Coronary Artery Disease

ACUTE BIOLOGIC CRISIS
IAN VAN V. SUMAGAYSAY, MAN, RN, LPT, EMR

West Visayas State University – College of Nursing
June 2017
Acute Biologic Crisis
• Condition that may result to patient

mortality if left unattended in a
brief period of time.
• Condition that warrants immediate

attention for the reversal of
disease process and prevention of
further morbidity and mortality.
Conditions that are considered to
be ABC’s:
• Cardiac Failure
• Acute Myocardial Infarction
• Acute Pulmonary Failure
• Acute Renal Failure
• Stroke
• Increased Intracranial Pressure
• Metabolic Emergencies – DKA/HHNK
• Massive Bleeding
Conditions that are considered to
be ABC’s:
• Extensive Surgeries
• Extensive Burns
• Poisoning
• Emerging Illnesses (MERS-CoV, SARS,
Avian Flu)
• Multiple Injuries
MANAGEMENT OF PATIENTS WITH
CORONARY VASCULAR
DISORDERS
Learning Objectives:
1. Describe the pathophysiology, clinical

manifestations, and treatment of coronary
atherosclerosis.
manifestations, and treatment of angina
pectoris.
3. Use the nursing process as a framework
for care of patients with angina pectoris.

manifestations, and treatment of
myocardial infarction.
5. Use the nursing process as a framework
for care of patients with myocardial
infarction (acute coronary syndrome).
6. Describe the nursing care of a patient who
has had an invasive interventional
procedure for treatment of coronary artery
disease.
7. Describe coronary artery revascularization

procedures.
8. Describe the nursing care of the patient
treated with cardiac surgery.
Walls of Arteries and Veins
• Tunica Externa/Adventitia
– Outermost layer
– CT w/elastin and collagen
– Strengthens, Anchors
• Tunica Media
– Middle layer
– Circular Smooth Muscle
– Vaso-constriction/dilation
• Tunica Intima
– Innermost layer
– Endothelium
– Minimize friction
• Lumen
Artery / Vein Differences
Arteries (aa.) Veins (vv.)

Direction Blood Away from Blood to Heart
of flow Heart
Pressure High Low
Walls THICKER: Tunica THINNER: Tunica

media thicker than externa thicker
tunica externa than tunica media
Lumen Smaller Larger
Valves No valves Valves

Coronary Artery Disease
• Coronary Artery Disease a.k.a. Coronary

Heart Disease
• Most prevalent type of cardiovascular
disease.
• It refers to a spectrum of illnesses that range
from the least life threatening to the most life
threatening Acute Coronary Syndrome
such as AMI / Heart attack.
• Refers to the variety of pathologic

conditions that causes narrowing or
obstruction of the coronary arteries
which causes decreased perfusion in
the myocardium
• Results from narrowing of the large and
medium sized coronary arteries due to
plaque formation
• Primarily caused by atherosclerosis
• A broad term that includes stable angina

pectoris and acute coronary syndromes.
• Affects the arteries that provide blood,
oxygen and nutrients to the myocardium.
• Partial Occlusion – Ischemia
• Complete Occlusion – Infarction
• The heart may pump harder to meet
demands which may cause Heart Failure
Stages of Development of Coronary Artery

Disease:
1. Myocardial Injury - Atherosclerosis
2. Myocardial Ischemia – Angina Pectoris
3. Myocardial Necrosis – Myocardial Infarction
CORONARY
ATHEROSCLEROSIS
Coronary Atherosclerosis
• An abnormal accumulation of lipid, or fatty

substances and fibrous tissue in the vessel
wall. (Plaque / Atheroma Formation)
• A repetitious inflammatory response to
artery wall injury and an alteration to its
biophysical and biochemical properties
• Atheromas / Plaques
– Consist of lipids, cells,
fibrin, cell debris
– Lipids usually
transported with
lipoproteins
– Deposited in the intima
of the arterial wall
– Initiated by smoking,
hypertension and other
lifestyle factors
Pathophysiology:
• Fatty streaked formation in the vascular
intima→ T-cells and monocytes ingest lipids
in the area of deposition→ Atheroma
formation→ narrowing of the arterial
lumen→ reduced blood flow→ myocardial
infarction
ATHEROSCLEROSIS
- narrowing of artery
- lipid or fat deposits (plaques)
- tunica intima
ARTERIOSCLEROSIS
- hardening of artery, thicken
- calcium and protein deposits
- tunica media
Predisposing Factors:
1. Sex – male
2. Race – black
3. Smoking
4. Obesity
5. Hyperlipidemia
6. Sedentary lifestyle
7. Diabetes Mellitus
8. Hypothyroidism
9. Diet – increased saturated fats
10. Type A personality
Risk factors:
- Age: 30-50 y.o.; Male (55), Female (65)
- Gender: Males and Post-Menopausal
Females (HRT)
- Race: Non-whites has higher mortality rates
- Family History of CAD
- Hypertension, DM
- Smoking, Obesity
- Sedentary Lifestyle
- Hyperlipidemia, Elevated Uric Acid Levels
Signs and Symptoms:

1. Chest pain
2. Dyspnea
3. Tachycardia
4. Palpitations
5. Diaphoresis
Clinical Manifestations:
• Signs and symptoms would vary depending
on the location, degree of narrowing and
obstruction of the arterial lumen.
• Deprivation of heart muscle cells will result
in Myocardial Ischemia.
• Chest pain brought about by myocardial
ischemia is known as Angina Pectoris.
Clinical Manifestations:
• Sudden decrease of the blood to the heart
may cause Sudden Cardiac Death
• Typical S/Sx: Dyspnea, Nausea, Weakness,
SOB
Prevention:
• Correction of Cholesterol Abnormalities
• Cessation of Cigarette Smoking
• Management of Hypertension
• Control of Diabetes Mellitus
Dietary Measures:
• Referral to Registered Dietician
• Intake of 20 to 30mgs of soluble dietary fiber
such as fresh fruits, cereal grains, vegetables
and legumes
Physical Activity:
• Regular moderate physical activity at least 30
mins., 3-4 times per week
• Start and end activity with a 5 min. stretching
exercise
• Stop when adverse signs or symptoms appear
Management of Hypertension:
• Prolonged hypertension will result to the
stiffness of the vessel walls, leading to injury
and inflammation of the intima.
• Increased workload of the heart can also result
in the enlargement and thickening of the heart
which may lead to heart failure.
Treatment Regimen:
• Decrease total cholesterol, HDL, LDL
and triglycerides
• Manage hypertension
• Control diabetes
• Quit smoking
• Oral anticoagulant
• Exercise
Medications:
– 3-Hydroxy-3-Methylglutaryl coenzyme A (HMG-
CoA) e.g. atorvastatin (Lipitor); simvastatin (Zocor)
– Nicotic acids - niacin (Niacor, Niaspan)
– Fibric Acids – fenofibrate (Tricor)
– Bile Acid Sequestrants – cholestyramine
(LoCholest)
Surgical intervention:
– Percutaneous transluminal coronary angioplasty
(PTCA)
– Cardiac catheterization
– Laser beam technology
– Coronary artery bypass grafting
• Percutaneous transluminal coronary

angioplasty (PTCA) is a minimally invasive
procedure to open up blocked coronary
arteries, allowing blood to circulate
unobstructed to the heart muscle.
Objectives of PTCA:
1. Revascularize myocardium
2. To prevent angina
3. Increase survival rate
- Done to single occluded vessels
- If there is 2 or more occluded blood vessels
CABG is done
Laser Therapy:
3 Complications of CABG:
1. Pneumonia – encourage to perform deep
breathing, coughing exercise and use of
incentive spirometer
2. Shock
3. Thrombophlebitis
ANGINA PECTORIS
Angina Pectoris
• A clinical syndrome usually
characterized by episodes of chest pain
or pressure on the anterior chest
• Caused by insufficient coronary blood
flow resulting in a decreased oxygen
supply where there is increased
myocardial demand for oxygen supply in
response to physical exertion or
emotional stress
• “the need for oxygen exceeds the
supply”
Types of Angina Pectoris:
• Stable angina: predictable and consistent

pain that occurs on exertion and is relieved
by rest
• Unstable angina (also called pre-infarction
angina or crescendo angina): symptoms
occur more frequently and last longer than
stable angina. The threshold for pain is
lower, and pain may occur at rest.
Types of Angina Pectoris:
• Intractable or refractory angina: severe

incapacitating chest pain
• Variant angina (also called Prinzmetal’s
angina): pain at rest with reversible ST-
segment elevation; thought to be caused by
coronary artery vasospasm
• Silent ischemia: objective evidence of
ischemia (such as electrocardiographic
changes with a stress test), but patient
reports no symptoms
Angina Pectoris
Pathophysiology:
• Coronary blood flow becomes
inadequate to meet myocardial oxygen
demand → myocardial ischemia →
myocardial cells alter from aerobic to
anaerobic metabolism producing
chemical end products → a progressive
impairment of metabolic, mechanical and
electrical functions → angina pectoris
Angina Pectoris
Risk factors:
• Atherosclerosis, CAD
• Men are high risk, Increasing age
• Hypertension, Hypercholesterolemia
• DM
• Thromboangitis obliterans
• Severe anemia
• Aortic insufficiency
• Smoking, Sedentary lifestyle
• Family history of premature ischemic
heart disease
Angina Pectoris
Predisposing Factors:
1. Sex – male
2. Race – black
3. Smoking
4. Obesity
5. Hyperlipidemia
8. Hypothyroidism
Angina Pectoris
Potential Complications:
• Acute pulmonary edema
• Congestive heart failure
• Cardiogenic shock
• Dysrhythmias and cardiac arrest
• MI
• Myocardial rupture
• Pericardial effusion and cardiac
tamponade
Angina Pectoris
Precipitating Factors: 4E’s
• Exertion - physical exertion
• Eating - consumption of a heavy meal
• Extreme Temperature - very cold or very
hot
• Excitement - strong emotions and sexual
activity
Angina Pectoris
Assessment of Angina Pectoris:
• P – Position/ Location and Provocation
• Q – Quality/ Quantity
• R – Radiation/ Relief
• S – Severity/ Symptoms
• T – Timing
*Attacks usually occur between midnight

