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					  MYOCARDIAL
  INFARCTION
(HEART ATTACK)
       A Case Study


 By Rolly M. Policarpio RN
I. INTRODUCTION


        The numerous numbers of literary works that drew inspiration from the work of
the heart demonstrate the magnificent and life-sustaining function of this organ. More
than a metaphor of love, it is a metaphor of life. indeed heart maintains life by keeping
the blood dynamic at all times even without our conscious awareness. But the hear itself
has a life that need to be sustained and maintained. This is possible because of the
networks of blood vessels specially the coronary artery, that nourish every single cell of
the heart. Sometimes, the coronary artery become inadequate by the formation of
blockage from a complex process brought about by conglomeration of differen factors.
This can lead to coronary artery diseases and worst to myocardial infarction.


        Myocardial infarction, sometimes called as Acute Myocardial Infarction(AMI) or
Myocardial Ischemia is also known as heart attack, coronary occlusion, or simply
"coronary," which is a life-threatening condition characterized b! the formation of
localized necrotic areas within the myocardium (Black, 2005) and occurs when
myocardial tissue it abruptly and severed deprived of oxygen. Angina pectoris is
characterized by a chest pain resulting from reducer coronary blood flow, which causes
a temporary imbalance between myocardial blood supply and demand. Moreover it is a
chest pain resulting from myocardial ischemia (inadequate blood supply to the
myocardium), (Black, 2005).


        Worldwide, heart diseases and stroke are also found to be the leading causes of
death. It is estimated tha 7.1 million people worldwide die of heart disease each year. In
2008, almost 48% of all continental deaths were dun to cardiovascular disease
(Billiones, 2008).


        In the United Stated of America (USA), 7,900,000 had heart attack (American
Heart Association), about one of every five dies from Myocardial infarction.. Incidence is
1,260,000 new and recurrent coronary attacks per year (National Heart, Lung, and Blood
institute's Atherosclerotic Risk in Communities PANICS Study and Cardiovascula Health
Study (CHS). About 37 percent of people who experience a coronary attack in a given
year die from it.
       In the Philippines. as to the 10 leadings causes of Mortality in the Philippines
(2008), Heart Diseases rank< 1^S^t. On the other hand, as to the 10 leading causes of
Morbidity in the Philippines (2008), Hypertension and Hear Diseases ranks, 5th and 8th,
respectively. The region with the highest morbidity for CVD is Region 7, followed b!
Regions 1, CAR, 2 and 6, (NSO, Philippines, 2008).


       One of the major technological breakthroughs regarding the treatment of acute
myocardial infarction is the development of hybrid stent called Stentys. The new
capabilities of this stent is self-expanding platform, solving Stent-malapposition. Two
patients were successfully treated during acute myocardial infarction procedures by Drs.
S Verheye (Antwerp, Belgium) and K. E. Hauptmann (Trier, Germany). The problem with
the old stent used is the malposition of the device several days after it was placed to the
affected artery. One of the greatest problems ir myocardial infarction is the urgent
diagnosis of the disease condition. Usually, the patient is diagnosed of having
myocardial infarction after being positive with troponin T marker and significant
ECG(electrocardiagram) tracin^( pattern. The problem is the Troponin T marker will only
be evident in the blood 3 hours after the myocardial infarction. This delayed some
important medical interventions which greatly improve the patient's diagnosis. Thi
problem is solved by a new sensitive cardiac troponin assays and copeptin, a marker of
endogenous stress, i^l combination with standard cardiac troponin. Both approaches
seem to largely overcome the sensitivity deficit o current standard cardiac troponin. With
the sensitive cardiac troponin assays, the time to detect the troponin T marks is greatly
reduced to one hour. This is very significant because life saving measures can be iniated
early. Both marke need to be presents in order to diagnosed myocardiakl infarction.


