Pulmonary Restrictive Flashcards
Overview of restrictive disease chracteristics?
- Decrease in all lung volumes – especially total lung capacity
- Decrease in lung compliance
- Preservation of expiratory flow rates
- HALLMARK: INABILITY TO INCREASE LUNG VOLUME IN PROPORTION TO AN INCREASING PRESSURE IN THE ALEVOLI
TLC in restrictive diseae severity?
- Decreased TLC
- Mild: 65-85%
- Moderate: 50 -65%
- Severe: < 50%
Examples of acute intrinsic restrictive lung diseaes?
- ARDS
- Aspiration
- Neurogenic problems
- Opioid overdose
- High altitude
- Negative pressure pulmonary edema
- CHF
Examples of chronic intrinsic lung disease?
- Sarcoidosis
- Hypersensitivity pneumonitis
- Eosinophilic Granuloma
- Drug induced pulmonary fibrosis
Extrinsic restrictive lung disease?
- Skeletal structures
- Neuromuscular disorders
- Flail chest
- Pneumothorax
- Mediastinal mass
Other causes of restrictive lung disease?
- Obesity
- Ascites
- Pregnancya
Preop goals for patient with restrictive lung disease?
- Similar to those for asthma/COPD
- Assess the severity of lung disease
- Identify comorbid conditions
- Optimize prior to surgery
Important notes to take from history of patient with restrictive lung diseaes?
Respiratory
- Current symptoms - dyspnea, cough, wheezing, or hemoptysis
- Activities or positions that worsen
- Need for oxygen therapy
- Recent history of disease – need for ER visit or hospitalization
- History of tobacco use
- Exposure to drugs/radiation that can damage lungs
Cardiovascular
- Pulmonary HTN
- Cardiomyopathy
- Heart failure
Other
- Rheumatic disease
- Musculoskeletal pain/weakness
Things to note on physical assessment of patient with restrictive lung diseaes?
- BMI
- PFT’s
- Most will already have baseline PFT’s
- Type & Severity of disease
- Patients with sever restrictive disease that should not undergo elective surgery
- ABG
- Resting SpO2 < 93 or elevated serum bicarb on CMP
- Imaging
- X-ray or CT – will most likely have
- Exercise capability
What does a PFT in restrictive lung disease look like?
- Decreased FVC
- Decreased FEV1
- NORMAL TO INCREASED FEV1/FVC ratio

MAC anesthesia in restrictive lung disease?
- Appropriate for selected procedures
- Closely monitor SpO2, ETCO2, & respiratory pattern
- Be ready to provide urgent airway management and respirator support
-
Sedatives will decrease RR and drive
- Prevent hypoxia and hypercapnia
- SMALL FRC
- Use short acting agents
- Dexmedetomidine is advantageous
Always consent for GA as well
Regional/Neuroaxial technique in pt with restrictive lung dsieae?
- Advantageous for surgical anesthesia and postoperative pain control
- Spinal/Epidural
- Maintain diaphragmatic function, but may decrease accessory muscles and inspiratory capacity
- Lower Extremity
- Well tolerated
Upper Extremity
- Brachial plexus
-
Interscalene
- 100% phrenic nerve block – reduces FEV1 and FVC
- Use cautiously in patients with limited reserve
- Supraclavicular & Infraclavicular blocks
- 17 -50% have reduced FEV1 and FVC
- Most likely due to spread of local anesthetic- LA can go back up and get back to phrenic nerve
-
Axillary or wrist
- Acceptable- and preferred
-
Interscalene
Induction of GA in pt with restrictive lung disease?
- Place in reverse Trendelenburg- unloads lung/volume
- Adequately preoxygenate- less reserve iwth apnea d/t small lung volumes
- Agents
- Avoid long acting
- Choice based on patient and procedure
Maintenance during GA in pt with restrictive lung disease?
- TIVA
- Short acting agents- propofol can build up over time
- Volatiles
- Sevoflurane is excellent choice; limit desflurane – high concentrations can cause irritation
- May inhibit hypoxic pulmonary vasoconstriction
- Nitrous
- Typically avoided – increase in pulmonary vascular resistance - also takes away amount of O2 you’re able to give
- Opioids
- Short acting- sufentanil, alfentanil for example
- Muscle relaxants
- Short acting
- Adjuncts
- Lidocaine, ketamine & dexmedetomidine are highly encouraged
- toradol, tyenol for adjuncts
- dexmedetomidine as well
Considerations for ventilation during GA for patient with restrictive lung disease?
- Goal: Optimal oxygenation and minimization of ventilatory induce lung injury
- TV: Low tidal volumes 4-6 ml /kg
- I:E Ratio: 1:1 or 2:1
- HAVE POOR COMPLIANCE
- need slow, gentle breath in, need time for lungs to fill lungs
- Rate: 14 – 18 (Adjusted to maintain baseline PaCO2 values)
- Patients may have chronic respiratory acidosis-keep at baseline!!
- FiO2: Adjusted to maintain PaO2 > 60 mmHg or SpO2 > 90%- high levels of O2 can cause oxygen toxicity from free radicals
- PEEP: Judicious use of 5 – 10 cm H2O
- Prevent alveolar collapse and maintain adequate FRC
- High intrathoracic PEEP may impair venous return and decrease CO
- may need vasopressor support in order to tolrate peep
Emergence in patient with restrictive lung dx?
- May have serious complication
- Place in reverse Trendelenburg position
- Adequate reversal of NMBD’s- need to make sure EVERY NMJ is open and working because they’re already compromised
-
Adequate pain control
- Short acting agents- balance with resp depression
- When patient is alert and cooperative
- Stable
- Not tachycardic, hypoxic or hypercapnic
-
May extubate to CPAP
- Prevent atelectasis
Postop concerns for patient with restrictive lung dx?
- Adequate oxygenation
- High flow NC to BiPap
- Adequate analgesia
- Incentive spirometry
- Early ambulation
Summary of anesthesia needs for pt with restrictive disease?
- Short acting agents
- Neuraxial/regional
- Don’t take away respriatory drive
- UE- interscalene has high risk blocking phrenic nerve /supra also has high risk
- LE regional work well
- Opioid sparing techniques
What is a laryngospasm?
- Primitive protective airway reflex that exists to protect against aspiration but can occur in light anesthesia
- Sustained closure of the vocal cords resulting in the partial or complete loss of the patients airway
- Complete
- Chest movement without any air movement
- Partial
- Chest movement with some stridorous noise
- Noticeable mismatch between patient effort and volume of air movement
- Complete
Epidemiology and incidence of laryngospasm?
Epidemiology
- Difficult to get true incidence- different reporting requirements by hospital
- Depends on case mix, hospital, experience of the provider, and hospital reporting requirements
- Newer drugs- lower with propofol c/t thiopental
Varying Incidence
- 1% in adults
- 2% in children
- 3% in very young- highest
-
Can be as high as 25% in patients undergoing tonsillectomy & adenoidectomy
- secretion, swelling, ETT, area with sx has high innervation, causes laryngospasm
Pathophys laryngospasm?
- Protective airway reflex
- Mechanical, chemical, or thermal receptor stimulation in the supraglottic airway
- Closure of the glottic opening by constriction of the intrinsic laryngeal muscles
- True vocal cords
- False vocal cords
- Aryepiglottic folds
What are the two anatomical levels where a laryngospasm can happen?
False vocal cords
- Anterior movement and backwards tilt of the arytenoids
- Posterior movement of the base of the epiglottis
- Adduction of glottic opening
True vocal cords
- Lower and posterior to false cords
- Closure may not be mandatory for laryngospasm to occur
-
Case reports of laryngospasm in patients with bilateral vocal cord paralysis
- the false vocal cords can close hard enough to cause spasm that true vocal cord spasm isn’t necessary
What is the laryngospasm reflex pathway?
