NCM112j - CARDIO
Module 2: Coronary Artery Disease
CORONARY ARTERY DISEASE
• also known as :
Atherosclerotic Heart Disease
Coronary Atherosclerosis
Coronary Arteriosclerosis
Coronary Heart Disease (CHD)
Ischemic Heart Disease (IHD)
Myocardial Ischemia
ARTERIOSCLEROSIS
 refers to the loss of elasticity or
hardening of the arteries that
accompanies the aging process.
ATHEROSCLEROSIS
 is a condition in which the lumen of
arteries fill with fatty called plaque
deposits called plaque (chiefly
composed cholesterol, a fatty (lipid)
substance).
CORONARY OCCLUSION
 closing of the coronary artery which
reduces or totally interrupts blood
supply to the distal muscle area
 most common cause is
atherosclerosis (abnormal
accumulation of fats)
CORONARY ARTERY DISEASE
(CAD)
 narrowing or obstruction of one or
more coronary arteries
 refers arteriosclerotic and
atherosclerotic changes in the
coronary arteries supplying the
myocardium.
 as a result of atherosclerosis, which is
an accumulation of lipid- containing
plaque in the arteries.
CAUSES:
narrowing of the large and medium-
sized coronary arteries due to:
1. deposition of atheromatous plaque in
the vessel wall
1
 thrombus
 clots
platelet plugs
ATHEROMA
 is a fatty substance that builds up in
the arteries over time
 commonly known as atherosclerotic
plaque, or simply plaque.
 atheromas form along the inside
lining of the arteries and interrupt
blood flow
PATHOPHYSIOLOGY
1. The disease causes decreased
perfusion of myocardial tissue and
inadequate myocardial oxygen
supply leading to hypertension,
angina, dysrhythmias, mi, heart
failure, and death.
2. Collateral circulation, more than one
artery supplying a muscle with
blood, is normally present in the
coronary arteries, especially in older
persons.
3. The development of collateral
circulation takes time and develops
when chronic ischemia occurs to
meet the metabolic demands;
there- fore an occlusion of a
coronary artery in a
 Younger individual is more likely to
be lethal
 Than in an older individual.
MODIFIABLE RISK FACTORS
 Hyperlipidemia
 cigarette smoking, tobacco use
 hypertension
 diabetes mellitus
 metabolic syndrome obesity
 physical inactivity
NON- MODIFIABLE RISK FACTORS
 family history of cad (1st degree
relative)
NCM112j - CARDIO
Module 2: Coronary Artery Disease
 increasing age
- more than 45 years for men COMPLICATIONS
- more than 65 years for women  Heart Attack
 gender: men  Heart Failure
 race: African, American  Heart Rhythm Abnormal

