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KChan Saves the World > KC Critical Care > Flashcards

KC Critical Care Flashcards

1
Q

Summarize the evidence for cooling post cardiac arrest

A

TTM2 - Hypothermia versus normothermia after out of hospital cardiac arrest
Dankiewicz et al.

Population: 18+ OOHCA rosc >20 mins unconscious
Intervention: TTM 33 degrees via cold IV fluids or IV cooling devices with invasive temp monitoring, then slow rewarming from 28-40 hours
Control: Normothermia, active cooling only if temp 37.8 or greater
Outcome: All cause mortality at 6 mo.

International multicentre RCT

No difference in primary outcome between the two groups. No difference in secondary outcomes (ex. disability). Hypothermia group did have higher rates of arrhythmia

Bottom line: in OOHCA, focus should be on achieve normothermia with TTM only in patients with temp of 37.8 or higher

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2
Q

*6 predictors of difficult BVM

A

MOANS
Mask seal (beard, distorted anatomy)
Obesity or obstruction
Aged (<55yo)
No teeth (consider putting the BVM inside the patient’s lower lip)
Stiff lungs (COPD, CHF)

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3
Q

*5 strategies to improve BVM

A

Strategies
- Optimize positioning
- Lift mandible to mask via jaw thrust when bagging via “C-E” clamp technique
- Trial two person technique
- Suction
- Insert oropharyngeal airway
- Insert nasopharyngeal airway
- Insert nasogastric tube
- Remove foreign body
- If edentulous keep dentures in
- Attach PEEP valve

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4
Q

*4 ways to improve direct laryngoscopy with assuming normal c-spine

A
  • Optimize position (e.g. sniffing position, ear to sternum, patient head at lower part of intubator’s sternum)
  • Ensure appropriate blade size/type
  • Enter mouth with laryngoscopy from right side and sweep tongue to left
  • Visualize epiglottis and place blade in vallecula intubation. What are SIX maneuvers to - Lift in direction of laryngoscope handle
  • Ensure good lighting
  • BURP
  • If edentulous, remove dentures
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5
Q

*6 predictors of difficult laryngoscopy

A

L - Look for gestalt airway difficulty
E - Evaluate 3-3-2 (pts fingers)
- 3 Fingers between open incisors =mouth opening
- 3 Fingers for thyromental distance
- 2 Fingers from laryngeal prominence to floor of mandible
M - Malampati
O - Obstruction/Obesity (epiglottis, neck CA, Ludwig’s etc)
N - Neck mobility (ank spon, RA, downs syndrome, c-collar etc)

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6
Q

*What are 4 reasons of false negative colourimetric ETCO2 (ie. Tube in trachea)

A

Low flow state (cardiac arrest states, a low pulmonary flow due to PE, or large alveolar dead space)
Airway obstruction
Equipment problem

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7
Q

*Causes of false positive ETCO2?

A
  1. Supraglottic area
  2. ingestion of carbonated beverage followed byoesophageal intubation
  3. administrationof Bicarb before intubation (CO2=HCO3)
  4. Oesophageal intubationproceeded by significant BVM prior to intubation—> extra gas in stomach
  5. Contamination with gastric secretions
  6. Contamination with acidic medications (ex: Epi)
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8
Q

*Adverse events of succinylcholine

A

Hyper K, MH

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9
Q

*4 reliable means to confirm tube placement

A

Direct visualization
Bronchoscopy/fiberoptic
ETCO2 (colour change or continuous)
Chest X-ray
POCUS
Chest rise
Auscultation
Misting in ETT
Aspiration of air
Bougie

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10
Q

*List 4 complications of trach placement <3 weeks

A

Bleeding
Infection
Tracheal wall injury
Dislodgement
Subcutaneous emphysema
Pneumothorax
Pneumomediastinum

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11
Q

*List 4 complications of trach placement >3 weeks

A

Stenosis
Granuloma
Tracheomalacia
Pneumonia
Tracheo arterial fistula
Dysphagia

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12
Q

*What is the most common cause of major bleeding following a trach placement

A

Tracheoinnominate fistula

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13
Q

*List 5 things that you can do for the bleeding described above

A

Overinflate balloon
Deflate balloon, remove, and intubate again
Place direct pressure with digit
Blood transfusion
Anticoagulant reversal
TXA
ENT consult

