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Coronary Syndrome PDF
Coronary Syndrome PDF
6 HOURS
Continuing Education
ACUTE CORONARY
SYNDROME
Even nurses outside the ED should recognize its signs and symptoms.
C
oronary artery disease, in which standard of care for all patients who present with
atherosclerotic plaque builds up inside symptoms of any of the three stages of ACS.2-5
the coronary arteries and restricts the Nurses not specializing in the care of patients with
flow of blood (and therefore the deliv- cardiovascular disease may not be familiar with cur-
ery of oxygen) to the heart, continues rent practice guidelines and nomenclature, but they
to be the number-one killer of Americans. One nevertheless play significant roles in detecting patients
woman or man experiences a coronary artery dis- at risk for ACS, facilitating their diagnosis and treat-
ease event about every 25 seconds, despite the time ment, and providing education that can improve out-
and resources spent educating clinicians and the comes. Many patients admitted with a diagnosis of
public on its risk factors, symptoms, and treatment. NSTEMI or unstable angina are cared for by physi-
Coronary artery disease can lead to acute coronary cians other than cardiologists and are therefore less
syndrome (ACS), which describes any condition likely to receive evidence-based care. Nurses caring
characterized by signs and symptoms of sudden for these patients can be instrumental in promoting
myocardial ischemia—a sudden reduction in blood adherence to practice guidelines.
flow to the heart. The term ACS was adopted
because it was believed to more clearly reflect the WHO’S AT RISK FOR CORONARY ARTERY DISEASE?
disease progression associated with myocardial Nonmodifiable factors that influence risk for coro-
ischemia. Unstable angina and myocardial infarc- nary artery disease include age, sex, family history,
tion (MI) both come under the ACS umbrella. and ethnicity or race. Men have a higher risk than
Left circumflex
artery
Left anterior
Right coronary descending artery
artery
Atherosclerotic plaque
occluding the artery
Area of ischemia,
injury, and infarction
Posterior
descending artery
women. Men older than age 45, women older than PATHOPHYSIOLOGY OF ACS
age 55, and anyone with a first-degree male or ACS begins when a disrupted atherosclerotic plaque
female relative who developed coronary artery dis- in a coronary artery stimulates platelet aggregation
ease before age 55 or 65, respectively, are also at and thrombus formation. It’s the thrombus occlud-
increased risk. Modifiable risk factors include ele- ing the vessel that prevents myocardial perfusion
vated levels of serum cholesterol, low-density (see figure 1). In the past, researchers supposed that
lipoprotein cholesterol, and triglycerides; lower lev- the narrowing of the coronary artery in response to
els of high-density lipoprotein cholesterol; and the thickening plaque was primarily responsible for the
presence of type 2 diabetes, cigarette smoking, obe- decreased blood flow that leads to ischemia, but
sity, a sedentary lifestyle, hypertension, and stress. more recent data suggest that it’s the rupture of an
Ischemia
The inverted T wave
is caused by altered
repolarization.
Injury
ST segment elevation
is a sign of myocardial
injury.
Infarction
Abnormal Q waves
result from the absence
of depolarization current
from dead tissue and the
presence of opposing
currents from other areas
of the heart.
and anxiety prior to an acute MI and may not Framingham Heart Study was initiated in 1948 to
attribute those symptoms to heart disease.11 It’s also explore contributing factors for cardiovascular disease
important for clinicians to realize that women tend and has provided the scientific community with much
to experience pain in the back rather than subster- of what is known today about heart disease (for more
nally or in the left side of the chest and do not char- information, visit www.framinghamheartstudy.org).
acterize it as pain, but may instead report a numb, Findings from this longitudinal study of 5,209 partic-
tingling, burning, or stabbing sensation12; in fact, a ipants found that 50% of patients diagnosed with an
recent study found that, when compared with men, MI experienced silent ischemia and did not exhibit
women diagnosed with ACS more often reported any of the classic symptoms of ACS.3 Populations
indigestion, palpitations, nausea, numbness in the more likely to experience a silent MI include people
hands, and atypical fatigue than chest pain.13 with diabetes, women, older adults, and those with a
Silent ischemia. Ischemia can also occur without history of heart failure.3 As the prevalence of diabetes
any obvious signs or symptoms. The classic rises, silent ischemia may also become more common.
Unstable angina, non–ST-segment myocardial infarction (NSTEMI), and ST-segment myocardial infarction (STEMI)
differ with regard to duration, severity, and treatments, yet those differences can be difficult to remember. Here
they are presented side by side. Look for the highlighted areas to see where they differ from one another.
Anderson JL, et al. Circulation 2007;116(7):e148-e304; Hazinski MF, et al., editors. Handbook of emergency cardiovascular care for healthcare providers. Dallas:
American Heart Association; 2008.
DIAGNOSING ACS markers into the blood. These markers help practi-
The patient’s clinical history, presenting symptoms, tioners determine whether the patient is having or
biomarker levels, and electrocardiographic results has recently had an acute MI (either an NSTEMI
are all evaluated. or a STEMI). The utility of various biomarkers is
Cardiac biomarkers. Injured myocardial cells determined by the timing and duration of their ele-
release proteins and enzymes known as cardiac bio- vation as well as by the extent of their cardiac speci-
46 AJN ▼ May 2009 ▼ Vol. 109, No. 5 ajnonline.com
Levels of troponins I and T increase within four to
six hours of myocardial injury; troponin I levels
remain elevated for four to seven days, and troponin
T levels remain elevated for 10 to 14 days. Normal
reference ranges for cardiac biomarkers vary among
laboratories; in order to diagnose myocardial necro-
sis a single troponin elevation greater than the 99th
percentile of an agreed-upon reference control
ST-Segment Elevation Myocardial group is required.14
Cardiac troponins are the preferred biomarkers
Infarction (STEMI) for diagnosing acute MI because elevated levels cor-
relate with a more accurate diagnosis, predict a
Cause high risk of future cardiac events even when levels
of the myocardium-specific biomarker creatine
• Thrombus fully occludes the coronary artery
kinase-MB (CK-MB) are normal or only mildly ele-
Signs and Symptoms
• Pain with or without radiation to arm, neck,
back, or epigastric region Nurses can use the mnemonic
• Shortness of breath, diaphoresis, nausea, light-
headedness, tachycardia, tachypnea, hypoten- ‘MONA’ to recall initial treatment
sion or hypertension, decreased arterial oxy-
gen saturation (SaO2), and rhythm abnormali- strategies
ties
• Occurs at rest or with exertion; limits
activity
vated, and elicit fewer false positives when concur-
• Longer in duration and more severe than in
rent skeletal muscle injury is present (after trauma
unstable angina (irreversible tissue damage
or surgery, for example). But if a laboratory is
[infarction] occurs if perfusion is not restored)
unable to process troponins, CK-MB is considered
a reasonable alternative. CK-MB is a cardiac-specific
Diagnostic Findings
enzyme that’s released within four to six hours
• ST-segment elevation or new left bundle of injury and remains elevated for 48 to 72 hours
branch block on electrocardiography after injury. Two consecutive levels of CK-MB greater
• Cardiac biomarkers are elevated than the 99th percentile of a reference control group
contribute to the diagnosis of acute MI.14
Treatment Myoglobin, a heme protein, is not cardiac spe-
• Oxygen to maintain SaO2 level at > 90% cific, yet it’s still considered a valuable biomarker
• Nitroglycerin or morphine to control pain because it’s the first to rise after myocardial damage.
• β-blockers, angiotensin-converting enzyme If a patient presents with ACS symptoms that
inhibitors, statins (started on admission and started less than three hours earlier, CK-MB and tro-
continued long term), clopidogrel (Plavix), ponin levels may not yet be elevated. In such a case,
unfractionated heparin or low-molecular- myoglobin can rule out or lead to an early diagno-
weight heparin sis of acute MI and prompt decisive therapy.14
• Percutaneous coronary intervention within 90 Electrocardiographic findings. The AHA and the
minutes of medical evaluation ACC recommend that a 12-lead electrocardiogram
• Fibrinolytic therapy within 30 minutes of med- (ECG) be performed in patients with symptoms con-
ical evaluation sistent with ACS and interpreted by an experienced
physician within 10 minutes of ED arrival.2 Findings
on a 12-lead ECG help the practitioner to differenti-
ate between myocardial ischemia, injury, and infarc-
tion; locate the affected area; and assess related
conduction abnormalities. Electrocardiographic find-
ficity. The cardiac troponins, troponin T and tro- ings reflective of unstable angina or NSTEMI include
ponin I, are the most cardiac-specific biomarkers. ST-segment depression and inverted T waves. ST
These structural proteins are not normally found in depression will normally resolve when the ischemia
serum; therefore elevated serum levels may predict or pain has resolved, although T-wave inversion may
the degree of thrombus formation and microvascu- persist. Providers should review electrocardiographic
lar embolization associated with coronary lesions. findings as well as levels of cardiac biomarkers to dis-
Aspirin 162–325 mg orally, crushed or chewed; Contraindicated in active peptic ulcer disease,
then 81–325 mg daily hepatic disease, bleeding disorders, and aspirin
allergy
or
Morphine sulfate 2–4 mg IV push (may repeat every 5–15 Indicated when pain not improved with nitroglyc-
min until pain controlled) erin
ble angina, NSTEMI, or STEMI whose low-density binding of fibrinogen and subsequent platelet aggre-
lipoprotein cholesterol level is above 100 mg/dL.5 In gation. If a percutaneous coronary intervention (PCI)
patients with a diagnosis of NSTEMI or STEMI, a is planned and can be performed without delay, the
lipid panel should be ordered during hospitalization. glycoprotein IIb/IIIa inhibitor of choice is abciximab
Clopidogrel (Plavix) inhibits platelet aggregation (ReoPro).2 If the PCI is not planned or is delayed, the
and can be administered to unstable angina and glycoprotein IIb/IIIa inhibitors eptifibatide (Integrilin)
NSTEMI patients with a known allergy to aspirin. or tirofiban (Aggrastat) are preferred. These agents
Clopidogrel may also be added to aspirin therapy in may also be considered in patients opting for conser-
ACS patients scheduled for diagnostic angiography vative treatment. Glycoprotein IIb/IIIa inhibitors con-
or in those receiving conservative treatment. fer the greatest benefits in patients scheduled for PCI
Contraindications are similar to those for aspirin who have elevated cardiac troponin levels.2
therapy, and clopidogrel should not be administered Options for anticoagulant therapy in patients
if coronary artery bypass surgery is planned within with unstable angina or NSTEMI include enoxa-
the next five to seven days because it increases a parin (Lovenox), unfractionated heparin, bivalirudin
patient’s risk of bleeding.2 (Angiomax), and fondaparinux (Arixtra).2 These
Glycoprotein IIb/IIIa inhibitors are the antiplatelet agents are recommended in patients scheduled for
agents used in unstable angina and NSTEMI patients diagnostic testing. Enoxaparin or unfractionated
who are scheduled for an invasive diagnostic proce- heparin is strongly recommended in patients who
dure. These drugs bind to the platelet surface integrin choose conservative treatment, but fondaparinux is
glycoprotein IIb/IIIa receptor sites and inhibit the preferred in those at higher risk for bleeding.
β-blockers Administer oral dose within Contraindicated when heart rate < 60 beats per minute, systolic
• metoprolol (Lopressor) 24 hours of symptom onset blood pressure < 100 mmHg, and in heart blocks, moderate-to-
• atenolol (Tenormin) and continue upon dis- severe left ventricular failure, pulmonary edema, acute asthma,
• propranolol (Inderal) charge or reactive airway disease
Angiotensin-converting Administer oral dose within Assess for hypotension, decreased urine output, cough, hyper-
enzyme inhibitors 24 hours of symptom onset kalemia, and renal insufficiency
• enalapril (Vasotec) and continue upon dis-
• captopril (Capoten) charge Contraindicated in renal failure, hyperkalemia, angioedema, and
• lisinopril (Prinivil, Zestril) pregnancy
• ramipril (Altace)
Monitor vital signs and blood glucose
Statins Administer oral dose upon Instruct patients to take at bedtime and limit grapefruit consump-
• atorvastatin (Lipitor) discharge when low-density tion
• pravastatin (Pravachol) lipoprotein cholesterol >100
• simvastatin (Zocor) mg/dL Contraindicated in pregnancy
Clopidogrel (Plavix) Administer loading dose, Contraindicated in active peptic ulcer disease, bleeding disorder,
followed by 75 mg/day; hepatic disease, or if coronary artery bypass graft surgery is
continue on discharge planned within 5–7 days
Glycoprotein IIb/IIIa Abciximab (ReoPro) pre- Contraindicated with active bleeding, bleeding disorder, surgery
inhibitors ferred if PCI is planned and or trauma within last month, or platelets < 150,000/mm3
• abciximab (ReoPro) can be performed without
• eptifibatide (Integrilin) delay Monitor blood tests for anemia and clotting disorders
• tirofiban (Aggrastat)
eptifibatide (Integrilin) or
tirofiban (Aggrastat) pre-
ferred if PCI is not planned
or is delayed
Anticoagulation agents Indicated for unstable Monitor complete blood count, platelets, bleeding times, blood
• unfractionated heparin angina, NSTEMI, and urea nitrogen, and creatinine levels
• low-molecular-weight STEMI
heparin
• enoxaparin (Lovenox)
• fondaparinux (Arixtra)
• bivalirudin (Angiomax)
Alteplase (Activase) Yes 4–8 min IV bolus dose, then 90-min con-
tinuous infusion
(Committee to revise the 1999 guidelines for the manage- Continuing Education
ment of patients with acute myocardial infarction).
Circulation 2004;110(9):e82-e292. EARN CE CREDIT ONLINE
4. Antman EM, et al. 2007 Focused update of the ACC/AHA Go to www.nursingcenter.com/ce/ajn and receive a certificate within minutes.
2004 guidelines for the management of patients with ST-
elevation myocardial infarction: a report of the American
College of Cardiology/American Heart Association Task GENERAL PURPOSE: To provide registered professional
Force on Practice Guidelines. Circulation 2008;117(2):296- nurses with current information on acute coronary syn-
329. drome, including risk factors, pathophysiology, manifes-
5. Krumholz HM, et al. ACC/AHA 2008 performance mea- tations, and diagnostic and treatment approaches.
sures for adults with ST-elevation and non-ST-elevation
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• summarize the characteristics, pathophysiology, mani-
myocardial infarction). J Am Coll Cardiol festations, and diagnostic strategies related to acute
2008;52(24):2046-99. coronary syndrome.
6. Hansson GK. Inflammation, atherosclerosis, and coronary • plan the appropriate interventions for patients diag-
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