Nursing care of client with Coronary Artery Disease Part 1 of 2

NURSING CARE OF CLIENT
WITH ACUTE CORONARY
SYNDROME

ASSESSMENT, DX EXAMS

Maria Carmela L. Domocmat, RN, MSN
Instructor
School of Nursing
Northern Luzon Adventist College

CORONARY ARTERY DISEASE

CLDomocmat 8/9/2012 2

Coronary Artery Disease

AKA

Ischemic Heart Disease
Coronary Heart Disease (CHD)
Coronary Occlusive Disease (C.O.D.)
Atherosclerotic Heart Disease (A.H.D.)



Refers to the diseases of the heart that
result from a decrease in blood supply to
the heart muscle
Disease caused by inadequate supply of
blood to the heart.


CAD

Include the disorders
1. Angina pectoris
2. Acute coronary syndrome
a. Unstable angina
b. MI (STEMI, NSTEMI)


Incidence
Primary cause of morbidity mortality in the
Philippines

Etiology
Results from development of obliterative
lesions within the coronary arteries


Ten Leading Causes of Mortality
Philippines, 2000
1. Diseases of the Heart
2. Diseases of the Vascular System
3. Malignant Neoplasm
4. Pneumonia
5. Accidents
6. Tuberculosis, all forms
7. Chronic Obstructive Pulmonary Disease & Allied
Conditions
8. Certain conditions originating in the Perinatal period
9. Diabetes Mellitus
10. Nephritis, Nephrotic Syndrome and Nephrosis

http://www.doh.gov.ph/files/table1_4.pdf CLDomocmat 8/9/2012 7

Occlusion of the coronary artery or any of its
branches
Decrease or absence of blood supply to myocardium

1. Transient Hypoxia:
Angina Pectoris
2. Hypoxia with decreased function:
Myocardial Ischemia
3. Death and necrosis of myocardium:
Myocardial Infarction

Causes of CAD

Arteriosclerosis
Atherosclerosis


Atherosclerosis – deposition of fat
containing substances along the intima of
blood vessels causing its narrowing ; a type
of arteriosclerosis


atherosclerosis


Atheroma Formation


Atherosclerosis develops in the coronary
arteries, causing them to become
narrowed or blocked. Blood flow to the
area of the heart supplied


Arteriosclerosis

Is hardening of arterie
primarily affects the intimal layer of the blood vessels
Includes:
a. Atherosclerosis – accumulation of fat
deposits
b. Monckebergs sclerosis – calcium
accumulation in medial layers of the arteries
c. Arteriolar sclerosis- thickening of the
sclerosis-
small artery vessels


Theories of Pathogenesis

1. Response to injury theory
2. Neoplasia Theory


Theories of Pathogenesis
1. Response to injury theory
Injurious Stimuli (HPN, Hypercholesterolemia)

Endothelial damage

Increased permeability/adhesion molecule

Lipids and platelets travel to the areas affected

Migration of macrophages into vessel wall

Plaques begin to form from cells which are imbibed
into the endothelium

Lipids are engulfed by the cells (foam cells) and
smooth muscle cells develop

Narrowing of blood vessels

Plaque disruption


Thrombus formation

Obstruction of coronary arteries

Decreased Myocardial Oxygenation
Angina pectoris
Myocardial Infarction


2. Neoplasia Theory
- vessel injury cause cell proliferation
stemming from a single cell (monoclonal
origin)


Aortic atherosclerotic plaques


Cross section of a coronary artery. A thrombus occludes the
lumen and rests upon a mature atherosclerotic plaque. Note
the relative thickness of the intima and media.

Etiology and risk factors
Nonmodifiable risk factors
Modifiable risk factors


Nonmodifiable risk factors

Heredity
Increasing age
Gender


Heredity

family history of first degree relative
with CVD at 55 yrs old or younger (M),
65 yrs old or younger (F)


Increasing age

›45 yrs old (M); ›55 yrs old (F)


Gender

affects men more than women before
they have menopause
with OCP use after menopause increase
risk of developing CAD especially with
smoking history
with early menopause- 3x’s increase risk
menopause-
of developing CAD
lifestyle changes that increase risk of CAD
in women
a. more women have entered the work force
b. increase number of smokers



Cigarette smoking Homocysteine levels
Hypertension Metabolic syndrome
Increase serum Physical inactivity
cholesterol
Lack of exercise
Obesity
Diabetes
Stress
Inflammatory
Response


Cigarette smoking

Nicotine – initiate release of
catecholamine
Endothelial dysfunction and increased
vessel wall thickness
Increase blood CO level
Beware! Passive smoking
Oral contraceptives (OC) + smoking


Hypertension

men >45 y/o with BP exceeding 140/90
all adult women with pressures above
160/95 have a 50% increase in
mortality
the higher the BP = the higher the risk
of CAD


Increase serum cholesterol

> 259mg/dl = 3x’s more likely to develop
CAD
Patients with LDL to HDL ratios greater than
4:1 are prone to CAD


Modifiable Risk Factors cont.

