Cardiovascular 9. Acute Myocardial Infarction

Acute Myocardial Infarction

12/01/09

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Acute Myocardial Infarction Definition The term myocardial infarction is derived from myocardium (the heart muscle) and infarction (tissue death due to oxygen starvation) Ischemic myocardial necrosis usually resulting from abrupt reduction of coronary blood flow to a segment of myocardium.

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Acute Myocardial Infarction Epidemiology It is a medical emergency, and the leading cause of death for both men and women all over the world

Important Risk factors: • • • • • • • • 12/01/09

Older age Male gender Family history Cigarette smoking Hypercholesterlemia (especially high LDL and low HDL) Diabetes High blood pressure Obesity (defined by a BMI of more than 30 kg/m2) Free Template from www.brainybetty.com

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Acute Myocardial Infarction Most common cause of AMI is an occlusive coronary thrombus at the site of a pre-exixting atherosclerotic plaque

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Other causes: • Coronary artery spasm Variant angina Cocaine abuse

• Coronary artery embolus Atrial myxoma Atrial or ventricular thrombus

• Vasculitis • Hypercoagulable states Polycythemia vera Thrombocytosis

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Acute Myocardial Infarction Mechanism of AMI Over decades atherosclerosis causes gradual buildup of cholesterol and fibrous tissue in plaques in the wall of coronary arteries

Coronary artery lumen narrows as a result of decades of advancing atherosclerosis

Plaques can become unstable due to inflammation, rupture, and promote a thrombus that occludes the artery; this can occur in minutes

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Plaque rupture leads to myocardial infarction A collagen scar forms in its place Free Template from www.brainybetty.com

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Acute Myocardial Infarction

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Acute Myocardial Infarction

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Clinical Findings Symptoms • Chest pain: •

prolonged (>20 min) sensation of tightness, pressure, squeezing Radiation to left arm, lower jaw, neck, right arm, back, epigastrium

• • • • • • • •

Dyspnea: shortness of breath Diaphoresis: an excessive form of sweating Weakness or Fatigue Light-headedness Nausea and vomiting Palpitations Loss of consciousness Sudden death

• Silent, without chest pain or other symptoms 12/01/09 Free Template from www.brainybetty.com

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Acute Myocardial Infarction

Diagram of pain zones in myocardial infarction dark red = most typical area, light red = other possible areas 12/01/09

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Signs General: Appearance: Anxious and sweating Tachycardia or Bradycardia Blood pressure high or low Fever: low grade Jugular venous distention (JVD)± Edema ± Cyanosis ± 12/01/09

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Chest: Clear lungs, or basilar rales

Heart: May be normal Abnormally located ventricular Impulse Soft heart sounds Atrial gallop S4 or ventricular gallop S3 Systolic murmur due to papillary muscle or ventricular septal rupture Pericardial friction rub

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Acute Myocardial Infarction ECG Change

Onset

Disappearance

Electrocardiogram (ECG) Hyper acute T Immediately 6-24 hours waves (Tall Peaked T waves in leads facing infarction)

ST Segment elevation

Immediately 1-6 weeks

Q waves longer than 0.04 sec

One to Years to never several days

T wave inversion 6-24 hours

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Months to years

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Acute Myocardial Infarction Main Coronary blood supply Right Coronary Artery

Left Coronary Artery

Arises from Aorta behind the right aortic sinus of valsalva

Arises from the Aorta behind the left aortic Sinus of valsalva

Supplies: •Posterior Inferior wall of LV •Right Ventricle and atrium via marginal branch •SA and AV node

Left anterior descending (LAD) Supplies: Anterior wall of left ventricle Anterior two thirds of interventricular septum Left Circumflex (LCX) Supplies: Lateral wall of left ventricle

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Acute Myocardial Infarction

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Acute Myocardial Infarction Location of Myocardial Infarction Area of Infarction

ECG Changes in leads

Artery involved

Inferior wall

II, III, aVf

Right Coronary

Anteroseptal

V1-V3

Left anterior descending

Anterior wall

V2-V4

Left anterior descending

Lateral wall

I, aVL, V4, V5 and V6

Left anterior descending or circumflex

Posterior wall

V1-V2: Tall broad initial R wave, ST depression, Tall Upright T wave, in association with Inferior or lateral MI

Posterior descending

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Cardiac Enzymes • Cardiac markers or cardiac enzymes are proteins from cardiac tissue found in the blood • These proteins are released into the bloodstream when damage to the heart occurs, as in the case of a myocardial infarction • Serial measurement of cardiac enzymes is the most valuable diagnostic test • Creatinine Kinase (CK-MB) and Troponin I or T (TNI) are the most specific and widely used assays 12/01/09

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CK-MB begins to elevate at 4-6 hours after onsetof chest pain and peaks at 12-24 hours

Troponin I begins to elevate 4-6 hours after onset of pain and Remains elevated for 1-2 weeks

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Chest X-Ray: May be normal or may show signs of Congestive heart failure

Echocardiography: Provides assessment of ventricular function and wall motion. Doppler echo is used to diagnose post infarction mitral regurgitation or ventricle septal defect

Other Laboratory tests: Leukocytosis

Scintigraphic studies: Angiography: 12/01/09

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Acute Myocardial Infarction A chest X-ray showed large Cardiac silhouette and bilateral interstitial markings consistent with pulmonary edema.