       Being an ICU nurse trainee before in a tertiary private hospital in Angeles City,
the nurse researche encountered many patients suffered from myocardial infarction.
This study is very essential in the sense that, i empowers the nurse to give appropriate
nursing interventions in the prevention and management of patients havin^( myocardial
infarction. This case study will serve as a tool to broaden up the knowledge of the
researcher and all the people who are involve in this study. This study will also serve as
a reference for the future researcher who will goin to indulge in the same topic. The
researcher made this case study to meet the following objectives.
Objectives


Nurse Centered


       After the completion of the study, the nurse researcher will be able to:


      perform a comprehensive assessment of the patient with myocardial infarction.
      enumerate the signs and symptoms of myocardial infarction
      identify the diagnostic procedures that would help in the diagnosis of myocardial
      identify nursing problems utilizing the subjective cues and objective cues of
       myocardial infarction.
      perform appropriate therapeutic interventions for each of the formulated nursing
       diagnosis.
      evaluate the effectiveness of nursing care for myocardial infarction formulate
       conclusion based on findings and enumerate recommendations concerning
       myocardial infarction.


Client Centered
      After the completion of the study, the client will be able to maintain functional
       health status and progress within client's own limit through the application of the
       nursing process.
      After the completion of the study, the client's significant others will be able to
       increase awareness on the different predisposing factors that can cause
       myocardial infarction, gain knowledge on the different signs and symptoms of
       myocardial infarction, gain knowledge on the course of myocardial infarction and
       will be able to state the importance of proper diet, activity in the prevention of
       heart problem specially myocardial infarction
      After the completion of the study, other patients who suffer from myocardial
       infarction and their significant other will be able to have increase knowledge on
       the course myocardial infarction, prevention and management.
II. NURSING ASSESSMENT


1.   PERSONAL DATA


       a.    Demographic Data


       Mang Undoy is a 51-year-old male patient, a Filipino, and a member of the
Catholic religion. He currently resides in Pulong Maragul, Angeles City. He was born on
August 10, 1958 in Angeles City Pampanga. Mang Undo was admitted last October 07,
2009 at 3:00pm in a secondary hospital situated in Angeles City with the chief complaint
of chest pain which is heavy, substernal, radiating to the left arm and unrelieved by rest.
He was initiall diagnosed of to consider Acute Myocardial Infacrtion. He was discharged
on October 16, 2009 with the fine diagnosis of Acute Myocardial Infacrtion.


       b.    Socio - Economic and Cultural Factors


       Mang Undoy belongs to a nuclear family. He is married for 30 years with Aling
Fujiwara and has 6 children Mang Undoy and his wife and 4 children live in a 3m x 4m
shanty made from galvanized iron scraps and semi woods. The house has two windows
(2ft by 2 ft) made from galvanized iron fastened by woods.


       Mang Undoy finished 2nd year high school. When he was 20 yrs old, he started
working as a pig agent. Non he earns 50Phplpig sold with an average of 2000 php per
week. He usually works from 8am till 9pm looking for pig t sell. The monthly breakdown
of their expenses are as follows: water bill: Php 400, electric bill: Php 600, food: Ph
5,000. He smokes 1 pack of cigarette per day for 30 years now. He occasionally drinks
alcohol about 5 bottles of bee per week 500mllbottle.


       The family believe in witchcraft and sorcery. His elder sister works as a fortune
teller. They do consult to the alternative forms of medicines such as traditional healers
(albularyo and manghihilot) if illnesses arises but also reso^l to the hospital to seek
medical attention and assistance as necessary. The family uses common herbal plants
sucl as vitex negundo (lagundi) for fever through decoction preparation (3-51eaves), and
sidium guava (bayabas) fo cleaning wounds, decoction preparation as well (3-5 leaves).
The family also uses over the counter (OTC) drugs to manage common illness like
Paracetamol for fever, Loperamide for diarrhea, Robitusin for cough and coulds and
Mefenamic acid for pain such as headache.


