An Evidence Based up-date for first year EM residents on why we do, what we do, in emergency medicine in the care of the chest pain patient.

1. AHA / ECC
Guidelines
2014
• Troy W. Pennington DO, MS, FAAEM

2. ACC/AHA Guidelines
2010 revision
• Onset & Recognition of Symptoms
– ACS need not present with CHEST PAIN
• 1/3 of all MI’s present with symptoms other
than chest pain
• Remember Anginal Equivalents
– Dyspnea
– Extreme Fatigue
– Diaphoresis
– Syncope
Teach Your patients to access the system early,
Half of all patients who die of ACS do it before
reaching the hospital!

4. AHA / ACC Update
• Top Five Factors on initial History
– Nature of anginal symptoms
– Prior history of CAD
– Male gender
– Older age
– Increasing number of traditional risk factors
u HPI is the most important…risk factor profile or lack of risk factors
has limited utility in the acute setting

5. What are typical Signs &
Symptoms of Chest Pain in
ACS?
• Chest Pressure
• Radiation to the left neck, jaw, shoulder or arm
• Dyspnea
• Diaphoresis
• Nausea
• Vomiting
• Lightheadness

6. “Atypical” Chest Pain
• Pleuritic
• Sharp
• Positional
• Reproducible

7. What are the Top Four Signs
& Symptoms to Predict
ACS?
• Chest Pain that radiates (especially
bilaterally or to the RIGHT side)
• Pain on Exertion
• Diaphoresis
• Vomiting

8. Copyright ©2010 American Heart Association
O'Connor, R. E. et al. Circulation 2010;122:S787-S817
Acute Coronary Syndromes Algorithm

9. Level’s of Evidence

10. ED Evaluation & Risk
Stratification
Upon Presentation Organize
patient into one of three
groups...
1. ST Segment Elevation
or Presumed new LBBB
2. Ischemic St- Segment
Depression > 0.5mm
3. Nondiagnostic EKG

11. ST Segment Elevation
or
Presumed new LBBB
• Threshold Values
• ST-segment elevation consistent with
STEMI are J-point elevation 0.2 mV (2
mm) in leads V2 and V3 and 0.1 mV (1
mm) in all other leads (men >40 years old)
• J-point elevation 0.25 mV (2.5 mm) in
leads V2 and V3 and 0.1 mV (1 mm) in all
other leads (men <40 years old); J-point
elevation 0.15 mV (2.5 mm) in leads V2
and V3 and 0.1 mV (1 mm) in all other
leads (women)

12. Ischemic ST-segment Depression
• >0.5 mm (0.05 mV) or dynamic T-
wave inversion with pain or discomfort
is classified as UA/NSTEMI.
• Nonpersistent or transient ST-segment
elevation >0.5 mm for <20 minutes is
also included in this category.
• Threshold values for ST-segment
depression consistent with ischemia are
J-point depression 0.05 mV (-.5 mm) in
leads V2 and V3 and -0.1 mV (-1 mm)
in all other leads (men and women).

13. The Nondiagnostic ECG
• This ECG is nondiagnostic and inconclusive for
ischemia, requiring further risk stratification.
• This classification includes patients with normal
ECGs and those with ST-segment deviation of <0.5
mm (0.05 mV) or T-wave inversion of <0.2 mV.
• This category of ECG is termed nondiagnostic.

14. “Within a STEMI system of care, the first physician
who encounters a patient with STEMI determines the
need and strategy (fibrinolytic or PPCI) for
reperfusion therapy!”
✴ Routine consultation with a cardiologist or
another physician is not recommended except
in equivocal or uncertain cases
✴ Consultation delays therapy and is associated
with increased hospital mortality rates

15. Risk Stratification
• Diagnosis of ACS and risk
stratification become an
integrated process in patients
presenting to an acute care
setting with possible ACS and
an initially nondiagnostic
evaluation
• This nondiagnostic evaluation
includes a normal or
nondiagnostic 12-lead ECG and
normal serum cardiac biomarker
concentrations

