ACS-STEMI Guidelines
Dr. KAZI ALAM NOWAZ
MD FINAL PART STUDENT CARDIOLOGY
NHFH & RI
• The term acute coronary syndrome (ACS) is a
unifying construct representing a
pathophysiologic and clinical spectrum
culminating in acute myocardial ischemia
• Unstable angina (UA), Non ST Elevation
Myocardial Infarction (NSTEMI) and ST
Elevation Myocardial Infarction (STEMI)
collectively constitute the diagnosis of Acute
Coronary Syndrome (ACS).
Universal definition of myocardial
infarction
• A combination of criteria is required to meet the diagnosis of acute
MI, namely the detection of an increase and/or decrease of a
cardiac biomarker, preferably high-sensitivity cardiac troponin, with
at least one value above the 99th percentile of the upper reference
limit and at least one of the following:
• Symptoms of ischaemia.
• New or presumed new significant ST-T wave changes or left bundle
branch block on 12-lead ECG.
• Development of pathological Q waves on ECG.
• Imaging evidence of new or presumed new loss of viable
myocardium or regional wall motion abnormality.
• Intracoronary thrombus detected on angiography or autopsy.
Pathophysiology of Myocardial
ischemia and infarction
DEFINITION
• STEMI represents the most lethal form of ACS,
in which a completely occlusive thrombus
typically results in total cessation of coronary
blood flow, manifested electrically as elevation
of the ST segment on the ECG.
Types
• Type 1 MI
Type 1 MI is characterized by atherosclerotic
plaque rupture, ulceration, fissure,erosion or
dissection with resulting intraluminal
thrombus in one or more coronary arteries
leading to decreased myocardial blood flow
and/or distal embolization and subsequent
myocardial necrosis
• Type 2 MI
Type 2 MI is myocardial necrosis in which a
condition other than coronary plaque instability
contributes to an imbalance between myocardial
oxygen supply and demand. Mechanisms include
coronary artery spasm, coronary endothelial
dysfunction, tachyarrhythmias, bradyarrhythmias,
anaemia, respiratory failure, hypotension and
severe hypertension, injurious effects of
pharmacological agents and toxins.
• Type 3
sudden cardiac death with symptoms of
ischaemia, new ST elevation or LBBB or
coronay thrombus
• Type 4a MI associated with PCI
• Type 4b MI associated with stent thrombosis
• Type 5 MI associated witH CABG
Classification of Myocardial Infarction
• Type I: Spontaneous Myocardial Infarction
• Type 2: Myocardial Infarction Secondary to an Ischemic
Imbalance
• Type 3: Myocardial Infarction Resulting in Death When
Biomarker Values Are Unavailable
• Type 4a: Myocardial Infarction Related to Percutaneous
Coronary Intervention (PCI)
• Type 4b: Myocardial Infarction Related to Stent Thrombosis
• Type 5: Myocardial Infarction Related to Coronary Artery
Bypass Grafting (CABG)
Non-modifiable risk factors:
• Gender
• Age
• Family history of CVD
• Diabetes
• Human immunodeficiency virus (HIV).
Modifiable risk factors:
• smoking
• poor diet
• high cholesterol
• physical inactivity
• high blood pressure
• being overweight
• depression, social isolation and
• lack of social support
SIGNS
• Signs of sympathetic activation : Pallor, Sweating,
Tachycardia
• Signs of vagal activation : Vomiting, Bradycardia
• Signs of impaired myocardial function :
-Hypotension, oliguria, cold periphery.
-Narrow pulse pressure
-Raised JVP
-Third heart sound
-Lung Crepitation
• Sign of tissue damage : Fever
• Complications : Murmur ,Pericardial rub
Risk Stratification
• Five simple baseline parameters have been reported to
account for > 90% of the prognostic information for 30-
day mortality. These characteristics are given in
descending order of importance:
-Age
-Systolic blood pressure
- Killip classification
-Heart rate
-Location of MI
• In addition, various risk models have been created to
improve risk prediction.
TIMI Risk Model for Prediction of Short-Term
Mortality in ST-Segment Elevation Myocardial
Infarction Patients
DIAGNOSIS
• It is based on :
Clinical Findings
Classical ECG Changes
Rising Titre of Cardiac Enzymes
• The classic ECG findings:
ST segment elevation, followed by T wave
inversion and Q waves.
