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Pulmonary Reduced Flashcards Preview

!!!! Oral - SIMPLY SLIDES (co-existing + principals) > Pulmonary Reduced > Flashcards

Flashcards in Pulmonary Reduced Deck (36)
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1

Characteristics COPD and asthma:

Chronic Obstructive diseases characterized by:

  • Chronic airway inflammation
  • Airway wall thickening (epithelial, submucosa and smooth muscle) → impairs gas exchange
  • Expiratory airflow obstruction
    • ​Asthma = reversible
    • COPD = not reversible or incompletely reversible​​
  • Airway hyperreactivity

2

Causes of asthma exacerbations:

  1. Allergens
  2. Exercise
  3. Nightime/sleep
  4. Chemicals (ASA/NSAIDs, VAs, irritants)
  5. Cold
  6. Infection

3

S/s of asthma:

  1. Wheezing
  2. Breathlessness/Air Hunger
  3. Chest tightness
  4. Early AM or nighttime cough
  5. Reversible airflow obstruction
  6. Tachypnea
  7. Prolonged expiratory phase
  8. Fatigue

4

Pre-op assessment of asthma:

  1. Triggers
  2. Severity (med requirements)
  3. Degree of reversibility w/ tx
  4. Current status, symptoms
  5. Prior anesthesia history
  6. Breath sounds
  7. general appearance, etc

5

Pre-op labs for asthma:

  1. PFTs
  2. ABG
  3. ECG (RH failure)
  4. CBC (eosinophils)
  5. CXR (hyperinflation of lungs)

6

Pre-op meds for asthmatics:

  1. Benzos
    1. anxiety can precipitate bronchospasm bronchospasm)
  2. Opioids
    • be sure to titrate carfully
  3. H2 antagonists
    • unopposed H1 antagonism may cause bronchoconstriction- Use Caution!
  4. Bronchodilators
    • albuterol) - 15-30 min before 
  5. Pre-op steroids - prohylaxis
    • Hydrocortizone 100 mg q8h if FEV1 predicted 

7

Overall goal for induction of anesthesia in asthmatics

GOAL= Blunt airway reflexes and avoid bronchoconstriction during airway instrumentation

  1. Consider Regional (good choice)
  2. Whenever possible, use LMA for smoother emergence/extubation
  3. GA should:
    1. ​depress airway reflexes 
      • Lidocaine 1-1.5 mg/kg IV (consider LTA)
      • Opioids -judiciously (fentanyl and analogues)
    2. Avoid hyperreactivity 
      • Use High MAC >1.5 for bronchodilation and bronchial reflex inhibition (Sevo and halothane are the least irritating)
      • ​AVOID desfluane/isoflurane - airway irritant
      • Propofol and ketamine is best for induction
        • avoid Sodium metabisulfite prep 
        • Higher end of induction doses
      • Ketamine will increase secretions which may irritate the airway, but does bronchodilate - maybe give some glyco?
      • Maybe AVOID ketoralac/NSAIDS - increased leukotrienes via lipooxygenase pathway
    3. Treat bronchoconstriction 
      • ​albuterol
      • sevoflurane
    4. AVOID histamine realease
      • ​​Sux, atricurium, mivicurium, D-tubo, morphine, demerol, thopental
    5. ​​​Neostigmine is ok for reversal, but MUST be given with anticholinergic - glycopyrolate

8

Maintenance of anesthesthesia in asthmatics:

  1. High concentration VA
    1. Sevo/halo are least pungent/irritating
  2. Avoid histamine releasers (sux, atra, miva)
  3. Avoid bronchospasm

9

Ventilation goals for asthmatics:

Ventilation

  1. Avoid PEEP !! →prone to air trapping
    • these pts may have intrinsic peep r/t air trapping
    • during an acute attack, may see “breath stacking”
  2. Decrease RR (8-10 bpm) - allows for adequate exhalation 
  3. Longer I:E ratio
  4. Increase TV - to maintain Normal PaCO2
    1. TV and inspiritory flow rates are limited by excessive peak airway pressures
    2. Upper Limit - 40 cm H2O

  5. If you can choose a mode – consider using PCV over  volume controlled ventilation

  6. Liberal hydration of pt and circuit

    • Place a humidifier in the breathing circuit

10

Treatment of intra-op bronchospasm:

  1. FiO2 to 100%
  2. Deepen anesthesia with VA or drugs
  3. Give a ß-agonist
  4. If no air movement:
    1. Epinephrine IV: 2-8 mcg/min (SQ 0.3-0.5mg q20-30min)
    2. Terbutaline (SQ)
    3. Corticosteroids: 1-2 mg of cortisol
  5. Other IV broncholilators
    1. Ketamine
    2. Propofol
    3. Lidocaine  

11

Emergence/post-op care for asthma:

  1. Smooth emergence - ETT promotes bronchoconstriction and airway resistence
  2. Pre-emptive albuterol, IV lido 10-15 minutes prior to wake up
  3. Deep extubation if possible
  4. If not, try to get patient to SV as early as possible

