EMS overview of Asthma and COPD lecture.ppt

Editor's Notes

• #2: ? Take out albuterol slides - or decrease to 1 slide
• #12: Tripodding Pallor Cyanotic Pursed lips Anxious look on face Accessory muscles Barrel chest
• #16: Bronchospasm: -drastic increase in resistance to air flow in the bronchioles, -makes inhalation and particularly exhalation extremely difficult -resulting in wheezing and feeling of “shortness of breath” Edema: -Due to leaky capillaries in the lung related to the chemicals that trigger asthma attack -Bronchial wall edema causes smaller airways to collapse, which leads to increased WOB during exhalation Mucus plugging: -These thick secretions lead to the characteristic cough of asthma -Plugs usually made of mucus, serum proteins, inflammatory cells, and cellular debris
• #18: Histamine, prostaglandins, leukotrienes
• #19: There is also a component of chronic asthma changes with increases in connective tissue, thicker mucosal layer, and thicker muscular layer.
• #20: Normal gas exchange, CO2 out, O2 in. Normal thin walled airways vs thickened, inflammed airways. Gas exchange is less effective in thickened airways, longer distance for CO2 and O2 to move.
• #21: Active: -Inhalation uses diaphragm and chest wall muscles. -Muscle expansion causes negative intrathoracic pressure, which sucks air in. Passive: -Once full breath is in, muscles relax, and recoil of chest returns chest to resting position. -The negative pressure returns to neutral pressure, chest wall contracts to original position. - -Exhalation of air is passive process. Asthma exacerbation: -With narrowing and collapse of airways, exhalation becomes difficult and requires energy, which leads to increased work of breathing and shortness of breath. -Exhalation becomes active, requiring accessory muscles of respiration. -This can lead to respiratory tiring, exhaustion, and eventually respiratory failure.
• #22: Wheezing: asthma, respiratory infections, CHF Stridor: epiglottitis, anaphylaxis, aspirated foreign body, tracheomalacia,
• #25: Management of asthma: 1.) Objective measures of lung function - formal pulmonary function tests (PFTs) performed by a pulmonologist. -Helps patients to know baseline lung function and response to therapies aimed at improving baseline lung functions and preventing asthma attacks.
• #26: FEV1 is not a measure that we use in prehospital and emergency care. The reason I’m explaining this, is that FEV1 is a surrogate marker for peak flow, and that a lot of the studies that I’ll mention later use FEV1 as a measure of lung function. Just know that is is a measure of lung function commonly used.
• #28: Spectrum of illness ranging from mild intermittent with symptoms less than twice per week, and nighttime symptoms less than twice per month to severe persistent asthma with continuous daytime symptoms and frequent nighttime symptoms. In mild, normal PF is at least 80% of expected although can be much lower in setting of acute asthma attack. In severe, normal PF is less than 60% expected, and much less in acute exacerbation.
• #30: 2.) Environmental control measures. -Involves patient paying attention to what individual triggers are and how to minimize / avoid these triggers. -Often with the help of an allergist - allergen testing, desensitization through allergy shots
• #34: 3.) Comprehensive pharmacologic therapy -Treating acute asthma attack is life-saving treatment, paramount to prehospital care -May also be able to advise patient on the importance of having a better regiment of medications if your history reveals frequent episodes or suboptimal therapy.
• #35: Rescue meds: either bronchodilators / beta-agonists or quick acting antiinflammatory agents. Preventative meds: long-acting bronchodilators, long-acting anti-inflammatory, and meds to reduce triggered cascade with release of inflammatory mediators.
• #38: Leukotriene modifiers and mast cell stabilizers are designed to prevent inflammatory cells from being so hyper-responsive in the initial trigger of asthma attack. Release fewer of inflammatory mediators (histamine, etc) Leukotriene modifiers are also used for seasonal allergies, chronic urticaria, and exercise-induced bronchospasm. Mucomyst is a mucolytic, reduces viscosity of pulmonary secretions, but can actually increase volume of bronchial secretions and worsen acute asthma.
• #39: 4.) Patient education - linked to all 3 above components. - Educate on objective measures of lung function (know baseline peak flow) - Environmental measures (pets, dust?) need allergist? - Pharmacologic therapy - I’ve met patients in the ED who use their albuterol MDI twice daily faithfully, but only use inhaled steroid when “things get really bad,” which you know is totally backwards
• #40: Examples of inadequate patient education: Albuterol bid regardless of symptoms Flovent or Advair only when severe Not using Singulair or other preventative regularly or stopping because their asthma attacks have become less frequent. (Well, if you don’t like your attacks being so infrequent, then by all means, stop taking the preventative medication)
• #41: Remember… tripodding, tachycardic, sats 87%…..
• #42: SAMPLE history (signs/symptoms, allergies, meds, past medical history, last oral intake, events leading up to) OPQRST history: Onset, Provocation, Quality, Region/Radiates, Severity, Time
• #43: SAMPLE history (signs/symptoms, allergies, meds, past medical history, last oral intake, events leading up to) OPQRST history: Onset, Provocation, Quality, Region/Radiates, Severity, Time
• #44: So, you now have a history of present illness, but what other things about this person’s disease will be important to you and should clue you in to a sicker patient?
