1. Management of
Patients with
Coronary
Vascular
DisordersMa. Tosca Cybil A. Torres, RN

2. Coronary Artery Disease (CAD)
• Coronary artery disease (CAD) (or
atherosclerotic heart disease) is the end
result of the accumulation of atheromatous
plaques within the walls of the coronary
arteries that supply the myocardium with
oxygen and nutrients. It is sometimes also
called coronary heart disease (CHD), but
although CAD is the most common cause of
CHD, it is not the only cause.

3. ATHEROSCLEROSIS (AS)
• is a disease of large and medium-sized
muscular arteries (e.g., coronary, carotid,
arteries of the lower extremities) and the
elastic arteries such as the aorta and iliac
vessels (supplying blood to the lower trunk
and lower limbs arising from the
bifurcations of aorta).
• it is a slowly progressive disease that
begins in childhood, but does not manifest
until middle age or later, when the arterial
lesions precipitate clinical manifestations
by virtue of organ injury.

4. • the basic lesion – the atheroma
(fibrinofatty plaque) – consists of a raised
focal plaque within the intima, having a
core of lipid (mainly cholesterol) and a
covering fibrous cap.
• atheromas compromise arterial blood flow
and weaken affected arteries. Many
eventually undergo a variety of
complications (e.g., calcification,
ulceration, thrombus formation, and
aneurysmal dilation)

5. Atheroma

6. Atherothrombosis (1)

7. Atherothrombosis (2)

8. Athérothrombosis (3)
a
b
c
d
e

9. Athérothrombosis (4)
a b
c
d
e

10. Thrombus position
and consequences
Infarct

11. Many risk factors have been
associated with CAD.
Nonmodifiable risk factors
Age
Gender
Ethnicity
Family history and genetic
inheritance.

12. Modifiable risk factors include elevated serum lipids,
hypertension, tobacco use, physical inactivity, obesity,
diabetes, metabolic syndrome, psychologic states, and
homocysteine level.
• Elevated serum lipid levels are one of the four most firmly
established risk factors for CAD.
• Lipids combine with proteins to form lipoproteins and are
vehicles for fat mobilization and transport. The different types of
lipoproteins are classified as high-density lipoproteins (HDLs),
low-density lipoproteins (LDLs), and very-low-density
lipoproteins (VLDLs).
– HDLs carry lipids away from arteries and to the liver for
metabolism. High serum HDL levels are desirable.
– HDL levels are increased by physical activity, moderate alcohol
consumption, and estrogen administration.
– Elevated LDL levels correlate most closely with an increased
incidence of atherosclerosis and CAD.

13. • Hypertension, defined as a BP greater than or
equal to 140/90 mm Hg, is a major risk factor in
CAD.
• Tobacco use is also a major risk factor in CAD.
The risk of developing CAD is two to six times
higher in those who smoke tobacco than in those
who do not.
• Obesity is defined as a body mass index (BMI) of
less than 30 kg/m2. The increased risk for CAD is
proportional to the degree of obesity.
– Diabetes, metabolic syndrome, and certain
behavioral states (i.e., stress) have also been found
to be contributing risk factors for CAD.
•

14. ARTERIAL OCCLUSIVE DISORDERS
The most common cause is arteriosclerosis
obliterans (ASO).
The lower extremities are more commonly
affected. The aorta may also be affected.
Atheromatous plaque develops at the points
of branching, bifurcations, or vessel
narrowing.
More prevalent among men, 50-70 years old.

15. Clinical manifestations:
• Pain – intermittent claudication is an aching,
persistent, cramp-like, squeezing pain that
occurs after a certain amount of exercise of
the affected extremities. It is relieved by rest.
• Coldness or cold sensitivity – coldness in the
feet with exposure to a cold environment,
associated with blanching or cyanosis due to
tissue ischemia.
• Impaired arterial pulsations – impaired or
absent pulse indicates decrease blood flow
due to arterial spasm.

