Narcan 1hr rule
-Safe to discharge patient 1hr after Narcan administration if provider feels comfortable and if has not needed further Narcan in the department and meets 6 criteria:
1. Able to walk
2. Temp >36C and <38C
3. RR 10-20
4. Sats 95%
5. HR 60-100
6. GCS 15

Fluid Comparison
-Across multiple studies Balanced Fluids (example LR) is non-inferior to NS and Odds Ratio would suggest possible superiority in terms of decreasing rate of AKI and reducing mortality.
-NS also associated with hyperchloremic metabolic acidosis, with balanced fluids leading to higher pH, lower chloride, and higher bicarb levels
-Balanced fluids more costly than NS (LR ~25% more expensive than NS)

NightShift Pro-Tips
-Phase delay scheduling is better than Phase advance (better to go morning shift then evening shift then night shift then morning shift, etc)
-Nap prior to shift, and nap on shift if possible (short 20min nap is best)
-Use Bright Lights (prior to 4am) to help keep you awake
-Caffeine early in shift and avoid big meals. Aim for snacks high in protein and fat and low in carbs (avoid big sugar swings)
-Minimize bright lights after shift and on drive home (sunglasses can help)
-Consider Melatonin 30min prior to sleep (shown to help fall asleep faster and stay asleep longer)
-Sleep in dark, cool room (blackout curtains and/or facemasks can help, and body needs cool temps to aid in sleep
-Try to avoid >3 night shifts in a row, but avoid 1 solo night shift (messes up your rhythm)

Neurogenic shock v spinal shock/stun

Spinal stun/shock: After spinal cord injury can have transient loss of function below the injury (loss of continence, anesthesia, paralysis). Can last hours to weeks.
-Can see priapism in males. (especially C-spine injury)
-Thought to be due to loss of K and thus reduced axonal transmission, with return of some if not all movement once K re-equilibrates
-Do Bulbocarvenosus Reflex checks to determine when distal spinal function has returned and gives idea of prognosis

Neurogenic shock: true shock from TBI/spinal cord injury. Interruption of autonomic pathways –> decreased SVR and alters vagal tone.            
-MAP goal 85, need to resuscitate with fluids in case there’s hypovolemic/hemorrhagic component to the trauma, otherwise need pressors (NE first line)

Lyme Disease Review

Lyme rarely transmitted in first 48hrs, ~25% chance in first 72hrs
Prophylactic ABx only if they meet all criteria:
-36hrs or more with tick attached, PPx started within 72hrs of removal, no contraindication to doxy (<8yrs old, pregnant, lactating), only if ixodes, inf disease society of America doesn’t recommend PPx unless in state with >20% lyme rate in ticks (which doesn’t count Kentucky, TN, IN, IL. Only surrounding state is WV)

-After removal (tweezers/foreceps, don’t crush or twist, just steady straight pull), clean and then have patient observe x30days for EM
-Observing for EM better plan of action than PPX ABx, serologic testing not recommended (don’t develop markers early in course)

If you believe they have early stage 1 lyme then doxy 100mg BID x10-14days
Stage 2/early disseminated (carditis/meningitis/bells): Doxy 100mg x14-28 days (14 days appropriate, will need ID f/u anyway) (Ceftriaxone if need IV)
Stage 3: severe arthritis 14-28days of doxy 100mg BID PO (again 14days shown to be appropriate, will need ID f/u), encephalitis x14-28days of ceftriaxone IV initially and Doxy PO when able
If contraindication to doxy then amox is second line

Serotonin Syndrome
autonomic hyperactivity, mental status changes, neuromuscular abnormalities

Mental status change (anxiety/restless/agitated delirium), autonomic (tachy, hyperthermic, diaphoretic, htn, vom, diarrhea), NM (clonus, rigidity, hyper-reflexive, tremor)
Fentanyl can cause serotonin release because 5-HT1A receptor agonist
Tx: stop offending agent, support, sedate with benzos PRN, cyproheptidine (12mg initial dose)

SCAPE

Increased afterload –> to pulm edema –> stress response with epi/NE/etc –> vasoconstriction –> afterload increase and the cycle continues

Workup: basic labs (including BNP), ekg, cxr, can do US/echo (can be normal or reduced EF)
-Concern if BNP >500
Treatment: BIPAP/CPAP for PPV, nitro drip (start at 100mcg/min and titrate from there, can give sublingual in the meantime while setting up drip)
-most are fluid down so don’t diurese (i.e. no Lasix right away, confirm fluid status first)
-Can wean BIPAP/CPAP once pt’s BP is at their normal and nitro <50mcg/min. Wean PEEP by 2 q10min, if patient doesn’t tolerate then turn back up. Once below PEEP 5 then can attempt switch to NC
-Can start ACE-I (enalapril/captopril) as patient improves
-Morphine can make some more comfortable but poor support for it overall

WPW and SVT

SVT: AVNRT and AVRT
AVNRT: abnormal circuit going round and round in the AV node, goes down septum so narrow
AVRT: doesn’t use AV node but rather accessory pathway (WPW), so often wide

