I) Initial assessment and stabilization of the patient begins immediately upon arrival, focusing on airway, breathing, circulation, and identifying high-risk features. II) Initial therapy includes pain relief, hemodynamic support, and preparations for reperfusion. III) Reperfusion therapy with either primary percutaneous coronary intervention (PCI) or thrombolysis is recommended if possible within 12 hours of symptoms onset, with PCI preferred if readily available.

1. M. Sherif Mokhtar, MD
Professor of Cardiology,
Professor of Critical Care Medicine,
Cairo University

2. 1. Relief of ischemic pain.
2. Assessment of the hemodynamic state and
correction of abnormalities that are present.
3. Initiation of Reperfusion Therapy with primary
percutaneous coronary intervention (PCI) or
thrombolysis
4. Antithrombotic Therapy to prevent rethrombosis
of an ulcerated plaque or subtotal stenosis
(Antman et al., 2004; ACC/AHA task force)

3. This is then followed by the administration of
different drugs that may improve the long-term
prognosis:
5. Prevention of Left Ventricular Remodeling with
an angiotensin converting enzyme (ACE) Inhibitor
6. Prevention of Recurrent Ischemia and life-
threatening ventricular arrhythmias with Beta
Blockers

4. Administration of different drugs that may improve
the long-term prognosis:
7. Cholesterol Lowering with a Statin to prevent
or slow disease progression.
8. Anticoagulation in the presence of left
ventricular thrombus or chronic AF.

5. 9. Long-term Therapy: in collaboration with a cardiac
rehabilitation program, involves Atherothrombotic
Risk Reduction including cessation of
smoking, control of hypertension and
diabetes, nutritional counseling, and an exercise
and stress reduction program.

6. 10. Additional Therapy is based upon the
identification of patients at continued ischemic
risk with:
• Assessment of clinical factors.
• A predischarge exercise tolerance test.
• Measurement of left ventricular function.

7. I) Initial Assessment.
II) Initial therapy.
III) Reperfusion therapy.
IV) Anticoagulation.
V) Arrhythmia management.
VI) Further medical therapy.
VII) Angiography after thrombolysis.
VIII) Managing recurrent chest pain.

8. • Begins as soon as the patient arrives in the
emergency department.
• Continues in the coronary care unit.
• Consists Of Acute Triage And Early Risk
Stratification.

9. I) Acute Triage
A focused evaluation on presentation:
A. Responsiveness, Airway, Breathing and
Circulation: in patients in respiratory or
cardiorespiratory arrest (the appropriate CPR
algorithms should be followed).

10. Acute Triage
B. Evidence of Systemic Hypoperfusion
(cardiogenic shock complicating acute MI
requires aggressive evaluation and
management).

11. Acute Triage
C. Sustained Ventricular Tachyarrhythmias in the
periinfarction period must be treated immediately:
• Deleterious effect on cardiac output,
• Possible exacerbation of myocardial
ischemia, and
• The risk of deterioration into VF.

12. II) Early Risk Stratification
• High Risk Features include older age, low blood
pressure, tachycardia, heart failure (HF), and an
anterior MI.
• Specific Scoring Systems, such as the TIMI Risk
Score, permit a fairly precise determination of the
risk of in-hospital mortality.
(Morrow et al., 2001; Wu et al.,2002)

13. Early Risk Stratification
• Patients at high risk are usually considered to
require, Aggressive Management Strategy in
addition to standard medical management.
• Direct Transport or, less optimally, prompt
Interhospital Transfer to a facility with
revascularization capabilities is recommended for
such patients.
(Antman et al., 2004)

15. I) Initial Assessment.
II) Initial therapy.
III) Reperfusion therapy.
IV) Anticoagulation.
V) Arrhythmia management.
VI) Further medical therapy.
VII) Angiography after thrombolysis.
VIII) Managing recurrent chest pain.

