Transcript Acute Coronary Syndrome

Angina Pectoris
Acute Coronary Syndrome
Coronary Artery Disease
Cardiac Pharmacology
Myocardial Infarction
Lecture 2
Joy Borrero, RN, MSN 9/10
Coronary Artery Disease
 Etiology
 Risk factors
 Nonmodifiable vs. modifiable risk factors
 Clinical manifestations
 Goals of therapy
 Medications
ATHEROSCLEROSIS
START
END
STATINS aka: (COENZYME INHIBITOR)
Mevacor, Zocor, Lipitor
BLOCKS BIOSYNTHESIS OF CHOLESTEROL
• HIGH FIRST PASS EFFECT
*MONITOR LFT
•SIDE EFFECTS
•N/V/D & ABDOMINAL CRAMPS
•MYALGIA, ARTHRALGIA,Cataracts
•HEADACHES, DIZZINESS, INSOMNIA
•Liver and kidney dysfunction
Angina Pectoris
 Episode of chest pain or pressure due to insufficient artery
flow of oxygenated blood.
 Myocardial 02 demand exceeds 02 supply. CAD is the most
common cause.
 One coronary artery branch becomes completely occluded;
therefore, 02 is not perfused to the myocardium, resulting in
transient ischemia and subsequent retrosternal pain.
Angina Pectoris
Precipitating Factors: Warning Sign for MI
Clinical Signs & Symptoms: do not occur until lumen is 75%
narrowed. Sternal pain: mild to severe. May be described as heavy,
squeezing, pressing, burning, crushing or aching. Onset sudden or
gradual. May radiate to L. shoulder and arm. Radiates less commonly
to R. shoulder, neck, jaw. Pt may have weakness/numbness of wrist,
arm, hands. pain usually short duration and relieved by removal
precipitating factors,rest or NTG. Can be gradual (CAD) or
sudden(vasospasm)
Associated Symptoms: dyspnea, N & V, tachycardia, palpitations,
fatigue, diaphoresis, pallor, weakness, syncope, factors
Types of Angina
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Stable: There is a stable pattern of onset, duration and
intensity of sx, pain is triggered by a predictable degree of exertion
or emotion.
Variant Angina (Prinzmetal's)
Cyclical, may occur at rest.
Ventricular arrhythmia, brady arrhythmia and
conduction
disturbances occur.
Syncope associated with arrhythmia may occur
Nocturnal Angina only at night. Possible associated
with REM sleep.
Unstable Angina AKA Pre infarction angina
Pain is more intense, lasts longer
Assesment

1.
Hx
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2.
Physical Exam
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3.
EKG
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4.
Exercise EKG
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5.
6.
Thallium Scan
Coronary Angiography
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7.
Cardiac Enzymes
Medications for Angina
1. Nitrates decrease myocardial 02 demand via
peripheral vasodilation and reverse coronary artery spasm
thus increase 02 supply to myocardial tissue.
2. Understanding how Nitrates Work: peripheral
vasodilation results in:
-decreased 02 demand
-decreased venous return to heart
-decreased ventricular filling which results
decreased wall tension and thus
-decreased 02 demand
in
NTG Forms:
• SL (Nitrostat)
• Lingual Sprays - similar to SL in use (Nitrolingual)
• Sustained release capsules/tablets (Nitrobid)
• Ointments 2% (Nitrobid)- wear gloves when applying
• Transdermal Patch (Nitro-Dur)
• IV (Tridil) For attacks unresponsive to other tx
Side/Adverse Effects
 Vascular HA (may be severe)
 Hypotension (may be marked)
 Tachycardia
 Palpitations
Acute Angina Treatment
Goal: Enhance 02 supply to myocardium:
M- Morphine for pain
O- Oxygen 4-6L as ordered
N- NTG sublingual, repeat q5 minutes x3
A- Aspirin to prevent platelet aggregation
Angina Treatment
The focus is to relieve acute attacks and prevent further attacks.
1. Activity/exercise tolerance - a regular exercise
prescription is established after stress testing
and/or cardiac cath.
Baseline
Gradual increase
Avoid
Alternate
ADLS
NTG before exercise
Patient education
Lifestyle modifications for controllable risk factors.
Support groups are helpful, Example: Weight
watchers,
Smoke-enders, stress workshops, cardiac
rehabilitation. Supply patients with
information, name of contact person and
phone numbers
Identify precipitating factors for Anginal pain
Medication compliance
Cardiac Pharmacology
Beta-adrenergic Blockers
Therapeutic effect - decrease the rate and force of
the cardiac contraction (resulting in decreased
02 demand) and decrease vasoconstriction in
the myocardium and vasculature.
Mechanism of Action - inhibit circulating
catecholamines from stimulating beta receptor
sites. There are two type of beta receptors (B1
& B2).
Beta-adrenergic Blockers
B1 receptor stimulation by catecholamines
results in increased HR & myocardial contractility so,
blocking the B1 effect results in slowed HR &
decreased myocardial contractility.
 Cardio-selective
 Excess blockade can result in bradycardia, heart block,
heart failure and/or hypotension.

