dr_hani
09-18-2002, 11:42 PM
Background: Acute myocardial infarction (AMI) is the rapid development of myocardial necrosis caused by a critical imbalance between the oxygen supply and demand of the myocardium. This usually results from plaque rupture with thrombus formation in a coronary vessel, resulting in an acute reduction of blood supply to a portion of the myocardium.
Pathophysiology: The most common cause of AMI is narrowing of the epicardial blood vessels due to atheromatous plaques. Plaque rupture with subsequent exposure of the basement membrane results in platelet aggregation, thrombus formation, fibrin accumulation, hemorrhage into the plaque, and varying degrees of vasospasm. This can result in partial or complete occlusion of the vessel and subsequent myocardial ischemia. Total occlusion of the vessel for more than 4-6 hours results in irreversible myocardial necrosis, but reperfusion within this period can salvage the myocardium and reduce morbidity and mortality.
Sex:
Male predilection exists in persons aged 40-70 years.
In persons older than 70 years, no sex predilection exists.
Age:
AMI occurs most frequently in persons older than 45 years.
Certain subpopulations younger than 45 years are at risk, particularly cocaine users, insulin-dependent diabetics, patients with hypercholesterolemia, and those with a positive family history for early coronary disease. A positive family history includes any first-degree male relative aged 45 years or younger or any first-degree female relative aged 55 years or younger who experienced a myocardial infarction.
In younger patients, the diagnosis may be hampered if the physician does not maintain a high index of suspicion.
History:
Chest pain, usually across the anterior precordium, is described as tightness, pressure, or squeezing.
Pain may radiate to the jaw, neck, arms, back, and epigastrium. The left arm is affected more frequently than the right arm.
Dyspnea, which may accompany chest pain or occur as an isolated complaint, indicates poor ventricular compliance in the setting of acute ischemia.
Nausea and/or abdominal pain often are present in infarcts involving the inferior wall.
Anxiety
Lightheadedness and syncope
Cough
Nausea and vomiting
Diaphoresis
Wheezing
Elderly patients and those with diabetes may have particularly subtle presentations and may complain of fatigue, syncope, or weakness.
Physical:
Frequently, physical examination findings are normal.
Patients with ongoing symptoms usually will lie quietly in bed and appear pale and diaphoretic.
Hypertension may precipitate AMI, or it may reflect elevated catecholamines due to anxiety, pain, or exogenous sympathomimetics.
Hypotension indicates ventricular dysfunction due to ischemia. It usually indicates a large infarct and may be observed with a right ventricular infarct.
Acute valvular dysfunction may be present.
This dysfunction usually involves the papillary muscle.
Mitral regurgitation due to papillary muscle ischemia or necrosis may be present.
Congestive heart failure (CHF) may occur.
Neck vein distention
Third heart sound (S3)
Rales on pulmonary examination
New or worsening mitral regurgitant murmur may be noted.
A fourth heart sound is a common finding in patients with poor ventricular compliance that is due to a preexisting heart disease or hypertension.
Dysrhythmias may be present.
With heart block or right ventricular failure, cannon jugular venous a waves may be noted.
Causes:
The predominant cause is a rupture of an atherosclerotic plaque with subsequent spasm and clot formation.
Ventricular hypertrophy (eg, left ventricular hypertrophy [LVH], idiopathic hypertrophic subaortic stenosis [IHSS], underlying valve disease)
Hypoxia due to carbon monoxide poisoning or acute pulmonary disorders (Infarcts in this setting usually occur when myocardial demands dramatically are increased relative to blood supply.)
Emboli to coronary arteries, which may be due to cholesterol or infectious causes
Coronary artery vasospasm
Arteritis
Coronary anomalies, including aneurysms of the coronary arteries
Cocaine, amphetamines, and ephedrine
Increase afterload or inotropic effects, which increase myocardial demand
Primary vasospasm of the coronary artery
Risk factors for atherosclerotic plaque formation include the following:
Age
Being male and younger than 70 years
Smoking
Hypercholesterolemia and hypertriglyceridemia
Diabetes mellitus
Poorly controlled hypertension
Type A personality
Family history
Sedentary lifestyle
Lab Studies:
-Creatine kinase–MB (CK-MB)
This is the criterion standard for detection of myocardial necrosis.
Levels begin to rise within 4 hours after injury, peak at 18-24 hours, and subside over 3-4 days.