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14
Q

List 4 predictors of difficult LMA insertion

A

restricted mouth opening, obstruction/obesity, distorted anatomy, stiffness to ventilation

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15
Q

List 5 predictors of difficult cric

A

hx of surgery, mass (abscess, hematoma), access/anatomy problems (edema, obesity), radiation, tumor

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16
Q

Describe the Cormack and Lehane grading of glottic view

A

Grade 1 = you see the entire glottic aperture —> 100% intubation success
Grade 2 = arytenoid and epiglottis +/- portion of the vocal cords
Grade 3 = you only see epiglottis —> extremely difficult intubation
Grade 4 = not even epiglottis = impossible intubation
Note grade 2 has (a, b)

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17
Q

Describe the 7 Ps of RSI. Provide specific numbers with regards to O2

A

Preparation: assessment of patient, all drugs are prepared, all equipment is assembled.
Preoxygenation: ~3mins of 100% O2 or 8 vital capacity breaths
Pretreatment: consider fentanyl in ICP, atropine in children, Ventolin for asthmatics
Paralysis with induction: Sedative followed by NMBA
Positioning: Neck flexionin the sniffing position
Placement of the tube: 45-60 seconds after NMBA
Post intubation management: confirm placement, sedatives (opioids, sedatives) mechanical ventilation

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18
Q

What is delayed sequence intubation

A

Procedural sedation for preoxygenation (i.e. Bipap). Use of early dissociative doses of ketamine 1mg/kg/IV to reduce agitation and assist with pre oxygenation. This is someone who did not tolerate pre oxygenation and needs induction for this phase.

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19
Q

List 3 agents that can be used for induction and their doses

A

Ketamine 1-2mg/kg
Propofol 1-2mg/kg
Etomidate 0.3mg/kg

Think 1-2-3

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20
Q

List 2 paralytics and their doses

A

Succinylcholine 1.5mg/kg
Rocuronium 1mg/kg

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21
Q

List 5 contraindications to succinylcholine

A

NM disorders (MS, ALS, muscular dystrophy, myasthenia gravis), hyperkalemia (burns >10% BSA, crush injury, intraabdominal sepsis), malignant hypothermia

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22
Q

Describe the Mallampati score

A

see photo
I: Hard palate, Soft palate, Uvula, fauces, pillars
II: Hard palate, Soft palate, Uvula, fauces
III: Hard palate Soft palate , base of the uvula —>Moderate difficulty
IV: Hard palate only —>severe difficulty

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23
Q

Describe the mechanisms of succinylcholine and rocuronium

A

succ:persistent depolarization of neuromuscular junction; mimics the effects of acetylcholine.

roc: nondepolarizing agent which competitively bind to ACh receptors preventing and blocking the receptors so there will be no access to ACh to bind to the receptors, and prevents muscular activity

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24
Q

List 5 complications of succinylcholine

A
  1. Cardiovascular effects (sinus bradycardia, especially in children)
  2. Fasciculations
  3. Hyperkalemia —>increase serum K by 0.5
  4. Increased IOP
  5. Malignant hyperthermia
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25
Q

Contraindication to NIPPV

A
  • Respiratory arrest,
  • cardiac arrest,
  • altered level of consciousness,
  • craniofacial trauma or deformity (mask seal impossible),
  • inability to protect airway (secretions, blood),
  • acute MI,
  • recurrent vomiting,
  • upper airway obstruction
  • patient refusal
  • recent UGI surgery
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26
Q

Evidence-based patient outcomes of NIPPV in COPD (2)

A

Prevention intubation
Reduced mortality
Reduced admission to ICU

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27
Q

Other reasons to use NIPPV than pulmonary edema (2)

A

Severe asthma
COPDe
Post extubation
Chest trauma/flail chest
Neuromuscular disease

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28
Q

What are 3 control variables in PC ventilation?

A

Rate
Pressure target
Insp. time
PEEP

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29
Q

What are 2 dependent variables in PC ventilation?

A

Tidal volume
Insp flow rate

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30
Q

The patient suddenly becomes hypotensive after intubation; what is the ONE thing you need to do first?

