Transcript Crisp White & Navy - University of Windsor

Coronary Artery
Disease and Acute
Coronary Syndrome
The Heart as a Pump
► The
heart is a hollow
muscular organ about
the same size as your
fist.
► It is a 2 sided pump,
with a muscular wall
called the septum
separating the right
and left sides
The Coronary Arteries
►
►
►
As a muscle the heart
needs oxygen and
nutrients to work
The heart muscle has its
own blood supply through
the coronary arteries
Women’s coronary arteries
tend to be smaller
Description
► Coronary
Artery Disease (CAD)
 A type of blood vessel disorder that is
included in the general category of
atherosclerosis
Description
► Atherosclerosis
 Can occur in any artery in the body
 Atheromas (fatty deposits)
►Preference for the coronary arteries
Description
► Atherosclerosis
 Terms to describe the disease process:
►Arteriosclerotic heart disease (ASHD)
►Cardiovascular heart disease (CHD)
►Ischemic heart disease (IHD)
►CAD
Description
► Cardiovascular
diseases are the major cause
of death in the US and Canada
► Heart attacks are still the leading cause of
all cardiovascular disease deaths and deaths
in general
Etiology and Pathophysiology
► Atherosclerosis
is the major cause of CAD
 Characterized by a focal deposit of cholesterol
and lipids, primarily within the intimal wall of
the artery
Process of Coronary Artery
Disease - Atherosclerosis
►
Over time ….a series of
events within the artery
 A fatty streak
(permanent)– can start in
infancy & young children
 Fatty – ( lipid) deposits
throughout the years
 Narrowing and impaired
blood flow occurs with
the gradual occlusion as
plaque thickens and blood
clots form
Etiology and Pathophysiology
► Endothelial
lining altered as a result of
chemical injuries
 Hyperlipidemia
 Hypertension
Etiology and Pathophysiology
► Bacteria
and/or viruses may have role in
damaging endothelium by causing local
inflammation
► C-reactive protein (CRP)
 Nonspecific marker of inflammation
 Increased in many patients with CAD
 Chronic exposure to CRP triggers the rupture of
plaques
Etiology and Pathophysiology
► Endothelial
alteration 
 Platelets are activated
 Growth factor stimulates smooth muscle
proliferation
 Cell proliferation entraps lipids, which calcify
over time and form an irritant to the
endothelium on which platelets adhere and
aggregate
Etiology and Pathophysiology
► Endothelial
alteration 
 Thrombin is generated
 Fibrin formation and thrombi occur
Response to Endothelial Injury
Fig. 33-3
Stages of Development in
Atherosclerosis
Fig. 33-4
Etiology and Pathophysiology
Collateral Circulation
► Analogous
to “detours” around
atherosclerotic plaques
► Occur normally in coronary circulation
► But collaterals increase in the presence of
chronic ischemia
► When occlusion occurs slowly over a long
period, there is a greater chance of
adequate collateral circulation developing
Collateral Circulation
Fig. 33-5
Risk Factors for Coronary Artery Disease
► Risk
factors can be divided:
 Unmodifiable risk factors
 Modifiable risk factors
Risk Factors for Coronary Artery Disease
► Unmodifiable




risk factors:
Age
Gender
Ethnicity
Genetic predisposition
Risk Factors for Coronary Artery
Disease
► Modifiable







risk factors:
Elevated serum lipids
Hypertension
Smoking
Obesity
Physical inactivity
Diabetes mellitus
Stressful lifestyle
Diabetes Treatment
►
►
►
►
►
►
►
Prescribed Meal Plan (sit down with a Dietitian)
Home Blood Sugar monitoring
Regular exercise – at least 150 mins./wkly
? Medications – pills or Insulin or both
Ongoing Education- Diabetes classes
Support – family and friends
Physician follow-up or Specialist referral
A person with Diabetes is considered
high risk like someone who has
already had a heart attack!
Stress
- “We do not laugh because we’re happy –
we’re happy because we laugh” William James
Stress may not be the main
cause of disease ……. but,
managing stress helps us;

maintain health

deal with health problems.
Anger, anxiety and depression
are major emotions that need
to be dealt with for a healthy
heart
►
“75% of all good health
is under our control!”
Risk Factors for Coronary Artery Disease
► Health
Promotion
 Identification of high-risk persons
 Management of high-risk persons
►Risk




factor modification
Physical fitness
Health education in schools
Nutrition (weight control, ↓ fat, ↓ chol intake)
Cholesterol-lowering medications
Types of Angina
► Results
when the lack of oxygen supply is
temporary and reversible
► Types of Angina
 Stable Angina
 Prinzmetal Angina
 Unstable Angina
Coronary Artery
Stable Angina Pectoris
► Chest
pain occurs intermittently over a long
period with the same pattern of onset,
duration, and intensity of symptoms
► Can be controlled with medications on an
outpatient basis
► Pain usually lasts 3 to 5 minutes
 Subsides when the precipitating factor is
relieved
 Pain at rest is unusual
Silent Ischemia
► 80
% of patients with myocardial ischemia
are asymptomatic (with pain or without pain
the ischemia has the same prognosis)
Prinzmetal’s Angina
► Occurs
at rest usually d/t spasm of major
coronary artery
► Spasm may occur in the absence of CAD
Unstable Angina
► Angina






that is:
New in onset
Occurs at rest
Has a worsening pattern
Unpredictable
Considered to be an acute coronary syndrome
Associated with deterioration of a once stable
atherosclerotic plaque
Clinical Manifestations
Angina
► Chest
pain or discomfort (d/t ischemia)
 A strange feeling, pressure, or ache in the chest
 Constrictive, squeezing, heaving, choking, or
suffocating sensation
 Indigestion, burning
However…
► Up
to 80% of patients with myocardial
ischemia are asymptomatic
► Associated with diabetes mellitus and
hypertension
Location of Chest Pain
Fig. 33-12
Diagnostic Studies
Angina
► ECG
► Coronary
angiography
► Cardiac markers (CK MB, Troponin)
► Treadmill exercise testing (stress test)
► Serum lipid levels
► C-reactive protein (CRP)
► Nuclear imaging
Coronary Angiography
►
►
►
A diagnostic test using xrays to record the passage of
a contrast dye in the heart
To identify the presence,
location and nature of any
coronary artery disease
The heart valves and heart
muscle can also be assessed
Coronary Angiogram
Coronary Angioplasty Video Link
► http://www.healthscout.com/animation/1/3
8/main.html
Collaborative Care
Angina
► Treatment
for stable angina:
  oxygen demand and/or  oxygen supply
 Nitrate therapy
 Stent placement
Collaborative Care
Angina
► Treatment




for stable angina:
Percutaneous coronary intervention
Atherectomy
Laser angioplasty
Myocardial revascularization (CABG)
Coronary Artery Bypass Surgery
►
►
Is open heart surgery, which
a bypass ( detour) is made to
go around an area of
blockage in a coronary artery
Bypasses are usually taken
from the leg veins or an
artery from the inside of the
chest wall
Collaborative Care
Angina
► Drug
Therapy
 Antiplatelet aggregation therapy
►Aspirin:
drug of choice (for MI prevention)
►First line of treatment for angina
Collaborative Care
Angina
► Drug
Therapy
 Nitrates
►1st
line therapy for treatment of acute anginal
symptoms
►Dilation of vessels
Collaborative Care
Angina
► Drug
Therapy
 -Adrenergic blockers
 Calcium channel blockers
Collaborative Care
Angina
► Percutaneous
coronary intervention
 Surgical intervention alternative
 Performed with local anesthesia
 Ambulatory 24 hours after the procedure
Collaborative Care
Angina
► Stent
placement
 Used to treat abrupt or threatened abrupt
closure and restenosis following PCI
The Coronary Stent Procedure
►
A coronary stent is a
small tubular wire
object inserted into a
coronary artery at the
time of angioplasty to
keep the previously
narrowed artery open
Collaborative Care
Angina
► Atherectomy
 The plaque is shaved off using a type of
rotational blade
 Decreases the incidence of abrupt closure as
compared with PCI
Collaborative Care
Angina
► Laser
angioplasty
 Performed with a catheter containing fibers that
carry laser energy
 Used to precisely dissolve the blockage
Collaborative Care
Angina
► Myocardial
revascularization (CABG)
 Primary surgical treatment for CAD
 Patient with CAD who has failed medical
management or has advanced disease is
considered a candidate
Clinical Manifestations
Myocardial Infarction
► Pain
 Severe, immobilizing chest pain not relieved by
rest, position change, or nitrate administration
►The
hallmark of an MI
Serum Cardiac Markers
(Lewis p.817)
►
►
Creatine Kinase (creatine phosphokinase) (CK-MB)
 Increased in > 90% of MI patients.
 Begins to rise 4-6 hours
 Peaks 24 hours
 Returns to normal in 2 - 3 days
Troponin
Myocardial muscle protein released after an injury
Troponin T and Troponin I are cardiac specific indicators
of an MI
Much more specific than CK-MB
Rises quickly and remains elevated for 2 weeks
Serum Cardiac Markers
► Lactic





Dehydrogenase (LD or LDH)
Found in heart muscle as well as others
It is increased in >90% of MI patients.
Begins to rise 24 hours
Peaks in 3 days
Returns to normal in 8-9 days
Diagnostic Cardiac enzymes
(See Lewis p. 817 Figure 33-15 also)
Clinical Manifestations
► Acute
Coronary Syndrome (ACS)
 Develops when the oxygen supply is prolonged
and not immediately reversible
Clinical Manifestations
► ACS
encompasses:
 Unstable angina
 Myocardial infarction (MI)
Relationships Among CAD, Stable
Angina, and MI
Fig. 33-8