ACEP 2018 Cardiology v31prd-medweb-cdn.s3.amazonaws.com/documents/emprodev/files/ACEP 2018... ·...

9/28/2018

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ACEP 2018

Cruising the LiteratureCardiology 2018Corey M. Slovis, M.D.

Vanderbilt University Medical CenterMetro Nashville Fire DepartmentNashville International Airport

Nashville, TN

CPREpinephrine

Heads Up CPRPCI S/P Arrest

TORArrest S/P Sex

EpinephrineNew Engl J Med 2018;379:711-21

• Large double blind placebo controlled trial

• 8,014 pts, UK EMS, adults ≥ 16 yo

• 4,015 pts, 1 mg epi Q 3-5 min

• 3,999 placebo receiving patients

What is the role of epinephrine in cardiac arrest?

The study evaluated 30 day outcomes and functional neurologic outcomes at

discharge and at 3 months

New Engl J Med 2018;379:711-21

Times and Dose

6.6 min Call to EMS arrival (median)

21.4 min Call to epinephrine or placebo

4.9 ± 2.5 mg Epinephrine dose (mean)

New Engl J Med 2018;379:711-21

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0%

10%

20%

30%

40%

50%

60%

Hu

nd

red

s

30.7

ROSC and EMS Transport

ROSC EMS Transport

11.7

Placebo Epi Placebo Epi

New Engl J Med 2018;379:711-21

36.3

50.8

0%

1%

2%

3%

4%

5%

2.4%

30 Day Survival

Placebo

3.2%

Epinephrine

New Engl J Med 2018;379:711-21

OR = 1.39p = 0.02

NNT = 112

New Engl J Med 2018;379:711-21

30 Day Neurologic Outcomes

0.0

0.5

1.0

1.5

2.0

2.51.9%

Rankin 0 - 3

Placebo

2.2%

Epinephrine

New Engl J Med 2018;379:711-21

OR = 1.18CI = 0.86-1.61

0.00.10.20.30.40.50.60.70.80.91.01.11.21.31.41.51.6

1.35%

Favorable Neurologic OutcomeRankin 0 - 2

Placebo

1.29%

Epinephrine

New Engl J Med 2018;379:711-21

0%

10%

20%

30%

40%

50%

60%

17.8%

Severe Neurologic Disability (30 d)Rankin 4, 5

Placebo

31.0%

Epinephrine

New Engl J Med 2018;379:711-21

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Adjusted AnalysisParamedic Witnessed

Favors Placebo Favors Epinephrine

New Engl J Med 2018;379:711-21

Adjusted AnalysisVF/pVT vs Non Shockable

Favors Placebo Favors Epinephrine

New Engl J Med 2018;379:711-21

Adjusted AnalysisMedical vs Traumatic

Favors EpinephrineFavors Placebo

New Engl J Med 2018;379:711-21

Epinephrine in Cardiac ArrestTake Homes

The role of epinephrine in cardiac arrestwill continue to be debated

Epinephrine increases survival butdoes not increase the rate of

neurologically intact survival

Epinephrine increases the number of neurologically devastated survivors

Positive Result Conclusion

Epinephrine in OOHCA arrest improves ROSC and likelihood

for hospital discharge

Neutral Result Conclusion

Epinephrine does not improve neurologically intact survival

in OOHCA

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Negative Result Conclusion

Epinephrine in OOHCA just increases the likelihood of being neurologically

devastated without significantly increasing the number of neurologically

intact survivors

Heads Up CPR

Resuscitation 2018;128:51-5

• Heads up CPR ICP and CPP

• Porcine study of 20 pigs

• Confirms ICP and CPP

• However no improvement in cerebral oxygenation and/or metabolism

• Heads-up CPR is not yet of proven benefit in pigs or humans

PCI S/P Cardiac Arrest

JACC 2018;72:471-2

• 110,636 Medicare database AF pts

• 9,147 developed new AF in ED

• 25% new AFib diagnosed in ED

• Average age 77, 63% female

How often do ED physicians prescribe anticoagulants for stroke prophylaxis in newly

diagnosed Atrial Fibrillation?

Results

• High stroke risk and low/int bleed risk not correlation with increase likelihood of Rx

• Almost 2/3 of Rxs: Warfarin

JACC 2018;72:471-2

Less than 1 in 5 prescribed anticoagulation

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• 599 OHCA registry pts

• UPMC and Mercy Hospitals

• Early vs Later vs no Cath/PCI

• STEMI and no AMI pts

How valuable is PCI s/p cardiac arrest?

