RESP Study PDF

Week 1 - Sept 6 2024: Lower respiratory disorders & respiratory failure Week 1 - Sept 6 2024 Lower respiratory disorders & respiratory failure - Synchronous session 10:00 - 11:30 - In class activities: - Course overview - Directed discussion - Nursing interventions...

Week 1 - Sept 6 2024: Lower respiratory disorders & respiratory failure Week 1 - Sept 6 2024 Lower respiratory disorders & respiratory failure - Synchronous session 10:00 - 11:30 - In class activities: - Course overview - Directed discussion - Nursing interventions in respiratory failure - Advanced airway management - Mechanical ventilation overview - Topics: - Lower respiratory disorders and respiratory failure including artificial airways and invasive ventilation - Readings: - Ch. 28 - Ch. 29 (p. 575 @ airway obstruction - p. 580) - Ch.30 (p. 610-629) - Ch. 40 (p. 914-922) - Ch. 68 (p. 1713-1722) - Ch. 70 Objectives - Review structures & functions of the respiratory system - Review fundamental components of a respiratory assessment - Differentiate between hypoxia and hypoxemia - Differentiate between hypoxemic and hypercapnic respiratory failure - Identify the following V/Q relationships: normal unit; V/Q mismatch; shunt; dead space - Identify common pathologies and disorders that contribute to respiratory failure (including venous thromboembolism & chest trauma) - Describe ARDS - Describe key concepts related to non-invasive & invasive respiratory support including modes of ventilation - Describe nursing interventions related to respiratory failure - Analyze arterial blood gasses Upper respiratory tract - Provides protection to lower airways - Nasal passages - Epiglottis - Air is warmed & humidified & filtered *main fx of URT - Olfactory receptors *Use of advanced airways in relation to the main fx of tract is that it is no longer provided by natural mechanisms so be mindful in pt care (as well as pts losing ability to also vocalize and smell) Lower respiratory tract - Carina (landmark for lower respiratory tract) - Ventilation *movement of air between atmosphere & alveoli, and distribution between lungs - Respiration *process of gas exchange; movement of oxygen from atmosphere to blood stream and movement of carbon dioxide from blood stream to atmosphere - Compliance *measure of elasticity of lungs and thorax, when its decreased in eg. states of inflammation; it is very difficult to inflate our lungs, fluid filled situations; problem with compliance or things like pulmonary edema and ARDS - Elastance *pathology that affects elasticity are fibrosis and sarcoidosis *Left side of lungs has 2 lobes (LU, LL) and 8 segments *Right side of lungs has 3 lobes (RU, RM, RL) and 10 segments *Big concept of oxygenation, ventilation, and respiration is the importance of distinguishing them Key landmarks - Carina *Sits at the bifurcation of the left and right main stem bronchi (when looking at pt with advanced airway support and eg. they have an endotracheal tube in place, they are likely being provided sedation and analgesia so they have an altered LOC purposefully; stimulating the carina is one mechanism we can look at to test a pts ability to protect their airway, elicit stimulation of carina with eg. suction catheter should under normal circumstances produce a cough. In intubated/ sedated pts, this is how we perform some cranial nerve testing) - Left & right main bronchus *There is a different angle on the left in which it has an acute angle vs right mainstem is a bit straighter; keep in mind that there is a higher risk of aspiration to the right side than left due to anatomical differences (eg. pt that has aspirated food), other thing to keep in mind when looking at advanced airways is the possibility of intubating the right side inadvertently instead of tube coming down about 2 cm above carina (if pt has gone through a procedure and was placed on mechanical ventilator, first intervention is have a look for symmetry in chest expansion to ensure no marked differences between left and right; if we see more movement/ ventilation on right side we might have right mainstem intubation) - Anterior vs posterior trachea *Anterior has cartilaginous rings that provide protection and keep trachea open, vs posteriorly we have smooth muscles; keep in mind for risks using advanced airways (eg. endotracheal tube pt) as there is an inflated cuff and pressure against posterior trachea, so we run the risk of tissue damage and tracheoesophageal fistulas; must be mindful of pressure and impact it can have on posterior trachea Respiratory airways *Conducting airways; trachea, segmental bronchi, non respiratory subsegmental bronchi (bronchioles) *Respiratory unit: respiratory subsegmental