STEMI pdf - D. Tahsin

ACUTE ST ELEVATION

MYOCARDIAL INFARCTION

(STEMI

)

By The End of This Lecture You Should Be

Able To

• Differentiate ACS from other acute chest pain emergency

conditions

• Diagnose STEMI using clinical, ECG, and biochemical tools
• Recognize the various steps of management of the patients

before and after reaching hospital

Objectives

• Appreciate the vital importance of time in the proper

management of STEMI

• Appreciate that STEMI is caused by complete obstruction of

a coronary artery by thrombus

• Understand that thrombus removal is the cornerstone of

management

• When the ECG shows ST elevation, attempts at reperfusion

should take priority over further investigations

Clinical Scenario 1

• A 60-year-old man with Hx of diabetes, hypertension, and

smoking is brought to the emergency room by his family
because of severe chest pain

What Conditions Cause Acute chest pain?

• ACS (STEMI, NSTEMI)
• Aortic dissection
• Acute pericarditis
• Pulmonary embolism and infarction
• Pneumothorax
• Extracardiac causes: esophageal spasm, visceral obstruction

or perforation, musculo-skeletal chest pain

Clinical Presentation of ACS, including STEMI

Pain:
• Chest, back, shoulder, epigastrium, neck, throat, mandible,

arms, hands

• Prolonged
• Severe
• Not relieved!

ACS (STEMI): Clinical features

Other features
• Severe anxiety
• Nausea and vomiting
• Breathlessness
• Collapse
• Syncope

STEMI: PHYSICAL SIGNS

• Signs of sympathetic activation:

• Pallor
• Sweating
• Tach

ycardia

• Signs of vagal activation

• Vomiting
• B

radycardia

STEMI: PHYSICAL SIGNS

• Signs of impaired myocardial function

• Hypotension, oliguria, cold sweat
• Narrow pulse pressure
• Raised JVP
• S3
• Faint S1
• Diffuse apical impulse
• Lung

crepitations

STEMI: DIFFERENTIAL Dx

• Aortic dissection:

• Pain is abrupt & severe from the onset, tearing in nature, more in

the back

• Pulmonary embolism

• Dyspnea, tachypnea, tachycardia, hypotension

• Acute pericarditis:

• Important to differentiate, as thrombolytic therapy may cause

cardiac tamponade

• Pain is sharp, related to breathing , posture and swallowing

• Pericardial friction rub

STEMI: Diagnosis & Basic Investigations

• Clinical presentation
• ECG
• Troponin (indicating myocardial cell injury)
• Enzymes indicating myocardial cell necrosis: CPK, AST,

LDH

STEMI Diagnosis, additional investigations

• Echocardiography
• CXR
• Blood tests: WBC, ESR

Tetrad of Diagnosis

•Chest pain
•Classical ECG showing ST elevation
•Raised troponin
•Raised markers of myocardial cell necrosis

The ECG in STEMI

Sequence of changes in STEMI:
1. Tented, peaked T waves
2. Acute ST elevation (the current of injury)
3. Loss of amplitude of the R wave
4. Development of a Q wave
5. T wave inversion
6. Reduction in the magnitude of the ST elevation (ST resolution)
7. Deepening of Q waves

The ECG in STEMI

• Hyperacute T waves

STEMI: ECG

• ST segment elevation: the earliest ECG change

STEMI

normal

angina

STEMI: ECG

• Next: reduction of R wave amplitude, appearance of Q

waves, T inversion

STEMI: ECG

• Then: deepening of Q waves, T inversion & resolution of ST

segment

STEMI: ECG

• 12 weeks after MI, the ST segment returns completely to

normal

Acute Anterior MI

Acute inferior MI

STEMI Diagnosis:

Biochemical markers

• Troponin T (Tn T)
• Troponin I (Tn I)
• Creatinine Kinase (CK)
• Creatinine kinase MB (CK-MB)
• Others: AST, LDH

Biochemical Markers

Biochemical Markers: Troponins

cTn-T & cTn-I:
• More specific than CK & CK-

• Start to rise in 4-6 hours
• Persist in the circulation for 2

weeks

• Troponins are elevated in

unstable angina but to less
severe degree.