and 8 am.
Angina Pectoris
Canadian Cardiovascular Society

Classification of Angina:
Class Activity Limits to Activity
I Prolonged Exertion None
II Walking <2 Blocks Slight
III Walking >2 Blocks Marked
IV Minimal or Rest Severe

Angina Pectoris
Assessment:
• Chest pain
• Mild indigestion
• Choking or heavy sensation in the upper
chest that ranges from discomfort to
agonizing pain
• Pain is poorly localized, Unrelieved by
rest and NTG
• Dyspnea, diaphoresis, nausea and
vomiting, cold clammy skin, anxiety,
dizziness and syncope
Angina Pectoris
Signs and Symptoms:

1. Levine’s Sign – initial sign that shows the hand
clutching the chest
2. Chest pain characterized by sharp stabbing pain
located at sub sterna usually radiates from back,
shoulder, arms, axilla and jaw muscles, usually
relieved by rest or taking nitroglycerine
3. Dyspnea
4. Tachycardia
5. Palpitations
6. Diaphoresis
Angina Pectoris
Diagnostic Procedure:
1. History taking and physical exam
2. ECG tracing reveals ST segment
depression
3. Stress test – treadmill test, reveal
abnormal ECG
4. Serum cholesterol and uric acid is
increased
Angina Pectoris
Nursing intervention:
• Monitor VS, ABG, ECG, O2
• Provide health teaching
• Minimize precipitating events
• Provide dependent nursing intervention
Angina Pectoris
Treatment:
• Nitroglycerin tablets: SL; up to 3 tablets
every 5 mins within 15 mins
• Reduce stress, anxiety; Avoid exertion,
extreme temperatures (4E’s)
• Avoid smoking, Maintain a low
cholesterol, low saturated fat diet
• Exercise
• Maintain bed rest, Avoid Straining
• Place on semi or high fowler’s position
• O2 at 2LPM
Angina Pectoris
Nursing Management:
1. Enforce complete bed rest
2. Administer medications as ordered
a. Nitroglycerine (NTG) – when given in small
doses will act as venodilator, but in large doses
will act as vasodilator
- Give first dose of NTG (sublingual) 3 – 5
minutes
- Give second dose of NTG if pain persist after
giving first dose with interval of 3 - 5 minutes
- Give third and last dose of NTG if pain still
persists at 3 – 5 minutes interval
Angina Pectoris
Nursing Management when giving NTG

- Keep the drug in a dry place, avoid
moisture and exposure to sunlight as it
may inactivate the drug
- Monitor side effects
• Orthostatic hypotension
• Transient headache and dizziness
- Instruct the client to rise slowly from
sitting position
- Assist or supervise in ambulation
Angina Pectoris
Nursing Management when giving NTG

- Keep the drug in a dry place, avoid
moisture and exposure to sunlight as it
may inactivate the drug
- Monitor side effects
• Orthostatic hypotension
• Transient headache and dizziness
- Instruct the client to rise slowly from
sitting position
- Assist or supervise in ambulation
Angina Pectoris
- When giving nitrol or transdermal patch

o Avoid placing near hairy areas as it may
decrease drug absorption
o Avoid rotating transdermal patches as it
may decrease drug absorption
o Avoid placing near microwave ovens or
during defibrillation as it may lead to burns
(most important thing to remember)
Angina Pectoris
b. Beta-blockers
- (lol)
- Propanolol - side effects PNS – broncho
constriction, vasodilation
- Not given to COPD cases because it causes
Bronchospasm
c. ACE Inhibitors
- (pril)
- Enalapril, captopril
d. Calcium Antagonist
- calcibloc
- Nifedipine, diltiazem
Angina Pectoris
3. Administer oxygen inhalation