16. The patient with an STEMI should be started on
therapy to:
• Relieve ischemic pain,
• Stabilize hemodynamic status, and
• Reduce ischemia while being assessed as a
candidate for Thrombolysis or Direct PCI.
(Antman et al., 2004)

17. Other routine hospital measures include:
• Anxiolytics,
• Oxygen,
• ECG, and BP monitoring, and
• Intravenous access.
All initial therapy can be carried out in the emergency
department based upon a predetermined, Institution-
Specific, written protocol.
(The 2004 ACC/AHA guidelines)

18. Reperfusion Therapy with either (PCI) or
thrombolysis, if less than 12 hours has elapsed from the
onset of symptoms. Primary PCI is preferred to thrombolysis
when readily available.
Antiplatelet Therapy including
aspirin, clopidogrel, and, in patients undergoing primary
PCI, a GP IIb/IIIa inhibitor.
Sublingual Nitroglycerin followed by IV Nitroglycerin
in patients with persistent chest pain after three sublingual
nitroglycerin tablets, as well as in patients with hypertension
or HF.

19. Nitrates must be used with caution or
avoided in settings in which hypotension is likely or
could result in serious hemodynamic
decompensation, such as RV Infarction or severe
Aortic Stenosis.
Nitrates are contraindicated in patients who
have taken a phosphodiesterase inhibitor for erectile
dysfunction within the previous 24 hours.

20. Intravenous Morphine Sulfate at an initial dose of 2
to 4 mg, with increments of 2 to 8 mg repeated at 5 to 15
minute intervals, to relieve chest pain and anxiety.
Beta Blockers are administered universally to all
pts without contraindications who experience an acute
STEMI, irrespective of concomitant fibrinolytic therapy or
performance of primary PCI.
Treatment should include Early Intravenous Beta
Blockade.
(Antman et al., 2004)

21. Electrolyte Replacement
Although there are no clinical trials documenting
the benefits of Electrolyte Replacement in acute
MI, the ACC/AHA guidelines recommend maintaining
the serum Potassium concentration above 4.0 meq/L
and a serum Magnesium concentration above 2.0
meq/L (2.4 mg/dL or 1 mmol/L).
(Antman et al., 2004)

22. Glucose Control
Randomized trials have demonstrated that both
diabetics and nondiabetics who have had an acute MI or
are critically ill benefit from Tight Blood Glucose control.
A class I recommendation to the use of an Insulin
Infusion to normalize blood glucose in patients with an
STEMI and a complicated course, regardless of whether
they have a diagnosis of diabetes mellitus
(The 2004 ACC/AHA guidelines)

23. I) Initial Assessment.
II) Initial therapy.
III) Reperfusion therapy.
IV) Anticoagulation.
V) Arrhythmia management.
VI) Further medical therapy.
VII) Angiography after thrombolysis.
VIII) Managing recurrent chest pain.

24. Percutaneous Coronary Intervention
PCI
The ACC/AHA task force gave a class I recommendation
to the use of Primary PCI for:
Any patient with an acute STEMI (defined as >1 mm ST
elevation in two contiguous leads after nitroglycerin to rule
out coronary vasospasm).
• Who presents within 12 hours of symptom onset and
• Who can undergo the procedure within 90 minutes of
presentation.
• By persons skilled in the procedure.

25. For patients presenting 12 to 24 hours after
symptom onset, the performance of primary PCI is
reasonable if the patient has:
• Severe Heart Failure,
• Hemodynamic or Electrical Instability, or
• Persistent Ischemic Symptoms.
(Antman et al., 2004)

26. All patients are pretreated at diagnosis
with aspirin, clopidogrel, and a GP IIb/IIIa
inhibitor.
There appears to be No Role for
Pretreatment Thrombolysis before planned
primary PCI (Facilitated PCI).