Biochemical Markers

CK (creatinine kinase):
• Found in skeletal muscles (MM isoenzyme), in the brain (BB

isoenzyme) and in the myocardium (MB isozyme)

• Starts to rise at 4-6 hours,

peaks at 12 hrs, and
disappears in 36-48 hrs

Biochemical Markers

CK is not specific for cardiac muscle, it may rise in

• Intramuscular injection
• Physical exercise
• Defibrillation

CK-MB is more specific and sensitive for cardiac muscle

injury

Biochemical Markers

CK-MB is not elevated with the administration of DC shock or

skeletal muscle injury.

Further Testing?

• If the ECG shows ST elevation, time should be

reserved for immediate management!

• Other investigations should be done after reperfusion

therapy

Other Blood Tests

• Leukocytosis:

• Neutrophilia
• Reaches a peak on the first day
• Correlates

with the extent of myocardial damage, i.e. with prognosis

• Erythrocyte Sedimentation Rate (ESR)
• C-Reactive Protein (CRP)

Chest X-Ray

• Pulmonary edema

• Heart size:

• Usually normal
• Cardiomegaly

due to old myocardial infarctions

Echocardiography

• Usually done after reperfusion therapy
• Can be performed at the bedside
• Useful to assess the status of the LV & RV
• Detects mechanical complications

• LV mural thrombus
• Ventricular septal rutpture
• Mitral regurgitation
• Pericardial effusion
• RV infarction

Clinical Scenario 2

• A 70-year-old man suffers severe chest pain with sweating

and severe weakness while at rest.

This patient Probably
Sustained ACS (Infarction,
Heart Attack)

Immediate (Prehospital) management

• DO NOT PANIC!
• Call for help, ambulance
• Transfer to a safe place,

remove tight clothes,
administer sublingual
angised if available…..

Immediate (Prehospital) management

• Observe pulse, BP (if

possible) and level of
consciousness

• Transfer to hospital as

soon as possible

• What is the immediate danger to the patient?

What is the imminent danger to this patient?

Acute cardiovascular collapse & death, caused by
• Arrhythmia (VF)
• Cardiac standstill

• Patient becomes pulseless and unconscious

Immediate (Prehospital) management: CPR

• In case patient becomes pulseless and unresponsive:

administer CPR (cardio-pulmonary rescuscitation)

Immediate (Prehospital) management

AED: automatic
external Defibrillator:
If available, give DC
shock, continue CPR
until restoration of
pulse, repeat DC if
necessary

Prehospital management

• Advanced Life Support (ALS)

Transferring The Patient

• Rapid transfer of the patient to hospital: ambulance

• Ambulance should be well

equipped:

• Defibrillators
• Analgesia
• Oxygen
• Monitors
• ECG machines
• Thrombolytic therapy?

Early managemnt: immediate measures

• Cannula
• Oxygen
• ECG monitoring
• Standard (12-lead) ECG
• Analgesia: morphine sulphate

REPERFUSION

THERAPY

STEMI

• Myocardial necrosis caused by thrombotic occlusion of a

coronary artery

• Occlusive thrombus is formed at site of rupture of

atherosclerotic plaque

Reperfusion

• Once diagnosis is established, reperfusion should be

attempted

• Should be done as soon as possible
• The situation is an emergency: minutes mean muscle

THE KEY TO PROPER MANAGEMENT OF ACUTE

MYOCARDIAL INFARCTION IS THE TIMELY AND

IMMEDIATE REMOVAL OF THROMBUS

OBSTRUTION AND RESTORATION OF BLOOD FLOW

TO THE INFARCTED SEGMENT. THIS IS EXPECTED

TO PREVENT LOSS OF MYOCARDIUM, IMPROVE LV

FUNCTION, IMPROVE QUALITY OF LIFE, AND

PROLONG SURVIVAL.

