ANGINA PECTORIS/

MYOCARDIAL
ISCHEMIA
□Insufficient blood
flow resulting to
inadequate oxygen
supply to the
myocardium causing
transient chest pain
due to obstruction or
spasm of coronary
arteries
 CAUSES ATHEROSCLEROSIS
HYPERTENSION DIABETES MELITUES
THROMBOANGITIS OBLITERANS
POLYCYTHEMIA VERA
AORTIC REGURGITATION

REDUCED CORONARY TISSUE

DIMINISHED MYOC ARDIAL OXYGENATION

INCREASED LATIC ACID PRODUCTION ( LATIC ACIDOSIS )

CHEST PAIN
 Types of Angina Pectoris
Stable Angina
□ the most common form of angina
□ characterized by burning, heavy, or squeezing
feeling in the chest.
 Types of Angina Pectoris
Unstable angina
□ chest pains occur with increased frequency
□ requires hospital admission and more aggressive
therapy
 Types of Angina Pectoris
STABLE ANGINA UNSTABLE ANGINA
□ Chest pain last for less than □ Chest pain is last more than 15
15 minutes minutes but not more than 30
minutes
□ Recurrence is less frequent □ Recurrence is more frequent
□ Relieved by Rest or □ not relieve by rest or
nitroglycerin nitroglycerin.
 Types of Angina Pectoris
Prinzmetal’s or Vasospastic Angina
□Is uncommon pattern of episodic angina that occurs at
rest due to coronary artery spasm.
□Responds promptly to coronary vasodilators and
calcium-channel blockers.
 Intractable Angina
□ Also called Refractory Angina unresponsive to
intervention.
□ Respond poorly invasive procedures such as
angioplasty or by pass surgeries.
 VARIANT ANGINA
□Chest pain is longer duration
□Occur at rest
□Attack occurs in early hours of the day
□May result from Coronary artery spasms
Nocturnal Angina
□ Occurs only at night and possibly associated with REM
sleep
Angina Decubitus
□ Paroxysmal chest pain that occurs in sitting or lying
down
Post infarction angina
□ Occurs after MI, when residual ischemia may cause
episodes of angina.
 Precipitating factors of Angina
4 E’s
□ Exertion
□ Emotion
□ Eating heavy meal
□ Environment
 Clinical Manifestations
Chest pain
□ Transient (temporary), paroxysmal substernal or pre cordial pain,
squeezing, burning, pressing, choking aching or bursting left
sternal chest pain
□ Heaviness or chest tightness
□ The patient often says, “It feels like gas or heartburn or indigestion”
□ Radiates down one or both arms, left shoulder jaw, neck and back
□ Precipitated by physical exertion
□ Relieve by rest and Nitroglycerine
 Clinical Manifestations
□Pallor
□Diaphoresis
□Dyspnea
□Faintness
□Palpitation
□Dizziness
 ANGINA CHEST PAIN
□Sub-sternal
□Anterior chest pain
□Vague ( Radiates)
□Exertion
□Relieved by rest and Nitroglycerine
□Short duration (less than 15 minutes)
 Assessment of Chest Pain
□Precipitating factors of Angina- 4 E’s
□Provocative
□Quality
□Region
□Severity
□Timing and Treatment
 SUBSEQUENT ASSESSMENT
□ Obtain 12 lead ECG
□ Assess patient knowledge on the disease
□ Medical history- previous attacks and Drug
therapy
 Nursing Diagnosis
□Pain related to decreased oxygen supply and
demand
□Decreased cardiac output related to reduced
preload, afterload and contractility
□Anxiety related to chest pain
 NURSING INTERVENTIONS
To Relieve Chest pain
□Assess the level of chest pain and its duration
□Place in comfortable position
□VS q 5-10 minutes until anginal pain subsides
□Administer oxygen and Nitroglycerine as ordered
□Monitor relief of pain
 NURSING INTERVENTIONS
To maintain Tissue Perfusion
□ Avoid over fatigue
□ Stop activity immediately
□ Monitor BP and HR in response to drug therapy
□ Monitor ECG- ST segment depression and Elevation
 To Decrease Anxiety
□ Minimize emotional outburst, worry and tension
□ Verbalize fears and concerns
□ Maintain an optimistic outlook
□ Explain the reasons for hospitalization, diagnostic test,
and therapies administered
□ Teach relaxation techniques such as yoga, DBE
□ Administer sedative and tranquilizer.
ACTIVITY
□Encourage within patient’s limitation
DIET
□ DASH diet-rich in vegetables, fruits and whole
grains, fat-free or low-fat dairy products, fish, poultry,
beans and nuts.
□ Low sodium, low fat and cholesterol, High Fibers
□ Avoid saturated fat (animal fats)
□ White meat ( chicken without skin, turkey, fish are low in
cholesterol)
□ Read labels
 NITROGLYCERINE
□ Promotes venous and arterial relaxation of coronary vessel and
