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

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
Stable:

Assesment
1.

Hx

2.

Physical Exam

3.

EKG

4.

Exercise EKG

5.

Thallium Scan

6.

Coronary Angiography

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
in decreased wall tension
and thus
-decreased 02 demand

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
IV

(Tridil)
other tx

(Nitro-Dur)

For attacks unresponsive to

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

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 its 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 effectdecreases 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

Whats 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

Obtain EKGs
Batman
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 bypass 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 localthrombosis.

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 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 clients 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
clients 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. Theres 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 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.