CLINICAL MANIFESTATIONS
 Chest pain
 Palpitations SURGICAL MANAGEMENT
 Dyspnea 1. PTCA: Percutaneous
 Syncope Transluminal Coronary
 Excessive fatigue Angioplasty
DIAGNOSTIC STUDIES FOR CAD  IA minimally invasive procedure to
1. ELECTROCARDIOGRAPHY open blocked or stenosed coronary
 ST- segment depression, arteries allowing unobstructed blood
 T-wave inversion, or both is noted flow to the myocardium
 when blood flow is reduced and  to compress the plaque against the
ischemia occurs walls of the artery and dilate the
 ST segment returns to normal when vessel
the blood flow returns. 2. LASER ANGIOPLASTY - to
 when blood flow returns. vaporize to plaque
 with infarction : cell injury results in: 3. ATHERECTOMY - to remove the
 ST- segment elevation, followed by plaque from the artery
T- wave inversion and abnormal Q 4. CORONARY ARTERY BYPASS
wave GRAFTING ( CABG)
2. CARDIAC CATHETERIZATION  A major surgical operation where
 Provides the most definitive source atheromatous blockages in a patient's
for diagnosis. coronary arteries are bypassed with
 Shows the presence of harvested venous or arterial conduits.
atherosclerotic lesions.  To improve blood flow to the
myocardial tissue at risk for ischemia
or infarction because of the occluded
artery.
5. VASCULAR STENT - to prevent the
artery from closing and to prevent
restenosis.
MEDICATIONS
 Nitrates to dilate the coronary
arteries and decrease preload and
3. BLOOD LIPID LEVELS afterload.
 May be elevated.  Calcium channel blockers to dilate
 Cholesterol-lowering medications may coronary arteries and reduce
be prescribed to reduce the vasospasm
development of atherosclerotic  Statins: Cholesterol-lowering
plaques. Medications - to reduce the
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NCM112j - CARDIO
Module 2: Coronary Artery Disease
development of atherosclerotic  CHOLESTEROL : 140-199 MG/DL
plaques.  LOW-DENSITY LIPOPROTEINS:
 Beta-blockers to reduce the bp in LOWER THAN 130MG/DL
individual with hypertension  HIGH-DENSITY LIPOPROTEINS:
 Imipramine - using this medication 30 TO 70 MG/DL
to treat depression may improve your  TRIGLYCERIDES : LOWER THAN
mood, sleep, appetite, and energy 200 MG/DL
level and may help restore your
interest in daily living
PHARMACOLOGIC THERAPY
 Nitrates
 Betablockers INTERVENTIONS
 Calcium Channel Blockers 1. Instruct the client regarding the
 Ace Inhibitors. purpose of diagnostic medical and
 Statins surgical procedures and pre-
 Imipramine procedure and post procedure
expectations.
HEALTH TEACHINGS 2. Assist the client to identify risk
 Life Style Change factors that can be modified.
 Weight Control 3. Assist the client to set goals to
 Stress Management promote lifestyle changes to reduce
 Healthy Diet the impact of risk factors.
 Exercise 4. Assist the client to identify barriers
 Smoking Cessation to compliance with the therapeutic
plan and to identify
Atherosclerosis impedes coronary 5. Instruct the client regarding a low-
blood flow by which of the calorie, low- sodium, low-
following mechanisms? cholesterol, and low-fat diet, with
a. Plaques obstruct the vein an increase in dietary fiber.
b. Plaques obstruct the artery 6. Instruct the client regarding
c. Blood clots form outside the vessel prescribed medications.
wall 7. Provide diet instructions , stressing
d. Hardened vessels dilate to allow the that dietary changes are not
blood to flow through temporary and must be maintained
Which of the following actions is for life.
the first priority care for a client 8. Assist the client to identify risk
exhibiting signs and symptoms of factors that can be modified.
coronary artery disease? 9. Assist the client to set goals that
a. Decrease anxiety will promote changes in lifestyle to
b. Enhance myocardial oxygenation reduce the impact of risk factors.
c. Administer sublingual nitroglycerin 10. Stress to the client that dietary
d. Educate the client about his changes are not Temporary and
symptoms must be maintained for life; instruct
the client regarding prescribed
VALUES medications.
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Module 2: Coronary Artery Disease
11. Assist the client to identify barriers
to compliance with the therapeutic
plan and to identify methods to
overcome barriers.
12. Provide community resources to the
client regarding exercise, smoking
cessation, and stress reduction as
appropriate.

II. ANGINA (Myocardial Ischemia)

Angina Pectoris or Simply Angina CLINICAL MANIFESTATIONS:
 Transient chest pain caused by ANGINA
insufficient blood flow to the 1. Pain
myocardium.  Transient paroxysmal substernal or
 Results myocardial ischemia precordial pain
( decreased blood low and oxygen  Described as heaviness or lightness
supply to the myocardium) of the chest “indigestion’, crushing
 Ischemia is a condition in which  Radiates down one or both arms, left
blood flow (and thus oxygen) is shoulder, jaw, neck and back.
restricted or reduced in a part of the  Precipitated by rest and activity or
body. exertion
 Cardiac ischemia is decreased  Relieved by rest or nitroglycerine
blood flow and oxygen to the heart CLINICAL MANIFESTATIONS:
muscle ANGINA PECTORIS
ETIOLOGY: 2. Pallor
• Angina is caused by an imbalance 3. Diaphoresis
between oxygen supply and demand. 4. Dyspnea
CAUSES: 5. Faintness
 Atherosclerosis - obstruction of 6. Palpitations
coronary blood flow 7. Dizziness
 Coronary artery spasm (sudden 8. Digestive Disturbance
tightening of the arteries that send
blood to the your heart.) ANGINA PQRST PAIN ASSESSMENT
 Conditions increasing Method Of Assessment Of Chest
 Myocardial oxygen consumption. Pain
PATHOPHYSIOLOGY OF ANGINA P – ROVOCATIVE
 what activities bring on the pain?
Q - UALITY
O what does the pain feel like?
R–EGION/RADIATION
S – EVERITY
 how does the pain rate of 1 to 10?
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Module 2: Coronary Artery Disease
T – iming/treatment?
 when did the pain begin? O how long
does it last?
 what do you do to relieve the pain
 are these measures effective?
 may occur at rest
4. INTRACTABLE ANGINA IS A
CHRONIC, INCAPACITATING
ANGINA UNRESPONSIVE TO
INTERVENTIONS.
5. POSTINFARCTION ANGINA
 occurs after mi
 associated with acute coronary
insufficiency
 lasts longer than 15 minutes
 symptom of worsening cardiac
ischemia
 occurs after an mi, when residual
ischemia may cause episodes of
angina

