STEMI

By Dr. Hamdy Abdalla

Badawy

Definition Pathophysiology Anatomy Etiology Clinical presentation DDx Workup Treatment and medication

Definition

Myocardial Infarction Irreversible necrosis of heart muscle secondary to prolonged ischemia occurs when there is a diminished blood supply to the heart which leads to

myocardial cell damage and ischemia. Ischemia usually occurs due to blockage of the coronary vessels. This blockage

is often the result of thrombus that is superimposed on an ulcerated or unstable atherosclerotic plaque formation in the coronary artery.

Pathophysiology Ischemia develops when there is an increased demand for oxygen or a decreased supply of oxygen. Ischemia can develop within 10 seconds and if it lasts longer than 20

minutes, irreversible cell and tissue death occurs.

Myocardial cell death begins at the endocardium. The area most distal to the arterial blood supply.

As vessel occlusion continues cell death spreads to the myocardium and eventually to the epicardium.

Severity of the MI depends on three factors. - Level of occlusion - Length of time of occlusion - Presence or absence of collateral circulation

Pathophysiology

Anatomy

Etiology

Atherosclerosis is the disease primarily responsible for most (ACS) cases. Approximately 90% of myocardial infarctions result from an acute thrombus that

obstructs an atherosclerotic coronary artery.

Nonmodifiable risk factors for atherosclerosis include the following: Age Sex Family history of premature coronary heart disease

Modifiable risk factors for atherosclerosis include the following: Hypertension Diabetes mellitus Smoking Dyslipidemia

obesity Psychosocial stress Sedentary lifestyle and/or lack of exercise

Etiology

Causes of myocardial infarction other than atherosclerosis

Coronary occlusion secondary to vasculitis Ventricular hypertrophy Primary coronary vasospasm (variant angina) Drug use (eg, cocaine, amphetamines, ephedrine) Coronary anomalies, including aneurysms of coronary arteries Factors that increase oxygen requirement, such as heavy exertion, fever, or

hyperthyroidism Factors that decrease oxygen delivery, such as hypoxemia of severe anemia Aortic dissection, with retrograde involvement of the coronary arteries

Clinical presentation History

Symptoms are unique to each individual patient. Ranging from no symptoms to sudden cardiac arrest.

Retrosternal pain more severe and lasts longer i.e. > 30 - 60 min, present at rest, heavy, squeezing & crushing, stabbing or burning radiating to arms, back, lower jaw, neck & epigastrium.

Associated with nausea, vomiting, anxiety & palpitation. Painless STEMIs in diabetics and older age group Sudden onset of breathlessness Sudden loss of consciousness & confusion state

Other symptoms of myocardial infarction include the following: Diaphoresis Anxiety Wheezing Cough Light-headedness with or without syncope

Clinical presentation Physical Examination

Vital signs

Perform focused examination ( Heart- chest- Abdomen - Extremities ): Look for signs of hemodynamic compromise and left heart failure; determine

baseline neurologic function, particularly if fibrinolytic therapy is to be given.

Differential diagnosis Acute Chest Pain

Cardiac – Aortic Dissection* – Pericarditis - Myocarditis Pulmonary – Pulmonary Embolism* – Pneumonia – Pneumothorax* Chest wall – Rib fracture – Costochondritis – Herpes zoster (before rash) Gastrointestinal – Peptic Ulcer* – Pancreatitis – Esophageal • Spasm • Rupture – Biliary

Workup

Initial care should include the early and simultaneous achievement of four goals:

● Confirmation of the diagnosis by ECG and biomarker measurement ● Relief of ischemic pain ● Assessment of the hemodynamic state and correction of abnormalities that may be present ● Initiation of antithrombotic and reperfusion therapy if indicated　　 Workup - ECG - Cardiac biomarker - Other lab studies ( electrolytes , cbc , LFT , renal , coagulation ) 　 - CXR - Cardiac imaging

Workup

Workup

Electrocardiogram

Why A Pre-hospital EKG?

EMS should Obtain a 12 lead EKG EMS looking for ST segment elevation Indicates injury that can be reversible if found early and acted upon

early TIME IS MUSCLE The earlier the discovery of an acute cardiac event, the quicker the

patient can receive the most appropriate care EKG’s sent to the ED before patient arrival allows for the right

personnel to be available to properly care for the patient in the most time efficient manner

Electrocardiogram

Myocardial Insult

Ischemia - lack of oxygenation - ST depression or T wave inversion - permanent damage avoidable Injury - prolonged ischemia - ST elevation - permanent damage avoidable Infarct death of myocardial tissue; damage permanent; may have Q wave

Electrocardiogram

Evolution of AMI A - pre-infarct (normal) B - Tall T wave (first few minutes of infarct) C - Tall T wave and ST elevation (injury) D - Elevated ST (injury), inverted T wave (ischemia), Q wave (tissue death) E - Inverted T wave (ischemia), Q wave (tissue death) F - Q wave (permanent marking)

