aaem resuscitation final · • absence of stemi does not rule out culprit coronary lesion and may...

4/9/2018

1

AAEM 2018Keeping Up With The Literature

Resuscitation

Corey M. Slovis, M.D.Vanderbilt University Medical Center

Metro Nashville Fire DepartmentNashville International Airport

Nashville, TN

VanderbiltEM.com

The Modified Valsalva

PSVT Management

Stable Unstable

Younger Older Conscious Unconscious

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PSVT ManagementStable

Younger• Valsalva

• Carotid massage

• Both Valsalva and Carotid

• Consider ice water

• Adenosine 12 mgs IVP

OlderValsalva

--

--

--

Adenosine 12 mgs IVP

Lancet 2015;386:1747-53

Can lying the patient down and raising their legs 45˚ for 15 seconds immediately post

Valsalva increase its effectiveness?• 428 Patients with PSVT

• Randomized 1:1 for standard vs. modified

• Sitting vs sitting then lie back with legs raised0

5

10

15

20

25

30

35

40

45

50

15%

Valsalva Effectiveness(n=214 each group)

Standard Lie back, Legs up

47%%

Lancet 2015;386:1747-53

p < 0.0001 or = 4.9

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Use new drugs as soon as possible before they develop side effects or

lose efficacy

Am J Emerg Med 2017;35:1662-65

Is the modified Valsalva really as effective as first reported?

• 56 patients, Turkish single center study

• Std Valsalva vs modified Valsalva

• Narrow complex PSVT up to rate of 220

• Lancet study: 47% effectiveness

0

5

10

15

20

25

30

35

40

45

50

10.7%

Standard Valsalva Modified Valsalva

42.9%

%

Am J Emerg Med 2017;35:1662-65

p < 0.007

Modified ValsalvaTake Homes

• Works in almost ½ of patients

• Less need for adenosine

• Efficacy reaffirmed in another study

• This is a practice changing maneuver

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CPRAHA New VT Guidelines

VFibBicarb

Circulation Oct 2017:Online

• 467 pages, 622 references

• ACS generally causes VF or polymorphic VT

• A scar from old MI generally causes monomorphic VT

• If in doubt with wide complex tachycardia: assume it’s VT (class I).


• For hemodynamically stable VT: procainamide is the preferred pharmacologic agent (class IIa). However, cardioversionremains a class I recommendation.

• Unstable ventricular arrhythmias: electricity is undoubtedly first priority. If that fails, amiodarone is the preferred pharmacologic agent (class IIa).


• Consider emergent PCI in all patients after out-of-hospital cardiac arrest, particularly with initial shockable rhythm.

• Absence of STEMI does not rule out culprit coronary lesion and may be seen in 30% of patients.

*Stolen from: Spoon-feed via Journal Feed by Clay Smith

4/9/2018

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Refractory VFib

• Move pads Ant-Lat Ant-Post

• Consider Beta Blockade

• Consider Double Sequential Defibrillation (DSD)

• PCI

• ECMO

Resuscitation 2017;117:97-101

Is double sequential defibrillation (DSD) beneficial in refractory VF/pVT?

• 45 patients treated with DSD

• Retrospective observational study

• London Ambulance Service

• Compared to 175 who got standard defibrillation

• Only patients with ≥ 6 shocks compared

• 3 standard Ant-Lat defibrillations

• Anti-arrhythmic administration

• 3 standard Ant-Post defibrillations

• Double sequential defibrillation

• Done 3 – 4 seconds apart

Double Sequential ProtocolResuscitation 2017;117:97-101

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0

5

10

15

20

25

30

35

40

45

50

55

60

35%38%

Standard vs DSD in VF/pVT

EMS ROSC

56%59%


%

STD STDDSD DSD

6.6% 7%

Discharged

STD DSD

Hosp ROSC

Double Sequential DefibrillationTake Homes

• Not a randomized trial

• Many pts got up to 10 shocks pre DSD

• The role of Double Sequential Defibrillation is not yet clarified and needs a randomized larger trial

Annals Emergency Medicine 2018;71:109-12

Is Dual Sequential Defibrillation (DSD) dangerous to the defibrillators?