PRECIPITATING EVENTS OF
ANGINA PECTORIS
1. Exertion- vigorous exercise done
very sporadically
2. Emotions- excitement, sexual
TYPES OF ANGINA activity.
1. STABLE ANGINA (Effort Angina) 3. Eating-a heavy meal
 Classic type of angina related to 4. Environment– extreme
myocardial ischemia temperatures
 Occurs during exertion  These events increase myocardial
 Relieved by rest and drugs oxygen demands. Further
 Severity does not change disequilibrium between oxygen
 Chest pain lasts for less than 15 supply and demand occurs .
minutes
 Recurrence is less frequent
2. UNSTABLE ANGINA
(Periinfarction Angina)
 Chest pain lasts for more than 15
minutes but less then 30 minutes
 Recurrence more frequent, may
occur at night
 Intensity of pain increases
3. VARIANT ANGINA (Prinzmetal’s
Angina) DIAGNOSTIC TEST FOR ANGINA
 Results from coronary artery spasm, PECTORIS
 Attacks may be associated with st  Electrocardiogram (ECG)
segment elevation noted on the  Stress Test (without imaging or blood
electrocardiogram ü chest pain longer tests to help diagnose angina)
in duration  Coronary CT Angiography,
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NCM112j - CARDIO
Module 2: Coronary Artery Disease
 Cardiac Magnetic Resonance Imaging  Store in cool dry place , do not
 Coronary angiography refrigerate it may be destroyed by
 Echocardiogram heat, light and moisture,
 Stress Test with Imaging may be  Change stocks every 3 months
performed  Observe for side effects : headache,
flushed face, dizziness, faintness,
MEDICATIONS: ANGINA tachycardia, common during the first
1. VASODILATORS : few doses of the medication. Do not
NITROGLYCERINE, AMYL NITRATE, discontinue the drug.
ISOSORBIDE
EFFECTS BETA – ADRENERGIC BLOCKING
 Direct relaxing effect on vascular AGENTS
smooth muscle, resulting in  PROPRANOLOL (INDERAL)
generalized vasodilation.  METOPROLOL (LOPRESSOR)
 Decrease peripheral resistance,  NADOLOL (CORGARD)
decrease systolic pressure, produce  ATENOLOL (TENORMIN)
venous pooling and decrease preload.  PINDOLOL (VISKEN)
 Coronary vasodilation redistributes  ESMOLOL (BREVIBLOC)
myocardial blood flow more  EFFECTS: decrease myocardial
efficiently. demand by decreasing heart rate, bp,
myocardial contractility and calcium
output.

