Crisis Scenarios Flashcards

1
Q

Anaphylaxis Patho

A

Type 1 hypersensitivity (immediate) occurs w/in 15-30min after exposure to antigen (latex exposure delayed d/t absorption via skin)
Antigen introduced to helper T cells
Memory B cells prompt IgE production
IgE attached to mast cells & basophils
Antigen enters bloodstream & attaches to IgE antibodies
Mast cell & basophil lysis → histamine & leukotriene release

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2
Q

Anaphylaxis Causes

A
NMBs - Rocuronium & Succinylcholine
Antibiotics
Latex exposure
Medications - Propofol, Heparin & Protamine, Opioids, LAs
Colloids & blood products
Antiseptics
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3
Q

Anaphylaxis S/S

A
Grade 1-4
CV hypotension & tachycardia
Respiratory bronchospasm & pulmonary edema
Integumentary flushing & hives
Inflammation ↑permeability
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4
Q

Anaphylaxis Treatment

A
Discontinue triggering agent
Assessment 
100% FiO2
Fluid administration
Epinephrine 10-100mcg Q2min IV push → infusion
Antihistamine (Benadryl 50mg H1 blocker)
Ranitidine 50mg H2 blocker
Methylprednisolone (Solu-medrol) 100mg corticosteroid
Bronchodilators (β2 agonists)
Nebulized albuterol
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5
Q

Bronchospasm Patho

A

Stimulus
↑afferent to NTS releases glutamate
Vagus nerve excitation
↑ACh release stimulates M2 & M3 receptors → VSMC contraction ↑tone
Severe bronchoconstriction → bronchospasm

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6
Q

Bronchospasm Causes

A

Airway manipulation - induction, emergence, & repositioning
Insufficient anesthesia depth
Anaphylaxis (presents as bronchospasm w/ hypotension)
Medications - Desflurane, AChEi, histamine releasing (Meperidine), β2 adrenergic antagonists, & Hemabate
Cold air
Aspiration

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7
Q

Bronchospasm S/S

A
↑WOB
Wheezing
Prolonged expiration w/ ↓Vt
V/Q mismatch
Shark fin capnograph
↑PIP
Difficult to manually mask-ventilate
Hypotension 
↑pulmonary vascular resistance → R ventricle overload
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8
Q

Bronchospasm Treatment

A

PREVENTION

  • Preop assessment (reactive airway, asthma, COPD, recent URI, smoker)
  • Allergies
  • Aspiration risk
  • Pre-treat
  1. High flow 100% FiO2
  2. Manual ventilation ensure adequate exhalation time (disconnect circuit - hypotension d/t air trapping)
  3. Help!
  4. Assess & remove stimulus
  5. Deepen anesthesia ↑volatile anesthetic or admin Ketamine
  6. Inhaled short-acting β2 adrenergic agonist (Albuterol)
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9
Q

Laryngospasm Patho

A

Bilateral RLN damage - loss intrinsic muscle tone
SLN external branch innervates cricothyroid muscle
Adduction

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10
Q

Laryngospasm Causes

A

Airway manipulation
Noxious stimuli
Inadequate anesthetic depth → laryngeal stim
Secretions on the vocal cords

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11
Q

High Laryngospasm Risk

A
Reactive airway disease
Smokers
Infection, inflammation, exposure to irritants
Airway abnormality
GERD
Surgical procedures

Reduce the risk - deepen anesthesia, avoid Desflurane, postpone surgery, optimize the patient, pre-treat (Albuterol)

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12
Q

Laryngospasm S/S

A

Hypoxia
↓SpO2
Negative pressure pulmonary edema (pink, frothy sputum)
CV effects

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13
Q

Laryngospasm Treatment

A
  1. Help!
  2. Remove stimulus
  3. Admin 100% FiO2
  4. Open & clear airway
  5. Perform jaw thrust
  6. Apply PPV 10-30cmH2O
  7. Deepen anesthesia (↑volatile anesthetic or Propofol bolus)
  8. Admin Succinylcholine 0.1-2mg/kg IV
  9. Mask ventilate & monitor patient

