STEMI

1. STEMI
By
Dr. Hamdy Abdalla Badawy

2.  Definition
 Pathophysiology
 Anatomy
 Etiology
 Clinical presentation
 DDx
 Workup
 Treatment and medication

3. 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.

4. 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

5. Pathophysiology

6. Anatomy

7. 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

8. 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

9. 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

10. 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.

11. 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

12. 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

13. Workup

14. Workup

15. 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

16. 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

17. 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)

18. 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

19. 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)

20. 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 .

21. 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

22. 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

23.  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

25.  Benign Early Repolarisation
Concave ST elevation Large amplitude T wave
Notching or slurring of J point

26.  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

27. 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

28. 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

29. 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.

31.  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).

32. 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.

33. 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;

34. 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.

35. 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

36. 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 min
60-90 min
90-120 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

37. 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

38. 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

39. 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.

40. 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

41.  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

42. 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

43. Thank you