the AV node ■ ECG: ● Atrial rate 300-600bpm, ventricular rate can reach 120-200bpm if untreated ● Rhythm irregular ● No discernable P waves ● QRS can be normal or abnormal ● PR cannot be measures ● Multiple P:QRS ● Pulse deficit may present ■ Increases risk for HF, MI, stroke; decreases SV and CO ■ Patient may be symptomatic or asymptomatic ■ Treatment ○ Prevention of embolic events ○ Antiarrhythmics to control ventricular rate ○ Cqrdioversion ■ Wolf-parkinson white syndrome: if the QRS is wide and the ventricular rhythm is very fast and irregular, an accessory pathway should be suspected ● The accessory pathway is typically congenital tissue between the atria, bundle of His, AV node, Purkinje fibers, or ventricular myocardium ● Electrical cardioversion is treatment of choice if hemodynamically stable ● Medications that block AV conduction should be avoided bc ventricular rate can increase ● Procainamide, propafenone, flecainide, and amiodarone are recommended to restore sinus rhythm if hemodynamically stable ● Cath ablation for long term management ○ Junctional dysrhythmias: proginate in AV nodal tissue ■ Premature junctional complexes: impulse that starts in the AV nodal area before the next normal sinus impulse reaches the AV node ● Causes include digitalis toxicity, heart failure, and coronary artery disease ● ECG like PAC except P wave absence, may follow or occur before QRS, PR interval >.12s ● Rarely significant symptoms ● Treatment: see frequent PACs ■ Junctional rhythms: AV node becomes pacemaker ● Occurs when Snus slows or when impulse cannot be conducted (complete heart block) ● ECG if not caused by complete heart block ○ Ventricular rate 40 to 60 bpm; atrial rate also 40 to 60 bpm if P waves are discernible ○ Ventricular and atrial rhythm: Regular ○ QRS shape and duration: Usually normal, but may be abnormal ○ P wave: May be absent, after the QRS complex, or before the QRS; may be inverted, especially in lead II ○ PR interval: If the P wave is in front of the QRS, the PR interval is less than 0.12 seconds. ○ P:QRS ratio 1:1 or 0:1 ● Treatment: same as sinus brady (needed due to symptoms of decreased cardiac output) ○ May need emergency pacing ■ Nonparoxysmal junctional tachycardia: enhances automaticity in junctional area, similar to junctional rhythm but rate is 70-120bpm ● May indicate a serious underlying condition, such as digitalis toxicity, myocardial ischemia, hypokalemia, or chronic obstructive pulmonary disease. ● Because junctional tachycardia is caused by increased automaticity, cardioversion is not an effective treatment ● Hemodynamically stable ■ AV nodal reentry tachycardia: common dysrhythmia, occurs when an impulse is conducted to an area in the AV node that causes the impulse to be rerouted back into the same area over and over again at a very fast rate ● Causes fast ventricular rate too ● Paroxysmal atrial tachycardia (PAT): AVNRT that abruptly starts and ends with normal QRS duration ● QRS can be >.12 seconds and block in bundle branch is known to be present ● Causes/factors: caffeine, nicotine, hypoxemia, stress ● ECG ○ V rate: 120-1220, A rate 150-250 ○ Rhythm normal ○ QRS usually normal ○ P wave difficult to discern ○ PR >.12 ○ P:QRS 1:1 or 2:1 ● Treatment: alleviate symptoms and improve QOL, vagal maneuvers ● Aim of therapy is to break reentry ○ Catheter ablation ● If P waves cannot be identified the rhythm may be called Supraventricular tachycardia (SVT) or paroxysmal supraventricular tachycardia (PSVT) until cause if determined ● Ventricular dysrhythmias: originate in foci in ventricles ○ Premature ventricular complex: impulse that starts and is conducted through ventricles before next normal sinus impulse ■ Can occur in healthy people esp with caffeine, nicotine, alcohol ● Can also be caused by cardiac ischemia, infarction, increased workload, digitalis toxicity, hypoxia, acidosis, electrolyte imbalances (esp hypokalemia) ■ ECG: ● Irregular rhythm due to early QRS ● PP may be regular if PVC did nor depolarize sinus node ● QRS duration >.12s and shape is abnormal ● P wave may be hidden or abnormal in shape if it follows the QRS ● PR interval <.12s if before QRS ● P:QRS should be 1:1 or 0:1 ■ Treatment: long term not indicated but if frequent and persistent may be given amiodarone or sotalol short term ● PVC + MI does not mean increase in sudden cardiac death ● May precede cardiomyopathy or increased incidence of HF and mortality ○ Ventricular tachycardia: 3 or more PVC in a row, occurring at a rate >100bpm ■ Causes similar to PVC ■ Emergency, patient is almost always unresponsive and pulseless ■ ECG ● QRS duration >.12s, bizarre abnormal shape ● P waves difficult to detect, usually more QRS waves if apparent ■ Hemodynamic stability does not predict mortality risk ■ Treatment: ● Patient may need antiarrhythmic medications, antitachycardia pacing, or direct cardioversion or defibrillation. ○ Procainamide may be used for monomorphic stable VT in patients who do not have acute MI or severe HF ○ IV amiodarone is the medication of choice for a patient with impaired cardiac function or acute MI. ○ Sotalol may also be considered for stable monomorphic VT. ○ Although lidocaine had been the medication most commonly used for immediate, short-term therapy, especially for patients with impaired cardiac function, it has no proven short- or long-term efficacy in cardiac arrest ● If patient is stable continue assessment ● Cardioversion for monophasic VT in symptomatic patient ● Defib if pulseless ● Implantable cardioverter defibrillator if EF <35% ○ Amiodarone if >35% ● Small percentage need alation ■ If rate >200 suspect accessory pathway ● If V rhythm is irregular suspect a-fiv ■ Torsades de pointes is a polymorphic VT preceded by a prolonged QT interval, which could be congenital or acquired. ○ Ventricular fibrillation: most common dysrhythmia in patients with cardiac arrest ■ Disorganized quivering of ventricles ■ Causes: most common is CAD and MI, but also cardiomyopathy, valvular heart disease, acid- base imbalances, electric shock, proarrhythmic meds, unsuccessfully treated VT ● Brugada syndrome: common in asians ■ ECG: ● V-rate >300 ● Rhythm irregular ● No QRS/P/anything really ■ Treatment ● Early defibrillation and CPR ● Amiodarone and epi for refractory v-fib after defibrillation ○ Idioventricular rhythm (ventricular escape rhythm) occurs when the impulse starts in the conduction system below the AV node; when sinus node fails to create an impulse or when the impulse is created but cannot be conducted through the AV node the Purkinje fibers automatically discharge an impulse ■ When idioventricular rhythm is not caused by AV block, ECG ● 20-40 bpm ● >40 bpm: accelerated idioventricular rhythm ● Rhythm regular ● QRS abnormal shape, >.12s ■ Same treatment as asystole or pulseless electrical activity ● Iv epi, atropine, vasopressors, emergency pacing ○ Ventricular asystole: flatline ■ ECG: ● No QRs, no P waves or few ■ Treatment: CPR, cause treatment ■ Causes ● Hypoxia, hyperthermia, hydrogen ion imbalance, hyper/hypoglycemia, hyperkalemia ● Trauma, toxins, tamponade, tension pneumo, thrombus Cardiac Rhythm Therapies ● Catheter ablation: destroys cells that are causing the tachydysrhythmias ○ Most common for a-fib, but also used in AVNRT, recurrent VT ○ Moderate sedation and IV heparin are commonly given ○ Patient monitored for 30-60 minutes after and retested for dysrhythmia ■ Obstructive sleep apnea is a risk factor for recurrence ○ Risks: AV block, pericardial tamponade, phrenic nerve injury, stroke, hematoma, pulmonary vein stenosis, atrioesophageal fistulas, retroperitoneal bleeding ● Cryoablation: ablation but cold ● Mini maze: open heart surgical procedure for refractory a-fib ○ Reserved only for those undergoing cardiac surgery for other reasons ○ May need permanent pacemaker after due to SA node injury ● Convergent procedure: utilizes hybrid approach to ablation ● Left atrial appendage occlusion: alternative to warfarin in patients with nonvalvular a-fib ○ LAA most common site for stroke-causing clots in patients with nonvalvular a-fin Adjunctive modalities and management: for when meds alone aren't enough ● Pacemakers: electronic devices that provide electrical stimuli to the heart ○ Types ■ Permanent ● Transvenous pacemaker (implanted) ○ ■ Temporary ○ Pacemaker generator functions ■ NASPE-BPEG code for pacemaker function ○ Complications ■ Infections, bleeding, hematoma, dislocation of leads, cardiac tamponade, pacemaker malfunction, skeletal muscle or phrenic nerve stimulation ● Cardioversion and defibrillation ○ Treat tachydysrhythmias by delivering electrical current that depolarizes (Electrically Stimulates) critical mass of myocardial cells ■ When cells depolarize, sinus node is usually able to recapture role as heart pacemaker ○ In cardioversion, current delivery is synchronized with patient’s ECG ○ In defibrillation, current delivery is unsynchronized ○ Safety measures ■ Ensure good contact between skin, pads, and paddles ● Use conductive medium, 20 to 25 pounds of pressure ■ Place paddles so they do not touch bedding or clothing and are not near medication patches or oxygen flow ■ If cardioverting, turn synchronizer on ■ If defibrillating, turn synchronizer off ■ Do not charge device until ready to shock ■ Call clear 3 times, follow checks required for clear ● Ensure nobody is in contact with patient, bed, or equipment ○ Implantable cardioverter/defibrillator: detects and terminates life-threatening episodes of tachycardia and fibrillation ■ Most Common Complication is Oversensing of Dysrhythmia ■ NASPE-BPEG code ■ Antitachycardia pacing ■ ● Nursing management for devices implanted ○ ECG assessment, CXR ○ Assessment: CO and hemodynamic stability, monitor incision site, signs of ineffective coping, level of knowledge and education needs of family and patient Assessment ● Causes of dysrhythmia, contributing factors, the dysrhythmia's effect on the heart's ability to pump an adequate blood volume ● Assess