Larson maneuver
- Stylohyoid & mylohyoid elevate the larynx & open the airway w/ inspiration

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14
Q

Negative Pressure Pulmonary Edema Patho

A

Attempted inspiration against occluded airway
↑negative intrathoracic pressure (normal -4cmH2O → -140cmH2O)
↑VR & afterload
↑pulmonary blood volume & PVR
↑hydrostatic pulmonary pressures
Edema

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15
Q

Negative Pressure Pulmonary Edema Causes

A

Strong inspiratory effect against an occluded airway/closed glottis

Adults:

  • Laryngospasm
  • Upper airway tumors
  • Postop vocal cord paralysis
  • Obesity

Pediatrics:

  • Epiglottitis
  • Croup
  • Laryngotracheobronchitis
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16
Q

Negative Pressure Pulmonary Edema S/S

A
Cough & pink frothy sputum
Mechanically ventilated patient
- Difficulty bagging
- ↑airway pressures
Tachypnea
Desaturation
Rales or rhonchi
Tachycardia
Pulmonary infiltrates
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17
Q

Negative Pressure Pulmonary Edema Treatment

A
Elevate HOB
Maintain patent airway
Provide supplemental FiO2
Initiate PPV
Admin steroid & diuretics
Limit fluid intake
Bronchodilator
Obtain/monitor ABGs
Maintain lower Vt & plateau airway pressures
Laryngospasm - perform Larson maneuver
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18
Q

Equipment Malfunction Definition

A

Inability equipment to perform intended function
Contribute to morbidity & mortality
Difficult to manage equipment malfunction in complex environment
Malfunctions = inevitable
Prompt recognition & response to the malfunction

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19
Q

AANA Standards

A

Standard 6 EQUIPMENT

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20
Q

Airway Equipment Malfunction

EXAMPLES

A
ETT cuff rupture
Dysfunctional ETCO2 capnography
Video laryngoscope malfunction
Check equipment before to ensure properly functioning
Back-up equipment available
PREPARATION & VIGILENCE
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21
Q

AGM Equipment Malfunction

A
Disconnection or misconnection
Leaks
Occlusion or obstruction
Failure to initiate ventilation
Pipeline or tank failure
Relief valve malfunction
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22
Q

Power Failure

A
Manually ventilate w/ bag-mask
Auxiliary oxygen
Transition to IV anesthetic (Propofol TIVA)
Use transport monitors
IV infusion pumps back-up battery 4hr
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23
Q

Airway Fire Causes

A

TRIAD:

  1. Oxidizer - oxygen or nitrous oxide
  2. Fuel - alcohol based prep solutions, surgical drapes, sponges, towels, gauze, ETTs & LMAs, organic matter
  3. Ignition - ESUs, lasers, fiber-optic lights
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24
Q

Airway Fire S/S

A

FIRE!
Smell smoke, melted plastic, burning fuels
Flash, smoldering embers, darkened ETT/LMA, breathing circuit w/ soot, orange or red glow to ETT or LMA
Audible pop
Inability to adequately ventilate

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25
Q

Airway Fire Prevention

A

PREVENTION
Silverstein fire risk assessment
Laser proof vs. resistant
ETT cuff filled w/ saline or methylene blue
Fire extinguishing materials available
Sterile saline & saline-moistened cotton gauze
Minimum oxygen
Avoid N2O during high risk procedures
Allow preparation solutions adequate drying time
Bipolar ESU not monopolar

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26
Q

Airway Fire Treatment

A
  1. Remove ETT/LMA, turn off gases, remove flammable material, & pour saline into airway
  2. Extinguish burning ETT/LMA in sterile saline basin
  3. Resume ventilation w/ 21%
  4. Ventilate w/ 100% FiO2 via face mask only when fire extinguished
  5. Examine airway & remove residual debris w/ rigid bronchoscope
  6. Consider lavage w/ normal saline
  7. Re-intubate w/ smaller ETT when indicated
  8. Assess thermal trauma extent