16. • Color changes – cyanosis or rubor may be
observed when the extremities are placed in
dependent position.
• Ulceration and gangrene – may be due to
ischemia or trauma. Impaired tissue
perfusion inhibits healing process.
• Edema – results from severe obstruction.
• Sexual dysfunction - occlusive disease of
the terminal aorta decreases the blood
supply to the vascular tree supplying penile
circulation. Unsustained erection may be
experienced by the client

17. Prevention:
Primary Prevention
– Provide information on the effects of :
• a. cigarette smoking- nicotine causes vasoconstriction, spasms of the
arteries, reduced circulation to the extremities. The carbon monoxide
inhaled in cigarette smoking reduces O2 transport to the tissues.
• b. hypertension – causes elastic tissue in the arteries to be replaced by
fibrous collagen tissue. This reduces arterial elasticity and increases
resistance to blood flow.
• c. hyperlipidemia – cholesterol and triglycerides contribute to the
development of atherosclerotic plaque in the vessels.
• d. obesity – places an added burden on the heart and blood vessels. It
enhances propensity to DM, hypertension, and hyperlipidemia.
• e. physical inactivity – compresses circulation
• f. emotional stress – stimulates the sympathetic response which results
to vasoconstriction. Stress may also cause increase cholesterol and
platelet levels and hypertension.
• g. DM – changes in glucose and fat metabolism enhance
atherosclerotic process.

18. Secondary Prevention
• Encourage client with early symptoms to seek
medical care. This is to prevent complications like
infection, injury, thrombosis and amputation.
Tertiary Prevention
• Rehabilitation is an important aspect of
management of clients with arterial occlusive
disorder. Exercises develop collateral circulation
will be beneficial.

19. Management:
• Quit smoking
• Control of serum lipid levels
• Skin and foot care
• Diet- low fat, low cholesterol
• Activity – daily walking program

20. If levels remain elevated despite modifiable
changes, drug therapy is considered
– Statin drugs work by inhibiting the synthesis of cholesterol in
the liver. Liver enzymes must be regularly monitored. (ex.
Simvastatin)
– Niacin, a water-soluble B vitamin, is highly effective in
lowering LDL and triglyceride levels by interfering with their
synthesis. Niacin also increases HDL levels better than many
other lipid-lowering drugs.(Ex. Niacin SR)
– Fibric acid derivatives work by accelerating the elimination
of VLDLs and increasing the production of apoproteins A-I
and A-II. (ex. Lipofen, Tricor)
– Bile-acid sequestrants increase conversion of cholesterol to
bile acids and decrease hepatic cholesterol content. The
primary effect is a decrease in total cholesterol and LDLs. (ex.
Questran)

21. Angina Pectoris
Definition:
Angina: Choking or suffocation.
Pectoris: Chest.
Angina pectoris, is the medical term used to describe
acute chest pain or discomfort.
Angina occurs when the heart’s need for oxygen
increases beyond the level of oxygen available from
the blood nourishing the heart.
It has 3 types
• Stable Angina
• Un stable angina &
• Variant Angina (Prinzmetal’s or resting angina) :

22. Types of Angina
• Stable angina:
– People with stable angina have episodes of
chest discomfort that are usually
predictable. That occur on exertion or under
mental or emotional stress.
Normally the chest discomfort is relieved
with rest,
nitroglycerin (GTN) or both.
– It has a stable pattern of onset, duration
and intensity of symptoms.

23. • Unstable angina:
– It is triggered by an un predictable
degree of exertion or emotion.
– (progressive), more severe than
stable. Characterized by increasing
frequency & severity. Provoked by
less than usual effort, occurring at
rest &
– interferes with pt lifestyle.

24. • Variant Angina (Prinzmetal’s or resting
angina) :
occur spontaneously with no
relationship to activity. Occurs at rest
due to spasm. Pt discomfort that
occurs rest usually of longer duration.
Appears to by cyclic & often occurs at
about the same time each day (usually
at night). Thought to be caused by
coronary artery spasm

25. CHRONIC STABLE ANGINA
• Chronic stable angina refers to chest pain
that occurs intermittently over a long period
with the same pattern of onset, duration, and
intensity of symptoms.
– Angina is rarely sharp or stabbing, and it usually
does not change with position or breathing.
Many people with angina complain of indigestion
or a burning sensation in the epigastric region.
– Anginal pain usually lasts for only a few minutes
(3 to 5 minutes) and commonly subsides when
the precipitating factor is relieved. Pain at rest is
unusual.