       The patient loves to eat fatty foods; his favorite food actually is ~bulalo~ and
"chicharo~ He is also love drinking coffee, usually 2-3cups of coffee within a day. He
eats 2-3 times a day, usually large meals. He love! drinking siftdrinks as well about
500ml/day.


       As to the routine activities of daily living of the patient, his usual routine are the
following. At about 6:00 am the patient wakes up, do morning care, and eat his
breakfast. By 8:00, he will meet his other friend and start going house to house to find
pigs that can be sold. At around 11:30am, he will go home and eat his lunch. By
12:00nn-3pm he would take a rest, watch t.v. or take a nap. reading newspapers, and
listening to radio and take his lunch z around 12:00-1:00pm. By 3:30pm the patient
resumes roaming around until 9pm. And at around 10pm, the patient retires from the
whole day's activities and usually wakes up at around 6am in the morning. As to the
urinar elimination and bowel elimination of the patient, he usually urinates 5-6 times
within a day and defecates 1-2 times; day. The patient lives in community which he
described as polluted. Houses are not properly spaced and people usually dump their
trashes almost anywhere.


2.   FAMILY - HEALTH ILLNESS HISTORY (Refer to schematic diagram below)


       Mang Undoy belongs to a nuclear type of family wherein he lives with his wife
and six children. The patien has no information on the medical history of their
grandparents on both sides. His father died from heart attack hi mother has a DM and
died from the complications. They all have diabetes meliitus and his 3 older brothers and
sister died also from complications of DM
                                                             AMI/DM


                                                   54y/o      51y/o     49y/o    48 y/o
                                                   yo         yo        yo




3. HISTORY OF PAST ILLNESS


       When the patient was young, he suffered from occasional cough and cot,
measles, mumps and fever. At the age of 27 (1985), he was diagnosed of having DM II
and was prescribed oral medications. At the age of 47 (2005), hi had ameobiasis and
was prescribed metronidazole 500mg capsules twice a day for 7 days.


4. History of Present illness


       January-August 2009: Patient experienced chest pain which is bearable and can
be relieved by rest. He also experienced occasional headaches and difficulty of
breathing. He never sought professional advices for these symptoms because he usually
manages them with paracetamol for headache and rest for the other symptoms.


       October 7, 2009: at about 10:00 am, while the patient is drinking a glass of water
inside their house, hi suddenly experienced ch~stpain. He rested for a while and after
about 6 minutes the pain disappeared. At 2:00 pm while the patient is watching t.v. the
chest pain recurred, the patient felt weird because he has not done anything tha usually
provoke the(~ccg*nce of the pain. He became so worried because after 10 minutes of
resting and nc moving at all the pain did not disappear. After 20 minutes, the pain
became worst. He described the pain as Shari stabbing pain. He felt the pain becoming
worst and radiating to his left amn. He had also difficulty of breathing. Hi quickly called
the attention of his wife and together with his sister living nearby went to a secondary
public hospital ir Angeles City. He was admitted at 3:00 pm with primary diagnosis of to
consider acute myocardial infarction.


5. PHYSICAL EXAMINATION


Day 1: Upon Admission (Intensive Care Unit): October 07, 2009 at 3:00pm


(Lifted from the chart)


Vital signs:
BP: 140/100mmHg
Temp: 37.5°C/axilla
P R: 109bpm
R R: 38bpm
02 Sat: 97%


General Survey: Patient is conscious and coherent, appears weak and with guarded
behaviours.