bronchi (bronchioles), alveolar ducts - Respiratory bronchioles - Primarily smooth muscle *keep in mind they are prone to bronchoconstriction or bronchodilation (eg. pt with acute exacerbation of asthma with profound bronchoconstriction and we are using bronchodilators to mitigate that), another thing to keep in mind is some pt airways become very sensitive and we can actually cause bronchospasm as we manipulate pts/ their airways - Alveoli *functional unit itself  - Surfactant *phospholipid, fx is to stabilize alveoli to increase lung compliance and ease the work of breathing, also provides surface tension that we need to keep alveoli open - Blood supply *alveoli are rich in blood supply (eg. when pulmonary embolism occurs, what happens in this capillary network is fast and it receives the entire cardiac output to give us indication on role it plays) - Type I & II alveolar epithelial cells *type 1 cells make up 90% of total lung surface area and are main structural cells; play a major role in gas exchange, type 2 cells are less in # but they produce, store and secrete surfactant (when we have injury to alveolar wall, type 2 cells will divide and line the surface to become type 1 cells) - Alveolar macrophages *play a phagocytic role, keep the alveoli clean, keep in mind that although alveolar network are individual units there is communication between them through the pores of kohn, so alveolar macrophages help keep these spaces clean normally Pulmonary circulation - *In consideration of the pulmonary circulation, the alveolar capillary membrane is extensive - Each red blood cell spends ~¾ of a second *in this interface - *During that time it is exposed to alveolar gas of 2-3 alveoli because of how they communicate (we look at venous oxygen saturation; blood returning to pulmonary vasculature to be reoxygenated, goes from 75% to >96% in less than ¾ of a second *Our pulmonary artery wanting to situate that, is the only artery in the body that receives venous/ deoxygenated blood, it divides into the left and right branches and the branching continues to form the capillary that surround the alveoli (oxygenated blood returns to the left atrium via the 4 pulmonary veins), largest vascular bed and receives the entire cardiac output Muscles of ventilation: inhalation & exhalation mechanisms - Inhalation is primarily diaphragmatic (innervated by medulla and phrenic nerve) *becomes an issue with C spine injuries - Exhalation is more of a passive event (becomes more active with exercise) *when looking at pulmonary disease that decrease compliance; it is often in our muscles of ventilation, so in actually observing inhale and exhale processes that we will notice increased work of breathing in pts *Diaphragm contracts on inspiration, external intercostals elevating ribs to provide expansion Oxygen hemoglobin dissociation curve - “Right releases” - Y axis = oxygen saturation % - X axis = PaO2 mmHg - Factors shifting curve to the left: 1. ↑ pH 2. ↓ pcO2 3. ↓ temperature 4. ↓ 2, 3 DPG (hexokinase deficiency, hypothyroidism, bank blood) 5. Some congenital hemoglobinopathies (hemoglobin rainier, hiroshima, san francisco) 6. Carboxyhemoglobin - Factors shifting curve to the right: 1. ↓ pH  2. ↑ pcO2 3. ↑ temperature 4. ↑ 2, 3 DPG (pyruvate kinase deficiency, hyperthyroidism, anemia, chronic hypoxemia; high altitude and congenital heart disease) 5. Some congenital hemoglobinopathies (hemoglobin kansas, seattle) *Important things when considering respiratory failure: - Looking at partial pressure of oxygen (amount of oxygen dissolved in the plasma), eg. recall arterial blood gasses (paO2, paCO2) we look at oxygen and or carbon dioxide dissolved in the plasma - From respiratory perspective, when looking at normal curves (B curve), a paO2 of 80 to 100 being normal, then we look at paO2 of 60, and another axis with O2 sat, we will see that between a paO2 of 100/ 90/ 80, we see little change in spO2/ oxygen saturation - With paO2 of 60 mmHg (definition of hypoxemic respiratory failure), very little change in spO2 at that point - Pt can have O2 sat of 90% but if we look at ABG it can be concerning as we have a PaO2 of 60 mmHG, past 60 is a steep decline in oxygen saturation - In situations where there is a curve shift to left or right, it has other implications on our saturation and how well the body is able to compensate - When looking at right shift, recall that hemoglobin under these circumstances (acidosis, increase pcO2, elevated temp), hemoglobin will let go of oxygen molecule - Whereas in left shift (eg. alcoholic pt, decreasing pcO2, hypothermic), hemoglobin doesn't want to let go of oxygen; supplemental oxygen is so important here - Under normal