16. The Nondiagnostic Evaluation
• Normal or nondiagnostic
12-Lead ECG
• Normal Serum Biomarker
Concentrations
★ Most... not All... Most of these
patients will not be experiencing
ACS
• But they may have
underlying CAD or other
clinical features putting
them at risk for major
advents over the course of
the next few days

17. ACC/ACC Risk
Stratification
Guidelines

18. TIMI Risk Score
In Unstable Angina & Non-St
Elevation MI

19. Selection of Strategy
for patients with Non-St Elevation
ACS

20. ACS Therapy- The
Evidence
Oxyge
n

21. Guidelines Say
• Oxygen should be
administered to patients
with breathlessness, signs
of heart failure, shock, or an
arterial oxyhemoglobin
saturation <94%
(Class I, LOE C).
• In the absence of
compelling evidence for
established benefit in
uncomplicated cases,
ACC/AHA Guidelines have
noted that there appeared
to be little justification for
continuing routine oxygen
use beyond 6 hours.

22. Aspirin & NSAIDS
• DO I Give ASA...
• And How Much
Should I Give?
• What about a
NSAID...Kinda
Makes Sense,
Decrease
inflammation...BUT!

23. Aspirin.....Of Course!

24. Aspirin
Aspirin was found to substantially reduce vascular events in
all patients with AMI, and in high-risk patients it reduced
nonfatal AMI and vascular death.
Aspirin is also effective in patients with NSTEMI. The
recommended dose is 160 to 325 mg
Chewable or soluble aspirin is absorbed
more quickly than swallowed tablets.
Aspirin suppositories (300 mg) are safe and can be
considered for patients with severe nausea, vomiting, or
disorders of the upper gastrointestinal tract.

25. Initial Evaluation and Management
Immediate Management
• Give ASA 325mg PO
– In true asa allergy………. 300mg plavix po
• Nitrates
– NTG sublingual .4mg x 3
• Initiate SL NTG as usual, and consider IV NTG
for persistent ischemia after 3 sublingual tablets,
for patients with heart failure (HF), and for
patients with hypertension.

26. NSAIDS
• Don’t Give & DC if they are
part of their regular meds
on admit!

27. Nitroglycerin

28. Nitroglycerin

29. Nitroglycerin

30. Nitroglycerin

31. Nitrate
Contraindications
Nitrates should not be given to
patients with:
 SBP < 90 mm Hg or more
than a 30mm Hg decrease
from the patient’s baseline
 Bradycardia < 50 beats/min
[out of concern for worsening
bradycardia due to vagal
response?
 Tachycardia > 100 beats/min
[out of concern for
hypovolemia or RV MI?]
unless HF is present;
 Right Ventricular MI...

32. AHA / ACC Quick
Facts
• Response to Nitro and/or
GI cocktail is neither
sensitive nor specific
• Up to 6% of NSTEMI’s are
associated with normal
EKG’s
• Unstable angina has a
normal EKG up to 4% of
the time

33. Morphine
• Reasonable in patients with
uncontrolled ischemic chest
pain despite NTG…..
• Morphine was downgraded from
a Class I to a Class IIa
• Crusade registry showed an
association between MS usage
and mortality in ACS patients

34. Reperfusion
Therapies

35. Fibrinolytics

36. Fibrinolysis for
Reperfusion
• If Given to eligible
patients as early as
possible
• Goal Door to Needle
Less than 30 Minutes
• Patients tx’d within the
first 70 minutes of onset
of sx. have > 50%
reduction in infarct size,
75% reduction in
mortality!

37. Fibrinolysis for
Reperfusion
• Estimates that 65
lives saved per
1000 patients
treated if done in
3 hours of onset
of symptoms!

38. Contraindication
s
to Fibrinolytic
Therapy

39. Contraindications
to Fibrinolytic
Therapy
• The Mortality
Benefit is time
Sensitive!

40. Benefits of Fibrinolytic
Therapy
Fibrinolytics have been
shown to be beneficial
across a spectrum of
patient subgroups with
comorbidities such as
previous MI, diabetes,
tachycardia, and
hypotension.

41. Risks of Fibrinolytic
Therapy
• Small but definite
increase in risk of
hemorragic stroke.
• More intensive regiems
such as alteplase and
heparin pose greater
risk than streptokinase
and aspirin.