4. Place client on semi fowler‘s position
5. Monitor strictly vital signs, intake and output
and ECG tracing
6. Provide decrease saturated fats sodium and
caffeine
Angina Pectoris
7. Provide client health teachings and discharge

planning
a. Avoidance of 4 E‘s
b. Prevent complication (myocardial infarction)
c. Instruct client to take medication before
indulging into physical exertion to achieve the
maximum therapeutic effect of drug
d. The importance of follow up care
Angina Pectoris
Pharmacologic Treatment:
• Nitrates: dilate the coronary arteries, reduces
O2 requirements of the heart (Isosorbide
Dinitrate, NTG)
• Anticoagulants : prevent thrombus formation
(Aspirin, Clopidogrel, Heparin)
• Beta-blockers: reduces BP and HR
(Propranolol, Metoprolol, Acebutolol)
• Calcium channel blockers: dilate coronary
artery and reduce vasospasm, lowers HR
(Diltiazem, Nifedipine, Verapamil, Amlodipine)
• Laxatives: lessens constipation and straining
Angina Pectoris
Nursing Diagnoses:
• Ineffective myocardial tissue perfusion secondary
to CAD, as evidenced by chest pain or equivalent
symptoms
• Anxiety related to fear of death
• Deficient knowledge about the underlying disease
and methods for avoiding complications
• Noncompliance, ineffective management of
therapeutic regimen related to failure to accept
necessary lifestyle change
Angina Pectoris
Expected Patient Outcomes:
1. Reports that pain is relieved promptly
a. Recognizes symptoms
b. Takes immediate action
c. Seeks medical assistance if pain
persists o
2. Reports decreased anxiety
a. Expresses acceptance of diagnosis
b. Expresses control over choices within
medical regimen
c. Does not exhibit signs and symptoms that
indicate a high level of anxiety changes in quality
Angina Pectoris
3. Understands ways to avoid complications and

demonstrates freedom from complications
a. Describes the process of angina
b. Explains reasons for measures to prevent
complications
c. Exhibits normal ECG and cardiac enzyme levels
d. Experiences no signs and symptoms of acute MI
4. Adheres to self-care program
a. Takes medications as prescribed
b. Keeps health care appointments
c. Implements plan for reducing risk factors
ACUTE MYOCARDIAL INFARCTION
Acute Myocardial Infarction
• Death of myocardial tissue in regions of
the heart with abrupt interruption of
coronary blood supply brought about by
inadequate oxygenation and is often
caused by sudden, complete blockage
• Characterized by localized formation of

necrosis with subsequent healing by scar
formation and fibrosis
• Acute Myocardial Infarction a.k.a. Heart

Attack, Coronary occlusion
• Caused by undiagnosed and untreated
angina
• Occurs when the myocardial tissue is
abruptly and severely deprived of oxygen
• Ischemia develops if blood flow is acutely
reduced by 80 – 90 %
Types
1. Transmural Myocardial Infarction – most
dangerous type characterized by occlusion of
both right and left coronary artery
2. Subendocardial Myocardial Infarction –
characterized by occlusion of either right or
left coronary artery
The Most Critical Period Following

Diagnosis of Myocardial Infarction:
- 6 – 8 hours because majority of death
occurs due to arrhythmia leading to PVC’s
Pathophysiology: AMI
Interrupted coronary blood flow →

myocardial ischemia → anaerobic
myocardial metabolism for several hours →
pain → ischemia and triggering of ANS
responses that exacerbate the imbalance
between myocardial oxygen supply and
demand → persistent ischemia →
myocardial death → depressed cardiac
function → further triggering of ANS
response → imbalance of myocardial oxygen
demand and supply
1. Sex – male
2. Race – black
3. Smoking
4. Obesity
5. Hyperlipidemia
8. Hypothyroidism
Modifiable Risk Factors of AMI:
• Stress • Hyperlipidemia
• Diet • Diabetes Mellitus
• Exercise • Obesity
• Cigarette Smoking • Personality Type or
• Alcohol Behavioral Factors
• Hypertension • Contraceptive Pills
Signs and Symptoms
1. Chest pain
- Excruciating visceral, viselike pain located at
substernal and rarely in precordial
- Usually radiates from back, shoulder, arms, axilla, jaw
and abdominal muscles (abdominal ischemia) and
hands
- Not usually relieved by rest or by nitroglycerine
2. Dyspnea
3. Increase in blood pressure (initial sign)
4. Hyperthermia
5. Ashen skin (pale), cool, clammy, diaphoretic
6. Mild restlessness and apprehension,

anxiety
7. Occasional findings
a. Pericardial friction rub
b. Split S1 and S2
c. Rales/Crackles upon auscultation
d. S4 or atrial gallop
Assessment:
- Chest pain: severe, persistent, crushing,
substernal discomfort
- Dyspnea, rales or crackles
- Increased BP then gradual drop in BP
- Diaphoresis, cold clammy skin, N/V, elevated
temperature, anxiety
Assessment and Diagnostics:

• Patient History of illnesses
• Family Health History
• Echocardiogram
• ECG – done within 10 minutes upon
presentation of symptoms
– Usual changes are: T-wave inversion, ST
segment elevation and an abnormal Q wave
1. Cardiac Enzymes
a. CPK – MB
- Creatinine phosphokinase is increased
- Heart only, 12 – 24 hours
b. LDH – Lactic dehydroginase is increased
c. SGPT – Serum glutamic pyruvate
transaminase is increased
d. SGOT – Serum glutamic oxal-acetic
transaminase is increased
Serum Test Earliest Test Running Peak (HR) Return to