prevention of coronary spasm
□ causes coronary vasodilation and increases blood flow to the
heart
□ Decrease peripheral resistance, decrease systolic pressure and
preload
□ ointment, sublingual, IV, patch, or oral “Imdur”
□ Relief of chest pain or angina and reduce the risk of
heart attack and sudden death.
 NURSING CONSIDERATION
IN NITROGLYCERINE
THERAPY
□Administer SL (at the first sign of chest pain.)
□Sitting position when taking the drug.
□Offer sips of water before giving SL nitrates
□Take maximum of 3 doses at 5 minutes interval
□Advise the pt to always carry 3 tablet in his pocket
□Instruct the patient that a burning sensation under
the tongue will be felt.
 NURSING CONSIDERATONS
□Store nitroglycerine in a cool dry place, use
dark/amber colored air tight container.
□Change stock of nitroglycerine every 3 months
□Observe for side effects: Headache, flushed face,
dizziness, faintness, tachycardia.
□Transderm Nitro patch-once a day, usually in the
morning.
 NURSING CONSIDERATONS
□Best taken before any strenuous activity
□Burning sensation is a sign of potency of the drug. Facial
flushing is a side effect.
□Do not chew the tablet.
□Monitor the BP and HR.
□Evaluate the effectiveness- Pain relief
 Beta Adrenergic Blocking Agent
□ ends with “lol”
□ decrease myocardial oxygen demand by
decreasing the heart rate, bp, myocardial
contractility and calcium output.
□ Propanolol, Atenolol, Metoprolol, Esmolol,
Nadolol, Pindolol, Timolol
 NURSING
CONSIDERATION
(BETA-BLOCKERS)
□Assess the PR before giving the drug.
□Best taken with food
□Do not give to clients with asthma and DM patients
□Observe for SE: NV, mental depression, mild diarrhea,
fatigue, impotence.
□GLUCAGON- antidote for beta blocker poisoning.
 Calcium Channel Blockers
□ Norvasc, Cardizem, Verapamil (Isoptin, Calan),
Amlodipine, Nicardipine, Nifedipine, Diltiazem
□ stops the transport of calcium to the myocardium and into
smooth muscle which causes vasodilation on the
coronary arteries to improve oxygen demand and supply
□ Monitoring heart rate, orthostatic hypotension,
□ Educate about good oral hygiene
 NURSING CONSIDERATIONS
□ Assess HR and BP
□ Monitor hepatic and renal function
□ Administer 1 hr before or 2 hrs after meal.
□ Prepare GLUCAGON- antidote for calcium channel
blocker overdose
 Calcium Channel blockers
□ Inhibit calcium ion transportation into myocardial
cells to depress inotropic and chronotropic activity,
decreasing cardiac work load
□ Vasodilation effect, and reduces coronary spasm
□ Verapamil (Isoptin, Calan), Amlodipine
□ Nicardipine, Nifedipine, Diltiazem
 NSG CONSIDERATIONS
□ Assess HR and BP
□ Monitor hepatic and renal function
□ Administer 1 hr before or 2 hrs after meal.
□ GLUCAGON- for calcium channel blocker overdose
 PLATELET AGGREGATE
INHIBITORS/ ANTI
PLATELET
□ It prevents platelet from clumping and
blood clots from forming
□ ASA, Aspirin, Dypiridamole,
Clopidogril, Ticlopidine, Plavix
 NSG CONSIDERATIONS
□ Watch for signs and symptoms of GI bleeding, especially
if patient has a history.
□ Plavix: taken if can’t take aspirin
□ Assess for ss and sx of bleeding
□ Avoid straining of stool.
□ ASA with food.
□ Observe for TINNITUS. ASA toxicity
□ ASA may cause Bronchoconstriction. Observe for wheezing
 Anti coagulants
□ It prevent blood clotting
□ Inactivates thrombin and other clotting
factors inhibiting conversion of fibrinogen to
fibrin
□ Examples: Heparin, Coumadin
 Heparin Sodium
▪ Assess for signs of bleeding
▪ Keep protamine sulfate at the bedside. Antidote if
bleeding occurs in heparin therapy
▪ If administered SC, do not aspirate, do not massage the
site of heparin injection.
▪ Monitor PTT or APTT levels
▪ Used for maximum of 2 weeks
 Warfarin Sodium (Coumadin)
□ Assess for signs of bleeding
□ Keep Vit K. Antidote if bleeding occurs in Coumadine
therapy
□ Monitor Prothrombin Time
□ Minimize green leafy vegetables in the diet.
□ Don’t give ASA and Coumadin together to prevent
bleeding.
 MYOCARDIAL INFARCTION (MI)
□Results from prolonged lack of blood flow to a portion
of the myocardial tissue resulting to lack of OXYGEN,
DEATH or NECROSIS to the myocardial tissue.
 CAUSES
ATHEROSCLEROSIS, Thrombosis,