Afferent
- Internal branch of the superior laryngeal nerve
Efferent
- Recurrent laryngeal nerve
- Lateral cricoarytenoid (adducts the glottic opening)
- Thyroarytenoid muscles (adducts & shortens
- External branch of the superior laryngeal nerve
- Cricothyroid (tenses the vocal cords)

What happens during a laryngospasm when you’re awake?
- Higher level override
- Conscious state
- Can gain control after potential aspiration
- Protective
- Hypercapnia and hypoxia depress laryngeal adductor neurons
- People will say “laryngospasm will break under hypoxia or hypercarbia”
- Probably not the best approach- will allow kids to become hypoxic/hypercarbic to see if laryngospasm will break on it’s on.
Risk factors for development of laryngospasm? Anesthesia, patient and surgical r/f?
Anesthesia
- INSUFFICIENT DEPTH OF ANESTHESIA
- ACCUMULATIO OF SECRETIONS/BLOOD IN AIRWAY
- Drugs: desflurane, isoflurane & sugammadex
- Airway: LMA (induction) and ETT (extubating)
- Inexperienced providers- may be related to insuff. depth on intubation and not fully awake on extubation
Patient
- Children
- ASA Class 3 or 4- may be related to anesthetics we use for these cases. Lower doses of anesthetics= lighter anesthesia= more risk for laryngospasm
- GERD
- SMOKING (2nd hand in children)
- URI- especially last 3/4 weeks
Surgical
- Airway surgery
- Appendectomy
- Genitourinary
- Thyroid surgery
- Esophageal surgery
What is seen clinically during a laryngospasm?
- Chest movement with limited airflow at mouth and nose
- Limited anesthesia bag movement
- Silence or stridor on inspiration
- Absence of ETCO2
- Body movements – engorged neck veins
- Tracheal tugging
- Paradoxical breathing
- Desaturation
What are other clinical scenarios that may resemble a laryngospasm?
- Anaphylaxis
- Angioedema
- Foreign body in airway
- Vocal cord paralysis
- Breath holding
- Loss of upper airway tone
- Residual muscle relaxants or opioids
- Bronchospasm
Prevention of laryngospasm?
- Anticholinergic drugs
- Probably be limited to patients with copious secretions or ketamine administration
- Propofol induction vs thiopental (sulfa group can cause bronchospasm)
- Lidocaine
- IV – equivocal studies- some show good, some bad
- Topical - some benefits; danger – blood/secretions can accumulate in an insensate area - may not be able to cough/clear and increase risk laryngospasm
- Magnesium
- Smooth muscle relaxation; few/underpowered studies
-
Adequate depth of anesthesia
- Especially with inhalational induction
- Wait a few minutes after loss of lid reflex to start IV
- Cough on extubation to force secretions out
Treatment laryngospasm?
- Remove stimulus
- Suctioning is controversial (clenched jaws or induce further spasm)
- Call for help
- Jaw thrust and 100% oxygen- larson maneuver
- CPAP with tight fitting mask- give slow, easy, gentle ventilations
- Deepen the anesthetic
- Lidocaine 1-1.5 mg/kg
- Propofol 0.5 mg/kg
- Muscle relaxation
- Succinylcholine
- IV: Succinylcholine 20 mg – onset 30 – 60 seconds- realize may need to give amnestic too!!
- IM: Succinylcholine 4 mg/kg – 4 minutes
- In pediatrics – may also want to give atropine to prevent bradycardia
- Rocuronium 1 mg/kg- can stick around for awhile, make sure to give amnestic!
- Succinylcholine
- Intubation- if all of the above fail to break laryngospasm
Laryngospasm summary? def, epidemiology, mechanism, rf, presentation, treatment…
- Definition – unwanted muscular response of the larynx
- Epidemiology – difficult to ascertain
- Mechanism – afferent and efferent limbs
- Risk factors – anesthesia, patient & surgery
- Presentation – silence/stridor, limited bag movement, NO etco2
- Treatment – remove, ask for help, jaw thrust, 100% O2, deepen the anesthetic, paralyze & re intubation
What is pulmonary edema?
- edema- Leakage of intravascular fluid into the interstitium of the lungs and alveoli
Cause
- Increased capillary pressure
- Hydrostatic or cardiogenic
- Increased capillary permeability
- Aspiration
- Sepsis
What is negative pressure pulmonary edema?
- Manifestation of upper airway obstruction and generation of large negative intrathoracic pressure
- Young, healthy, athletic patients at high risk- can generate higher negative intrathoracic pressure
- Typically follows laryngospasm, biting ETT, or foreign body aspiration
Pathology
- Upper airway obstruction
- Trying to inhale against an obstruction
- Develops high levels of NEGATIVE intrathoracic pressure
- Venous return to the heart increases
- CO decreases
- Pressure in pulmonary vascular bed increases
- Alveolar membrane junction disrupted
- Fluid from interstitial space flows into alveoli
- Pulmonary edema develops
S/S Negative pressure pulmonary edema (NPPE)
- Inspiratory stridor
- Wheezing
- Use of accessory muscles
- PANIC…
- Hypoxia
- Pink frothy sputum
Differential for NPPE?
- Anaphylaxis
- Acute lung injury
- Residual paralysis
- Fluid maldistribution
- TURP syndrome
- Neurogenic
- Increases SNS activity
- MI
- Heart failure
Management of NPPE?
- Relieve obstruction
- May require emergent re-intubation
- Correct hypoxia
- Facemask to BiPap
- Chest x-ray- ground glass opacities
- Labs
- CMP & ABG
- Pharmacologic
- Diuretics
- B2 Agonists
- Placement
- PACU keep vs stepdown/ICU- Depending on clinical picture
Summary NPPE?
- Pathology – trying to inhale against a closed glottis
- S/Symptoms – Stridor, wheezing & pink frothy sputum
- Treatment – Remove obstruction, correct hypoxia, diuretics & placement
- Minor can go home after monitoring in PACU
- Severe may need ICU
What is ARDS? pathology?
- Life threatening respiratory disease process characterized by
- Hypoxemia
- Reduced lung compliance
- Increased hospitalization, ICU days & morbidity
- Mortality – 45%
Pathology
- Varies based on causative pathology
- Inflammatory process that (this doesn’t vary…)
- Damages endothelial cells
- Inhibits surfactant production
- Impairs coagulation
- Inhibits normal alveolar immune response
- Increased vascular permeability
- DAMAGED ALVEOLAR – CAPILLARY MEMBRANE

What happens in injured alevolus during acute phase ARDS?
- Damage to alveoli and inflmmatory responst from macrophages produces mediators(TNF, IL1, IL6, brings in more neutrophils)–. decrease capillary membrane permeability
- damaged hyaline membrane develops and releases protease that breakdown membrane
- damage to pulmonary capillary membrane

What are some direct and indirect risk factors for ARDS?
Direct
- Pneumonia
- Aspiration
- Inhalational injury
- Pulmonary contusion
- Drowning
Indirect
- Major trauma
- Pancreatitis
- Severe Burns
- Drug overdose
- TRALI
What is the berlin definition of ARDS?
- Based on:
- timing- within 1 week known insult
- chest imaging- bilateral opacities not explained by effusions/lung collapse/nodules
- origin of edema- not explained by cardiac failure or fluid overload
- oxygenation
- mild- PaO2/FiO2 200-300 with PEEP >5-
- mod- PaO2/FiO2 100-200 with peep >5
- severe- PaO2/FiO2 <100 with peep >5

What is difference between peak and plateau pressure?
- Peak pressure= resistive pressure
- shows maximal pressure in proximal airways
- equated to action of blowing up a balloon
- If peak pressure and plateau pressure are >5 mmHg, then elevated peak pressure
- high peak pressure= airway issue
- bronchospasm
- retained secretion
- mucus plug
- blocked ETT tip/sitting agianst wall
- Plateau pressure= elastic/compliance of lungs/how stiff lungs are
- surrogate for end alveolar presure (end expiratory alveolar pressure)
- equated to when you stop blowing the balloon, the pressure equalizes b/w balloon and your airway
- high plateau signifies:
- PNA
- Pneumothorax
- pulmonary edema
- ARDS
ARDS intraop considerations?
- Mechanical forces generated by positive pressure ventilation can contribute lung injury
- Especially at the interface between normal lung units and damaged lung units
- Limit stretch, strain, and biotrauma
Ventilation strategies in ARDS?
- FiO2
- Lowest to maintain SaO2 between 88 -95%
- Hyperoxia – oxidative damage & alveolar collapse
- PEEP
- Maintains open airways
- Prevent recurrent opening and closing of airways
- Increase intrathoracic pressure
- Mode
- Does not appear to change outcomes, but PCV most common
- TV
- Low tidal volumes 6-8 ml/kg ideal body weight
- Low plateau pressure
- < 16 cm H20 goal
- < 30 cm H20 decreased mortality
- Decrease shear stress
PaCO2 and recuirtment maneuvers in ARDS?
- PaCO2
- Permissive hypercapnia
- Unless head trauma or severe right heart failure
- Permissive hypercapnia
- Recruitment Maneuvers
- Prevention of atelectasis
- 40 cmH20 for 40 seconds
- Stepwise fashion – increase by 5 cm H20 to 40
- Controversial
- Some studies – routine
- May be associated with hemodynamic instability
- Data is inconclusive- if hard time oxygenating, recruitment maneuvers may be beneficial
- Prevention of atelectasis
ARDs managmeent based on severity?
- yellow- needs more data
- HFO= high frequency oxygenation

Anesthetic choice for ARDS patients?
- Little evidence to choose one type over another
- Inhaled
- May be protective against ischemic/reperfusion injury
- Anti-inflammatory
- Con – inhibits hypoxic pulmonary vasoconstriction
- TIVA
- Propofol – possibly anti-inflammatory
Fluid management in ARDS?
- Fluids
- Judicious
- Blood
- Hemoglobin trigger of 7 g/dl is described
- Independent risk of ARDS
What is aspiration?
- Defined as: entry of liquid or solid material into the trachea and lungs
- Typically occurs when patients without sufficient laryngeal protective reflexes passively (at night) or actively regurgitate gastric contents
- Occurring 1:2000 – 3000 surgeries requiring anesthesia
- About 50% of patients who aspirate develop a lung injury such as pneumonitis and aspiration pneumonia
What determines the degree of lung damage from aspiration?
- The degree of lung damage is modified by:
- Degree of acidity
- Volume of aspirate
- Presence/absence of particulate matter in aspirate fluid
- As little as 50 ml’s of gastric content can be considered severe
-
Remember 25
- Volume < 25 ml’s
- pH > 2.5
Pulmonary syndrome of Aspiration? Phases?
Pulmonary Syndromes
- Dry cough/bronchospasm
- Mild pneumonitis
- Pneumonia
- ARDS
- Cardiopulmonary collapse
- Death
Phases
- Phase 1: Immediate damage from low pH/ high pH
- Phase 2: Inflammatory response
- Infection
- Infiltration
Patho behind aspiration?
- Chemical irritaion causes loss of cilia
- dead and dmaged epithelial cells
- mucous lining lost
- allows capillary membrane to open and interstitial fluid to flow in
- body needs to repair damage, brings neutrophil, macrophages which break down capillary membrane further and release proteases. more fluid flows into alveoli
- proteases damage the capillary-membrane lining
- cyclic process that takes time to resolve

Med risk factors for aspiration?