Increase Time (Mins.) Normal
(HR)
Total CK 3-6 30-60 24-36 3 days

CK-MB:
Isoenzyme 4-8 30-60 12-24 3-4 days
Mass Assay 2-3 30-60 10-18 3-4 days
Myoglobulin 1-3 30-60 4-12 12 hours

Troponin T or I 3-4 30-60 4-24 1-3 weeks
2. Troponin Test – is increased (protein in

myocardial)
3. ECG tracing reveals
a. ST segment elevation
b. T wave inversion
c. Widening of QRS complexes indicates that
there is arrhythmia in MI
4. Serum Cholesterol and uric acid are both
increased
5. CBC – increased WBC
Diagnostic Tests:
-ECG: Elevated ST segments, T wave inversion, Q
wave presence
-Myocardial Enzymes: Increased Troponin T and I,
CK-MB, LDH and myoglobin
-Blood tests: Elevated WBC, Elevated erythrocyte
sedimentation rate (ESR), elevated serum
cholesterol, alanine aminotransferase (AST)
-Exercise stress test
Nursing Management
Goal: Decrease myocardial oxygen demand
1. Decrease myocardial workload (rest heart)
- Administer narcotic analgesic/morphine
sulfate
- Side Effects: respiratory depression
- Antidote: Narcan/Naloxone
- Side Effects of Naloxone Toxicity is tremors
2. Administer oxygen low inflow to prevent

respiratory arrest at 2 – 3 L/min
3. Enforce CBR without bathroom privileges
a. Using bedside commode
4. Instruct client to avoid forms of valsalva
maneuver
5. Place client on semi fowler‘s position
6. Monitor strictly vital signs, intake and output
and ECG tracing
7. Provide a general liquid to soft diet that is

low in saturated fats, sodium and caffeine
8. Encourage client to take 20 – 30 cc/week of
wine, whisky and brandy to induce
vasodilation
9. Administer medication as ordered :
a. Vasodilators
- Nitroglycerine
- ISD (Isosorbide Dinitrate, Isordil) sublingual
b. Anti Arrythmic Agents

- Lidocaine (Xylocane
- Side Effects: confusion and dizziness
- Brutylium
c. Beta-blockers
- (-lol)
d. ACE Inhibitors
- (-pril)
e. Calcium Antagonist
- amlodipine, verapamil, diltiazem
f. Thrombolytics/ Fibrinolytic Agents

- Streptokinase
- Side Effects: allergic reaction, pruritus
- Urokinase
- TIPAF (tissue plasminogen activating factor)
- Side Effects: chest pain
- Monitor for bleeding time
g. Anti Coagulant
- Heparin (check for partial thrombin time)
- Antidote: protamine sulfate
- Coumadin/ Warfarin Sodium (check for
prothrombin time)
- Antidote: Vitamin K
h. Anti Platelet
- PASA (Aspirin)
- Anti thrombotic effect
- Side Effects of Aspirin
• Tinnitus
• Heartburn
• Indigestion/Dyspepsia
- Contraindication
• Dengue
• Peptic Ulcer Disease
• Unknown cause of headache
10. Provide client health teaching and discharge
planning concerning
a. Avoidance of modifiable risk factors
- Arrhythmia (caused by premature ventricular
contraction)
b. Cardiogenic shock
- late sign is oliguria
c. Left Congestive Heart Failure
d. Thrombophlebitis
- homan’s sign
e. Stroke/CVA
f. Post MI Syndrome/Dressler’s Syndrome

- Client is resistant to pharmacological agents;
administer 150,000 – 450,000 units of
streptokinase as ordered
g. Resumption of ADL particularly sexual

intercourse is 4 – 6 weeks post cardiac rehab,
post CABG and instruct to
- make sex as an appetizer rather than dessert
- instruct client to assume a non weight bearing
position
• Client can resume sexual intercourse if can
climb staircase
- dietary modification
h. Strict compliance to mediation and importance
of follow up care
Nursing Intervention:
1. Monitor VS: ECG, blood test, physical
assessment, MIO
2. Minimize anxiety
3. Minimize metabolic demands: soft diet, low salt,
low cholesterol, low fat
4. O2 at 2LPM
5. Provide health teaching: MI, healing process,
treatment regimen
Pharmacology:
- Nitrates, thrombolytics, aspirin, ACE inhibitors,
anticoagulants
- Stool softeners, hypolipidemics
- Analgesics: morphine sulfate (drug of choice)
- MONA: Morphine, Oxygen, Nitroglycerin,
Aspirin
Surgical:
-Percutaneous Transluminal Coronary Angioplasty
-Coronary Artery Bypass Graft (CABG)
Health teaching:
-Effects of MI, healing and treatment
-Medication, risk factors, diet: low sodium, low
cholesterol, no caffeine
-Resumption of sexual activity: 4-6 weeks or could
tolerate an exercise of 3-4mph or could climb a
flight of stairs without difficulty
MI management: MONA
Morphine
O2
Nitroglycerine
Aspirin
Cardiovascular Assessment
Chest Pain • In MI, it is more

