Acute Myocardial Infarction
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Acute Myocardial Infarction DR.LIU LIXIN
DEFINITION
Acute myocardial infarction (MI) is defined as death or necrosis of myocardial cells. It is a diagnosis at the end of the spectrum of myocardial ischemia or acute coronary syndromes. From an anatomic or morphologic standpoint, the two types of MI are
transmural : STEMI nontransmural:NSTEMI
Fig, 9-2. Epicardial versus subendocardial injury currents
ACS Types
Pathophysiology Mechanisms of Occlusion: Most MIs are caused by a disruption in the vascular endothelium associated with an unstable atherosclerotic plaque that stimulates the formation of an intracoronary thrombus, which results in coronary artery blood flow occlusion. If such an occlusion persists long enough (20 to 40 min), irreversible myocardial cell damage and cell death will occur.
Vulnerable Plaque
Pathogenesis OF AMI
Clinical Manifestation
Premonitory Pain: a recent onset of angina, a worsening angina, or a worsening angina pectoris poorly responsive well to a nitrate. Pain Of Infarction:more severe, long lasting, and relieved little by rest or nitroglycerin.
Clinical Manifestation
Associated Symptom: Nausea and vomiting ,abdominal bloating,cold sweat,SOB Painless infarction: 20% silent or atypical Sudden death & early arrhythmias:ventricular fibrillation
Clinical Manifestation
Arrhythmias : 75~95% of patients develop cardiac arrhythmias . Any type of arrhythmias may be found Cardiac failure :Heart failure occurs in about 32-48% of hospitalized patients with acute MI Cardiogenic shock :A loss of myocardium greater than 40% generally leads to cardiogenic shock
Clinical Manifestation
Signs:HR is usually increased (but inferior MI commonly leads to bradycardia). S1 is low, S4 (atrial gallop) is noted and an S3 (Ventricular gallop) is present when develop LV failure
Laboratory findings
ECG for AMI • • • • •
Q wave duration of more than 0.04 seconds Q wave depth of more than 25% of ensuing r wave ST elevation in leads facing infarct (or depression in opposite leads) Deep T wave inversion overlying and adjacent to infarct Cardiac arrhythmias
Sequence of changes in evolving AMI R
R T
ST
R
P
P
P T
QS
Q
Q
1 minute after onset
ST
P
ST
1 hour or so after onset
P
A few hours after onset
R
ST
T P
T
T
Q
Q
Q
A day or so after onset
Later changes
A few months after AMI
Anterior infarction
Anterior infarction
I II III
Left coronary artery
aVR aVL aVF
V1 V2 V3
V4 V5 V6
Inferior infarction Inferior infarction
I II III
Right coronary artery
aVR aVL aVF
V1 V2 V3
V4 V5 V6
Lateral infarction
Lateral infarction
I II III
Left circumflex coronary artery
aVR aVL aVF
V1 V2 V3
V4 V5 V6
Echocardiography :to estimate ventricular wall motion abnormalities and left ventricular function. Radioisotope studies: Technetium 99m Hemodynamic Measurement:
Diagnosis and Differential Diagnosis
Complications
Dysfunction or rupture of papillary muscle Rupture of the heart Embolism Ventricular aneurysm Postmyocardial infarction syndrome Shoulder-hand syndrome
Treatment
Monitoring: coronary care unit (CCU) Rest and bedside care Oxygen Relief of pain :give morphine sulfate, 3~5mg IV slowly. nitroglycerin can be given sublingually
Drugs
Nitroglycerin Beta block Calcium channel blockers Angiotensin converting enzyme inhibitor (ACEI) :ventricular
remodeling
Anti-platelet agents Aspirin 300mg qd Clopidogrel 75mg qd
Drugs Anti-coagulation agents LMWH (Low-molecular-weight Heparins ) Enoxaparin 1 mg/kg SC q12h Fraxiparine 5000u SC q12h Lipid-lowering drugs:Statin agents Atorvastatin 20mg qn
Thrombolytic therapy
Thrombolytic therapy is indicated for MI and ST segment elevation greater than 0.1 mV in 2 contiguous EKG leads, or new onset of a bundle branch block, who present less than 12 hours but not more than 24 hours after symptom onset. Intravenous streptokinase and recombinant tissue-type plasminogen activator (rt-PA) the "door-to-needle" time is 30 minutes or less
Percutaneous Coronary Intervention(PCI)
Emergency PCI is recommended for patients present within 6h of onset of pain "door-to-balloon" time: 90 minutes PCI provides a definite survival advantage over fibrinolysis for MI patients who are in cardiogenic shock
PCI-6
TIMI grading system:
Grade 0 = complete occlusion of the infarct-related artery. Grade 1 = some penetration of the contrast material beyond the point of obstruction but without perfusion of the distal coronary bed. Grade 2 = perfusion of the entire infarct vessel into the distal bed but with delayed flow compared with a normal artery.