NURSING INTERVENTIONS IN
DRUG THERAPY NURSING INTERVENTIONS: BETA
 NITROGLYCERINE THERAPY BLOCKERS
 Assume sitting position when taking  Assess PR before administration,
the drug, prevents hypostatic withhold if bradycardia is present
hypotension. U  Administer with food to prevent GI
 Take maximum of three doses at 5 upset
minute interval.  Do not administer Inderal
 If taken sublingual, experience (propranolol) to clients with asthma,
stinging or burning sensation under it causes bronchoconstriction.
the tongue. This indicates that  Contraindicated to patients with DM,
medication is potent. causes hypoglycemia
 Sublingual route produces onset of  Extreme caution in clients with heart
action within 1-2 minutes, duration of failure
action 30 minutes.  Side effects: nausea, vomiting,
 Offer sips of water before giving mental depression, diarrhea, fatigue
sublingual nitrates, dryness of mouth and impotence.
inhibit drug absorption.  Antidote for beta blocker
 Advise to always carry 3 tablets in his poisoning : glucagon
pocket
NITROGLYCERINE CALCIUM- CHANNEL BLOCKERS
 VERAPAMIL (ISOPTIN)
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Module 2: Coronary Artery Disease
 NIFEDIPINE ( ADALAT, CALCIBLOC)
 DILTIAZEM ( CARDIZEM)
 AMLODIPINE ( NORVASC)
 NICARDIPINE ( CARDENE)
 EFFECTS: inhibit calcium ion
transportation into myocardial cells
decreasing cardiac workload.
 has vasodilation effect
 reduces coronary vasospasm
NURSING INTERVENTIONS
CALCIUM CHANNEL BLOCKER
 Assess HR, BP
 monitor hepatic, renal function
 administer 1 hours before or 2 hours
after meals, food delays absorption.
 Antidote for calcium - channel
blocker: glucagon (help regulate your
blood glucose (sugar) levels.
Glucagon increases in the blood
blood sugar level and prevents it
from dropping too low)
OTHER MEDICATIONS: ANGINA
PECTORIS
PLATELET AGGREGATION
INHIBITORS
 ASA (ASPIRIN)
 DIPYRIDAMOLE ( PERSANTIN)
 CLOPIDOGREL ( PLAVIX)
 EFFECTS : inhibit platelet
aggregation
NURSING INTERVENTIONS:
 Assess s/s of bleeding
 Avoid straining at stool, prevents
rectal bleeding
 Give asa with food, prevents gi upset
 Observe for asa toxicity – tinnitus
(ringing of the ears)
 May cause bronchoconstriction,
observe for wheezing.
ANTICOAGULANTS
7
 HEPARIN SODIUM (CLEXANE ,
FRAGMIN)
 EFFECTS: inactivates thrombin
formation and other clotting factors
inhibiting conversion of fibrinogen to
fibrin, fibrin clot formation is
prevented
 Assess for bleeding, keep protamine
sulfate available( antidote) , if
: bleeding occurs.
 Do not aspirate, massage site of
heparin injection, to prevent
hematoma formation
 Monitor ptt therapeutic effects ptt x2
to 2.5)
 WARFARIN SODIUM
 EFFECT: inhibit hepatic synthesis of
vitamin K
NURSING INTERVENTIONS:
 Assess s/s of bleeding
 Keep vit K (aquamephyton) readily
available, administered as an antidote
if bleeding occurs.
 Minimize green leafy vegetables in
diet, these contain vitamin k and
antagonize the effect of coumadin, to
prevent bleeding.
NURSING INTERVENTIONS:
ANGINA PECTORIS
A. IMMEDIATE MANAGEMENT
1. Assess pain; institute pain relief
measures.
2. Administer oxygen at 3 l/min by
nasal cannula as prescribed.
3. Assess vital signs and provide
continuous cardiac monitoring and
nitroglycerin as pre- scribed to
dilate the coronary arteries, reduce
the oxygen requirements of the
myocardium, and relieve the chest
pain.
4. Ensure bed rest is maintained,
place the client in semi-fowler’s
position, and stay with the client.
NCM112j - CARDIO
Module 2: Coronary Artery Disease
5. Obtain a 12-lead ecg.
6. Establish an IV access route. MYOCARDIAL INFARCTION
B. FOLLOWING THE ACUTE
EPISODE
1. Instruct the client regarding the
purpose of diagnostic medical and
surgical procedures and the
preprocedure and postprocedure
expectations.
2. Promoting tissue perfusion
 Assist the client to identify angina-
precipitating events.
 Avoid over- fatigue
 Stop immediately if chest pain,
dyspnea, light headedness, or MYOCARIDIAL INFARCTION
faintness may indicate low tissue  in myocardial infarction
perfusion.  an area of the myocardium is
 Instruct the client to stop activity and permanently destroyed
rest if chest pain occurs and to take  causing formation of localized
nitroglycerin as prescribed. necrotic areas within the
3. Instruct the client to seek medical myocardium.
attention if pain persists.  due to plaque rupture and
4. Promoting activity and rest subsequent
 Encourage slower activity or shorter  thrombosis formation
periods of activity with more rest  resulting in complete occlusion of an
periods, avoid over exertions.. artery infarction : tissue death or
 Take nitroglycerine before exercise necrosis due to inadequate blood
 Increase extent of exercise gradually supply to the affected area.
5. Promote relief of anxiety and
feeling of well – being.
 reduction of patient’s level of anxiety MYOCARDIAL INFARCTION
 minimize outbursts, worry, and ISCHEMIA
tension.
 encourage optimistic outlook to help INJURY
relieve the cardiac work load.
6. Diet INFARCT
 low sodium, low fat and low
cholesterol, high fiber diet PATHOPHYSIOLOGY
 avoid saturated fats( animal fats) Myocardial Ischemia (interrupted
white meat (chicken without skin, coronary blood flow: thrombotic
fish) are low in cholesterol occlusion caused rupture of a plaque)
 read labels injury (damage to cardiac
7. Activity muscle)infarct (necrosis/myocardial
 Activities are encouraged within the death)depression cardiac function
patient’s limitations
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NCM112j - CARDIO
Module 2: Coronary Artery Disease
 STRESS

