Airway/Resus

ACLS

Airway Sizes

Allergic Reaction

Anaphylaxis

Bougie Cricothyrotomy

Difficult Airway Algorithm

EtCO2

Oxylog 3000 plus (Own the Oxylog) LITFL.com

Ventilator Management

BER vs MI

• BER's STE has steeper downstroke than upstroke

Anaphylaxis

Definition

Highly likely when ANY ONE of the following criteria is fulfilled:

1. Criterion 1 (90% of pts)
   1. Acute onset of an illness involving the skin, mucosal tissue, or both AND at least one of the following:
      1. Respiratory compromise
      2. Reduced BP or associated symptoms (syncope, dizziness)
2. Criterion 2 (10-20% of pts)
   1. TWO OR MORE of the following that that occur rapidly after exposure to a LIKELY allergen for that pt
      1. Involvement of the skin-mucosal tissue (hives, swollen lips-tongue-uvula)
      2. Respiratory compromise
      3. Reduced BP or associated symptoms
      4. Persistent GI symptoms (vomiting, diarrhea, crampy abd pain)
3. Criterion 3
   1. Reduced BP after exposure to a KNOWN allergy for that pt (minutes to hours):
      1. Adults
         1. Systolic < 90 or > 30% from baseline
      2. Peds
         1. Less than 70 mmHg from 1 month up to 1 year
         2. Less than (70 mmHg + [2 x age]) from 1 to 10 years
         3. Less than 90 mmHg from 11 to 17 years

DDX

1. Generalized urticaria
2. Angioedema
3. Asthma exacerbation
4. Anxiety attack
5. MI
6. Scombroidosis
7. Other forms of shock

Presentation

• Cutaneous symptoms - 90%
• Respiratory symptoms - 70%
• GI symptoms - 40%
• Cardiovascular symptoms - 35%

Treatment

1. Epinephrine 1:1000 IM 0.3-0.5mg (0.3-0.5mL) Q5-15min
   1. Give as soon as possible
   2. Always IM initially
   3. Start epinephrine infusion 1:10,000 2-10µg/min if inadequate response to IM
   4. Peds
      1. IM - 0.01mg/kg/dose (max 0.5mg)
      2. IV infusion - 0.05-1 mcg/kg/min
2. Oxygen
   1. Consider intubation if e/o airway edema
3. NS bolus
   1. If unresponsive to Epi assume distributive shock (give NS 1-2L)
4. Glucagon 1-2mg IV over 5 min followed by infusion of 5-15µg/min
   1. If on B-blocker AND unresponsive to epi
5. Also consider:
   1. Albuterol: For bronchospasm resistant to IM epinephrine
   2. Antihistamines
      1. Only for sympton control (hives, itching) AFTER hemodynamically stable
         1. Diphenhydramine 25 to 50 mg IV
         2. Ranitidine 50 mg IV (minimal evidence to support this)
   3. Glucocorticoid: May blunt biphasic reaction
      1. Methylprednisolone 125 mg IV (2mg/kg in peds)
      2. Three day PO course (biphasic reaction always occurs within 72hrs)

Course

1. Uniphasic (80-90%)
   1. Symptoms peak within 30min-1hr after onset, resolves within 30min-1hr of receiving Tx
2. Biphasic (10-20%)
   1. Uniphasic response, followed by asymptomatic period of hour or more, then return of symptoms
   2. The second phase does not necessarily resemble the first!
   3. Possible risk factors
      1. Severe initial symptoms
      2. Late administration of epi
      3. Delayed resolution of initial symptoms
   4. Little evidence that glucocorticoids blunt a biphasic presentation
3. Protracted (case reports)
   1. Lasts hours to days without resolving completely

Disposition

1. Admit: Severe and moderate (especially if symptoms did not respond promptly to epi)
2. Home: Symptom-free for at least 4hr
   1. Send home with an epi autoinjector!

Sources

• Tintinalli
• Brown SGA, Mullins RJ and Gold MS, Anaphylaxis: diagnosis and management, MJA 2006; 185: 283–289
• Ewan PW, ABC of allergies – Anaphylaxis, BMJ 1998; 316: 1442-1445
• Simons FER, Gu X, Simons KJ, Epinephrine absorption in adults: Intramuscular versus subcutaneous injection, J Allergy Clin Immunol 2001;108:871-3
• Lieberman P et al, The diagnosis and management of anaphyalxis: An updated practice parameter, J Allergy Clin Immunol 2005;115;3:S483-S523
• Sheikh A, Shehata YA, Brown SGA, Simons FER. Adrenaline (epinephrine) for the treatment of anaphylaxis with and without shock.Cochrane Database of Systematic Reviews2008, Issue 4. Art. No.: CD006312. DOI:10.1002/14651858.CD006312.pub2.
• Second symposium on the definition and management of anaphylaxis: summary report--Second National Institute of Allergy and Infectious Disease/Food Allergy and Anaphylaxis Network symposium.

EtCO2

Qualitative: Purple to yellow (acid) after 3 breaths

Quantitative: waveform capnography

VENTILATION: Pulmonary exchange of CO2 and its expiration

- measured by colorimetric (qualitative) capnometry or continuous infrared spectroscopy (quantitative) aka wave form capnography

Colorimetric

- litmus paper, CO2 is from purple to yellow

- maybe used if not cardiac arrest or profound shock

- caveat:

1. has to be after 6 breaths (could be CO2 pushed to the stomach, so needs to clear those first)

2. it's a litmus paper, it turns yellow to any acid, like vomit

3. Adrenaline if it contaminates ET tube

4. Cardiac arrest: litmus paper could not measure the low levels of CO2 that the capnograph can

ETCO2

- concentration of CO2 at the end of exhalation

- underestimates PaCO2 among healthy by 4-5mmHg (ETCO2 is 5 less than PaCO2)

- unpredictable correlation for sick patients (complicated, V/Q mismatches)

* the only guarantee is PaCO2 is at least ETCO2, eg if ETCO2 is 45, PaCO2 is at least 45

(PaCO2 is always higher or equal to ETCO2)

- attaches to ET tube or nasal cannula, sucks out some of the exhaled gas

measured by spectrophotometry giving number + wave form of CO2

- consists of 2 contributing factors (difficult what extent one is represented)

1. PaCO2: concentration of CO2 in artery

2. Dead space: areas not perfused, not receiving CO2 back from venous blood

- main reason in ED of dead space is poor cardiac output/perfusion of lungs

THEREFORE, ETCO2 is not only a measure of PaCO2 (ETCO2 is not equal to PaCO2)

USES: normal: 35-45 (Dr Scott weingart from Amal Mattu's podcast)

1. Tube confirmation: 100% if wave form is present even in cardiac arrest (as long as CPR is done)

- you can also attach this to ET tube "during" intubation itself, if wave form is seen = confirmed

2. Procedural sedation:

- breath by breath monitoring of waveform and quantitative measure of CO2

* remember as long as you give supplemental O2, pulse ox couldn't be relied to on ventilation (REMEMBER APNEIC OXYGENATION)

* if patient is breathing room air, you can use pulse ox as surrogate measure of ventilation

as CO2 rises, they will only desaturate if they're not taking enough breaths, therefore stimulate them or bag them

3. CPR/ACLS prognosis: if 20 minutes of ACLS, ETCO2 is <10, then zero survival (get echo probe too)

- same token, ROSC: sudden increase of ETCO2, check pulse, likely ROSC

4. TBI:

- eg. after intubation, ETCO2 of 55, pCO2 is at least 55, therefore will need some ventilatory support

low ETCO2 is not useful

therefore, if ETCO2 is 55, manage first (don't send the abg)

if it's less than 35, send it

5. Intubation of acidotic patients

- eg DKA, Sepsis, Aspirin; after intubation if ETCO2 is high, these patients will crash due to acidosis-related dysrrhythmias

- get the baseline ETCO2, eg 10 with help of NIV -> intubate, bag them and don't let CO2 to rise -> then hook to mechanical ventilator and maintain ETCO2 to 10

- of course not perfect (CO2 can also be high), but you give patient possible shot

Sources:

LITFL

emcrit

medicscribe.com

capnography.com

Ventilator Management

2 sets of patients:

1. ALI/ARDS and everything else

2. Obstructive (COPD/Asthma)

Mode

= when not sure use A/C

= you set the TV and RR

= patient initiates, and machine gives preset of Vt eg 500c

4 things you have to know about ALI (ARDSnet)

Vt = lung protection; 6-8 cc/kg IBW

Flow rate = patient comfort

RR = ventilation

FiO2/PEEP = Oxygenation

Vt = PROTECTION

- goal is to lower to 6cc/kg

- not adjusted according to ventilation (eg CO2 of 60, don't increase Vt or if low, don't lower Vt)

Inspiratory flow rate/IFR/peak flow = COMFORT

- how quickly a breath is delivered

- if high breath duration is quick

- 60-80 lpm

- if patient is sucking, not getting enough air = increase IFR

RR = VENTILATION

- 60 cc/kg/min to maintain eucapnia

- once intubated, requirement doubles due to deadspace of the circuit -> 120 cc/kg/min

70 x 120 = 8400

8400cc/500cc = 17

therefore start 16-18/min to prevent hypercapnia

- if hyperventilating, go down; if hypoventilating CO2 is low, RR to go up

* for acidotic patients, needs high minute ventilation

minimum 240 cc/kg/min, at least 36/min and adjust up

to prevent hypercapnia, to prevent acidosis

FiO2/PEEP =OXYGENATION

- if low O2, increase FiO2/PEEP tandem

- start 100% FiO2, wait x 5 minutes, get ABG

- drop to 40%, after 2 minutes wait for result

- use the PEEP scale for PEEP/FiO2, target 90-95% saturation (not more than >95%, at saturation of 100%, you won't know if the PaO2 is 80% or 400% which is too much), adjust every 10 minutes

- PEEP does not pop lungs!

PEEP

- good: Improves V/Q, decreases shunt, decreases atelectasis/trauma, improves spont breathing

- bad: decreases venous return (you can work it out, give more fluid)

- myth: causes pneumothorax, head explodes

*alveoli is like balloon: easier to blow if there's some air already in there

How to avoid pneumothorax

- check plateau pressure (or alveolar pressure), should be <30cmH20

- check every 30 minutes, if >30, adjust PROTECTION which is Vt (if too high drop Vt from 8 to 7)

- peak pressure means nothing

Ventilation curve pattern/ventilation pressure wave form on VC mode

- air rushes to ET tube, tracheobronchial tree = high initial pressure = Peak pressure

- after system has equilibrated with alveolar, it plateaus = Plateau pressure

Peak pressure: PIP/Peak Inspiratory pressure

- means nothing to patient's safety

- does not affect the alveoli

- only purpose is to alarm the vent

Plateau pressure:

- this reflects small airway and alveolar pressure

- not measured by vent directly (after delivering the oxygen, vent drops very quickly)

- should be less than 30cmH20

- press inspiratory hold button (0.5-1 second) once patient breathes = plateau pressure

*Peak pressure: pressure on major airways (+ ET tube) = alarm

Plateau pressure: pressure on smaller airways (+ alveoli) = matters

PIP: peak airway pressure

Pplat: Plateau pressure

Paw: airway pressure

SUMMARY:

Vt: if plateau pressure >30, decrease Vt

IFR/Peak flow: if patient is sucking, not getting enough air = increase IFR

RR = ventilation, if CO2 too high, increase RR

FiO2/PEEP: increase this if <90% saturation with target 90-95%

analgesia:

- fentanyl or morphine

- comfort for pain, blunts effects of hypercapnia

then sedation:

- propofol, ativan, versed

OBSTRUCTION (asthma, COPD)

- goal: give patients time to expire

- mode: AC

Vt: 8cc/kg IBW

IFR/peak flow: make inspiration shorter therefore higher to expire slower: 80-100 lpm

FiO2: 40-100%, usually no Oxygenation problem, leave at 40% if you want (they desaturate because they tire out)

PEEP: zero

RR: - most important setting, set this low

- start at 10

IE ratio: 1:4 or 1:5

Permissive Hypercapnia

- CO2 of >50, as long as pH is 7.2, 7.1 (because of hypercapnia) that's fine

- bicarb has no pathophysiologic reason

AVOID air-trapping and autoPEEP

- air trapping: alveoli are closed off cuz of mucous plugging and air could not go out, needs suctioning/pulmonary toilet

- auto PEEP: dynamic overinflation of alveoli, goes away if they are allowed to breathe

Airtrapping: normally there is a space between fully expiring gas and the next inspiration

in obstructive disease, the air is not fully exhaled and inspiration comes in immediately, stacking air/gas

- if this happens, lower RR

AutoPEEP

- if vent doesnt have this, look at plateau pressure

*peak pressure

- does not mean anything

- represents ET tube, large airways

- constricted on obstructive disease, therefore this is high like 80-90, therefore this always alarms, just increase upper treshold of alarm, cuz this does not mean anything

* plateau pressure: if >30, significant auto PEEP, decrease RR

if <30, autoPEEP is not significant

Scenario

- Asthmatic, crashing on the vent (low sat low BP)

DISCONNECT the vent, leave the ET tube

- if air rushes, the air-stacked will go out

- if no air rush, no improvement of vital signs = use DOPE

Sedated completely (you intubated this patients due to muscle fatigue, so dont let them breathe)

- propofol: has bronchodilatory effect too

analgesia: fentanyl/morphine; blunts hypercapnia, for comfort

SUMMARY:

Vt: 8cc/kg

IFR: 80lpm

FiO2: just maintain sats >90

RR: 10

- if airtrapping on curve, decrease down to 8 to 6

- if >30 plateau pressure; down RR

-----

pdf Vent Handout from Dr Scott Weingart

Crashing post intubation

D - isplacement

O - osbstruction

P - PTX

E - Equipment failure

S - in asthma, stacked breaths

Stacked breaths - disconnect the vent circuit

- if air gushes out, patient improves

- if no improvement, no air gushing = proceed to DOPS

Equipment failure - attached BVM (eg kinked tube, machine failure, no O2 in vent etc)

D - tube Displacement: check ETCO2 colorimetric or wave form

O - obstruction: suction, if too thick plug, can push with bougie, but the plug will go deeper

P - tension PTX, check with US if with time, otherwise....

Perform bilateral finger thoracostomies!!!

Level of ET tube: from teeth, Caucasian 23 M, 21 F; Asian 22 M, 20 F

Allergic Reaction

1. Prednisolone 0.5-1 mg/kg x 5 days
2. Promethazine 25mg IM or Diphenhydramine 50mg IM/IV
3. +/- H2 blocker: Famotidine 40mg / Cimetidine 300mg
4. Rule out Anaphylaxis
5. 6 units FFP if Hereditary Angioedema

See Airway/Resus > Anaphylaxis

Bougie Cricothyrotomy

Materials

1. Bougie
2. Scalpel/Knife
3. ET tube size 6 (or size 6 Shiley) with syringe pre-attached ready to inflate
4. Ambu-bag with EtCO2 pre-attached

Steps

• Landmark: Feel for and stabilise Cricothyroid membrane* with non-dominant hand
• 2 cm horizontal incision and bluntly dissect with finger
• Insert bougie until it stops advancing feeling for the tracheal ring thugs
• Insert the ET tube (or Shiley) and stop once the balloon is inside
• Inflate balloon, connect to ambu-bag, check EtCO2

*Cricothyroid membrane: between thyroid cartilage (Adam's apple) and cricoid cartilage (inferiorly)

- If not obviously palpable, make a vertical incision first and blunt dissections to feel for landmarks

Indications:

1. Failed Airway

2. Difficult Anatomy

3. Excessive Blood in Mouth or Nose

4. Facial trauma

5. Airway Obstruction due to angioedema, trauma, burns or foreign body obstructing the airway

Note that cricothyrotomy is still above subglottic stenosis (eg. post intubation; large goitre) and therefore this procedure won't solve it. If it is above clavicle, it is ENT, if below = thoracic surgeon.

Link video

Airway Sizes

Airway Sizes

LMA: Female 3 or 4, Male 4 or 5

Oropharyngeal Airway: lip/teeth to angle of jaw

Nasopharyngeal Airway: tip of nose to tragus

ETT: Female 6.5, 7; Male 7.5, 8

Bougie Cricothyrotomy: ETT 6

ACLS

New Points

EtCO2

BLS

ECG

V-fib, Pulseless VT

Asystole and PEA

Bradycardia

Tachycardia

New Points

• No ventilations for untrained lay persons
• Compression: a priority, push hard (2cm), push fast (100/min)
• No Atropine, no pacing on PEA/Asystole
• Supraglottic airway (eg. LMA) is upgraded
• Cricoid Pressure not routine
• Bedside Echo

EtCO2 is cool

• Tube confirmation
• Gauge of quality CPR
• Marker of futility of resus (<10mmHg)
• Marker of ROSC (increase of 10mmHg)

BLS

• Compressions: minimize interruptions, push hard/fast
• Ventilation: 30:2 (8-10 breaths if intubated)

ECG

• rate: fast or slow
• WRS: wide or narrow
• rhythm: regular or irregular

V-fib, Pulseless VT

• Shock + CPR - Adrenaline - Shock + CPR - Amiodarone - Causes
• Shock (Unsynchronized 200J biphasic, 360J monophasic) + CPR x 2 mins
• Adrenaline 1mg if Shock + CPR x 2 minute does not convert
• Shock + CPR
• Amiodarone 300mg IV push, repeat 150mg as indicated;
• or Lignocaine 1-1.5mg/kg then 0.5-0.75mg/kg q5-10 mins;
• or Magnesium 2g IV, then infusion (polymorphic VT)

Asytole, PEA

• Adrenaline 1mg q3-5 mins
• 6H: Hypovolemia, Hypoxia, Hypothermia, Hypoglycaemia, H ions (Acidosis), HypoK/HyperK
• 5T: Tox, cardiac Tamponade, Tension PTX, Thrombosis (AMI), Thrombosis (PE)

Bradycardia

• Significant if chest pain, hypotension, AMS, pulmonary oedema
• Profound bradycardia <40 bpm
• Temporize with Atropine 0.5mg 3-5 mins if QRS is not wide
• 1. Transcutaneous Pacing
• 2. Chronotropes:
• 2a. Dopamine 2-10mcg/kg/min
• 2b. Adrenaline 2-10mcg/min
• Transvenous pacing if above fails

Tachycardia

• 3 questions
• 1. Sinus?
• 2. QRS wide or narrow?
• 3. Regular or irregular?

Narrow regular

• Sinus Tachycardia: Tx underlying
• SVT: Vagal maneuver (converts 25%)
• Adenosine: 6mg IVP, then 12mg
• If fails, Diltiazem 15-20mg IV, then infusion of 5-15mg/h
• or Metoprolol 5mg IVP x 3 followed by 50mg PO
• Synchronized cardioversion 100J Biphasic

Narrow irregular

• MAT: Tx underlying HypoK, hypoMg
• Sinus Tachycardia with frequent PACs
• Afib, Aflutter with variable conduction
• Diltiazem
• MTP (good in setting of ACS)
• Amiodarone (good in hypotension, CHF)
• Digoxin (good in CHF)
• Synchronized Cardioversion: 120-200J

Wide regular

• VT unless proven otherwise
• If stable, antiarrhythmics
• 1. Procainamide 20-50mg/min till rhythm is suppressed, hypotensive or max (17mg/kg), avoid if prolonged QT
• 2. Amiodarone 150mg x 10 mins, repeat as necessary
• 3. Sotalol 100mg IV x 5 mins: avoid if prolonged QT
• Synchronized Cardioversion: 100J
• Adenosine is okay for Dx and Tx if rhythm is regular and monomorphic
• .
• SVT with aberrancy: Tx as SVT

Wide Irregular

• No AV nodal blockers (Adenosine, B blocker, Ca blockers, Dig), can trigger V-fib
• 1. Afib with preexcitation
• 1a. First line: Electric Cardioversion
• 2b. Second line: Procainamide, Amiodarone, Sotalol
• 2. Afib with aberrance
• 3. Polymorphic VT/Torsades
• 3a. Emergent Defib (NOT synchronized)
• 3b. Correct electrolytes
• 3b. Stop QT prolonging meds

Source: AHA ACLS 2010