• Zoll M and/or Physio-Control LP 15s

• Two DSDs: 1 Zoll & 1 LP @ 560 J synched

• Two DSDs with 2 LPs at combined 720 J

• All 4 DSDs done A-P

• One LP found to become nonfunctional


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“LIFEPAK defibrillators comply with standards which require defibrillators to withstand defibrillation shocks from a second defibrillator connected to a patient. This

testing does not include delivering simultaneous/sequential or overlapping 360 J defibrillation shocks from two

LIFEPAK defibrillators. There are no design and/or safety standards for use of external defibrillators to perform

double sequential defibrillation. We cannot guarantee the reliability of functionality of devices subject to this off-

label use. Product warranty cannot legally cover damage to LIFEPAK defibrillators which occurs as a result of

performing an off-label use”

Dual Sequential DefibrillationTake Homes

• May not be more effective

• May damage defibrillator

• Is a crowd pleaser

Bicarbonate in CPR


How does bicarbonate administration during CPR affect outcome?

• 15,601 OOH cardiac arrests Vancouver

• 5,165 (37%) received IV bicarbonate

• Evaluated survival and good neuro outcome

• Also performed propensity scoring comparisons

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0123456789

1011121314

12.3%

10.8%

Bicarb vs No BicarbUnadjusted, Unmatched


Survival Good Neuro

1.6%

Bicarb No Bicarb Bicarb No Bicarb

%

1.3%

Adjustment via propensity analysis required, as patients getting

bicarbonate usually are in arrest longer with refractory arrests and higher total doses of epinephrine

Bicarbonate in Cardiac ArrestResuscitation 2017;119:63-9

0.0

0.5

1.0

1.5

2.0

2.5

3.0

3.5

4.03.5%

2.8%

Bicarb vs No BicarbPropensity Analysis


Survival Good Neuro

2.2%

Bicarb No Bicarb Bicarb No Bicarb

%

OR=0.64 OR=0.59

1.8%

Bicarbonate in Cardiac ArrestsTake Homes

• Don’t routinely use

• Decreases survival and favorable neuro

• Generates CO2 and is hyperosmolar

• Use for pre-existing acidosis or OD(DKA, sepsis, methanol, EG, TCA)

• Great in Hyperkalemia

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STEMI?

JAMA Int Med 2018;178:133-4

JAMA Int Med 2018;178:133-4

JAMA Int Med 2018;178:133-4

4/9/2018

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but…

STEMI = check K if RF(or really big T waves)

Time = Muscle

HyperK = ECG

ECG Changes Serum Level

Loss of P Wave 6.5 - 7.5

Widened QRS usually > 8

Tall Peaked T 5.5 -6.5

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What are the 5 ECG Changes Seen in Hyperkalemia

• Tall Peaked T-Waves

• Prolonged P-R Interval

• Loss of P Wave

• Widening of QRS

• Sine Wave

Symptomatic Bradycardia5 Rule Outs

• Abnormal VS: Hypoxia, Hypothermia

• Ischemia/Infarction

• Elevated ICP

• Beta Blocker-Calcium Blocker (and other) ODs

• Hyperkalemia

BRASH Syndrome

Bradycardia

Renal Failure

AV Blocker

Shock

Hyperkalemia

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STEMI Evolution

EMS ECG

ED ECG 12 minutes later

• 83 prehospital ECGs with STEMI

• 217 EMS agencies; UPMC Medical Control

•All patients went to cath lab

Prehosp Emerg Care 2014;18:174-179

How often does a prehospital STEMI arrive with a resolved ECG?

