Transcript Coronary Artery Disease/Acute Coronary Syndrome

Coronary Heart Disease
NUR -224
Coronary Heart Disease
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Affects 16 million people
Causes more than 600,000 death annually
Caused by impaired blood flow to the myocardium
Accumulation of atherosclerotic plaque in the
coronary arteries usual cause.
• May be asymptomatic or may lead to angina
pectoris, acute coronary care syndrome, myocardial
infarction (MI/heart attack), dysrhythmias, heart
failure and even sudden death
Coronary Atherosclerosis
• Atherosclerosis is the abnormal accumulation
of lipid deposits within arterial walls and
lumen.
• In coronary atherosclerosis, blockages and
narrowing of the coronary vessels reduce
blood flow to the myocardium.
Coronary Heart Disease
Risk Factors
• age (over 50)
• heredity
• smoking
• obesity
• high serum cholesterol levels
• hypertension
• diabetes mellitus
Angina Pectoris
• Characterized by chest pain and usually
precipitated by exercise and relieved by rest.
• Myocardial oxygen needs are greater than
partially occluded vessels can supply,
myocardial cells become ischemic and shift to
anaerobic metabolism 
• produces lactic acid that stimulates the nerve
endings in the muscle  pain
• Pain subsides when oxygen supply meets
myocardial demand.
Angina Pectoris
• Chest pain  reduced coronary blood flow 
temporary imbalance between myocardial
blood supply and demand
• This causes temporary/reversible myocardial
ischemia.
• More than 30 minutes of ischemia irreversibly
damages myocardial cells (necrosis)
Types of Angina
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Stable angina
Unstable angina
Silent Ischemia
Variant angina (Prinzmetal’s angina)
Stable Angina
• Occurs with a predictable amount of activity
or stress
• Predictable and common
• Occurs when the work of the heart is
increased by physical exertion, exposure to
cold, or by stress
• Sensation may occur  neck, jaw, shoulders
• Lasts for few minutes – 5/15 minutes
• Relieved by rest and/or nitrates
Unstable Angina
 Occurs with increasing frequency, severity and
duration
 Pain is unpredictable and occurs with
decreasing levels of activity or stress and may
occur at rest.
 Patients at risk for myocardial infarction
 May not be relieved by NTG or rest
Variant Angina (Prinzmetal’s)
• Atypical angina that occurs unpredictably
• Caused by coronary artery spasm with/out
atherosclerotic lesion
• Often occurs at night
Silent Ischemia
• Occurs in the absence of any subjective
symptoms (asymptomatic)
• Patient reports no pain
• May occur with either activity or mental stress
Clinical Manifestations
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Chest pain
Precipitated by an identifiable event.
Classic sequence
Women frequently present with atypical
symptoms of angina
Angina Pain
Manifestations
 Chest Pain
 Quality
 Associated manifestations
 Atypical manifestations
 Precipitating factors
 Relieving factors
Assessment/Diagnostic Findings
o Past medical history/family history
o Comprehensive description of chest pain
o Presence of risk factors
o Electrocardiography
o Echocardiography
o Cardiac stress testing
o Cardiac Angiography
Medical Management
 Focus on maintaining coronary blood flow and
cardiac function
 Measures to restore coronary blood flow
(later)
 Pharmacologic therapy
* nitrates
* beta blockers
* calcium channel blockers
* aspirin
Nitrates
• SL NTG -> acute angina attacks (Buccal spray)
• Acts within 1-2 minutes
Long acting nitroglycerin
• Used to prevent attacks not treat an acute
attack.
• Headache, hypotension, nausea, dizziness
• NTG, Nitrostat, Nitro-bid
Nitrates
• Nursing Responsibilities
• Patient Teaching
B –Adrenergic Blockers
 Decrease myocardial contractility, HR, BP 
which will reduce myocardial oxygen demand
 Side effects  bradycardia, hypotension,
wheezing, GI complaints.
 Contraindicated for patient with asthma
 Metoprolol (Lopressor), Atenolol(Tenormin),
Carvedilol (Coreg)
Beta Blockers
Nursing Responsibilities
Patient Teaching
Calcium Channel Blockers
• Decrease the workload of the heart
• Relax blood vessels  decrease BP and
increase coronary perfusion
• Potent coronary vasodilator
• Amlodipine (Norvasc), Diltiazem(Cardizem),
Felodipine (Plendil)
• Used to treat Variant Angina
Aspirin
• Prevent platelet aggregation/thrombus
formation
• Reduces the incidence of MI
• 80-325 mg of aspirin as soon as dx. is made
• If patient is taking Tylenol – should continue
to take aspirin
• GI upset – H2 blocker, PPI
Nursing Diagnosis
• Ineffective Cardiac Tissue Perfusion
• Deficient Knowledge
• Risk for Ineffective Therapeutic Regimen
Management
Acute Coronary Syndrome
 Condition of unstable cardiac ischemia
 Includes unstable angina and acute myocardial
ischemia c/out significant injury of myocardial
tissue
 Coronary blood flow is acutely reduced, but
not fully occluded. Myocardial cells are injured
by the acute ischemia that results.