coronary artery bypass graft
CABG
Myocardial Bridging
secondary prevention A Aspirin Anti － anginals B Betaloe Blood pressure －－ C Cholesterol Cigarette D Diet Diabetes E Education Exercise
DEFINITION
Acute myocardial infarction (MI) is defined as death or necrosis of myocardial cells. It is a diagnosis at the end of the spectrum of myocardial ischemia or acute coronary syndromes. From an anatomic or morphologic standpoint, the two types of MI are
transmural : STEMI nontransmural:NSTEMI
Fig, 9-2. Epicardial versus subendocardial injury currents
ACS Types
Pathophysiology Mechanisms of Occlusion: Most MIs are caused by a disruption in the vascular endothelium associated with an unstable atherosclerotic plaque that stimulates the formation of an intracoronary thrombus, which results in coronary artery blood flow occlusion. If such an occlusion persists long enough (20 to 40 min), irreversible myocardial cell damage and cell death will occur.
Vulnerable Plaque
Pathogenesis OF AMI
Clinical Manifestation
Premonitory Pain: a recent onset of angina, a worsening angina, or a worsening angina pectoris poorly responsive well to a nitrate. Pain Of Infarction:more severe, long lasting, and relieved little by rest or nitroglycerin.
Clinical Manifestation
Associated Symptom: Nausea and vomiting ,abdominal bloating,cold sweat,SOB Painless infarction: 20% silent or atypical Sudden death & early arrhythmias:ventricular fibrillation
Clinical Manifestation
Arrhythmias : 75~95% of patients develop cardiac arrhythmias . Any type of arrhythmias may be found Cardiac failure :Heart failure occurs in about 32-48% of hospitalized patients with acute MI Cardiogenic shock :A loss of myocardium greater than 40% generally leads to cardiogenic shock
Clinical Manifestation
Signs:HR is usually increased (but inferior MI commonly leads to bradycardia). S1 is low, S4 (atrial gallop) is noted and an S3 (Ventricular gallop) is present when develop LV failure
Laboratory findings
ECG for AMI • • • • •
Q wave duration of more than 0.04 seconds Q wave depth of more than 25% of ensuing r wave ST elevation in leads facing infarct (or depression in opposite leads) Deep T wave inversion overlying and adjacent to infarct Cardiac arrhythmias
Sequence of changes in evolving AMI R
R T
ST
R
P
P
P T
QS
Q
Q
1 minute after onset
ST
P
ST
1 hour or so after onset
P
A few hours after onset
R
ST
T P
T
T
Q
Q
Q
A day or so after onset
Later changes
A few months after AMI
Anterior infarction
Anterior infarction
I II III
Left coronary artery
aVR aVL aVF
V1 V2 V3
V4 V5 V6
Inferior infarction Inferior infarction
I II III
Right coronary artery
aVR aVL aVF
V1 V2 V3
V4 V5 V6
Lateral infarction
Lateral infarction
I II III
Left circumflex coronary artery
aVR aVL aVF
V1 V2 V3
V4 V5 V6
Echocardiography :to estimate ventricular wall motion abnormalities and left ventricular function. Radioisotope studies: Technetium 99m Hemodynamic Measurement:
Diagnosis and Differential Diagnosis
Complications
Dysfunction or rupture of papillary muscle Rupture of the heart Embolism Ventricular aneurysm Postmyocardial infarction syndrome Shoulder-hand syndrome
Treatment
Monitoring: coronary care unit (CCU) Rest and bedside care Oxygen Relief of pain :give morphine sulfate, 3~5mg IV slowly. nitroglycerin can be given sublingually
Drugs
Nitroglycerin Beta block Calcium channel blockers Angiotensin converting enzyme inhibitor (ACEI) :ventricular
remodeling
Anti-platelet agents Aspirin 300mg qd Clopidogrel 75mg qd
Drugs Anti-coagulation agents LMWH (Low-molecular-weight Heparins ) Enoxaparin 1 mg/kg SC q12h Fraxiparine 5000u SC q12h Lipid-lowering drugs:Statin agents Atorvastatin 20mg qn
Thrombolytic therapy
Thrombolytic therapy is indicated for MI and ST segment elevation greater than 0.1 mV in 2 contiguous EKG leads, or new onset of a bundle branch block, who present less than 12 hours but not more than 24 hours after symptom onset. Intravenous streptokinase and recombinant tissue-type plasminogen activator (rt-PA) the "door-to-needle" time is 30 minutes or less
Percutaneous Coronary Intervention(PCI)
Emergency PCI is recommended for patients present within 6h of onset of pain "door-to-balloon" time: 90 minutes PCI provides a definite survival advantage over fibrinolysis for MI patients who are in cardiogenic shock
PCI-6
TIMI grading system:
Grade 0 = complete occlusion of the infarct-related artery. Grade 1 = some penetration of the contrast material beyond the point of obstruction but without perfusion of the distal coronary bed. Grade 2 = perfusion of the entire infarct vessel into the distal bed but with delayed flow compared with a normal artery.
coronary artery bypass graft
CABG
Myocardial Bridging
secondary prevention A Aspirin Anti － anginals B Betaloe Blood pressure －－ C Cholesterol Cigarette D Diet Diabetes E Education Exercise
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