42. PCI
Coronary angioplasty with or without
stent placement is the treatment of
choice for the management of STEMI
when it can be performed effectively
with a door-to-balloon time <90
minutes

43. The Clot Box

44. The Clot Box

45. The Clot Box

46. TNKase Dosing
• Acute MI: Single IV bolus over 5
seconds based on body weight;
• <60 kg ……..30mg
• 60-69 kg……35mg
• 70-79 kg……40mg
• 80-89 kg…….45mg
• > 90 kg……...50mg

47. PCI versus
Fibrinolysis
• How long should we wait for
PCI?
• At what point is the survival
benefit lost. A study by Pinto
and Colleagues breaks it
down...

48. PCI versus
Fibrinolysis

49. PCI Following ROSC
After Cardiac Arrest
Each Year approximately 236,000 to 325,000
patients experience out-of-hospital cardiac
arrest...
The prognosis is GRIM with median survival to
discharge rate of about 8.4%

50. PCI Following ROSC
After Cardiac Arrest
• A 12-Lead ECG
should be
performed as soon
as possible after
ROSC!
• Clinical Findings of
COMA in patients
with OOHCA should
not be a
contraindication to
consider immediate
angiography and
PCI!

51. ROSC
After Cardiac
Arrest

52. Complicated
AMI
• Infarction of > 40% of the LV
myocardium usually results in
cardiogenic shock and a high
mortality rate.
• PCI is the treatment of choice
• Fibrinolysis though is not
contraindicated

53. RV
Infarction
• May occur up to 50%
patients with inferior MI
• In Inferior MI obtain
right sided ECG
• ST Elevation >1mm in
V4R is 88% Sensitive
and 78% Specific for
RV infarction
• Strong predictor of
complicated in patient
course and increased
mortality

54. RV Infarction
• RV infarction causes
RV dysfunction, these
patients need RV
filling pressure to
maintain cardiac
output
• Avoid nitrates,
diuretics, and other
vasodilators
(ace inhibitors)
• Hypotension is
treated with a fluid
bolus

55. Adjunctive Therapies for
ACS & AMI
• Clopidogrel- irreversibly
inhibits the adenosine diphosphate
receptor on the platelet, resulting in
a reduction in platelet aggregation
through a different mechanism than
aspirin…
• Patients with ACS and a rise in
cardiac biomarkers or ECG changes
consistent with ischemia had
reduced stroke and major adverse
cardiac events if clopidogrel was
added to aspirin and heparin within
4 hours of hospital presentation.

56. Adjunctive Therapies for
ACS & AMI
• Clopidogrel given 6 hours
or more before elective PCI
for patients with ACS
without ST elevation
reduces adverse ischemic
events at 28 days.
• The CURE Trail-
documented an increased
rate of bleeding (but not
intracranial hemorrhage) in
the 2072 patients
undergoing CABG within 5
to 7 days of administration.

57. Adjunctive
Therapies for ACS
& AMI

58. Adjunctive Therapies
for ACS & AMI
• On the basis of these findings, providers
should administer a loading dose of
clopidogrel in addition to standard care
(aspirin, anticoagulants, and reperfusion) for
patients determined to have moderate- to high-
risk non-ST-segment elevation ACS and STEMl
(Class I, LOE A).
In patients <75 years of age a loading dose of
clopidogrel 300 to 600 mg with non-STE ACS
and STEMI, regardless of approach to
management, is recommended.

59. Prasugrel
• Prasugrel is an oral thienopyridine prodrug
that irreversably binds to the ADP receptor to
inhibit platelet aggregation.
Small improvements in combined event rate
(cardiovascular mortality, nonfatal infarction, and
nonfatal stroke) and/or mortality are observed
when prasugrel (compared to clopidogrel) is
administered before or after angiography to
patients with NSTEMI and STEMI managed with
PCI.