 Most people have stenosis of one or more
coronary arteries.
Acute Coronary Syndrome
Cardinal manifestation
 Chest pain – substernal/epigastric
 Dyspnea
 Diaphoresis
 Pallor
 Cool skin
 Tachycardia
 Hypotension
Acute Coronary Care Syndrome
Diagnosis
• ECG
• Cardiac Markers
*Cardiac muscle troponins (sensitive indicators
of myocardial damage)
* Creatine Kinase (CK) & CK-MB (specific to
myocardial muscle)
Medications
• Reduce myocardial ischemia
• Reduce risk for blood clotting
• Nitrates
• Beta blockers
• Antiplatelet (po/IV)
Oral Antiplatelet -Medication
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Aspirin
Clopidogrel (Plavix)
Ticlopidine (Ticlid)
Suppress platelet aggregation, prevents the
development of thrombus.
• Nursing responsibilities
• Patient Education
IV Antiplatelet
• Tirofiban (Aggrastat)
• Eptifibatide (Integrilin)
• IV antiplatelets more effective than oral
administered meds but the risk of bleeding is
greater
Heparin
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Prevents the formation of new clots
Reducers the occurrence of MI
IV bolus/then continuous infusion
Infusion based on PTT – 2-2.5 times the
normal PTT value (25-35 sec.)
• LMWH – Lovenox/Fragmin
• All increase the risk of bleeding : bleeding
precautions
Revascularization Procedures
• Several procedures may be used to restore
blood flow and oxygen to ischemic tissue.
Nonsurgical techniques:
• percutaneous coronary revascularization
• coronary atherectomy
• intracoronary stents
• coronary artery bypass graft (surgical
procedure may be used)
Percutaneous Coronary
Revascularization
Is recommended for patients:
• Fail medical management
• Have left main coronary artery/three vessel
disease
• Are not candidates for PCI
• Have failed PCI with ongoing chest pain
Percutaneous Coronary
Intervention
Goal: open the affected artery within 90
minutes of arrival to a facility
Advantages:
• Alternative to surgical intervention
• Performed with local anesthesia
• Patient is ambulatory 24 hours after the
procedure
• Hospital stay shorter
• Patient can return to work
Percutaneous Coronary
Revascularization
• A balloon-tipped catheter is threaded over the
guide wire
• Balloon is inflated for about 30 sec.-2 minutes
to compress the plaque against the arterial
wall
• The stent is then placed over a balloon
catheter and expanded as the balloon is
inflated
• It remains in the artery when the balloon is
removed.
Percutaneous Coronary
Intervention
Post procedure care:
• Assess vital signs
• Bedrest/ flat in bed
• Affected leg straight
• Pressure dressing applied
• Monitor for bleeding/hematoma
• Resume self-care activities/ambulation few
hours after procedure
Percutaneous Coronary
Revascularization
Atherectomy
• Remove plaque from the identified lesion
• Catheter shaves the plaque off vessels walls
using a rotary cutting head - retaining the
fragments in it compartment and removing
them from the vessel.
• Rotation catheter pulverize the plaque into
particles small enough to pass through the
coronary microcirculation.
CABG
• Involves using a section of a vein /artery to
create a connection (bypass) between the
aorta and the coronary artery beyond
construction.
• This allows blood to perfuse the ischemic
portion of the heart.
• Internal mammary artery in the
chest/saphenous vein from the leg are the
vessels most commonly used.
CABG Surgery
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Internal mammary artery – is commonly used.
Remains palliative treatment and not a cure.
Improves quality of life/patient outcomes
Postoperative complications/mortality
increase as a function of age.
• Women have a higher mortality rate than men
CABG
Patient teaching
• Lifestyle changes and reduction of risk factors
• Explore, recognize, and adapt behaviors to
avoid to reduce the incidence of episodes of
ischemia
• Teaching regarding disease process
• Cardiac rehabilitation
• Stress reduction
• When to seek emergency care
Myocardial Infarction
• An area of the myocardium is permanently
destroyed  necrosis of the myocardial cells.