LOCATION OF MI
• Occurs in the left ventricle, often
depresses left ventricular function.
• due to occlusion of the LADA (left
anterior descending artery). This is
Referred to as an anterior wall
infarction.
• contractile function in the necrotic
area ceases permanently
CLINICAL MANIFESTATIONS OF MI
 Chest pain : crushing, severe
 Longer than 30 minutes
 Unrelieved by rest or nitroglycerine,
radiating to the left arm, back or jaw
neck
 ”(chest hand- clutching)
characterized by levine’s sign a
universal sign of distress in angina
pectoris and mi.
ASSESSMENT FINDINGS
 Pain occurs without a cause , usually
in the morning
 Relieved by opioids, unrelieved by
nitroglycerin
 associated with dyspnea, fear and
anxiety, palpitations, fatigue and sob
 decreased left ventricular function
and decreased CO
 cardiovascular system compensate by
increasing heart rate frank – Starlin
LAW

CLINICAL MANIFESTATIONS
 Anxiety and apprehension
 feeling of “doom”, Restlessness
Pathophysiologic Basis
 Severe pain of a heart attack is
terrifying most clients are aware of
the significance of a heart attack,
RISK FACTORS restlessness results from shock and
NON-MODIFIABLE RISK FACTORS pain.
 AGE  shock
 FAMILY HISTORY  systolic pressure below 80 mmhg,
 ETHNIC BACKGROUND  gray facial color, lethargy,
MODIFIABLE RISK FACTORS diaphoresis, peripheral cyanosis,
 HYPERTENSION tachycardia, bradycardia, weak pulse
 SMOKING Pathophysiology:
 HYPERLIPIDEMIA  due to severe pain, severe reduction
 OBESITY of cardiac output and inadequate
 DIABETES MELLITUS tissue perfusion, causing tissue
 PHYSICAL INACTIVITY
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NCM112j - CARDIO
Module 2: Coronary Artery Disease
hypoxia, oliguria ( less than 30ml/ decreased
hour. hours
oxygenation
 Fever
2-4hours
 with in 24 hours Most
after
 extends 3- 7 days accompanied by definite
TTROPONIN I heart
leukocytosis and elevated ESR findings for
attack
 result from severe pain and from MI
chest pain
vasovagal reflexes conducted from an
area of damaged myocardium to git. AST
Is also used
 gas pains around the heart” nausea (ASPARTATE
8 HOURS in liver
and vomiting” AMINO
damage
 Result from destruction of myocardial TRANSFERASE)
tissue and inflammatory process’ Cardiac
indigestion” speciific
isoenzyme
ECG AND CARDIAC ENZYMES (found
ASSESSMENTS CK-MB 24 HOURS mainly in
ECG CHANGES IN MI cardiac
 ST-SEGMENT ELEVATION Cells)
 T-WAVE INVERSION indicator for
 ABNORMAL Q WAVE mi
LDH Reflects
(Lactic tissue
3 days ( 72
Acid breakdown
hours )
dehydroge- and
nase ) hemolysis

OTHER DIAGNOSTIC EXAM

CARDIAC CATHETERIZATION:
 Provides definite diagnosis
 provides information about the
patency of the coronary arteries
 site of insertion: femoral artery (best)