• Most common intense, unrelated to
• Due to Ischemia or activities and can’t
MI be relieved by NTG
• Precipitated by
stress or can be • If it occurs during
relieved breathing, suspect
by Nitroglycerin respiratory problems
(NTG)
Rough diagram of pain zones in myocardial infarction
(dark red = most typical area, light red = other possible
areas, view of the chest).
Dyspnea
• Subjective feeling (inability to get
enough air).
• Dyspnea on exertion is due to increased
O2 myocardial demand.
• Orthopnea is related to blood pooling
in the pulmonary bed; suspect
Pulmonary Edema
• Any sudden or acute dyspnea may be a
sign of Pulmonary Embolism
Chest tightness
Cough / Sputum
• Mucoidal and/or Foamy
sputum can be a sign of CHF
• Pink-tinged frothy appearance may signal
Pulmonary Edema.
• Whitish, viral infection
• Change in color other than the above
mentioned may signify bacterial infection
Cyanosis
• Bluish discoloration of the skin and
mucous membrane
• Sat O2 is below 90%
Fatigue
• May be due to Anemias or related to
decreased Cardiac Output
Palpitations
• Awareness of rapid or irregular heart beat
• Autonomic Nervous System and Adrenal
Glands response (stress)
Syncope
• Transient loss of consciousness
• Due to decreased cerebral
tissue perfusion
Edema due to:

• Increased Hydrostatic Pressure (HP)
• Decreased Colloidal Oncotic Pressure
(COP)
• Obstructed Lymphatic or Vascular System
• Related to Inflammatory reaction
Types of Edema
• Bilateral edema
=CHF or Renal Failure
• Unilateral edema
=Vascular or Lymphatic
obstruction
• Non-pitting edema
=Inflammatory
• Pitting edema =HP and
COP derangement
Skin
• Color, temperature, hair growth, nails,
capillary refill
• spooning of fingers /clubbing of fingers
• Heart rate – 60-100

• Rhythm – regular or irregular
• Bruits and Thrills – murmur like; vascular
in origin- palpate a thrill, auscultate a bruit
• Blood Pressure
• Jugular venous pressure
Cardiac rate and rhythm

• Tachycardia=↑ 100 beats/minute
• Bradycardia=↓ 60 beats/minute
• Arrhythmias=irregular rate and rhythm
Laboratory & Diagnostic Test
Complete Blood Count-

• RBC suggest tissue oxygenation.
Elevated WBC may indicate infectious
heart disease and MI.
Erythrocyte Sedimentation Rate (ESR)
• It is elevated in infectious heart disorder or
MI. Normal range: Males: 15-
20mm/hr Females: 20-30 mm/hr
Blood Coagulation Test:

1. Prothrombin Time (PT, Pro Time)-
• It measures time required for clotting to
occur. Used to evaluate effectiveness
of COUMADIN
• Normal range 11-16 secs.
Blood Coagulation Test:

2. Partial Thromboplastin Time (PTT)-
• Best screening test for disorders of
coagulation. Used to determine the
effectiveness of HEPARIN
• Normal Range: 60-70 secs.
Blood Urea Nitrogen (BUN)- Indicator

of renal function Normal Range: 10-
20mg/dl (5-25mg/dl is also accepted).
Blood Lipids:
• Serum Cholesterol:
• 150-200mg/dl
• Serum Triglycerides
• 140-200mg/dl.
Serum Enzymes Studies

Aspatate Aminotransferase(AST)-
• Elevated levelindicates tissue necrosis.
Normal Range: 7-40mu/ml
CK-MB-
• Elevated 4-6hrs from the onset
of infarction; peaks 24-36 hrs. returns to
normal 4-7days. Normal Range: males:
50-325mu/ml; Females: 50-250mu/ml

• Lactic Dehydogenase (LDL)- Onset:
12hrs;Peak: 48hrs; returns to normal: 10-
14 days4. Hydroxybuterate
• Dehydroxynase (HBD)- it is valuable in
detecting silent MI because it is elevated
for a long period of time. Onset: 10-12hrs;
Peaks: 48-72hrs; Returns to Normal 12-13
days

• Troponin- Most specific lab test to detect
MI. Troponin has 3 compartments: I,C, &T
. Troponin I persist for 4-7 days.
Serum Electrolytes/ Blood Chemistry:

1. Sodium (Na)
2. Potassium (K)
3. Calcium (Ca)
4. Magnessium (Mg)
5. Glucose
6. Glycosylated Hemoglobin (Hemoglobin
A1c)
• ECG/ EKG- ST segment elevation and T

wave inversion
• Radiologic Findings (Chest X-Ray)