• Atypical ECG findings
– Bundle branch block
– Ventricular pacing
– Non diagnostic ECG
– Isolated posterior MI
– universal ST depression with ST-elevation in aVR
– Diagnosis in doubt → echo → primary PCI strategy
Routine Investigation
• ECG( Serial ECG may be required)
• CK-MB
• Troponin I( Serial measurement
may be required)
• ECHO-2D
• Fasting Lipid Profile
• HbA1c
• Serum Creatinine
• SGPT
• Serum Electrolyte
• CBC
• CXR-P/A view
• FBS/RBS
Other Investigation
• Echo color Doppler- Wall motion Defect,LV
Impairment, MR, VSR
• CAG
LOCALIZATION OF CORONARY CIRCULATION IN
M.I.
ANATOMIC ECG LEADS CORONARY ARTERY
• Septal V1-v2 Proximal LAD
• Anterior V3-V4 LAD
• Apical V5-V6 Distal LAD, LCx, or RCA
• Lateral I, Avl LCx
• Inferior II, III, aVF RCA(85%), LCx (15%)
• RV V4R Proximal RCA
• Posterior V1-V3 RCA or LCx
Management
The goals for the management of patients with
suspected STEMI include:
1. control of cardiac discomfort,
2. rapid identification of patients who are
candidates for urgent reperfusion therapy,
3. triage of lower-risk patients to the appropriate
location in the hospital, and
4. avoidance of inappropriate discharge of patients
with STEMI
Initial ER Management
• Aspirin 160 to 320 mg tablet (non-enteric coated, chewed);
• Clopidogrel 300 to 600 mg whether or not fibrinolysis will be
given;
• Clopidgrel 600 mg or prasugrel 60 mg or ticagrelor 180 mg when a
patient will undergo PCI;
• Nitrates, either via sublingual or intravenous(IV) routes. Nitrates
are contraindicated in patients with hypotension or those who
took a phosphodiesterase 5 (PDE5) inhibitor within 24 hrs (48 hrs
for tadalafil);
• Morphine 2 to 4 mg IV for relief of chest pain, and;
• Supplemental oxygen MAY BE RECOMMENDED during the first 6
hours to patients with arterial oxygen saturation of less than 90%.
Absolute contraindications
• Any prior ICH
• Known structural cerebral vascular lesion (eg, AVM)
• Known malignant intracranial neoplasm (primary or metastatic)
• Ischemic stroke within 3 months EXCEPT acute ischemic stroke
within 4.5 h
• Suspected aortic dissection
• Active bleeding or bleeding diathesis (excluding menses)
• Significant closed-head or facial trauma within 3 mo
• Intracranial or intraspinal surgery within 2 mo
• Severe uncontrolled hypertension (unresponsive to emergency
therapy)
• For streptokinase, prior treatment within the previous 6 mo
Relative contraindications
• History of chronic, severe, poorly controlled hypertension
• Significant hypertension on presentation (SBP 180 mm Hg or DBP 110 mm
Hg)
• History of prior ischemic stroke 3 mo
• Dementia
• Known intracranial pathology not covered in absolute contraindications
• Traumatic or prolonged (10 min) CPR
• Major surgery (3 wk)
• Recent (within 2 to 4 wk) internal bleeding
• Noncompressible vascular punctures
• Pregnancy
• Active peptic ulcer
• Oral anticoagulant therapy
TIMI
• TIMI FLOW GRADE — The degree of perfusion in the
infarct-related artery (IRA) is typically described by the
TIMI flow grade:
• TIMI 0 refers to the absence of antegrade flow beyond
a coronary occlusion. (complete occlusion)
• TIMI 1 flow is faint antegrade coronary flow beyond
the occlusion, although filling of the distal coronary
bed is incomplete.
• TIMI 2 flow is delayed or sluggish antegrade flow with
complete filling of the distal territory.
• TIMI 3 flow is normal flow which fills the distal
coronary bed completely.
Complication Of STEMI
Early Complication:
• Disturbance of rate, rhythm, and conduction
• Cardiogenic Shock
• Left Ventricular failure
• Right ventricular failure
• Pulmonary embolism and infarction
• Cerebrovascular accident
• Rupture of intraventricular septum
• Acute MR; LV free wall rupture
• Pericarditis
Continue….
Late Complication:
• Re infarction
• Recurrence of arrhythmia
• Heart Failure
• Post MI syndrome
• Ventricular Aneurysm
• Thromboembolism
• Sudden death
• Psychosis
Thank You

Stemi

  • 1.
