Transcript acute_mi_shock_mar_04

Chest Pain/ MI/Shock
Victor Politi, M.D., FACP
Medical Director SVCMC PA program
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Approximately 1 million hospitalized
patients each year have MI as a
principal diagnosis
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Approximately 200,000 - 300,000
people in US die from MI’s each year
MI Risk Factors
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Smoking
HTN
High fat diet
High LDL
Diabetes
Stress
Inactivity
Male gender
Age/Heredity
– Elevated homocysteine and C-reactive
protein levels
A patient presents with chest
pain
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What do you do?
Stable angina, unstable
angina, ACI, AMI
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An indistinguishable spectrum
– beginning with stable lumen-restricting
coronary artery plaques
– results in plaque fissuring
– initiates platelet adhesion & fibrin plugs
w/overlying but non-occlusive thrombus
– results in plaque disruption, occlusive
thrombus composed of fibrin, platelets &
erythrocytes
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Most heart attacks are caused by the
build up of atherosclerotic plaque inside
the arterial wall - which can trigger the
formation of a thrombus
Frequency of “Silent” AMIs
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Framingham Study: largest long term
prospective study of cardiovascular disease
Cohort of 5,127 participants
708 (13%) suffered AMI
213 (30%) were not recognized during AMI
Only 1/2 demonstrated classic AMI S/Sxs
allowing identification of AMI in retrospect
Classic Presentation
Retrosternal, epigastric chest pain or
tightness
 SOB
 Diaphoresis
 Nausea, vomiting
 Levine’s sign
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Atypical Symptoms of AMI
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Admits chest discomfort- denies pain
A little sweating previously - now gone
Previous indigestion - now ok
May or may not have mild SOB
Can’t describe symptoms - uses vague terms
EKG normal or non-specific changes present
– In fact - an atypical presentation is the most
typical presentation
Symptoms pain
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Chest pain– typically below the sternum
– intense/severe/subtle
– squeezing sensation/heavy pressure
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Angina not relieved by rest or nitroglycerin
Back pain
Abdominal pain
Pain radiating to
– shoulder/arms/chest
– neck/teeth/jaw
– back
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Pain that is prolonged > 20 min
Other Symptoms
Bad Indigestion
 Dyspnea
 Cough
 Syncope
 Nausea or vomiting
 Diaphoresis
 Anxiety
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Physical Exam
Rapid pulse
 BP - varies
 may reveal abnormal chest sounds on
auscultation
 Diaphoresis
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Studies
ECG
 Echocardiography
 Coronary angiography
 Stress test
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– EST
– Nuclear
– Studies which show heart damage or high risk
 Troponin I / troponin T
 CK and CK-MB
 Myoglobin-serum
Additional Lab Tests
CBC
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 Pt/Ptt
 Chest x-ray
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What is first in your work-up?
12 lead ECG
 Is it useful ?
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A “normal” ECG
Studies show that as many as 15% of
ECGs are completely normal and 60%
of ECGs are normal or show nonspecific
changes even in the presence of an
evolving AMI
 When are ECGs useful ?
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Treatment
Continuous ECG
 Continuous BP
 IV - fluids/meds
 oxygen
 Pulse ox
 Blood work
 urinary catheter - to monitor fluid
status
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ASA
Aspirin
40% relative reduction in mortality
 What’s the right dose?
 Probably the single most important
thing we can do
 Irreversible - inhibit platelet aggregation
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Aspirin -Contraindications
ASA Allergy
 GI bleed
 Bleeding disorder
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Nitrates
When should nitrates be given?
 Who should receive nitrates?
 Who should not receive nitrates?
 Dose
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– SL NTG
– Spray
– Paste
– IV
Morphine MSO4
Does morphine reduce pain? Yes
 Does morphine reduce
mortality/morbidity? NO
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Morphine vs NTG
Glycoprotein IIB/IIA Inhibitors
Utilized in ACISs without AMI
 Action is to “de-couple” platelets
 Three FDA-approved
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– Integrillin - eptifibatide
– Aggrestat - tirobifan hydrochloride
– Repro-abciximab
Heparin
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When should heparin be given?
Who should receive heparin?
What is the right way to give heparin?
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Is there a wrong way to give heparin?
Other forms of heparin, anticoagulants?
Therapeutic monitoring
Oral anticoagulation – Warfarin
– Coumadin
Low-molecular weight heparin
Enoxaparin dosed 1mg/kg SQ Q 12 hr
 No PTT monitoring necessary
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– potential of fewer labs drawn, run
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No IV necessary
– fewer IV starts, no pumps, outpatient
treatment
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Fragmin
The ESSENCE Trial
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Efficacy & safety of SQ Enoxaparin in non-Qwave coronary events
Significant relative risk reductions (RRR) &
cost savings compared to unfractionated
heparin
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>15% relative risk reduction in incidence of
death, AMI, recurrent angina & combined triple
endpoints
10% relative risk reduction in CABG
21% relative risk reduction in PTCA
Decreased resource utilization resulting in
cost savings exceeding $1000 per patient
Beta-blocker IVP
When should beta blockers be given?
 Who should receive beta blockers?
 Who should not receive beta blockers?
 What is the right dosing regimen?
 Primary, secondary benefits?
 B1-B2 Blocker
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Ace Inhibitors
Studies show decreased mortality if
given in first few days after AMI
 Benefit due to effects on myocardium
remodeling
 long term benefits show increased EF
and decreased incidence of CHF
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Cholesterol Lowering Agents
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Current thinking; the lower the total
and LDL cholesterol - the better !
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Many types available -currently the
statins seem to show the best reduction
Thrombolysis: Eligibility
Criteria
No age limit
 Clinical
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Chest pain, chest pain-equivalent c/w AMI of <
12 hrs from onset or < 24hrs if “stuttering”
EKG
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1mm or > ST elevation in 2 or + limb leads
2mm or > ST elevation in 2 or + precordial
leads
New onset bundle branch block
Contraindications to
Thrombolytics
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History of CVA/TIA within 6 months
Recent head trauma, known intercranial mass
Surgery, PTCA, severe trauma in past 2 weeks
Recent GI bleed or ulcer
Persistent, uncontrollable SBP >200, DBP>110
Non-compressible venous or arterial puncture
CPR greater than 10 minutes
Aortic dissection Dx=> CT of thorax
Pericarditis
Thrombolytics
TPA
 Retavase
 Streptokinase
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Door -to-Drug Time
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Time is Muscle!
Goal of Treatment
Stabilize patient
 Stop the progression of heart attack 
– prevent further heart damage
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Reduce demands on heart
– so it can heal
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Prevent complications
Other cardiac conditions
Bradycardia
Systolic rate < 60
 Symptomatic
 Atropine
 Isopril
 Pacemaker
 What medications has the patient
taken?
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Atrial Arrythmia
A Fib
 A flutter
 SVT
 PAT
 PAC
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Atrial Flutter
AV Blocks
1st degree AVB
 2nd degree AVB
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– Type 1
– Type 2
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3rd degree AVB
Ventricular Arrythmias
PVC
 V Tach
 V Fib
 Torsades
 Ventricular escape beat
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An 84 year old lady with hypertension-First degree AV block
Cardiogenic Shock
Symptomatic blood pressure <90
systolic
 due to low cardiac output
 Goal of treatment - increase perfusion
to vital organs
 Treatment options include
Dopamine/Dobutamine/Levophed/
balloon pump (aortic counterpulsation)
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Cardiac Tamponade
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Hypotension caused by reduction of
cardiac output secondary to inability of
the ventricle to provide adequate stroke
volume due to fluid in the pericardial
sac
Questions ???