A

Disconnect from the vent and compress chest

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31
Q

What are 2 causes for a patient becoming hypotensive on a ventilator?

A

Breath stacking
Tension pneumo
Bronchospasm
Inadequate sedation
Obstruction

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32
Q

Causes of high pressure alarm (4)

A
  • Tube obstruction
  • Pneumothorax
  • Equipment problem
  • Breath stacking
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33
Q

Patient arrests post-intubation, 3 things to do while CPR in progress

A
  • Disconnect the ventilator and proceed with slow BVM
  • Check tube placement, pass a suction catheter and remove obstruction or exchange tube as necessary
  • If concern for pneumothorax, perform a finger thoracostomy
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34
Q

Patient needs BiPAP. What are the three settings you need to put into the machine?

A
  • IPAP (inspiratory positive airway pressure) 10cm H2O
  • EPAP (expiratory PAP) 5cm H2O
  • FiO2 (fraction of inspired oxygen) start at 100% then titrate down
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35
Q

What are the two diseases that benefit the most from BiPAP?

A
  • Acute cardiogenic pulmonary edema
  • COPD exacerbation
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36
Q

BiPAP decreases preload – true or false?
BiPAP increases afterload – true of false?

A

True
False

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37
Q

What settings need to be calibrated when initiating BiPAP (case of COPDe)

A
  • IPAP (inspiratory positive airway pressure) 10cm H2O
  • EPAP (expiratory PAP) 5cm H2O
  • FiO2 (fraction of inspired oxygen) start at 100% then titrate down
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38
Q

Describe initial BiPAP settings

A

IPAP 10, EPAP 5, FiO2 100%

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39
Q

Draw curves for volume control and pressure control ventilation

A

see photo

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40
Q

What physiology is represented in the following graph?

A

see photo

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41
Q

For each of the following describe set parameters, variable parameters, and ideal patient population:
Pressure control ventilation

A

Set parameters: pressure, inspiratory time, RR, PEEP
Variable parameters: tidal volume, inspiratory flow rate
Ideal patients: risk of high PEEP (COPD, asthma), high respiratory drive as inspiratory flow is not fixed ex. Salicylate overdose

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42
Q

For each of the following describe set parameters, variable parameters, and ideal patient population:
Volume control ventilation

A

Set parameters: tidal volume, RR, inspiratory flow pattern
Variable parameters: PIP, end inspiratory alveolar pressure
Ideal patients: ARDS, obesity or severe chest wall burns where you want to ensure an adequate volume is delivered

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43
Q

Describe the following modes of ventilation:
Control
Synchronized
Support

A

Control: delivers mandatory breaths at a fixed rate with a set volume and allows spontaneous breaths to be triggered but will assist those breaths with the full set volume as well; breaths are all the same
Synchronized: ventilatory breaths at a pre set rate, and patient can breathe spontaneously in between breaths; breaths may look different
Support: breaths only delivered on a patient trigger; all breaths are spontaneous

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44
Q

List initial vent settings for an intubated patient

A

Mode: continuous (often the initial setting in the ED)
FiO2: 100%
Tidal volume 6ml/kg
RR: 12
I:E ratio: 1:4
PEEP 6

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45
Q

List 4 things that could go wrong in a crashing intubated patient

A

DOPE: Dislodgement (extubation), obstruction (iPEEP, mucous plug, PE), pneumothorax, equipment failure

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46
Q

Describe an approach to troubleshooting the vent

A

Disconnect the patient from the vent to release autoPEEP
Bag with 100% FiO2
Check tube position: direct look, pass a suction catheter
Auscultate for equal breath sounds

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47
Q

Describe modifications to vent settings for each of the following:
1) COPD
2) Asthma
3) ARDS

A

1) COPD: Pressure control, adequate respiratory time (low RR), higher PEEPs ex. 10, monitor plateau pressure
2) Asthma: low RR for longer expiratory time, volume control ventilation
3) Volume control ventilation TV 6-8ml/kg

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48
Q

*Local anesthetics: List 3 amides

A

Lidocaine, bupivacaine, ropivicaine

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49
Q

*Local anesthetics: List 3 esters

A

Cocaine, procaine, tetracaine

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50
Q

*What’s the maximum dose of lidocaine with and without epi?