0%

10%

20%

30%

40%

50%

60%

70%56.2%

Survival to Discharge

Early Cath Lab47.2%

31%

CCU Only52.8%

p = 0.0001


0%

10%

20%

30%

40%

50%

60%

70%

65.6%

Survival to DischargeEarly PCI vs CCU

Early Cath Lab

31%

CCU Only

p = 0.0001


Am Heart J 2018;202:144-7

• Witnessed EMS arrests or within 3 min of EMS

• Pathway activated immediately

• 86 pts EMS screened 38 accepted

• Arrest until PCI start: 63 min

• No survivors among 17 non-VF pts

How valuable is immediate PCI during cardiac arrest?

PCI and Survival

• 70% of VF pts had a culprit lesion

• 92% of survivors had VF

• 1/3 of non STEMI VF arrests had acute lesion

• Mechanical CPR but no ECMO = 0% survival

• Low 30% 30 d survival (3 x of Sweden)

Am Heart J 2018;202:144-7

Early Coronary AngiographyTake Homes

• Early CCL essential to find intervenable lesions

• If PCI indicated: survival doubles with good neuro

• Non ST elevation AMI: intervenable lesions about 30% of time

• They, too, greatly benefit

• Be aggressive for high ROI

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TOR

EMS requests termination of CPR in progress for a 47 yo man found down.

You are NOT the EMS Medical Director. They have given 2 doses of epinephrine, ventilated the patient and performed high

quality CPR. They are enroute to you. The rhythm is slow PEA.

Should you stop CPR on arrival?

What are the TOR criteria?


• 227 CPR patients, 39.2% TOR +

• Excludes pregnancy, suspected drug OD

• Overall 8% TOR/non-TOR pts admitted

• Overall survivor to discharge: 1.3%

• All with good neuro outcomes

Do the TOR criteria apply to patients transported to the ED?

TOR Criteria and Survival

• Non shockable rhythms

• Arrest not-witnessed by EMS

• NO ROSC prior to transporting


0.0% survival in TOR + patients


TOR TOR and ED PhysiciansTake Homes

• No response to epi in an unwitnessed non VF/VT arrest portends non survival

• Stop sooner, not later

• Use low ETCO2 (< 10 mm Hg)

• And no US viewed wall motion

• Terminate more before EMS transport

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Circulation 2018;137:1638-40

Only 47% received CPR in these witnessed arrests

Maybe put on defib pads and hook up AED during the warm up

STEMI?

ECG STEMI Changes

JAMA Int Med 2018;178:133-4

JAMA Int Med 2018;178:133-4

JAMA Int Med 2018;178:133-4

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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

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

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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

West J Emerg Med 2017;18:963-71

What ECG changes predict patient decompensation in HyperKalemia?

• 188 patients serum K ≥ 6.5 meq/L ( x = 7.1)

• Observational study, Brown University

• ECGs within 60 min of serum (mean = 18 min)

• Hemolyzed samples excluded

• Peaked Ts, P-R , QRS , Bradycardia, Junctional

Adverse Events

• 28 pts, average K = 7.5 meq/L

• Symptomatic Bradycardia in 22 pts

• VT: 2 pts

• Cardiac Arrest: 2 pts

• Death: 4 ptsall prior to calcium administration


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ECG Abnormalities and Adverse Events


ECG Predictors of Adverse Events

• QRS prolongation most common predictor- Seen in 79% of pts with adverse events- Average QRS 152 msec

• Bradycardia second most common predictor- Seen in 60% of pts with adverse event

• 86% of patients had > 1 ECG abnormality


No patient with only peaked Ts or prolonged P-R duration had an

adverse event


ECG Changes and HyperKalemiaTake Homes

• Widened QRS and Bradycardia in Hyperkalemia portends disaster

• Tall peaked T waves do NOT

• Do not use calcium for those patients who merely have peaked T waves and/or a prolongation of the P-R interval

Chest Pain andScoring Systems

JACC 2018;71:606-16

How does HEART, EDACS, simplified EDACS compare in predicting 60 day MACE

• 118,822 pts, Kaiser Group, retrospective study

• Electronic keyword text string search

• All patients chart evaluated using all 3 scores

• Used a Troponin I level < detectable

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JACC 2018;71:606-16JACC 2018;71:606-16