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0

10

20

30

40

50

60

70

80

90

100 n = 83 78.3% (65)

STEMI Resolution

Total AMI

ED STEMI

21.6% (18)

ST Resolution


• 1 in 5 prehospital STEMIs have ECG changes

• There was no difference in % occlusion in those

• Patients without STEMI resolution are more


that resolve prior to ED arrival

with and without ST resolution of STEMIECG changes

likely to have multivessel disease

ST segment resolution of a STEMI still

equals a STEMI and mandates rapid

transport to coronary catheterization

ST Segment Resolution = NO STEMI

Prehosp Emerg Care 2018;Jan 16:1-8

Do serial 12 leads during EMS transport add any useful information in diagnosing a STEMI?

• 728 STEMI transports, Quebec EMS

• Used BLS-EMTs transmitting Q 2 minutes

• 24 minute average transport time (15-38)

• “Persistent” STEMI vs “Evolution” vs “Loss”

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0%

1%

2%

3%

4%

5%

6%

7%

8%

9%

10%

Dynamic STEMI ECGs15.7% (114 / 728)

No STEMI STEMI STEMI No STEMI


4.5%

STEMI No (multiple changes)

7.7%8.0%

Results

• 84.3% of STEMIs were persistent

• 15.7% of STEMIs were dynamic

• 8% of STEMIs not evident on first ECG


STEMI Evolution

• 12.3 min was median time from No STEMI

• Females had more dynamic changes then men

• Longer transports = more dynamic changes


Some STEMIs stay persistent

Some STEMIs “come and/or go”


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No STEMI STEMITake Homes

One ECG begets another

STEMI No STEMITake Homes

A STEMI is a STEMI if seen even just once!!

Hypotension: Danger in TBI

Push Dose Pressors

Annal Emerg Med 2017;70:522-30

How deleterious is hypotension in patients with traumatic brain injury (TBI)?

• 7,251 TBI pts ages 10 and older• Statewide EMS database for Arizona• Median age 40 yo; IQR 24-58 yo

• 7.2% (539) of patients had BP < 90 mm Hg• Evaluated time and depth spent hypotensive

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“Dose of Hypotension”

90 – SBP = Depth of Hypotension x Minutes

Hypotension “Dose”

10 minutes at 80 SBP = dose of 10 x 10 = 100

10 minutes at 70 SBP = dose of 10 x 20 = 200

Thus 10 minutes at 70 mm Hg increases mortality 20% over 10 minutes at 80 mm Hg


Each 2 fold increase in hypotension dose, increased mortality by 20%

Depth and Duration of Hypotensionvs Mortality


Hypotension in TBITake Homes

• Dramatically increases mortality

• 20% for each doubling of dose (time x 90-SBP)

• Avoid hypotension, treat hypotension

• Is Sys BP 90, 100, or 120 SBP optimal s/p TBI?

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Depth and Length of Hypotension in TBI are both critical!

Am J Emerg Med 2018;epub ahead of print

Are “neo-sticks” safe and effective in hypotensive ED patients?

• Phenylephrine/neosynephrine-a pure alpha-1 agonist

• 1 cc amp = 10 mg (not 1 mg)

• Used 1000 mcg/10 cc

• Others use 100 mcg “neo sticks”

Primary Diagnosis for Phenylephrine

Phenylephrine-BP Effects in 181 pts

Dose (mcg) MAP HR

< 100 (40 pts) + 4 (1.7-6.2) + 2.2 (-2-6.3)

100 – 199 (83 pts) + 5.6 (2.3-8.8) - 0.2 (-2.6-2.1)

200 – 500 (26 pts) +12 (4.5-20) - 2.4 (-6-1.1)

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Adverse Effects of Phenylephrine

• Rare

• 5 patients: “potentially harmful” VS changes

• 2 bradycardias into 40s

• But were already HR

• 3 hypertensive s/p phenylephrine

• Only 1 proximate to medication admin

Phenylephrine in the EDTake Homes

• A great pressor if used carefully

• 100-200 mcg dose to start

• Be careful if you mix it (1 cc = 10 mg!)