indicators of cardiac output and oxygenation ● Health history: previous occurrences of decreased cardiac output, possible causes of the dysrhythmia ● All medications (prescribed and over-the-counter) ● Psychosocial assessment: patient’s “perception” of dysrhythmia ● Physical assessment ○ Skin ○ Fluid retention (edema, JVD, lung sounds) ○ Heart sounds ○ BP, pulse pressure Planning: major goals ● Eradicating or decreasing occurrence of dysrhythmia to maintain cardiac output ○ Decrease contributory factors ● Minimizing anxiety ● Patient acquires knowledge about dysrhythmia and its treatment Nursing interventions ● Monitor and manage the dysrhythmia ○ Assess vital signs on an ongoing basis ○ Assess for lightheadedness, dizziness, fainting ○ If hospitalized ■ Obtain 12-lead ECG ■ Continuous monitoring ○ Monitor rhythm strips periodically ○ Antiarrhythmic medications ■ “6-minute walk test” ● Reduce anxiety ○ Stay with patient ○ Maintain safety and security ○ Help them develop system to identify contributing factors to episodes ○ Maximize patient control ● Promote home- and community-based care ● Educate the patient about self-care ○ Treatment options ○ Medication levels (therapeutic) ○ How to take pulse before meds ○ Symptom recognition ○ Decreasing recurrence ○ Emergency plan ○ CPR (family) ○ Assess patient understanding regarding mechanical therapy ● Continuing care ○ Referral for home care ■ Hemodynamically unstable with signs of decreased CO ■ Significant comorbidities ■ Socio Economic issues ■ Limited self-management skills ■ Electronic device recently implanted Electrophysiology studies ● Identify the impulse formation and propagation through the cardiac electrical conduction system ● Assess the function or dysfunction of the SA and AV nodal areas ● Identify the location (called mapping) and mechanism of the arrhythmogenic foci (the exact site where the dysrhythmia originates) ● Assess the effectiveness of antiarrhythmic medications and devices for the patient with a dysrhythmia ● Treat certain dysrhythmias through the destruction of the causative cells (ablation) Chapter 27: Management of Patients with Coronary Vascular Disorders Atherosclerosis: abnormal accumulation of lipid deposits and fibrous tissue within arterial walls and lumen ● Most common cause of CVD Coronary atherosclerosis: blockages and narrowing of the coronary vessels ● Reduce blood flow to the myocardium ● Plaques are called arethomas Cardiovascular disease is the leading cause of death in the United States for men and women of all racial and ethnic groups ● Coronary artery disease (CAD) is the most prevalent cardiovascular disease in adults ○ Risk factors Chart 27-1 ■ Modifiable ● Cholesterol levels ○ Elevated LDL: primary target for cholesterol lowering medications ○ Good levels ■ LDL <100, <70 in high risk patients ■ HDL >40 males, >50 females ■ TGL <150 ■ TCL <200 ● Tobacco use ● Hypertension ● Diabetes, metabolic syndrome ○ Metabolic syndrome dx ■ Insulin resistance (fasting plasma glucose more than 100 mg/dL or abnormal glucose tolerance test) ■ Central obesity (waist circumference >35 inches in females, >40 inches in males) ■ Dyslipidemia (triglycerides more than 150 mg/dL, HDL less than 50 mg/dL in females, less than 40 mg/dL in males) ■ Blood pressure persistently greater than 130/85 mm Hg ■ Proinflammatory state (high levels of C-reactive protein [CRP]) ■ Prothrombotic state (high fibrinogen level) ● Peripheral artery disease ● AAA ● Carotid artery disease ● Physical inactivity, obesity ■ Nonmodifiable ● Family history of CAD ● Age >45 men, >55 women ● Gender: men develop CAD realier ● Race: higher in AA ■ Framingham risk calculator: estimates cardiac event risk in the next 10 years in those 20 or older ■ High-sensitivity C-reactive protein: CRP is a known inflammatory marker for cardiovascular risk including coronary events and stroke ● Liver produces CRP in response to tissue injury ● High levels may occur in diabetics and those who are likely to have acute coronary events ● View results together with other screening tools ○ Prevention ■ Control cholesterol ● Six types of medications ○ HMG CoA reductase inhibitors (statins) ■ Decrease total, ldl, tg, increase hdl ■ Inhibit lipid synthesis ○ Nicotinic acids ○ Fibric acids ■ Increase hdl, lower tg and other synthesis ○ Bile acid sequestrants ■ Decrease ldl, slight increase hdl ■ Inhibit fat absorption by oxidizing cholesterol into bile acids ○ Cholesterol absorption inhibitors -ezetimibe ■ Inhibits absorption in small intestines ○ Omega 3 acid ethyl esters ■ Inhibit TG production in liver ■ Dietary measures ● Total fat 25-35% of calories ○ S-fat: <7% of calories ○ P-u-fat <10% ○ M-u-fat <20% ● Carbs 50-60% ● Fiber 20-30g/day ● Protein 15-25% ● Cholesterol <200mg/day ■ Physical activity ● Moderate intensity aerobics 150 mins ● Or high-intensity 75 mins ■ Medications ■ Manage modifiable risk factors ○ Ischemia symptoms - atypical presentation ■ Patients who are older of have a history of diabetes or heart failure may report SOB ■ Women often have atypical symptoms including indigestion, nausea, palpitations, and numbness Coronary arteries ● Angina pectoris: characterized by episodes or paroxysmal pain or pressure in the anterior chest caused by insufficient coronary blood flow ● Causes: increased demand from ○ Physical exertion: increases myocardial oxygen demand ○ Emotional stress, physical stress: releases catecholamines, increases BP, HR, workload ○ Artherosclerotic disease (usually) ○ Exposure to cold: causes vasoconstriction, elevated bp, increased oxygen demand ○ Eating a heavy meal: moves blood to tummy and away from <3 ● Types (chart 27-2) ○ Stable angina: predictable and consistent pain that occurs on exertion and is relieved by rest and/or nitroglycerin ○ Unstable angina (also called preinfarction angina or crescendo angina): symptoms increase in frequency and severity; may not be relieved with rest or nitroglycerin ○ Intractable or refractory angina: severe incapacitating chest pain ○ Variant angina (also called Prinzmetal’s angina): pain at rest with reversible ST-segment elevation; thought to be caused by coronary artery vasospasm ○ Silent ischemia: objective evidence of ischemia (such as electrocardiographic changes with a stress test), but patient reports no pain ● S/S ○ Described as tightness, choking, heavy sensation ○ Often felt retrosternally and may radiate to neck, jaw, shoulder, back, arms (usually left) ○ Anxiety ○ Dyspnea, SOB ○ Dizziness ○ Nausea, vomiting ○ Typical angina pain subsides with rest ot NTG ○ Unstable pain is characterized by increased frequency and severity, not relieved by rest and NTG ● Gerontology ○ Diminished pain transition may affect presentation ■ Silent CAD ○ Teach patients to recognize chest pain-like symptoms ○ Stress testing, cardiac cath ○ Medication doses ● Treatment: decrease demand and increase oxygen supply ○ Medications ■ Nitro ■ B-adrenergic blocks: block beta adrenergic sympathetic stimulation, decrease HR, conduction of impulse, BP, and contractility ● Metoprolol ● atenolol ■ CCBs: decrease automaticity and AV conduction, slow HR and decrease contraction, workload; dilate smooth muscle ● Amlodipine ● diltiazem ■ Antiplatelet/anticoags ● Aspirin ● Clopidogrel and ticlopidine ● Prasugrel ● Heparin ■ Glycoprotein 2a/3a agents ○ O2 ○ Reduce and control risk factors ○ Reperfusion therapy ● Assessment ○ Vitals, signs of respiratory distress, ECG ■ ECG: T wave inversion, ST elevation, abnormal Q wave ○ Symptoms ■ Pain ○ Activities that precede attacks ○ Risk factors, lifestyle, health promotion ○ Patient and family knowledge ○ Plan of care ● Diagnosis: ○ Risk for decreased cardiac tissue perfusion ○ Anxiety related to cardiac symptoms and possible death ○ Deficient knowledge about the underlying disease and methods for avoiding complications ○ Noncompliance, ineffective management of therapeutic regimen related to failure to accept necessary lifestyle changes ● Collaborative problems ○ ACS, MI, both, dysrhythmias and arrest, HF, cardiogenic shock ● Planning: goals ○ Immediate and appropriate treatment ○ Prevention of angina ○ Prevention of anxiety ○ awareness/knowledge of disease process ○ Understanding care, adherence ○ Absence of complications ● Interventions ○ Treat angina: priority ■ Stop all activity and sit or rest in bed ■ Assess while performing other interventions ■ Nitro and other meds ■ Oxygen ○ Reduce anxiety ■ Calm manner ■ Stress-reduction techniques, patient teaching ■ Spiritual needs ■ Patient and family needs ○ Prevent pain ■ Identify level of activity that causes patient prodromal signs and symptoms ● Plan accordingly ■ Alternate activities and rest ■ Patient and family teaching ○ Self-care, education ■ Balance activity with rest ■ Follow exercise regimen ■ Avoid extreme temps for exercise ■ Use of emotional support ■ Avoid OTCs, may increase HR or BP ■ Diet low in fat and high in fiber ■ Medication teaching (nitro admin) ■ Maintain normal BP and BG ○ Continuing care ■ Follow up with HCP ■ Report increased s/s to provider Acute Coronary Syndrome and Myocardial Infarctions: emergent situations ● Characterized by an acute onset of myocardial ischemia that results in myocardial death if definitive interventions do not occur promptly ● Usually results from unstable angina and rupture of atherosclerotic plaque, clot formation ● AKA coronary occlusion, heart attack ● S/S ○ Chest pain: occurs suddenly, continues despite rest and medications ○ SOB, indigestion, n/v, anxiety ○ Cool, pale skin ○ Increased HR and RR ○ ECG changes: elevation of ST segment in two contiguous leads, t wave inversion, abnormal q waves 1-3 days development ○ Labs: cardiac enzymes, troponins I and T, CK-mb, myoglobin ● Nursing diagnoses ○ Risk for decreased cardiac tissue perfusion related to reduced coronary blood flow ○ Acute pain related to increased myocardial oxygen demand and decreased myocardial oxygen supply ○ Risk for imbalanced fluid volume ○ Risk for ineffective peripheral