60 Day MACE Plus RevascTrop I < 0.02

JACC 2018;71:606-16

NPV % of R/O Pts

HEART 99.08 51.8%

EDACS 98.88 60.6%

Simplified 98.88 48.1%EDACS

60 day MACE for an undetectable troponin I (< 0.002) and a low risk

score is 99.5% for all 3 tests

JACC 2018;71:606-16

JACC 2018;71:606-16

Take Homes

• Undetectable troponin x 2 plus a low risk HEART or EDACS provides more than a 99% negative predictive value for a major adverse event

• These patients may not really benefit for subsequent stress testing

• Beware positive troponins, even just barely detectable ones

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Acad Emerg Med 2018;epub June

How does the HEART pathway perform in a randomized trial-over a 1 year study?

• 282 patients, single center trial

• ACC/AHA std care vs HEART pathway

• 1 year MACE and downstream testing

• Used 0 and 3 hour troponins

• HEART 0-3 pts: DC’d, follow up with PCP

HEAR Performance1 Year Results

• 66/141 patients had negative 0-3 hour troponin and a HEAR score of 0-3

• None of these discharged patients had a major adverse cardiac event (MACE) by 1 year

• NPV % 100%; Sensitivity for MACE: 100%

• But only 8% reduction in 1 year for cardiac testing


0%

10%

20%

30%

40%

50%

60%

70%

80%63.1%

Objective Testing at 1 Year

Heart Pathway

71.6%

Usual Care

p = ns


HEART Score and PathwayTake Homes

• First 1 year study of HEAR

• No longer HEART

• A subjective “objective” test

• Beware positive Trop

Am J Emerg Med 2017;35:704-9

Is “Low Risk” by HEART and other scoring systems really low risk?

• 434 pts from 7 EDs

• Average age 57 (49-64)

• Used HEART, TIMI, GRACE, EDACS

• Compared HEART ≤ 3 vs ≤ 2

HEART ≤ 3 has a miss rate of 3.6%

HEART ≤ 2 had a miss rate of 0

Am J Emerg Med 2017;35:704-9

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Acad Emerg Med 2018;25:434-43

Can a single initial high sensitivity Troponin allow early ED discharge when combined with a risk score?

• 2,258 low risk CP patients

• Pooled data from 4 Australian/NZ studies

• Used hs Troponin T and hs Troponin I

• EDACS: ED Assessment of Chest Pain Score

• 30 day MACE results

Results

• Evaluated ranges of Troponins + EDACS

• Boot strapping to find ≥ 98.5% sensitivity

• Threshold Trop I ≤ 7 ng/L; Trop T ≤ 8 ng/L

• EDACS Threshold score ≤ 15

• Allowed 30% of patients to be D/C’d


Study found low levels of detectable hs Troponin plus low EDACS score almost as good as detecting no hs Troponin at all

(below level of detection)


Detectable Troponin – implicit risk – be careful

This study says you will miss 1.5% of ACS – it’s the same as most studies before high sensitivity

Troponin were available


JAMA 2017;318:1913-24

• Meta-analysis of 22,457 pts, 19 studies

• Abbott ARCHITECT-STAT HS Troponin

• Attempted to maximize patients at lowest risk

• Used < 5 ng; 5-99th percentile; > 99th

• 99th percentile HS Troponin I = 14-20 ng

What high-sensitivity Troponin I should be cut-off to R/O ACS?

A HS Troponin I of < 5 ng is seen in ½ of R/O ACS pts and yields a

NPV of 99.5 of AMI or Death at 30 d and a NPV of 99.9 for Death at 30 d

JAMA 2017;318:1913-24

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JACC 2018;72:620-32

• 0/1 hr Troponin I or T studied

• 4,368 serial Trop T pts; 3,500 serial Trop I pts

• Did not also use HEART pathway

• Used ESC 0-1 hr R/O pathway

Troponin Rule OutsJACC 2018;72:620-32

Troponin T: Trop I:

0 hr < 5 ng/L 0 hr < 2 ng/L

or or

0 hr < 12 ng/L 0 hr < 5 ng/L

and and1 hr < 3 ng/L 1 hr < 2ng/L

JACC 2018;72:620-32

NPV of 0/1 Hr R/OTroponin T and I

JACC 2018;72:620-32

hsT hsI

JAMA Cardiol 2018;3:112-113

• 1,690 R/O ACS pt; 15 US EDs HS Trop T

• Used 0, 3, 6-9, 12-24 hr levels

• Healthy volunteers 99th % = 19 ng/L

• Found 0 and 3 hr accuracy plateaued

Can a 0-3 hr HS Troponin T R/O 30 day ACS > 99% of patients?