27. Recommended for:
Any patient with an Acute Coronary Syndrome and:
• ST elevation in at least two contiguous or adjacent leads,
• New or presumably new LBBB, or
• A true posterior MI.
Who presents within 12 hours of symptom onset,
• Has no contraindications for thrombolysis, and
• Presents to a facility without the capability for
expert, prompt intervention with primary PCI within 90
minutes of first medical contact.
(Antman et al., 2004; Menon et al., 2004)

28. Indicated also for:
Patients who present to a facility in which the
relative delay necessary to perform primary PCI (the
expected Door-to-Balloon time minus the expected
door-to-needle time) is greater than one hour.
The survival benefit is greatest when thrombolytic
agents are administered within the first four hours after
the onset of symptoms, particularly within the first 70
minutes.

29. 1) The benefit of thrombolysis is greatest when
therapy is given within the First Four Hours
after the onset of symptoms, particularly within the
first 70 minutes as the resistance of cross-linked
fibrin is time-dependent
(Boersma et al., 1996; Weaver et al., 1993)

30. 2) Although patency is restored in up to 87
percent of infarct-related arteries, normalization
of blood flow (as assessed by the TIMI flow
grade) occurs in only 50 to 60 percent.
(The GUSTO Investigators et al., 1993; Chesebro et al., 1987)

31. 3) After apparently successful thrombolysis, Early
Recurrence of Ischemia or ST segment shifts
(Threatened Reocclusion) have been observed in
20 to 30 percent of patients, with frank Thrombotic
Coronary Reocclusion in 5 to 15 percent, and
reinfarction in 3 to 5 percent.
(Gibson et al., 2003)

32. 4) Major Hemorrhagic Complications occur in 2 to 3
percent. The most serious is intracerebral
hemorrhage, which occurs in:
• As many as 1 percent overall,
• 1.4 percent of the elderly, and
• Over 4 percent in patients with multiple risk factors.
(Brass et al., 2000)

33. 5) As many as 20 to 30 percent of patients
presenting with an acute STEMI, particularly the
elderly, are not candidates for thrombolytic
therapy because of contraindications such as
active internal bleeding, a recent stroke, or
hypertension.
(Cannon et al., 2002)

34. 6) Efficacy of Thrombolytic Therapy has not been
demonstrated in patients in cardiogenic shock
(unless coronary perfusion pressure is increased
with an IABP) or those with prior coronary artery
bypass surgery.

35. Recovery of LV function decreases with later
PCI, but late PCI may still be beneficial at a time
when thrombolytic therapy is no longer effective.
This is an important issue, since registry data
suggest that 9 to 31 percent of patients with an STEMI
present more than 12 hours after the onset of
symptoms.
(Schomig et al., 2003)

36. Possible mechanisms for benefit:
1) Residual antegrade or collateral blood flow, which was
present in 73 percent of patients in the BRAVE-2 trial.
The low rate of persistent flow may maintain myocardial
viability and therefore infarct size until blood flow is
restored by late PCI.
2) Prevention of ventricular remodeling, also may be
involved.
3) A potential benefit of late primary PCI is a reduction in the
risk of free wall rupture.
(Gibbons et al., 2005)

37. I) Initial Assessment.
II) Initial therapy.
III) Reperfusion therapy.
IV) Anticoagulation.
V) Arrhythmia management.
VI) Further medical therapy.
VII) Angiography after thrombolysis.
VIII) Managing recurrent chest pain.

38. Intravenous Unfractionated Heparin
In the following patients:
• Those with an STEMI undergoing PCI or surgical
revascularization.
• Those treated with thrombolytic therapy with
alteplase, Release, or Tenecteplase.
• Patients who receive No Reperfusion Therapy.
(The ACC/AHA and ACCP guidelines)
(Antman et al., 2004; Popma et al., 2004)

39. Low Molecular Weight Heparin
• A class IIb recommendation: In patients with
STEMI treated with thrombolytic therapy (usefulness
or effectiveness is not well established).
• It may be reasonable to use LMWH in patients who
do not receive reperfusion therapy.
• LMWH should be used only in patients under 75
yeas of age who are without significant renal
dysfunction.
(The ACC/AHA , 2004)

40. Bivalirudin
Bivalirudin is an acceptable alternative to heparin
plus GP IIb/IIIa inhibitor in patients undergoing
primary PCI (Initial bolus of 0.75 mg/kg IV
followed by IV infusion of 1.75 mg/kg per hour;
can be discontinued after PCI).