Upper limit of reference range values for CK-MB is 3-6% of total CK.
A level within the reference range in the ED does not exclude the possibility of myocardial necrosis.
A single assay in the ED has a sensitivity of 34%.
Serial sampling over periods of 6-9 hours will increase the sensitivity to nearly 90%.
Over 24 hours, the sensitivity is near 100%.
-Myoglobin
This is a very sensitive early marker of acute myocardial necrosis, but it is not specific for myocardial cell necrosis.
The myoglobin/carbonic anhydrase III ratio increases specificity. Myocardial cells do not release carbonic anhydrase.
-Troponin I
This is a contractile protein that normally is not found in serum. It is released only when myonecrosis occurs.
For early detection of myocardial necrosis, sensitivity of this study is superior to that of the CK-MB. Troponin I is detectable in serum 3-6 hours after an AMI, and its level remains elevated for 14 days.
Troponin T has similar release kinetics and specificity for myocardial necrosis, but it is slightly less sensitive than troponin I within the first 6 hours.
-Complete blood count
Leukocytosis may be observed within several hours after an AMI. It peaks in 2-4 days and returns levels within the reference range within 1 week.
CBC may be useful if anemia is suspected as a precipitant. Transfusion with packed red blood cells and supplemental oxygen may be the only treatment modalities in cases where anemia is considered the only precipitant.
Erythrocyte sedimentation rate (ESR) rises above reference range values within 3 days and may remain elevated for several weeks.
The serum lactase dehydrogenase (LDH) level rises above the reference range within 24 hours of an AMI, reaches a peak within 3-6 days, and returns to the baseline within 8-12 days.
Imaging Studies:
-Chest x-ray
CXR may provide clues to an alternative or complicating diagnosis (eg, aortic dissection, pneumothorax).
CXR also reveals complications of AMI, particularly pulmonary edema, and CHF.
-Echocardiography
Use 2-dimensional and M-mode echocardiography when evaluating wall motion abnormalities and overall ventricular function.
This also can identify complications of AMI (eg, valvular insufficiency, ventricular dysfunction, pericardial effusion).
-Technetium-99m sestamibi scan
Technetium-99m is a radioisotope that is taken up by the myocardium in proportion to the blood flow and is redistributed minimally after injection. This allows for time delay between injection and imaging.
It has potential use in identifying infarct in patients with atypical presentations or uninterpretable ECGs.
Normal scan findings are associated with an extremely low risk of subsequent cardiac events.
-Thallium scanning: Thallium accumulates in the viable myocardium.
Prehospital Care:
All patients being transported for chest pain should be managed as if the pain were ischemic in origin unless clear evidence to the contrary exists.
If available, an ALS unit should transport patients with hemodynamic instability or respiratory difficulty.
Prehospital notification by Emergency Medical Services (EMS) personnel should alert ED staff to the possibility of an AMI. EMS personnel should receive online medical advice for a patient with high-risk presentation.
Specific prehospital care includes the following:
IV access, supplemental oxygen, pulse oximetry
Immediate administration of aspirin en route
Nitroglycerin for active chest pain, given sublingually (SL) or by spray
Prehospital thrombolysis allows eligible patients to receive thrombolysis 30-60 minutes sooner than if treatment was given in the ED; however, prehospital thrombolysis is still under investigation (Thrombolysis in Myocardial Infarction [TIMI] and other trials).
Telemetry and prehospital ECG, if available
Emergency Department Care:
Delays in administration of thrombolysis often occur because of delay in obtaining an ECG, interpretation, lack of immediate availability of thrombolytic agents, and outdated protocols requiring cardiology consultation before thrombolytic treatment.
An ECG should be performed as soon as possible after the patient presents to the ED. The ECG should be hand-delivered to an experienced physician.
All patients should be placed on telemetry.
Two large-bore IVs should be inserted if the EMS has not already completed this.
Pulse oximetry should be performed, and appropriate supplemental oxygen should be given (maintain oxygen saturation >90%).
A CXR should be performed soon after arrival to screen for alternative causes of chest pain and identify possible contraindications to thrombolysis (eg, aortic dissection).
