This document provides an overview of STEMI (ST-segment elevation myocardial infarction). It defines STEMI and lists its clinical features and complications. It discusses the important investigations for STEMI including electrocardiogram, cardiac markers, echocardiogram, and MRI. It also outlines the management of STEMI both in the emergency department and hospital, including reperfusion therapies, medications, monitoring for complications, and addressing issues like hypotension and hypovolemia.

1. P R E PA R E D BY :
N U R I Z Z AT U L NA J WA , 0 3 6
ACUTE CORONARY SYNDROME
(STEMI)

2. LEARNING OBJECTIVES
 DEFINE STEMI
 ENUMERATE THE CLINICAL FEATURES
 UNDERSTAND THE COMPLICATIONS
 KNOW THE INVESTIGATIONS
 KNOW THE MANAGEMENTS

3. DEFINITION
Any group of clinical symptoms compatible with acute
myocardial ischemia and covers the spectrum of
clinical conditions ranging from :
UNSTABLE ANGINA
NON-ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION
ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION

5. STEMI
 Definition of STEMI – New ST elevation at the J point in
two contiguous leads of >0.1 mV in all leads in absence
of left ventricular hypertrophy or left budle branch
block, other than leads V2-V3 – For leads V2-V3 the
following cut points apply: ≥0.2 mV in men ≥40 years,
≥0.15 mV in women.
 STEMI is a life-threatening, time-sensitive emergency
that must be diagnosed and treated promptly

6. PATHOPHYSIOLOGY
 Role of acute plaque rupture

9. CLINICAL FEATURES
SYMPTOMS
CHEST PAIN (cardinal)
• Commonly occur at rest
• Severe, prolonged
• Tightness, heaviness or constriction
• Can come with pallor and peculiar
facial expression
• Radiates to left arm from central
chest.

10. BREATHLESSNESS
SYNCOPE
VOMITING
FATIGUE

11.  Signs of sympathetic activation
 Pallor
 Sweating
 Tachycardia
 Signs of vagal activation
 Vomiting
 Bradycardia
 Signs of impaired myocardial
function
 Hypotension, oliguria, cold
peripheries
 Narrow pulse pressure
 Raised jvp
 Third heart sound
 Diffuse apical impulse
 Lung crepitations
 Sign of tissue damage
 Fever
 Signs of complication
 Mitral regurgitation
 pericaritis
PHYSICAL SIGNS

12. COMPLICATION
 EARLY
 ARRTYHMIA
 CARDIOGENIC SHOCK
 ACUTE HEART FAILURE
 CARDIAC TAMPIONADE
 RUPTURE OF
INTERVENTRICULAR
SEPTUM
 PERICARDITIS
 PULMONARY EDEMA
 LATE
 DRESSLERS SYNDROME
 CHRONIC HEART FAILURE

14. INVESTIGATION

15. ELECTROCARDIOGRAM
 Should be done and interpreted within 10 minutes of
arrival
 12 lead ECG ;
 3 Standard limb lead
 3 Augmented limb lead
 6 precordial limb lead

16. ELECTROCARDIOGRAM

17. ELECTROCARDIOGRAM
 New ST elevation at the J point in two anatomical contiguous leads of >0.1 mV in
all leads in absence of left ventricular hypertrophy or left budle branch block,
other than leads V2-V3 – For leads V2-V3 (precordial lead) the following cut points
apply: ≥0.2 mV in men ≥40 years, ≥0.15 mV in women.
 In early MI, T waves become tall ( hyperacute myocardial infarction), transient and
last for few hours only.