A

Without: 3–5mg/kg
With: 7mg/kg

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51
Q

(What factor determines the potency of local anesthetic?

A

Lipid solubility

52
Q

*What factor determines the duration of action of local anesthetic?

A

Protein-binding affinity

53
Q

*What factor determines the time of onset of action of local anesthetic?

A

pKa (dissociation constant)

54
Q

List 5 symptoms of local anesthetic toxicity

A

Parasthesias, lightheadedness, tinnitus, decreased LOC, confusion, seizure, coma, cardiac arrest, methemoglobinemia

55
Q

What is the maximum dose of bupivacaine with and without epi

A

Without: 1.5-2mg/kg
With: 3mg/kg

56
Q

List 6 side effects of NSAIDS

A

GI: dyspepsia, peptic ulcer disease, GI bleeding
Renal: AKI, HTN, electrolyte abnormalities
CVS: platelet dysfunction
MSK: impaired bone healing
Drug interactions: ASA, anticoagulants, ACEi, steroids, lithium

57
Q

Describe the difference between COX1, COX2, and non selective NSAIDS

A

COX 1: present in all cells, increase bicarbonate and mucus production in the stomach
COX 2: specific for injury and inflammation
Nonselective NSAIDs are felt to balance side effects. COX-2 selective NSAIDs have less GI side effects but may have more cardiovascular side effects due to the inhibition of thromboxane

58
Q

*Identify a patient’s ASA classification

A

ASA I A normal healthy patient
ASA II A patient with mild systemic disease
ASA III A patient with severe systemic disease
ASA IV A patient with severe systemic disease that is a constant threat to life
ASA V A moribund patient who is not expected to survive without the operation
ASA VI A declared brain-dead patient whose organs are being removed for donor purposes

59
Q

*Just in case, here is the ASA definition of sedation and analgesia (in case the question was mis-read by whoever wrote these questions down for us)

A

Minimal sedation (anxiolysis)
Moderate sedation and analgesia - “conscious sedation”
Dissociative sedation - ketamine only
Deep sedation and analgesia - airway start to be impaired
General anesthesia
See photo

60
Q

*4 symptoms on Hx compatible with OSA

A

STOP BANG
Snoring loudly
Tired during the day
Observed apnea
Pressure (HTN)

BMI > 35
Age > 50
Neck > 40cm
Guy

61
Q

*4 conditions associated with OSA

A

HTN
Obesity
Stroke
EtOH or sedative abuse
Head and neck ca
GERD

62
Q

*4 things that could happen when you administer PSA to patient with OSA

A

Airway obstruction
Ventilatory arrest
Hypoxemia
?Hypotension

63
Q

*Induction agent of choice in asthma

A

Ketamine

64
Q

What is the fasting time recommended before sedation

A

Anesthesia guidelines: 6 hours for foods, 4 hours for breast milk, 2 hours for clear liquids
ACEP guidelines: should not delay procedures based on fasting time

65
Q

For each of the following, list the sedation dose and advantages and disadvantages: ketamine

A

1-2mg/kg
Advantages: hemodynamically neutral, preferred in asthmatics, analgesia
Disadvantages: risk of laryngospasm, risk of increased secretions, emergence reactions. No real evidence for increased ICP

66
Q

For each of the following, list the sedation dose and advantages and disadvantages: midazolam

A

0.05-0.1mg/kg
Advantages: hemodynamically neutral, amnesia and anxiolysis
Disadvantages: no analgesia, respiratory depression

67
Q

For each of the following, list the sedation dose and advantages and disadvantages: propofol

A

0.5-1mg/kg
Advantages: easily titratable, fast on and fast off, good for muscle relaxation
Disadvantages: more hypotension, respiratory depression, contraindicated in egg/soy allergy, no analgesia

68
Q

List 5 maneuvers that can be done to manage laryngospasm

A

Positive pressure: CPAP, BVM with peep
Jaw thrust, pressure at Larson’s point
Deeper sedation
Paralysis and intubation

69
Q

For each of the following, list the sedation dose and advantages and disadvantages: fentanyl