A single HS Troponin T < 6 ng/L has a NPV of 99.4 and both a 0 and 3 hr of < 19 ng/L has a

NPV of 99.3 for 30 d ACI


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The 0 and 1 hour rule out protocols yield at NPV for ACS of 99.8 for HS

Troponin T and 99.7 for HS Troponin I and allows early discharge for

1/2 - 2/3 of patients


Circ 2018;138:in press

• 536 pts, Parkland Hospital, HS and Trop T

• Uses delta changes

• Above 52 ng/L = AMI, < 6 ng/L ≥ 3 hrs = R/O

• < 3 ng at 1 hr = R/O

• < 7 ng from baseline at 3 hrs = R/O

Can a multi-step 0, 1 and 3 hour protocol deal with the “indeterminate” patients when using

high-sensitivity Troponin (hsTrop)

Protocol providing 100%Sensitivity for AMI and 100%

Negative predictive values for R/O



Circ 2018;138:in press Circ 2018;138:in press

9/28/2018

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Take Homes onHigh Sensitivity Troponins

• Undetectable at 0-1 or 0-3 rules out AMI

• Delta testing excludes evolving AMI

• Early AMI presenters need values over time

• Using the 99th percentile may not be optimal

• Beware detectable Troponin

At the current time there is no universally accepted high sensitivity

Troponin protocol and objective scoring system that is “proven” to be optimal

All important decisions are made onincomplete information….

Yet we are responsible for everydecision we make.

Sheldon Kopp 1972JACC 2018;71:606-16

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How Important is Stress Testing??

Does CCTA add anything to a chest pain work up once AMI has been ruled out?

The SCOT-HEART trial

New Engl J Med 2018;379:924-33

• 4,146 Scottish CP pts, 3-7 year f/u

• Randomized to CCTA or routine case

• NOT ED pts, all CP pts

• Compared mortality, AMI, ReVasc rates

Treatments

• More preventative Rx if CCTA

• More anti-angonal Rx if CCTA

• More early angiography and ReVasc, too

• At 5 years no diff in ReVasc rates

New Engl J Med 2018;379:924-33

0%

1%

2%

3%

4%

5%

Hu

nd

red

s

0.2%0.4%

Cardiac Death or AMICCTA vs No CCTA

Death

2.1%

3.5%

CCTA CCTANo No

2.3%

3.9%

Combined

CCTA No

Non Fatal AMI

p = 0.004

New Engl J Med 2018;379:924-33

CCTA for CP PtsTake Homes

• Not an ED CP study

• Knowing coronary anatomy helps post ED Rx

• Allows more aggressive care

• My thoughts are R/O AMI is not enough

• Are coronaries: WNL, some CASHD, obstructed?

JAMA Int Med 2018;178:212-19

• 1,000 pts (40-74 yo) from ROMICAT-II

• No hx CAD, no CRF

• 118 pts no testing vs 882 CCTA or stress test

• Evaluated 28 day MACE

• Also ACS dx %; Angiography/PCI %

Is stress testing necessary if ECG is non ischemic and 2 Troponins are negative?

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0

2

4

6

8

10

12

14

0%

9%

Stress Testing vs No TestingACS Angiography 30 d PCI

ACS Dx

0%

10%

No NoTest Stress

2%

5%

30 d PCIAngiography

All p < 0.001

JAMA Int Med 2018;178:212-19

0.0

0.2

0.4

0.6

0.8

1.0

1.2

1.4

1.6

1.8

2.0

2.22%

28 Day MACE

No Testing

1%

CCTA or Stess

P = NS

JAMA Int Med 2018;178:212-19

Stress TestingTake Homes

It is getting harder and harder to justify routine stress testing

May miss 1-2% 30 d ACS just using ECG and Troponin without scoring system

Adding low HEART Score is key

JAMA Int Med 2017;177:1175-82

• 926,633 pts retrospective observational study

• Database study of ED CP pts. 18-64 yo

• Followed pts for 1 year

• Evaluated rates of PCI, CABG and AMI

• Compared weekday to weekend pts

Does stress testing decrease PCI or AMI?