    ACS-STEMI Guidelines Dr. KAZIALAM NOWAZ MD FINAL PART STUDENT CARDIOLOGY NHFH & RI
  • 2.
    • The termacute coronary syndrome (ACS) is a unifying construct representing a pathophysiologic and clinical spectrum culminating in acute myocardial ischemia • Unstable angina (UA), Non ST Elevation Myocardial Infarction (NSTEMI) and ST Elevation Myocardial Infarction (STEMI) collectively constitute the diagnosis of Acute Coronary Syndrome (ACS).
  • 3.
    Universal definition ofmyocardial infarction • A combination of criteria is required to meet the diagnosis of acute MI, namely the detection of an increase and/or decrease of a cardiac biomarker, preferably high-sensitivity cardiac troponin, with at least one value above the 99th percentile of the upper reference limit and at least one of the following: • Symptoms of ischaemia. • New or presumed new significant ST-T wave changes or left bundle branch block on 12-lead ECG. • Development of pathological Q waves on ECG. • Imaging evidence of new or presumed new loss of viable myocardium or regional wall motion abnormality. • Intracoronary thrombus detected on angiography or autopsy.
  • 4.
  • 5.
    DEFINITION • STEMI representsthe most lethal form of ACS, in which a completely occlusive thrombus typically results in total cessation of coronary blood flow, manifested electrically as elevation of the ST segment on the ECG.
  • 6.
    Types • Type 1MI Type 1 MI is characterized by atherosclerotic plaque rupture, ulceration, fissure,erosion or dissection with resulting intraluminal thrombus in one or more coronary arteries leading to decreased myocardial blood flow and/or distal embolization and subsequent myocardial necrosis
  • 7.
    • Type 2MI Type 2 MI is myocardial necrosis in which a condition other than coronary plaque instability contributes to an imbalance between myocardial oxygen supply and demand. Mechanisms include coronary artery spasm, coronary endothelial dysfunction, tachyarrhythmias, bradyarrhythmias, anaemia, respiratory failure, hypotension and severe hypertension, injurious effects of pharmacological agents and toxins.
  • 8.
    • Type 3 suddencardiac death with symptoms of ischaemia, new ST elevation or LBBB or coronay thrombus • Type 4a MI associated with PCI • Type 4b MI associated with stent thrombosis • Type 5 MI associated witH CABG
  • 9.
    Classification of MyocardialInfarction • Type I: Spontaneous Myocardial Infarction • Type 2: Myocardial Infarction Secondary to an Ischemic Imbalance • Type 3: Myocardial Infarction Resulting in Death When Biomarker Values Are Unavailable • Type 4a: Myocardial Infarction Related to Percutaneous Coronary Intervention (PCI) • Type 4b: Myocardial Infarction Related to Stent Thrombosis • Type 5: Myocardial Infarction Related to Coronary Artery Bypass Grafting (CABG)
  • 10.
    Non-modifiable risk factors: •Gender • Age • Family history of CVD • Diabetes • Human immunodeficiency virus (HIV).
  • 11.
    Modifiable risk factors: •smoking • poor diet • high cholesterol • physical inactivity • high blood pressure • being overweight • depression, social isolation and • lack of social support
  • 13.
    SIGNS • Signs ofsympathetic activation : Pallor, Sweating, Tachycardia • Signs of vagal activation : Vomiting, Bradycardia • Signs of impaired myocardial function : -Hypotension, oliguria, cold periphery. -Narrow pulse pressure -Raised JVP -Third heart sound -Lung Crepitation • Sign of tissue damage : Fever • Complications : Murmur ,Pericardial rub
  • 14.
    Risk Stratification • Fivesimple baseline parameters have been reported to account for > 90% of the prognostic information for 30- day mortality. These characteristics are given in descending order of importance: -Age -Systolic blood pressure - Killip classification -Heart rate -Location of MI • In addition, various risk models have been created to improve risk prediction.
  • 15.
    TIMI Risk Modelfor Prediction of Short-Term Mortality in ST-Segment Elevation Myocardial Infarction Patients
  • 16.
    DIAGNOSIS • It isbased on : Clinical Findings Classical ECG Changes Rising Titre of Cardiac Enzymes • The classic ECG findings: ST segment elevation, followed by T wave inversion and Q waves.
  • 18.