• 1 cc into 10 cc = 1000 mcg (100 mcg/ml)

• We then take 1 cc into 10 cc again

Pediatr Crit Care Med 2018;epub ahead of print

• 24 patients in PICU

• 1.3 mcg/kg average dose

• HR by about 20

• MAP by about 25

• Very potent, significant tachycardia

MUDPILESMUKPILES

VasopressinEuglycemic DKA

4/9/2018

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Elevated Anion Gap(Na+-[Cl- + HCO3

-] 15)

M Methanol

U UremiaD DKA, AKA

P Phenformin/Metaformin, Paracetamol, Propylene Glycol

I INH and Iron

L Lactic AcidosisE Ethylene GlycolS Salicylates, Solvents

K , Starvation KetoacidosisPhenformin/Metaformin

Am J Emerg Med 2018;epub ahead of print

• Metformin increases lactate production

• Glucose metabolism changed to anaerobic

• Can cause a profound lactic acidosis in RF pts

• Reported when Cr > 1.5 mg/dl

• Think of when lactate > 15 and A.G.

Am J Emerg Med 2018;36:341-e5-341.e6

Consider Vasopressin when dealing with refractory lactic acidosis and shock in

metformin patients

SGLT2 InhibitorsSodium Glucose Cotransporter 2 Inhibitors

• The Good- Inhibits proximal tubular reabsorption of glucose- May decrease the rate of diabetic kidney disease

• The Bad- Increases reabsorption of ketones

- Increases glucagon levels

- Thus promoting hepatic ketogenesis

J Clin Endocrinol Metab 2015;100:2849-52

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Euglycemic DKA?

Case Rep Crit Care 2016:ID 1656182 J Diab and Comp 2017;31:611-14

• SGLT-2 may cause Euglycemic DKA

• Glucose values 200-300

• Yet severe acidosis

• May take longer to clear keto acids

• Be wary, use PE, VS & pH, not just glucose

640 reports of DKA with 3 SGLT 2 inhibitors:

Empagliflozin, Dapagliflozin and Canagliflozin

Int J Nephrol Renovasc Dis 2017;10:153-8

ED Fluids

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• Compartment Syndrome after D50%

• 57 yo woman required fasciotomy

• Important facts on D50 provided

• Suggests D10 as an alternative


• D50 osmolarity = 2,525 mOsm

• pH = 3.2 – 6.5

• Hypertonic and acidotic = phlebitis

• D10 = 505 mOsm

D50% vs D10%

Can D10W be substituted for D50W?

• 24 month trial of 871 pts, 100 ml D10W

• Contra Costa EMS and Highland Hospital

• Average initial glucose was 37; repeat 91 mg %

• 23% required a second bolus

• 0.8% (< 1:100) required a third


D10 vs D50

Take Homes

• Both raise glucose effectively

• D50 to 250 in 5 min; D10 to 100 in 10 min

• May need to repeat D10 in 1:4 patients

• D10 may be safer

• No definitive head to head large trial yet

4/9/2018

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• 23% of pts required a 2nd dose (200/871)

• 0.8% of pts required a third dose

• Median glucose change 55 mg% (32-80 IQR)

• No reported adverse effects

N Engl J Med 2018;378:819-28

Is LR or NSS more advantageous in non-criticalED patients admitted to the hospital?