41. Enoxaparin
Enoxaparin for patients not managed with PCI
and <75 years give 30 mg IV bolus followed
immediately by 1 mg/kg subcutaneously every 12
hours.
In patients ≥75 years of age, do not use an initial
IV bolus. Initiate dosing with 0.75 mg/kg
subcutaneous every 12 hours (maximum 75 mg
for the first two doses only).

42. Give antiplatelet therapy (in addition to aspirin)
to all patients:
1. Patients treated with fibrinolytic therapy: Give
clopidogrel loading dose 300 mg if age less than
75 years; if age 75 years or older, give loading
dose of 75 mg.
2. Patients treated with no reperfusion therapy:
Give ticagrelor loading dose 180 mg.

43. 3. Patients treated with primary percutaneous
coronary intervention: Give ticagrelor loading
dose of 180 mg or prasugrel loading dose of 60 mg
(if no contraindications: prior stroke or TIA, or
relative contraindications for prasugrel such as
those age 75 years or older, weight less than 60
kg). For patients at high risk of
bleeding, clopidogrel 300 to 600 mg (600 mg
preferred) is preferred to ticagrelor or praugrel.

44. Warfarin
Indications include:
• Left Ventricular Thrombus Or Aneurysm.
• Left Ventricular Ejection Fraction below 30 percent
with or without heart failure.
• A history of a thromboembolism.
• Chronic Atrial Fibrillation, in which warfarin therapy
is continued for an indefinite period of time.

45. I) Initial Assessment.
II) Initial therapy.
III) Reperfusion therapy.
IV) Anticoagulation.
V) Arrhythmia management.
VI) Further medical therapy.
VII) Angiography after thrombolysis.
VIII) Managing recurrent chest pain.

46. Prophylactic IV or ion Lidocaine to prevent
VT/VF in the acute MI patient is not recommended.
Recommended prophylactic measures include:
• Early administration of an intravenous Beta Blocker
and
• Correction of Hypokalemia and Hypomagnesemia.

47. I) Initial Assessment.
II) Initial therapy.
III) Reperfusion therapy.
IV) Anticoagulation.
V) Arrhythmia management.
VI) Further medical therapy.
VII) Angiography after thrombolysis.
VIII) Managing recurrent chest pain.

48. a) Oral Beta Blockers:
An oral Cardioselective Beta Blocker, such as:
• Metoprolol (25 to 50 mg BID with the short-
acting preparation) or
• Atenolol (50 to 100 mg daily),
should be continued or begun if the patient has not
received early intravenous therapy.

49. b) Nitrates:
• Should be given for 24 to 48 hours in patients with:
• Recurrent ischemia,
• Hypertension, or
• Heart failure.
• Long-term Nitrate Therapy is useful for the
treatment of Recurrent ischemia or Heart Failure.

50. c) ACE inhibitors:
A class I recommendation is given to the administration
of oral ACE inhibitors within the first 24 hours of MI onset
in patients with the following characteristics.
• ST elevation in two or more anterior precordial leads
(anterior STEMI)
• Clinical heart failure or pulmonary congestion
• Left ventricular ejection fraction less than 40 percent
(The ACC/AHA guidelines)
(Antman et al., 2004)

51. Recommendation:
An ACE inhibitor should be given to all patients with
an STEMI without a contraindication. Treatment
should be begun within the first 24 hours, since
there is appreciable benefit in high-risk patients who
cannot always be accurately identified in the first day.
(Antman et al., 2004)

52. However,
• Caution is necessary to avoid causing hypotension
in the first few hours after the infarction.
• Concern about concurrent aspirin therapy
attenuating the effect of an ACE inhibitor appears
largely unwarranted.
(Latini et al., 2000)