Patients not randomized, those who underwent stress testing were older,

M > F and had more risk factors

JAMA Int Med 2017;177:1175-82

JAMA Int Med 2017;177:1175-82

Stress testing of patients with non ischemic ECG and negative biomarkers

results in longer ED/hospital stays, more angiography, more PCI but

no decrease in AMI over 1 year

9/28/2018

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Does shared decision making lead to decreased testing without increased risk to

patients and/or physicians?

• 834 CP patients evaluated 45 days s/p ED

• Multicenter trial, 5 EDs across USA

• All eligible for Stress or MD CT

• All kept health care diaries

• Compared usual care to shared decision making

Chest Pain Choice (CPC) Tool

• Provides 45 d personalized ACS risk

• Compares Obs admit to 3 d follow up

• Clearly explains management options

• Explain Stress or CCTA vs 3 d follow up


Key FindingsAcad Emerg Med 2018;25:293-300

Shared decision making patients had 25.8% less advanced testing than

routine care over 45 days –without any worsening of outcomes

or increased number of adverse conditions

So what should you do:

- Do a very careful history

- Use HEART but diaphoresis &/or radiationto R arm or shoulder, Abn ECG = high risk

- Beware a single Troponin

- Be more careful in HS = 3

- Always involve the patient and family

Type 1 vs Type 2 MI?• It’s not STEMI vs NSTEMI

• Supply vs demand mismatch

• Mismatch due to non CASHD secondary process

• 2 x incidence vs AMI due to STEMI/NSTEMI

• Poorer survival (5 yr = 40% vs 60-65%)

JAMA 2018 online Jun 11

Male vs Femalein AMI Dx and Rx

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Circulation 2018;137:781-90

How different is AMI in males vs females less than age 55?

• 2,009 women, 976 men with AMI

• Young defined as 18-55

• About 90% of M and F pts has chest sx:- pain, pressure, tightness, discomfort

• Women had more additional symptoms

• 50% more F than M had no CP

Physicians much more likely to attribute AMI symptoms to another

disease in women than men

53.4% F vs 36.7% M, p < 0.001

Circulation 2018;137:781-90

Women and AMI

We need to be careful

“Atypical symptoms” may be typical in women

Be aware of our unconscious biases

Are women really treated differently for ACS if they are troponin positive?

• 7,272 pts from Vancouver, 2008-2013

• All pts troponin positive with ischemic CP

• 2,933 females: 4,339 males

• Evaluated % PCI, meds, mortality

• All had cTnI > 99th percentile


Symptoms & Diagnosis in EDTroponin Positive Females


• More respiratory symptoms(22.4% vs 14.8% F:M)

• Less classic chest pain symptoms(77.6% vs 85.2%)

• AMI less frequently diagnosed in ED(35.4% vs 52.5%)

• Less likely to be using evidence based meds:(ACE-I / ARB 0.32; BB 0.52, Statin 0.31)

Risk FactorsTroponin Positive Females

• Older 65 (70.8% vs 49.3%)

• More HT HT (39.8% vs 28.5%)

• More RF CRF (27.6% vs 18.7%)


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05

101520253035404550556065

64.3

Troponin PositivePCI and MACE

PCI MACE

48.4

Female Male Female Male

OR = 0.52(0.39 – 0.70)

HR = 1.24*(0.94 – 1.65)*p – NS onceadjusted for difference

18.822.7


How We Treat Women vs Men with ACS

Take Homes

• We as ED MDs are less aggressive with women and they do worse

• Even if Troponin positive, we are less aggressive with emergent PCI and/or cardiac meds

Lancet 2018;391:1693-1705

Does liberal oxygen therapy increase morbidity or mortality?

• 16,307 patients, 25 randomized trials

• Sepsis, CVA, Trauma, AMI, s/p CPR, Critically ill

• COPD, ECMO, Hyperbarics or Psych excluded

• Evaluated mortality in hospital, 30 d and/or longest

• Hospital stay, hospital acquired pneumonia, LOS

Lancet 2018;391:1693-1705

Study compares FiO2 given liberally at rates from 30% - 80% with a few at 100% FiO2 vs a majority of patients treated with no supplemental O2, or low flow (2-4 L/min) nasal prongs or titrated to O2 sat < 96%

Median FiO2 52% vs 21% for a median duration of 8 hours

Unrestricted oxygenation will increase mortality by about 21% at 30 days in

comparable patients with similar baseline O2 saturations

There were no differences in in-hospital complication

Lancet 2018;391:1693-1705

Oxygenation of Critically Ill PatientsTake Homes

94 – 96% Not higher

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PNAS 2018;115:8569-74

• Higher mortality seen when women with STEMI treated by male ED physician

• Female=Male when treated by female ED physicians

• Male physicians do better if more females in ED practice or they have treated more females in past

• Be careful of unconscious gender bias

Patient vs Doctor Gender

M Doc

F Pt

M Doc

M Pt

F Doc

F Pt

• 550 pts, Mecklenburg, NC EMS

• Mean E2B 80.8 min, SD 19.7 min

Prehosp Emerg Care 2018;in press Mar

Each 1 min increase in E2B above mean time increased mortality by 3%

or 30% for 10 minute delay

Pulmonary Embolus

Is Lytic Therapy indicated or justified in acute PE?

