Myocardial Infarction

I. Anatomy and Physiology

 The heart is the primary pump that circulates blood through the entire
vascular system. It is closely related to the size of the body and is roughly
the size of the individual’s closed fist.
 The heart lies in the pericardial cavity. It is formed by the pericardium, or
pericardial sac, tissues that surround the heart and anchor it within the
mediastinum.
 The pericardium consists of 2 layers. The tough, fibrous connective
tissue outer layer is the fibrous pericardium, and the inner layer of flat
epithelial cells, with a thin layer of connective tissue, is called the serous
pericardium.
 The portion of the serous pericardium lining the fibrous pericardium is
the parietal pericardium, whereas the portion covering the heart surface
is the visceral epicardium, or epicardium.
 Each half of the heart is made up of two chambers: superiorly the atria
and inferiorly the ventricles. Thus the four chambers of the heart include
the right atrium, right ventricle, left atrium, and left ventricle.
  The cardiac muscle in the wall of the heart is thick and metabolically very
active. Two coronary arteries supply blood to the wall of the heart.
 The left coronary artery originates on the left side of the aorta. It has 3
major branches: The anterior interventricular artery, circumflex artery,
and the left marginal artery. The right coronary artery originates on the
right side of the aorta. It gives rise to the posterior interventricular artery.

References:
Seeley's Essentials of Anatomy and Physiology, 9th Edition
Hillegass Essentials of Cardiopulmonary Physical Therapy, 3rd Edition

II. Definition
 Osteoarthritis is also called as degenerative joint disease, is
characterized by degeneration of cartilage that results in structural and
functional failure of synovial joints.
 Most prevalent form of arthritis and is a leading cause of impaired
mobility in the elderly.
 Can be divided into two classifications:
 Primary OA - a disorder of unknown cause, and the cascade of
joint degeneration events associated with it is thought to be
related to a defect in the articular cartilage.
 Secondary OA- has a known cause, which may be trauma,
infection, hemarthrosis, osteonecrosis, or some other condition.
References:
Robbins and Cotran Pathologic Basis of Disease, 9th Ed.
Lippincott’s Primary Care Orthopaedics
O’Sullivan Physical Rehabilitation, 6th Ed

III. Etiology
 Injury before adulthood may start the remodeling of a bone that modifies
joint mechanics and nourishment in a way that winds up risky only later in
life.
 Work-related tasks including heavy-lifting are associated with the
development of hip OA.
 There is expanding recognition of the role of femoroacetabular impingement
(FAI), a mechanical mismatch between the femoral head and acetabulum.
 Sports that involve high-intensity, acute, direct joint impact from contact with
different players do convey an increased risk of OA, particularly when
repetitive joint impact and twisting are combined.
 Labral tears can likewise disrupt the synovial seal that contains the synovial
fluid inside the joint. The resulting increase in joint friction can further harm
the joint and contribute to the advancement of osteoarthritic changes.
 Obesity
 References:
O’Sullivan Physical Rehabilitation, 6th Ed.
Goodman Pathology Implications for the Physical Therapist, 4th Ed.

IV. Epidemiology
 OA is the most well-known type of arthritis and is widespread among people
more than 40 years old.
 27 million adults age 25 or more of the U.S. populace have clinical OA of
some joint.
 As the normal age of the U.S. populace expands, an expected 67 million
Americans will gain some type of arthritis by the year 2030.
 Approximately 10% to 30% of those influenced with OA have significant pain
and disability.
 Understanding the risk factors related with OA can help in further clarifying
the disease process as well as helping to potentially slow down OA
progression.
References:
O’Sullivan Physical Rehabilitation, 6th Ed.
Frontera and De Lisa’s Physical Rehabilitation and Medicine, 5 th Ed.

V. Pathophysiology
 An increase in water content is involved in OA, with the proteoglycans
having been swollen with water far beyond ordinary.
 Articular cartilage loses its compressive stiffness and elasticity which brings
about the transfer of compressive forces to underlying bone.
 The joint space narrows as the articular cartilage is destroyed.
 Portrayed by biosynthesis and repair as the chondrocytes attempt to recover
the damaged matrix while the later stage is degradative in nature as
catabolic enzyme activity digests the matrix and dissolves the cartilage.
 Fibrous, cartilaginous, and bony prominences, known as osteophytes,
eventually develop around the periphery of the joints, but can likewise
develop along joint capsule insertions or project from the degenerating joint
surfaces.
 Mild fraying or “flaking” of superficial collagen fibers and deeper fraying or
“fibrillation” of the upper third of the cartilage follows and may advance to
full-thickness fissures.
 Fissuring and eburnation of the cartilage, which is portrayed as the
diminishing and loss of the articular cartilage, bringing about the exposure
of the subchondral bone, which becomes denser with the surface getting
worn and polished, can occur.
References:
O’Sullivan Physical Rehabilitation, 6th Ed.
Goodman Pathology Implications for the Physical Therapist, 4th Ed.
Frontera and De Lisa’s Physical Rehabilitation and Medicine, 5 th Ed.
 VI. Clinical Manifestation
 Pain present in combination with either:
 Hip internal rotation ≥15°
 morning stiffness ≤60 minutes
 Hip internal rotation <115°
 Decreased ROM with a tendency for the hip to be held in a somewhat
flexed, abducted, and externally rotated position.
 Internal rotation is usually restricted and painful.
 Pain arising from the hip joint is commonly experienced in the groin, but
can also be felt in the buttock, trochanteric, or knee region.
 Increased risk of falls
 Bony enlargement
 Crepitus on motion
 Tenderness on pressure
 Joint effusion
 Malalignment
 Joint deformity
 Decreased hip ROM is associated with:
 Decreased walking speed
 Decreased stride length
 Poor balance
 Increased energy expenditure
References:
O’Sullivan Physical Rehabilitation, 6th Ed.
Goodman Pathology Implications for the Physical
Rehabilitation, 4th Ed.

VII. Sequelae
 Cardiac failure
 Cardiogenic shock
 Cardiac rupture
 Pericarditis
References:
Goodman Pathology Implications for the Physical Therapist, 4th Edition
https://www.nursingtimes.net/clinical-archive/cardiovascular/complications-
associated-with-myocardial-infarction/205206.article

VIII. Prognosis
 The first 24 hours after onset of symptoms is the time of highest risk for
sudden death. The sooner someone reaches the hospital, the better the
prognosis. Of those experiencing an acute MI, 80% survive the initial
attack when transported to a coronary care unit. Substantial reductions
in post-MI death have occurred over the last 5 decades because of
improved intervention.
  Factors negatively affecting prognosis include age (clients older than 80
years have a 60% mortality); evidence of other CVDs, respiratory
diseases, or uncontrolled diabetes mellitus; anterior location of MI (30%
mortality rate); and hypotension (clients whose systolic blood pressure
is less than 55 mm Hg have a 60% mortality rate). The risk of re-
infarction is increased in women, people with elevated blood pressure,
and people with elevated serum cholesterol.

References:
Goodman Pathology Implications for the Physical Therapist, 4th
Edition
IX. Medical Assessment
 Electrocardiogram (ECG)

 Angiogram
 References:
Seeley's Essentials of Anatomy and Physiology, 9th Edition
Goodman Pathology Implications for the Physical Therapist, 4th Edition
Watchie Cardiovascular and Pulmonary Physical Therapy, 2nd Edition

X. Medical Treatment
 Anticoagulants (aspirins) to slow down or prevent clot formation
 Thrombolytic agents, such as tPA (tissue plasminogen activator),
facilitate break down of clots that have already formed
 “Clot busters” or “super-aspirins” e.g., Ticlid (ticlopidine), clopidogrel
 Angioplasty or bypass surgery

References:
Goodman Pathology Implications for the Physical Rehabilitation, 4th Edition
Seeley's Essentials of Anatomy and Physiology, 9th Edition

XI. PT Assessment
 History taking
 Inspection
 Auscultation
References:
Magee Orthopedic Physical Assessment, 6th Edition

XII. PT Treatment
 Cardiac Rehabilitation:
 Inpatient Phase (Phase I):
 Initiate self-care activities
 Progress from sitting to standing to minimize
deconditioning
 Provide supervised ambulation
  Outpatient Phase (Phase II):
 “Low-level” exercise training
 Progress the patient to an independent exercise program
 Outpatient Program (Phase III):
 Supervised exercise conditioning program continued in a
hospital or community setting
 Perform recreational activities
References:
Kisner Therapeutic Exercise Foundations and Techniques, 6th Edition

Prepered by:
Mercado, Danette L.
Pulgar, Danison P.