53. d) Angiotensin II Receptor Blockers:
The role for an Angiotensin II Receptor Blocker (ARB) in
patients with an STEMI is more limited.
Class I Recommendation:
In patients with an STEMI who are intolerant of ACE
inhibitors and who have clinical or radiological signs of
heart failure or a left ventricular ejection fraction less than
40 percent.
(The 2004 ACC/AHA guidelines)
(Antman et al., 2004)

54. e) Statin Therapy:
Should be initiated prior to hospital discharge in
all patients with an STEMI (Atorvastatin 80
mg/day, which was used in the PROVE IT-TIMI 22 and
MIRACL trials).
(Antman et al., 2004)
(Cannon et al., 2004)
(Schwartz et al., 2001)

55. f) Calcium Channel Blockers:
• Primarily serve as adjunctive therapy in patients with
ongoing or recurrent symptoms of ischemia despite
optimal therapy with beta blockers (with or without
nitrates),
• In patients who are unable to tolerate adequate
doses of one or both of these agents, or
• In patients with rapid AF when beta blockers are
contraindicated.

56. I) Initial Assessment.
II) Initial therapy.
III) Reperfusion therapy.
IV) Anticoagulation.
V) Arrhythmia management.
VI) Further medical therapy.
VII) Angiography after thrombolysis.
VIII) Managing recurrent chest pain.

57. Coronary angiography and, if appropriate, PCI after
thrombolysis in patients with:
• Recurrent MI,
• Moderate or severe spontaneous or provocable
myocardial ischemia during recovery, or
• Cardiogenic Shock or Hemodynamic Instability.
(A class I recommendation)
The 2004 ACC/AHA guidelines)

58. I) Initial Assessment.
II) Initial therapy.
III) Reperfusion therapy.
IV) Anticoagulation.
V) Arrhythmia management.
VI) Further medical therapy.
VII) Angiography after thrombolysis.
VIII) Managing recurrent chest pain.

59. Typically caused by either:
• Recurrent Ischemia And Reinfarction Or
• Infarction Pericarditis.
Recurrent chest pain within the first 12 hours of
onset of MI is considered to be related to the original
infarct and not evidence of reinfarction.
Pericarditis is probably not responsible for
significant chest discomfort in the first 24 hours.

60. Among patients with an STEMI who have undergone
apparently successful thrombolysis:
• Early recurrence of ischemia (Threatened Reocclusion)
has been observed in 20 to 30 percent of patients,
(Armstrong et al., 1998; Langer et al., 1998)
• Thrombotic Coronary Reocclusion in 5 to 15 percent, and
(Topol et al., 1987; Ohman et al., 1990; The GUSTO
Angiographic Investigators. 1993)
• Reinfarction in 3 to 5 percent.
(Gibson et al., 2003; Donges et al., 2001;
Hudson et al., 2001; Barbash et al.,m 2001)

61. Therapeutic Strategy
1. Escalation of Therapy: with beta blockers and nitrates to
decrease myocardial oxygen demand and reduce ischemia.
2. Intravenous Anticoagulation: should be initiated if it is not
already being administered.
3. Insertion Of An Intraaortic Balloon Pump should also be
considered for patients with:
• Hemodynamic instability,
• Poor LV function, or
• A large area of myocardium at risk.
(Antman et al., 2004)

62. Management Strategy:
4. PCI is the treatment of choice for patients with recurrent
ischemia or emergent CABG for reinfarction or
threatened reinfarction in the following settings, provided
that coronary anatomy is suitable:
• When there is objective evidence of recurrent MI.
• For moderate or severe spontaneous or provocable
ischemia.
• For cardiogenic shock or hemodynamic instability.
(The ACC/AHA guidelines a class I recommendation)
(Antman et al., 2004)

63. Management Strategy:
5. Patients with recurrent ST elevation can also be treated or
retreated with Thrombolytic Therapy.
However, an invasive strategy of angiography and
revascularization is usually preferred.
Patients should not be Retreated with Streptokinase.
(Antman et al., 2004; Barbash et al., 2001)

64. 1. Heart Failure and Cardiogenic Shock:
 Class III patients should be considered for
hemodynamic monitoring if they do not respond
promptly to medical therapy.
 Killip class IV patients generally require invasive
monitoring with pulmonary artery catheterization and
arterial blood pressure monitoring.