Electrocardiogram

ST segment elevations > 2 mm ( 2 small box) in 2 or more contiguous chest leads (V1-V6) >1mm (1 small box) in 2 or more anatomically contiguous leads (ie: II, III, aVF; I, aVL, V5, V6)

T wave changes Q wave development Reciprocals new left bundle branch block and presentation consistent with ACS

Electrocardiogram

EKG changes are significant when they are seen in at least two contiguous leads Two leads are contiguous if they look at the same area of the heart or they are

numerically consecutive chest leads

Groups of EKG Leads : Inferior wall - II, III, aVF Septal wall - V1, V2 Anterior wall - V3, V4 Lateral wall - I, aVL, V5, V6 Standard leads does not look at posterior wall or right ventricle of the heart - and need special lead placement for these views

Posterior wall: V7-V9 ( leads placed on the patient’s back 5th intercostal space creating a 15 lead EKG)

Electrocardiogram diagnosis of MI in LBBB :

What is normal for LBBB? - Wide complex - ST elevation - the ST segments and T waves show “appropriate discordance” — i.e. they are directed

opposite to the main vector of the QRS complex. This produces ST elevation and upright T waves in leads with a negative QRS complex (dominant S wave), while producing ST depression and T wave inversion in leads with a positive QRS complex .

Electrocardiogram Think Sgarbossa criteria 1- ST Elevation ≥ 1 mm and concordant with QRS complex Score 5 points 2- ST Elevation ≥ 5 mm and discordant with QRS complex Score 2 points 3- ST Depression ≥ 1 mm in V1, V2, V3 Score 3 points A total score of 3 or more suggests that the patient is likely experiencing an AMI based on

the ECG crtieria With a score less than 3, the ECG diagnosis is less certain requiring additional evaluation

Other Causes of ST elevation

- Benign Early Repolarisation - Acute Pericarditis - Brugada syndrome - Myocarditis - LVH \ Athlete’s heart syndrome - Hyperkalaemia - Acute intracranial event - LV Aneurysm - Aortic dissection

Pericarditis ECG features

- Usually global low magnitude ST elevation - Concave upward morphology - PR depression can be seen early - T wave changes later (days to weeks) - ST changes resolve fully so not persistent on future ECGS

Benign Early Repolarisation

Concave ST elevation Large amplitude T wave

Notching or slurring of J point

Brugada Syndrome A disease of myocardial sodium channels that leads to paroxysmal ventricular arrhythmias

and sudden cardiac death in young patients.

- Type I: ST – segment elevation is triangular and T waves may be inverted in V1 – V3 - Type II: downward displacement of ST – segment (does not reach baseline) - Type III: middle part of ST segment touches baseline

Serum Cardiac Markers

Myocardial cells produce certain proteins and enzymes associated with cellular functions. When cell death occurs, these cellular enzymes are released into the blood stream. CPK and troponin

Serum Cardiac Markers

CPK

- Creatine Phosphokinase - CPK-MB more specific for STEMI - Begin to rise 3 to 12 hours after acute MI. - Peak in 24 hours - Return to normal in 2 to 3 days

Troponin

Troponin-T & Troponin-I

Myocardial muscle protein released into circulation after injury. These are highly specific indicators of MI. Serum levels increase within 3-12 hours from the onset of chest pain, peak at

24-48 hours, and return to baseline over 5-14 days Myoglobin-lacks cardiac specificity.

Initial assessment:

- Consider the diagnosis in patients with chest discomfort, shortness of breath. Women, the elderly, and diabetic may have"atypical"presentations.

- Obtain 12 lead ECG within 10 minutes of arrival; repeat every 10 to 15 minutes if initial ECG nondiagnostic but clinical suspicion remains high (initial ECG often NOT diagnostic).

Initial interventions: Assess and stabilize airway, breathing, and circulation. Attach cardiac and oxygen saturation monitors; provide supplemental oxygen to maintain

O2 saturation >90 percent. Establish IV access.

Give aspirin 325 mg (non-enteric coated), to be chewed and swallowed Give clopidogrel loading dose 300 mg if age 75 years or less; if age over 75 years, give

loading dose of 75 mg.

S/L nitrates 0.4 mg up to 3 doses 5 min apart , IF patient has persistent chest discomfort, hypertension, or signs of heart failure AND there is no sign of hemodynamic compromise (eg, right ventricular infarction) and no use of phosphodiesterase inhibitors

Analgesia morphine 5-10 mg IV + metaclopramide 10 mg IV

IV β-blockers metoprolol 5 mg every 5 min for 3 doses IF no signs of heart failure , and no signs of hemodynamic compromise, bradycardia, or severe reactive airway disease.

Start 80 mg of atorvastatin as early as possible, and preferably before PCI.

