2. Learning Objectives
Define the differences of ischemia, injury,
and infarct.
Define angina pectoris, etiology, s/s,
diagnosis, and treatment
Differentiate between UA, NSTEMI, &
STEMI: s/s, diagnosis, and treatment
Localize area of infarct on a 12-lead EKG
Discuss women & heart disease
3. National Statistics
Coronary Artery Disease
Cardiovascular disease is the leading cause of
death among men and women in all racial
and ethnic groups.
Affects approximately 58 million Americans and
costs the nation $274 billion each year,
including health expenditures and loss of
productivity
(Woods et al, 2005, p.115)
4. National Statistics
According to the AHA, 785,000
Americans will have an MI this
year, and nearly 500,000 of
them will experience another
(Overbaugh, 2009, p. 42)
5. National Statistics
In 2006, nearly 1.4 million
patients were discharged with a
primary or secondary diagnosis
of ACS, including 537,000 with
unstable angina and 810,000
with either NSTEMI or STEMI
(Overbaugh, 2009, p. 42)
6. Atherosclerotic Plaque
The usual cause of an acute coronary
syndrome is the rupture of an
atherosclerotic plaque
(Phalen and Aehlert, 2006, p. 61)
8. Angina Pectoris
Latin phrase literally means “pain in the
chest”
Many different conditions are
responsible for causing angina
pectoris
9. Stable (Classic) Angina
Remains relatively constant and predictable in
terms of frequency of episodes, severity,
duration, time of appearance, precipitating
factors, and response to therapy
Usually related to emotional upset, exercise or
exertion, exposure to cold weather, consumption
of heavy meals
Duration of symptoms is typically 2 – 5 minutes;
occasionally 10 – 15 minutes
11. Prinzmetal’s Angina
AKA Variant Angina
It is the result of intense spasm of a segment of
an epicardial coronary artery
Occurs exclusively at rest; early morning
Lasts only a few minutes; however long enough
to produce dysrhythmias including v-tach or
v-fib, as well as sudden death
12. Prinzmetal’s Angina
Difficult to identify this type of angina
Has been reported to occur with migraine,
Raynaud’s phenomenon, and aspirin-
induced asthma
It is relieved by administration of
nitroglycerin
15. Acute Coronary Syndromes
ACS’s are a physiologic continuum of
conditions caused by a similar
sequence of pathologic events: a
transient or permanent obstruction of
a coronary artery
(Phalen and Aehlert, 2006, p. 60)
16. Acute Coronary Syndromes
These conditions are characterized by
an excessive demand or inadequate
supply of O2 and nutrients to the
heart muscle associated with:
Plaque Disruption
Thrombus Formation
Vasoconstriction
(Phalen and Aehlert, 2006, p. 60)
17. ACS’s: 3 Categories
Unstable Angina
Non-ST-Segment Elevation MI
(NSTEMI)
ST-Segment Elevation MI (STEMI)
19. Coronary Artery Obstruction
How does it happen?
Fatty Streak Fibrous Plaque Ruptured Plaque Advanced
Atheromatous
Plaque
20. Endothelial Damage
Progression from a fatty streak to an
advanced lesion is associated with
injured endothelium that activates the
inflammatory response
(Phalen and Aehlert, 2006, p. 61)
21. Rupture of Plaque
Rupture of the plaque surface occurs
frequently during plaque growth and
is probably the most significant
mechanism underlying the
progression of coronary lesions
(Phalen and Aehlert, 2006, p. 61)
22. Stable & Unstable Plaque
As plaque builds up, it can become either stable or unstable.
Unstable plaque is more prone to sudden rupture, a potentially
life-threatening even.