Lack of exercise
Obesity
Distribution of body fat
Waist measurement: N: less than 40 inches (M);
less than 35 (F)
BMI – N: 18.5 to 24.9
Diabetes
Stress: increases BP


Metabolic syndrome

Diagnosis of this includes 3 of the ff:
Insulin resistance (FBS › 100 mg/dl or
abnormal GTT)
Central obesity (waist circum › 35 inches for F;
› 40 for M
Dyslipedemia (Tg ›150 mg/dL; HDL ‹ 50
mg/dL for F; ‹ 40 mg/dL for M)
BP persistent ›130/85
Proinflammatory state (high CRP level)
Prothtombin state (high fibrinogen level)


Inflammatory responses

chronic inflammation cause increase C-
reactive protein (CRP) levels which tend
to disrupt plaque inside arterial walls
Lab test : high sensitivity C-reactive
protein (hs-CRP)


Homocystein levels

Essential amino High homocysteine
acid levels increase the
risks of a heart
High serum levels attack or stroke.
block production of
nitric oxide
Normal value: ‹ 12
mmol/dL


Physical inactivity

Goal: 30 minutes, regular moderate
aerobic exercise (ex: brisk walking)


Let’s Review



Cigarette smoking Homocysteine levels
Hypertension Metabolic syndrome
Increase serum Physical inactivity
cholesterol
Lack of exercise
Obesity
Diabetes
Stress
Inflammatory
Response


Prevention


An ounce of prevention is better
than a pound of cure


Preventive measures

Lifestyle modifications
Reduce stress
BP control, DM control
Lower Serum chole
Reduce CRP levels (hs-CRP)
hs-
Lower Homocystein levels
Boost “good cholesterol” levels (HDL)


Lifestyle modifications

Diet: low fat , low cholesterol, low salt
quit smoking , avoid passive smoking
exercise and weight reduction
adequate time for rest and relaxation


Medications

statins
Glycoprotein IIb/IIIa receptor
IIb/
antagonists
aspirin, plavix
Aspirin in low doses is the best known agent
for the prevention of coronary heart disease.


Cigarette smoking cessation

Educational program, Counseling,
Consistent motivation, reinforcement
messages, support group,
meds
nicotine patch [NicoDerm CQ, Habitrol]
antidepressant bupropim [Zyban])


Exercise and weight reduction

Goal: 30 minutes, regular moderate
aerobic exercise (ex: brisk walking)
EBP:
Men who had weights 30 min or
more per week had a 23% risk
reduction in coronary heart disease


Reduce Serum chole

Serum fasting lipid profile at least q 5
yrs
Lipid-lowering meds
Statins
Nicotinic acid
Fibric Acids
Bile acid sequestrants
Cholesterol absorption inhibitor
Omega-3-acid-ethyl esters

Statins

block a substance liver needs to make
cholesterol.
This reduces cholesterol in liver cells, which
causes liver to remove cholesterol from
your blood.

may also help body reabsorb cholesterol
from built up deposits on your artery
walls.
http://www.mayoclinic.com/health/hdl-
cholesterol/CL00030/NSECTIONGROUP=2

Statins

atorvastatin (Lipitor)
fluvastatin (Lescol)
lovastatin (Altoprev, Mevacor)
pravastatin (Pravachol)
rosuvastatin (Crestor)
simvastatin (Zocor)


EBP: Statins

Statin Drugs and Dietary Supplements – Vit.
E and C, selenium plus statin resulted into
reduced LDL levels compared to statins
alone.