Post airway fire

  • 24hr observation
  • Monitor delayed laryngeal-tracheal edema
  • Severe airway burns remain intubated & receive humidified FiO2
  • Monthly laryngoscopy or bronchoscopy indicated up to 6mos (tracheal stenosis occur months later)
  • All materials involved should be retained for further investigation
  • Report to the Joint Commission as sentinel event
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27
Q

Malignant Hyperthermia Patho

A

RYR1 gene located on 19q13.1 chromosome
CACNA1S gene
Dihydropyridine & ryanodine VGCa2+ channels
↓receptor threshold to release Ca2+
Resistance to feedback mechanisms ↓Ca2+ ion conductance

28
Q

Malignant Hyperthermia Causes

A

Exposure to volatile anesthetic agents
Succinylcholine
Stress?

29
Q

Malignant Hyperthermia S/S

A
↑ETCO2 not responsive to hyperventilation
Tachycardia or arrhythmias
Rigidity
Tachypnea
Labile blood pressure
↑temperature
Myoglobinuria
Skin mottling or cyanosis
SaO2 desaturation
Metabolic & respiratory acidosis
Hyperkalemia
↑creatinine kinase
↑serum & urine myoglobin
30
Q

Malignant Hyperthermia Treatment

A

Discontinue volatile anesthetic or Succinylcholine
HELP!
Admin Dantrolene 2.5mg/kg
Hyperventilate w/ 100% FiO2
Cooling
Activated charcoal filters on AGM circuit
Antidysrhythmic
Monitor & treat ABGs, blood glucose, coags, CK, serum & urine myoglobin, & liver enzymes
Maintain adequate urine output

31
Q

Aspiration Patho

A

Liquid or particulate matter enter tracheobronchial tree
R bronchus more susceptible d/t lesser angle & wider
1. Direct chemical damage to epithelium
2. Inflammatory cascade
3. Infectious fluid consolidation in alveoli
4. V/Q mismatch → shunting

32
Q

Aspiration Causes

A

Anesthesia ↓lower esophageal sphincter tone & loss protective reflexes

33
Q

High Aspiration Risk

A
Uncontrolled GERD
Stroke → dysphagia
Diabetes (gastroparesis)
Morbid obesity
↑abdominal pressure (ascites/edema)
Bowel obstruction
Pregnancy >13wks
Trauma - SNS response impairs gastric emptying (blood diverts to vital organs)
34
Q

Aspiration S/S

A

Oral secretions

  • Cough
  • Mild tracheal irritation
  • Transient laryngospasm

Acidic gastric contents

  • Arterial hypoxemia
  • Bronchospasm
  • Dyspnea
  • Abnormal breath sounds
  • ARDS
35
Q

Aspiration Treatment

A
PREVENTION
Preop assessment to identify at risk patients
NPO guidelines
Pharmacologic prophylaxis
Gastric U/S
RSI

Vigilance
Trendelenburg
Suction mouth & pharynx
Intubate & oxygenate

Post-aspiration
Monitor S/S
Cough or wheeze
Maintain SpO2
CXR
Extended LOS
ICU admission
36
Q

Myocardial Infarction Patho

A
Atherosclerotic disease NSTEMI vs. STEMI
Demand ischemia (supply vs. demand)
Supply:
- CorrPP
- ADBP
- LVEDP
- HR (diastole time)
- Coronary artery resistance
Demand:
- HR
- Preload
- Afterload
- Contractility/inotropy
37
Q

Myocardial Infarction Causes

A

Supply/demand mismatch

38
Q

Myocardial Infarction S/S

A
Sustained tachycardia or bradycardia
Hypertension or hypotension
Arterial hypoxemia
ST depression or elevation
Troponin levels
↑PAOP
TEE ventricular wall changes