60. Prasugrel
• Prasugrel (60 mg oral loading dose) may be
substituted for clopidogrel after angiography in
patients determined to have non-ST-segment
elevation ACS or STEMI who are more than 12
hours after symptom onset prior to planned PCI
(Class IIa, LOE B).
• There is no direct evidence for the use of
prasugrel in the ED or prehospital settings
• Prasugrel is not recommended in STEMI patients
managed with fibrinolysis or NSTEMI patients
before angiography

61. Algorithm for Patients With UA/NSTEMI
Managed by an Initial Invasive Strategy.
Anderson J L et al. Circulation 2011;123:e426-e579
Copyright © American Heart Association

62. Glycoprotein IIb/IIIA
Inhibitors
• There is no current evidence supporting the
routine use of GP IIb/ IIIa inhibitor therapy prior
to angiography in patients with STEMI and use
of these agents upstream is uncertain...
• Current evidence supports a selective strategy
for the use of GP IIb/IIIa inhibitors in the use of
dual platelet inhibitor treatment of patients with
planned invasive strategy taking into
consideration the ACS risk of the patient and
weighing this against the potential bleeding risk

63. Glycoprotein IIb/IIIA
Inhibitors
Use of GP IIb/ IIIa
inhibitors should be guided
by local interdisciplinary
review of ongoing clinical
trials, guidelines, and
recommendations.

64. Beta Blockers…..What
Now?
• The COMMIT Study 2005
– Early use of IV beta blockers was found to increase the
chances of developing cardiogenic shock, and there
was no overall benefit on mortality.
– Recommendations now are focused on simply
initiating the beta blockers within 24 hours to confer
the beneficial effects reduction in ventricular
dysrhythmias, sudden death, and reinfarction but
without the dangers of predisposing to cardiogenic
shock.

65. Contraindications to Beta Blockers
• Signs of HF
• Evidence of low-output state
• Risk of Cardiogenic Shock in NSTE-ACS
include:
– age > 70 yo
– SBP < 120
–sinus tachycardia > 110 or HR < 60
Other relative contraindications to beta blockade…
(PR interval > 240 msec, 2nd or 3rd degree heart block, active
asthma, or reactive airway disease).

66. B-Adrenergic Receptor
Blockers
• Recent evidence shows no particular benefit to the
IV administration of B-blockers on either mortality,
infarct size, prevention of arrhythmias, or
reinfarction
• IV Beta Blockers may show benefit in NSTEMI
Balancing the evidence overall for non-ST-segment
elevation ACS patients, current ACC/AHA
Guidelines recommend B-blockers be initiated
orally within the first 24 hours after hospitalization

67. Heparins

68. Unfractionated Vs. Low-Molecular
Weight Heparin in UA/NSTEMI
Lovenox
Lovenox
Arixtra
Arixtra
Angiomax Angiomax

69. Treatment Recommendations
for
UA / NSTEMI
• NSTEMI conservative
approach-
• Either fondaparinux (Class IIa,
LOE B) or enoxaparin (Class IIa,
LOE A) are reasonable
alternatives to UFH or placebo
• NSTEMI planned early
cath- either enoxaparin or
UFH are reasonable
choices
• Renal Insufficiency-
bivalirudin or UFH may be
considered (Class IIb, LOE

70. Treatment
Recommendations for
Heparin vs. LMH in STEMI

71. Enoxaparin
• For patients with STEMI managed with
fibrinolysis in the hospital, it is reasonable to
administer enoxaparin instead of UFH (Class IIa,
LOE A)
• Patients initially treated with enoxaparin should
not be switched to UFH and vice versa because
of increased risk of bleeding (Class III, LOE C)

72. Enoxaparin
• Dosing
• In younger patients <75 years the initial dose of
enoxaparin is 30 mg IV bolus followed by 1 mg/kg
SC every 12 hours (first SC dose shortly after the IV
bolus) (Class IIb, LOE A)
• Patients >75 years may be treated with 0.75 mg/kg
SC enoxaparin every 12 hours without an initial IV
bolus (Class IIb, LOE B).
• Patients with impaired renal function (creatinine
clearance <30 mL/min) may be given 1 mg/kg
enoxaparin SC once daily (Class IIb, LOE B).
Patients with known impaired renal function may
alternatively be managed with UFH (Class IIb, LOE
B).