Reperfusion

• Restoration of coronary patency
• Resolution of acute ST elevation
• Reduces myocardial infarct size
• Relieves pain
• Preserves LV function
• Improves survival

Reperfusion

• May reduce arrhythmias, but may exacerbate these

arrhythmias (reperfusion injury)

• Should be administered as soon as possible to achieve

maximal salvage of myocardium (minutes mean muscle)

Methods of Reperfusion

•Pharmacological (thrombolytic therapy)

Mechanical (primary PCI)

• Mechanical (primary PCI)

Reperfusion: Thrombolytic therapy

• Thrombolytic agents:

• Streptokinase
• Alteplase (tPA)
• Tenecteplase (TNK)
• Reteplase (rPA)

Reperfusion: Thrombolytic therapy

• Thrombolysis is of no benefit (and may be harmful):

• If given > 12 hours from the onset of STEMI

(preferably given within the first 6 hours)

• In cases of NSTEMI or unstable angina

Thrombolytic Complications

Bleeding:
• Cerebral hemorrhage :

• It may be wise to withhold treatment if there is significant risk of bleeding

• With streptokinase:

• the development of antibodies to the drug that render future administration

of the drug ineffective

• hypotension

Thrombolysis: Contraindications

Absolute contraindications:
• Known bleeding tendency
• Active bleeding (except menstruation)
• History of cerebrovascular occlusion within the previous year
• History of intracranial hemorrhage
• Cerebral or spinal tumor

Reperfusion therapy: primary PCI

• Associated with better results than thrombolytic

therapy

• Requires specialized experience and expensive

equipment

• Should be performed as soon as possible (minutes

mean muscles)

• Indicated in cases of failure of thrombolytic therapy or

when such therapy is contraindicated.

Objectives

• Be familiar with the management of the patient with

established myocardial infarction

• Understand STEMI complications in the CCU: Mechanical and

electrical

• Appreciate the long-term management of patients with

STEMI

Clinical Scenario 3:

• A 63-year-old diabetic woman sustained an anterior wall

STEMI.

• Was transferred in time to hospital
• Received thrombolytic therapy with t-PA with resolution of

ST changes and disappearance of chest pain

• Was transferred to the CCU
• Echo showed mild hypokinesia of the anterior wall with good

systolic function

• What is the next step in management?

Maintaining Vessel Patency

• Aspirin
• Clopidogrel
• Anticoagulants

Maintaining Vessel Patency: ASA

• Oral ASA (75-350 mg/day)
• Reduces mortality
• Should be continued for life
• Combination with clopidogrel: improves outcome

Maintaining Patency: Anticoagulants

• Heparin:

• Unfractionated heaprin and LMWH
• Improve survival of patients with STEMI
• Slight increase in the risk of intracranial bleeding
• Not given after successful primary PCI

Antithrombotic therapy

Oral Antithrombotic therapy?

• Warfarin
• Direct acting oral anti-coagulants:

• Direct thrombin inhibitors: dabigatran
• Factor Xa inhibitors: apixaban, rivaroxaban

Indications:
• Atrial fibrillation
• Extensive anterior wall MI with LV dysfunction
• The demonstration of mobile thrombus on echocardiography

Management of STEMI

• Early management
• Maintaining vessel patency
• Adjunctive therapy

Adjunctive Therapy

• β-blockers
• Nitrates (?)
• ACE inhibitors
• Lipid-lowering agents (statins)

Adjunctive Therapy: β-blockers

• During the acute presentation:

• i.v. administration
• Atenolol or metoprolol
• Reduce pain
• Reduce arrhythmia
• Improve short term survival

• Contraindicated:

• Congestive heart failure
• Heart block
• bradycardia

Adjunctive Therapy: β-blockers

Long term use of β-blockers :

•

Should be given to ALL patients unless contraindicated

•

Improve long term survival

Adjunctive Therapy: ACE inhibitors, Statins

• Essential for the secondary prevention of atherosclerosis
• ACE inhibitors are also useful to maintain LV function
• When side-effects develop to ACE inhibitors, ARBs should be

used

Complications of STEMI: Clinical Scenario 4

• A 55-year-old hypertensive and smoker sustains an extensive

anterior infarction. He is only transferred to hospital 24
hours after the attack. The ECG shows established anterior
wall MI, with deep Q waves, ST elevation, and T inversion in
the anterior leads. No thrombolytic therapy was
administered

• What are the expected complications?