Pharmacologic intervention is likely to include the following:
Immediate administration of aspirin if not taken by the patient or administered by EMS before arrival
beta-blockade for rate control and decrease of myocardial oxygen demand if not contraindicated
Additional ED intervention may include the following:
Morphine sulphate
Anxiolytic
Heparin
Thrombolysis
Platelet aggregation (IIb/IIIa receptor) inhibitor
ACE inhibitor
Antiarrhythmic agent
Pathophysiology: The most common cause of AMI is narrowing of the epicardial blood vessels due to atheromatous plaques. Plaque rupture with subsequent exposure of the basement membrane results in platelet aggregation, thrombus formation, fibrin accumulation, hemorrhage into the plaque, and varying degrees of vasospasm. This can result in partial or complete occlusion of the vessel and subsequent myocardial ischemia. Total occlusion of the vessel for more than 4-6 hours results in irreversible myocardial necrosis, but reperfusion within this period can salvage the myocardium and reduce morbidity and mortality.
Sex:
Male predilection exists in persons aged 40-70 years.
In persons older than 70 years, no sex predilection exists.
Age:
AMI occurs most frequently in persons older than 45 years.
Certain subpopulations younger than 45 years are at risk, particularly cocaine users, insulin-dependent diabetics, patients with hypercholesterolemia, and those with a positive family history for early coronary disease. A positive family history includes any first-degree male relative aged 45 years or younger or any first-degree female relative aged 55 years or younger who experienced a myocardial infarction.
In younger patients, the diagnosis may be hampered if the physician does not maintain a high index of suspicion.
History:
Chest pain, usually across the anterior precordium, is described as tightness, pressure, or squeezing.
Pain may radiate to the jaw, neck, arms, back, and epigastrium. The left arm is affected more frequently than the right arm.
Dyspnea, which may accompany chest pain or occur as an isolated complaint, indicates poor ventricular compliance in the setting of acute ischemia.
Nausea and/or abdominal pain often are present in infarcts involving the inferior wall.
Anxiety
Lightheadedness and syncope
Cough
Nausea and vomiting
Diaphoresis
Wheezing
Elderly patients and those with diabetes may have particularly subtle presentations and may complain of fatigue, syncope, or weakness.
Physical:
Frequently, physical examination findings are normal.
Patients with ongoing symptoms usually will lie quietly in bed and appear pale and diaphoretic.
Hypertension may precipitate AMI, or it may reflect elevated catecholamines due to anxiety, pain, or exogenous sympathomimetics.
Hypotension indicates ventricular dysfunction due to ischemia. It usually indicates a large infarct and may be observed with a right ventricular infarct.
Acute valvular dysfunction may be present.
This dysfunction usually involves the papillary muscle.
Mitral regurgitation due to papillary muscle ischemia or necrosis may be present.
Congestive heart failure (CHF) may occur.
Neck vein distention
Third heart sound (S3)
Rales on pulmonary examination
New or worsening mitral regurgitant murmur may be noted.
A fourth heart sound is a common finding in patients with poor ventricular compliance that is due to a preexisting heart disease or hypertension.
Dysrhythmias may be present.
With heart block or right ventricular failure, cannon jugular venous a waves may be noted.
Causes:
The predominant cause is a rupture of an atherosclerotic plaque with subsequent spasm and clot formation.
Ventricular hypertrophy (eg, left ventricular hypertrophy [LVH], idiopathic hypertrophic subaortic stenosis [IHSS], underlying valve disease)
Hypoxia due to carbon monoxide poisoning or acute pulmonary disorders (Infarcts in this setting usually occur when myocardial demands dramatically are increased relative to blood supply.)
Emboli to coronary arteries, which may be due to cholesterol or infectious causes
Coronary artery vasospasm
Arteritis
Coronary anomalies, including aneurysms of the coronary arteries
Cocaine, amphetamines, and ephedrine
Increase afterload or inotropic effects, which increase myocardial demand
Primary vasospasm of the coronary artery
Risk factors for atherosclerotic plaque formation include the following:
Age
Being male and younger than 70 years
Smoking
Hypercholesterolemia and hypertriglyceridemia
Diabetes mellitus
Poorly controlled hypertension
Type A personality
Family history
Sedentary lifestyle
Lab Studies:
-Creatine kinase–MB (CK-MB)
This is the criterion standard for detection of myocardial necrosis.
Levels begin to rise within 4 hours after injury, peak at 18-24 hours, and subside over 3-4 days.
Upper limit of reference range values for CK-MB is 3-6% of total CK.
A level within the reference range in the ED does not exclude the possibility of myocardial necrosis.