73. ACS- Heparin
• What did the
Cochrane review
say about heparin in
ACS?
• Found no difference
in overall mortality
between the groups
treated with heparin
and placebo.
• NO LIVES SAVED
BY HEPARIN in
ACS…
Magee et al. Heparin versus placebo for acute coronary syndromes.
Cochrane database Syst Rev. 2008 Apr 16;(2):CD003462.

74. Heparin- ACS
• Heparins reduced the occurrence of MI by about
3%
• This means a number needed to treat of 33
• At 7‐10 days there was a 3% lower rate of MI in
the heparin group, but at 30 days, 60 days, 90
days and six months it was not lower.

75. Heparin-
ACS
• While initially the heparin
group at 7‐10 days
appeared to have fewer
heart attacks, they had
caught up in the later
dates and there was no
apparent change in the
rates. So if the drug just
delays a heart attack that
they are going to have
anyway, that would not be
considered a
patient‐oriented benefit
except for in some
specialized circumstances.

76. To Heparin or not To
Heparin…
• What does Mel Say?
• Low Risk Patients….NO Heparin
• High Risk Patients….Maybe

77. JAMA Feb 22, 2012
Article
• AGE / Gender
• Presence or
Absence of
Chest Pain
• Mortality
Canto et al. Association of age and sex with myocardial infarction symptom presentation
and in-hospital mortality. JAMA. 2012 Feb 22;307(8):813-‐22.

78. ACS in Women
• Which of the Following
in Women and MI are
True?
1. Premenopausal Women
Don’t have Mi’s
2. It is only older women
present atypically
3. Painless MI has a Good
Prognosis
4. Older women present very
differently from men
Canto et al. Association of age and sex with myocardial infarction symptom presentation
and in-hospital mortality. JAMA. 2012 Feb 22;307(8):813-‐22.

79. ACS in Women
• Women are less likely to get EKG’s then
Men
• Can’t rely on pain
• Can’t ignore Premenopausal women

80. ACS
• 35% of the total population with MI’s had
no pain!
• 42% of the women in the study had no
Pain!
• 31% of the men had no pain!

81. ACS
in Women
• In Medico-Legal
literature in the US,
young women are at
higher risk for
lawsuits for missed
diagnosis of MI.
• Women are at
higher risk for dying
from their MI in
hospital.
• Patients that
presented without
Chest Pain had a

82. Patients under 45
• 20% of Women under 45 had no pain
• 13% of Men under 45 had no pain
• As the Groups got older, 50% of men and
women over 75 have chest pain
• ** Young women do get MI’s and cardiac
risk factors are predictive of long-term not
short-term outcomes…

83. ACS in Women
• What % of women in the study had NO
PAIN……
• 42%

84. CT Angiography For
Low Risk Chest Pain
• So who is the Low
Risk Chest Pain
patient?

85. What is Low Risk Chest Pain…
• Low Risk
patients for
ACS are those
with no
hemodynamic
derangements
or arrhythmias,
a normal or
near normal
EKG, and a
negative initial
cardiac injury
marker

86. Low Risk Chest Pain
• By The Numbers-
• 8 million ED visits
per year in the
U.S. for chest pain
• Only 1-2miilion
actually have
disease
• <5% have ST
segment elevation
• We Still miss 1-2%
of all MIs

87. CTA For Low Risk
Chest Pain
• AMAl Mattu,
MD
• Excerpt
From
EMRAP
July 2012
Excerpt from AHA Circulation 2010
Guidelines
Part 10: Acute Coronary Syndromes

88. The Missed 2%
• Typically patients with
Fewer Risk Factors
• Atypical Presentations
• More likely to be women
• Less concerning or nearly
normal EKGs
• Tend to be younger
• Mortality for admitted
patients with ACS 8-10%
• ACS Patients that were sent
home mortality 25-35%

89. Remember…
• Even though there are factors
that decrease the likelihood of
ACS… NONE of them Risk-
Stratify a patient to “NO RISK”…

90. Planning on sending
patient home…
• Document as many low-risk features as
possible…this will increase the defensibility
of your chart if there is an adverse outcome.

91. THANK YOU
Questions?
You can contact me at:
troypenn@aol.com
OnScene1097.com