Thorax 2018;73:464-71

• 22 RCTs: 16 full, 1 low dose vs heparin

• 4 studies compared low vs full dose

• 1 study used catheter directed lytics

• Evaluated mortality, major bleeding, 1 CH

Results

• No lytic protocol significantly better than heparin

• No significant trend toward lower mortality though

• Full dose lytics risk of major bleeding

• Low dose lytics best for lowest mortality & safety

Thorax 2018;73:464-71

9/28/2018

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Lytics in PETake Homes

• Use in arrest and peri arrest50 mg IV over 1 minute

• Full dose lytics only for massive PE(refractory hypoxia, hypotension)

• Half dose lytics appear as good as full

Critical Care Med 2018;46:1617-25

Can ½ dose TPA be used to treat PE?

• Retrospective cohort trial, 420 hospital database

• 699 pts treated with ½ dose TPA

• 3,069 full dose TPA

• Evaluated mortality, major bleeding, Escalation

• Propensity matching of 548 pts 1:1

0

2

4

6

8

10

12

14

16

18

20

0.5%BLS

Mortality and Cerebral Hemorrhage

Mortality ICH

13%

1/2 Full 1/2 Full

p = ns

p = ns

15.1%

0.4%


0%

10%

20%

30%

40%

50%

60%53.8%

Escalation in Therapy

½ Dose

41.4%

Full Dose

p=0.01


Half Dose Lytic PE TherapyTake Homes

• Not a ringing endorsement

• But not a controlled study

• 25.9% vs 7.3% required 2nd thrombolysis

• 14.2% vs 3.8% had mechanical fragmentation

• Role of ½ dose lytics remains very unclear

Acad Emerg Med 2018;25:995-1003

Can low risk PE patients be safely discharged from the ED?

• 114 randomized PE patients

• 51 ED D/C’d vs 63 admitted

• D/C pts placed on rivaroxaban 15 mg BID

• 90 day follow-up

• No high-risk PE patients

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Requiring Admission for PE

• Hemodynamically unstable

• Active or high-risk for bleeding

• Sys BP > 180; DBP > 110

• Hypoxic

• Already anti-coagulated

• Pregnant, Liver DSX, C-Cl < 30

Acad Emerg Med 2018;25:995-1003

Results

Acad Emerg Med 2018;25:995-1003

• No VTE reoccurrences in either group

• No VTE deaths in either group

• No differences in bleeding rates(1 minor in each group)

0

5

10

15

20

25

30

35

40

4.8

Hospital Stay in Hours

NOAC

33

Admit

p < 0.0001

Acad Emerg Med 2018;25:995-1003

± 16.8

± 48

Initial Visit Costs

• $1,496 ED with NOAC on DC

• $4,234 Admit Std of Care Rx

Acad Emerg Med 2018;25:995-1003

Sending Home PEsTake Homes

• First large study

• Safe in low-risk patients

• Cheaper, faster

• Avoids in-hospital days

• A “new” treatment consideration

Chest 2018;154:249-56

Can PE be an outpatient disease?The LOPE Study

• Prospective study, 200 pts, 5 EDs

• Intermountain Health, Salt Lake UT

• PESI < 86, TT Echo, Leg US

• 90 d mortality, Recurrent VTE, Major bleed

• Measured patient satisfaction; 100% follow-up

9/28/2018

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Methods

• Low risk PESI < 86, no hypotension or hypoxia

• Admit to Obs for 12-24 hr (x=13 hrs)

• TTE to R/O RV strain

• Leg US to R/O Proximal DVT

• Discharge on NOAC

Chest 2018;154:249-56

Results

• No recurrent VTE, no mortality

• 1 major bleed on OP NOAC

• 91% stated they preferred OP care

Chest 2018;154:249-56

Out Patient Management of PETake Homes

• Safe

• But only in very select pts

• Low risk PESI, WNL Echo, No DVT

• Troponin and BNP testing not helpful

• Can be followed as OP


Do subsegmental PEs (SSPE) require therapy?