19. ECG AND LOCATION OF MI

21. SHOWS ST ELEVATION BUT NOT STEMI !
Electrolyte abnormalities
Left bundle branch block
Aneurysm of left ventricle
Ventricular hypertrophy
Arrhythmia disease (Brugada syndrome, ventricular
tachycardia)
Takotsubo/Treatment (iatrogenic pericarditis)
Injury (MI or cardiac contusion)
Osborne waves (hypothermia or hypocalcemia)
Non-atherosclerotic (vasospasm or Prinzmetal’s
angina

22. CARDIAC MARKER

23. CARDIAC MARKER

24. PROPERTIES OF CARDIAC MARKER

25. ECHOCARDIOGRAM (ECHO)
 To detect the presence or
absence of wall motion
abnormalities and value of
ejection fraction

26. LATE ENHANCEMENT MAGNETIC RESONANCE
IMAGING ( MRI )
 The most accurate method for diagnosing MI or
nonischemic cardiomyopathies, quantifying the scar,
assessing viability and evaluating thrombus
 Hyperenchancement is seen as bright area of tissue
against background of dark normal myocardium
 Gadolinium is administered, images obtained after 10
mins

28. OTHERS
 Leukocytosis with a peak on 1st day
 Raised ESR that remain for some days
 Elevated C- reactive protein
 Chest radiography
 Heart size usually normal
 Enlargement cardiac shadow indicate previous myocardial
damage or pericardial effusion
 Evidence of pulmonary edema
 Radionuclide scanning
 Shows site of necrosis and extent of impairment of ventricular
function (lack of sensitivity and specificity)

29. Initial management (prehospital care)
Recognition of symptoms by pt and seek for medical attention.
Rapid deployment of emergency medical team capable of performing
resuscitative maneuvers, including defibrillation.
Transport patient to hospital facility accompanied by
physicians/paramedics skilled in providing cardiac life support/manage
arrhythmias.
Implementation of reperfusion therapy.

30. Management in emergency department
Control of cardiac discomfort.
Reperfusion therapy. This may involve transfer of pt from non-
PCI capable hospital to PCI capable hospital within 120 minutes.
Aspirin, B-blocker, t-PA. No heparin.
Supplementary O2 therapy.

32. Control of discomfort
Sublingual nitroglycerine up to 3 doses of 0.4mg at 5 minutes
interval.
Morphine in small dose (2-4mg) every 5 minutes.
Beta-blocker if pt do not have:
• - Sign of heart failure, evidence of low-output state, increased risk of
cardiogenic shock, and other contraindication to B-blockade.
If discomfort return with further ischemia (ST-segment/T-
wave shift), IV nitroglycerine should be considered.

33. Limitation of infarct size
1. PRIMARY
PERCUTANEOUS
CORONARY
INTERVENTION (PCI)
- Usually angioplasty.
- Applicable to pt with
contraindication to fibrinolytics.
- Preferred when diagnosis is in
doubt, cardiogenic shock is
present, bleeding risk increased,
or symptoms has been present at
least 2-3 hours when clot is more
mature and harder to lyse.

34. Limitation of infarct size (cont.)
2. FIBRINOLYSIS
- Should be initiated within 30 min of presentation.
- Tissue plasminogen activator (t-PA), streptokinase, tenecteplase
(TNK), reteplase (rPA).
- t-PA – 15mg bolus followed by 50mg IV over 30 min, 35mg next
60 min.
- Streptokinase – 1.5 million units (MU) IV over 1 hr.
- rPA – 10 MU bolus over 2-3 min, followed by 2nd 10 MU bolus
after 30 min.
- TNK – IV bolus 0.53mg/kg over 10 seconds.

35. Limitation of infarct size (cont.)
3. INTEGRATED REPERFUSION THERAPY
Cardiac catherization and coronary angiography to be
carried out if:
1. Failure of reperfusion  consider rescue PCI
2. Coronary artery reocclusion or development of recurrent
ischemia  consider urgent PCI

36. Limitation of infarct size (cont.)
4. Coronary Artery Bypass
Graft (CABG)
 When PCI fails to prevent
further ischemia, CABG is
considered.
 Great saphenous vein from the
leg is taken and grafted from
aorta or its major branch to
relevant obstructed coronary
artery to immediately restore
blood flow.