26. • The treatment of chronic stable angina is aimed at
decreasing oxygen demand and/or increasing oxygen
supply and reducing CAD risk factors.
– In addition to antiplatelet and cholesterol-lowering drug therapy, the
most common drugs used to manage chronic stable angina are
nitrates.
• Short-acting nitrates are first-line therapy for the treatment of angina.
Nitrates produce their principal effects by dilating peripheral blood
vessels, coronary arteries, and collateral vessels. (Isordil)
• Long acting nitrates are also used to reduce the incidence of anginal
attacks. (Imdur)
• -Adrenergic blockers are the preferred drugs for the management of
chronic stable angina. (Inderal)
• Calcium channel blockers are used if -adrenergic blockers are
contraindicated, are poorly tolerated, or do not control anginal
symptoms. The primary effects of calcium channel blockers are (1)
systemic vasodilation with decreased SVR, (2) decreased myocardial
contractility, and (3) coronary vasodilation. (Norvasc, Plendil)
• Certain high-risk patients (e.g., patients with diabetes) with chronic
stable angina may benefit from the addition of an angiotensin-converting
enzyme (ACE) inhibitor. (Capoten)

27. Diagnostic tests
 chest x-ray
 12-lead ECG
 laboratory tests (e.g., lipid profile)
 nuclear imaging
 exercise stress testing
 coronary angiography

28. ACUTE CORONARY SYNDROME
• Acute coronary syndrome (ACS) develops when ischemia
is prolonged and not immediately reversible. ACS
encompasses the spectrum of unstable angina, non–ST-
segment-elevation myocardial infarction (NSTEMI), and ST-
segment-elevation myocardial infarction (STEMI).
• ACS is associated with deterioration of a once stable
atherosclerotic plaque. This unstable lesion may be partially
occluded by a thrombus (manifesting as UA or NSTEMI) or
totally occluded by a thrombus (manifesting as STEMI).
• Unstable angina (UA) is chest pain that is new in onset,
occurs at rest, or has a worsening pattern. UA is
unpredictable and represents an emergency.

29. ISCHEMIA VS INFARCTION
ISCHEMIA INFARCTION
PAIN SUBSTERNAL
PRESSURE/ HEAVINESS
SQUEEZING
SUBSTERNAL
CONSTRICTIVE (+ SX
OF SHOCK)
DURATION 3-5 MIN > 5 MIN
PRECIPITANTS STRESS/ EXERTION NO
REST
NITROGLYCERINE
RELIEVED NOT RELIEVED
CARDIAC TISSUE
DAMAGE
NOT PERMANENT PERMANENT

30. Myocardial infarction (MI)
• Myocardial infarction (MI) Myo means muscle, “Cardiac” heart,
infarction means “death of tissues due to lack of blood supply”.
• occurs as a result of sustained ischemia, causing irreversible
myocardial cell death. Eighty percent to 90% of all MIs are due to
the development of a thrombus that halts perfusion to the
myocardium distal to the occlusion. Contractile function of the
heart stops in the infracted area(s).
– Cardiac cells can withstand ischemic conditions for
approximately 20 minutes. It takes approximately 4 to 6 hours
for the entire thickness of the heart muscle to infarct.
– Infarctions are described based on the location of damage
(e.g., anterior, inferior, lateral, or posterior wall infarction).
– Severe, immobilizing chest pain not relieved by rest, position
change, or nitrate administration is the hallmark of an MI. The
pain is usually described as a heaviness, pressure, tightness,
burning, constriction, or crushing.

31. Myocardial infarction (MI)

32. PATHOPHYSIOLOGY
Coronary artery cannot supply enough blood to the heart in
response to the demand due to CAD
Within 10 seconds myocardial cells experience ischemia
Ischemic cells cannot get enough oxygen or glucose
Ischemic myocardial cells may have decreased electrical &
muscular function
Cells convert to anaerobic metabolism.
Cells produce lactic acid as waste
Pain develops from lactic acid accumulation
Pt feels anginal symptoms until receiving demand increase 02
requirements of myocardial cells

33. MYOCARDIAL INFARCTION
IRREVERSIBLE CARDIAC DAMAGE FROM OCCLUSION OF 1
OR MORE CORONARY ARTERY
E.C.G.
Recent M.I. – ST elevation (injury)
T wave inversion (ischemia)
Previous M.I. – Q wave (necrosis / old infarct)
BLOOD STUDIES
Troponin T & I
LDH
CPK MB

