Transcript Acute Myocardial Infarction

Acute Myocardial Infarction
By Jonathan Phillips
Definition
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MI is irreversible necrosis of heart muscle secondary to
prolonged ischemia.
Results in imbalance of oxygen supply and demand.
Appearance of cardiac enzymes in the circulation generally
indicates myocardial necrosis.
MI is considered part of a spectrum referred to as ACS which
includes unstable angina and non-Q wave MI.
Majority of ST-segment elevation will develop Q waves.
Those w/o ST elevation will be diagnosed with unstable angina
or NQWMI on the basis of the presence of cardiac enzymes.
Etiology
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Atherosclerosis is the disease primarily
responsible for the majority of ACS cases.
Approximately 90% of MI result from acute
thrombus that obstructs an atherosclerotic
coronary artery.
Plaque rupture is considered to be the major
trigger of coronary thrombosis.
Signs and Symptoms
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Shortness of Breath
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Shortness of breath may be the patient’s anginal
equivalent or symptom of heart failure
Due to elevated end-diastolic pressures
secondary to ischemia, which then lead to
elevated pulmonary pressures
Signs and Symptoms
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Chest Pain
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Usually described as a substernal pressure sensation that
also may be described as squeezing, aching, burner or
even sharp pain
Prolonged chest discomfort lasting longer than 30 minutes
is most compatible with infarction
Radiation to the left arm or neck is common
Sensation is precipitated by exertion and relieved by rest
and nitroglycerin
Chest pain may be associated with nausea, vomiting,
diaphoresis, dyspnea, fatigue, or palpitation
Atypical chest pain is common, especially in patient with
diabetes and the elderly
Signs and Symptoms
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Atypical Presentations
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Common and lead to frequently lead to misdiagnosis
Example: elderly patient may present with altered mental
status
Example: patient may present with abdominal discomfort or
jaw pain as his/her anginal equivalent
Low threshold should be maintained when evaluateing high
and moderate risk patients, as their anginal equivalents may
mimic other presentations
Risk Factors
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Nonmodifiable
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Age
Sex
Family history of CAD
Modifiable
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Smoking and other tobacco use
Diabetes mellitus
HTN
Dyslipidemia
Obesity
Risk Factors
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New and other risk factors
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Elevated homocysteine levels
Male pattern baldness
Sedentary lifestyle and/or lack of exercise
Psychosocial stress
Presence of PVD
Poor oral hygiene
Risk Factors
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Nonatherosclerotic causes
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Vasculitis
Coronary emboli
Congenital coronary anomalies
Coronary trauma
Coronary spasm
Drug use (cocaine)
Heavy exertion, fever, hyperthyroidism
Hypoxemia of severe anemia
Differentials
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Anxiety disorders
Aortic dissection
Aortic stenosis
Cholectystitis
Esophageal spasm
Esophagitis
Acute gastritis
GERD
Myocarditis
Pneumothorax
PE
Criteria for MI Diagnosis
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EKG Changes
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ST segment elevation > 1 mm in 2 or more
contiguous precordial or or limb leads
New (or presumed new) LBBB
ST segment depression with prominent R waves
in leads V1 and V2, if thought to represent a
posterior wall infarction rather than unstable
angina
Criteria for MI Diagnosis
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Lab Studies
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Troponins
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Considered criterion standard for diagnosing MI
Serum levels increase within 3-12 hours from the onset
of chest pain, peak at 24-48 hours and return to to
baseline over 5-14 days
Creatine kinase
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CK-MB levels increase within 3-12 hours at onset of
chest pain and return to baseline withing 48-72 hours
Criteria for MI Diagnosis
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Labs Studies (cont.)
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Myoglobin
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Highly sensitive but not very specific. May be useful
along with other studies in early detection of MI
Imaging Studies
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CXR: chest film used to assess patient’s heart
size, CHF and pulmonary edema
Criteria for MI Diagnosis
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Imaging Studies (cont.)