• Normal
• Cardiomegaly
• Signs of CHF
Hemodynamic Monitoring
• Swan-Ganz Catheterization
• Right side of the heart
• Pulmonary artery pressure
• Pulmonary artery occlusive pressure
• Right atrial pressure
• Cardiac output
Swan-Ganz Catheterization
Coronary Angiogram
• allows to visualize narrowings or
obstructions
• therapeutic measures can follow
immediately.
Goal of Treatment
• Pain relief
• Reduction of myocardial oxygen
consumption
• Prevention and treatment of complications
Intervention
Admit to the CCU/ ICU

• Activity
– Day 1: bed rest, if stable
– Day 2-3: bed rest, but patient may be allowed
to sit on a chair for 15-20 minutes
• Early mobilization is recommended for
uncomplicated AMI
Intervention
Monitoring Vital Signs:

• First 6 hours- q30-60 minutes
• Next 24 hours- q 2 hours
• Thereafter q 4 hours
Diet:
• NPO: 1st 24 hours
• If stable low salt, low cholesterol diet
Intervention
IV Fluids:
• D5W to KVO
• If unable to take food/fluid per orem
• 1000ml/8 hours
• K supplement
Intervention
Pain Medication:
• Morphine SO4
• (2-5mg/IV dose)
• Potent analgesic
• Peripheral venous vasodilation
• Pulmonary venous distention
• Inferior wall MI: may increase vagal
discharge
Intervention
Tranquilizers:
• To decrease anxiety
• Diazepam (5-10 mg per IV/orem)
Laxatives:
• To prevent straining during defecation
• Lactulose (HS)
Intervention
Drugs to Limit Infarct Size:

• Beta Blockers
– Hyperdynamic states, HPN w/o evidence of
heart failure
– Reduce myocardial oxygen consumption by
decreasing: BP. Heart Rate, Myocardial
Contractility and calcium output.
– Ex: Propranolol, Metoprolol, Atenolol
Intervention
Nursing Consideration:
• Assess Pulse Rate before administration;
with hold if bradycardia is present.
• Administer with food, may cause GI upset.
• Do not administer with asthma it causes
Bronchoconstriction.
• Do not give to patient with DM, it causes
hypoglycemia.
• Antidote for Beta Blocker poisoning is
Glucagon
Intervention
Nitrates:
• Act by augmenting perfusion at the border
of ischemic zone.
• Generalized vasodilation
• Reducing myocardial O2 demand
• Lowering preload
• Lowering afterload
• Ex: IV Nitroglycerine,
Sublingual Niotroglycerine,Oral/Transdermal
Nitroglycerine
Intervention
Nursing Considerations:
• Only a maximum of 3 doses at 5 min. interval.
• Offer sips of water before giving it
sublingually.
• Store the medication in a cool, dry place; use
dark /amber container.
• If side effects is noticed do not discontinue
the drug this is usual in the first few doses
of medication.
• Rotate skin sites for nitro patch.
Intervention
ACE inhibitors:
• reduce mortality rates after MI.
• Administer ACE inhibitors as soon as possible
• ACE inhibitors have the greatest benefit in
patients with ventricular dysfunction.
• Continue ACE inhibitors indefinitely after MI.
• Angiotensin-receptor blockers may be used as
an alternative adverse effects, such as a
persistent cough.
Intervention
Aspirin and/or antiplatelet therapy:

• Continue aspirin indefinitely
• Clopidogrel may be used as an alternative
only if resistance or allergy to aspirin.
Intervention
Nursing Considerations:
• Assess for signs and symptoms of Bleeding.
• Avoid straining at stool to avoid
rectal bleeding.
• It should be given with food.
• Observe for toxicity- Tinnitus (ringing of ears).
• May cause Bronchoconstriction- Observe
for wheezing.
Intervention
Heparin:
• Assess for S/Sx of Bleeding.
• Keep Protamine Sulfate available.
• If used SQ. do not aspirate to prevent
hematoma formation.
• Monitor for PTT or APTT
• Used for a maximum of 2 weeks.
Intervention
Coumadin (Warfarin Sodium):

• Assess for bleeding
• Keep Vitamin K available.
• Monitor for Prothrombin Time
• Do not give together with aspirin to prevent
bleeding.
• Minimize green leafy vegetables in the diet.
Intervention
Thrombolytic therapy:
• Effectiveness highest in the first 2 hours
• After 12 hours, the risk associated with
thrombolytic therapy outweighs any benefit
Intervention
Contraindicated:
• unstable angina and NSTEMI
• and for the treatment of individuals with
evidence of cardiogenic shock
• streptokinase, urokinase, and alteplase
(recombinant tissue plasminogen activator ,
rtPA),reteplase,tenecteplase
Drugs
Intervention
Surgical Care:
• Percutaneous Transluminal Coronary
Angioplasty -treatment of choice
• PCI provides greater coronary patency
• lower risk of bleeding and instant knowledge
about the extent of the underlying disease.
• A specially designed balloon – tipped
catheter is inserted under fluoroscopic
guidance and advance to the site of the
obstruction.
Intervention
Intravascular Stenting
• Biologic Stent is produced through
coagulation of collagen, ellastin and other
tissues in the vessel wall by
laser, photocoagulation or radio frequency.
• It is done to prevent restenosis
after Percutaneous Transluminal Coronary
Angioplasty.
Intervention
Surgical Care
• Percutaneous Transluminal Coronary
Angioplasty
Intervention
Emergent or Urgent
Coronary Artery Graft Bypass Surgery
• (CABG) is indicated if angioplasty fails
• Severe narrowing of 1 or more coronary
artery.
• Commonly used: Saphenous vein and
internal mammary artery.
Intervention
Coronary Artery Graft Bypass Surgery

