Pulmonary Flashcards
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
Causes of asthma exacerbations:
- Allergens
- Exercise
- Nightime/sleep
- Chemicals (ASA/NSAIDs, VAs, irritants)
- Cold
- Infection
S/s of asthma:
- Wheezing
- Breathlessness/Air Hunger
- Chest tightness
- Early AM or nighttime cough
- Reversible airflow obstruction
- Tachypnea
- Prolonged expiratory phase
- Fatigue
Pre-op assessment of asthma:
- Triggers
- Severity (med requirements)
- Degree of reversibility w/ tx
- Current status, symptoms
- Prior anesthesia history
- Breath sounds
- general appearance, etc
Pre-op labs for asthma:
- PFTs
- ABG
- ECG (RH failure)
- CBC (eosinophils)
- CXR (hyperinflation of lungs)
Pre-op meds for asthmatics:
-
Benzos
- anxiety can precipitate bronchospasm bronchospasm)
-
Opioids
- be sure to titrate carfully
-
H2 antagonists
- unopposed H1 antagonism may cause bronchoconstriction- Use Caution!
-
Bronchodilators
- albuterol) - 15-30 min before
-
Pre-op steroids - prohylaxis
- Hydrocortizone 100 mg q8h if FEV1 predicted
Overall goal for induction of anesthesia in asthmatics
GOAL= Blunt airway reflexes and avoid bronchoconstriction during airway instrumentation
- Consider Regional (good choice)
- Whenever possible, use LMA for smoother emergence/extubation
-
GA should:
-
depress airway reflexes
- Lidocaine 1-1.5 mg/kg IV (consider LTA)
- Opioids -judiciously (fentanyl and analogues)
-
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
- <span>avoid Sodium metabisulfite prep </span>
- <span>Higher end of induction doses</span>
- 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
-
Treat bronchoconstriction
- albuterol
- sevoflurane
-
AVOID histamine realease
- Sux, atricurium, mivicurium, D-tubo, morphine, demerol, thopental
- Neostigmine is ok for reversal, but MUST be given with anticholinergic - glycopyrolate
-
depress airway reflexes
Maintenance of anesthesthesia in asthmatics:
-
High concentration VA
- Sevo/halo are least pungent/irritating
- Avoid histamine releasers (sux, atra, miva)
- Avoid bronchospasm
Ventilation goals for asthmatics:
Ventilation
-
Avoid PEEP !! →prone to air trapping
- these pts may have intrinsic peep r/t air trapping
- during an acute attack, may see “breath stacking”
- Decrease RR (8-10 bpm) - allows for adequate exhalation
- Longer I:E ratio
-
Increase TV - to maintain Normal PaCO2
- TV and inspiritory flow rates are limited by excessive peak airway pressures
- Upper Limit - 40 cm H2O
- If you can choose a mode – consider using PCV over volume controlled ventilation
- Liberal hydration of pt and circuit
- Place a humidifier in the breathing circuit
Treatment of intra-op bronchospasm:
- FiO2 to 100%
- Deepen anesthesia with VA or drugs
- Give a ß-agonist
-
If no air movement:
- Epinephrine IV: 2-8 mcg/min (SQ 0.3-0.5mg q20-30min)
- Terbutaline (SQ)
- Corticosteroids: 1-2 mg of cortisol
-
Other IV broncholilators
- Ketamine
- Propofol
- Lidocaine
Emergence/post-op care for asthma:
- Smooth emergence - ETT promotes bronchoconstriction and airway resistence
- Pre-emptive albuterol, IV lido 10-15 minutes prior to wake up
- Deep extubation if possible
- If not, try to get patient to SV as early as possible
Characteristics of COPD:
- Progressive airway obstruction
- Chronic bronchitis and/or emphysema
- Smoking #1 risk factor
COPD staging:
- Stage 1: FEV1 > 50% predicted
- Stage 2: FEV1 35-49%
- Stage 3: FEV 1
“Blue bloaters”:
- Chronic bronchitis
- Copious secretions cause obstruction
- Cough
- Diminshed breath sounds
- PaO2 →cyanosis and dusky appearance
- PaCO2 > 45
- Pulmonary hypertension d/t HPV
- Marked cor pulmonale/righ sided heart failure
- Overweight
- CXR: increased bronchovascular markings