atenolol (Tenormin)

metoprolol (Lopressor, Toprol)
Beta-adrenergic Blockers
B2 receptor stimulation by catecholamines results in dilation of
the bronchial tree, the coronary arteries and the
peripheral vasculature
Blocking the B2 effect results in bronchoconstriction,
coronary artery vasoconstriction and peripheral vascular
constriction.
Drugs that have a B2 blockade effect are used
cautiously/contraindicated in clients with COPD.
Non-selective Beta Blockers - Block B1 and B2
receptors
propanolol (Inderal)
carvedilol (Coreg)
Beta-adrenergic Blockers
Side Effects - many may be predicted based upon understanding the
mechanism of action.
Hypotension
Bradycardia
Heart Failure
Weakness/Fatigue
Depression
Impotence
Hypoglycemia
Hallucinations
Patient Teaching:
Use with caution in clients prone to coronary artery spasm due to
vasoconstrictive effects.
Contraindicated in clients with CHF and second or third degree
heart block due to the rate slowing and reduction in contractility.
Non-selective beta blockers contraindicated with COPD.
Do not abruptly discontinue beta blockers
Calcium Channel Blockers
Action - inhibit flow of Ca+ across cell
membrane. Ca+
is essential for cardiac stimulation, conduction, contractility
and relax vascular smooth muscle which results in decreased
02 demand and increased coronaryblood supply
VASODILATION
Indications: angina, HTN, arrhythmia
Drugsverapamil (Calan, Isoptin)
diltiazem (Cardizem)
nifedipine (Procardia)
amlodipine (Norvasc)
Calcium Channel Blockers
Side Effects of Calcium Channel Blockers
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Constipation (with Verapamil)
Dizziness
Facial Flushing
HA
Edema of ankles/feet
Bradycardia
Hypotension
Epinenepherine (adrenalin)
 Vasoconstriction- Increase BP
 Alpha, Beta 1 and Beta 2 agonist
 Decrease congestion of nasal mucosa
 Catacholamine- produced by……
 Tx of AV block and cardiac arrest
ACE INHIBITORS –The “prils”
Angiotensin Converting Enzymes Inhibitors
Action: Blocks production of Angiotensin II in kidneys
Indications: HF, HTN, MI, DM neuropathy
Causes: Vasodilation (mostly arteriole)
Decreased BP
Excretion of Na and H2O (but not K)
Ex.: captopril (Capoten)
enalapril (Vasotec)
fosinopril (Monopril)
ramapril (Altace)
SE : ortho hypotension, dry cough, hyperkalemia
Angiotensin Receptor Blockers- ARBs
Action- Block the binding of Angiotensin II
to it’s receptor in the vascular and adrenal tissues
Examples: candesartan (Atacand)
losartan (Cozaar)
Cardiac Glycoside
digoxin (Lanoxin)
Action :+Inotropic effect
Increases force of myocardial contraction
- Chronotropic effect- decreases HR
Tx: heart failure, afib
Nsg: Apical Pulse for 1 full minute, hold for <60, same time
daily
Monitor Dig levels 0.5-0.8 ng/ml
Monitor K levels
Monitor for Dig toxicity: anorexia, fatigue, weakness,
vision changes (halos)
Myocardial Infarction
 Leading cause of death in US
 Thrombosis in atherosclerotic artery causes 90% of MIs.
 A region of the myocardium is abruptly deprived of blood
supply due to restricted coronary blood flow
 Ischemia results and may lead to necrosis within 6 hours
 JCAHO Core Measures for AMI (4/10)
Gender Differences in MI
Females, when compared to males:
-present with MI later in life
-have poorer prognosis and high morbidity
-are 2x as likely to die in the first weeks
-are more likely to die from the first MI
-have higher rates of unrecognized MI
-NSTEMI MI vs STEMI
EKG changes with MI
Location of MI
Depends on which artery is affected
LV receives most of the CA supply and so it is the most affected
Left Anterior Descending (LAD)
Left Circumflex artery (LCA)
Right Coronary Artery (RCA)
General Types of MI
 Transmural-invades full thickness of myocardium
 Subenedocardial-invades partial thickness
Collateral Circulation
 A network of blood vessels present at birth that can dilate
and become functional a/r/o coronary artery occlusion and
ischemia. “collateral circulation”
 Natural “bypass” mechanism helps decrease the size of the MI
Risk Factors and Etiology
 CAD and its risk factors
 Any situation requiring increased O2 in the presence of
decreased O2 supply.
 Non atherosclerotic coronary artery occlusions
Effects of MI
 Cell death
 Contractility in the affected areas reduced or absent