COMPLICATIONS OF STEMI

• Short-term complications

• Arrhythmias
• Mechanical complications
• Residual ischemia
• Pericarditis
• embolism

• Long term complications

• Recurrnet ischemia
• LVdysfunction

complications

• Arrhythmias
• Mechanical complications
• Acute circulatory failure
• Residual ischemia
• Pericarditis
• embolism

complications

tachy arrhythmias

ventricular

• Arrhythmias

atrial

brady arrhythmias

Tachyarrhythmias

• Ventricular:

– Premature ventricular ectopics (PVCs)
– Accelerated idioventricular rhythm
– Ventricular tachycardia
– Ventricular fibrillation

• Atrial

– Atrial fibrillation

Tachyarrhythmias

The patient collapsed in the CCU!
• What is the diagnosis
• What’s the urgent treatment?
• What drug is given to prevent recurrence?

Tachyarrhythmias

Ventricular fibrillation:
• The major cause of death in

patients with STEMI before

reaching hospital

• Occurs in 5-10% of patients who

reach hospital

• Lethal arrhythmia unless treated

by prompt defibrillation

• Does not affect the long term

prognosis of acute MI.

Tachyarrhythmias

Atrial fibrillation:
• Common in acute MI
• Frequently transient
• May be serious if it

occurs in the context of
LV failure

Atrial Fibrillation: Treatment

• May be transient and needs no treatment
• Indications to treat:

• Rapid ventricular rate
• Hemodynamic deterioration (hypotension, CHF, pulmonary

edema)

• Emergency treatment:

• Synchronized DC shock

• Non-emergency situation:

• Infusion of β-blocker or amiodarone

Bradyarrhythmia: AV block

In the setting of inferior MI:
• Usually temporary
• Resolves with thrombolytic

therapy

• May need atropine if persists
• If there is hemodynamic

deterioration:

temporary pacemaker insertion

Bradyarrhythmia: AV block

In the setting of anterior wall MI:
• More serious than in inferior MI
• May be complicated by sudden asystole
• Prophylactic temporary pacemaker should be inserted

complications

• Arrhythmias
• Mechanical complications
• Acute circulatory failure
• Residual ischemia
• Pericarditis
• embolism

Mechanical complications

• Papillary muscle rupture
• Interventricular septal rupture
• Ventricular free wall ruputre

Papillary Muscle Rupture

Papillary muscle rupture

• Sudden severe mitral regurgitation (MR)
• Presents with pulmonary edema & shock
• O/E: pansystolic murmur at the apical area radiating to the

axilla or back. S3 & S4

• The murmur is frequently faint or even absent
• Dx: echo and Doppler
• Treatment: urgent surgery

Ventricular Septal Rupture

Ventricular Septal rupture

• Sudden deterioration:

hypotension, right ventricular
failure, shock

• Clinically: pansystolic murmur at

the left sternal border

• Diagnosis: echo and Doppler
• Treatment: surgery

complications

• Arrhythmias
• Mechanical complications
• Acute circulatory failure
• Residual ischemia
• Pericarditis
• Embolism

Acute circulatory failure

(Cardiogenic Shock)

• Indicates extensive myocardial damage
• Usually fatal without intervention
• Mortality of 90% if untreated
• With primary PCI: can be reduced to 25%

Management of cardiogenic shock

• Calculating cardiac output & systemic vascular resistance

(Swan-Ganz catheter)

• The use of inotropic drugs, diuretics, &/or vasodilators

according to the calculations

• Circulatory assistance with intra-aortic balloon pump
• Primary PCI

100

complications

• Arrhythmias
• Mechanical complications
• Acute circulatory failure
• Residual ischemia
• Pericarditis
• Embolism