23. Stable Plaque
Hard, consist primarily of collagen-
rich sclerotic tissue, and have a
thick fibrous cap over the lipid
core that separates it from
contact with blood
70%-diameter stenosis is required
to produce anginal symptoms
(Phalen and Aehlert, 2006, p. 62)
24. Unstable Plaque
Soft and have a thin fibrous
tissue over the lipid core that
separates it from the vessel
lumen
Rupture tends to occur near the
normal part of the vessel wall
It is unknown whether plaque
rupture is triggered on
spontaneously
(Phalen and Aehlert, 2006, p. 63, 64)
26. Ischemia
Myocardial ischemia is the result of an
imbalance between the metabolic needs of
the myocardium and the flow of oxygenated
blood to it
EKG Changes: ST-segment depression
& T-wave inversion
(Related to delays in depolarization and repolarization)
27. Ischemia
May occur as a result of either or both of the following:
Demand Ischemia: Increased myocardial O2 demand
(Anemia, hypoxemia, coronary artery narrowing due to a
thrombus, vasospasm, or rapid progression of atherosclerosis)
Supply Ischemia: Reduced myocardial O2 supply
(Exercise, smoking, heavy meals, fever, HF, tachydysrhythmias,
OCM, cocaine, amphetamines, emotional stress, hypertension,
cold weather, aortic stenosis, pheochromocytoma,
thyrotoxicosis)
28. Injury
Ischemia prolonged more than just a few minutes
results in myocardial injury.
Injured myocardial cells are still alive but will infarct if
the ischemia is not quickly corrected
EKG Changes: ST-segment elevation
(Injured myocardial cells do not depolarize
completely, remaining electrically more positive
than the uninjured areas surrounding them)
29. Infarction
A myocardial infarction occurs when blood flow to
the heart muscle stops or is suddenly decreased
long enough to cause cell death
Infarcted cells are without function and cannot
respond to electrical stimulus or provide any
mechanical function
(Thalen and Aehlert, 2006, p, 67)
EKG Changes: ST-segment elevation,
T-wave inversion, abnormal Q waves
30. Abnormal Q Waves
An abnormal Q wave indicates the presence of dead
myocardial tissue and subsequently a loss of
electrical activity (Thalen and Aelhert, 2006, p. 77)
Pathological Q waves represent transmural MI and are
most commonly seen with STEMI (Davis, 2004)
Sometimes occurs within hours of onset of chest pain
More commonly appears 1-3 days after the event
Most Post MI Q waves are permanent
31. Pathologic Q Waves
1/3 or greater than the amplitude of
an R wave
R Wave
5 mm
Q Wave
2.5 mm
And/or greater than 40 ms (0.04 secs)
41. Cardiac Enzymes
Ordered for patients c/o chest pain and
suspected AMI
CE’s are drawn in sets of three 6 to 8 hours
apart
Sometimes initial results are negative
CK-MB & Troponins are released within hours of
a cardiac event
42. Cardiac Enzymes
CK-MB or CPK-MB
Creatine Phosphokinase
Rise within 4-6 hours after an AMI
Peak @ 18 – 24 hours (6x > normal)
Return to normal within 3 – 4 days
43. Cardiac Enzymes
Troponin I
Rise within 3 hours of an AMI
Preferred cardiac enzyme in diagnosis
of an AMI
44. Cardiac Enzymes
Lab will call nursing for critical lab
values
Physician needs to be notified
immediately for elevated Troponin
levels
45. Cardiac Enzymes
Patients with elevated CE’s usually
undergo a stress test and/or cardiac
catheterization for further
investigation of cause of chest pain.
47. Signs & Symptoms
UA, NSTEMI, & STEMI
Pain with or without radiation to arm,
neck, back, or epigastric region
SOB, tachypnea, decreased SaO2
Tachycardia, hypotension or hypertension
Diaphoresis, nausea, lightheadedness,
Rhythm abnormalities
48. Signs & Symptoms: Chest Pain
UA: NSTEMI STEMI
Occurs with rest Occurs with rest Occurs with rest
or exertion; limits or exertion; limits or exertion; limits
activity activity activity
Longer duration Longer duration
and more severe and more severe
than in unstable than in unstable
angina angina
(irreversible tissue
damage [infarction]
occurs if perfusion
is not restored)
(Overbaugh, 2009, pp. 46, 47)
50. Goals for Treatment
Minimize Infarct Size
Salvage ischemic Myocardium
Alleviate Vasoconstriction
Reduce Myocardial O2 Demand
Prevent & Manage Complications
Improve Chances of Survival
(Phalen and Aehlert, 2006, p. 60)
51. Treatment
UA NSTEMI STEMI
Oxygen to Same as UA plus: Same as UA &
maintain O2 sat > Cardiac cath & NSTEMI except:
90% possible PCI for No glycoprotein
NTG or MSO4 to IIb/IIIa inhibitors
patients with
control pain ongoing CP, PCI should be
BB’s, CCB’s,
hemodynamic done within 90
ACEI’s, statins, instability, or minutes of medical
clopidogrel, evaluation
increased risk of
unfractionated
heparin or LMWH, worsening clinical Fibrinolytic
glycoprotein condition therapy within 30
IIb/IIIa inhibitors minutes of
evaluation
(Overbaugh, 2009, pp. 46, 47)
52. Pharmacologic Treatment
Beta-Adrenergic Blockers
Negative Inotropic and Chronotropic Effects
Reduces myocardial contractility and heart
rate resulting in decreased demand for
oxygen
53. Pharmacologic Treatment
Calcium Channel Blockers
Non-dihydropyridines
Negative Inotropic and Chronotropic Effects
Reduces myocardial contractility and heart
rate resulting in decreased demand for
oxygen
Also work to decrease workload of the heart
by coronary arterioles
54. Pharmacologic Treatment
Nitroglycerin
Promotes decrease O2 demand by dilating
veins which decreases venous return to the
heart thus decreasing ventricular filling
(decreases preload)
Decrease in wall tension decreases O2 demand
(Frank-Starling Effect)
55. Pharmacologic Treatment
Morphine Sulfate
Decreases pain and anxiety – decreasing heart
rate and oxygen consumption
Reduces cardiac preload and afterload –
decreasing workload of the heart
Relaxes bronchioles – increasing oxygenation
56. Pharmacologic Treatment
Antiplatelet Agents
Aspirin (acetalsalicylic acid): Low dose, long-
term aspirin use irreversibly blocks formation
of thromboxane A2 in platelets, producing an
inhibitory effect on platelet aggregation
57. Pharmacologic Treatment
Antiplatelet Agents
Plavix (clopidogrel): Inhibits 1st and 2nd Phases
ADP-induced affects of platelet aggregation
58. Pharmacologic Treatment
HMG-CoA Reductase Inhibitors
“Statins”
Decreases the rate of cholesterol
production
Liver needs HMG-CoA reductase
to make cholesterol
When less cholesterol is
produced liver needs to
“recycle” LDL from the blood
circulation
60. National Statistics
American Heart Association:
About 7.3 million females alive
today have a history of heart
attack, angina pectoris, or both
61. National Statistics
Women with diabetes and CVD, especially African
American and Hispanic, die at a higher rate than
men or non-diabetic women
Since 1984, the number of CVD deaths for females
has exceeded those for males.
In 2004, CVD was the cause of death in 459,096
females. Females represent 52.8 percent of
deaths from CVD.
62. National Statistics
According to the American Heart Association:
More women than men have angina
pectoris in total numbers (4.6 million
versus. 4.4 million)
About 25,000 females diagnosed with
angina pectoris were discharged from
short-stay hospitals in 2005
63. Atypical Chest Pain
Women experience cardiac chest pain differently!!
Discomfort varies greatly and be more generalized or
subtle
Chest heaviness, squeezing
Pain in left chest, midabdomen, back, or shoulder
Arm pain
Sharp, fleeting pain
Palpitations
(Cheek and Sherrod, 2008)
64. Atypical Chest Pain
During an MI:
Discomfort is more likely to occur in neck, back, arm,
shoulder, jaw, or throat
Sometimes occurring with n/v, indigestion, upper
abdominal pain, dyspnea, fatigue, diaphoresis,
dizziness, or fainting
(Cheek and Sherrod, 2008)
65. Atypical Findings
An older women or one with diabetes may not
experience any pain during an MI
EKG findings are different for men and women
Women are less likely to have ST-segment elevation
(Cheek and Sherrod, 2008, pp. 38, 39)
66. TJC Core Measures
for AMI
Aspirin within 24 hours
PCI within 90 minutes for STEMI
LVF Assessment (echocardiogram)
ACEI or ARB for EF < 40%
If +MI, aspirin & BB ordered at D/C
“STATIN” prescribed at discharge
Discharge medications to include aspirin &
beta-blocker if positive for MI
Adult smoking cessation advice/counseling
76. Limb Leads:
I, II, III, aVR, aVL, aVF
I, II, III
aVR, aVL, aVF
EKG
77. Limb Leads: I, II, III
Bipolar
Each of these leads has a distinct
negative pole and a distinct positive
pole
These were the 1st leads to be used when
EKG’s were developed
Limb Leads (Phalen and Aehlert, 2006, p. 24)
78. Limb Leads: aVR, aVL, aVF
“a” = augmented Unipolar
“V” = voltage Have a distinct
positive pole but
“R” = right arm
do not have a
“L” = left arm distinct negative
pole
“F” = left foot (leg)
Limb Leads (Phalen and Aehlert, 2006, p. 24, 26)
81. Chest Leads: V1-V6
Aka Precordial Leads
Unipolar
The positive electrode for each lead is
placed on a specific location on the
chest and the heart is the theoretical
negative electrode
Chest Leads (Phalen and Aehlert, 2006, p. 25)
85. I V1 V4
aVR
Lateral Septal Anterior
None
LAD or RCA branch LAD LAD
II aVL V2 V5
Inferior Lateral Septal Lateral
RCA LAD or RCA branch LAD LAD or RCA branch
III aVF V3 V6
Inferior Inferior Anterior Lateral
RCA RCA LAD LAD or RCA branch
86. Anterolateral Wall MI
Leads: I, V3-V6, AVL
Reciprocal ST-segment Depression in
Inferior Leads
87. Inferior/Posterior Wall MI
Leads: II, III, AVF
Reciprocal ST depression in Posterior Leads
If ST elevation is seen in II, III, and/or AVF, then look for reciprocal
changes (ST-depression) in V1 – V4, indicates a posterior MI
88. Posterior Wall MI
Hyperacute: Mirror image of acute injury in leads V1-V3
Fully Involved: Tall R-wave, Tall upright T-wave in leads
V1-V3
89. STEMI & New BBB
Infarct-induced BBB – increased mortality
rate between 40% and 60%
Increased rate of cardiogenic shock – up
to 70%
New-Onset BBB is an indication of a
bigger problem – extensive infarction
– Tissue lost due to infarct is what increases the
mortality rate and cardiogenic shock
90. STEMI & New BBB
Patients that have septal or anteroseptal
infarcts are more likely to develop new-
onset BBB
New-Onset BBB also indicates a higher
likelihood of developing AV blocks
On the other hand, an old LBBB can
produce ST-segment elevation and wide Q
waves that are similar to infarction
91. References
Cheek, D., & Sherrod, M. (2008). Women and heart disease: What’s new. Nursing 2008,
38(1), 36-42.
Davis, L. (2004). Cardiovascular nursing secrets. St. Louis, MO: Mosby Elsevier
Haworth, K., & Pratowski, E. R., (Eds.). (2000). Myocardial infarction: An incredibly
easy mini-guide. Springhouse, PA: Springhouse Corporation.
Lackey, S. A. (2006). Suppressing the scourge of AMI. Nursing 2006, 36(5), 37-41.
Lilley, L. L., Harrington, S., & Snyder, J. S. (2007). Pharmacology and the nursing
process, (5th ed.). St. Louis, MO: Mosby Elsevier.
Overbaugh, K. J. (2009). Acute coronary syndrome. American Journal of Nursing, 109(5),
42-52.
Phalen, T., & Aehlert, B. (2006). The 12-lead ECG in acute coronary syndromes, (2nd ed.).
St. Louis, MO: Elsevier Mosby.
Woods, S. L., Sivarajan Froelicher, E. S., Underhill Motzer, S., & Bridges, E. J. (2005).
Cardiac nursing (5th ed.). Philadelphia, PA: Lippincott, Williams, and Wilkins.