circumstances when oxygen is bound to hemoglobin, 97% of oxygen is bound to hemoglobin (when we look at paO2/ partial pressure of oxygen dissolved in the plasma, only about 3% of available oxygen is dissolved in plasma but the rest is bound) - Hemoglobin abnormalities are possible, in which they affect oxygen carrying capacity (eg. sickle cell anemia; we have impaired oxygen carrying capacity, methemoglobin; where iron in hemoglobin molecule changes from ferrous (2+) to ferric (3+) state and it does not have the ability to carry oxygen, carboxyhemoglobin; hemoglobin has greater affinity to carbon dioxide molecule than it does the oxygen molecule therefore we can easy have oxygen monoxide bound to hemoglobin and it doesn't want to let it go therefore keep in mind with carbon monoxide injury and spO2 is that the spO2 monitors cannot distinguish what is bound to hemoglobin so it can be carbon monoxide that is bound and not oxygen and still have a reading of 100% spO2 Respiratory assessment review - Subjective health information - Past health history *relevant to problem history and what they are experiencing now - Medications *what is effective or not - Surgeries or other treatments - Current health history - Objective health information - Vital signs - Inspection *chest wall configuration (eg. COPD pt has barrel chest), spinal deformities that can result in catharsis or lumbar lordosis, looking at normal WOB and RR we see ranges from 10 to 20 being normal, on infection we look for rhythm and symmetrical chest movement,  looking at pt body positions (eg. sitting up in tripod), are they able to lie flat (unlikely in resp distress pts), what is effort of breathing (eg. muscle use or intercostal retraction), trachea (midline or deviation), unequal movement of chest (eg. flail chest, intubation of right mainstem and it needs to be pulled back) - Palpation *look at thoracic expansion, is chest symmetrical, trachea is palpable and midline, tactile fremitus (palpable vibration using the word“99”, increased over areas of consolidation eg. pneumonia) - Percussion and auscultation: Auscultation - Fine crackles = series of short, explosive, high pitched sounds heard just before end of inspiration; rapid equalization of gas pressure when collapsed alveoli or terminal bronchioles suddenly snap open; sounds similar to rolling hair between fingers just behind ear *heard at bases esp when we have fluid filled lugs or pts with early signs of pulm edema - Coarse crackles = series of short, low pitched sounds on inspiration and sometimes expiration; air passing through airway intermittently occluded by mucus, unstable bronchial wall, or fold of mucosa; sounds similar to blowing through straw under water (increase in bubbling quality with more fluid) *severe pneumonia or significant pulm congestion - Wheezes = continuous high pitched squeaking sound caused by rapid vibration of bronchial walls; first evident on expiration; possibly evident on inspiration as obstruction of airway increases; possibly audible without stethoscope - Stridor = continuous musical sound of constant pitch; result of partial obstruction of larynx or trachea *significant airway obstruction, heard as though its very far away - Absence of breath sounds = no sound evident over entire lung or area of lung *pleural effusion, widespread atelectasis, non functional alveoli - Pleural friction rub = creaking or grating sound occurs when roughened, inflamed surfaces of pleura rub together; evident on inspiration, expiration, or both; no change with coughing; usually painful, especially on deep inspiration - *bronchial breath sounds = not over trachea or throat but listening in other lung fields, clear breath sounds, very hallow and easily heard, may think breath sounds are amazing and heard everywhere but if they are outside of normal anatomical location they are concerning finding/ adventitious sound Percussion sounds - Resonance = low pitched sound heard over normal lungs - Hyperresonance = loud, lower pitched sound than normal resonance heard over hyperinflated lungs, as in chronic obstructive lung disease and acute asthma *think air - Tympany = drumlike, loud, empty quality heard over gas filled stomach/ intestine or pneumothorax - Dull = medium intensity pitch and duration heard over areas of "mixed" solid and lung tissue, like over top area of liver, partially consolidated lung tissue (pneumonia), or fluid filled pleural space - Flat = soft, high pitched sound of short duration heard over very dense tissue where air is not present Configurations of the thorax: Normal adults - Thorax has elliptical shape with anteroposterior to transverse ratio of 1: 2 to 5:7 Barrel chest  - Note equal anteroposterior