REDUCED CORONARY TISSUE

DIMINISHED MYOCARDIAL OXYGENATION

Left atrium and ventricle

INCREASED LATIC ACID PRODUCTION ( LATIC ACIDOSIS )

CK-MB, troponins, myoglobin production

Ischemia, injury, Necrosis
 What happens to the heart muscle after an MI?
Early signs of an MI
□no physical changes to heart muscle yet (until about 6-8 hours).
□If the myocytes die, cardiac enzymes are released-
CK-MB (4 to 6 hours after MI), troponins (2-4 hour most
regarded) myoglobin (1 hour after injury)
 Within 24-36 hours
□inflammation sets in and neutrophils come on the
scene and congregate at the damaged tissue site.
□complication is possible pericarditis.
□within 24 hours the heart fails to pump efficiently
resulting to cardiogenic shock and arrhythmias
Within 10 days
□granulation occurs when the macrophages come on
the scene.
□WBCs came to clean up the dead cells and
other components.
□The new tissue formed from granulation is not
well formed and is weak. This increases the
chance of cardiac rupture.
Within 2 months
□ scarring occurs, and the heart is affected in size
and functionality due to increased collagen.
 ETIOLOGY/CAUSES
□Thrombus formation- the most common
causes of MI
□Severe CAD
□Intramural hemorrhage
□Coronary artery spasm
□Coronary artery embolism
 Degree of Damage to the Heart Muscle
Myocardial
ischemia/Zone
of ischemia
❖ Temporary deprivation of
oxygen and transient
absence of blood supply
and other nutrients to the
heart
Degree of Damage to the Heart Muscle
Myocardial injury/zone of
injury
❖ Inflamed and Damage to
the heart muscle
(myocardium)
❖ Most commonly results
from myocardial
ischemia
Degree of Damage to the Heart Muscle
Myocardial
Necrosis/Zone of
infarction
❖ Death of myocardial
tissue (MI)
❖ Complete oxygen
deprivation
❖ Irreversible damage
 Classification of MI according to the
Heart muscle involve
Transmural (Q wave) infarction
❖ necrosis occurs throughout the entire thickness of the heart
muscle
❖ extends from endocardium to epicardium
 Classification of MI according to the
Heart muscle involve
Sub endocardial infarction
❖ necrosis is in the innermost layer of the heart lining
chambers.
❖ Affects the endocardial muscles
Intramural infarction
❖ patchy areas of the myocardium associated with long
standing angina pectoris.
 ANGINA AND MI
ANGINA PECTORIS MI
□ Chest pain- usually last less 15 □ Chest pain-last more than 2
minutes hours

