Myocardial infarction

Maj Aswathy Ganesh

I year MSc(N)
CON ,AFMC
Introduction
Coronary Circulation
Coronary Circulation
 Definition

• Acute Myocardial Infarction historically is defined as a clinical

syndrome that meets a certain set of criteria, usually a
combination of symptoms, electrocardiographic changes and
cardiac biomarkers in the proper clinical context

(Universal Definition Of MI –AHA)

 Incidence
• 3 million worldwide
• 1 million death in US annually
• More in developed countries
• Men is at greater risk
Risk factors
NonModifiable
 Risk factors
Modifiable

• Smoking
• Tobacco use
• Dyslipidemia
• Physical inactivity
• Obesity
• Diabetes Mellitus
• Hypertension
 Etiology

• Atheroma
• Atherosclerosis
• Coronary artery spasm
 Pathophysiology
• Acute occlusion of one or more large major coronary arteries
• The occlusion is usually thrombotic and due to rupture of a
plaque formed in coronary arteries
• Occlusion leads to lack of oxygen in the myocardium, in
ischemic conditions cardiac cells are viable for approximately
20-40 minutes
• The lack of oxygen in myocardium results in sacrolemnal
disruption and myofibril relaxation. These are one of the first
ultrastructural changes in the process of MI
 Pathophysiology
• The prolonged ischemia ultimately results in necrosis of
myocardial tissue
• With total occlusion of coronary arteries contractility ceases
after several minutes, depriving myocardial cells of glucose for
aerobic metabolism
• Anaerobic metabolism begins and lactic acid accumulates
• Myocardial nerve fibers are irritated by increased lactic acid and
transmit a pain messages to the cardiac nerves and upper
thoracic posterior nerve routes
 Pathophysiology
• The necrosis spreads from sub endocardium to sub
epicardium.The sub epicardium is believed to have increased
collateral circulation, which delays its death
• Depending on teritiary affected by infarction, the cardiac
function is compromised.
• Due to the negligible regeneration capacity of myocardium the
infarcted area heals by scar formation and often heart is
remodeled characterized by dilation segmental hypertrophy of
remaining viable tissue and cardiac dysfunction
 Pathophysiology
• Due to the negligible regeneration capacity of myocardium the
infarcted area heals by scar formation and often heart is
remodeled characterized by dilation segmental hypertrophy of
remaining viable tissue and cardiac dysfunction
• And if blood flow is restored timely, aerobic metabolism
resumes and contractility is restored ,cellular repair also begins.
 Classification