 Electrical instability
Dysrhythmias occur in 90% of patients
 PVCs
 V tach
 V fib
 Bradycardia
Complications of MI
 CHF
 Mitral Valve Insufficiency
 Dysrhythmias
 Pericarditis
 Post Infarction MI
 Thromboembolic Complications
 Rupture of Ventricular Wall
MI Precipitating Factors
 None in most cases
 Severe exertion and stress
 59% occur at rest or while asleep
Clinical Manifestations
 Angina-Chest Pain
 Vital Signs
 Heart and Lung
 Associated S&S
What’s the difference?
Angina
Myocardial Infarction
Diagnosis of MI
Based on 2 out of 3 criteria
1. Chest pain indicative of ischemic heart disease
2. Characteristic EKG changes (ST elevation)
3. Marked rise and eventual decline in serum markers of
cardiac injury
Diagnostic studies
 EKG
 Serum Enzymes/Cardiac Biomarkers
 Cardiac Catheterization
 Other lab tests
 Echocardiogram
 CXR
 Pulse Ox
Goals
 Limit size of infarct/prevent further damage
 Increase O2 supply and decrease O2 demand
 Prevent and /or recognize complications early
 Reduce pain
Nursing Diagnosis
Nursing Interventions
Remember: MONA and Oh Batman
 Obtain EKGs
 Monitor mentation
 Assess heart sounds
 Assess lungs
 Assess peripheral circulation/skin
 Assess urinary output
 Assess GI function
 Assess pain
OH BATMAN!
 O
 H
 B
 A
 T
 M
 A
 N
Nursing Interventions
 Activity
 Safety
 Reduce anxiety
 Patient Education
 Nutrition
Pharmacology Therapy for MI
 Thrombolytic Agents a/k/a Plasminogen Activators
(Streptokinase, T-PA,Retavase)
-decrease infarct size
-improved ventricular function
-increased survival rates
 Glycoprotein IIB and IIIA
Pharmacology Therapy
 ASA
 Nitrates
 Morphine Sulfate
 Beta blockers
 Calcium channel blockers
 ACEs and ARBs
Antiarrhythmics
 Class IA- Na channel blockers
 Class IB- Na channel blockers
 Class II- Beta blockers
 Class III- Amiodarone
 Class IV- Ca Channel blockers
Anticoagulants
 Heparin
 LMWH- Lovenox, Fragmin
Post MI Cardiac rehab
 Begins in acute phase and continues indefinitely as outpatient
 Includes:
education
activity progression
counseling
medical management
Non-Pharmacologic Therapy
 Percutaneous transluminal coronary angioplasty (PTCA)
 Dilates coronary arteries obstructed by plague. 30%
restenosis rate within first 6 months.
 Patient Criteria
 Non-calcified lesions less than 2 cm. The ideal candidate
would have less than a one year history of angina and be
able to undergo coronary artery by-pass grafting if
necessary. Patients with calcified lesions or lesions in
branch vessels are not considered good candidates
Non-Pharmacologic Therapy
 Cardiac Catheterization/ Balloon Angioplasty
 Performed in the cardiac cath lab. A catheter with a
balloon tip is passed into the obstructed artery and is
alternately inflated and deflated to increase arterial
diameter and perfusion.
 Complications
 Arterial rupture, spasm, emboli, MI
 Post-procedure care
Other Procedures
 Coronary Artery Stents
 Stainless steel mesh stent is placed in lumen to prevent
restenosis after angioplasty. Requires anticoagulation and
antiplatelet tx to prevent local-thrombosis.
 Coronary Laser Surgery
 Laser can destroy atherosclerotic plaque. Research is being
conducted in transluminal laser angioplasty to coronary
arteries.
 Atherectomy - surgical removal of atheroma.
Coronary Artery By-Pass Grafting (CABG)
 Procedure - Surgical revascularization to increase coronary
blood flow.
 Patients with severe disease may not be candidates.
Longevity after surgery still being debated. Surgery does not
cure atherosclerosis and patients must still control risk
factors
Post-op CABG
 Post-Operative Nursing Assessments & Care
 Cardiovascular function
 Respiratory function - pt may be on mechanical ventilator for
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
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short time.
Renal Function
Neurologic Function
Peripheral Vascular Function
Fluid & Electrolyte Balance
Pain management
Psychological Status
Safety - Pt may be restrained to present self extubation
Cardiac Tamponade of CABG
 Etiology - heart is compressed by fluid within the pericardial
sac. Ventricular filling is thus impaired resulting in decreased
cardiac output and circulatory collapse.
 Clinical Signs