A single assay in the ED has a sensitivity of 34%.
Serial sampling over periods of 6-9 hours will increase the sensitivity to nearly 90%.
Over 24 hours, the sensitivity is near 100%.
-Myoglobin
This is a very sensitive early marker of acute myocardial necrosis, but it is not specific for myocardial cell necrosis.
The myoglobin/carbonic anhydrase III ratio increases specificity. Myocardial cells do not release carbonic anhydrase.
-Troponin I
This is a contractile protein that normally is not found in serum. It is released only when myonecrosis occurs.
For early detection of myocardial necrosis, sensitivity of this study is superior to that of the CK-MB. Troponin I is detectable in serum 3-6 hours after an AMI, and its level remains elevated for 14 days.
Troponin T has similar release kinetics and specificity for myocardial necrosis, but it is slightly less sensitive than troponin I within the first 6 hours.
-Complete blood count
Leukocytosis may be observed within several hours after an AMI. It peaks in 2-4 days and returns levels within the reference range within 1 week.
CBC may be useful if anemia is suspected as a precipitant. Transfusion with packed red blood cells and supplemental oxygen may be the only treatment modalities in cases where anemia is considered the only precipitant.
Erythrocyte sedimentation rate (ESR) rises above reference range values within 3 days and may remain elevated for several weeks.
The serum lactase dehydrogenase (LDH) level rises above the reference range within 24 hours of an AMI, reaches a peak within 3-6 days, and returns to the baseline within 8-12 days.
Imaging Studies:
-Chest x-ray
CXR may provide clues to an alternative or complicating diagnosis (eg, aortic dissection, pneumothorax).
CXR also reveals complications of AMI, particularly pulmonary edema, and CHF.
-Echocardiography
Use 2-dimensional and M-mode echocardiography when evaluating wall motion abnormalities and overall ventricular function.
This also can identify complications of AMI (eg, valvular insufficiency, ventricular dysfunction, pericardial effusion).
-Technetium-99m sestamibi scan
Technetium-99m is a radioisotope that is taken up by the myocardium in proportion to the blood flow and is redistributed minimally after injection. This allows for time delay between injection and imaging.
It has potential use in identifying infarct in patients with atypical presentations or uninterpretable ECGs.
Normal scan findings are associated with an extremely low risk of subsequent cardiac events.
-Thallium scanning: Thallium accumulates in the viable myocardium.
Prehospital Care:
All patients being transported for chest pain should be managed as if the pain were ischemic in origin unless clear evidence to the contrary exists.
If available, an ALS unit should transport patients with hemodynamic instability or respiratory difficulty.
Prehospital notification by Emergency Medical Services (EMS) personnel should alert ED staff to the possibility of an AMI. EMS personnel should receive online medical advice for a patient with high-risk presentation.
Specific prehospital care includes the following:
IV access, supplemental oxygen, pulse oximetry
Immediate administration of aspirin en route
Nitroglycerin for active chest pain, given sublingually (SL) or by spray
Prehospital thrombolysis allows eligible patients to receive thrombolysis 30-60 minutes sooner than if treatment was given in the ED; however, prehospital thrombolysis is still under investigation (Thrombolysis in Myocardial Infarction [TIMI] and other trials).
Telemetry and prehospital ECG, if available
Emergency Department Care:
Delays in administration of thrombolysis often occur because of delay in obtaining an ECG, interpretation, lack of immediate availability of thrombolytic agents, and outdated protocols requiring cardiology consultation before thrombolytic treatment.
An ECG should be performed as soon as possible after the patient presents to the ED. The ECG should be hand-delivered to an experienced physician.
All patients should be placed on telemetry.
Two large-bore IVs should be inserted if the EMS has not already completed this.
Pulse oximetry should be performed, and appropriate supplemental oxygen should be given (maintain oxygen saturation >90%).
A CXR should be performed soon after arrival to screen for alternative causes of chest pain and identify possible contraindications to thrombolysis (eg, aortic dissection).
Pharmacologic intervention is likely to include the following:
Immediate administration of aspirin if not taken by the patient or administered by EMS before arrival
beta-blockade for rate control and decrease of myocardial oxygen demand if not contraindicated
Additional ED intervention may include the following:
Morphine sulphate
Anxiolytic
Heparin
Thrombolysis
Platelet aggregation (IIb/IIIa receptor) inhibitor
ACE inhibitor
Antiarrhythmic agent