65. Heart Failure and Cardiogenic Shock:
Invasive hemodynamic monitoring may also be
warranted for patients with suspected mechanical
complications of MI resulting in shock, such as:
 Papillary muscle rupture or Dysfunction,
 Ventricular septal defect, or
 Cardiac tamponade.

66. Killip-Kimball Hemodynamic Subsets
Class Description
I No dyspnea; physical examination results are normal
II No dyspnea; bibasilar crackles or S3 on examination
Dyspnea present; bibasilar crackles or S3 on
III
examination; no hypotension
IV Cardiogenic shock

67. Pharmacologic Treatment:
Should be tailored to the patient's clinical and hemodynamic
state.
Patients with:
 Systolic arterial pressure >100 mmHg,
 Pulmonary artery occlusion pressure >15 mm Hg, and
 Cardiac index <2.5 L/min/mz.
Should be treated initially with a vasodilator, either
intravenous nitroglycerin or intravenous nitroprusside.

68. Inotropic support:
If arterial pressure decreases or the increase in
cardiac output is inadequate, inotropic support with
dobutamine should be initiated at 1 to 2 pg/kg/min and
titrated to 5_15 pg/kg/min. Milrinone is an alternative
inotropic agent.
Loop diuretics, such as furosemide (20-40 mg
intravenously or orally every 2-4 hours), should be used to
reduce pulmonary congestion. Diuretics should be used
with caution in hypotensive patients.

69.  Systolic arterial pressure <90 mm Hg,
 Pulmonary arterial occlusion pressure >15 mm Hg, and
 Cardiac index <2.5 L/min/m2.
 These patients should be treated as soon as possible
with Intra-aortic Balloon Counterpulsation (IABC).

70. Severely hypotensive patients (systolic arterial
pressure <70 mmHg) should be treated with
norepinephrine to rapidly raise the systolic arterial
pressure. If the systolic arterial pressure is 70 to 90 mmHg
with signs of shock, dopamine may be considered initially.
Once the systolic blood pressure has stabilized to at
least 90 mm Hg, dobutamine can be added to further
increase cardiac output and reduce the dosage of
vasopressor.

71. Patients with STEMI who develop shock within 36
hours of MI:
 Benefit from Early Invasive Reperfusion performed
within 18 hours of onset of shock.
 In patients with 1- or 2-vessel disease, PCI is preferred.
 Patients who remain symptomatic and have 3-vessel
disease or significant left main coronary artery disease
should undergo urgent coronary bypass surgery.

72.  Volume Expansion until the blood pressure is
stabilized, pulmonary arterial occlusion pressure
is >20 mmHg, or right atrial pressure is >20
mmHg.
 Associated Bradycardia or high-degree heart
block may require chemical or electrical
intervention.

73.  Agents such as nitrates and diuretics that reduce
preload should be avoided.
 If volume expansion is inadequate to stabilize a
patient, dobutamine can be administered.
 lntra-aortic balloon counterpulsation should - be
considered for refractory hypotension.

74.  Occurs in < 20% of patients treated with thrombolytic
therapy.
 Patients treated with primary PCI have a lower
incidence of recurrent ischemia.
 Reinfarction may present special diagnostic
difficulties (cardiac troponin levels can be elevated
for 5 to 14 days).
 Pericarditis should also be considered as a potential
cause of recurrent chest pain after an MI.

75.  Medical treatment is similar to management of
unstable angina.
 But also includes cardiac catheterization and
reperfusion,
 Recurrent infarction with ST elevation on ECG can be
treated with repeat thrornbolysis. Streptokinase-
based drugs should not be used a second time
because of the risk of allergic reactions.
 Acute reperfusion with PCI or CABG maybe required
for stabilization.