Presentation/sensation potentially masked by anesthetics & other drugs

39
Q

Myocardial Infarction Treatment

A

PREVENTION = key

STEMI

  • TPA fibrinolytic therapy
  • Percutaneous coronary intervention
  • Coronary artery bypass graft

Goal re-establish blocked coronary blood flow ↓MVO2

Bed rest, analgesia, supplemental oxygen, β blocker therapy, IV nitroglycerin (short-acting vasodilator), antiplatelets/anticoagulants, ACE inhibitors, ANG II receptor blockers, Ca2+ channel blockers

40
Q

Hemorrhage Patho

A

Excessive blood loss
↓CO → baroreflex
SNS response ↑HR ↑renin, ANG II, vasopressin
RAAS activation

41
Q

Hemorrhage Causes

A

Risk factors include anticoagulants, coagulopathies, certain surgeries, tissue/collagen disorders
Incompetent surgeons

42
Q

Hemorrhage S/S

A
Hypotension
Acute blood loss & hemodynamic instability
Tachycardia ↑HR
RAAS activation
Na+/H2O retention
MAP <50mmHg → CNS ischemic response
"Oh shit"
"Call vascular surgery"
*Suction*
43
Q

Hemorrhage Treatment

A

Phase I - immediate life-threatening & uncontrolled hemorrhage → activate MTP
Massive transfusion protocol
Phase II - ongoing hemorrhage → tailored management
Phase III - controlled hemorrhage → restore physiology

44
Q

Massive Transfusion Protocol

A
10 units PRBCs in 24hr
Goal = maintain end organ perfusion
Control airway
100% FiO2
Large bore IVs
Blood warmer & rapid infuser
Send type & screen
IV fluids, Trendelenburg, vasopressors
Ideal ratio PRBC:FFP:Platelets 1:1:1
Minimize lethal triad - metabolic acidosis, hypothermia, & coagulopathy
45
Q

Thyrotoxicosis Patho

A

Thyroid gland hyperactivity = hyperthyroidism
Thyroid hormones directly excite the heart
↑HR/inotropy
Heart muscle strength impaired d/t protein catabolism
↑β adrenergic receptor
Upregulation - exaggerated response to circulating catecholamines

46
Q

Thyrotoxicosis Causes

A

Grave’s disease
- Autoimmune disorder antibodies bind to TSH receptor & stimulate the thyroid
Toxic nodular hyperthyroidism
Thyroiditis - release stored thyroid hormones
Thyroid cancer

47
Q

Thyrotoxicosis S/S

A
Weight loss
Anxiety
Fatigue
Heat intolerance
↑oxygen consumption
↑SBP 10-15mmHg
↓DBP 
Vasodilation
Sinus tachycardia
Cardiac dysrhythmias
↑CO
Muscle weakness
Hand tremor
Difficulty sleeping
48
Q

Thyrotoxicosis Treatment

A

Thyroid gland ablation w/ radioactive iodine
Thyroidectomy
Anti-thyroid drugs
- Thionamides (Methimazole, Carbimazole, Propylthiouracil)
β adrenergic blockade
- Propranolol, Metoprolol, Atenolol
High relapse rate in patients treated only w/ medications

49
Q

Thyroid Storm Patho

A

Precipitating event rapid ↑thyroid hormone & SNS activity
Hypothesized
Acute stress or infection causes ↑SNS response & ↑thyroid hormone sensitivity → cytokine release & other immune dysfunction (immunological disturbances)

50
Q

Thyroid Storm Causes

A

Surgery
Abrupt anti-thyroid medication discontinue
Trauma
Acute illness
Parturition
Recent use iodinated contrast or radio-iodine therapy
Burns
Medication SE (amiodarone, anesthetics, salicylates)

51
Q

Thyroid Storm S/S

A
Fever >38.5°C
Tachycardia/dysrhythmias
Heart failure
Hypertension
N/V
Confusion/agitation
Weakness
Tremor
52
Q