to transverse ratio and that ribs are horizontal instead of the normal downward slope, this is associated with normal aging and also with chronic emphysema and asthma as a result of hyperinflation of lungs Pectus carinatum - Forward protrusion of the sternum, with ribs sloping back at either side, and vertical depressions along costochondral junctions (pigeon breast), less common than pectus excavatum, this minor deformity necessitates no treatment (surgery if severe) Pectus excavatum - Markedly sunken sternum and adjacent cartilages (also called funnel breast), depression begins at second intercostal space, becoming depressed most at junction of xiphoid process with body of sternum, more noticeable on inspiration, congenital and usually not symptomatic, when severe sternal depression may cause embarrassment and a negative self concept (surgery may be indicated) Scoliosis - Lateral S shaped curvature of the thoracic and lumbar spine usually with involved vertebrae rotation, note unequal shoulder and scapular heights, unequal hip levels, and rib interspaces flared on convex side, onset is more prevalent in adolescent age groups (esp girls), mild deformities are asymptomatic, if deviation is severe (>45 degrees) scoliosis may reduce lung volume; then pt at risk for impaired cardiopulmonary function (primary impairment is cosmetic deformity, negatively affecting self image, refer early for treatment which is often surgery) Kyphosis - Exaggerated posterior curvature of the thoracic spine (humpback) that causes significant back pain and limited mobility, severe deformities impair cardiopulmonary function, if neck muscles are strong the pt compensates by hyperextension of head to maintain level of vision, kyphosis has been associated with aging esp in cases of "dowager's hump" in postmenopausal women with osteoporosis, common well before menopause, related to physical fitness; women with adequate exercise habits are less likely to have kyphosis Focused respiratory assessment Subjective (ask pt and note responses): - Shortness of breath - Wheezing - Sputum production (color, quantity) - Pain with breathing *pulm embolism has sharp chest pain when breathing - Cough *productive or non productive Objective - Diagnostic (check lab results for critical values) - Arterial blood gas measurements - Chest radiographic examination - Hematocrit, hemoglobin measurements *must be adequate for oxygen carrying capacity - Physical exam - Observe: - Respirations for rate, quality and pattern - Facial expression, level of consciousness, position pt takes to breath *altered LOC/ behavioral changes are earliest sign of hypoxemic process occurring - Inspect:  - Skin and nails for integrity and color *clubbing, angle of nail bed - Accessory muscle use and position of trachea - Shape, symmetry and movement of chest wall - Palpate: - Chest and back for masses - Tactile fremitus - Auscultate: - Lung (breath) sounds *look for decrease in breath sounds at bases or adventitious Arterial blood gas values - pH = 7.35 to 7.45 - Partial pressure of oxygen (paO2) = 80 to 100 mmHg *3% of available oxygen, oxygen dissolved in plasma - Oxygen saturation = ≥95% *can see very little change until we have paO2 of 60 - Partial pressure of carbon dioxide (paCO2) = 35 to 45 mmHg - HCO3 = 21 to 28 mmol/ L (VBG same) Mixed venous blood gas values *only attainable when pt has pulmonary artery catheter - pH = 7.31 to 7.41 - Partial pressure of oxygen (paO2) = 40 to 50 mmHg - Oxygen saturation = 60 to 80% - Partial pressure of carbon dioxide (paCO2) = svO2 is better indicator for change in acid base balance - HCO3 = 21 to 28 mmol/ L Critical values for paO2 and spO2 РаO2 SpO2 Considerations: ≥70% ≥95% Adequate unless ptt is hemodynamically unstable or has O2 unloading problem. With a low cardiac output, dysrhythmias, a leftward shift of the oxygen hemoglobin dissociation curve, or carbon monoxide inhalation, higher values may be desirable. Benefits of a higher arterial O2 level must be balanced against risk of O2 toxicity 60% 90% Adequate in almost all pts. Values are at steep part of oxygen hemoglobin dissociation curve. Oxygenation is adequate, but margin of error is less than for higher values 55% 88% Adequate for pts with chronic hypoxemia if no cardiac problems occur. These values are also used as criteria for prescription of continuous O2 therapy *tolerate sat of 88 for COPD pts 40% 75% Inadequate but may be acceptable on a short term basis if pt also has CO2 retention. In this situation, respirations may be stimulated by a low paO2. Thus, the paO2 cannot be raised rapidly. O2 therapy at a low concentration (24%-28%) will gradually increase paO2. Monitoring for dysrhythmias is necessary