Review of System:


HEENT: anicteric sclerae, pale palpebral conjunctive. Chest/Lungs: Symmetrical chest
expansion SCE, (-) retractions, (+1 basal rales (BLF),with orthopnea when in low
fowlers position, difficulty of breathing, use of accessory muscles in breathing,
chest pain scale of 10/10. Abdomen: flabby, normal abdominal bowel sounds, soft (-)
abdominal pain Genitourinary: (-)dysuria, (-) changes in bowel movement. Extremities: -
cyanosis, full and equal peripheral pulses Neurological: Glasgow Coma Scale (GCS) 15


Day 1 :(lntensive Care Unit): October 07, 2009


Nurses Notes (Lifted from the chart)
Vital signs: BP: 140/100mmHg Temp: 36.5°C/axilla P R: 109bpm R R: 36bpm 02 Sat:
97%


The patient appears weak; guarded behaviours noted; pale paipebral conjunctive;
bibasal rales noted; wit orthopnea when in low fowlers position; difficulty of
breathing; use of accessory muscles in breathing; coughing; chef pain scale of
10/10; Glasgow Coma Scale (GCS) 15


Day 2 :(lntensive Care Unit): October 08, 2009


Vital signs: BP: 140/100mmHg Temp: 36.9°C/axilla P R: 106bpm R R: 38bpm 02 Sat:
98%


The patient appears weak; guarded behaviours noted; pale palpebral conjunctive;
bibasal tales noted; Ate orthopnea when in low fowlers position; difficulty of
breathing; use of accessory muscles in breathing; coughing; chest pain scale of
6/10; Glasgow Coma Scale (GCS) 15


Day 3 :(lntensive Care Unit): October 09, 2009


Vital signs: BP: 130/100mmHg Temp: 38.1°C/axilla P R: 107bpm R R: 34bpm 02 Sat:
97%


General Survey: The patient was wearing white t-shirt and shorts and was sited on the
bed. He appears weak wit easy fatigability at times as noted during the interview
(pauses at times during conversation) but oriented a to time, place, name and person.


a. Skin: Has brown complexion, no lesions, cysts or nodules and edema noted. He has
good skin turgor.


b. Head/Scalp: Hair is thin, curly and short with some white hairs generally black in color
equally distribute upon inspection. No pediculosis, dandruff, scratches, lesions, swelling
or depressions. No abnormal masses, cysts, nodules and pain felt upon palpation of
scalp.
c. Eyes: Eyebrows and eyelashes are black in color, thin and evenly distributed, anicteric
sclera and pal, palpebral conjunctive noted. Pupils are equally round and reactive to light
and accommodation. The eye are able to move in cardinal directions and with (+)
blinking reflex. Upon palpation of the eyeballs, no pal is elicited.


d. Ears: Symmetrical and no abnormal discharges noted. No excess cerumen was
observed in the auditor canal upon inspection. Pain is not felt upon palpation of ears.


e. Nose: No nasal deviation. No nasal discharges, deformities and obstruction noted..
Nasal septum is intac and at the midline.


f. Mouth: With dark colored lips without cracks, dryness and smooth texture. Can purse
lips, with teeth siightl yellow in color without dental caries. Gums are dark in color and
tongue is pink and moist upon inspection Tonsils are not inflamed and uvula is located at
the midline under lighted penlight upon inspection.


9. Neck: Midline position, no deformities noted. With palpable carotid pulse, with minimal
jugular distensio^l noted. There is no weakness noted on sternocleidomastoid as
evidenced by head turning, neck flexior and extension. No abnormal mass, cysts,
nodules noted upon neck muscle palpation.


h. Chest and Lungs: With symmetrical chest expansion. No lesions and masses noted.


Heart: Adynamic precordium and heart rate is of normal rate and rhythm. No murmurs or
abnormal hear sounds heard upon auscultation such as S3 and S4 gallop.


j. Abdomen: Has normal contour, flabby. No lesions, masses, cysts, nodules and
deformities noted. Witl normal abdominal bowel sounds 10-15bowels sounds in all
quadrants, no masses, cysts nodules ant tenderness noted upon palpation.


k. Back and Spine: With normal curvature of the back and spinal column is straight. No
report of pain upo introduction of direct hit to the costovertebral area.
I. