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
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
26
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
27
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
28
Prevention of laryngospasm?
* Anticholinergic drugs * Probably be limited to patients with c**opious 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
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!* * Intubation- *if all of the above fail to break laryngospasm*
30
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
31
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
32
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
33
S/S Negative pressure pulmonary edema (NPPE)
* Inspiratory stridor * Wheezing * Use of accessory muscles * PANIC… * Hypoxia * **Pink frothy sputum**
34
Differential for NPPE?
* Anaphylaxis * Acute lung injury * Residual paralysis * Fluid maldistribution * TURP syndrome * Neurogenic * Increases SNS activity * MI * Heart failure
35
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*
36
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*
37
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
38
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
39
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
40
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
41
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
42
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
43
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
44
PaCO2 and recuirtment maneuvers in ARDS?
* 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
ARDs managmeent based on severity?
* yellow- needs more data * HFO= high frequency oxygenation
46
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
47
Fluid management in ARDS?
* Fluids * Judicious * Blood * Hemoglobin trigger of 7 g/dl is described * Independent risk of ARDS
48
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
49
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_**
50
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
51
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
52
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
53
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*
54
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*
55
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?
56
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
57
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??*
58
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*
59
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
60
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?