- Risk Factors: Medications
- Drugs that either induce loss of consciousness or alter LES tone
- Propofol/thiopental/etomidate/ketamine
- Volatile anesthetics
- Opioids
- Thiopental
- Atropine/glycopyrrolate
Predisposing conditions that increase risk for aspiration (patient factors)
Any condition that increases gastric pressure (overcome LES) or lessen LES tone and allow acid regurg.
- GERD
- Gastrointestinal obstruction
- Altered level of consciousness
- Patients taking opioids/sedatives
- Need for emergency surgery/trauma
- Hiatal hernia
- Lack of coordination of swallowing
- Obesity
- Diabetes
- Pregnancy- pushes up gastric contents, higher intragastric pressure and causes backflow up LES
- Unrecognized difficult airway- pushing lots of air into stomach while ventilating
Provider risk factors increasing r/f aspiration
- Improper decision making
- Not using preventative measures
- Lack of experience
- Inadequate patient preparation- trauma
- Cricoid pressure
- Neural reflex that is not well understood- may be triggering swallowing reflex from UES causing LES to relax and risk increased aspiration
Prevention/Harm reduction from aspiration?
- Preoperative fasting
- ASA guidelines
- Nasogastric tube ?
- No evidence to support routine use; HOWEVER – IF PRESENT – USE!
- Medications
- H2 blockers, PPI, prokinetics, non-particulate antacids, & anticholinergics
- h2 blockers- decrease volume, increase pH, takes time to work
- PPI- increase pH and decrease volume, take time
- bicitra- used for immediate relief, good for emergencies, may make pt vomit d/t taste
- reglan- decrease pyrloric sphincter and move things though stomach/intestine
- Positioning
- Head down – recommended, allows aspirant to go out of the mouth
- 15 – 45 degrees –with mouth at level of larynx
- RSI
- Cricoid pressure – benign practice & should be used
- Released if creating difficulties in securing the airway
- 50% incorrectly applied
- What’s a Newton?

ASA fasting guidlines?
- Clear liquids= 2 h
- breast milk= 4 h
- infant formular 4-6 h
- non human milk 6 h
- light meal 6 h
- heavy meal (fat and meat) 8 h
Recognition, s/s and differntial for aspiration?
- Recognition
- Identification of gastric content in oropharynx – 70%
- Silent – micro
- Signs & Symptoms
- Hypoxia
- Increased peak airway pressures
- Adventitious lung sounds
- Laryngospasm/bronchospasm
- Differential
- Anaphylaxis
- PE
- ETT obstruction
- light anesthesia??
Treatment for aspiration?
- Place head down and turn to the side
- Suction the airway
- Secure the airway
- recognize that contents can leak around the cuff
- Suction the airway prior to initiating positive pressure ventilation- don’t start ventilating once tube placed, suciton first!!!
- Administer bronchodilators as needed
- Peep
- Neutrophil inhibitors – lidocaine or sivelestat (neutrophil elastase inhibitor)
- Bronchoscopy
- Flexible- just looks around in the lung
- Rigid- if particulate matter have to convert to rigid to pull it out
What to consider if patient has aspirated?
- Proceed with case??
- dpeends on urgency of surgery and patient status (maintain saturation, having bronchospasms, etc)
- Chest x-ray
- When is best time to get?– takes time to develop damage. get up front and then 2-3 hours later
- Antibiotics/steroids
- NOT routinely used
- PACU/ICU
- Oxygenation status
- Majority does not require treatment
- Circulatory collapse
- ACLS
- ECMO
Summary of aspriation?
- Aspiration – entry of liquid or solid material to trachea/lungs
- Complex pattern – Mild to ARDS to circulatory collapse
- Risk factors – Medications, patient, provider
- Prevention – Risks assessment, fasting, medications, RSI & positioning
- Management – Clear secretions, secure airway, suction, steroids and antibiotics are not routinely used, what about case, and where do they need to go?