• 13,347 adult ED patients, 1 hospital

• Pragmatic, multiple cross overs• ED pts admitted to non ICU beds

• 1,089 ml LR (Plasma-Lyte) vs 1,071 ml NSS (medians)

• Hospital free days and major adverse kidney events

NSS LR

• Na

• Cl

• OSM

• pH

• Lactate

• K

• Ca

• 155 meq

• 155 meq

• 310

• 5 – 5.5

• ---

• ---

• ---

• 130 meq

• 109 meq

• 273

• 6.5 7.4+

• 28 meq

• 4 meq

• 3 meq

155 meq

5 – 5.5

28 meq

PlasmaLyte / NormosolNa 140 meq/L

Cl 98 meq/L

Osm 294 mOsm

pH 7.4

Acetate 27 meq/L

Gluconate 23 meq/L

K 5 meq/L

Mg 3 meq/L

4/9/2018

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Major Adverse Kidney Events

• Death

• New Renal Replacement Therapy

• Final serum Cr > 200% baseline

0

5

10

15

20

25

30

Hospital Free DaysMajor Kidney Events

N Engl J Med 2018;378:819-28

Hosp Free Day Major Kidney Event

25d

5.6%

P=0.01

25d

4.7%

Getting a median of about 1100 cc of NSS(mean 1600 cc) results in a significant

increase of renal dysfunction at 30 days when saline is used vs a balanced

electrolyte solution of LR or Plasma-Lyte

N Engl J Med 2018;378:829-39

Is LR or NSS more advantageous in ED patients admitted to the ICU?

• 15,802 adult pts from 1 hospital• Pragmatic, multiple cross overs• ED pts who were then ICU admitted

• 1,000 ml LR/Plasma-Lyte vs 1,020 ml NSS (median)

• Compared mortality, new RRT, persistent Cr 2 x

4/9/2018

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N Engl J Med 2018;378:829-39

N Engl J Med 2018;378:829-39

0%

2%

4%

6%

8%

10%

12%

14%

16%

18% 15.4%

Major Adverse Kidney Events

NSS

N Engl J Med 2018;378:829-39

14.3%

LR

P=0.04

0%

1%

2%

3%

4%

5%

6%

7%

8%

9%

10%

11%

12%

Hu

nd

red

s

11.1%

10.3%

Death, Renal Replacement Therapy and Cr 2 x

Mortality

2.9% 2.5%

N Engl J Med 2018;378:829-39

NSS NSSLR LR

6.6%6.4%

Cr

NSS LR

RRT

p < 0.6

p < 0.08

p < 0.06

4/9/2018

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Balanced Crystalloids vs NSSTake Homes

• Same cost, same color, same manufacturers

• NSS is hyperchloremic and acidotic

• LR (or Plasma-Lyte) appears safer in 29,000 pts

• I see no benefit to routine NSS

Love it s/p vomiting with dehydration

TXA

Tranexamic AcidTXA

• An anti-fibrinolytic

• Blocks fibrin clot dissolution

• TXA binds to plasminogen

• Blocks plasminogen – fibrin interaction

• FDA approved in 1989 for hemophilia

TXADecreasing Blood Loss

• Tooth extractions in hemophilia

• Refractory nose bleeds

• Decrease surgical blood loss (orthopedics: spine and hip; ob/gyn: hysterectomy)

• During cardiopulmonary bypass

• Post major trauma?

4/9/2018

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Plasminogen Plasmin Fibrin

Clot Dissolution

Fibrin Split Products

TPA

TXA

HyperfibrinolysisAcute Coagulopathy of Trauma

• Seen in 25 - 40% of severe trauma patients

• Hypoperfusion

• Acidosis

• Hypothermia

• Activation of protein C fibrinolysisLY30 > 3%

Hyperfibrinolysis (HF) in patients with severe trauma = 70-100% mortality

LY30 > 3%

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Lancet 2017;389:2105-16

Does TXA decrease mortality in post-partum hemorrhage?