Pulsus Paradoxus
Blood Pressure

Neck Veins
Heart Sounds

Respirations
Mental Status

Pain
 Treatment

Thoracotomy Pericardiocentesis
NCLEX TIME
Modifiable risk factors associated with CAD include:
A. age, weight, cholesterol level
B. Smoking, diet, BP
C. Family hx, weight, BP
D. Blood glucose, activity level, family hx
NCLEX TIME
A patient has just returned from cardiac cath. Which nursing
intervention is most appropriate?
A. Assist pt to ambulate to the BR
B. Restrict fluids
C. Monitor peripheral pulses
D. Insert an indwelling catheter
NCLEX TIME
A 63 man is resuscitated successfully after cardiac arrest.
Blood studies show that he is acidotic. Why?
A. Decreased tissue perfusion causes lactic acid
production
B. The pt typically has an irregular heart beat
C. The pt was treated inappropriately with Na Bicarb
D. Fat forming ketoacids are breaking down
NCLEX TIME
Rosie is preparing her client for discharge following his
inpatient stay with angina, which is now stable. Rosie is
reviewing both modifiable and nonmodifiable risk
factors. Select all factors below that are nonmodifiable.
A.Age
B.Gender
C.Obesity
D.Family history
E.Hypertension
NCLEX TIME
Following her inferior wall MI, Mrs. Green is quiet, reserved,
and avoiding contact with her family. Understanding the
psychosocial aspects of ACS, which intervention would be
best for the nurse to do first?
 A.Have the client’s cardiologist write for a psychiatric
referral.
 B.Provide an atmosphere of acceptance.
 C.Foster mechanisms to suppress anger and hostility.
 D.Provide factual information to the client’s family alone.
NCLEX TIME
When Rosie is assessing her client with chest pain, she is
evaluating whether or not the client is suffering from
angina or MI. Which symptom would be indicative of an
MI?
 A.Substernal chest discomfort
 B.Chest pain brought on by exertion or stress
 C.Substernal chest discomfort relieved by nitroglycerin
or rest
 D.Substernal chest pressure relieved only by opioids
NCLEX TIME
All of the following clients are being cared for on the coronary care
“stepdown” unit. When making client assignments, which client will
be best for the charge nurse to assign to a new graduate RN who has
completed 6 months of orientation to the unit?
A.A client who has a new diagnosis of heart failure and needs discharge
teaching about medications
B.A client who has just returned to the unit after having a coronary
arteriogram and has orders for vital signs every 15 minutes
C.A client with a history of angina who is requesting nitroglycerin for
left anterior chest pain
D.A client who has many questions about the electrophysiology studies
that are scheduled
NCLEX TIME
4.An RN and an LPN who both have several years of experience in the
intensive care unit are caring for a group of clients. Which task will
be most appropriate for the RN to delegate to the LPN?
A.Obtaining pulmonary artery wedge pressures every hour for a client
admitted with pulmonary edema
B.Monitoring vital signs and assessing the catheter insertion site for a
client who returned from a coronary arteriogram an hour ago
C.Teaching the family members of a client who is scheduled for
myocardial nuclear perfusion imaging about the procedure
D.Completing the admission assessment for a client admitted to the
unit with acute coronary syndrome
NCLEX TIME
The nurse is caring for a client who has been admitted with
chest pain of unknown etiology. All of the following
laboratory tests are obtained. Which test results require the
most immediate action by the nurse.
A.Troponin T is elevated.
B.Creatinine kinase is decreased.
C.Myoglobin is increased.
D.High-density lipoproteins are decreased.
Cardiac Case Study
A 57yo male is admitted to your unit c/o dull pain in the left
side of his chest and radiating to his neck. There’s no
diaphoresis or SOB. Risk factors include
hypercholesteremia and a 70 pack year hx of smoking.
PE reveals BP 140/86, HR 110, normal heart sounds and
clear lungs bilat. Cardiac markers drawn ½ hour after the
onset of pain show Myoglobin 45mcg. Troponin I at
0.01ng/mL and CPK-MB of 10u/L. EKG shows
nonspecific ST wave changes in the anterior leads.