If circulation to the affected myocardium is
not promptly restored , the heart loses the
ability to maintain effective cardiac output.
• Life-threatening event
• May lead to cardiogenic shock and death
Myocardial Infarction
• Annually 785,000 experience their first MI
• Majority of deaths from MI occur during the
initial period after symptoms begin:
60% within the first hour
40% prior to hospitalization
• Medical treatment and training in CPR are
vital to decrease deaths due to MI.
Myocardial Infarction
• The area of infarction develops over minute
to hours.
• Cellular ischemia  affects conduction and
myocardial contractility
• Myocardial contractility decreases, increasing
the risk for dysrhythmias, subsequently
reducing cardiac output, B/P, and tissue
perfusion
Myocardial Infarction
• When a larger artery is compromised,
collateral vessels connecting smaller arteries
in the coronary system dilate to maintain
blood flow to the cardiac muscle.
• The degree of collateral circulation determines
the extent of myocardial damage.
• Occlusion of coronary artery without any
collateral vessels  massive tissue damage
and death
Clinical Manifestations
• Pain – sudden and usually not associated with
activity
• Women/older adults atypical chest pain,
elevated BP & HR initially, then ↓’es
• Nausea/vomiting
• Fever
• Dyspnea, shortness of breath
• Anxiety , sense of impending doom
Collaborative Care
Goals
• Relieve chest pain
• Reduce the extent of myocardial damage
• Maintain cardiovascular stability
• Decrease cardiac workload
• Prevent complications
Assessment/ Diagnostic Findings
• ECG
• Laboratory tests— serum cardiac biomarkers
CK-MB
Myoglobin
Troponin
CBC
Echocardiogram
Laboratory Tests
Serum Cardiac Markers
• Are proteins released into the blood from
necrotic heart muscle
• They occur after cellular death indicates
cardiac damage
• Creatine kinase (CK-MB) and troponin are
measured to diagnose an MI.
Serum Cardiac Markers
Creatine kinase (CK )
• Important enzyme for cellular function
• Found mainly in cardiac muscle (skeletal
muscle/brain)
• Begin to rise rapidly with damage to these
tissues at about 4/6 hours after an MI , peak
at about 12/24 hours and return to normal
within 36/48 hours
• CK correlates with the size of the infarction
Serum Cardiac Markers
CPK-MB
• Subset of CK specific to cardiac muscle
• Most sensitive indicating of MI
• Elevated CK –alone is not specific for MI
• Elevated CPK-MB  positive indicator of MI
• Does not normally rise with chest pain from
angina or other causes other than MI
Serum Cardiac Markers
Troponin
• Regulates the myocardial contractility process
• Proteins released during myocardial infarction
– are sensitive indicators of myocardial
damage.
• Necrosis of cardiac muscle, troponins are
released and blood levels rise.
• Is a highly cardiac specific indicator of an MI
• Increases with 4-6 hours during an acute MI,
remains elevated for a long period -- 3 weeks
Serum Cardiac Markers
Myoglobin
• Helps transport oxygen
• Found in cardiac and skeletal muscle
• Levels start to increase within 1-3 hours of
symptom onset return to normal within 24
hours after onset of symptoms.
• Is one of the first cardiac markers to appear
after MI, it lacks cardiac specificity.
• Kidneys rapidly excrete it in urine  blood
levels return to normal range within 24 hours.
Ischemia, Injury , Infarction
COMPLICATIONS
• Heart failure
• Cardiogenic shock
• Dysrhythmias and cardiac arrest
Interdisciplinary Care
Immediate treatment goals for the MI
 Relieve the chest pain
 Reduce the extent of myocardial damage
 Decrease the cardiac workload
 Prevent complications
Treatment of Acute MI
• Obtain diagnostic tests including ECG within
10 minutes of admission to the ED
• Oxygen
• Aspirin, nitroglycerin, morphine, beta-blockers
fibrinolytic therapy
• Revascularization Procedures
• As indicated: IV heparin, LMWH
• Bed rest
Nursing Interventions
• Pain stimulates the SNS, increasing cardiac
work. Pain relief is a priority.