STEMI NTEMI
• Results from complete and • Results from severe coronary
prolonged occlusion of artery narrowing,transient
coronary artery occlusion,or micro
• Occurs in one or more major embolization of thrombus or
artery atheromatous material.
• Block in minor artery or partial
obstruction of major artery
 Clinical Manifestations
• Chest pain
severe,crushing
not relieved by rest
heaviness and tightness
radiating to left arm(men)
jaw, back, arm(women)
constricting
Levine’s sign
 Clinical Manifestations
• nausea and vomiting
• Shortness of breathe
• Diaphoresis
• Palpitations
• Light headness
• Loss of consciousness
• Cold calmy skin
• Sudden cardiac death
 Diagnostic evaluation
Patient history
ECG
Cardiac enzymes
2 D Echo
Cardiac enzymes and isoenzymes
Other lab investigation
Chest x -ray
 Diagnostic Evaluation
Nuclear imaging studies
Coronary angiography
Digital substraction angiography
Exercise stress test
MRI
PET scan
 Diagnostic Evaluation
• Patient history
onset of pain
character, type
medical history
personal history
previous history of CAD
family history
 Diagnostic Evaluation
ECG
ST segment elevation
Leads Location of events
V1-V4 Anterior
I,aVL,V5-V6 Lateral
I,aVL,V1-V6 Anterolateral
V1-V3 Anteroseptal
II,III,aVF, Inferior
I,aVL,V5-V6,II,III,aVF Inferolateral
??
 Diagnostic evaluation
Cardiac enzymes and isoenzymes
• CKMB – isoenzyme elevates within 4-8 hours,peak in 12-20
hours ,returns to normal in 48-72 hours
• LDH – elevation 8-24 hours peaks within 72-144 hours and
returns to normal in 14 days
• Trponin I & T- elevates in 4-6 hours, peak at 14-18 hours and
return to baseline over 6-7 days
• Myoglobin-elevated within 2 hours and peaks at 3-15 hours
 Diagnostic Evaluation
Other lab investigations
• WBC- leukocytosis
• ESR- raised
• Liver enzymes-elevated
• Lipid profile-elevated
Chest xray
May be normal or show enlarged cardiac shadow suggestive of
heart failure
 Diagnostic Evaluation
2D Echo
• Wall motion abnormalities
• Chamber size
• Ventricular function
• Ejection fraction
Nuclear imaging studies
• Myocardial viability
• Blood flow
 Diagnostic Evaluation
Coronary Angiography
• Procedure that uses contrast material and x-rays to visualize
coronary artery ,and see how blood flows through arteries ,via
transradial or transfemoral approach.
 Diagnostic Evaluation
Exercise stress test
• Measures the heart’s ability to respond to external stress in a
controlled clinical environment
MRI
• Visualization of blood flow ,plaque formation, areas of necrosis,
infarction, blood clots
PET Scan
• Evaluate cardiac metabolism, tissue perfusion, coronary artery
flow reserve, myocardial viability
 Medical Management
Goals of medical management
• To restore myocardial blood flow
• To reverse myocardial damage
• To minimize myocardial damage
• To preserve myocardial function
• To prevent complications
 Medical Management
Goals
• Prevention of major adverse cardiovascular events
• Identification of patient with STEMI and triage for ealy
reperfusion
• Relief of ischemic chest discomfort
• Treatment of acute lifethreathening complications of ACS such
as VF/pVT ,unstable bradycardia, shock
 Medical Management
• Assess ABC .Be prepared to provide CPR and defibrillation
• Administer aspirin 162 to 325mg chewable
• Consider O2 , nitroglycerin and morphine if needed
• Obtain 12 lead ECG
• Establish IV access
• Review complete fibrinolytic check list
• Obtain a initial cardiac markers level
• Obtain a potable chest x-ray
• Consider administration of p2y12 inhibitors
 Medical Management
NSTEMI
• Initiate DAPT and anticoagulant therapy
• PCI with stenting
 Medical Management
STEMI
• Early reperfusion therapy
• For PCI the goal is first medical contact-to-balloon inflation time
is 90 minutes
• For fibrinolysis door to needle time is 30 minutes
 Medical Management
Morphine
• 3 mg IV bolus
• Produce CNS analgesia
• Reduces adverse effects of neurohumoral activation
• Alleviates dyspnea
• Produces venodilation which reduce LV preload and oxygen
requirement
 Medical Management
Aspirin
• 162-325mg non-enteric coated or chewable aspirin
• Immediate and near total inhibition of thromboxaneA2 production
by inhibiting platelet cyclooxygenase
 Medical Management
Oxygen
• Administer o2 if patient is dyspneic, hypoxic, or has an obvious
sign of heart failure
• Spo2 is less than 90%
 Medical Management
Recombinant tissue plasminogen activator
• Tenectaplase 30-50 mg IV bolus over 5 secs
<60 kg - 30 mg
60-70kg 35mg
70-80kg 40mg
80-90kg 45mg
• Alteplase 0.05 0.1mg/kg/hr
• Streptokinase 250000 IU in slow IV infusion
 Medical Management
P2Y12 inhibitors / ADP receptor antagonists
• Inhibit platelet activation and aggregation by antagonizing the
platelet P2Y12 inhibitors.This prevents the binding of ADP to
the receptor which attenuates platelet aggregation
• Tab clopidogrel 300mg PO stat then 75 mg bd
• Tab ticagrelor 90 mg bd
• Tab prasugrel
• canagrelor
 Medical Management
Glycoprotein GP IIB/IIA inhibitors
• Prvent the binding of fibrinogen to platelet
• Inj abciximab
• Inj Tirofiban
Low molecular weight heparin
• Binds to antithrombin III enhancing its effect prevents
conversion of fibrinogen to fibrin
• Dose 60mg bd
 Medical Management
ACE inhibitors
• Prevents conversion of angiotensin I to angiotensin II and decreases
endothelial dysfunction
• Eg: Ramipril, Enlapril
Beta adrenergic blockers
• Inhibit sympathetic nerve stimulation of heart ,reduces both heart rate and
contractility to decrease afterload
• Eg: metaprolol ,atenolol
• Calciumchannel blocker
• Prevents entry of Ca into vascular smooth muscle
Amlodipine, diltiazem
 Medical Management
• Percutaneous coronary intervention is the recommended
reperfusion therapy in acute MI.
• Primary PCI – patient is taken to cath lab immediately arrival to
ED
• Rescue PCI – patient is initially treated with fibrinolytic therapy,
patient does not show any signs of reperfusion
• Pharmacoinvasive therapy- the patient is initially treated with
fibrinolytic therapywith intention to perform PCI if appropriate.
 Surgical Management
• CABG
• Primary surgical treatment for CAD
• Patient who had failed medical management is considered for
surgical revascularisation
 Nursing Management
• Acute pain related to myocardial ischemia and decreased
myocardial oxygen supply as manifested by severe chestpain
and tightness, radiation of pain to neck and arms, facial
grimacing , change in pulse and BP
• Activity intolerance related to imbalance between myocardial
oxygen supply and demand ,presence of ischemia on
myocardial tissues, cardiac depressant effect of certain drugs
as evidence by exertional angina generalized weakness,
alteration in heart rate and BP with activity
 Nursing Management
• Anxiety related to threat or change in health ,the threat of loss,
death, diagnosis of heart attack as evidenced by fearful attitude,
apprehension, uncertainity , feeling of inadequacy, somatic
complaints, sympathetic stimulation, expression of concern