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Echo: can define an extended infarction and
assess overall LV and RV function. Can detect
such complications as acute MR, LV rupture or
pericardial effusion
Myocardial perfusion: obtain prior to discharge to
assess extent of ischemia if the patient has not
undergone a cardiac cath
Criteria for MI Diagnosis
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Imaging Studies
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Cardiac angiography: cardiac cath defines
patient’s coronary anatomy and the extend of
vessel disease. Patient’s with cardiogenic shock,
intractable angina despite medications or severe
congestion should undergo cardiac cath
immediately
Treatment
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Goal: restoration of the balance between the
O2 supply and demand to prevent further
ischemia; pain relief; and prevention,
treatment of other complications that arise
Treatment
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Bedrest
NPO until stable
ASA
IV Heparin
Warfarin
Beta blockade (avoid agents known to cause reflux
tachycardia)
Digoxin-maybe of value for tachycardia associated
with hypotension or CHF
Analgesics
Treatment
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ACE inhibitor
Supplemental O2
Relieve pulmonary vascular congestion
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Acute revascularization
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Diuretics, IV NTG, MSO4
Thrombolytic- standard of care
Mechanical revascularization- cath, CABG
Intra-aortic balloon pump
Treatment
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Medications to avoid:
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CCB
Lidocaine
IV magnesium
Treatment
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Thrombolytic therapy
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Criteria for use:
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< 6 hours most beneficial
6 to 12 hours less beneficial but still worthwhile
> 12 hours: little apparent benefit unless ongoing chest
discomfort or a “stuttering” course
Treatment
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Thrombolytic therapy agents:
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SK (streptokinase) and APSAC (anistreplase)
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t-PA (alteplase, tissue plasminogen activator
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Double bolus, 30 minutes apart)
TNK-tPA (tenecteplase)
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IV bolus and double infusion (accelerated dose)
r-PA (reteplase)
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IV infusion (SK), Single bolus (APSAC)
Singe bolus (over 5 to 10 seconds)
n-PA (lanoteplase)
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Single bolus
Treatment
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Thrombolytic therapy (t-PA)
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Tissue plasminogen activator is superior to
streptokinase in achieving a higher rate of
coronary artery patency
Recent trials show an even greater patency rate if
a llb/llla receptor antagonist (abciximab) is
combined with a half dose of thrombolytic agent
as initial reperfusion strategy
Treatment
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Aspirin
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Shown to decrease mortality and re-infarction rates after MI
Clopidogrel may be used as alternative in cases of aspirin
resistance or allergy
Platelet glycoprotein, ASA, UFH to patients with continuing
ischemia and to whom PCI is planned
Abciximab can be used 12-24 hours in patient with unstable
angina or NSTMI in whom PCI planned within next 24
hours.
Treatment
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Beta-blockers
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Reduce rates of reinfarction and recurrent
ischemia if administered within 12 hours after MI
Administer routinely to all patients with MI unless
contraindication is present
Treatment
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Heparin
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Established as adjunctive agent in patients
receiving t-PA but not with streptokinase
Indicated in patients undergoing primary
angioplasty
LMWHs have been shown superior to UFHs in
patients with unstable angina or NQWMI
Treatment
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Nitrates
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No apparent impact on mortality rate
Provides symptomatic relief and reload reduction
Administer within first 48 hours, unless
contraindicated (ie. RV infarction)
Treatment
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ACE Inhibitors
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Reduce mortality rates after MI
Administer as soon as possible if patient has no
contraindications
Greatest benefit in patients with ventricular
dysfuction
Continue indefinately after MI
Surgical Care
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PTCA
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Provides greater coronary patency (>96%
thrombolysis in MI (TIMI) 3 flow) and lower risk of
bleeding
Studies show that primary PTCA has a mortality
benefit over thrombolytics
Stenting and adjunctive llb/llla therapy are
improving the results of primary PTCA
Surgical Care
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Cardiac Cath and Angioplasty
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For patients who don’t fit criteria for thrombolytic
therapy or have persistent ischemia
Treatment of choice for patients with cardiogenic
shock, patients whom thrombolysis failed and
those with high rise of bleeding or
contraindications to thrombolytic therapy
Surgical Care
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CABG
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For patients where angioplasty fails
For patients who develop mechanical
complication such as a VSD, LV rupture or
papillary muscle rupture
Concerns
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Right Ventricular Infarction
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1/3 of patients with inferior Mi develop RV infarction
Right-sided ECG with greater than 1mm ST elevation in
V3R or V4R leads describes an RV infarction
ECHO may be helpful in diagnosis
PE shows inc.in JVD, right-sided S3, Kussmaul sign or
hypotension
Avoid nitrates or any medications that lower the reload
Pulmonary artery cath can be helpful in guiding therapy
Questions
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What is the most common cause of MI?
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b.
c.
d.
Hyperlipidemia
Acute thrombus that obstructs an atherosclerotic
coronary artery
Hypertension
Plaque rupture
Answer
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What is the most common cause of MI?
a.
b.
c.
d.
Hyperlipidemia
Acute thrombus that obstructs an atherosclerotic
coronary artery
Hypertension
Plaque rupture
Question
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What is the proven therapy shown to reduce
mortality in acute MI?
a.
b.
c.
d.
Aspirin
Beta-blockers
ACE inhibitors
Thrombolytics
Answer
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What is the proven therapy shown to reduce
mortality in acute MI?
a.
b.
c.
d.
Aspirin
Beta-blockers
ACE inhibitors
Thrombolytics
Question
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What is the most specific marker for the
heart which goes up in 6 hours and peaks
at 24 hours.
a.
b.
c.
d.
Myoglobin
CPK
LDH
Troponin I
Answer
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What is the most specific marker for the
heart which goes up in 6 hours and peaks
at 24 hours.
a.
b.
c.
d.
Myoglobin
CPK
LDH
Troponin I