37. Hospital phase management
1. Monitoring cardiac rhythm and hemodynamic.
2. Limit movement of pt for 1st 3 days.
3. Diet – pt to receive nothing or clear liquid by
mouth in 1st 4-12 hrs. Controlled diet are given.
4. Bowel Management – diet rich in bulk, and stool
softener are given to offset the effect of
narcotics used in treatment.
5. Sedation, because pt need to sleep – Diazepam
(5mg), Oxazepam (15-30mg), or Lorazepam
(0.5-2mg) 3-4 times a day. Additional dose may
be given at night for better sleep.

38. Pharmacotherapy
1. ANTITHROMBOTIC AGENTS
 Use of antiplatelet and anticoagulant agents to maintain
patency of infarct-related artery and reduce tendency of
thrombosis.
 Aspirin as antiplatelet
 P2Y12 ADP receptor inhibitor (Clopidogrel) to prevent
activation and aggregation of platelet.
 Glycoprotein IIb/IIIa receptor inhibitor to prevent
thrombotic complication during PCI.
 Heparin (unfractionated and low molecular weight)

39. Pharmacotherapy (cont.)
2. BETA-ADRENOCEPTOR BLOCKERS
 Unless contraindicated (heart failure or severely compromised
LV function, heart block, orthostatic hypotension, or a history of
asthma)
 Reduce myocardial oxygen demand and prevent tendency of
ischemia.

40. Pharmacotherapy (cont.)
3. INHIBITION OF RENIN-ANGIOTENSIN-
ALDOSTERONE SYSTEM
 Maximum benefit seen in high-risk pt. (those who are elderly or
who have an anterior infarction, a prior infarction, and/or
globally depressed LV function)
 The mechanism involves a reduction in ventricular remodeling
after infarction with a subsequent reduction in the risk of CHF.
 A multidrug regimen for inhibiting the reninangiotensin-
aldosterone system has been shown to reduce both heart failure–
related and sudden cardiac death–related cardiovascular
mortality after STEMI.

41. Pharmacotherapy (cont.)
4. OTHER AGENTS
 IV Nitroglycerine (5-10 µg/min initial dose, up to 200 µg/min)
for the 1st 24-48 hours after onset of infarction shows favourable
effect on ischemic process and ventricular remodelling.
 Usage of calcium antagonist have failed to establish a favourable
result, so it is not recommended.

42. Complications and their management
1. VENTRICULAR DYSFUNCTION
 Soon after STEMI, LV begins to dilate (Ventricular remodelling) as a
result of expansion of infarct.
 Overall chamber enlargement that occurs is related to the size and
location of the infarct, causing more marked hemodynamic
impairment, more frequent heart failure, and a poorer prognosis.
 Progressive dilation and its clinical consequences may be
ameliorated by therapy with ACE inhibitors and other vasodilators
(e.g., nitrates)

43. Complications and their management (cont.)
2. HEMODYNAMIC ASSESSMENT
 Pump failure is now the primary cause of in-hospital death
from STEMI.
 Positioning of a balloon flotation (Swan-Ganz) catheter in
the pulmonary artery permits monitoring of LV filling
pressure; this technique is useful in patients who exhibit
hypotension and/or clinical evidence of CHF.
 Cardiac output can also be determined with a pulmonary
artery catheter. With the addition of intra-arterial pressure
monitoring, systemic vascular resistance can be calculated
as a guide to adjusting vasopressor and vasodilator therapy.

44. Complications and their management (cont.)
3. HYPOVOLEMIA
 May be secondary to previous diuretic use, to reduced fluid
intake during the early stages of the illness, and/or to
vomiting associated with pain or medications.
 Hypovolemia should be identified and corrected in patients
with STEMI and hypotension before more vigorous forms of
therapy are begun.
 Optimal LV filling or pulmonary artery wedge pressure
(generally ~20 mmHg) is reached by cautious fluid
administration during careful monitoring of oxygenation and
cardiac output.

45. SUMMARY