76. Hemodynamically significant bradycardia or A-
V Block:
Can be initially treated with intravenous
atropine in a dose of 0.5 mg every 3-5 minutes to
a total dose of 3 mg while preparing for
transcutaneous pacing.
Atropine rarely corrects complete heart
block or type II second-degree A-V block.

77. Temporary Transvenous Pacing is indicated for:
 Complete heart block,
 Bilateral Bundle Branch Block,
 New or indeterminate-age Bifascicular Block with first-
degree A-V block,
 Type II second-degree AN block, and
 Symptomatic sinus bradycardia that is unresponsive to
atropine.

78.  Immediate Cardioversion is indicated in unstable
patients.
 Depending upon the specific arrhythmia, intravenous
adenosine, b-blockers, or diltiazem may be effective.
 Ventricular tachycardia and ventricular fibrillation
should be treated according to current ACLS
guidelines.
 After defibrillation, if indicated, amiodarone is the drug
of choice in patients with an MI.

79.  Can occur prior to surgery, intraoperatively, and during
the postoperative period.
 Postoperative MI is the most common, with the peak
incidence on the third postoperative day.
 Perioperative MI is often associated with atypical
presentations and is frequently painless.
 New-onset, or an increase in, Ventricular Arrhythmias
is often the presenting finding, as is postoperative
Pulmonary Edema.

80.  The diagnosis can be confirmed with serial ECG and
cardiac marker determinations.
 Treatment is similar to standard treatment.
 Thrombolytic therapy may be contraindicated
depending on the type of surgery.
 Primary PCI should be considered.
 The mortality for perioperative MI is very high, up to
60% in some studies.

81. 1. The preliminary diagnosis of unstable
angina/non-ST-elevation MI is based on the clinical
symptoms, assessment of risk factors for coronary
artery disease, and ECG interpretation.
2. A 12-lead ECG should be obtained and interpreted
within 10 minutes in patients with possible
myocardial ischemia.
3. Non-enteric-coated aspirin at a dose of 162 to 325
mg should be initially administered (by chewing) as
soon as possible to all patients with suspected or
diagnosed ACS.

82. 4. High-risk patients (continuing
ischemia, elevated troponin levels) with
UA/NSTEMI may be candidates for additional
therapy with (GP) IIb/lIIa inhibitors and an early
invasive strategy.
5. The combination of aspirin and heparin is more
beneficial in ACS than aspirin alone.
6. b-Blockers should be administered to all
patients with ACS unless there are strong
contraindications.

83. 7. A plan for early reperfusion of patients with
STEMI should be developed by healthcare
providers based on resources available in their
facility and community.
8. A goal of 90 minutes or less from hospital
presentation to balloon inflation is optimum for
primary PCI for STEMI.
9. Thrombolytic therapy for reperfusion in SI'EMI
should ideally be initiated within 30 minutes of the
patient's arrival to the hospital.

84. 10. Patients who undergo PCI with angioplasty with or
without stent placement should be treated with a
GP IIb/IIIa inhibitor and an antiplatelet agent
such as clopidogrel.
11. Use of angiotensin-converting enzyme inhibitdrs
decreases mortality in all patients with STEMI.
12. Evidence suggests that patients with STEMI who
develop shock within 36 hours of MI benefit from
early invasive reperfusion performed within 18
hours of onset of shock.

85. Myocardial infarction (MI) with LV failure
remains the most common cause of CS. In
general, CS complicates 8.6% of ST-segment
elevation MIs (STEMI)2 and 2.5% of non–ST
segment elevation MIs.3
(Hasdai et al., 2000)

86. It is increasingly clear that CS represents a wide
clinical spectrum, including preshock (patients at
significant risk of developing CS), mild CS
(responsive to low-dose inotropes/vasopressors),
profound CS (responsive to high-dose inotropes/
vasopressors and IABP, and severe refractory CS
(SRCS; unresponsive to high-dose inotropes/
vasopressors and IABP).