□ Relieve by nitroglycerine □ Not relieve by nitroglycerine

□ Nitroglycerine □ Morphine
□ Precipitated by stress and □ Not
exercise
□ Relieve by rest □ Not
□ Maybe accompanied by □ Accompanied by dysrhythmias
dysrhythmias
 Clinical Manifestations
Chest pain (intense, heavy)
Radiating chest pain that goes to left arm, jaw, back
Unrelieved by nitroglycerin or rest (chest pain)
Sweating (cold)
Hard to breathe (shortness of breath)
Increased heart rate, blood pressure or irregular heart rate
Nausea with vomiting
Going to be anxious and scared
 CLINICAL MANIFESTATIONS
□ Shock- hypotension, tachycardia-bradycardia, tachypnea, lethargy, cold
skin and diaphoresis, peripheral cyanosis and weak pulse.
□ Anxiety and Apprehension
□ Oliguria
□ FEVER
□ Suffocation, dyspnea, orthopnea, gurgling or bubbling
respiration
 Diagnostic Evaluations
ECG changes
□Elevation of ST segment- due to injury area or Acute
MI
□Inverted T wave- From the zone of ischemia
□Pathologic Q wave- Develops due to area of
infarction/tissue necrosis and are permanent
Elevated Troponins
□gold standard now used by most hospitals in
assessing for an MI
□Most specific test to detect MI.
□Elevated Troponin T, I, C- sensitive as CK MB
for the detection of MI
□usually drawn every 6 hours for 3 sets.
CK-MB
□it elevates 4-6 hr after injury
□the most sensitive enzyme for determining for heart
muscle damage
Elevated LDH 1 and LDH 2
□sensitive isoenzyme that indicates myocardial damage
Elevated WBC and ERS
□ due to inflammatory process
 OTHER TEST
□Echocardiogram
□Heart Catheterization
□Stress test with Myocardial Perfusion
Imaging
 Nursing Interventions
□ Monitoring & Assessing Cardiovascular
system-12-lead EKG, and continuous bedside cardiac
monitoring.
□ Semi fowlers
□ OXYGEN via nasal cannula- at 2- 4 L/Minute
□ Working IV access
□ Monitor lung sounds “crackles”
□ Bedrest for 24-48hrs
 Nursing Interventions
□ Collect cardiac enzymes as ordered by the physician
□ Administering medications per MD order:
□ Oxygen, Morphine sulphate, MEPERIDINE
(DEMEROL), THROMBOLYTIC
THERAPY
Streptokinase (streptase), Urokinase, and Tissue
plasminogen activator (Activase).
MORPHINE SULFATE
□ Narcotic Agonist, analgesic,
□ DOC of MI
□ Used relieve pain
□ To improve hemodynamics by reducing pre
load and afterload and promotes venous
pooling of blood in the periphery
 NURSING CONSIDERATIONS
□ Best taken with Food
□ Report nausea and vomiting and respiratory
depression
□ Keep Naloxone HCL (antidote) at the bedside
□ Instruct the patient to lie down during IV
administration.
□ Contraindicated to patient with PANCREATITIS
 MEPERIDINE (DEMEROL)
□Has Vagolytic effect –causing tachycardia
□Narcotic Analgesic
□Negative Pain
□Avoid alcohol
□Keep the antidote: Naloxone hydrochloride
□Supine position- prevent hypotension
 THROMBOLYTIC THERAPY
□ Streptokinase (streptase), Urokinase, and Tissue
plasminogen activator (Activase)
□ It dissolve obstructing thrombus
□ Effectiveness of the drug: Absence of chest pain
□ Detect for occult bleeding during and after thrombolytic
therapy
□ Assess neurologic status changes
 ANTI-THROMBOTIC AGENTS
□ prevent formation of clot
□ Lovenox and Heparin
□ monitor for bleeding (assess gums of mouth, stool (dark
tarry), drop in blood pressure and increase in
heart rate, blood in urine
□ watch platelet count which may start to decrease after
several days
 ANTI PLATELET
□ It decrease platelets aggregation and thrombus
formation
□ It prevents platelet from clumping and blood clots from
forming
□ Aspirin (ASA), Plavix, Dypiridamole, Clopidogril
□ Watch for signs and symptoms of GI bleeding, and
Thrombotic Thrombocytopenic Purpura (TTP)
 NSG CONSIDERATIONS
□ Watch for signs and symptoms of GI bleeding,
especially if patient has a history.
□ Assess for ss and sx of bleeding
□ Avoid straining of stool.
□ ASA with food.
□ Observe for TINNITUS. ASA toxicity
□ ASA may cause Bronchoconstriction.
 Anti-Coagulants
□ It prevent blood clotting
□ Inactivates thrombin and other clotting factors
inhibiting conversion of fibrinogen to fibrin
□ Examples: Heparin, Coumadin
Heparin Sodium
▪ Assess for signs of bleeding
▪ Keep protamine sulfate at the bedside.