34. P Q
R
S
T
E.C.G.

35. P Q
R
S
T
E.C.G.
ST SEGMENT
ELEVATION

36. P Q
R
S
T
E.C.G.
INVERTED
T - WAVE

37. P
Q
R
S
T
E.C.G.
Q wave

38. Signs and Symptoms
• Classic symptom of heart attack
are chest pain radiating to neck,
jaws, back of shoulder, or left arm
 The pain can be felt like:
 Squeezing or heavy pressure
 A tight band on the chest
 An elephant sitting on the chest

39. ContOther symptoms include:
• Shortness of breath
(SOB)
• Weakness and
tiredness
• Anxiety
• Lightheadedness
• Dizziness
• Nausea vomiting
• Sweating, which may be
profuse

40. MYOCARDIAL INFARCTION
NURSING CARE
1. Pain relief –
Morphine ( + preload
& afterload)
Demerol causes vomiting
2. Oxygen
3. Inotropics
4. Beta Blockers
5. Antiarrhythmics
6. No ice or very hot
drinks
7. Anticoagulants
8. ECG and CVP
monitoring
9. Laxatives – Lactulose
10. PTCA
11. Thrombolytic Therapy
BEFORE CELLULAR
DEATH, US. 6 HRS AFTER
THE ATTACK

41. Collaborative Management
• Assessment:
• History
• Clinical manifestation
• Cardiovascular assessment
• Laboratory assessment
• Troponin T & I
• CK-MB

42. Radiographic Assessment
 ECG
 Stress Test
 Myocardial perfusion imaging
 MRI
 Cardiac Catheterization

43. IMMEDIATE MANAGEMENT OF MI:
GOALS:
• To prolong life.
• Minimize infarct size.
• Reverse ischemia.
• Reduce cardiac work.
• Prevent and treat complications.
A) INITIAL TREATMENT:
• Rapid triage.
• OMI (oxygen, monitor and I/V line).
• Check vital signs and O2 saturation.
• ECG within 10 minutes and repeat ECG.
• Blood samples for enymes, CBC, lytes, and lipid
profile.

44. Drug therapy
Analgesic – for relief of pain, this is a priority. Pain may cause shock.
Examples, morphine sulfate, lidocaine, Nitroglycerine IV
Thrombolytic Therapy – to disintegrate blood clot by activating the
fibrinolytic processes.
• Ex. Streptokinase, urokinase and tissue plasminogen activator (TPA).
 Administration is most crucial between 3-6 hours after the initial infarction has
occurred.
 Detect for occult bleeding during and after thrombolytic therapy.
 Assess neurologic status changes which may indicate GI bleeding or cardiac
tamponade.
Anticoagulant and antiplatelet medications – are administered after
thrombolytic therapy to maintain arterial patency.
Other Medications:
• Beta-adrenergic blocking agents
• Diazepam

45. Coronary
revascularization
with coronary artery
bypass graft
(CABG) surgery is
recommended for
patients who (1) fail
medical
management, (2)
have left main
coronary artery or
three-vessel
disease
Surgical Therapy

46. The off-pump coronary
artery bypass (OPCAB)
procedure uses full or
partial sternotomy to
enable access to all
coronary vessels. OPCAB
is also performed on a
beating heart using
mechanical stabilizers and
without cardiopulmonary
bypass (CPB).
Surgical Therapy

47. Transmyocardial laser revascularization (TMR) is an indirect
revascularization procedure used for patients with advanced
CAD who are not candidates for traditional bypass surgery and
who have persistent angina after maximum medical therapy.
Surgical Therapy

48. Surgical management
• PTCA (Percutaneous Transluminal
Coronary Angioplasty

49. Balloon Angioplasty – involves insertion of a special catheter
through fluoroscopy into the site of occlusion. The balloon tip of
the catheter is inflated to compress and rupture the
atheromatous plaque.

50. Stent – involves use of rigid but flexible structure that
maintains the integrity of the vascular wall and patency
of the artery.