WPW: 2 conduction pathways (AV node and accessory pathway), accessory pathway doesn’t have the pause that AV node provides thus PR is shortened and QRS broadens (can be wide, usuall 110s) and sloping upstroke (delta wave).
-Orthodromic and Antidromic
-Orthodromic has the impulse come back up the accessory pathway and going back into AV node. Antidromic is the opposite.
-Orthodromic is narrow because conducting through the AV node and bundle of His (looks like normal AVNRT)
-Antidromic is wide because it conducts through the ventricle, looks like VTach
-WPW+AFib: accessory pathway allows a lot of the atrial impulses to go down that are normally blocked by AV node. Looks like AFib with aberrancy but rate between some beats can be up to 300bpm. Also get some variation beat to beat in QRS structure, some will be narrow and some will be wide, overall different QRS morphologies of the different beats.

Adenosine blocks AV node, CCB and amiodarone slow AV node conduction. So Adenosine will return orthodromic WPW tachycardia to normal WPW ekg/rhythm. If antidromic then shock if unstable or procainamide because procainamide blocks the accessory pathway. Also, use procainamide or shock if WPW and AFib.

Pharmacy Pressor Lecture (A=alpha, B=Beta, doses in mcg/kg/min unless specified)

Vasopressors: vasopressin and phenylephrine (increase SVR)
Ionotropines: dobutamin, milrinone, isoproterenol (increase CO)
Inopressors: NE, epi, dopa (SVR and CO increase)
Beta-1 increases myocardial contractility and chronicity
Alpha-1 is arterial smooth muscle contracture

Vasopressin acts on V1 (vasoconstrict) and V2 (fluid resorption in kidney, slower) receptors
Dose is 0.3U/min, no more, no less. NE sparing effect. Can cause tissue ischemia and other ischemia at higher doses.

Dopamine: 0.5-5mcg/kg/min primarily hits dopamine receptors, but as you increase it hits B-1 (5-10mcg), and at 10-20 you hit A receptors. More arrhythmia than NE. Usually start around 5mcg/kg/min, max 20mcg/kg/min.

NE: strong A with some B. Start at 0.02mcg/kg/min (can start 0.1 or 0.2 if really needing it) and max 0.8mcg/kg/min. Too high can cause peripheral and GI ischemia.
-Safe to give up to 24hrs peripherally

Epi: mainly B activity below 0.05, then above you get more A activity. Starting dose 0.02, max 0.8

Phenylephrine: strong A only, start 0.5mcg/kg/min, max at 3. Reflex bradycardia and tachyphlaxis are possible adverse reaction.

Dobutamine (Do-beta-mine): Almost all Beta (1>2), start 2.5, max 20, used for HF and symptomatic brady, does increase myocardial demand

Milrinone: PDE-3 inhibitor, Start 0.125, max 0.75. Increases contractility and improves relaxation. Vasodilation leading to hypotension is adverse effect

Weight-based dosing: ideal BW for the morbid obesity. Can always titrate.
If extravasation: Stop infusion, aspirate as much fluid as possible, warm compresses for 30mn q4hrs for 24hrs, give phentolamin (5-10mg diluated in 10ml NS) injected in affected site

Cardiogenic shock: first line is NE, if low output can consider adding Epi
Hypovolemic shock: Stop the bleed and replace volume, pressors not recommended, adequately resuscitate before any pressor
Neurogenic shock: MAP goal >85, NE phenylephrine or dopa (>10mcg) but NE #1
Septic shock: NE then add vaso if needed. If refractory to pressors -> hydrocortisone 50 q6hrs

Push-dose pressors: Phenylephrine and epi
-Phenylephrine: concentration 100mcg/ml, giving 0.5-2ml q2-5min, onset 1min, lasts 10-20min. Good for patients who are hypotensive and tachy
Our code phenylephrine sticks are 1mg/10ml which are the correct concentration
-Epi: 10mcg/ml, dose 0.5-2ml every 2-5min.
Our code epi sticks are 1mg/ml, to make the push dose concentration mix 1ml from code epi into 9ml of NS and you get appropriate concentration.

Arrhythmias:
Think IV, O2, monitor, then look at rhythm strip: fast or slow, narrow or wide, regular or irregular, P waves present? Is patient stable?
Fast and unstable gets shocked, Slow and unstable gets paced

Bradycardia: wide is less responsive to meds and block is below AV node, narrow is normally faster and more responsive to Atropine

Sinus(narrow) Brady DDx think “DIE”
Drugs: BB/CCB OD, med SE
Ischemia: RCA supplies SA node, sick sinus syndrome
Electrolyte abnormality: Hyperkalemia causes no response to pacer or meds due to inability to repolarize

Wide, Fast, Regular: VTach, WPW antidromic, SVT with aberrancy
Tx: Amio, Procainamide, synchronized cardioversion

Wide, Fast, Irregular: AFib w/BBB, polymorphic VTach, AFib with WPW, Torsades
Tx: Cardioversion or Block AV node depending on stability, (Torsades gets Magnesium)