Reduce CRP levels (hs-CRP)
hs-

Low fat, low chole diet
Smoking cessation
Exercise
Statin
Aspirin


Lower Homocystein levels

B-complex vitamin (esp folic acid)


Boost your “good cholesterol”
levels (HDL): Set your target
HDL cholesterol level
At risk Desirable
Less than 40
60 mg/dL (1.6
Men mg/dL (1.0
mmol/L) or above
mmol/L)
Less than 50
60 mg/dL (1.6
Women mg/dL (1.3
mmol/L) or above
mmol/L)
cholesterol/CL00030

levels (HDL)
Don't smoke.
Lose weight
Get more physical activity.
Drink alcohol only in moderation
Choose healthier fats.
Monounsaturated and polyunsaturated fats —
found in olive, peanut and canola oils
Nuts, fish and other foods containing omega-3
fatty acids

EBP: Alcohol

Compared with men who consume
alcohol less than once a week, men
who consume alcohol 3-7 days a week
had a 32%-37% reduction of MI.



Choose healthier fats.
Monounsaturated and polyunsaturated fats —
found in olive, peanut and canola oils
Nuts, fish and other foods containing omega-3
fatty acids




Niacin (Niaspan)
Fibrates
The medications fenofibrate (Lofibra, Tricor)
and gemfibrozil (Lopid) can also help increase
HDL cholesterol level.


Stable and Unstable Angina Pectoris
See separate presentation


Acute Myocardial Infarction


Acute Myocardial Infarction

Occurs when myocardial tissue is abruptly
and severely deprived of O2
When blood flow is reduced by 80-90%
80-
ischemia develops


prolonged ischemia lasting more than 35-
35-
45 minutes produces irreversible cellular
damage and necrosis of the
myocardium
ischemic injury evolves over several hours
toward complete necrosis and infarction


The autonomic nervous system attempts
to compensate for the depressed cardiac
performance.
This results to further imbalance between
myocardial oxygen supply and demand
The 3 areas which develop in MI are:


http://pathologyproject.files.wordpress.com/2011/03/early-signs.jpg


Zone of infarction

Zone of hypoxic
injury
Zone of ischemia


Most common site for MI is the anterior
wall of the left ventricle.
MI may be classified as follows:
Transmural infarct – extends from endocardium
to epicardium
Subendocardial – affects the endocardial muscles
Intramural – seen in patchy areas of the
myocardium and is usually associated with
longstanding angina pectoris
Healing requires formation of scar tissues
that replace the necrotic myocardium; scar
tissue inhibits contractility


javascript:eml2('dorland','infarction_myocardial.jpg')


Clinical Manifestations



Pain
crushing, severe, prolonged, unrelieved by
rest or nitroglycerine, radiating to one or
both arms, neck, back

Signs of shock - hypotension, cold
diaphoresis, peripheral cyanosis,
tachy/brady,
tachy/brady, thready pulse


Women often present with a “triad” of
symptoms, including indigestion or
abdominal fullness, chronic fatigue despite
adequate rest, and inability to catch one’s
breath.



fever
apprehension
indigestion
dob
n/v
pallor, cyanosis, coolness of extremities
increase BP, HR, S4, transient murmur


PE

thorough and focused health hx and PE
goal: presence of CAD risk factors, angina,
previous infarctions
focused assessment
chest pain
general appearance
determination of frequent VS
cont monitoring of cardiac and pulse
ongoing eval of mental status, heart, lungs,
abd UO, extremities
Maria Carmela L.Domocmat, RN, MSN 8/9/2012 75

Diagnostic exams


Diagnostic exams
ECG
Serum Markers of Myocardial Damage :
Cardiac biomarkers
Cardiac catheterization with coronary
arteriography
Echocardiography
Radionuclide imaging
PET Scan
CT scan
Magnetic Resonance Imaging
Intravascular ultrasound (IVUS)


Stress ECG

ST segment
depression of 1mm or
more during exercise
ECG changes during
testing may indicate
ischemia


12 lead ECG changes

T wave inversion
ST segment elevation (subepicardial
(subepicardial
injury)
ST segment depression
(subendocardial injury)
abnormal Q wave (infarction)


http://www.technion.ac.il/~eilamp/mi_qwave.html

Abnormal Q wave


12- lead ECG

Note: 1 single ECG is NOT sufficient to
confirm or exclude dx of AMI
cardiac conduction system is dynamic process
that is subject to change overtime
Recommendation
serial ECGs q 30 min for pt at high risk for AMI


Acute Cardiac Ischemia Time-
Insensitive Predictive
Instrument (ACI-TIPI)

Adobe Acrobat Adobe Acrobat
Document Document


Serum Markers of Myocardial
Damage : Cardiac biomarkers


Cardiac Serum markers

during infarction process – cell
membranes rupture, allowing intracell
enzymes to spill out into blood stream
are substances that are released into the
blood when the heart is damaged or
stressed.
Measurement of these biomarkers is
used to help diagnose, risk stratify,
monitor and manage people with
suspected acute coronary syndrome
(ACS) and cardiac ischemia.