A

1mcg/kg
Advantages: rapid onset, short duration, minimal CV side effects
Disadvantages: respiratory depression, rigid chest syndrome

70
Q

*List the SIRS and qSOFA criteria

A

SIRS criteria
- T >38 or <36 degrees Celsius
- HR >90 beats/min
- RR >20 breaths/min or PaCO2 < 32 mmHg
- WBC >12,000/mm3, <4,000/mm3 or >10% bands

2 or more criteria meet SIRS definition

qSOFA criteria
- AMS/GCS <15
- RR >= 22 breaths/min
- SBP <= 100 mmHg

71
Q

*Describe the scale of sepsis severity

A

No.

72
Q

List 5 signs of tissue hypoperfusion

A

[Box 6.4]
see photo

73
Q

What is the difference between neurogenic shock and spinal shock

A

Neurogenic shock = interrupted sympathetic and parasympathetic input from spinal cord to heart and vasculature. Classically - vasodilation and bradycardia (but can have a wide variation in heart rate depending on other factors).

Spinal shock = loss of sensation and motor function following spinal cord injury. reflexes are depressed or absent distal to site of injury. This may last for hours to weeks post-injury. The end of spinal shock is marked by the return of the bulbocavernosus reflex (internal/external anal sphincter contraction in response to squeezing the glans penis or clitoris, or tugging on an indwelling foley)

74
Q

What is the definition of shock

A

Inadequate perfusion to meet tissue metabolic demand

75
Q

Define each of the following: cardiac output, MAP, shock index

A

CO = HR * SV
MAP = CO * SVR
Shock index = HR/SBP

76
Q

List 4 types of shock

A

Cardiogenic
Obstruction (ex. Tamponade, tension pneumo, PE, critical AS)
Hypovolemic (ex. Volume loss, third spacing)/ Hemorrhagic
Distributive including septic, anaphylaxis, neurogenic

77
Q

List the 2 categories of adrenergic receptors that are the target of vasopressors

A

Beta: increases heart rate and contractility; may increase blood flow but higher risk of ischemia
- Beta 1: Improves contractility, heart rate
- Beta 2: bronchodilation, vasodilation, contractility
Alpha: Increase vascular tone, may decrease cardiac output with higher systemic vascular resistance
- Alpha 1: vasoconstriction
- Alpha 2: sympathetic inhibition, inhibits the release of catecholamines in the periphery(peripheral vasoconstriction)

78
Q

For each of the following describe beta affects and alpha effects
1) Norepinephrine
2) Epinephrine
3) Phenylephrine
4) Dopamine
5) Vasopressin
6) Dobutamine
7) Milrinone

A

Norepinephrine: mostly alpha, some beta (beta 1>beta 2)
Epinephrine: alpha at high doses, and beta at low doses (beta 1>beta 2); mostly beta
Phenylephrine: pure alpha
Dopamine: some alpha at high doses, mostly beta (beta 1>beta 2)
Vasopressin: ‘alpha like’ active through V1 receptors
Dobutamine: minimal alpha (vasodilatory), mostly beta (beta 1 >beta 2)
Milrinone: no alpha (vasodilatory), ‘beta like’ through phosphodiesterase inhibition

79
Q

What is the starting dose of norepinephrine

A

0.01-0.1 mcg/kg/min

80
Q

What is the start dose of an epinephrine infusion

A

0.05-0.5 mcg/kg/min

81
Q

*What is the calculation for CPP (Patients ICP is 40. BP is now 120/60. Calculate CPP.)

A

CPP = MAP – ICP
MAP = 1/3 (SBP – DBP) + DBP.
CPP = 80 - 40 = 40 mmHg

82
Q

*What is the range over which CPP is auto regulated

A

50 -160

83
Q

*5 CT signs patient has increased ICP on CT

A
  • Compressed basal cisterns
  • Diffuse sulcal effacement
  • Diffuse loss of differentiation between gray and white matter
  • Midline shift
  • Compressed ventricle
  • Brain herniation
84
Q

*Four treatments for increased ICP

A

Combination of
- Elevate head of bed
- Maintain neutral head and neck position to avoid jugular venous compression
- Mannitol
- Hypertonic saline
- Hyperventilate to PCO2 30-35 mmHg
- Sedation
- Analgesia
- Anti-emetics
- Treat fever
- Surgical decompression
- Reverse anticoagulation
- Phenobarb coma