• Systemic review and meta-analysis

• 15,563 patients from 14 studies

• 4.6% of PEs are SSPEs


Do subsegmental PEs (SSPE) require therapy?

• 90 d VTE%:- 5.3% if treated vs 3.9% if not

• 90 d Bleed rate:- 8.1% if treated

• Death: 2.1% treated vs 3% not

“These data suggest clinical equipoise for decision to anticoagulate

patients with SSPE”

“However…lack of a controlled clinical trial”


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JAMA 2018;319:559-66

Should we rely on using PERC in low risk for PE patients?

• 1,916 pts from 14 French EDs

• Used R/O PE pts with PE probability < 15%

• Each ED did 6 mos PERC vs no-PERC

• D-dimer for all non-PERC low risk pts

• 3 month follow-up

Results

• 1 VTE over 3 mos in PERC neg pt

• 0 VTEs in control group

• This PERC “miss” was VS–and CTA equivocal

• PERC stayed 43 minutes less

• Similar mortality: 0.3 vs 0.2 (1 pt)

JAMA 2018;319:559-66

0%

5%

10%

15%

20%

25%

13%

PERC vs D-Dimer For All

PERC

23%

No PERC

JAMA 2018;319:559-66

ED CTPA

PERC Take Homes

• Use it

• Especially when you want to D/C

• Study clearly supports its use

• But only in very low risk pts!

Atrial Fibrillation

West J Med 2018;19:417-22

Can PO Diltiazem be substituted for an IV Infusion to control Atrial Fibrillation with RVR?

• 111 adult pts with AF and RVR > 110 bpm

• Single center observational study from VCU

• Used 4 hour HR to measure efficacy

• PO dose: 30 mg (53%), 60 mg (41%)

• IV dose: 10 mg/hr median (2.5-20 hour range)

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Mean initial loading doses were 0.22 mg/kg oral and

0.24 mg/kg IV

West J Med 2018;19:417-22

0%

10%

20%

30%

40%

50%

60%

70%

80%

73.2%

HR Less Than 110 at 4 Hours

131 Initial HR

West J Med 2018;19:417-22

55.3%

145 Initial HR

P=0.049

PO IV

70 pts41 pts

PO Diltiazem vs IV Continuous InfusionTake Homes

• Small not well controlled study

• Variable loading dose, low IV infusion

• IV group had higher initial HR (140 vs 131)

• However- Consider PO Diltiazem in patients vs

continuous infusion in selected cases

Median infusion was 10 mg/hr

Loading dose was 16.8 mg

in 70 kg pt infusion rate was only 5.8 mg/hr

Too Little IV Diltiazem


Can a simple to follow protocol allow more discharges in AFib/AFlut patients?

• 1,108 patients

• Retrospective before-after trial

• Academic community hospital

• Evaluated percent of pts admitted in 1 year

• Also 3 and 30 day returns

Study Assumptions and Hypothesis

• 20 yr AFib admits 60% in US

• No defined AHA/ACC discharge pathway

• Great care variations US vs Canada

• Future stroke is greatest risk

• AFib/AFlut rarely acutely life-threatening


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• Arranged follow up within 3d

• Seen then in cardiology clinic

• Anticoagulation held until then

• Discharged on BB or Calcium Blocker

• Metoprolol 50 BID

• Diltiazem 120-180 ext release


Current Common AFib PathwayMost EDs

• H/P, CXR, ECG, basic labs, thyroid

• IV rate control meds

• Cardiology consult

• Echo

• Admit

St. Joseph Murphy AlgorithmExclusions and Admit

• Underlying Acute Illness(sepsis, PE, etc.)

• Acute Coronary Syndrome

• Acute Heart Failure

• Syncope

• Hemodynamic instability



• Synchronized cardioversion not focus

• Rate-control IV meds discouraged

• Not specifically stated by patientsalmost all < 48 hr onset of AFib/AFlut

• About ½ “low morbidity”

• ¼ HF Hx, ¼ CAD, 1/8 DM0

10

20

30

40

50

60

70

80 63.6%

BLS

Hospital Admit Rates

All Patients Low Acuity

80%

Pre Post Pre Post


16.1%P < 0.001

31.3%P < 0.001

67.4%

43.7%

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NOTE

• Pharmacological conversions not attempted

• IV rate control discouraged

• 50 mg PO Metoprolol

• 120-180 mg PO Diltiazem ER

• D/C cardioversion not increased


Additional Findings

• Cardioversion rates pre : post:- 21.2% vs 17.2%

• 3 day ED return for any reason:- 1.19 vs 1.0%

• 30 day ED returns- 3.8% vs 3.0%

• 90% followed up in AFib clinic

• 10% went outside system


Simplified AFib Discharge PathwaysTake Homes

• Single center trial

• Very simple, very impressive

• < 48 hr not specifically cited

• stroke risk ?