tissue perfusion related to decreased cardiac output from left ventricular dysfunction ○ Anxiety related to cardiac event and possible death ○ Deficient knowledge about post-ACS self-care ● Collaborative problems/complications ○ Pulmonary edema, HF, cardiogenic shock, dysrhythmias, arrest, pericardial effusion, cardiac tamponade ● Planning: goals ○ Minimize MI damage, preserve function, and prevent complications ○ Relief of pain, signs, symptoms ○ Prevention of myocardial damage ○ Maintain effective respiratory function and tissue perfusion ○ Reduce anxiety ○ Adhere to self-care ○ Early recognition of complications ● Interventions ○ Relieve pain, s/s of ischemia ○ Improve respiratory function and promote perfusion ○ Reduce anxiety ■ Give patient time to express fears ○ Monitor and manage complications ○ Patient/family education ● Management ○ Initial management: Oxygen and medication therapy - supplemental oxygen, aspirin, nitroglycerin, and morphine ○ Frequent VS assessment ○ Physical rest in bed with head of bed elevated ○ Relief of pain helps decrease workload of heart ○ Monitor I&O and tissue perfusion ○ Frequent position changes to prevent respiratory complications ○ Report changes in patient’s condition ○ Evaluate interventions ○ Thrombolytics when Percutaneous coronary intervention is not available or will not be available soon enough ○ Encourage cardiac rehabilitation to extend and improve quality of life ■ Limit progression of atherosclerosis, return to work and pre-illness lifestyle, prevent another cardiac event ■ Phase I: starts at diagnosis ● Essentials of self care ● Signs and symptoms ● Medication regimen ● Follow up ● Rest-activity balance ■ Phase 2: status at discharge ● Supervised, ECG monitored, exercise ● Educational sessions ■ Phase 3: long term for stability and long term conditioning Invasive Coronary Artery procedures ● Coronary artery stent ● Coronary artery bypass graft (CABG) ○ ○ The major indications for CABG are: ■ Alleviation of angina that cannot be controlled with medication or PCI ■ Treatment for left main coronary artery stenosis or multivessel CAD ■ Prevention of and treatment for MI, dysrhythmias, or heart failure ■ Treatment for complications from an unsuccessful PCI ○ Recommendation is made according by the number of diseased vessels, symptoms, previous treatment, degree of LV dysfunction, and presence of other health problems ■ LV main artery must be 50% occluded and others must be 70% ○ Current guidelines recommend internal mammary arteries should be used ■ Greater and lesser saphenous veins are commonly used, but artherosclerotic changes are quicker to develop, often within 5-10 years ● Cardiac surgery ○ Bypass system: maintains perfusion, circulation, and oxygenates blood while bypassing heart and lungs ■ Hypothermia at about 28C (82.4 F) must be maintained ■ ● Percutaneous coronary interventions: performed through skin puncture rather than surgical incision ○ Complications after the procedure may include abrupt closure of the coronary artery and a variety of vascular complications, such as bleeding at the insertion site, retroperitoneal bleeding, hematoma, and arterial occlusion ■ Kidney injury from contrast agent used ○ Percutaneous Transluminal Coronary Angioplasty (PTCA) ■ Balloon-tipped catheter is used to open blocked coronary vessels and resolve ischemia. ■ It is used in patients with angina and as an intervention for ACS ○ Coronary artery stent: placement of a metal mesh that provides structural support to vessel at risk of acute closure Management of patients requiring invasive interventions ● Assessment of patient ○ Neurologic status ○ Cardiac status ○ Respiratory status ○ Peripheral status ○ Renal function ○ Pain ○ Fluids and electrolytes ○ Gas exchange ● Reduce fear and anxiety ○ Describe sensations ○ Reinforce that medication to relieve pain will be provided and they will be closely monitored ○ Encourage discussion of scars and correct misconceptions ○ Normalize fear of dying ○ Anti-anxiety meds ● Monitor and manage potential complications ● Provide patient education ● Maintain cardiac output ○ Prevent venous stasis ■ Exercise ■ Compression devices ○ Report indications of decreased output ○ Admin meds ● Promote adequate gas exchange ○ Deep breathing, coughing, suctioning ○ ET tube maintenance ○ Change positions every 1-2 hours when hemodynamics stabilize ● Maintain fluid and electrolyte balance ○ Record all fluid input and output ○ Monitor hemodynamic parameters, serum electrolytes ● Minimize sensory–perception imbalance ○ Delirium typically appears after 2-5 day stay in the ICU, is more common in the elderly ○ Assess for causes ■ Increased sensory input ■ Medications ■ Sleep deprivation ■ Hypoxemia ■ Metabolic imbalances ○ Treatment ■ Medications ■ Analgesic ■ Sedatives ■ Sleep ■ Family interaction ● Relieve pain ○ Verbal and noverbal cues ○ Support incision ○ Give meds, watch for side effects ● Maintain adequate tissue perfusion ○ Discourage crossing of legs ○ Apply compression devices ○ Avoid elevating knees ■ No pillows in popliteal space ○ Passive and active exercises ○ Observe for ■ Acute onset of chest pain and respiratory distress, as occur in pulmonary embolus or MI ■ Abdominal or back pain, as occur in mesenteric emboli ■ Pain, cessation of pulses, blanching, numbness, or coldness in an extremity ■ One-sided weakness and pupillary changes, as occur in stroke ● Maintain body temperature: increased risk for hyperthermia as a result of tissue inflammation or infection after surgery ○ Hypothermia risk during/right after surgery ● Promote health and community-based care ○ Set realistic goals ○ Education planning ○ Incision care ○ Infection s/s ○ Diet ○ Activity progression ○ Deep breathing/coughing ○ Tobacco cessation ○ Medication regimen ○ Follow up visits, HHC ○ Monitoring weight and temperature Chapter 28: Management of Patients with Structural, Infectious, and Inflammatory Cardiac Disorders Valvular disorders ● Chordae tendineae of the AV valves anchor leaflets to papillary muscles ● Regurgitation: valve does not close completely and blood backflows; likely due to thickened and fibrosed chordae tendineae ○ Mitral regurgitation: permits blood flow back into LA from LV ■ Most common causes in developed countries are degenerative changes (prolapse_ and ischemia of LV; in developing countries is rheumatic heart disease and its sequelae ● Infective endocarditis, scarring, collagen disease, cardiomyopathy, and ischemic heart disease can result in papillary muscles or chordae tendineae/leaflets to stretch, shorten, or rupture ■ Not enough blood flows forwards (decreased CO): angina pectoris, postural hypotension, fatigue, dizziness ● Increase BP in LA, leading to LA hypertrophy and dilation, increases BP in pulmonary veins ○ Pulmonary congestion (SOB, pulmonary edema) and pulmonary vascular hypertension ○ Increased right ventricle work and strain, RV failure ■ Chronic: usually asymptomatic ■ Acute: severe CHF manifestation ● Dyspnea ● Fatigue ● Weakness ● SOB on exertion ● Cough from pulmonary congestion ● Palpitations ■ Systolic murmur is high pitched and best sounds at the apex, can radiate to left axillae ■ Pulse may be regular and good volume, or irregular from extrasystolic beats or a-fib ■ diagnosed and monitored via echo ■ Management ● Same as HF: reduce afterload using ACEIs, ARVs, BBs ● Surgical repair ○ Aortic regurgitation: permits blood flow back into the left ventricle from the aorta ■ May result from inflammatory lesions, infective or rheumatic endocarditis, congenital abnormalities, diseases like syphilis, dissecting aneurysm, blunt chest trauma, or deterioration of surgically replaced valve ■ Increases BP in left ventricle leading to LV hypertrophy and dilation; blood from LA cannot flow forward ● Increase BP in LA, leading to LA hypertrophy and dilation, increases BP in pulmonary veins ○ Pulmonary congestion (SOB, pulmonary edema) and pulmonary vascular hypertension ○ Increased right ventricle work and strain, RV failure ○ Reflex vasodilation of peripheral arterioles ■ Not enough blood flows forwards (decreased CO): angina pectoris, postural hypotension, fatigue, dizziness ■ Clinical manifestations ● Aortic insufficiency ○ Forceful beat in head or neck ○ Marked arterial pulsations visible or palpable at caroti or temporal arteries ● Exertional dyspnea, fatigue ● s/s of LVHF ○ SOB ○ Orthopnea ○ PND ■ Assessment and diagnosis ● High-pitched, blowing diastolic murmur at third or fourth intercostal space at left sternal border ● Widene pulse pressure ● Water hammer pulse (corrigan’s pulse): pulse strikes an suddenly collapses ● Echo (transesophageal is best) ○ Symptomatic: every 6 months ○ Asymptomatic: every 2-5 years ● Cardiac MRI ● Cardiac Cath ■ Prevention and treatment ● Preventing and treating infections, esp rheumatic fever ● Avoid exertion, sports, isometric exercise ● Dysrhythmia and HF treatment ● CCBs, ACEIs to reduce preload if jypertensive ● Reduce sodium to avoid volume overload (symptomatic) ● Surgery: valvuloplasty or replacement especially in those with LV dilation whether symptomatic or not ● Stenosis: valve does not open completely and blood flow is reduced ○ Mitral stenosis: limits flow of blood into LV ■ Most often caused by rheumatic endocarditis which thickens valve leaflets and chordae tendineae, leaflets may fuse together ● Orifice can narrow to width of a pencil, LA has trouble pushing blood leading to decreased CO ■ Increase BP in LA, leading to LA hypertrophy and dilation, increases BP in pulmonary veins ● Pulmonary congestion (SOB, pulmonary edema) and pulmonary vascular hypertension ● Increased right ventricle work and strain, RV failure ■ First symptom is usually yspnea on exertion as a result of pulmonary venous hypertension ■ Manifestations ● Fatigue: progressive ● Decreased exercise tolerance ● Dry cough or wheezing as a result of enlarged LA pressure on bronchial tree ● Hemoptysis ● Palpitations ● Orthopnea ● Paroxysmal nocturnal dyspnea ● Dyspnea ● Pulmonary vein hypertension ● Repeat respiratory infections ● Atrial dysrhythmias ■ Low pitched, rumbling diastolic murmur can be heard at apex; patient may have s/s of HF ■ Echo used to diagnose ■ ECG, stress test, cardiac cath with angiography may help determine severity ■ Treatment: treat infections an minimize risk, antibiotic prophylaxis for group A strep ● 10+ years of coverage for rheumatic fever with rheumatic carditis may be needed ● Anticoags, angina treatment ● Cardioversion ● BB, digoxin, CCBs ● Avoid strenuous activity, pregnancy, sports ● Surgery ○ Valvuloplasty: commissurotomy, PTV, valve replacement ○ Aortic stenosis: limits for of blood from left ventricle into aorta ■ Adults: results usually from calcifications caused by proliferative an inflammatory changes in response to years of normal mechanical stress )similar to atheroscleotic arterial disease changes) ● Risk: age, diabetes, bad cholesterol, hypercholesterolemia, HTN, smoking ● Congenital malformations or abnormal number of leaflets ● Rheumatic adhesions, fesiuns, stiffening, an calcific nodules ■ Increases BP in left ventricle leading to LV hypertrophy and dilation; blood from LA cannot flow forward; LV contracts more slowly but with more power ● Increase BP in LA, leading to LA hypertrophy and dilation, increases BP in pulmonary veins ○ Pulmonary congestion (SOB, pulmonary edema) and pulmonary vascular hypertension ○ When compensation fails, clinical signs evelop ● Increased right ventricle work and strain, RV failure ● Not enough blood flows forwards (decreased CO): angina pectoris, postural hypotension, fatigue, dizziness ■ Clinical manifestations: many are asymptomatic ● Exertional dyspnea caused by increased pulmonary venous pressure ● orthopnea ● PND ● Pulmonary edema ● Dizziness and syncope due to reduced flow to brain ● Angina pectoris ● BP can be low ● Pulse pressure can be low ■ Assessment and diagnosis ● Loud harsh systolic murmur over aortic area, may radiate to carotid arteries ○ Low pitched ● S4 may be heard ● Vibration from aortic space to superasternal notch ● Echo, MRI, CT ○ Symptoms: 6-12 months echo ○ None: 1-5 years echo ● 12 lea: LV hypertrophy ● Surgery ● Cath for left side ● Pressure tracings ● Stress tests ■ Prevention: reduce risk factors ■ Management: treat dysrhythmia and LV failure ■ Surgical valve replacement ■ Can't do surgery? 1 or 2 balloon percutaneous valvuloplasty with or without TAVI (transcatheter aortic valve implantation) ● Valve prolapse: stretching of an AV valve leaflet into the atrium during diastole ○ Mitral valve prolapse: one or both leaflets balloon back into left atrium during systole ■ First an only sign may be mitral click (heart sound), murmur of regurge during systole ● Diagnosis via echo ● Treatment to correct symptoms ■ Manifestations: usually produces no symptoms but can produce these ● Fatigue: whether rested or not, regardless of activity level ● SOB: not correlated to activity levels or pulmonary function ● Light Headed or dizziness, syncope ● Palpitations ● Chest pain: normally localized to the chest but not correlate with activity and can last for days ● Anxiety: maybe symptom related or dysautonomia related ● Progression to sudden death (rare) ● 15% of patients who develop murmurs eventually experience heart enlargement, a-fib, pulmonary hypertension, or HF ■ 2.5% of population, 2x more common in women ● Cause may be a hereditary connective tissue disorder resulting in enlargement of one or both leaflets but the cause if often unknown ■ Management/Treatment ● Teaching ○ If dysrhythmias ■ Avoid caffeine ■ Eliminate alcohol ■ Stop the use of tobacco products ● Prophylactic antibiotics not recommended before dental procedure ● Some may need antiarrhythmics ● Chest pain may need nitrates, but if not responsive to nitrates may use CCBs or BBs ● Severe or with HF may need repair or replacement of valve ■ Nursing ● Educate on heredity, 1st degree relatives may need echo ● Risk for endocarditis ○ Minimize risk ● Recognition and report of symptoms by patient ● To avoid alcohol, caffeine, ephedrine, an epinephrine double check OTC product labels and normal product labels ● Lifestyle factor teaching ● Pregnancy: delivery is ok vaginal if no regurge or complications ● Management ○ Patient education ■ Diagnosis, progressive nature, treatment plan ● bacterial risk of adherence to valve ○ Prevention ● Report new symptoms ■ Medication schedule: develop schedule, drug info teaching ● Risk to patients who have aortic stenosis and take nitro ○ Further decreases cardiac output, increases risk for syncope and decreased coronary artery flow ○ Treat with rest and relaxation first ■ Planned rest periods ○ Monitor vital sign trends ○ Watch for complications, teach patient to recognize s/s ■ Heart failure: fatigue, OW, decreased activity tolerance, hemoptysis, multiple resp infections, orthopnea, PND ■ Dysrhythmias: palpate pulse for strength and rhythm, ask whether they've had palpations or forceful beats ■ Dizziness, syncope, increase weakness, angina pectoris ○ Daily weights: watch for weight gain ○ HOB elevation for sleep if experiencing pulmonary congestion ● Surgical management ○ Valvuloplasty: repair of valve; does not require continuous anticoagulation; most require general anesthesia and bypass but some do not requires general anesthesia or bypass and ca be done in cardiac lab or hybrid room (or w/ imaging) ■ Commissurotomy: repair made to commissures between leaflets and separate them ● Does not require bypass ● More common in developing nations ● Preferred technique for patients with ○ Congenital mitral stenosis ○ Severe calcified mitral stenosis ○ Left atrial thrombus ○ Moderate-to-severe coexisting mitral regurgitation ○ Coexisting moderate-to-severe tricuspid regurgitation who would also benefit from tricuspid valve repair ● Open commissurotomy requires general anesthesia and bypass due to direct visualization ○ Thrombus an calcifications can be removed and chordae tendineae and papillary muscles can be repaired ■ Balloon valvuloplasty: most commonly performed in US as a bridge to replacement for close commissurotomy ● Often used for mitral and aortic stenosis but has also been used in tricuspid and pulmonic stenosis ○ Beneficial for mitral valve stenosis in younger patients and for patients with complex medical conditions that place them at high risk for complications of surgery ○ Contraindicated for patients with left atrial or ventricular thrombus, severe aortic root dilation, significant mitral valve regurgitation, severe valvular calcification, thoracolumbar scoliosis, rotation of the great vessels, and other cardiac conditions that require open heart surgery ● Performed at cardiac cath lab under light or moderate sedation and local anesthetic ● Balloons expand stenosed valves ○ 10-30s in mitral ○ 35-60s in atrial; not as effective as mitral valve procedure ■ Rate of restenosis is about 50% in the first 6 months ● All patients have some degree of regurgitation after mitral procedure ● Management: Nursing ○ Telemetry unit or ICU ○ Monitor for HF and emboli ○ Assess heart sounds every 4 hours ○ Same care as cardiac cath ○ After undergoing percutaneous balloon valvuloplasty patient usually remains in the hospital for 24-48 hours ● Possible complications from mitral balloon valvuloplasty include nclude bleeding from the catheter insertion sites, emboli resulting in complications such as strokes, and, rarely, left- to-right atrial shunts through the atrial septal defect created during the procedure. ● Aortic complications include aortic regurgitation, emboli, ventricular perforation, rupture of the aortic valve annulus, ventricular dysrhythmia, mitral valve damage, and bleeding from the catheter insertion sites ■ Annuloplasty: repair made to annulus ● General anesthesia and bypass required for most ● Two techniques ○ Ring insertion: leaflets sutured to ring to created annulus of desired size, tension from heart and blood born by ring rather than valve ■ Prevents progressive regurge ○ Tighten annulus: folds elongated tissue over onto itself in leaflets or tacks leaflets to atrium with sutures ■ Can degenerate more quickly due to forces ■ Leaflet repair: leaflet is partially resected and sewn together for repair ● Damage to leaflets from stretching, shortening, or tearing ● Elongated tissue may be ticked and sutured or a wedge may be removed and closed (resection) ● Chordoplastly: cuts short chordae to help short leaflets unfurl ● Extension: suture piece of pericardium to short leaflets ● Pericardial or synthetic patch, or sutures, can repair tears or holes ■ Chordoplasty: repair made to cord; usually mitral valve ● Stretched chordae tendineae can be shortened, transposed to the other leaflet, or replaced with synthetic chordae ● Torn chordae can be reattached to the leaflet ● Shortened chordae can be elongated. ● Stretched papillary muscles, which may also cause regurgitation, can be shortened or relocated ■ Some Valvuloplasty procedures do not require general anesthesia or cardiopulmonary bypass and can be performed in a cardiac catheterization laboratory or hybrid room ○ Valve replacement: most use general anesthetic, bypass, and median sternotomies ; mitral valve and rarely the aortic valve may be replaced with minimally invasive techniques ■ TAVI: minimally invasive aortic valve replacement that is performed in cath lab or hybrid room does not involve bypass or sternotomy ● Risky patients with aortic stenosis ● Balloon valvuloplasty + bioprosthesis ■ Mechanical: ● Designs: kinda cool look them up ○ Bileaflet ○ Tilting disc ○ Ball and cage ● Thought to be more durable than tissue prosthetics and often used in younger patients, patients with kidney injury, hypercalcemia, endocarditis, sepsis, or those who need valve replacement ● Do not deteriorate or become infected as easily ● Mitraclip is a mechanic bridge transcath procedure to treat degenerative mortal regurge in severe symptomatic patients with high risk ○ Decreased regurge blood, improvement of symptoms, decreased rates of hospitalization for HF ● Risks for thromboemboli and need for long term anticoags ■ Tissue: less likely to generate thromboemboli so no need for long term anticoags, nor as durable and require replacement for frequently ● Bioprosthesis: aortic, mitral, tricuspid replacement ○ Women of childbearing age because of potential complications of long-term anticoagulation associated with menses, placental transfer to a fetus, and delivery of a child ○ Patients older than 70 years and others who cannot tolerate long-term anticoagulation. ○ Most bioprosthesis are from pigs (porcine), but some are from cows (bovine) or horses (equine). T ○ May be stented or non-stented. ○ Last7 to 15 years ● Homografts (allografts): aortic and pulmonic replacement ○ From cadaver tissue; harvested and stored cryogenically ○ Not always available and very expensive ○ Last 10-15 years ● Autografts: ○ Obtained by excising the patient’s own pulmonic valve and a portion of the pulmonary artery for use as the aortic valve ○ Alternative for children (it may grow as the child grows), women of childbearing age, young adults, patients with a history of peptic ulcer disease, and people who cannot tolerate anticoagulation. ○ Aortic valve autografts have remained viable for more than 20 years ○ Mostly double valve replacement with pulmonic valve homograft also performed ■ If pulmonary vascular pressures are normal surgeon may not replace pulmonic valve ○ Complications: related to sudden changes intracardiac BP ■ All prosthetics create a degree of stenosis ■ Signs of backward HF resolve usually in a few hours or days if replacement was for stenotic valve ■ If for regurge, may need months for chamber to achieve best post-op function ● s/s resolve gradually ■ Bleeding, thromboembolisms, infection, HF, HTN, dysrhythmias, hemolysis, mechanical obstruction of valve ○ Post-surgical: ICU admission ■ Focus is hemodynamic stability and recovery from anesthesia ■ Frequent assessments every 5-15 minute for vitals until recovery from anesthesia ● Pay attention to neurologic, resp, and CV systems; assessment ever 1-4 hours ■ Patient education: ● Anticoag therapy ● Prevention of infective endocarditis ● Repeat echos ● Follow up ■ Transesophageal echo to evaluate effectiveness ■ IV meds to alter BP, treat dysrhythmias, correct HR are given and effects monitored ● Meds gradually decreased until no longer needed or oral route is an option ■ Eventually transferred to telemetry unit: usually within 24-72 hours when stable physical assessment, hemodynamics, no IV meds ● Wound care, diet, activity, medications, and self care education all should be reinforced ■ Discharge 307 days ■ Educate on anticoag therapy, frequent follow ups, and blood labs ● Warfarin rations 2-3.5 for mitral and 1.8-2.2 for aortic replacement ● Annuloplasty or tissue valves usually only need 3 months anticoags ● Aspirin warfarin for bioprosthesis or high risk ■ Mechanical replacement: prevention of infective endocarditis ● Prophylaxis before dental procedures (antibiotic) and invasive procedures or respiratory teact Cardiomyopathy: series of progressive events that culminates in impaired cardiac output and can lead to heart failure, sudden death, or dysrhythmias ● Types, classified according to structural and functional abnormalities ○ Lead to HF ■ Dilated cardiomyopathy (DCM): most common; significant dilation of ventricles without hypertrophy; systolic dysfunction ● Ventricles have elevated systolic and diastolic volumes but decreased EF ● Caused by 75+ conditions, 30% are idiopathic and can be linked to genetics ○ Screen first degree relatives ● Diminished contractile elements (actin and myosin filaments) of the muscle fibers and diffuse necrosis of myocardial cells lead to poor systolic function ○ Increase pulmonary and systemic venous pressure ○ Regurgitation can result ○ Poor glow can cause atrial or ventricular thrombi which can embolize to other locations ● Early diagnosis and treatment is key ■ Hypertrophic cardiomyopathy (HCM): autosomal dominant condition with prevalence rate of 0.2%; often detected after puberty ● Echos, ECGs, physical exams are performed every 12-18 months from age 12-18 and up to every 5 years from 18-70 ○ Doppler echo, tissue doppler imaging, and CV MRI ○ Genetic testing for risk ● Heart muscle asymmetrically increased in size and mass especially along septum, affects non adjacent areas of ventricle ○ Delayed relaxation of muscle ○ Decreased cavity size ○ Cells are disorganized, increase risk of dysrhythmias, decrease effectiveness of contractions ● Artery walls thicken and restrict blood supply ■ Restrictive/constrictive cardiomyopathy (RCM): diastolic dysfunction caused by rigid ventricular walls that impair diastolic filling and ventricular stretch; systolic function is usually normal ● Because s/s similar to constrictive pericarditis (dyspnea, nonproductive cough, and chest pain) echo and measurements of pulmonary artery systolic pressure, pulmonary artery wedge pressure, and central venous pressure is used to differentiate ● May be associated with amyloidosis (amyloid, a protein substance, is deposited within cells) and other such infiltrative diseases but is usually idiopathic ● Patients with restrictive cardiomyopathy are sensitive to digitalis. ○ Monitor these patients for digitalis toxicity: dysrhythmia, anorexia, nausea, vomiting, headache, and malaise ■ If present lower dose ○ Avoid nifedipine ○ Arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D): occurs when the myocardium is progressively infiltrated and replaced by fibrous scar and adipose tissue; starts with localized areas of RV and progresses to the whole heart ■ Inherited, uncommon ■ RV dilates and develops poor contractility, wall abnormalities, and dysrhythmias ■ Palpitations or syncope develop between 15-40 years ■ Should be considered in patients with v-tach originating in RV or sudden death among the young and athletes ■ ICD placement can help with dysrhythmias ○ Unclassified cardiomyopathy: have characteristics of more than one of the previously described types and are caused by fibroelastosis, noncompacted myocardium, systolic dysfunction with minimal dilation, and mitochondrial diseases ■ Ischemic cardiomyopathy: enlarged heart caused by CAD and usually accompanied by HF ■ LV noncompaction ■ Stress induced (Takotsubo) ● Pathophys: all cumulate in impaired CO, decreased SV that stimulates SNS, RAAS, increased systemic resistance, sodium, and fluid retention; lead to HF ○ Sodium is the major electrolyte involved ■ HF develops partly due to fluid overload ● Assessment ○ History (patient and family) ○ Early stages: tachycardia and extra heart sounds ■ DCM: diastolic murmurs ■ DCM and HCM: systolic murmurs ■ HF signs: JVD, crackles, pitting edema, enlarged liver ○ Chest pain ○ ROS: orthopnea, syncope ○ Diet: Na reduction, vitamin supplements ○ Psychosocial history: impact on family, stressors, depression ○ Physical ■ VS, pulse pressure ■ Pulsus paradoxus ■ Weight changes ■ Previous MI ○ Rule out other causes ○ CMRI especially useful with HCM ○ Echo is most helpful ○ ECG ○ CXR: enlargement, pulmonary congestion ○ Cathto rule out CAD ○ Biopsy to analyze cells ● Medical management: identify and manage causes, control dysrhythmias, anticoagulation, fluid limits for pulmonary congestion ○ HCM or RM limit physical activity ○ HCM avoid dehydration, BBs ro minimize risk of LV outflow obstruction ○ Amiodarone only drug shown to reduce incidence of arrhythmogenic sudden cardiac death ○ Pacemaker ○ Biventricular pacing in DCM and HCM to increase ejection fraction and reverse some structural changes ○ Septal ablation HCM ○ Surgery ■ Left ventricular outflow tract surgery ● Myectomy: excision of septal tissue ● May need mitral surgery ■ Heart transplant ● Cyclosporine immunosuppression ● Orthotopic transplant ○ Biatrial technique: leaves VC and PV in place ○ Bicaval technique: removes it all ■ Less AV regurg, conduction abnormalities, dysrhythmias ● Risk of rejection: minimize ○ Corticosteroids ○ Anti Proliferative ○ Calcineurin inhibitors ● Nerves, atropine does not affect hearts, only catecholamines ○ Many do not have angina with ischemia ○ Accelerated atherosclerosis ○ Some meds affect kidneys = hypertension (cyclosporine, tacrolimus) ● Osteoporosis risk increases ● 1 year survival 90% ○ Mechanical assistive devices ■ Intra aortic balloon pump most common ■ Ventricular (VADs) ● One ventricle per VAD ○ Bridge to recovery ○ Bridge to transplant ○ Destination therapy ● Internal or external ● Four types ○ Pneumatic ○ Electric or electromagnetic ○ Axial flow ○ Centrifugal ■ Total artificial hearts ■ Complications: bleeding, emboli, hemolysis, infection, kidney injury, mechanical failure, RSHF, multisystem failure ● Nursing Dx ○ Decreased cardiac output ○ Risk for ineffective cardiac, cerebral, peripheral, and renal tissue perfusion ○ Impaired gas exchange ○ Activity intolerance ○ Anxiety ○ Powerlessness ○ Noncompliance with medication and diet therapies ● Collaborative problems and complications ○ Heart failure ○ Ventricular dysrhythmias ○ Atrial dysrhythmias ○ Cardiac conduction defects ○ Pulmonary or cerebral embolism ○ Valvular dysfunction ● Goals/interventions/evaluation ○ Improvement or maintenance of cardiac output and peripheral blood flow ■ Rest, positioning (legs down), supplemental O2, medications, low Na diet, avoid dehydration (patients with HCM avoid diuretics) ■ HR and RR WNL, decreased dyspnea and increased comfort, maintain or improve gas exchange, absence of weight gain, maintain or improve peripheral blood flow ○ Increased activity tolerance and improving gas exchange ■ Cycle rest and activity, ensure patient recognizes symptoms that indicate the need for rest ■ Carry out activities of daily living (e.g., brush teeth, feed self), reports increased tolerance to activity ○ Reduction of anxiety ■ Eradicate or alleviate perceived stressors, educate family about