85
Q

*3 inclusion criteria for TTM

A

Suggested:
Post cardiac arrest (any cause)
ROSC < 30 mins from team arrival
Time < 6 hours from ROSC
Patient is comatose
MAP >= 65mmHg

86
Q

*2 Methods of cooling post ROSC

A

IV cold saline 2-3 mL/kg stat
cooling vest and cooling machine
sedation and paralysis

87
Q

*3 Complications of cooling

A

CVS
bradycardia
hypotension
decreased cardiac output (matched by reduced metabolic demand)
AF is common
severe dysrhythmias are more common below 30°C (86°F)
Other ECG changes in hypothermia include prolongation of the PR, QRS and QT intervals, as well as Osborn waves (or J-waves)
Laboratory tests
Potassium and magnesium levels fall (should be corrected)
low WBC, high PT/APPT and LFTs (do not require treatment)
Blood gas analysis may show low pH and HCO3- and high pCO2 and pO2 — these values may or may not be temperature adjusted, depending on your blood-gas analyzer.
Drugs
Drug metabolism is generally slowed, leading to increased half-life, and hence drug accumulation.

88
Q

List 5 principles of neuroresuscitation

What are BP targets in bleed?

A

Maintain oxygenation PaO2 80-120
Maintain normocarbia
Maintain blood pressure. SBP >100 (pt 50-69) or >110 (all other patients). SBP <140 in ICH. This generally corresponds to a MAP 65-100
Reduce ICP to maintain CPP
Maintain normothermia
Avoid hyperglycemia

89
Q

*What are 4 sites for IO insertion?

A

Sternum
Humeral head
Distal femur
Proximal tibia
Distal tibia

90
Q

*What are 4 contraindications for IO insertion?

A

Fracture in the same bone
IO within past 24h to same bone
Orthopedic prosthesis
Overlying infection
Osteogenesis imperfecta

91
Q

*What are 4 complications of IO insertion?

A

Compartment syndrome
Extravasation
Epiphyseal injury in children/growth plate injury
Pain with infusion
Fat embolism

92
Q

*3 things that have evidence-based decrease in mortality in cardiac arrest

A
  1. High quality CPR – rate 100-120, depth 4-5cm, full chest recoil
  2. Minimize interruption of compressions
  3. Early defibrillation / cardioversion from shockable rhythms
    “AHA Chain of Survival”
  4. Early recognition & activation of emergency response (911 activation)
  5. Immediate high quality CPR
  6. Rapid Defibrillation
  7. EMS medical services –> basic & advanced EMS rx, including ACLS
  8. ALS & post cardiac arrest care (cooling etc)
93
Q

*6 components of good CPR

A
  1. rate 100-120
  2. compression 4-5cm (5-6cm)
  3. allow full chest recoil
  4. don’t allow unnecessary interruptions to CPR
  5. change CPR providers q2 mins to reduce provider fatigue
  6. BVM ventilation with 30:2 ratio
94
Q

*4 reasons for cardiac arrest on POCUS

A
  1. large pericardial effusion with tamponade physiology
  2. massive pulmonary embolism with “D” sign, McConnel’s sign, right heart strain on POCUS
  3. HOCM / LV outlet obstruction
  4. Type A aortic dissection
95
Q

*TTM targets and for how long (OLD QUESTION)

A

33-36 for 24h

96
Q

*Post arrest targets (optimal range)

A

• PaCO2 range 35-45
• Sat 94-98%
• MAP > 65 mmHg
• Hgb > 80
• PcO2 60-200

97
Q

*What are five things that you should watch for as the team leader re: CPR quality

A
  • Compression ratio: 30:2 if no advanced airway
  • Compression rate: 100-120
  • Maximize compression time/fraction (> 75% target)
  • Deep, but not too deep (compression depth of 5-6 cm or 2-2.5 inches)
  • Allow full chest recoil
  • Use audio-visual devices (e.g. metronome, compression-depth analyzer) to optimize CPR quality
  • No pulse checks and using ETCO2 to monitor CPR (goal 12-15 mmHg) quality ROSC (35-40 mmHg)
98
Q

*Name 10 potentially reversible causes of PEA/Asystole

A

• Hypovolemia
• Acidosis
• Hyperkalemia/hypokalemia
• Hypothermia
• Hypoxia
• MI
• Thrombosis - Pulmonary embolism
• Tension Pneumonthorax
• Tamponade
• Toxins

99
Q

*3 medications that are specifically NOT recommended for routine use in 2015 ACLS guidelines

A

• HCO3
• Atropine
• Calcium
• IV fluids
• Fibrinolysis

100
Q

*3 interventions that are specifically NOT recommended for routine use in 2015 ACLS guidelines

A
  • Pacing
  • Precordial thump
101
Q

*5 complications and treatments in IJ or subclavian CVC placement

A

Pneumothorax – Needle + chest tube
Bleeding/art puncture – direct pressure
Air embolus – LL decubitus and aspirate/thoracotomy
Lost wire – call thoracics
Infection – Remove, Abx

102
Q

*3 physiologic mechanisms and example of each for hypoxemic respiratory failure

A
  • Low FiO2 (e.g. high altitude)
  • Hypoventilation (e.g. opioid misuse, obesity hypoventilation, impaired neural conduction e.g. ALS, Guillain-Barre, high C-spine injury, muscular weakness e.g. myasthenia gravis)
  • V/Q mismatch (e.g. COPD, pulmonary embolism, interstitial lung disease)
  • Shunt i.e. blood passes from right to left side without being oxygenated (e.g. intracardiac shunt, pulmonary AVM, atelectasis, pneumonia, ARDS)
  • Diffusion limitation (e.g. pulmonary fibrosis)
103
Q

*3 physiologic mechanisms and example of each for hypercarbic respiratory failure

A
  • Increased CO2 production (e.g. fever, sepsis, burns, over-feeding)
  • Decreased alveolar ventilation i.e. decreased RR (e.g. CNS lesion, overdose), decreased tidal volume (e.g. myasthenia gravis, ALS, Guillain-Barre, botulism, spinal cord disease, respiratory muscle fatigue in COPD/asthma exacerbation) increased dead space (e.g. pulmonary embolism, hypovolemia, poor cardiac output)
104
Q

What is the target ventilatory rate in CPR

A

30:2 if no advanced airways, 10 breaths per min (1 breath every 6 seconds) if advanced airway

105
Q

What should the EtCO2 level signifies ROSC

A

> 40

106
Q

What are 5 targets during CPR that indicate a good resuscitation

A

Palpable carotid or femoral pulse
CPP >15
Diastolic pressure >20
EtCO2 >10
ScvO2 >40

107
Q

Explain the results of the TTM2 trial

A

Hypothermia versus Normothermia after Out-of-Hospital Cardiac Arrest. N Engl J Med. 2021;384(24):2283-2294
Population: 1850 w OHCA, multicentre RCT. Excluded unwitnessed cardiac arrest, ECMO, febrile on admission, ICH, severe COPD
Intervention: hypothermia with target temp 33 degrees
Control: cooling only if temp >37.8
Outcome: no different in all cause morality at 6 mo (primary). No difference in functional outcome, health reality quality of life. Higher incidence of arrhythmia and hemodynamic instability in the hypothermia group
Bottom line: hypothermia does not lead to lower mortality. Aim for normothermia unless temperature >37.9

108
Q

Briefly describe the results of the original TTM1 trial in 2013

A

Large RCT in 36 ICUs internationally that showed no difference in the primary outcome of mortality (50% vs 48%) and no difference in neurologic outcomes between cooling patients to 33 vs 36 degrees Celsius.

