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Acute Myocardial Infarction
By Jonathan Phillips
Definition
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
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
Shortness of Breath– 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
Chest Pain– 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
Atypical Presentations– 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
Nonmodifiable– Age– Sex– Family history of CAD
Modifiable– Smoking and other tobacco use– Diabetes mellitus– HTN– Dyslipidemia– Obesity
Risk Factors
New and other risk factors– Elevated homocysteine levels– Male pattern baldness– Sedentary lifestyle and/or lack of exercise– Psychosocial stress– Presence of PVD– Poor oral hygiene
Risk Factors
Nonatherosclerotic causes– Vasculitis– Coronary emboli– Congenital coronary anomalies– Coronary trauma– Coronary spasm– Drug use (cocaine)– Heavy exertion, fever, hyperthyroidism– Hypoxemia of severe anemia
Differentials
Anxiety disorders Aortic dissection Aortic stenosis Cholectystitis Esophageal spasm Esophagitis Acute gastritis GERD Myocarditis Pneumothorax PE
Criteria for MI Diagnosis
EKG Changes– 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
Lab Studies– Troponins
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 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
Labs Studies (cont.)– Myoglobin
Highly sensitive but not very specific. May be useful along with other studies in early detection of MI
Imaging Studies– CXR: chest film used to assess patient’s heart
size, CHF and pulmonary edema
Criteria for MI Diagnosis
Imaging Studies (cont.)– 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
Imaging Studies– 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
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
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
ACE inhibitor Supplemental O2 Relieve pulmonary vascular congestion
– Diuretics, IV NTG, MSO4 Acute revascularization
– Thrombolytic- standard of care– Mechanical revascularization- cath, CABG
Intra-aortic balloon pump
Treatment
Medications to avoid:– CCB– Lidocaine– IV magnesium
Treatment
Thrombolytic therapy– Criteria for use:
< 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
Thrombolytic therapy agents:– SK (streptokinase) and APSAC (anistreplase)
IV infusion (SK), Single bolus (APSAC)– t-PA (alteplase, tissue plasminogen activator
IV bolus and double infusion (accelerated dose)– r-PA (reteplase)
Double bolus, 30 minutes apart)– TNK-tPA (tenecteplase)
Singe bolus (over 5 to 10 seconds)– n-PA (lanoteplase)
Single bolus
Treatment
Thrombolytic therapy (t-PA)– 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
Aspirin – 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
Beta-blockers– 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
Heparin– 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
Nitrates– No apparent impact on mortality rate– Provides symptomatic relief and reload reduction– Administer within first 48 hours, unless
contraindicated (ie. RV infarction)
Treatment
ACE Inhibitors– 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
PTCA– 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
Cardiac Cath and Angioplasty– 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
CABG– For patients where angioplasty fails– For patients who develop mechanical
complication such as a VSD, LV rupture or papillary muscle rupture
Concerns
Right Ventricular Infarction– 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
What is the most common cause of MI?a. Hyperlipidemia
b. Acute thrombus that obstructs an atherosclerotic coronary artery
c. Hypertension
d. Plaque rupture
Answer
What is the most common cause of MI?a. Hyperlipidemia
b. Acute thrombus that obstructs an atherosclerotic coronary artery
c. Hypertension
d. Plaque rupture
Question
What is the proven therapy shown to reduce mortality in acute MI?
a. Aspirin
b. Beta-blockers
c. ACE inhibitors
d. Thrombolytics
Answer
What is the proven therapy shown to reduce mortality in acute MI?
a. Aspirin
b. Beta-blockers
c. ACE inhibitors
d. Thrombolytics
Question
What is the most specific marker for the heart which goes up in 6 hours and peaks at 24 hours.
a. Myoglobin
b. CPK
c. LDH
d. Troponin I
Answer
What is the most specific marker for the heart which goes up in 6 hours and peaks at 24 hours.
a. Myoglobin
b. CPK
c. LDH
d. Troponin I