51. Nursing Diagnoses
• Acute pain R/T imbalance between myocardial
oxygen supply and demand
• Ineffective tissue perfusion R/T interruption of
arterial blood flow
• Ineffective coping R/T effects of acute illness and
major changes in life style
• Impaired gas exchange related to ineffective
breathing pattern and decreased systemic tissue
perfusion.
• Anxiety related to present status and unknown
future, possible lifestyle changes, pain, and
perceived threat of death.
• Activity intolerance related to fatigue

52. Nursing Management: Chronic Stable
Angina and Acute Coronary Syndrome
The following nursing measures should be
instituted for a patient experiencing angina:
(1) administration of supplemental oxygen,
(2) determination of vital signs
(3)12-lead ECG
(4) prompt pain relief first with a nitrate
followed by an opioid analgesic if needed,
(5) auscultation of heart sounds
(6) comfortable positioning of the patient.

53. • Initial treatment of a patient with ACS includes pain
assessment and relief, physiologic monitoring, promotion of
rest and comfort, alleviation of stress and anxiety, and
understanding of the patient’s emotional and behavioral
reactions.
– Nitroglycerin, morphine sulfate, and supplemental oxygen should be
provided as needed to eliminate or reduce chest pain.
– Continuous ECG monitoring is initiated and maintained throughout
the hospitalization.
– Frequent vital signs, intake and output (at least once a shift), and
physical assessment should be done to detect deviations from the
patient’s baseline parameters. Included is an assessment of lung
sounds and heart sounds and inspection for evidence of early HF
(e.g., dyspnea, tachycardia, pulmonary congestion, distended neck
veins).

54. Nursing Management
1. Promoting oxygenation and tissue perfusion
• instruct the patient to avoid over fatigue; stop activity immediately in the
presence of chest pain, dyspnea, lightheadedness and faintness.
• O2 therapy by cannula for the first 24-48 hours or longer if pain,
hypotension, dyspnea or dysrhythmias persist. Monitor VS changes,
indicative of complication.
• Position the client in semi-fowler’s position to allow greater diaphragm
expansion thereby lung expansion and better CO2 - O2 exchange.
2. Promoting adequate CO
• Monitor the following parameters: dysrhhythmias on ECG tracings, VS,
effects of daily activities on cardiac status, rate and rhythm of pulse.
• Administer pharmacotherapy as prescribed
• Promote rest and minimize unnecessary disturbances.
3. Promoting comfort:
• relieve pain; administer Morphine SO4 as ordered. This is to reduce
sympathetic
• stimulation, which increases myocardial O2 demand. In addition, this will
prevent
• shock which may result from severe pain.

55. 4. Providing rest:
• place patient in bed rest with commode privileges for 24
– 48 hours.
• administer diazepam(Valium) as ordered.
• provide psychosocial support to the client and his family.
Calmness and competency are extremely reassuring.
5. Promoting Activity
• gradual increase in activity is encouraged after the first
24-48 hours. May be allowed to sit on a chair for
increasing periods of time and begins ambulation on the
4th or 5th day.
• monitor for signs of dysrhythmias, chest pain, and
changes in VS during activity.

56. 6. Promoting nutrition and elimination
a. provide small, frequent feedings
b. provide low – calorie, low-cholesterol, low Na diet
c. avoid stimulants
d. avoid taking very hot or very cold beverages and gas forming foods. Vasovagal
stimulation may occur, thereby bradycardia.
e. use of bedpan and straining at stool should be avoided. Valsalva maneuver changes
BP and HR which may trigger ischemia; dysrhythmias, pulmonary embolism or
cardiac arrest.
f. use of bedside commode
g. administer stool softener as ordered (ex. Lactulose)
7. Promoting relief of anxiety and feeling of well-being:
 provide an opportunity for the client and family to explore their concerns and to
identify alternative methods of coping as necessary.
8. Facilitating learning
• teaching is started once the client is free of pain and excessive anxiety
• promote a positive attitude and active participation of the client and the family.

57. CARDIAC REHABILITATION:
Cardiac rehabilitation provides a venue
for continued education, re-enforcement
of lifestyle modification, and adherence
to a comprehensive prescription of
therapies for recovery from MI, which
includes exercise training
Goals of Rehabilitation program:
•Develop a program for progressive
physical activity
•Lives as full, vital and productive life
•Remain within the limits of the heart’s
ability to respond to increases in activity
and stress.

58. FOLLOW UP