• 20,021 women, TXA vs placebo• Randomized, double blind controlled• 193 hospitals, 21 countries• Also looked at hysterectomy incidence• 1 gram IV over 10 minutes• 2nd gram for continued bleed and/or restart

Death from bleeding was significantly reduced by TXA,

especially in those who received it within 3 hours

(1.2% vs 1.7%; p=0.008; RR 31%)

Lancet 2017;389:2105-16

Results

• No effect on hysterectomy incidence

• No decrease from 42 day all cause mortality

• No increase in PE, DVT, or AMI

• TXA significantly need for laparotomy(0.8% vs 1.3% p=0.002; RR 36%)

Lancet 2017;389:2105-16

Does time to treatment affect the efficacy and/or safety of TXA?

• 40,138 pts from 2 trials

• 1 trauma study: CRASH-2 20,127 pts

• 1 OB post-partum trial: WOMAN 20,011 pts

• No other large trial results available

• Stratified pts by age, systolic BP and time to TXA

Lancet 2018;391:125-32

4/9/2018

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Benefits of TXA decrease by 10% for every 15 minute delay in TXA

administration

No benefits are seen after 3 hours

Lancet 2018;391:125-32

Lancet 2018;391:125-32

Reduction in Effectiveness of TXA with Increased Treatment Delay

TXA Use and Time DelaysTake Homes

• If you are going to use TXA, sooner is better

• Prehospital > ED > OR

• The efficacy of TXA in a US level 1 trauma system is not yet proven nor widespread

What about TXA in a Level 1 Trauma Centerand evaluating based on

level of fibrinolysis?

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J Surg Res 2017;220:438-43

• 232 consecutive pts, Denver Health, 43 MTP

• Compared 3 fibrinolytic states

• Shutdown vs Physiologic vs Systemic fibrinolysis

• Compared each group of fibrinolysis types

• Analysis done with matching for injury severity

J Surg Res 2017;220:438-43

TXA Effect on Mortality

TXA Use and MortalityInjury Severity Adjusted

• Physiologic Fibrinolysis (LY30: 0.9%-2.9%)Significant increase in mortality (p=0.018)

• Hyperfibrinolysis (LY30: > 2.9%)Increased mortality (p-ns; 0.116)

• Fibrinolysis Shutdown (LY30 < 0.9%)No affect on mortality (p=0.5971)

J Surg Res 2017;220:438-43

TXA Use in Level 1 Trauma CenterDenver Take Homes

“There was no clear benefit in this study”

“TXA remains a significant predictor of mortality for patients with physiologic

fibrinolysis”

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“The role of TXA in mature trauma systems remains unclear and

emerging data supports it may have adverse effects”

J Surg Res 2017;220:438-43

“The role of TXA in mature trauma systems remains unclear and

emerging data supports it may have adverse effects?

TXA 2018 in Level 1 Urban TraumaMy Take Home

Stroke Therapy 2018

• 206 pts with deficit mismatch to infarct• Internal carotid or first MCA segment• Known well 6-24 hrs ago

• No infarct > 1/3 of MCA territory• Used Stryker Trevo device

New Engl J Med 2018;378:11-21

Can thrombectomy after 6 hrs, from hr 6-24, improve outcome? The DAWN Trial

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All patients had more ischemic tissue than already infarcted areas

New Engl J Med 2018;378:708-18

0%

10%

20%

30%

40%

50%

60% 49%

Functional Independence at 90 DaysModified Rankin 0, 1, 2

Thrombectomy

New Engl J Med 2018;378:11-21

13%

No Thrombectomy

P > 0.001

New Engl J Med 2018;378:11-21

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• No in serious adverse effect

• Almost ½ less neurologic deterioration

• Approximately ½ were wake up strokes

New Engl J Med 2018;378:11-21

For every 2.8 pts who underwent thrombectomy, 1 additional pt had functional independence

• 182 pts randomized from 38 US hospitals• 92 pts endovascular therapy vs standard care• Internal carotid or proximal MCA pts only