Give anticoagulant therapy to all patients:

1. patients with primary PCI, we prefer unfractionated heparin (UFH) to bivalirudin.

Dosing of UFH: (IV) bolus of 50 to 70 units/kg up to a maximum of 5000 units. Dosing of bivalirudin: Initial bolus of 0.75 mg/kg IV followed by IV infusion of

1.75 mg/kg per hour

2. patients with fibrinolysis, we prefer enoxaparin for patients not at high bleeding risk

Dosing of enoxaparin Patients <75 years: Loading dose of 30 mg IV bolus followed by 1 mg/kg

subcutaneously every 12 hour Patients ≥75 years: No IV loading dose. Administer 0.75 mg/kg subcutaneously

every 12 hours;

3. For patients not receiving reperfusion therapy, we use enoxaparin or UFH. - Dosing of enoxaparin: Dose same as for patients treated with fibrinolysis - Dosing of UFH: IV bolus of 50 to 70 units/kg to a maximum of 5000 units,

followed by an IV infusion of 12 units/kg per hour

Other important considerations: - Cocaine-related ACS: Give benzodiazepines (eg, lorazepam 2 to 4 mg IV every 15 minutes or so) as needed do NOT give beta blockers. - Stop NSAID therapy if possible. - Correct any electrolyte abnormalities, especially hypokalemia and hypomagnesemia, which often occur together.

Choosing the Optimal Reperfusion Strategy

Goal is rapid reperfusion Time targets from first medical contact to treatment

Fibrinolysis 30 minutes Primary angioplasty (PPCI) 90-120 minutes

Delayed reperfusion associated with increased mortality When time to PPCI will exceed 90-120 minutes fibrinolysis should be

given immediately Time delay for PPCI to achieve greater benefit than fibrinolysis may be

less than 90 minutes when Anterior MI Patient age <65 yrs Time from symptom onset <120 minutes

Impact of Delay to Primary PCI

90 DAY MORTALITY RELATED TO DOOR-TO-BALLOON TIME

Hudson MP et al. Hudson MP et al. Circ Cardiovasc Qual Outcomes 2011;4:183-92

SURVIVAL(%)

0 10 20 30 40 50 60 70 80 90

(n=1071)(n=1354)(n=1186)(n=1762)

<60 min60-90 min90-120 min≥120 min

99%

98%

97%

96%

95%

94%

93%

92%

100%

3.2%

90-day mortality

4.0%4.6%

5.3%

DAYS

P<0.0001

Reperfusion strategy:

Primary PCI strongly preferred Activate cardiac catheterization team for

- patients with cardiogenic shock, heart failure - contraindications to fibrinolysis. . - patients with symptoms of >12 hours fibrinilysis not indicated, but emergent PCI may be considered - Door to balloon time <90min - Person skilled in procedure(>75PCI/yr) - Supporting lab (>200PCI/yr of which 36 primary) - Cardiac surgical backup available

Reperfusion strategy:

fibrinolytic therapy - STEMI patients presenting to a facility without PCI or capability to transfer for

PCI in 90 min should undergo fibrinolysis in 30 min - ( compared with fibrin specific PCI may not reduce mortality if delay>60min) - In the absence of contraindications fibrinolytic therapy should be administered

if symptom onset within prior 12hrs - The occurrence of a change in neurological status during or after reperfusion

therapy within 24hrs is considered to be ICH unless proved otherwise . Fibrinolytic, antiplatelet and anticoagulants should be discontinued until brain imaging disproves ICH

Types of fibrinolysis

Fibrin specific agents tPA, tenecteplase, reteplase.

- tPA 15 mg loading followed by 50 mg IV over 30 min followed by 35 mg over 60 min.

- rPA double bolus regimen 10 MU bolus over 2 min followed by 2nd 10 MU over 30 min.

- TNK single IV bolus of 0.53 mg/kg over 30 min. UFH is usually indicated after thrombolysis.

Contraindications

Absolute contraindications

- Hx any intracranial hemorrhage - Ischemic stroke within the preceding three months - cerebral vascular malformation or a primary or metastatic

intracranial malignancy - Symptoms or signs suggestive of an aortic dissection - A bleeding diathesis or active bleeding - Closed-head or facial trauma within the preceding three months

Relative contraindications

- Severe hypertension or uncontrolled hypertension at presentiaton (blood pressure >180 mmHg systolic and/or >110 mmHg diastolic

- History of ischemic stroke more than three months previously - Traumatic or prolonged (>10 min) cardiopulmonary resuscitation - Major surgery within the preceding three weeks - Internal bleeding within the preceding two to four weeks - Pregnancy - Current warfarin therapy

Need for PCI after Fibrinolysis

Rescue PCI

Failed fibrinolysis

• Persistence of chest pain• Failure of ST elevation to decrease more than 50%

at 1 hr after fibrinolysis

2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction

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