CORONARY VASCULAR

DISORDERS

By, Evelin Malinti

Coronary Artery Disease
AKA
• Atherosclerotic heart disease
(ASHD)
• Coronary heart disease (CHD)
• Coronary occlusive disease
• Ischemic heart disease (ICHD)
Coronary Artery Disease
• CAD is a blood vessel disease of
the epicardial arteries responsible
for supplying the myocardium with
blood rich in oxygen and nutrients
• Disease caused by inadequate
supply of blood to the heart
CAD
• Include the disorder:
1. Angina Pectoris
2. Acute coronary syndrome
(unstable angina)
3. Myocardial Infarction (STEMI,
NSTEMI)
Incidence
• # 6 in the top 10 cause of death
in Indonesia in 2010 (CDC,
2013)
 Etiology & Risk Factors
• Diseases of the coronary
arteries is almost always due
to plaque and its
complications , particularly
thrombosis.
• Atherosclerosis is a
progressive inflammatory
disorder of arterial wall that is
characterized by focal lipid
rich deposits of atheroma
that remain clinically silent
until they become large
enough to impair tissue
perfusion
 Coronary Artery Disease
• Occlusion of the coronary artery or any of its branches
• Decrease or absence of blood supply to myocardium

• Transient hypoxia:
Angina Pectoris
• Hypoxia with decrease function:
Myocardial Ischemia
• Death and necrosis of myocardium:
Myocardial Infarction
Risk Factors for developing
atherosclerosis

Non Modifiable

• Increasing Age
• Gender
• Hereditary
• Increasing age
• > 45 yo (M)
• > 55 yo (F)
• Gender
• Affects men more than
women before they
have menopause
• Early Menopause- 3X
increase risk of
developing CAD
• Hereditary
• Family history of first degree relative
with CVD at 55 yo or younger (M),
65 yo or younger (F)
• Family history of HPN,
hypercholesterolemia, DM
Risk Factors for developing
atherosclerosis
Modifiable
• Cigarette Smoking
• Hypertension
• Hypercholesterolemia
• DM
• Physical inactivity
• Obesity
• Metabolic Syndrome
• Inflammatory response
• Homocysteine
Pathophysiology
1. Response to Injury Theory
Injurious Stimuli (HPN, Hypercholesterolemia, Smoking)

Endothelial damage

Increased permeability/Adhesion Molecules

Lipids & platelet travel to the area affected

Migration of macrophages into vessel wall

 Plague 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

Plague disruption

Thrombus formation

Obstruction of the coronary arteries

Myocardial Ischemia, Angina Pectoris, Myocardial Infarction

• An Ounce of
prevention is better
than a pound of cure
Prevention Measures

• Lifestyle • Maintain body wt

Modification • Reduce CRP level
• BP control, DM • Lower
control Homocysteine
• Reduce Stress Level
• Lower Serum • Boost “good
Cholesterol cholesterol” (HDL)
Angina Pectoris
AKA: stable Angina ( Classic Angina)

Definition
• It is a clinical syndrome, characterized
by paroxysm of chest pain, or a felling of
pressure in the anterior chest. It may
occur whenever there is an imbalance
between myocardial oxygen supply and
demand.
Causes and Pathophysiology

• The cause is considered to be

insufficient coronary blood
flow, resulting inadequate O2
supply of the myocardium.
Angina is usually caused by
atherosclerotic plaque.
Precipitating factors
• Common factor
• Physical exertion can precipitate an attack by
increase myocardial O2 demands.

• Exposure to cold can cause vasoconstriction

and increased B.P with increased demands.