“Pink puffers”:
- Emphysema
- Obstruction due to loss of recoil
- Severe dyspnea
- PaO2 > 60
- Normal PaCO2
- Very diminished breath sounds
- Tend to be thin
- anxious, pursed lips
- CXR: hyperinflation with a low diaphragm
Smoking cessation timeline:
-
12-24 hours:
- decreased carboxyhemoglobin levels to normal
-
2-3 weeks:
- ciliary function improves, increased airway secretions, hyperreactivity
- 4 weeks: PFTs improve
-
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)
Induction in COPD patients:
GOAL= minimize risk of post op respiritory failure
- 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
- Ketamine is good for pts who tolerate the CV effects, otherwise propofol
- Regional is a good choice: Avoid levels > T6
-
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
-
AVOID histamine realeasers
- Sux, atricurium, mivicurium, D-tubo, morphine, demerol, thopental
-
Use Short acting NMB-
- monitor with TOF so you know you are able to reverse
- Neostigmine is ok for reversal, but MUST be given with anticholinergic - glycopyrolate
Maintenance in COPD patients:
-
Cautious with N2O;
- Given in high concentration→limits the amount of oxygen delivery
- can cause rupture of bullae from emphysema→ pneumothorax
- VAs bronchodilate but also attentuate Hypoxic Pulmonary Vasoconstriction reflex
- Increased gradient between PaCO2 and ETCO2
- this is r/t air-trapping & ↑deadspace ventilation
- Opioids - less useful than VA’s for maintenance phase b/c can be associated w/prolonged depression of ventilation & delayed emergence
- Humidification
Ventilation goals in COPD patients:
- No PEEP
- Large TVs (10-15ml/kg)
- Large TV’s = ↓ likelihood of turbulent airflow and help maintain optimal VQ matching
- low RR (6-10 bpm)
- sufficient time for venous return;
- Humidifier in circuit
- Consider patient’s baseline CO2 and tolerate hypercarbia based on it
- are they a blue bloater or pink puffer?
- 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)
Emergence and post-op management in COPD patients:
Postoperative ventalitory status is the Priority issue
- 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 <strong>soon as possible</strong>, they wil do better!
- <strong>Education</strong> →Post op ventilation is NOT a complication, but rather an expected result
- Adjust vent based on blood gasses
-
Adequate pain control
- allows for pain free breathing and improved coughing & to avoid splinting → reduced atelectasis risk
Causes of reduced lung compliance:
Normal compliance = 100-200ml/cmH2O
- Increased fibrous tissue
- long-standing COPD, sarcoidosis, bleomycin toxicity
- Alveolar edema
- sepsis, re-expansion pulm edema, negative pressure pulm edema
- Low lung volumes
- atalectasis
- Increased pulm venous pressure
- pulm HTN secondary to chronic Hypoxic Pulmonary Vasoconstriction
Four types of restrictive lung disorders with examples:
- Acute intrinsic (pulm edema, ARDS, aspiration pneumonitis)
- Chronic intrinsic (pulm fibrosis, sarcoidosis)
- Chronic extrinsic (chest wall/ab/neuromusc diseases, obesity, kyphosis)
- Disorders of pleura/mediastinum (tumors, pneumothorax, pleural effusions)
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
- Treament:
- O2
- PEEP
- no diuretics unless volume overload is primary issue
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)
-
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
-
Most often caused by:
- post-extubation laryngospasm
- attempting to breath against closed airway- muscle guys
- Obstructve sleep apnea, hiccups, epiglotitis, tumors
- self-limiting to 12-24 hour duration
-
Treatment:
- O2
- airway monitoring/maintinence (C-Pap if needed)
- mechanical ventilation + PEEP if needed