87. The first published clinical trial of IABPs in
patients with CS demonstrated augmentation
of cardiac output by 0.5 L/min7.
(Scheidt et al., 1973)

88. Subsequent data from the Should We
Emergently Revascularize Occluded Coronaries
for Cardiogenic Shock (SHOCK) Trial Registry
demonstrated lower in-hospital mortality in
patients with MI who received IABP in
combination with thrombolytic therapy or early
revascularization with percutaneous transluminal
coronary angioplasty/coronary artery bypass
graft surgery8. (Sanborn et al., 2000)

89. Similarly, in the Global Utilization of
Streptokinase and TPA for Occluded Coronary
Arteries (GUSTO-I) trial, early institution of IABP
and thrombolytic therapy in patients with acute
MI (AMI) complicated by CS was associated with
an increased risk of bleeding and adverse
events but also a trend toward lower 3-day and
1-year all-cause mortality9.
(Anderson et al., 1997)

90. Common Causes of Cardiogenic Shock
MI without mechanical complications
MI with mechanical complications (ventricular
septal rupture or papillary muscle/chordal rupture).
Acute decompensation of chronic heart failure

91. Common Causes of Cardiogenic Shock
Acute myocardities
Postcardiotomy
Takotsubo/stress-induced cardiomyopathy
Peripartum cardiomyopahty

92. Common Causes of Cardiogenic Shock
Refractory arrhythmias
Cardiac tamponade
Massive pulmonary embolism

93. Common Causes of Cardiogenic Shock
Acute rejection after orthotopic heart
transplantation
Hypertrophic cardiomyopathy with severe outflow
obstruction
Aortic dissection complicated by acute severe
aortic insufficiency and/or MI

94. A recent meta-analysis suggested that
although IABPs may have a beneficial effect
on hemodynamic parameters in infarct-
related CS, the existing data to not support a
mortality benefit12.
(Unverzagt et al., 2011)

95. Finally, another recent meta-analysis
evaluating the use of IABPs in patients with
STEMI complicated by CS suggested no
improvement in 30-day survival or LV ejection
fraction and an increased risk of stroke and
bleeding complications13.
(Sjauw et al., 2009)

96. Given the minimal circulatory support
afforded by IABPs, next generation of
external VADs was designed to be surgically
implanted and powerful enough to provide full
circulatory support.

97. Despite advances in surgically implanted
external VAD technology and improvement in
the morbidity and mortality attributable to
these devices, important clinical problem
remain.

98. Including the need for general
anesthesia, systemic inflammation associated
with an open surgical procedure, and the
often prolonged delay associated with
operating room activation.

99. Widely regarded as the first PVAD, the
Hemopump Cardiac Assist System (Johnson
and Johnson Interventional Systems. Rancho
Cordova, CA) was a catheter-mounted, axial
flow device positioned across the aortic valve
and capable of providing up to 3.5 L/min of
short-term (hours to days) cardiac support for
patients with CS25.
(Wampler et al., 1994)

100. The TendemHeart PVAD
(CardiaAssist, Inc, Pittsburgh, PA) is a left
atrial-femoral bypass centrifugal pump
capable of providing up to 3.5 to 4.5 L/min of
cardiac output when inserted percutaneously.

101. Inflow/outflow cannula
configurations for the
TandemHeart and
Impella Recover 2.5
percutaneous
ventricular assist
devices (PVADs)

102. Although ECMO technology was developed
in the 1960s, there has been a recent
resurgence of this technology owing to better
cannulation techniques, smaller
cannulas, improved oxygenator
machines, and device miniaturization.

103. Together, these improvements have resulted
in lightweight, portable, reliable, and rapidly
implantable percutaneous ECMO systems in
2 possible configurations: veno-venous for
pulmonary support and veno-arterial for
cardiac and pulmonary support.

104. The major advantage of these systems over
other modern PVADs is the lack of need for
transseptal puncture or transfer to a cardiac
catheterization laboratory.