• Eating heavy meal which the blood flow to the

mesenteric area places a heavier demands on
the heart.
• Stress and emotional provoking situation
cause the release of adrenaline and B.P
may accelerate the heart rate
Precipitating factors (cont…)

• Uncommon factor

• Lying flat (angina decubitus)

• Vivid dreams ( nocturnal angina)

Clinical manifestations
• The pain is usually felt deep in the
chest behind the sternum. Although
the pain frequently is localized, it may
radiate to the neck, jaw, shoulders,
and inner aspects of the upper
extremities

• Patient often experience a tightness

or strangling sensation
Clinical manifestations (cont…)

• Feeling of weakness or numbness

in the arms, wrists, and hands may
be accompanied by pain

• Patient also has a sense of

impending death and an
apprehension
Acute Coronary Syndrome
& MI
• Acute Coronary Syndrome
Unstable angina (Pre-MI)
• Myocardial Infarction
- STEMI
- NSTEMI
Chest Pain Characteristic
• Unstable angina is characterized by
new-onset or rapidly worsening
angina, angina on minimal exertion
or angina at rest. It is most
dangerous and does not follow a
pattern, do not go away with rest or
medicine. the common features of
unstable angina are breathlessness,
nausea & vomiting
Chest pain... Cont’
• The pain occurs in the same sites as
angina but is usually more severe and
lasts longer; it is often described as a
tightness, heaviness or constriction in
the chest.
Myocardial Infarction
• An area of the myocardium is permanently
destroyed, typically because plaque
rupture and subsequent thrombus
formation result in complete occlusion of
the artery
• Signs & symptoms of MI cannot be
distinguished from those of unstable
angina
• When Blood flow is reduced by 80-
90% ischemia develops
• Prolong Ischemia > 35-45 min =
irreversible cellular damage &
necrosis of myocardium
• Ischemic injury evolves over several
hours toward complete necrosis and
infarction
Zone of Infarction

Zone of hypoxic
injury
Zone of Ischemic
 Clinical Manifestation
• 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, 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.
Nursing Assessment
• 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, extremities
Diagnostic Exam: ECG
• Unstable angina: The patient has clinical
manifestations of coronary ischemia, but ECG
and cardiac biomarkers show no evidence of
acute MI.
• STEMI: The patient has ECG evidence of acute
MI with characteristic changes in two contiguous
leads on a 12-lead ECG. In this type of MI, there
is significant damage to the myocardium.
• NSTEMI: The patient has elevated cardiac
biomarkers
• but no definite ECG evidence of acute MI.
Laboratory Test
• Creatine Kinase • Myoglobin
(CK-MB) • Myoglobin is a heme
• Elevated CKMB protein that helps transport
indicator of acute MI oxygen. Its found in cardiac
& skeletal muscle
• The level begins to
• The myoglobin level starts
increase within a few to increase within 1 to 3
hours and peaks hours and peaks within 12
within 24 hours of an hours after the onset of
MI. symptoms.
Laboratory test
• Troponin (I, T)
• a protein found in the myocardium, regulates
the myocardial contractile process.
• An increase in the level of troponin in the serum
can be detected within a few hours during acute
MI. It remains elevated for a long period, often
as long as 3 weeks, and it therefore can be
used to detect recent myocardial damage.
 Medical Managements
• Goal: to minimize myocardial damage,
preserve myocardial function, and prevent
complication
• Pharmacology therapy: (Nitroglycerin,
Morphine, ACE Inhibitor, Thrombolytic
Agent).
• Procedures: (PCI, Cardiac rehabilitation)
Medical managements
First line & initial treatments
• Semi folwer’s position
• O2 (2-4 lpm)
• IV access
• obtain 12-lead EKG
• VS and pulse oximetry
• labs (serum cardiac markers)
• ECG monitoring
• conduct hx and PE
• reduce pain
• administer meds
Nursing Managements