101

Residual Ischemia

• Presents as post infarction angina
• Causes of residual ischemia:

• Significant stenosis of an artery after successful thrombolysis
• Blockage of an artery that was responsible for the collateral supply of another

coronary artery

• Occurs in ~ 50% of patients with AMI

102

Residual Ischemia: Management

High risk group of unstable angina
• i.v. nitrates, β-blockers, Oxygen (if necessary)
• Aspirin
• Clopidogrel
• Anticoagulation
• Invasive strategy (PCI or CABG)

103

complications

• Arrhythmias
• Mechanical complications
• Acute circulatory failure
• Residual ischemia
• Pericarditis
• embolism

Pericarditis Following STEMI

• Acute pericarditis
• Post MI syndrome (Dressler’s Syndrome)

105

Acute Pericarditis

• Usually occurs in the 2

& 3

days

• Chest pain of different quality than ischemic:

• Sharp
• Localized
• Positional
• Related to breathing: worse on inspiration

• Pericardial friction rub
• ECG changes of acute pericarditis

106

Acute Pericarditis: Management

• The use of steroids or NSAID is contraindicated in AMI:

• Weakening of scar
• Increase the risk of aneurysm formation

• Aspirin in high dose
• colchicine
• Opiate-based analgesia

107

Post-MI-Pericarditis

(Dressler’s syndrome)

• Auto-immune reaction
• May occur 6 days-6 months after MI
• Pain (pleuro-pericarditis)
• Pyrexia
• Pericarditis
• Pleurisy
• Treatment: High dose ASA, NSAID, colchicine,

or even steroids

108

Complications: Ventricular

Remodelling

• Infarct expansion: thinning

& stretching of the

infarcted segment

Complications: Ventricular Remodelling

• Compensatory hypertrophy
of the remaining muscle
• Increased myocardial wall

tension

109

Complications: Ventricular Remodelling

• Eventual dilatation and
dysfunction of LV,

with the formation
of aneurysm

110

Drugs Used to Prevent Remodelling

• Angiotensin converting enzyme inhibitors
• Angiotensin receptor blockers
• Beta receptor blockers
• Mineralocorticoid antagonists
• Neprilysin inhibitors (sacubitril)

112

Management After Discharge From

Hospital

• Risk stratification
• Secondary prevention
• Rehabilitation

113

Risk Stratification after MI

Assessment for
•Residual ischemia
•Left ventricular function
•arrhythmias

114

Residual Ischemia

• Symptomatic patient: Coronary angio with a view to

revascularization

• Asymptomatic:

• Stress testing: routinely done after 4 weeks
• If high risk criteria coronary angio
• If not repeat ETT every year or if new

symptoms appear

115

Assessment of LV function

• Clinically
• ECG
• CXR
• Echo

• Radioisotope study

116

In Patients with LV dysfunction

• Look for reversible ischemia: coronary angio
• ACE inhibitors (captopril, enalapril, lisinopril)
• Angiotensin receptor blocker (ARBs) (valsartan,

losartan, candisartan) in patients who can’t

tolerate ACEI

• β-blockers: metoprolol, bisoprolol, & carvedilol
• Aldosterone receptor antagonist:

spironolactone, eplerenone

• ARB/neprilysin inhibitor (valsartan/sacubitril)

117

Arrhythmias

• Recurrent ventricular arrhythmias, causes:

• Residual ischemia
• LV dysfunction
• The presence of scar tissue

• Significant ventricular arrhythmias:

mangement

• Treatment of LV dysfunction, residual ischemia
• Electrophysiological study
• Specific anti-arrhythmic therapy
• Implantable cardiovertor-defibrillator (ICD)

118

Natural history & prognosis

• 25% of patients die within a few minutes
• 40% die within first month
• Early death is usually caused by arrhythmia
• Later on: the outcome is determined by the extent of

myocardial damage

119

Determinants of poor prognosis

• Poor LV function
• Arrhythmias
• Persistent AV block
• Anterior infarction > inferior infarction
• Old age
• Depression
• Social isolation