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Acute Myocardial Infarction Diagnostic criteria 1. Clinical history of ischaemic type chest pain lasting for more than 20 minutes 2. Changes in serial ECG tracings 3. Rise and fall of serum cardiac biomarkers such as CK-MB and Troponin I specific for the heart

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Acute Myocardial Infarction Types of AMI STEMI : ST-elevation myocardial infarction NSTEMI : Non-ST-elevation myocardial infarction Q-wave infarction Non-Q wave infarction

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Acute Myocardial Infarction Treatment A heart attack is a medical emergency which demands immediate attention The ultimate goal of the management in the acute phase of the disease is to salvage as much myocardium as possible and prevent further complications. 12/01/09

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Acute Myocardial Infarction General Measures • • • • • 12/01/09

CCU(coronnary care unit) Monitoring Oxygen(2-4 L/min) Aspirin Glyceryl trinitrate (nitroglycerin) Analgesia (usually morphine) Free Template from www.brainybetty.com

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Acute Myocardial Infarction Reperfusion therapy The concept of reperfusion has become so central to the modern treatment of acute myocardial infarction, that we are said to be in the reperfusion era

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Acute Myocardial Infarction Reperfusion therapy • Thrombolytic therapy • Percutaneous coronary intervention (PCI) • Bypass surgery

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Acute Myocardial Infarction Fibrinolysis is the process where a fibrin clot, the product of coagulation, is broken down by an enzyme plasmin Fibrin-specific thrombolytic agents have have the property of fibrin-enhanced conversion of plasminogen to plasmin.

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Thrombolytic Agents Recombinant tissue plasminogen activator (rtPA) Patients <70 years, Anterior MI, within 4 hours of onset and with pump failure.

Streptokinase Older patients with concomitant hypertension (>160mmHg), no previous exposure to streptokinase or recent streptococcal infection.

Urokinase Alteplase Reteplase TenecteplaseFree Template from www.brainybetty.com 12/01/09

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Thrombolytic therapy Indications 1. 2. 3.

Within 12 hours of the onset of typical chest pain of AMI ST elevation of > 1mm in two contiguous leads or Q waves New Left bundle branch block

Contraindications 1. 2. 3. 4. 5. 6. 7. 8. 12/01/09

Dissecting aortic aneurysm Uncontrolled hypertension > 180/110 Active peptic ulcer Bleeding Diathesis History of cerebrovascular disease Recent trauma or surgery especially of head or spine Traumatic CPR Pregnancy Free Template from www.brainybetty.com

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Percutaneous coronary intervention (PCI) • PCI done to abort a myocardial infarction is known as primary PCI • Goal of primary PCI: open the artery preferably within 90 minutes of the patient presenting to the emergency room • Primary PCI involves performing a coronary angiogram to determine the anatomical location of the infarcting vessel, followed by balloon angioplasty (and frequently deployment of an intracoronary stent) of the thrombosed arterial segment

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Other pharmacologic agents given in AMI

• • • •

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Beta blockers Angiotensen-converting enzyme inhibitors Anticoagulation (typically with heparin) Antiplatelet agents such as Clopidogrel

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Complications 1. Infarct extension and post infarction Ischemia • • •

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Inadequate blood flow though a recanalized vessel or reocclusion Medical therapy with nitrates, beta blockers, calcium channel blockers as well as heparin and aspirin is given If medical therapy fails then early catheterization and revascularization by Percutaneous transluminal coronary angioplasty (PTCA) or Coronary artery bypass graft (CABG) is performed

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2. Life threatening arrhythmias Electrical characteristics of the infarcted tissue is changed so arrhythmias are a frequent complication The re-entry phenomenon may cause too fast heart rates like ventricular tachycardia and even ventricular fibrillation and ischemia in the electrical conduction system of the heart may cause a complete heart block

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3. Myocardial Dysfunction Cardiac dysfunction is proportionate to the extent of myocardial necrosis ■Congestive

heart failure:

signs/symptoms: Dyspnoea, Diffuse rales in the lung, Arterial hypoxemia Treatment: Oxygen, Diuretics, morphine sulphate, vasodilators nitrates, ionotropic agents dopamine or dobutamine ■Hypotension

and shock:

Systolic BP<100 mmHg, low urine output, cold extremities and confusion Treatment: Dopamine, Norepinephrin, Intra-aortic baloon counterpulsation IABC

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4. Mechanical defects •

Paplillary muscle rupture and Interventricular septum rupture can occur in AMI

•

Detected by appearance of new systolic murmer with clinical deterioration and pulmonary edema

•

Treatment is by surgical repair

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5. Myocardial rupture  • • • •

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Myocardial rupture is most common three to five days after AMI Shear stress between the infarcted segment and the surrounding normal myocardium makes it a nidus for rupture Occur in the free walls of the ventricles The weakness may also lead to ventricular aneurysm Rupture is usually a catastrophic event that may result a life-threatening process known as cardiac tamponade

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6. •

• •

As a reaction to the damage of the heart muscle, inflammatory cells are attracted and may reach out and affect the heart sac causing pericarditis In Dressler's syndrome this occurs several weeks after the initial event. Treated with aspirin, NSAIDs and later steroids

7. • • • •

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Pericarditis

Mural Thrombus

Common in large anterior infarctions Systemic embolization is a potential threat Detected by echocardiography Treatment is anticoagulation with heparin followed by warfarin therapy

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Acute Myocardial Infarction Post Infarction Management Stress testing Coronary angiography Medical Therapy Antiplatelet drug therapy: Aspirin or clopidogeral Beta Blocker ACE- Inhibitors Lipid lowering Therapy Smoking cessation Regular exercise Sensible diet for patients with heart disease, Limitation of alcohol intake

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