Cardiac biomarkers

Current cardiac biomarker tests used
to help diagnose, evaluate, and monitor
individuals suspected of having acute
coronary syndrome (ACS) include:
Troponin I or T
CK-MB


Cardiac biomarkers
Other biomarker tests that may be used:
Myoglobin
BNP (or NT-proBNP) — although usually used to recognize
heart failure, an increased level in people with ACS indicates
an increased risk of recurrent events
hs-CRP
Homocysteine
Phased out biomarkers—the tests below are not
specific for damage to the heart and are no longer
recommended for evaluating people with suspected
ACS:
AST
LDH


Cardiac Troponin T and I

most sensitive to cardiac muscle damage
Not found in normal heart
quick, rapid test
if elevated – indicate AMI
become elevated in the blood within 3
or 4 hours after injury and may remain
elevated for 10 to 14 days.


Troponin

Troponin T
similar to CK-MB – with regard sensitivity
useful and more accurate than LDH in
confirmation of distant AMI
Troponin I
very specific and sensitive indicator of
AMI
not affected by any other dse or injury to any
other muscle except cardiac muscle


CK MB

Enzyme specific to cells of heart
(+) in blood indicates tissue necoris or
injury


Myoglobin

found in both skeletal and cardiac
muscle
Detected 2-3 hours post MI
2-


Myoglobin

start to rise within 2-3 hours of a heart
attack or other muscle injury, reach their
highest levels within 8-12 hours, and
generally fall back to normal within one day.
Increase is detectable sooner than troponin,
but it is not as specific for heart damage and
it will not stay elevated as long as troponin.
Although a negative myoglobin result
effectively rules out a heart attack, a positive
result must be confirmed by testing for
troponin.
http://labtestsonline.org/understanding/analytes/myoglobin/tab/test

Test Time to Peak Duration Sampling
detection

CK-MB
CK- 6-12 hours 1 day 3 days Every 12 hrs x 3
days start 6 hrs
after chest pain

Troponin T 3-12 hours 24 hours 10-14 days
10- One at least 12 hrs
after onset of pain

Troponin I 3-12 hours 24 hours 5-10 days One at least 12 hrs
after onset of pain

Myoglobin 1-3 hrs 12 hrs


Lactate dehydrogenase (LDH
or LD)
is an enzyme that is found in almost all of
the body's cells, but only a small amount
of it is usually detectable in the blood.
is released from the cells into the
bloodstream when cells are damaged or
destroyed. Because of this, the LDH test
can be used as a general marker of injury
to cells.
http://labtestsonline.org/understanding/analytes/ldh/tab/test


LDH

LDH1 subunit – plentiful in heart muscle
and released into serum when myocardial
damage occurs
LDH-1: heart, red cells, kidney, germ cells
LDH-2: heart, red blood cells, kidney (lesser amounts than LDH-1)
LDH-3: lungs and other tissues
LDH-4: white blood cells, lymph nodes, muscle, liver (lesser amounts
than LDH-5)
LDH-5: liver, skeletal muscle


Nrg considerations: LDH

Inform that no need to restrict food or
fluids
Muscle trauma caused by MI injections
can raise LD levels
Prosthetic valves or recent surgery or
pregnancy can cause elevated result


Test Time to Peak Duration Sampling
detection
SGOT 24 hours 2 days 4 days 1-2 days
after chest
pain
LDH 36 hours 3 days 10 days 1-2 days
after chest
pain


Other lab tests

Serum lipids
Hs CRP
Homocystein
WBC
Serum elec


Fasting lipid profile

total cholesterol: ‹ 200 mg/dL
triglycerides : ‹ 150 mg/dL
LDL : ‹ 100 mg/dL
HDL chole: ‹ 60 mg/dL

HDL: LDL ratio shld be 3:1


Homocystein levels

Normal value: ‹ 12 mmol/dL
Labs: NPO 1-12 hrs


High sensitive C- reactive protein
C-
(hs-CRP)
hs-
correlates with CK-MB levels but it
CK-
peaks several days later
Most standard marker of inflammation
Normal value: 1 mg/dl
> 3 – increase risk CAD