12

COPD pathology

  • Progressive airway obstruction
    • not reversible or incompletely reversable
  • Cell death and destruction of alveoli d/t
    • impaired lung parenchyma, degraded matrix, toxic action of macrophages nad neutrophils (inflammatory respnse)
  • Resultant enlargement of airspaces, fibrosis and mucous production
  • Inflammatory process →
    • steroids have limited effect(reduce frequency of exacerbations
    • bronchodilators have only modest effects
  • Chronic bronchitis and/or emphysema
  • Smoking #1 risk factor

13

COPD staging:

  1. Stage 1: FEV1 > 50% predicted
  2. Stage 2: FEV1 35-49%
  3. Stage 3: FEV 1 <35% predicted

14

"Blue bloaters":

  1. Chronic bronchitis
  2. PaO2  <60 →cyanosis and dusky appearance
  3. PaCO2 > 45
  4. Copious secretions cause obstruction
  5. Cough
  6. Diminshed breath sounds
  7. Pulmonary hypertension d/t HPV
  8. Marked cor pulmonale/righ sided heart failure
  9. Overweight 
  10. CXR: increased bronchovascular markings

15

"Pink puffers":

  1. Emphysema
  2. PaO2 > 60
  3. Normal PaCO2 
  4. Obstruction due to loss of recoil
  5. Severe dyspnea
  6. Very diminished breath sounds
  7. Tend to be thin
  8. anxious, pursed lips
  9. CXR: hyperinflation with a low diaphragm

16

Smoking cessation timeline:

  1. 12-24 hours:
    • decreased carboxyhemoglobin levels to normal
  2. 2-3 weeks:
    • ciliary function improves, increased airway secretions, hyperreactivity
  3. 4 weeks: PFTs improve
  4. 8 weeks:
    •  decreased rate of postoperative complications
    • immune, metabolic function normalizes

​(if patient cannot quit for four weeks before surgery, it is better to only have them quit for 24 hours before)

17

Induction in COPD patients:

GOAL= minimize risk of post op respiritory failure

  1. Caution with pre-medication
    • They don’t tolerate respiratory depressant effects of drugs (medulla is “reset” d/t chronic hypercarbia, so these pts are less sensitive to ↑ levels of CO2)
    • Hold opioids until the pt is hooked to monitors and with oxygen on
  2. Ketamine is good for pts who tolerate the CV effects, otherwise propofol
  3. Regional is a good choice: Avoid levels > T6
  4. Depress airway reflexes/reactivity
    • Lidocaine 1-1.5 mg/kg IV (consider LTA)
    • Opioids -judiciously (fentanyl and analogues)
    • Consiter comorbitities for other agents (Heart failure??)
    • Sevo may be best for bronchodilation (least irritating)​
    • AVOID desfluane/isoflurane - airway irritant​
    • albuterol
  5. AVOID histamine realeasers
    • ​Sux, atricurium, mivicurium, D-tubo, morphine, demerol, thopental
  6. Use Short acting NMB-
    1. monitor with TOF so you know you are able to reverse
  7. ​Neostigmine is ok for reversal, but MUST be given with anticholinergic - glycopyrolate

18

Maintenance in COPD patients:

  1. Cautious with N2O;
    1. Given in high concentration→limits the amount of oxygen delivery 
    2. can cause rupture of bullae from emphysema→ pneumothorax
  2. VAs bronchodilate ​but also attentuate Hypoxic Pulmonary Vasoconstriction reflex
  3. Increased gradient between PaCO2 and ETCO2
    • ​ this is r/t air-trapping & ↑deadspace ventilation

  4. Opioids - less useful than VA’s for maintenance phase b/c can be associated w/prolonged depression of ventilation & delayed emergence

  5. ​​Humidification

19

Ventilation goals in COPD patients:

  1. No PEEP
  2. Large TVs (10-15ml/kg) 

    • Large TV’s = ↓ likelihood of turbulent airflow and help maintain optimal VQ matching

  3. low RR (6-10 bpm)
    • sufficient time for venous return; 
  4. Humidifier in circuit
  5. Consider patient's baseline CO2 and tolerate hypercarbia based on it
    • are they a blue bloater or pink puffer?
  6. Monitor for air trapping
    • ​monitor for intrinsic PEEP or dynamic hyperinflation r/t air-trapping (expiratory volume never reaches baseline again, so next breath starts out at a higher baseline volume)

20

Emergence and post-op management in COPD patients:

Postoperative ventalitory status is the Priority issue

  1. May need to stay intubated/ventilated for prolonged period (they are susceptible to acute respiratory failure during post-op pd (d/t atelectasis, hypercapnia, hypoxemia, retention of secretions, bronchospasm​)
    • esp. after abdominal/thoracic surgeries →but the goal is to get them extubated as soon as possible, they wil do better!
    • Education →Post op ventilation is NOT a complication, but rather an expected result
  2. Adjust vent based on blood gasses
  3. Adequate pain control 
    • allows for pain free breathing and improved coughing & to avoid splinting → reduced atelectasis risk 

21

Causes of reduced lung compliance:

Normal compliance = 100-200ml/cmH​2O

  1. Increased fibrous tissue

    • long-standing COPD, sarcoidosis, bleomycin toxicity

  2. Alveolar edema
    • sepsis, re-expansion pulm edema, negative pressure pulm edema
  3. Low lung volumes
    • atalectasis
  4. Increased pulm venous pressure
    • pulm HTN secondary to chronic Hypoxic Pulmonary Vasoconstriction

22

Four types of restrictive lung disorders with examples:

  1. Acute intrinsic (pulm edema, ARDS, aspiration pneumonitis)
  2. Chronic intrinsic (pulm fibrosis, sarcoidosis)
  3. Chronic extrinsic (chest wall/ab/neuromusc diseases, obesity, kyphosis)
  4. Disorders of pleura/mediastinum (tumors, pneumothorax, pleural effusions)

23

Describe re-expansion pulm edema:

Acute Intrinsic restrictive disorder

Occurs after rapid evacuation of > 1L from pneumothorax/effusion that's > 24 hours old, due to enhanced capillary membrane permeability 

  1. Treament:
    1. O2
    2. PEEP
    3. no diuretics unless volume overload is primary issue

24

Describe negative pressure pulmonary edema:

Acute Intrinsic restrictive disorder 

Occurs minutes to 2-3 hours after acute upper airway obstruction (in a spontaneously breating patient)

  1. Highly negative intrapleural pressure causes: 
    • decreased interstitial hydrostatic pressure
    • increased venous return
    • increased LV afterload
    • incerased SNS outflow→HTN and displacement of blood volume
    • Acute pulmonary edema
  2. Most often caused by:
    • post-extubation laryngospasm
    • attempting to breath against closed airway- muscle guys
    • Obstructve sleep apnea, hiccups, epiglotitis, tumors
  3. self-limiting to 12-24 hour duration
  4. Treatment:  
    • O2
    • airway monitoring/maintinence (C-Pap if needed)
    • mechanical ventilation + PEEP if needed

25

Aspiration Pneumonitis s/s and treatment: 

Acute Intrinsic restrictive disorder

Gastric Acid aspirate is rapidly distributed through the lungs it destroys surfactant producing cells and injures lung epithelium

  1. Results in capilary permability/atelectesis
  2. s/s:
    • arterial hypoxemia (decreased sats)
    • Tachypnea
    • Bronchospasm
    • Pulmonary vascular constriction can causel pulmonary HTN
    • X-ray shows changes 6-12 hours later 
  3. Treatment: 
    • Increase FiO2
    • PEEP
    • B2 agonists (albuterol) bronchodilation
    • Bronchoscopy if suspect solid material
    • generally abx and steroid use is not used

26

sarcoidosis

  • what is it?
  • how do these patients present?  
  • what are the anesthetic considerations?

Chronic Intrinsic restrictive disorder

Systemic granulomas disorder that leads to pulmonary fibrosis leading to cor pulmonale and pulmonary hypertension

  • Laryngeal sarcoid = Decrease diameter of airway (smaller tube and difficult  airway/intubation)
  • Myocardial sarcoid = heartblocks, dysrhythmias, restrictive cardiomyopathy → cardiac involvement
  • Liver, spleen, unilateral optic and facial nerves palsey
  1. Often present w/ dyspnea, cough & rapid shallow breathing
  2. Cor pulmonale and pulm HTN are likely
  3. Decreased alveolar diffusion capacity
  4. Often haveng a mediasinoscopy →lymph node biopsy
  5. Often times on corticosteroids→STRESS DOSE!
  6. Check electrolytes; check for hyperclacemia r/t metabolism of granulomas

27

Consiterations with chronic extrinsic lung disease:

  1. Chest wall disorders
    • decreased lung voume corespond with increased airway resistence
  2. Neuromuscular disorders -
    • Inefective cough/clearance of secretions
    • prone to infection/pneumonia  
    • high risk for aspiration d/t ineffective swallowing.
  3. Mediastinal tumors
    • ​​can compress the pumonary artery, myocardium or SVC
    • can occulde airway if given a muscle relaxant

28

S/s of pneumothorax:

  1. Acute dyspnea
  2. Ipsilateral chest pain
  3. Decreased PaO2
  4. increased PaCO2
  5. Hypotension
  6. Tachycardia
  7. Uneven/decreased chest wall movement
  8. Hyperresonant percussion
  9. Decreased or absent breath sounds

29

Regional anesthesia in restrictive lung disease:

  1. AVOID > T10 level =  loss of accessory muscles
    • vital esp in spont breathing patients
  2. Good to note they don't tolerate sedation well so regional may be benificial for post op pain control 

30

Induction in restrictive lung disease:

  1. Pre-meds: Titrate pre-meds carefully to avoid respiratory depression (lose accessory muscle function easily)
    • they need high minute vent to compensate for low volumes
  2. Pre-oxygenation critical d/t reduced FRC & decreased safe apnea time
  3. Will have a shorter apnea time - work efficiently
  4. Use nitrous with caution - risk for barotrauma!!
  5. May need etomidate if CV comorbidities
  6. Use short actinng NMB

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