• Goals
• Recognize and treat cardiac ischemia
• Admin thrombolytic therapy as ordered, or
prepare client for PTCA and observe for
complications
• Recognize and treat potentially life
threatening dysrhythmias
• Goals
• Monitor for complications of reduced CO
• Maintain a therapeutic critical care
• Identify the psychosocial impact of AMI on
• client and family
• Educate the client in lifestyle changes and
• rehabilitation
 Nursing Diagnosis
• Acute Pain
• Ineffective Tissue perfusion (Cardiopulmonary)
• Activity Intolerance
• Ineffective Coping
Acute Pain
• related to imbalance between
myocardial oxygen supply and
demand
Intervention

• 1. Obtain description of chest discomfort

• 2. Vital signs and cardiac monitoring
• 3. Check vascular access
• 4. Place in semi fowler’s position
• 5. 12 lead ECG
• 6. O2 inhalation
Intervention cont’
7. Provide pain meds and aspirin
a. Nitroglycerine – increases collateral blood flow,
redistributes blood flow toward the subendocardium
and causes dilation of the coronary arteries
b. Morphine sulfate – relieves MI pain, decreases
sympathetic stimulation which decreases O2
demand and reduces circulating catecholamines
8. Assess the client’s VS and intensity of pain 5
minutes after administration of meds
9. Notify physician if patients condition
deteriorates
Ineffective Tissue Perfusion

• (Cardiopulmonary) related to
interruption of blood flow
• Goal : to restore perfusion to the injured
area to reduce the size of the infarct and
improve left ventricular function
Ineffective Tissue Perfusion
• 1. Thrombolytic therapy
• 2. Glycoprotein IIB/IIIA Inhibitors
• 3. Antiplatelets
• Aspirin
• Clopidogrel
• 4. Beta blockers
• 5. ACE Inhibitors
Ineffective Tissue Perfusion

1. Thrombolytic therapy
- Tissue plasminogen activator,
streptokinase, reteplase
- Indicated for patients who have chest pain
of greater than 30 minutes, unrelieved by
nitroglycerin and transmural MI (Q wave
MI)
Thrombolitic therapy
• dissolves thrombus and promote
reperfusion
• the golden period is 30 minutes from
onset of pain till thrombolytic therapy
within 30 minutes or PTCA within 1 hour
• Watch out for signs of bleeding and
hypersensitivity reaction ( Streptokinase )
• IV infusion
Ineffective Tissue
Perfusion
2. Glycoprotein IIB/IIIA Inhibitors
- targets the platelet component of the
thrombus to prevent fibrinogen from
attaching to activated platelets at
the site of the thrombus
- Examples: Abciximab, Eptifibatide,
Tirofiban
- Administered through IV
 Aspirin
• Swallow the tablets with a full glass of water.
• Taken as regular (not enteric-coated) lowdose
aspirin.
• Swallow the extended-release tablets whole with a full
glass of water. Do not break, crush, or chew them.
• Chewable aspirin tablets may be chewed, crushed, or
swallowed whole.
• Drink a full glass of water, immediately after taking
these tablets.
Nrg Considerations: Aspirin and Plavix
teach: may bleed more easily or for a longer time
than usual while you are taking if having surgery,
including dental surgery, tell doctor or dentist that
taking clopidogrel. Be careful not to cut or hurt aspi
or Plavix
Activity Intolerance
• related to imbalance between
oxygen supply and demand
 Actvity Intolerance
1. Bed rest with commode privilege for only 24-48
hours unless with complications.
2. Explain that the purpose of CCU confinement is
for continuous monitoring and safety during the
early recovery period.
3. Administer diazepam as ordered
4. Provide psychosocial support to the patient and
his family. Calmness and competency are
extremely reassuring.
 Program of Physical activity
1. Increase activities gradually after the first 24-48
hours
2. Early mobilization after an MI. May be allowed to sit
on a chair for increasing periods of time and begins
ambulation on the 4th or 5th day
3. Monitor V/S before activities.
4. An exercise session is terminated if any one of the
following occurs:cyanosis, cold sweats, faintness,
extreme fatigue, severe dyspnea, pallor, chest pain,
PR > 100, dysrhythmias, Bp > 160/90