Leukocytosis

10, 000 to 20, 000 mm3
appears on 2nd day
disappears in 1 wk
Myeloperoxidase – a leukocyte enzyme –
recently shown to ne a predictive ofAMI
even in clients without elevation in
Troponin T


Cardiac catheterization with
coronary arteriography


direct visualization of
the coronary arteries
by selective injection
of radiographic
contrast material
most sensitive and
specific test


pre post
Determine allergy to iodine Bed rest
and seafoods (prep Supine HOB elevate
antihistamine) Leg insertion site keep
straight
Informed consent
VS q 15v min for 1 hr; then
2-6 hrs bedrest q 30 for 2 hrs til stable
NPO post MN Analgesics
VS, auscultate heart and Assess insertion site
lungs, eval peripheral VS, auscultate heart and
pulses, withheld digitalis or lungs, eval peripheral
diuretics pulses,
Observe complication


Health educ post cath

For the next 24 hrs
Don’t bend at waist
Strain
Lift heavy objects
Avid tub bath
Call doctor if
Bleeding, swelling, new bruising from
peripheral site, temp >38.6C


Cardiac catheterization

Coronary angiography

Let’s watch

YouTube - Heart Animation_ Coronary Angiography _Cardiac Catheterization_.flv

http://video.about.com/heartdisease/Angiography.htm


Echocardiography


Echocardiography - produces images of wall
motion abnormalities


Transesophageal Echocardiography



Stress scintigraphy - use of thallium
201 or sestamibi
-decrease uptake of dye in ischemic tissue
Stress radionuclide ventriculography
- pyrophosphate injected peripherally
binds the radionuclide technetium to RBC
used to produce a scintigraphic image of
the left ventricle
90% sensitive

PET Scan


PET Scan

3 dimensional images
Inject isotopes
Avoid tobacco and caffeine 4 hrs before


CT scan


CT scan

Xray
Cross sectionial images of the chest
(heart, great vessels)
Evaluate cardiac masses and dse of aorta
, pericardium


Magnetic resonance angiography



No metal can enter the exam room
clothing with metal snaps or pins should not be
worn.
Jewelry, watches, rings etc should be left in a
locker.
Hairpins and dentures, should also be removed
and left in a locker or outside the exam room
Heavy facial makeup should not be worn as it may
create artifacts on the image.
Labs are not required unless have a history
of impaired kidney function. However, allergy
history records are necessary for contrast
studies.

Contraindication
Patients cannot have halter monitors, telemetry units,
nerve stimulation units or a IV pump in the magnet
room
If have a heart pacemaker or pacing wires, cerebal
aneurysm or Swan Ganz catheter cannot have an MRI
under any circumstances!
Pregnancy is a contraindication and will require patient
consent for an MRI.
All other history of metal fragments in the eye require
orbit screening x-rays prior to your MRI.
All other history of implants or surgery must be
indicated to the technologist. The make and model of
implants may be necessary (i.e. ear implants, heart
valve replacements).

B-mode ultrasonography



Ultrasound -
coronary artery;
Endovascular
ultrasound;
Intravascular
echocardiography


IVUS

Alternative to injecting medium
More reliable than angiography in
indicating distribution and composition,
arterial dissection, degree of stenosis of
the occluded artery


Intravascular ultrasound
(IVUS)
A tiny ultrasound wand is attached to a
catheter. This ultrasound catheter is
inserted into an artery in your groin area
and moved up to the heart.
A computer measures how the sound
waves reflect off blood vessels, and
changes the sound waves into pictures.
IVUS gives the health care provider a look
at coronary arteries from the inside-out.

IVUS

IVUS is almost always done at the end of angioplasty with stent placement, or coronary
catheterization. Angioplasty gives a general look at the coronary arteries, but it cannot
show the walls of the arteries. IVUS images show the artery walls and can reveal
cholesterol and fat deposits (plaques). Buildup of these deposits can increase your risk of a
heart attack.
IVUS has provided a lot of insight into how stents become clogged (stent restenosis).


Let’s review


Diagnostic exams
ECG
Serum Markers of Myocardial Damage :
Cardiac biomarkers
Cardiac catheterization with coronary
arteriography
Echocardiography
PET Scan
CT scan


Prognosis of CAD


Prognosis of CAD

>80 y/o = 60 %mortality
other diseases Dm, COPD= 30%
mortality
anterior wall MI= 30% mortality


Nursing care of client with Coronary Artery Disease Part 1 of 2

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Nursing care of client with Coronary Artery Disease Part 1 of 2