▪ If administered SC, do not aspirate and massage the site
of heparin injection.
▪ Monitor PTT or APTT levels
▪ Used for maximum of 2 weeks
 Warfarin Sodium (Coumadin)
□ Assess for signs of bleeding
□ Keep Vit K. Antidote if bleeding occurs in Coumadine
therapy
□ Monitor Prothrombin Time
□ Minimize green leafy vegetables in the diet.
□ Don’t give ASA and Coumadin together to
prevent bleeding.
 NITROGLYCERINE
□ Promotes venous and arterial relaxation of coronary
vessel and prevention of coronary spasm
□ causes vasodilation and increases blood flow to the heart,
hence better blood flow to the area experiencing ischemia
□ ointment, sublingual, IV, patch, or oral “Imdur”
□ Relief of chest pain
 NURSING CONSIDERATONS
□ Best taken before any strenuous activity
□ Place a tablet under the tongue at the first sign of chest pain.
□ Burning sensation is a sign of potency of the drug. Facial flushing
is a side effect.
□ Do not chew the tablet.
□Keep the tablets in dark container.
□ Monitor the BP and HR.
 Ace Inhibitors
□ ends in “pril”
□ Lisinopril, Ramipril, Enalapril, Captopril
□ It work by allowing more blood to get to the heart
muscle
□ It does this by blocking the conversion of Angiotensin I or
Angiotensin II
 Beta Adrenergic Blocking Agent
□ ends with “lol”
□ decrease myocardial oxygen demand by
decreasing the heart rate, bp, myocardial
contractility and calcium output.
□ Propanolol, Atenolol, Metoprolol, Esmolol,
Nadolol, Pindolol, Timolol
 NURSING
CONSIDERATION
(BETA-BLOCKERS)
□Assess the PR before giving the drug.
□Best taken with food
□Do not give to clients with asthma and DM patients
□Observe for SE: NV, mental depression, mild diarrhea,
fatigue, impotence.
□GLUCAGON- antidote for beta blocker poisoning.
 ARBS Angiotensin II Receptor Blockers
□ end in “sartan” like Losartan, Valsartan
□ It blocks angiotensin II receptors which causes
vasodilation.
□ Monitor sodium, K, and blood pressure
Statins (“tins)
□ Simvastatin, Atorvastatin,
□ helps lower LDL, total cholesterol, triglycerides, and
increase HDL.
□ Educate not to replace diet and exercise
□ Notify doctor if they develop muscle pain or tenderness
□ Monitor CPK (creatine kinase) levels if elevated
□ Monitor liver function
 Calcium Channel Blockers
□ Norvasc, Cardizem, Verapamil (Isoptin, Calan),
Amlodipine, Nicardipine, Nifedipine, Diltiazem
□ stops the transport of calcium to the myocardium and into
smooth muscle which causes vasodilation on the
coronary arteries to improve oxygen demand and supply
□ Monitoring heart rate, orthostatic hypotension,
□ Educate about good oral hygiene
 NURSING CONSIDERATIONS
□ Assess HR and BP
□ Monitor hepatic and renal function
□ Administer 1 hr before or 2 hrs after meal.
□ Prepare GLUCAGON- antidote for calcium channel
blocker overdose
 Surgical Management
Percutaneous
Transluminal Coronary
Angioplasty
□ A balloon tip catheter is placed
in a coronary vessel narrowed by
plaque
□ The balloon is inflated and
deflated to stretch the vessel
and flatten the lesion
□ Blood flows freely through
the unclogged vessel to the
heart.
 Surgical Management
Intra Coronary Stent
□ A diamond mesh tubular
device is placed in the
coronary artery
□ Prevents re-stenosis (after
PTCA) by providing
skeletal support
 Surgical Management
Intra Coronary
Atherectomy
□ A blade tip catheter is
guided in a coronary
vessel to the site of the
plaque
□ The plaque is cut, shave, or
pulverized then
removed
 Surgical Management
Coronary Artery Bypass Graft
□ A graft is surgically attached to
the aorta and the other end of the
graft is attached to a
distal portion of a coronary
vessel.
□ By passes obstructive lesion in
the vessel and returns to
adequate blood flow to the
heart muscle supplied by the
artery.
 Self Management Education Guide To Decrease
the Anginal Attack and MI
□ Manage Hypertension □Avoid extreme activities such as
□ Stop active and passive sudden exertion, walking
smoking against the wind, extreme
temperature, high altitude,
□Avoid alcohol and stress emotionally stressful situations
□ Plan a regular exercise under
medical supervision □ Lose weight if overweight
□ Healthy diet.
□ Adequate time to rest and
relaxation