Fast, Narrow, Regular: SVT, orthodromic WPW, AFlutter, Narrow complex VTach
Tx: unstable gets cardioverted, stable gets adenosine, dilt, verapamil, or metoprolol depending on rhythm

Nursing Update:
-Broselow tape in the top drawer of the Peds code carts
-2+ SIRS with suspected infection -> within 3hrs needs lactate, blood culuture, broad spectrum ABx, 30cc/kg if lactate >4.
-Monotherapy ABx in sepsis that meet bundle criteria: Ceftriaxone for PNA or urinary (Cefepime if pseudomonas concern), Zosyn, Unasyn. (Just Vanc doesn’t cut it)

(Pediatric emergency medicine playbook is good podcast for Peds EM education)
Peds congenital heart disease (CHD):
Normal baby caloric intake is 100kcal/kg/day, CHD babies can need closer to 150
QTc cutoff in peds 460
Most common CHD in bicuspid aortic valve, most common cyanotic lesion is Tetrology.
CHD is leading cause of death in babies
Risk Factors: prematurity, 1st degree relative with CHD, genetic syndrome, maternal DM, HTN, obesity, thyroid d/o, epilepsy, in-utero infection (TORCH)

Ductal Dependent Lesions:
-Ductus Arteriosus closes around 42wks gestation (~2wks old)
-Left->Right shunting seen around 6-8weeks with sweating with feeds, tachypnea/cardia, FTT
-If reliant on duct for pulmonary flow: severe cyanosis and shock when it closes (critical pulm stenosis or pulm atresia, tetralogy)
-If reliant on duct for systemic flow: tachypnea, cardiogenic shock, lactic acidosis (hypoplastic L heart, critical aortic stenosis)

CHD signs and symptoms: HR >160, ASD causes fixed S2 splitting, extra heart sounds, pathologic murmur, decreased pulses, cyanosis/pallor, sweating with feeds, tachypnic, decreased activity, increased irritability, weight loss/FTT, hepatomegaly

Workup: PE (want BP and pulse ox in all 4 extrem), CXR, EKG, CBC, CMP, iCal, Mg, vbg, consider hyperoxia test to r/o pulm cause (100%, PaO2 should be >150 if pulm path), Echo stat
Tx: Control airway PRN (likely needed), Cyanotic 75-85% is okay (over oxygenating causes vasodilation and that can cause issues and more R-side shunting) (goal is 85% if you don’t know what’s going on), ABx for r/o sepsis, PGE-1 0.05-0.1mcg/kg/min (start high and wean down, titrate to palpable femoral pulses and SpO2 improves. This can cause apnea so make sure to be ready for airway)

CXR findings: Boot-shaped heart in tetrology, Eggs on a string in Transposition (see below)

Tet Spell: AMS, LOC, and death from cyanosis
Tx: knees to chest (increase SVR to push blood to R-side of heart), 100% O2 (vasodilate pulm to push blood to R-side), Morphine .1mg/kg IM or IV (helps relax the kid), 5-10cc/kg NS bolus, phenylephrine.5-5mcg/kg/min (same effect as knees to chest), propranolol (if needed, decrease HR and increase ventricle filling), RSI with ketamine 1-2mg/kg (if needed)

Hypoplastic L Heart Emergency: Needs fluids (clot if dehydrated), heparin (break up and prevent clotting), consider pressors, Call CV-surg ASAP, ECMO

Infective Endocarditis:
Dx with Duke Criteria: diagnostic if 2 major, 1 major and 3 minor, or all 5 minor
-Major criteria: Both BCx’s positive, Endocardial involvement (vegetation, abscess, prosthetic valve dehiscence, new valve regurg)
-Minor criteria: Fever, predisposing heart condition or IVDU, Vascular Phenomena (Major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, and Janeway’s lesions), Immunologic Phenomena (Glomerulonephritis, Osler’s nodes, Roth’s spots, and rheumatoid factor), Blood culture + but not meeting major criteria

Growing more common in elderly with increase in valves and stents (higher risk of subacute). L-sided more common since mitral and aortic valve issues more common in older individuals.

Acute decompensated Heart failure is #1 COD (think valve rupture, need CV surg ASAP, can consider nitroprusside or dobutamine in the interim)

Valve Ring Abscess: needs CV surg repair or will recur and destroy heart. Also surgery for recurrent septic emboli or metastatic infection.

Increased risk in first 3months post-surgery because that’s how long endothelialization takes

STEMI Mimics:
Read “Dr Smith’s ECG blog”!!!!!! and OMI manifesto
STEMI mimics: hyperacute T waves, posterior MI, LCMA occlusion, DeWinters, wellens, sgarbossa and smith
Hyperacute T waves: occur early in MI
Posterior MI: look for ST depression in V1-V4
LMCA occlusion: aVR ST elevation predicts left main involvements
DeWinter: hyperacute T wave with broad base and low J-point/ST depression
Sgarbossa: use with BBB or paced rhythm or PVCs
Wellens: biphasic T wave (up and then down), not stemi equivalent, it represents reperfusion T waves, can be spontaneous or after cath. Has poor R wave progression