diagnosis, assist with anticipatory grieving ■ Discusses prognosis, verbalizes fears and concerns, participates in support groups, demonstrates appropriate coping mechanisms ○ Adherence to the self-care program\ ■ Takes medications as prescribed, modifies diet to accommodate sodium and fluid recommendations, modifies lifestyle, identifies S&S to be reported ○ Increased sense of power with decision making ■ Assist patients in identifying things that have been lost (i.e., ability to play sports), assist patients in identifying amount of control they still have left ■ Identifies emotional response to diagnosis, discusses control that he or she has ○ Absence of complications ○ Promote health and community based care ■ Educate patients about ways to balance lifestyle and work while accomplishing therapeutic activities ■ Assess patient and family and their adjustment to lifestyle changes, educate family about CPR and AEDs, establish trust Infectious diseases of the heart ● Key points ○ Any of the three layers of the heart may be affected by an infectious process ○ Diseases are named by the layer of the heart that is affected ● Diagnosis is made by patient symptoms and echocardiogram ● Management for all infectious diseases is prevention ○ IV antibiotics usually are necessary once an infection has developed in the heart ● Endocarditis: ○ Rheumatic endocarditis ■ Occurs most often in school-age children after group A beta-hemolytic streptococcal pharyngitis ● Need to promptly recognize and treat “strep” throat to prevent rheumatic fever ■ New murmur, cardiomegaly, pericarditis, heart failure ○ Infective endocarditis: microbial infection of endothelium ■ Usually develops in people with prosthetic heart valves or structural cardiac defects; also occurs in patients who are IV drug abusers and HAI in those with debilitating diseases, indwelling catheters, or prolonged IV therapy; patients on immunosuppressants or on corticosteroids are more susceptible to fungal endocarditis ■ Infections tend to be bacterial ○ Deformity or injury allows bacteria to attach to clots ○ Onset is insidious ○ Emboli common with left sided infective endocarditis when vegetative growth are larger than 10cm ○ Can result in destruction of valves, embolization of vegetative growth, toxic infection ○ Pulmonary embolism with right sided ● Pericarditis:Inflammation of the pericardium ○ Many causes, primary and secondary ■ Can be acute, chronic recurring ○ Classified as adhesive (constrictive) or by what accumulates in pericardial sac: serous, purulent, calcific, fibrinous, sanguineous, or malignant; may also be described as exudative or non effusive ○ Potential complications: pericardial effusion and cardiac tamponade ○ Clinical manifestations: can be asymptomatic, chest pain is common and constant but can worsen with inspiration or lying down ■ Most characteristic manifestation: creaky/scratchy friction tub at left lower sternal border ■ Dyspnea, nonproductive cough, hiccup, tachycardia, mild fever, increased WBC ESR and CRP, anemia ○ Medical ■ Treat cause, recognize complications ■ Fluid relief ● NSAIDs (not indomethacin) ● Colchicine and steroids if severe ● Pericardiocentesis ○ Nursing: analgesics, positioning, psychological support ● Myocarditis: inflammatory process involving the myocardium ○ Most common pathogens involved in myocarditis tend to be viral but can also be bacterial, rickettsial, fungal, parasitic, metazoal, protozoal, or spirochetal ■ Can also be immune after systemic infections such as rheumatic fever; patients on immunosuppressants; those with infective endocarditis, crohns, SLE ■ Inflammatory reaction to toxins ○ Begins in small area and spreads ■ DCM and HCM may be latent manifestations of myocarditis ○ Complications: cardiomyopathy and heart failure, heart dilation, thrombi on the wall ■ Degeneration of muscle fibers, infiltration of blood in vessels and between fibers ○ Dyspnea, syncope, palpitations, discomfort, flu-like; sudden cardiac death or CHF ○ Tachycardia and chest pain can occur ○ Hard to detect: Patients without any abnormal heart structure (at least initially) may suddenly develop dysrhythmias or ST–T-wave changes. ■ If the patient has structural heart abnormalities (e.g., systolic dysfunction), a clinical assessment may disclose cardiac enlargement, faint heart sounds (especially S1), pericardial friction rub, a gallop rhythm, or a systolic murmur. ■ WBC count, C-reactive protein, leukocyte count, and ESR may be elevated ○ Prevention: immunization and early treatment ○ Medical management: treat cause ■ Bed rest ● At least 6 months activity limits ● Increase activity slowly ■ NSAIDs not effective and can increase mortality ○ Nursing MGMT: resolution of symptoms, assessment for complications ■ Anti-embolism stockings, exercises to prevent thrombus, maybe meds ● Clinical manifestations ○ Fever ○ New heart murmur, friction rub at left lower sternal border (pericarditis) ○ Osler nodes (small, painful on pads of fingers and toes), Janeway lesions (irregular, red or purple, painless flat macules on hands and feet), Roth spots (hemorrhages with pale centers caused by emboli in fundus of eyes), and splinter hemorrhages in nail beds (rheumatic) ○ Petechiae on conjunctiva and mucous membranes ○ Cardiomegaly, heart failure, tachycardia, splenomegaly ○ Fatigue, dyspnea, syncope, palpitations, chest pain (myocarditis) ○ CNS: headache, Transient cerebral ischemia, strokes ○ Diagnostic tools: blood cultures (2 sets or anaerobic and aeroic), echocardiogram, CBC, rheumatoid factor, ESR, CRP, urinalysis, ECG, cardiac catheterization, CMR imaging, TEE, CT scan, antimicrobials ■ Negative cultures cannot rule out infective Endocarditis ■ Elevated WBC, anemia ■ Echocardiography, TWW ● Prevention ○ Antibiotic prophylaxis before certain procedures (dental) ○ Ongoing oral hygiene ■ Avoid nail biting ■ Avoid toothpicks or sharps in oral cavity ○ Avoid piercings, tattoos, branding, illicit drug use ○ Minimize acne and psoriasis ○ Female patients are advised NOT to use IUDs ○ Meticulous care should be taken in patients “at risk” who have catheters ○ Catheters, tubes, drains, and other devices should be removed as soon as they are no longer needed ○ Immunization? ○ Refer fevers >7 days ○ Proper antibiotic administration and adherence ● Medical management ○ Eradicate organisms ○ Antibiotics 2-6 weeks every 4 hours of continuously by IV ○ Monitor Temp for febrile reactions and therapy effectiveness ○ Surgery ■ CHF ■ Emboli ■ Valve obstructions ■ Aortic, periannular, myocardial abscess ■ Uncontrolled, persistent, recurrent, fungal infections ● Nursing ● Monitor temp ● Meds ● Fluids ● Rest ● NDAIDs for fever ● Infection control ● Assess heart sounds ● Assess lung sounds and lungs ● Assess for organ damage and strokes ● Emotional support ● Patient teaching Chapter 29: Management of Patients with Complications from Heart Disease Heart failure: a clinical syndrome resulting from structural or functional cardiac disorders that impair the ability of the ventricles to fill (diastolic failure) or eject blood through contraction (systolic failure) ● In the past, HF was often referred to as congestive heart failure (CHF), because many patients experience pulmonary or peripheral congestion with edema ○ Mostly caused by CAD, HTN, cardiomyopathy, valvular dysfunctions, and renal dysfunction with fluid overload ● HF is characterized by signs and symptoms of fluid overload or inadequate tissue perfusion ○ Clinical manifestations ■ Right sided: lung circulation reduced, backflow into system ● Viscera and peripheral congestion ● Jugular venous distention (JVD) ● Dependent edema, pitting edema after about 4.5 kg or L of fluid is retained ● Hepatomegaly ● Ascites ● Weight gain ■ Left sided: systemic circulation reduced, backflow into lungs ● Pulmonary congestion, crackles ● S3 or “ventricular gallop” ● Dyspnea on exertion (DOE) ● Low O2 sat-affects oxygen transportation to the brain ● Dry, nonproductive cough initially -> pink frothy sputum ● Oliguria: decreased blood flow to the kidneys ● Decreased flow to the other organs including the brain: dizziness, confusion, restlessness, anxiert ● Orthopnea, PND ■ Ejection fraction is normal with diastolic HF (55-65%) but low with systolic ○ Classification ■ I: No limitation of physical activity; Ordinary activity does not cause undue fatigue, palpitation, or dyspnea. ■ II: Slight limitation of physical activity,;Comfortable at rest, but ordinary physical activity causes fatigue, palpitation, or dyspnea. ■ III: Marked limitation of physical activity; Comfortable at rest, but less than ordinary activity causes fatigue, palpitation, or dyspnea. ■ IV: Unable to carry out any physical activity without discomfort; Symptoms of cardiac insufficiency at rest; If any physical activity is undertaken, discomfort is increased. ■ AHA classification ● ● Some cases are reversible ● Mostly chronic and progresive; managed with lifestyle changes and medications ○ Incidence increases with age, most common in those >75 ■ Most common reason for hospitalization in those over 65 and seconds most common reason for visits to physician’s office ○ 25% of those discharged after HF treatment are readmitted <30 days ○ Medications: ■ Angiotensin-converting enzyme (ACE) inhibitors: vasodilation; diuresis; decreases afterload; monitor for hypotension, hyperkalemia, and altered renal function; cough ● Helpful in particular for Systolic dysfunction ■ Angiotensin II receptor blockers: prescribed as an alternative to ACE inhibitors; work similarly ■ Hydralazine and isosorbide dinitrate: alternative to ACE inhibitors ● Nitrated cause venous dilation, lower preload; hydralazine lowers systemic vascular resistance and afterload ■ Beta-blockers: first line therapy prescribed in addition to ACE inhibitors; may be several weeks before effects seen; use with caution in patients with bronchospastic diseases such as asthma ● Relax blood vessels, lower BP, decrease afterload and cardiac workload ● Can cause