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Coexisting Test 3 > Pulmonary Restrictive > Flashcards

Pulmonary Restrictive Flashcards

1
Q

Overview of restrictive disease chracteristics?

A
  • 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
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2
Q

TLC in restrictive diseae severity?

A
  • Decreased TLC
  • Mild: 65-85%
  • Moderate: 50 -65%
  • Severe: < 50%
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3
Q

Examples of acute intrinsic restrictive lung diseaes?

A
  • ARDS
  • Aspiration
  • Neurogenic problems
  • Opioid overdose
  • High altitude
  • Negative pressure pulmonary edema
  • CHF
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4
Q

Examples of chronic intrinsic lung disease?

A
  • Sarcoidosis
  • Hypersensitivity pneumonitis
  • Eosinophilic Granuloma
  • Drug induced pulmonary fibrosis
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5
Q

Extrinsic restrictive lung disease?

A
  • Skeletal structures
  • Neuromuscular disorders
  • Flail chest
  • Pneumothorax
  • Mediastinal mass
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6
Q

Other causes of restrictive lung disease?

A
  • Obesity
  • Ascites
  • Pregnancya
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7
Q

Preop goals for patient with restrictive lung disease?

A
  • Similar to those for asthma/COPD
  • Assess the severity of lung disease
  • Identify comorbid conditions
  • Optimize prior to surgery
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8
Q

Important notes to take from history of patient with restrictive lung diseaes?

A

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
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9
Q

Things to note on physical assessment of patient with restrictive lung diseaes?

A
  • 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
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10
Q

What does a PFT in restrictive lung disease look like?

A
  • Decreased FVC
  • Decreased FEV1
  • NORMAL TO INCREASED FEV1/FVC ratio
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11
Q

MAC anesthesia in restrictive lung disease?

A
  • 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

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12
Q

Regional/Neuroaxial technique in pt with restrictive lung dsieae?

A
  • 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
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13
Q

Induction of GA in pt with restrictive lung disease?

A
  • 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
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14
Q

Maintenance during GA in pt with restrictive lung disease?

A
  • 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
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15
Q

Considerations for ventilation during GA for patient with restrictive lung disease?

A
  • 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
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16
Q

Emergence in patient with restrictive lung dx?

A
  • 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
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17
Q

Postop concerns for patient with restrictive lung dx?

A
  • Adequate oxygenation
    • High flow NC to BiPap
  • Adequate analgesia
  • Incentive spirometry
  • Early ambulation
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18
Q

Summary of anesthesia needs for pt with restrictive disease?

A
  • 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
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19
Q

What is a laryngospasm?

A
  • 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
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20
Q

Epidemiology and incidence of laryngospasm?

A

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
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21
Q

Pathophys laryngospasm?

A
  • 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
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22
Q

What are the two anatomical levels where a laryngospasm can happen?

A

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
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23
Q

What is the laryngospasm reflex pathway?

A

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)
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24
Q

What happens during a laryngospasm when you’re awake?

A
  • 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.
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25
Q

Risk factors for development of laryngospasm? Anesthesia, patient and surgical r/f?

A

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
26
Q

What is seen clinically during a laryngospasm?

A
  • 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
27
Q

What are other clinical scenarios that may resemble a laryngospasm?

A
  • Anaphylaxis
  • Angioedema
  • Foreign body in airway
  • Vocal cord paralysis
  • Breath holding
  • Loss of upper airway tone
    • Residual muscle relaxants or opioids
  • Bronchospasm
28
Q

Prevention of laryngospasm?

A
  • 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
29
Q

Treatment laryngospasm?

A
  • 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!
  • Intubation- if all of the above fail to break laryngospasm
30
Q

Laryngospasm summary? def, epidemiology, mechanism, rf, presentation, treatment…

A
  • 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
31
Q

What is pulmonary edema?

A
  • 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
32
Q

What is negative pressure pulmonary edema?

A
  • 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
33
Q

S/S Negative pressure pulmonary edema (NPPE)

A
  • Inspiratory stridor
  • Wheezing
  • Use of accessory muscles
  • PANIC…
  • Hypoxia
  • Pink frothy sputum
34
Q

Differential for NPPE?

A
  • Anaphylaxis
  • Acute lung injury
  • Residual paralysis
  • Fluid maldistribution
    • TURP syndrome
  • Neurogenic
    • Increases SNS activity
  • MI
  • Heart failure
35
Q

Management of NPPE?

A
  • 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
36
Q

Summary NPPE?

A
  • 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
37
Q

What is ARDS? pathology?

A
  • 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
38
Q

What happens in injured alevolus during acute phase ARDS?

A
  • 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
39
Q

What are some direct and indirect risk factors for ARDS?

A

Direct

  • Pneumonia
  • Aspiration
  • Inhalational injury
  • Pulmonary contusion
  • Drowning

Indirect

  • Major trauma
  • Pancreatitis
  • Severe Burns
  • Drug overdose
  • TRALI
40
Q

What is the berlin definition of ARDS?

A
  • 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
41
Q

What is difference between peak and plateau pressure?

A
  • 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
42
Q

ARDS intraop considerations?

A
  • 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
43
Q

Ventilation strategies in ARDS?

A
  • 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
44
Q

PaCO2 and recuirtment maneuvers in ARDS?

A
  • PaCO2
    • Permissive hypercapnia
      • Unless head trauma or severe right heart failure
  • 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
45
Q

ARDs managmeent based on severity?

A
  • yellow- needs more data
  • HFO= high frequency oxygenation
46
Q

Anesthetic choice for ARDS patients?

A
  • 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
47
Q

Fluid management in ARDS?

A
  • Fluids
    • Judicious
  • Blood
    • Hemoglobin trigger of 7 g/dl is described
    • Independent risk of ARDS
48
Q

What is aspiration?

A
  • 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
49
Q

What determines the degree of lung damage from aspiration?

A
  • 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
50
Q

Pulmonary syndrome of Aspiration? Phases?

A

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
51
Q

Patho behind aspiration?

A
  • 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
52
Q

Med risk factors for aspiration?

A
  • Risk Factors: Medications
  • Drugs that either induce loss of consciousness or alter LES tone
    • Propofol/thiopental/etomidate/ketamine
    • Volatile anesthetics
    • Opioids
    • Thiopental
    • Atropine/glycopyrrolate
53
Q

Predisposing conditions that increase risk for aspiration (patient factors)

A

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
54
Q

Provider risk factors increasing r/f aspiration

A
  • 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
55
Q

Prevention/Harm reduction from aspiration?

A
  • 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?
56
Q

ASA fasting guidlines?

A
  • 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
57
Q

Recognition, s/s and differntial for aspiration?

A
  • 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??
58
Q

Treatment for aspiration?

A
  • 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
59
Q

What to consider if patient has aspirated?

A
  • 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
60
Q

Summary of aspriation?

A
  • 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?

Coexisting Test 3 (8 decks)

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