• #45: Other than IV, O2, monitor Airway management per local protocol if needed
• #47: Decreased RR good sign in setting of improving sats, patient comfort, and other clinical measures. Bradypnea can also be a foreboding sign in the setting of respiratory fatigue, decreasing O2 sats, and other signs of clinical worsening.
• #48: Conversely, if you heard wheezing before, and now you do not hear wheezing, do not assume patient is better, could actually be worse, with little to no air movement at this time. Do not delay administration of oxygen and/or albuterol if peak flow not readily available.
• #50: Pediatric patients are extremely sensitive to manipulation of airway, and any manipulation (OPA, etc) can produce hypoxia and respiratory arrest. If child is maintaining their airway, let them be, while, of course, providing them with oxygen, albuterol if needed, and any other appropriate therapies.
• #51: If become hypokalemic, may see arrhythmias, and/or EKG abnormalities.
• #52: If you have a patient with minimal improvement after 3 nebs, then give them a 4th, 5th,, 6th…
• #53: Albuterol overdose management “Generally considered safe” Keep in mind, however, that as a sympathomimetic, tachycardia and hypertension may adversely affect some individuals. If during albuterol administration, patient develops chest pain, should check 12 lead EKG, get more history about the CP, consider stopping the albuterol. Pediatric potential toxic dose <6 years old = 1mg/kg. Over 6 years old, treat as adult. Each dose of nebulized albuterol is 2.5 mg. In a 2 year old child (weight 12kg), max amount is 12 mg = 5 nebs.
• #54: Population included all acute asthma attacks with an FEV1 < 50% predicted. If you break down the results by severity of asthma attack, there was an even higher benefit in patients whose initial FEV1 was <30% expected (those asthma attacks with a more severe obstruction), and in those with duration of symptoms > 24 hours.
• #58: Benefit in giving - the earlier the better for the patient Any adverse effects? Does not appear to be any in the acute treatment of asthma. No clinical difference in PO and IV steroids. Both have onset of action at 4 hours so are targeted at reducing phase 2 of asthma attack. So, if you’re called to evaluate a patient in resp distress due to asthma who is already on oral Prednisone, should you administer Solu-medrol?? Yes, won’t hurt, can only help. If someone is admitted to hospital for asthma attack, they will sometimes get steroids q 6 hours.
• #59: 2 year old child 12 kg
• #60: FEV1 measured, which is volume exhaled in 1 second, good measure of lung expiratory function. Can consider this similar to PF.
• #61: No ipratropium - you could argue that trying to replace ipratropium with magnesium was a failure, that much better results when ipratrpium was added to albuterol. Need to see a study with real maximal treatment of severe asthma attacks (steroids, albuterol, ipratropium) with and without magnesium. On the flip side, doesn’t seem to have really any adverse effects, so it won’t hurt…why not give it?
• #64: Can consider adding also if you’re providing maximal therapy with steroids, albuterol, ipratropium, and patient is getting worse. May help if patient is progressing towards respiratory failure and could prevent need for intubation. Plus, if patient goes into respiratory failure, cardiac arrest is eminent without prompt airway management, and epinephrine would, of course, then be indicated. (PEA, asystole) So if you foresee a patient headed this way, might as well give epinephrine a little earlier.
• #68: Hyperinflated lungs of severe asthma attack are susceptible to barotrauma (trauma from positive pressure ventilation) and subsequent pneumothorax. In resp failure and impending resp failure, intubation can be used in conjunction with standard therapy. Last ditch effort as intubation does not treat the underlying mechanism of disease. Still have airway inflammation and edema, still have inqdequate gas exchange, etc.
• #69: “Standard therapy” included albuterol, ipratropium nebulized, IV steroids, oxygen as needed, and all were reassessed frequently using FEV1 to follow response to therapy.
• #73: So, basically - no change in management. Transport rapidly, be prepared. Call med control.
• #75: Diagnosis of chronic bronchitis is made with presence of chronic productive cough for at least 3 months in each of previous 2 years after other causes of chronic cough have been excluded. Emphysema is defined as abnormal permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied with destruction of their walls, without evidence of fibrosis. Chronic bronchitis is defined by symptoms, whereas emphysema is defined by anatomic pathology. Conversely, the World Health Organization does not differentiate between chronic bronchitis and emphysema. The WHO definition of COPD is airflow limitation/obstruction that is not fully reversible, that is generally progressive and associated with abnormal inflammatory response to noxious particles or gases (which most of the time is cigarette smoke)
• #76: Emphysema - destruction of alveoli walls and sacs, functional lung tissue replaced by dilated, non-functioning areas of dead space. With enlargement / dilation of alveoli (air sacs), you get hypoxia from decreased surface area for gas exchange. Compared with normal lung tissue with many small, healthy, functioning alveoli. Able to adequately perform simple gas exchange; CO2 out, O2 in.
• #77: Pink puffers: emphysema, usually very thin, muscle wasting, distant lung sounds due to hyperinflation. Blue bloaters: chronic bronchitis, usually not as thin as patients with emphysema, have more bronchial / rhonchorus breath sounds due to chronic inflammation. 85% of COPD is chronic bronchitis, 15% is emphysema
• #81: PPV - CPAP and BiPAP have become very accepted in prehospital treatment of COPD.