hypotension, fatigue, dizziness, bradycardia ○ Slowly titrate up ■ Diuretics: decreases fluid volume, monitor serum electrolytes ■ Digitalis: improves contractility, slows conduction through AV node ● Monitor for digitalis toxicity especially if patient is hypokalemic: anorexia, condusion, visual disturbances, bradycardia, confusion ■ IV medications: indicated for hospitalized patients admitted for acute decompensated HF ● Milrinone: decreases preload and afterload; causes hypotension and increased risk of dysrhythmias ● Dobutamine: used for patients with left ventricular dysfunction; increases cardiac contractility and renal perfusion ● Gerontology: Older patients may present with atypical signs and symptoms such as fatigue, weakness, and somnolence ○ Decreased renal function can make older patients resistant to diuretics and more sensitive to changes in volume ○ Administration of diuretics to older men requires nursing surveillance for bladder distention caused by urethral obstruction from an enlarged prostate gland ● Assessment ○ Focus ■ Effectiveness of therapy ■ Patient’s self-management ■ S&S if increased HF ■ Emotional or psychosocial response ○ Health history ○ Physical exam: mental status; lung sounds: crackles and wheezes; heart sounds: S3; fluid status or signs of fluid overload; daily weight and I&O; assess responses to medications ● Diagnoses/Interventions ○ Activity intolerance related to decreased CO ■ Promote activity and reduce fatigue ● Bed rest for acute exacerbations ● Encourage regular physical activity; 30 to 45 minutes daily ● Exercise training ● Pacing of activities ● Wait 2 hours after eating for physical activity ● Avoid activities in extreme hot, cold, or humid weather ● Modify activities to conserve energy ■ Positioning; elevation of the head of bed (High Fowler position) to facilitate breathing and rest, support of arms ■ Goal: maintain stable vitals in target range ○ Excess fluid volume related to the HF syndrome ■ Assessment for symptoms ● Daily Weight, I&O ■ Relieve overload symptoms ● Diuretic therapy; timing of meds ● Fluid intake; fluid restriction ● Maintenance of sodium restriction ○ Anxiety-related symptoms related to complexity of the therapeutic regimen ■ Decrease anxiety or increase the patient’s ability to manage anxiety ○ Powerlessness related to chronic illness and hospitalizations ■ Encourage the patient to verbalize his or her ability to make decisions and influence outcomes ■ Need to consider end of life issues and when palliative or hospice should be considered ○ Ineffective family therapeutic regimen management ■ Educate the patient and family about management of the therapeutic regimen ● Low sodium diet ● Medications ● s/s of excess fluid, hypotension, disease exacerbation, daily weights ● Exercise program ● Stress management ● Preventing infarctions and when to contact a HCP ● Collaborative problems ○ Hypotension, poor perfusion, and cardiogenic shock (see Chapter 14) ■ Cardiogenic shock: decreased CO leads to inadequate perfusion and initiation of shock; life threatening and high mortality ● See shock chapter; symptoms of HF, shock, hypoxia ● Management: correct underlying problem ○ Reduce preload and afterload ○ Improve oxygenation and perfusion ○ Monitor hemodynamic parameters, monitor fluid status, and adjust medications and therapies based on the assessment data ○ Medications: diuretics, positive inotropic agents, and vasopressors ○ Circulatory assist devices ■ Intra-aortic balloon pump (IABP) ○ Dysrhythmias (see Chapter 26) ■ Hypokalemia ■ Hyperkalemia (ACEIs, ARBs, spironolactone) ■ Hyponatremia from diuretics ■ hypomagnesemia ○ Thromboembolism (see Chapter 30): decreased mobility and decreased circulation increase the risk for thromboembolism in patient with cardiac disorders, including those with HF ■ Pulmonary embolism: blood clot from the legs moves to obstruct the pulmonary vessels ■ S&S: dyspnea, pleuritic chest pain, tachypnea, cough ■ Treatment: anticoag therapy ■ Unfractionated heparin, low--molecular-weight heparin, fondaparinux (Arixtra), or rivaroxaban (Xarelto) ○ Pericardial effusion and cardiac tamponade ■ Pericardial effusion is the accumulation of fluid in the pericardial sac ■ Cardiac tamponade is the restriction of heart function because of this fluid, resulting in decreased venous return and decreased CO ■ Clinical manifestations: ill-defined chest pain or fullness, pulsus paradoxus, engorged neck veins, labile or low BP, shortness of breath ■ Cardinal signs of cardiac tamponade: falling systolic BP, narrowing pulse pressure, rising venous pressure, JVD, distant heart sounds ■ Management ● Pericardiocentesis: puncture of the pericardial sac to aspirate pericardial fluid ● Pericardiotomy: under general anesthesia, a portion of the pericardium is excised to permit the exudative pericardial fluid to drain into the lymphatic system ○ Pulmonary edema: as LV begins to fail blood backs up in the lungs, leads to pulmonary interstitial edema and often severe hypoxia; follows MI or HF ■ Clinical manifestations: restlessness, anxiety, dyspnea, cool and clammy skin, cyanosis, weak and rapid pulse, cough, lung congestion (moist, noisy respirations), increased sputum production (sputum may be frothy and blood tinged), decreased level of consciousness ■ Management: ● Prevention and early recognition ○ Monitor lung sounds and for signs of decreased activity tolerance and fluid retention ○ Hacking cough, dyspnea, fatigue, weight gain, increased edema ● Minimize exertion and stress ● Medications ○ O2, NRBM ○ Diuretics, vasodilators ● Positioning to promote circulation: upright with legs dangling decreases venous return, right ventricular SV, and lung congestion ● Psychological support, anticipatory care, reassurance ● Monitor meds ○ Sudden cardiac death or arrest ■ Emergency management: cardiopulmonary resuscitation ■ A: airway ■ B: breathing ■ C: circulation ■ D: defibrillation for VT and VF Chapter 30: Assessment and Management of Patients with Vascular Disorders and Problems of Peripheral Circulation Vascular System ● Two interdependent parts ○ Right side for pulmonary circulation ○ Left side for body tissues and systemic circulation ● Types of vessels ○ Arteries and arterioles ○ Capillaries ○ Veins and venules ○ Lymphatic Vessels ● Function ○ Circulatory needs ○ Blood flow and pressure ○ Capillary filtration and reabsorption ○ Hemodynamic resistance ○ Peripheral vascular regulation ● Gerontology: aging produces changes in the walls of the blood vessels that affect the transport of oxygen and nutrients to the tissues; changes cause vessels to stiffen and results in: ○ Increased peripheral resistance ○ Impaired blood flow ○ Increased left ventricular workload Vascular diseases ● Pathophys of Vascular Disease ○ Pump failure ○ Alterations of vessels ○ Circulatory insufficiency of extremities ● Assessment ○ Health history ■ Claudication ■ Rest pain ■ Location of pain ○ Physical assessment ■ Pulses ■ Skin: cool, pale, pallor, rubor, loss of hair, brittle nails, dry or scaling skin, atrophy, and ulceration ■ Edema ● Diagnosis ○ Doppler ultrasound flow studies ■ Continuous-wave Doppler ultrasound detects blood flow; combined with computation of ankle or arm pressures this diagnostic technique helps characterize the nature of peripheral vascular disease ○ Ankle brachial index (ABI) ○ Exercise testing ○ Duplex ultrasonography ○ Computed tomography scanning ○ Angiography and magnetic resonance angiography ○ Contrast phlebography (venography) ○ Lymphoscintigraphy Peripheral Arterial Occlusive Disease ● Hallmark symptom is intermittent claudication described as aching, cramping, or inducing fatigue or weakness ○ Occurs with some degree of exercise or activity ○ Relieved with rest ○ Pain is associated with critical ischemia of the distal extremity and is described as persistent, aching, or boring (rest pain) ● Ischemic rest pain is usually worse at night and often wakes the patient ● Medications ○ Pentoxifylline (Trental) ○ Cilostazol (Pletal) ○ Aspirin ○ Clopidogrel (Plavix) ○ Statins ● Assessment ○ Health history ○ Medications ○ Risk factors ○ Signs and symptoms of arterial insufficiency ■ Claudication and rest pain ■ Color changes ■ Weak or absent pulses ■ Skin changes and skin breakdown ● Diagnoses ○ Altered peripheral tissue perfusion ○ Chronic pain ○ Risk for impaired skin integrity ○ Knowledge deficient ● Goals ○ Promotion of vasodilatation ○ Prevention of vascular compression, relief of pain, attainment or maintenance of tissue integrity ○ Adherence to self-care program ○ Increase arterial blood supply, circulation ■ Exercises and activities: walking, graded isometric exercises. ● Note: consult primary health care provider before prescribing an exercise routine ■ Positioning strategies: keep extremities in lowered or dependent position ■ Temperature; effects of heat and cold ■ Stop smoking ■ Stress reduction Arterial Disorders ● Arteriosclerosis: Diffuse process whereby the muscle fibers and the endothelial lining of the walls of small arteries and arterioles become thickened and harden ● Atherosclerosis: accumulation of lipids, calcium, blood components, carbohydrates, and fibrous tissue on the intimal layer of the arteries ○ Atheromas or plaques ○ Common sites: ■ ○ Risk factors (also risk for PVD) ■ Modifiable: Nicotine, diet, HTN, diabetes, obesity, stress, sedentary lifestyle, CRP, hyperhomocysteinemia ■ Nonmodifiable: age, gender, genetics ○ Atheromas or plaques ● Peripheral arterial occlusive disease ● Upper extremity arterial occlusive disease ● Aortoiliac disease ● Aneurysms (thoracic, abdominal, other): a localized sac or dilation formed at a weak point in the wall of the artery ○ Classified by shape or form ■ Most common: saccular and fusiform ● Saccular aneurysm projects from only one side of the vessel ● When an entire arterial segment becomes dilated, a fusiform aneurysm develop ● Dissecting aorta ● Arterial embolism and arterial thrombosis ● Raynaud phenomenon and other acrosyndromes ○ Raynaud’s: Intermittent arterial vaso occlusion, usually of the fingertips or toes; phenomenon is associated with other underlying disease such as scleroderma ■ Manifestations: sudden vasoconstriction results in color changes, numbness, tingling, and burning pain ■ Episodes are usually brought on by a trigger such as cold or stress ● Protect from cold and other triggers, avoid injury to hands and fingers ■ Occurs most frequently in young women Venous Disorders ● Venous thromboembolism ○ Patho ○ Risk Factors ■ >65 years ■ Surgery or central venous cath placement ■ Septicemia ■ Pregnancy ○ Endothelial damage ■ Stasis ■ Altered coagulation ○ Manifestations ■ Deep veins: ■ Superficial veins: ○ If S/S present inform HCP immediately ○ Prevention: compression stockings, pneumatic compression devices, early ambulation, heparin or LMWH ■ Lifestyle changes: weight loss, smoking cessation, regular exercise ● Chronic venous insufficiency/postthrombotic syndrome ● Leg ulcers ○ Assessment: ■ History ■ Pain, pulses, edema ■ Presence of infection ■ Nutrition ○ Treatment depending on type of ulcer ■ Anti-infective therapy ■ Compression therapy ■ Debridement, dressings ■ Other ○ Diagnoses/ interventions/ outcomes ■ Impaired skin integrity related to vascular insufficiency ● Restore skin integrity ○ Cleanse wound ○ Positioning ○ Avoid trauma ○ Avoid heat ● Demonstrated restored skin integrity ■ Impaired physical mobility related to activity restrictions of the therapeutic regimen and pain ● Improve Mobility: initially restricted to promote healing ○ Encourage patient to move in bed and exercise upper extremities ○ Gradual progression ○ Activity to improve blood flow ○ Pain meds before ● Increases physical mobility ■ Imbalanced nutrition: less than body requirements related to increased need for nutrients that promote wound healing ● Promote adequate nutrition: high protein, high calorie, Vitamins C and A, iron (especially in older population due to increased anemia prevalence), Zinc ● Attains adequate nutrition ■ Promote home and community based care ○ Collaborative issues ■ Infection ■ Gangrene ● Varicose veins ○ Prevention: Avoid activities that cause venous stasis (wearing socks that are too tight at the top or that leave marks on the skin, crossing the legs at the thighs, and sitting or standing for long periods) ■ Elevate the legs 3 to 6 inches higher than heart level ■ Encourage to walk 30 minutes each day if there are no contraindications ■ Wear graduated compression stockings ■ Overweight patients should be encouraged to begin weight reduction plans Lymphatic Disorders ● Lymphangitis: inflammation or infection of the lymphatic channels ○ Characteristic red streaks that extend up the arm or the leg from an infected wound outline the course of the lymphatic vessels as they drain ● Lymphadenitis: inflammation or infection of the lymph nodes ● Lymphedema: tissue swelling related to obstruction of lymphatic flow ○ Primary: congenital ○ Secondary: acquired obstruction Cellulitis ● S&S: localized swelling or redness, fever, chills, sweating ● Treat with oral or IV antibiotics based on severity ● Nursing ○ Elevate affected area ○ Warm, moist packs to site every 2 to 4 hours ○ Educate regarding prevention of recurrence ○ Reinforce education about skin and foot care Chapter 31: Assessment and Management of Patients with Hypertension Hypertension aka high blood pressure: most common chronic disease in the US among adults, 33% have it and 46% of those don’t have it under control; most prevalent in African Americans ● Classification - review in patho notes ○ Blood pressure control ■ ○ Risk factors ■ Smoking ■ Obesity ■ Physical inactivity ■ Diabetes mellitus ■ Microalbuminura or GFR <60 mL/min ■ Older age ■ Family History ■ Dyslipidemia: elevated lipid levels ● Primary hypertension: essential ○ 95% unidentifiable causes ● Secondary: has a specific cause, mostly renal disease, sleep apnea, and pregnancy related ○ 5% of patients ● Clinical manifestations ○ Usually none other than elevated BP ○ Late stage ■ Retinal and other eye changes ■ Renal damage ■ Myocardial infarction ■ Cardiac Hypertrophy ■ Stroke ● Assessment ○ History and physical ■ Retinal exam ■ Assessment of potential systems from organ damage ● Angina, SOB, altered speech or vision, nosebleeds, headaches, dizziness, balance problems, nocturia ● CV: apical and peripher pulses ○ Lab tests ■ Urinalysis ■ Blood chemistry ○ ECG ● Management ○ Maintain blood pressure ■ <140/90 mm Hg ■ <150/90 mm Hg for older adult patients ○ Lifestyle modifications ■ Weight reduction: BMI within 18.5-24.9 ■ DASH diet, decreased sodium intake to less than 100 mmol/day ■ Regular physical activity ■ Reduced alcohol consumption ○ Medications to decrease peripheral vascular resistance and blood volume, decrease strength and rate of myocardial contractions ■ Diuretics, beta-blockers, alpha1-blockers, combined alpha- and beta-blockers, vasodilators, ACE inhibitors, ARBs, calcium channel blockers, dihydropyridines, and direct renin inhibitors ■ Stage 1 HTN ● African American and patients >60 yr : calcium channel blocker or thiazide diuretic ● Non African American and patients <60 yr: ACE-I or ARB ● Low doses are initiated, and the medication dosage is increased gradually if blood pressure does not reach target goal ● Multiple medications may be needed to control blood pressure ● Uncomplicated HTN: start thiazides ● Nursing Diagnosis/Goals ○ Deficient knowledge regarding the relation between the treatment regimen and control of the disease process ■ Understanding of the disease process and it’s treatment ■ Participation in self care program ■ Support and educate the patient about the treatment regimen ■ Reinforce lifestyle changes ■ Follow up care ○ Noncompliance with therapeutic regimen related to side effects of prescribed therapy ■ Absence of complications ■ Lower and controlling BP without adverse effects or undue cost ■ Take medications as prescribed ● Collaborative problems and potential complications ○ Left ventricular hypertrophy ○ Myocardial infarction ○ Heart failure ○ Transient ischemic attack (TIA) ○ Cerebrovascular disease (CVA, stroke, or brain attack) ○ Renal insufficiency and chronic kidney disease ● Evaluation and Outcomes ○ Reports knowledge of disease management sufficient to maintain adequate tissue perfusion ■ Maintains blood pressure at less than 140/90 mm Hg (less than 150/90 mm Hg for adults older than 60 years of age) with lifestyle modifications, medications, or both ■ Demonstrates no symptoms of angina, palpitations, or vision changes ■ Has stable BUN and serum creatinine levels ■ Has palpable peripheral pulses ○ Adheres to the self-care program ■ Adheres to the dietary regimen as prescribed: reduces calorie, sodium, and fat intake ■ Exercises regularly (30 mins most days a week) ■ Takes medications as prescribed and reports side effects ■ Measures BP routinely ■ Abstains from tobacco and excessive alcohol intake ■ Keeps follow up appointments ○ Has no complications ■ Reports no changes in vision; exhibits no retinal damage on vision testing ■ Maintains pulse rate and rhythm and respiratory rate within normal ranges; reports no dyspnea or edema ■ Maintains urine output consistent with intake; has renal function test results within normal range ■ Demonstrates no motor, speech, or sensory deficits ■ Reports no headaches, dizziness, weakness, changes in gait, or falls ● Gerontology ○ Medication regimen can be difficult to remember ■ Expenses can be a challenge ■ Monotherapy, if appropriate, may simplify the medication regimen and make it less expensive ■ Ensure that older adult patients understand the regimen and can see and read instructions, open medication containers, and get prescriptions refilled ○ Include family and caregivers in educational program Hypertensive emergency ● Blood pressure >180/120 mm Hg and must be lowered immediately to prevent damage to target organs ● Goals: reduce bp 20-25% in first hour and to 160/100 over 6 hours ○ Gradual reduction to normal over a period of days ○ Exception: Ischemic stroke and aortic dissection ● Medications ○ IV vasodilators: sodium nitroprusside, nicardipine, fenoldopam mesylate, enalaprilat, nitroglycerin ● Need very frequent monitoring of BP and cardiovascular status Hypertensive urgency ● Blood pressure is very elevated but no evidence of immediate or progressive target organ damage ● Oral agents can be administered with the goal of normalizing blood pressure within 24 to 48 hours ○ Fast-acting oral agents: ■ Beta-adrenergic blocker: labetalol ■ Angiotensin-converting enzyme inhibitor: captopril ■ Alpha2-agonist: clonidine ● Patient requires close monitoring of blood pressure and cardiovascular status ● Assess for potential evidence of target organ damage [Show More]

Last updated: 1 year ago

Preview 1 out of 94 pages

Add to cart

Instant download

We Accept:

We Accept
document-preview

Buy this document to get the full access instantly

Instant Download Access after purchase

Add to cart

Instant download

We Accept:

We Accept

Reviews( 0 )

$18.00

Add to cart

We Accept:

We Accept

Instant download

Can't find what you want? Try our AI powered Search

OR

REQUEST DOCUMENT
93
0

Document information


Connected school, study & course


About the document


Uploaded On

Mar 18, 2023

Number of pages

94

Written in

Seller


seller-icon
securegrades

Member since 4 years

118 Documents Sold


Additional information

This document has been written for:

Uploaded

Mar 18, 2023

Downloads

 0

Views

 93

Document Keyword Tags

Recommended For You

Get more on MED-SURG EXAM »

$18.00
What is Browsegrades

In Browsegrades, a student can earn by offering help to other student. Students can help other students with materials by upploading their notes and earn money.

We are here to help

We're available through e-mail, Twitter, Facebook, and live chat.
 FAQ
 Questions? Leave a message!

Follow us on
 Twitter

Copyright © Browsegrades · High quality services·