• Ischemic tissue > infarct by factor 1.8

New Engl J Med 2018;378:708-18

Does thrombectomy 6-16 hrs post stroke improve outcome if ischemic tissue still

present without infarct?The DEFUSE 3 Trial

0%

10%

20%

30%

40%

50%

17%

Rankin 0-2Thrombectomy 6-16 Hours

Usual Care

New Engl J Med 2018;378:708-18

45%

Thrombectomy

P < 0.001OR = 2.77Absolute = 28%

New Engl J Med 2018;378:708-1

4/9/2018

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Thrombectomy After 6 HoursTake Homes

• The window is staying open longer

• Major strokes (LVOs) need a comprehensive stroke center

• CT perfusion is an essential test in stroke

Mechanical TherapyTake Homes

Mechanical Therapy in those patients who have significant not yet infarcted brain equal to almost 2 x the infarct size have a dramatic increase in return to normal-near normal function

All large vessel strokes (LVOs) in either MCA-like distributions or posterior circulation should undergo perfusion studies, even if outside the lytic window of 4.5 hours

We can now aggressively treat wake up strokes

PE

• 560 pts, mean age 76

• 11 Italian hospitals

• Admitted patients only

• All had Wells criteria PE work-ups

• D-dimer performed if not low risk

NEJM 2016;375:1524-31

How common is PE in patients in the ED admitted for syncope?

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PE – Syncope Findings

• 1 in 6 (17.3%) of syncope pts had a PE

• 25% of syncope of unknown origin had PE

• PE in 13% of syncope pts with alternative Dx

• Note: only hospitalized pts

• Most had underlying illness or trauma

NEJM 2016;375:1524-31

A PE workup (D-dimer or CTA) needs to be performed in any patient with

unexplained syncope and all syncope patients who are being admitted

PE and SyncopeInitial Take Homes

So should you really do a pulmonary CTA on all of your PE patients being admitted?

• Meta-analysis of 12 additional studies

• Compared NEJM to 9 ED and 3 IP studies

• 6,608 ED pts with PE and 975 IP pts

Am J Emerg Med 2017;epub September

How common is PE in syncope patients seen in ED and in those requiring admission?

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Problems with NEJM

• NEJM high PE incidence is an outlier

• Many criticize study due to selection bias(Many CA pts. High number of insignificant sub segmental PEs, V/Q scanning in 25% of “PE” pts and used wrong n)

• No pts had RV strain on ECG, yet had syncope?

Incidence of PE in Syncope Pts

• NEJM PE prevalence in ED pts: 3.8%

• Pooled prevalence in meta-analysis: 0.8%

Am J Emerg Med 2017;epub September

• NEJM PE prevalence of PE in Admitted pts: 17.3%

• Pooled prevalence in meta-analysis: 1.0%

JAMA Intern Med 2018;epub ahead of print

• 1,671,944 adult ED syncope pts

• 5 data-sets, 4 different countries

• Canada, Denmark, Italy, USA

• Found PE rate of only 0.06%-0.55%

• 0.15-2.10% in admitted syncope pts

Am J Emerg Med 2018;36:253-6

• 348 syncope pts over 5.5 years

• 1.4% had a PE

• All PEs were PERC+ and had SOB

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Am J Emerg Med 2018;36:297-300

• Hypotension (SBP < 90 mm Hg)

• Hypoxia (O2 sat < 88 on RA)

• RV dysfunction

• Need for intubation

• Need for thrombolysis

Syncope and PE

PE in SyncopeTake Homes

• Rare 0.15-2%

• BP, HR, O2 sat, ECG and history to decide workup

• Use clinical judgement and not NEJM

Do modified Valsalva

Summary

Double sequential…not sure

NO Bicarb in most arrests

Bradycardia…R/O HyperK

STEMI…R/O HyperK

STEMIs can disappear or appear

Summary

Beware Hypotension in TBI

TXA’s role stays unclear

LR – yes NSS – no

Stroke window much wider

4/9/2018

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VanderbiltEM.com

aaem resuscitation final · • absence of stemi does not rule out culprit coronary lesion and may...

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