    • Atypical ECGfindings – Bundle branch block – Ventricular pacing – Non diagnostic ECG – Isolated posterior MI – universal ST depression with ST-elevation in aVR – Diagnosis in doubt → echo → primary PCI strategy
  • 19.
    Routine Investigation • ECG(Serial ECG may be required) • CK-MB • Troponin I( Serial measurement may be required) • ECHO-2D • Fasting Lipid Profile • HbA1c • Serum Creatinine • SGPT • Serum Electrolyte • CBC • CXR-P/A view • FBS/RBS
  • 20.
    Other Investigation • Echocolor Doppler- Wall motion Defect,LV Impairment, MR, VSR • CAG
  • 22.
    LOCALIZATION OF CORONARYCIRCULATION IN M.I. ANATOMIC ECG LEADS CORONARY ARTERY • Septal V1-v2 Proximal LAD • Anterior V3-V4 LAD • Apical V5-V6 Distal LAD, LCx, or RCA • Lateral I, Avl LCx • Inferior II, III, aVF RCA(85%), LCx (15%) • RV V4R Proximal RCA • Posterior V1-V3 RCA or LCx
  • 23.
    Management The goals forthe management of patients with suspected STEMI include: 1. control of cardiac discomfort, 2. rapid identification of patients who are candidates for urgent reperfusion therapy, 3. triage of lower-risk patients to the appropriate location in the hospital, and 4. avoidance of inappropriate discharge of patients with STEMI
  • 24.
    Initial ER Management •Aspirin 160 to 320 mg tablet (non-enteric coated, chewed); • Clopidogrel 300 to 600 mg whether or not fibrinolysis will be given; • Clopidgrel 600 mg or prasugrel 60 mg or ticagrelor 180 mg when a patient will undergo PCI; • Nitrates, either via sublingual or intravenous(IV) routes. Nitrates are contraindicated in patients with hypotension or those who took a phosphodiesterase 5 (PDE5) inhibitor within 24 hrs (48 hrs for tadalafil); • Morphine 2 to 4 mg IV for relief of chest pain, and; • Supplemental oxygen MAY BE RECOMMENDED during the first 6 hours to patients with arterial oxygen saturation of less than 90%.
  • 41.
    Absolute contraindications • Anyprior ICH • Known structural cerebral vascular lesion (eg, AVM) • Known malignant intracranial neoplasm (primary or metastatic) • Ischemic stroke within 3 months EXCEPT acute ischemic stroke within 4.5 h • Suspected aortic dissection • Active bleeding or bleeding diathesis (excluding menses) • Significant closed-head or facial trauma within 3 mo • Intracranial or intraspinal surgery within 2 mo • Severe uncontrolled hypertension (unresponsive to emergency therapy) • For streptokinase, prior treatment within the previous 6 mo
  • 42.
    Relative contraindications • Historyof chronic, severe, poorly controlled hypertension • Significant hypertension on presentation (SBP 180 mm Hg or DBP 110 mm Hg) • History of prior ischemic stroke 3 mo • Dementia • Known intracranial pathology not covered in absolute contraindications • Traumatic or prolonged (10 min) CPR • Major surgery (3 wk) • Recent (within 2 to 4 wk) internal bleeding • Noncompressible vascular punctures • Pregnancy • Active peptic ulcer • Oral anticoagulant therapy
  • 43.
    TIMI • TIMI FLOWGRADE — The degree of perfusion in the infarct-related artery (IRA) is typically described by the TIMI flow grade: • TIMI 0 refers to the absence of antegrade flow beyond a coronary occlusion. (complete occlusion) • TIMI 1 flow is faint antegrade coronary flow beyond the occlusion, although filling of the distal coronary bed is incomplete. • TIMI 2 flow is delayed or sluggish antegrade flow with complete filling of the distal territory. • TIMI 3 flow is normal flow which fills the distal coronary bed completely.
  • 52.
    Complication Of STEMI EarlyComplication: • Disturbance of rate, rhythm, and conduction • Cardiogenic Shock • Left Ventricular failure • Right ventricular failure • Pulmonary embolism and infarction • Cerebrovascular accident • Rupture of intraventricular septum • Acute MR; LV free wall rupture • Pericarditis
  • 53.
    Continue…. Late Complication: • Reinfarction • Recurrence of arrhythmia • Heart Failure • Post MI syndrome • Ventricular Aneurysm • Thromboembolism • Sudden death • Psychosis
  • 69.