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M. Sherif Mokhtar, MD
     Professor of Cardiology,
Professor of Critical Care Medicine,
         Cairo University
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)
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
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.
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.
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.
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.
• 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.
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).
Acute Triage

B. Evidence   of   Systemic     Hypoperfusion

  (cardiogenic shock complicating acute MI

  requires    aggressive      evaluation   and

  management).
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.
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)
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)
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.
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)
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)
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.
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.
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)
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)
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)
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.
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.
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)
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).
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)
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.
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)
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)
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)
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)
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)
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.
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)
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)
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.
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)
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)
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).
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).
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.
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.
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.
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.
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.
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.
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.
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.
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)
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)
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)
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)
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)
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.
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.
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)
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.
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.
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)
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)
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)
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)
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.
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.
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
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.
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.
 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).
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.
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.
   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.
   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.
   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.
 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.
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.
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.
   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.
 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.
 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.
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.
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.
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.
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.
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)
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).
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)
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)
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)
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
Common Causes of Cardiogenic Shock

Acute myocardities

Postcardiotomy

Takotsubo/stress-induced cardiomyopathy

Peripartum cardiomyopahty
Common Causes of Cardiogenic Shock

Refractory arrhythmias

Cardiac tamponade

Massive pulmonary embolism
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
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)
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)
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.
Despite advances in surgically implanted
external VAD technology and improvement in
the morbidity and mortality attributable to
these devices, important clinical problem
remain.
Including    the     need      for    general
anesthesia, systemic inflammation associated
with an open surgical procedure, and the
often   prolonged   delay    associated   with
operating room activation.
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)
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.
Inflow/outflow cannula
configurations for the
  TandemHeart and
 Impella Recover 2.5
    percutaneous
  ventricular assist
  devices (PVADs)
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.
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.
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.

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Mokhtar overview & acs-2012-final

  • 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)
  • 14.
  • 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.