ENZYMES THAT INDICATE

MYOCARDIAL INFARCTION GOALS OF MEDICAL MANAGEMENT
Time of  Minimize myocardial damage
Enzyme Description
occurrence  Preserve myocardial function
Myoglobin First First  Prevent complications
1-3 after enzyme to achieved by:
heart elevate due
attack to
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NCM112j - CARDIO
Module 2: Coronary Artery Disease
 re-perfusing the area with the 4. BETA-ADRENERGIC BLOCKING
emergency use of thrombolytic AGENTS
medications  DIAZEPAM ( VALIUM)
 reducing myocardial oxygen demand
and increasing oxygen supply with: SURGICAL MANAGEMENT FOR MI
 Medications • PTCA
• CORONARY ARTERY BYPASS GRAFT
 O2 administration
 Bed rest TREATMENT
TREATMENT : MI ACUTE STAGE :
1. ANTIPLATELET DRUGS • GOALS :
2. ANTICOAGULANTS  prevention further tissue injury and
3. NITRATES limitation of infarct size.
4. BETA- BLOCKERS  maximize myocardial tissue perfusion
5. STATINS and reduce myocardial tissue
6. REPERFUSION THERAPY: demand.
EMERGENCY REPERFUSION FOR 1. Supplemental oxygen by nasal
ST- SEGMENT ELEVATION MI cannula
a. FIBRINOLYTIC DRUGS - increases myocardial oxygen supply
(thrombolytic treatment that - nasal cannula dose not intensify
dissolves dangerous intravascular feeling of suffocation in client with mi
clots to prevent ischemic damage 2. Cardiac monitoring
by improving blood flow) - detects occurrence of dysrhythmias
b. PTCA 3. Promoting comfort
c. CABG - relieve pain
- administer morphine sulfate as
MEDICATIONS FOR MI ordered
A. MEDICATIONS : - decreases sympathetic stimulation
1. ANALGESIC : for relief of pain. this which increases myocardial oxygen
is a priority. demand this will prevent shock resulting
 morphine sulfate IV (drug of choice) from pain.
2. THROMBOLYTIC THERAPY 4. Rest
 to disintegrate blood clot by - bed rest during acute phase with
activating the fibrinolytic processes. commode( 24- 48 hours)
 streptokinase, urokinase and tissue Interventions Following the Acute
plasminogen activator Episode
• check for occult blood during and  bed rest first 24 to 36 hours .
after thrombolytic therapy
 use a bed- side commode if
• absence of chest pain : medication
prescribed.
is effective
3. ANTICOAGULANT AND  range-of-motion exercises to prevent
ANTIPLATELET MEDICATIONS thrombus formation and maintain
 Administered after thrombolytic muscle strength.
therapy to maintain arterial patency.  progress to dangling legs at the side
of the bed or out of bed to the chair

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NCM112j - CARDIO
Module 2: Coronary Artery Disease
for 30 minutes three times a day as
prescribed.
 progress to ambulation in the client’s
room and to the bathroom and then
in the hallway three times a day.
5. Monitor the following
parameters
- dysrhythmias/ ecg tracings
- VS
- effects of daily status
- PR ( rate and rhythm)
6. Promoting oxygenation and
tissue perfusion
- avoid overfatigue, stop activity
immediately in the presence of chest
pain - O2 inhalation 2l/ min by nasal
cannula first 24 -48 hours, longer if with
Dysrhythmias.
- position client in semi- fowler’s position
to allow greater diaphragm expansion
(lung expansion and better co2- oxygen
exchange . Promoting cardiac output).
7. Promoting activity
- increase in activity
- after 1st 24 – 48 hours patient maybe
allowed to sit on a chair for increasing
period of time and begins ambulation on
the 4th or 5th day.
- monitor for dysrhythmias, vs , pain
during activity.
8. Promoting nutrition and
elimination
- small and frequent feedings
- low- calorie, low cholesterol, low
sodium diet : limits metabolic demands
- avoid stimulants
- avoid very hot/ very cold
foods( vasovagal stimulation ( vagus
Nerve) may occur may lead in
bradycardia or cardiac arrest)
- having bowel movement
- standing for a long time
- no using of bedpan/ straining at stool.
Valsalva maneuver causes changes in
12
bp, hr may trigger ischemia,
dysrhythmias, cardiac arrest.
- use bedside commode
- may use stool softener as ordered.
11. Promote relief of anxiety and
feeling of well- being.
Myocardial Infarction
Nursing Interventions After Acute
Episode
1. Maintain bed rest for first 3 days
2. Provide passive rom exercises
3. Progress with dangling of the feet at
side of bed
4. Proceed with sitting on the bed, on
the chair for 30 minutes tid
5. Proceed with ambulation in the room
 toilet  hallway tid
Nursing interventions after acute
episode Cardiac Rehabilitation
Goal---to extend and improve
 Quality of life
 physical conditioning
 patients who are able to walk 3-4
mph are usually ready to resume
sexual activities
 primary reason for administering
morphine to a client with myocardial
infarction: to decrease oxygen
demand on the client’s heart
 the first intervention for a client
experiencing myocardial infarction:
administer oxygen
 most common complication of a
myocardial infarction: arrhythmias
NCM112j - CARDIO
Module 2: Coronary Artery Disease

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