Acute Pain
 Assess for verbal and nonverbal signs of pain
 Administer oxygen2-5L/min via nasal cannula
 Promote physical and psychologic rest
 Titrate IV nitroglycerin as ordered
 Administer morphine by IV push for chest pain
as needed
Nursing Interventions
Ineffective Tissue Perfusion
 Assess and document vital signs
 Assess for changes in LOC
 Auscultate heart and breath sounds
 Monitor ECG Administer antidysrhythmic
medications
 Monitor oxygen saturation
Nursing Interventions
Fear
 Acknowledge the client’s perception of the
situation
 Encourage questions/ provide consistent,
factual answers
 Encourage self-care
 Administer anti-anxiety medications as
ordered
 Teach non-pharmacologic methods
HEART FAILURE
Heart Failure
• Complex syndrome resulting from cardiac
disorders that impair the ventricles’ ability to fill
and effectively pump blood
• Inability of the heart to pump sufficient blood to
meet the metabolic demands of the body.
• 5.7 million people in the US have heart disease.
• HF is increasing in incidence and prevalence.
• Primarily a disease of older adults.
• HF is associated with high morbidity/mortality
rates
HEART FAILURE
• Heart failure develops  cardiac output falls 
decrease in tissue perfusion.
• Is a disorder of cardiac function
• Hypertension and CHD are the leading causes of heart
failure
• The prognosis for the client with heart failure
depends on the underlying cause and how effectively
the precipitating factors can be treated.
• Most clients with heart failure die within 8 years of
the diagnosis.
• Ejection fraction – provides information about the (L)
ventricle during systole. Normal 55-65%.
Pathophysiology
• Decrease cardiac output activation of
compensatory mechanisms neurohormonal
response decrease in renal perfusion &
increase vasoconstriction  sodium and
water retention  fluid overload increase
the workload of the heart
Etiology
• CAD and advancing age are the primary risk
factors for HF
• CAD is found in more than 60% of patients
• Other factors: hypertension, diabetes,
cigarette smoking, obesity,
Manifestations of Heart Failure
• CHD/hypertension are common causes of
L-sided heart failure whereas R- heart failure
caused by conditions that restrict blood flow to
the lungs (acute/chronic pulmonary disease).
Left sided heart failure can lead to right sided
heart failure.
Classification of Heart Failure
Left-sided heart failure
• Most common form of HF
• LV cannot pump blood effectively to the
systemic circulation. Pulmonary venous
pressures increase and result in pulmonary
congestion with dyspnea, cough, crackles, and
impaired oxygen exchange.
• This increase pulmonary pressure 
pulmonary congestion and edema
Types of Heart Failure
Manifestation of L-sided heart failure result from
pulmonary congestion (backward effects) and
decreased cardiac output (forward effects).
 Fatigue and activity intolerance
 Dizziness and syncope
 Pulmonary congestion
 Cyanosis
 Rales/wheezing
Types of Heart Failure
Right sided heart failure
• Causes a back up of blood to the ( R) atrium
• RV cannot eject sufficient amounts of blood
into the pulmonary circulation  blood backs
up in the venous system.
• Increase venous pressure causes abdominal
organs to become congested /peripheral
edema develops
• This results in peripheral edema, ® upper
quadrant pain, ascites, anorexia, nausea,
weakness, and weight gain.
Multisystem Effects of Heart
Failure
 Neurologic
 Respiratory
 Cardiovascular
 Gastrointestinal
 Genitourinary
 Integumentary
 Metabolic
Diagnostic Studies
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BNP levels – key diagnostic indicator of HF
Serum electrolytes
Liver function tests
Echocardiogram
Chest x-ray
Electrocardiogram
Heart Failure
Hemodynamics Monitoring
 Used to assess cardiovascular function in the
critically/unstable client and evaluate their
interventions
 Hemodynamic parameters  heart rate,
arterial blood pressure, central venous
pressure, pulmonary pressure and cardiac
output
Management of Heart Failure
• Eliminate or reduce etiologic or contributory
factors.
• Reduce the workload of the heart by reducing
afterload and preload.
• Optimize all therapeutic regimens.
• Prevent exacerbations of heart failure.
• Medications are routinely prescribed for heart
failure.
Medications
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Angiotensin-converting enzyme inhibitors
Angiotensin II receptor blockers
Beta-blockers
Diuretics
Digitalis
Other medications
Other Treatment
 Surgery
 Circulatory
assistance
 Cardiac transplantation
 Hemodynamic
Monitoring
Complications
Compensatory Mechanism
• Hepatomegaly/splenomegaly
• Dysrhythmias
• Pulmonary problems
Nursing interventions
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Decreased Cardiac Output
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Excess Fluid Volume
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Activity Intolerance
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Diet
ACUTE CORONARY SYNDROME
• ACS  occurs when ischemia is prolonged and
not immediately reversible resulting in
myocardial cell death .
• The spectrum of ACS encompasses: unstable
angina(UA), non-ST-segment-elevation MI
(NSTEMI), ST-segment-evaluation MI (STEMI).