Intervention
Complications
• Inflammation
• Mechanical
• Electrical abnormalities
Cardiac Rehabilitation
• A process which a person restored to

health and maintains optimal
physiologic, psychosocial and
recreational functions.
• Begins with the moment a client is
admitted to the hospital for emergency
care, it continues for months and even
years after the client is discharged from
the health care facility.
Goals of Rehabilitation
• To live as full, vital and productive life

as possible.
• Remain within the limits of the hearth’s ability
to respond to activity and stress.
Activities:
• Exercise may gradually implemented from
the hospital onwards.
• Exercise session is terminated if anyone of
the following occurs: cyanosis, cold sweats,
faintness, extreme fatigue, severe dyspnea,
pallor, chest pain, PR more than 100/ min.,
dysrhythmias greater than 160/95mmHg.
Teaching and Counseling
• Self management education guide.
• Control hypertension with continued medical
supervision.
• Diet
• Weight reduction program
• Progressive exercise
• Stress management techniques
• Resumption of sexual activity after 4-6 weeks
from discharge, if appropriate.
Teaching guide on resumption of sexual

activities:
• Assume less fatiguing position.
• The non- MI partner take the active role
• Take nitroglycerine before sexual activity
• If dyspnea, chest pain or palpitations occur,
moderation should be observed; if
symptom persist stop sexual activity
• Develop other means of sexual expression.
YOU ARE GOING TO EXPERIENCE A
HEART ATTACK IN..
3
2
1
QUIZ NO. 1
CARE OF CLIENTS WITH ACUTE

CORONARY SYNDROMES
Questions???
Thank you and Good Day!

Coronary Artery Disease

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Coronary Artery Disease

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ACUTE BIOLOGIC CRISIS

IAN VAN V. SUMAGAYSAY, MAN, RN, LPT, EMR

• Condition that may result to patient

• Condition that warrants immediate

1. Describe the pathophysiology, clinical

4. Describe the pathophysiology, clinical

7. Describe coronary artery revascularization

Arteries (aa.) Veins (vv.)

Walls THICKER: Tunica THINNER: Tunica

Valves No valves Valves

• Coronary Artery Disease a.k.a. Coronary

• Refers to the variety of pathologic

• A broad term that includes stable angina

Stages of Development of Coronary Artery

• An abnormal accumulation of lipid, or fatty

Signs and Symptoms:

• Percutaneous transluminal coronary

• Stable angina: predictable and consistent

• Intractable or refractory angina: severe

*Attacks usually occur between midnight

Canadian Cardiovascular Society

I Prolonged Exertion None

II Walking <2 Blocks Slight

III Walking >2 Blocks Marked

IV Minimal or Rest Severe

Signs and Symptoms:

Nursing Management when giving NTG

Nursing Management when giving NTG

- When giving nitrol or transdermal patch

3. Administer oxygen inhalation

7. Provide client health teachings and discharge

3. Understands ways to avoid complications and

• Characterized by localized formation of

• Acute Myocardial Infarction a.k.a. Heart

The Most Critical Period Following

Interrupted coronary blood flow →

6. Mild restlessness and apprehension,

Assessment and Diagnostics:

Serum Test Earliest Test Running Peak (HR) Return to

Total CK 3-6 30-60 24-36 3 days

Myoglobulin 1-3 30-60 4-12 12 hours

2. Troponin Test – is increased (protein in

2. Administer oxygen low inflow to prevent

7. Provide a general liquid to soft diet that is

b. Anti Arrythmic Agents

f. Thrombolytics/ Fibrinolytic Agents

f. Post MI Syndrome/Dressler’s Syndrome

g. Resumption of ADL particularly sexual

Chest Pain • In MI, it is more

Edema due to:

• Heart rate – 60-100

Cardiac rate and rhythm

Complete Blood Count-

Blood Coagulation Test:

Blood Coagulation Test:

Blood Urea Nitrogen (BUN)- Indicator

Serum Enzymes Studies

Serum Enzymes Studies

Serum Enzymes Studies

Serum Electrolytes/ Blood Chemistry:

• ECG/ EKG- ST segment elevation and T

• Radiologic Findings (Chest X-Ray)

Admit to the CCU/ ICU

Monitoring Vital Signs: