The Pre-brief
#ResusX20 STARTS TOMORROW! Join us on October 6-8, 2020, for an incredible virtual resuscitation and critical care conference, filled with quick, high-yield lectures and the opportunity to interact one-on-one with the experts. Check out the conference website for more details!
In the meantime, check out these learning pearls from day one of last year’s conference (originally posted on the Mercy St. Vincent Medical Center EM Residency Blog).
Blood Pressure in Neuro Emergencies; What’s My Target? by Dr. Evie Marcolini
- Lots of flavors of neuro disasters; each has its own blood pressure target
- Hemorrhagic stroke – mostly caused by untreated hypertension
– SBP<140; if patient has chronic HTN then SBP<180
– Our job is to prevent secondary injury by reversing AC and treating blood pressure
– ATACH-2 trial – Nicardipine: goal <180 and <140; no difference. Lower is not better. - Ischemic stroke
– Need to keep BP higher to allow perfusion via collateral flow
– Keep SBP relatively high, but must be <185 for tPA - Traumatic Brain Injury
– SBP>100 for ages 50-69; SBP>110 for everyone else (from BTF guidelines)
– SBP<90 increased mortality
– Every 5mmHg above SBP 90 (up to 135) decreases mortality - Subarachnoid hemorrhage
– SBP<140 – Goal is to prevent re-rupture
– Do it quickly: give a bolus and infusion (Nicardipine or Clevidipine)
– AVOID Nitroglycerin and Nitroprusside; these are vasodilating, making the vessels take up more space in the brain
How to Intubate the Injured Head and Why Your Decision Matters by Dr. Erin Sabolick
- It is critically important to prevent secondary injury (too late to prevent primary injury when patient is in front of us in the ED)
- Neuro exam is extremely valuable, and we lose that when we intubate the patient
- Important components of the neuro exam: eye opening, pupils, voice, motor response on both sides, upper and lower extremities
– Exam can be performed while preoxygenation (flush rate NC & NRB) and premedication (fentanyl, NO lidocaine) takes place
- Use video laryngoscope
- Ramped intubation: gravity helps with venous drainage
- Ketamine
– No ICP spikes (MYTH BUSTED: Systematic Review, LITFL)
– Hemodynamically neutral
– Allows for spontaneous respiration - Have your post-intubation sedation ready before the intubation
– Paralytics may last longer than sedative, so you will either need to redose the sedative or start your infusions
– Have extra induction and paralytic ready at the bedside - Be present at the bedside when the consultant performs a repeat neuro exam
Mastering Acids & Bases by Dr. Rory Spiegel
Dr. Spiegel gave a two-part lecture on digesting acid-base problems in our patients. There is absolutely no good way to do justice to Dr. Spiegel’s engaging lecture by typing out notes. Instead, I would highly recommend you watch his Acid-Base lecture from The Hospitalist and The Resuscitationist Conference.
- The actual pH number doesn’t matter
- Study conducted on rabbit hearts: heart beat better in neutral solution vs acidic solution; inotropes worked better in neutral solution
– However, in humans, results are different - “Apneic Oxygenation in Man” Frumin et al.
– heart did just fine with extreme acidosis and elevated pCO2
– The acidosis doesn’t really cause issues in humans - The name of the game is: Cations (Sodium) must equal Anions (Cl-, HCO3-, Anion gap)
– you can only become acidotic in two ways: either chloride increases and HCO3 decreases or gap increases and HCO3 drops
– alkalosis occurs by the opposite mechanism - SID (Strong Ion Difference) = Na-Cl. Normal is 36-40
– SID >40 = Alkalosis
– SID <40 = Acidosis - Ex: SID>40 occurs in (Cl decreases, HCO3 increases):
Vomiting: lose H+ and Cl
Dehydration: “Contraction alkalosis”, Aldosterone retains Na, so Na and HCO3 increase
Chronic resp acidosis: Na and HCO3 increase - Ex: SID<36 occurs in (Cl increases, HCO3 decreases):
Diarrhea: Losing Na and HCO3
AKI: not absorbing back Na and HCO3
RTA: peeing out Na and HCO3
Saline Infusion: significant Cl load (Normal Saline is a SID 0 fluid, will lower body SID). In LR, sodium lactate is the buffer –> lactate gets broken down and body gets free sodium; similar in Plasmalyte.
NaHCO3 administration –> CO2 blown off, you get free Na - Take home: if you use SID, no need for calculating a delta delta. We are looking at the chloride and how it influences the acid/base.
- All nongap acidosis is due to increases in chloride
- Gap alkalosis: gap (composed of weaker acids: lactate, albumin, ketones, alcohols) decreases and bicarb increases (eg. drop in albumin).
- Elevated anion gap acidosis (Mnemonic MUDPILES) – THESE WILL KILL YOUR PATIENT
> Methanol –> Formate
> Uremia –> phosphates and sulfates (high BUN; it’s not urate)
> DKA –> Ketones
> Paraldehyde (used for alc withdrawal)/Phenformin (inhibit Kori cycle) –> Lactate
> INH/Iron –> Lactate (due to seizures)
> Lactic acidosis –> Lactate, CO, CN, ischemia
> Ethylene Glycol –> Oxalate, Glycolate
> Salicylate –> Ketones, lactate - What labs do we need? – BUN – Lactate – Ketone – ASA Level If all are negative, only one left is toxic alcohol
Status Epilepticus: Where’s the evidence? by Dr. Erin Sabolick
- Definition: continuous seizure for 5 minutes or two seizures without interval return to baseline
- RAMPART trial showed that IM midazolam terminated more seizures without rescue therapy than IV lorazepam. IV midazolam hasn’t been looked at properly.
- Dr. Sabolick uses an algorithm similar to Dr. Justin Morgenstern from First10EM.com:
- Establish IVs, bilateral nasal airways, NRB, place patient on monitor
- Two doses of benzos, followed by phenytoin, propofol and RSI. If the seizure continues, start barbiturates.
- Some extra tips: – Start looking for reversible causes early
> Home medications/toxicology
> ETOH vs Benzo withdrawal
> INH toxicity
> Decreased Na/Ca/Glucose
> Consider eclampsia in any pregnant or postpartum patient
   – Involve consultants early
   – Consider taking the airway early if indicated - If hypotensive, can switch propofol to midazolam
- Consider adding ketamine
- STAT EEG (ensure no underlying seizure after paralysis)
- ESETT Trial: results coming out soon – compares fosphenytoin vs valproic acid vs levetiracetam
Traumatic Brain Injury by Dr. Evie Marcolini
- New guidelines from Brain Trauma Foundation in 2016 (be on the lookout for my BTF TBI guidelines summary soon!!!)
- Avoid hypotension. As from above: SBP>100 for ages 50-69; SBP>110 for everyone else.
- Optimize cerebral perfusion pressure (CPP = MAP-ICP), 60-70mmHg
- Don’t use induction agents that will drop BP. Use etomidate for induction. Ketamine is now an option; ICP increase has been debunked.
- Lidocaine: no longer used in RSI; can cause hypotension in RSI, so don’t use it.
- Laryngoscopy will increase blood pressure. Use fentanyl, which can help decrease pain and blood pressure and mitigate seizures.
- Some extra tips and tricks:
– Intubate with HOB up
– Hydrate your patient
– Place an arterial line early if possible
– Have esmolol ready (even prime tubing) to bring BP down quickly if the patient spikes
– Have meds drawn up and ready with push-dose agents - Hyperventilation: do not use anymore. Keep CO2 35-40. Only use if you are headed to ventriculostomy or craniectomy. Rebound vasodilatation that takes up space in the brain can occur.
- If there is a brain bleed:
– Reverse anticoagulant
– Seizure prophylaxis if clinically indicated
– Give Osmotics: Mannitol will cause diuresis, so you need to replace the fluids; Hypertonic saline is a volume expander, you can bolus 250mL at a time to decrease swelling/ICP - Ventriculostomy is indicated for sick patients, bad CT, bad exam
- Therapeutic hypothermia doesn’t work, but fever is bad – treat with tylenol
- Do not prognosticate within the first 24 hours
TXA in TBI: Are we there yet? by Dr. Erin Sabolick
- CRASH2 and MATTERs trials show some support for TXA in trauma
- Precise dosing regimen is uncertain at this time
- No increase in vasoocclusive events (strokes, MI, etc)
- CRASH3 results due very soon
– Since the compilation of these notes, CRASH3 results have come out, check out some of the reviews of the study here: RebelEM, First10EM, St. Emlyn’s Blog, TheSGEM - Bottom line: TXA for TBI? Not yet.
- Check out this Journal Club review of the Cal-PAT trial
Refractory Hypoxia by Dr. Rory Spiegel
- Step 1: lower your standards – don’t try to get all the lab numbers right
- Step 2: dry them out: diurese, use pressors early, and administer less fluids
- Step 3: phenotype your shunt physiology: determine if pathology is single lung vs double Lung
- Double lung
– ARDS – Berlin definition
– Lung is not stiffer, it is just smaller. There is loss of some lung parenchyma due to fluid.
– You are now dealing with “baby lungs,” so use smaller tidal volumes
– 4 large randomized trials that failed to show benefit of high vs low PEEP
– Start with ARDSnet protocol but monitor your patient and make changes as below
– Monitor your DRIVING PRESSURE = Plateau pressure – PEEP
> Normal DP ~14cmH2O.
> Answers the question “Is the tidal volume I am giving to this patient appropriate for their lungs?”
Start by increasing PEEP to decrease Driving pressure. If PEEP gets too high, then Plateau pressures can also rise (due to overdistension of the lungs). Solve this by lowering tidal volume. Plateau pressure will decrease and you can continue to increase PEEP and attempt to lower Driving pressure.
- Single lung – PEEP increase will cause worsening hypoxia – Place patient on his/her side with good lung down (lateral decubitus) > Increases blood flow to good lung > Increases airway pressure in good lung due to weight of mediastinum and other lung, allowing more air to reach bad lung
- Patients frequently just need time to re-recruit the alveoli
Posterior Stroke – What’s all the Fuss? by Dr. Evie Marcolini
CAT scans don’t work for posterior fossa. If you’re thinking posterior stroke, get the MRI.
Vestibular syndrome
– Triggered: positional, motion triggered, resolves in between motion: BPPV, orthostatic hypotension, GI bleed
– Episodic: discrete episode that resolves: panic attack, arrhythmia, TIA
– Acute: onset with some kind of trigger (maybe motion), can get better or worse with movement but does not resolve, symptoms persist: Vestibular neuritis, labyrinthitis, posterior strokeDr. Marcolini led a small group discussion about neurological emergencies and focused on the HINTS exam, giving specific recommendations about appropriate technique.
– 100% sensitive and 96% specific for posterior stroke, better than MRI
– However, only do the exam if the patient has active symptoms. If asymptomatic, don’t do exam!
– This video by Dr. Peter Johns has a great demonstration of the right exam techniques:
We look forward to seeing you this week for ResusX20! Visit ResusX.com for more information and to register!