Thyroid Storm Treatment

A

Identification
β adrenergics blunt response
Anti-thyroid medications inhibit thyroid hormone synthesis
Supportive measures - IVF replacement, electrolyte imbalance correction, reverse any acid-base imbalance, ensure adequate oxygenation ↑FiO2 demand
Manage hyperthermia
Vasoactive medications & advanced monitoring often necessary

53
Q

Postop Residual NMB Patho

A

Inadequate neuromuscular blocker reversal

nAChR antagonist

54
Q

Postop Residual NMB Causes

A

Incomplete relaxant reversal or failure to reverse NMB post-procedure

55
Q

Postop Residual NMB Risk Factors

A
Long-acting NMB
Improper dose or timing r/t paralytic or reversal dose
Deeper block = higher risk
Inhalational agents ↑risk
Elderly
Longer surgeries
Medical conditions:
- Renal or liver dysfunction/failure
- Neuromuscular disorders
- Sepsis or trauma
- Adrenocortical dysfunction
- Cholinesterase deficiency or genetic variation
- Metabolic disturbances
- Electrolyte abnormalities
- Obesity
Medications:
- Antibiotics
- Antidysrhythmics
- Antihypertensives
56
Q

Postop Residual NMB S/S

A
Postop pulmonary complications
- Hypoxemia
- Upper airway muscle weakness or obstruction
- Aspiration risk
Generalized muscle weakness
- Facial weakness
- Numbness
- Difficulty speaking, coughing, drinking
- Inability to perform deep breathing
- ↓ventilatory response to hypoxia
Awareness during emergence
57
Q

Postop Residual NMB Treatment

A

Peripheral nerve stimulator
- Ensure proper placement (stimulate the nerve NOT the muscle)
- Avoid monitoring facial muscles (overestimates recovery)
Quantitative TOF <0.9 objective measurement

58
Q

Epinephrine

A

IV concentration 1:10,000 or 0.1mg/mL = 1mg/10mL
IM concentration 1:1,000 or 1mg/mL
Bronchospasm 10-100mcg
Anaphylaxis 10-100mcg IV Q2min → Epi infusion (stabilizes the mast cells)
Code dose = 1mg
Pediatrics 1-10mcg/kg

59
Q

Don’t Forget

A
Call for help!
100% FiO2
Discontinue anesthetics
Verbalize differentials
Notify the surgical team
DELEGATE
60
Q

Assess Potential ETT Issues

A

Displacement
Obstruction ↑peak airway pressures d/t secretions or kinked ETT/tubing
Pneumothorax
Equipment failure

61
Q

Refractory Bronchospasm Treatment

A
  • Epi 10-20mcg
  • Terbutaline 0.25mg
  • Intubate
  • Methylprednisolone 125mg
  • Inhaled muscarinic antagonist (Ipratropium)
  • Magnesium sulfate 2g over 15-20min
62
Q

Hemorrhage Class I

A

<15% blood volume

- No significant vital sign changes

63
Q

Hemorrhage Class II

A

15-30%

  • Tachycardia, tachypnea, ↑pulse pressure
  • Loss 20% ↓BP
64
Q

Hemorrhage Class III

A

30-40%

- Tachycardia, tachypnea, systolic hypotension, oliguria, mental status changes

65
Q

Hemorrhage Class IVa

A

> 40%

  • Immediately life-threatening
  • Severe sustained hypotension, tachycardia, narrow pulse pressure, no UOP, cold & pale skin, ↓mental status
66
Q

Massive Transfusion Protocol

Complications

A
  • Hyperkalemia → arrhythmias or sudden cardiac arrest
  • Hypocalcemia → muscle weakness, tetany, myocardial dysfunction, coagulopathy
  • Hypothermia → coagulopathy, arrhythmias, hepatic dysfunction, myocardial depression, ↓drug metabolism