109
Q

Explain the results of the Hyperion temperature trial

A

Lascarrou J-B. “Targeted Temperature Management for Cardiac Arrest with Nonshockable Rhythm”.N Engl J Med. 2019.
Population: 581 patients in French ICUs with non shockable rhythms. RCT
Intervention: Cool to 33 degree
Control: Normothermia 36.5-37.5 degrees
Outcome: Survival with favourable neurologic outcome was improved 10.2% in hypothermia vs 5.7% in normothermia. No difference in 90 day mortality, adverse events, survival to ICU discharge

Bottomon line: therapeutic hypothermia should be utilized

Bottomon line:

110
Q

What are ILCOR recommendations for hypothermia post ROSC

A

Prevent fever by targeting temp <37.5
Do not actively warm to achieve normothermia

111
Q

Describe the ACLS algorithm for cardiac arrest

A

see photo

112
Q

What is the shock energy for defib

A

200 if biphasic, 360 if monophasic

113
Q

List 2 causes each of narrow and wide complex PEA

A

Narrow: tamponade, tension pTX, PE, MI
Wide: hyperkalemia, sodium channel blocker toxicity, MI

114
Q

What is VT storm

A

3 or more episodes of VF or sustained VT within 24 hours (or >3 shocks from ICD)

Generally patients can be shocked out of VT/VF easily, but they keep flipping back into VT/VF (unlike refractory VT where they can never get back into sinus)

115
Q

List 5 causes of VT storm

A

acute MI, heart failure, electrolyte abnormality, medication toxicity, medication non adherence, drugs (esp. hydrocarbons), thyrotoxicosis, sepsis

116
Q

List 5 management steps for VT storm

A

Stop Epi: increases myocardial oxygen demand and electrical instability
Amiodarone (first line): 150mg bolus then infusion
Esmolol (second line): 0.5 mg/kg (max 50mg) bolus then infusion 50-100 mcg/kg/min (max 0.3 mg/kg/min)
Lidocaine (third line): 1-1.5mg/kg bolus then infuse 0.02 mg/kg/min

Dual sequential defib
Stellate ganglion block

Correct electrolytes, mag supplementation
Sedation

117
Q

What does pulse oximetry measure

A

% of arterial hemoglobin that is in the oxygenated state (SpO2)

LEDs give off wavelengths of oxyhemoglobin and deoxyhemoglobin, the amount at which these wavelengths are absorbed and transmitted gives you the oxygen saturation

118
Q

List 5 limitations of SpO2

A

Poor pickup: low flow state, deep skin pigmentation, nail polish
Incorrect pickup: carboxyhemoglobin, methemoglobin
Artifact

119
Q

What is the concordance between EtCO2 and PaCO2

A

EtCO2 is less by PaCO2 by 2-5 mmHg (due to dilution in an open circuit)

120
Q

Describe the phases to this EtCO2 waveform (see photo)

A

Phase 1: inspiratory baseline, this should normally be devoid of carbon dioxide
Phase 2: expiratory upstroke, the beginning of expiration. Prolongation of this upstroke represents obstruction to expiratory gas flow ex. COPD
Phase 3: alveolar plateau
Phase 4: inspiratory downstroke

121
Q

Interpret these EtCO2 tracings (see photo)

A

see photo

122
Q

List 5 causes of elevated EtCO2

A

Metabolism: pain, hyperthermia, shivering
Respiratory: respiratory insufficiency (ex. Post seizure), COPD, analgesia/post sedation
Circulatory: increased CO
Meds: bicarb

123
Q

List 5 causes of low EtCO2

A

Metabolism: hypothermia, metabolic acidosis (ex. DKA)
Respiratory: bronchospasm, mucus plugging
Circulatory: hypotension, hypovolemia, cardiac arrest, pulmonary emboli

124
Q

List indications for EtCO2 monitoring in the ED

A

Confirm tube placement in trachea and continuous tube placement
immediate notification of accidental extubation
Procedure sedation monitoring
Quality of CPR: >10 good, <10 inadequate, ETCO2 <10 at 20 min = non-survivable. sudden increase in ETCO2 = ROSC
Target ventilation in head injured patients
Diagnosis of DKA/metabolic acidosis
Help detect bronchospasm and improvement after puffers

125
Q

What are 4 causes of low pressure alarm on the vent

A

diconnected
Cuff leak
Chest tube leak
Bronchopulmonary fistula

126
Q

Two long term effects of ketamine

A

chronic cystitis
Biliary sclerosis

127
Q

5 discharge criteria post procedural sedation

A

Walking
Normal vitals
GCS 15
Following commands
Tolerate PO

KChan Saves the World (24 decks)

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