• This protocol will have users

Acad Emerg Med 2018;in press August

• 450 pts, double-blind, placebo controlled

• 3 groups of pts from 3 Tunisian hospitals

• High dose vs Low dose vs Placebo

• MgSO4 9 grams vs 4.5 grams vs Placebo

• Given over 30 minutes

Is Magnesium effective for rate control in “Rapid” Atrial Fibrillation?

Measured effectiveness as HR < 90or rate lowering by > 20%


0%

10%

20%

30%

40%

50%

60%

70% 59.5%64.2%

EffectivenessHR < 90 or HR > 20%

9 Grams 4.5 Grams

43.6%

--


High Dose Mg Low Dose Mg Placebo

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This paper is not what it seems


• Essentially all patients got other rate control agents

• 45-50% received Digoxin

• 30% received Diltiazem

• 20% received Beta Blockade

Magnesium for Rate Control in AFTake Homes

• Adjunct? – maybe; Primary – NO

• 2.5 grams or 4.5 grams?

• 9 grams = lots of flushing (10-15%)

• Was very safe, < 1% hypotension

• Read this paper carefully

Annal Emerg Med 2018;71:96-108

How effective and safe is Ibutilide for ED conversion of Atrial Fibrillation and Atrial Flutter?

• 361 pts, 21 community EDs, 2009-2015

• Recent onset AFib/Flutter

• 61 yo median age (53-71 IQR); QTc > 480: 30%

• Evaluated conversion rate and complications

Ibutilide

• Class III antiarrhythmic, K channel blockade

• Slowed repolarization with QTc

• Usual dose: 1 mg x 2, 10 minute interval

• VTACH and/or Torsade's up to 5% each

• Almost always within 45 min – 1 hr


ECG monitoring s/p Ibutilide is 4 hours


Highest Risk for Ibutilide(% in this study)

• Heart Failure patients (5%)

• Prolonged QTc (29.4% > 480 mg)

• Hypokalemia (3.1% < 3.5 meq)

• Hypomagnesemia (0.9% < 1.6 meq/L)


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Methods

• 69% received rate reducing meds

• Most received Diltiazem

• Half also received 1-2 grams MgSO4

• 2/3 pre-Ibutilide Cardiology consult


Results

• 44% conversion to NSR at 90 min

• 54.8% to NSR at 4 hrs

• 75% for Atrial Flutter

• 91.8% electrical cardioversion s/p Ibutilide

• 0.6% VTach incidence – both s/p 2nd dose


IbutilideTake Homes

• Great pre cardioversion

• Not impressive alone

• Similar to procainamide

• Requires 4 hrs of monitoring

• Can be used if hypoK/hypomag **But give 2 grams MgSO4 pre-drug!


• EM, Card, EP, IM, APP, RN, Pharm D

• Provides Flow Chart

• Includes med and/or DC Cardioversion if possible

• Recommends use of Ibutilide or Flecainide

• D/C on NOAC if no contraindication

Clear onset < 48 hrsor

Adequately anticoagulated ≥ 4 weeksAcad Emerg Med 2018;25:1065-75

Cardioversion Recommendations

200 J A-P pad placement


Electrical Conversion

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Pharmacological Conversion• Pretreat with 2 grams MgSO4 over 30 min

• 1 gram Ibutilide over 10 min

• May repeat 10 min after 1st dose

• Monitor for Torsades x 4 hrs

• Do not use if:QTC > 450 msec; Hypo K; EF < 30%

Summary

Epi survival but bad Neuro too

Summary

PCI all VF/VT survivors

Not witnessed, no shock, no ROSC

HyperK: R/O if CRF STEMI

HEART works – beware scores > 2

Beware detectable HS Troponin

Summary

Stress tests: do less

Use shared decision making

Low risk PE can go home

Develop an AFib pathway

VanderbiltEM.com

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