MYOCARDIAL INFARCTION
MYOCARDIAL INFARCTION
the heart located to the left of the midline. o Stroke Volume (SV): 70 mL of
• Apex: Positioned just above the diaphragm. blood ejected per beat.
Cardiac Cycle
Cardiac Cycle and Physiology
• Systole: Contraction to pump blood out.
• Cardiac Cycle: Describes the events
• Diastole: Relaxation to fill the heart
between one heartbeat and the next,
chambers with blood.
involving both contraction (systole) and
• Blood Pressure: Increases during systole,
relaxation (diastole) of the heart.
decreases during diastole.
o Systole: Heart muscles contract to
pump blood out of the chambers.
o Diastole: Heart muscles relax to
allow the chambers to fill with
blood.
Cardiac Output ECG Components:
The continuum from angina to myocardial infarction (MI) is acute coronary syndrome. Manifestations of
acute coronary syndrome are due to an imbalance between myocardial oxygen supply and demand.
When blood flow to the heart is compromised, ischemia causes chest pain. Anginal pain is often described
as a tight squeezing, heavy pressure, or constricting feeling in the chest. The pain can radiate to the jaw, neck, or
arm. Pain unrelieved by rest or nitroglycerin and lasting for more than 15 min differentiates an MI from angina.
Females and older adults do not always experience manifestations typically associated with angina or MI.
The area of infarction in clients experiencing a myocardial infarction (MI) develops over minutes to hours. Early
recognition and treatment of an acute MI is essential to prevent death.
Research shows improved outcomes following an MI in clients treated with aspirin, betablockers, and
angiotensin-converting enzyme inhibitors or angiotensin receptor blockers.
An abrupt interruption of oxygen to the heart muscle produces myocardial ischemia. Ischemia can lead to
tissue necrosis (infarction) if blood supply and oxygen are not restored. Ischemia is reversible. An infarction
results in permanent damage. When the cardiac muscle suffers ischemic injury, cardiac enzymes are released into
the bloodstream, providing specific markers of MI.
PATHOPHYSIOLOGY
Ischemia beyond 20 minutes to several hours can cause irreversible cellular death (necrosis)
MI CLASSIFICATION
o Transmural MI: Full thickness hypercholesterolemia, elevated damage of the myocardium. (from
endocardium to epicardium) AKA Q-wave MI
o Non-Transmural MI: Partial thickness damage. Affects only part of the myocardium. AKA non Q-wave
MI. ST depression and T wave inversion may be seen.
✓ T-wave inversion is an indicator of ischemic damage to myocardium. Typically, few changes to P
waves occur during or after an MI, whereas Q-wave changes with no change in the ST or T wave
indicate an old MI.
4. Cardiac catheterization
• A coronary angiogram, also called a cardiac
catheterization, is an invasive diagnostic
procedure used to evaluate the presence and
degree of coronary artery blockage.
• Angiography involves the insertion of a
catheter into a femoral (sometimes a brachial)
vessel and threading it into the right or left
side of the heart. Coronary artery narrowing
and occlusions are identified by the injection
of contrast media under fluoroscopy.
Nursing actions: 1. Oxygen therapy- 2-4Lpm
2. Sublingual nitroglycerin therapy
• Ensure the client understands the procedure
3. Adequate analgesia (with morphine sulfate or
prior to signing informed consent.
Meperidine)
• Ensure that the client remains NPO 8hr prior
4. Aspirin, 160 to 325 mg orally
to procedure.
5. 12-lead electrocardiogram (ECG) should be
• Assess for iodine/shellfish allergy (contrast
performed
media).
6. Immediate reperfusion therapy, either by
thrombolytic or primary percutaneous
Interprofessional care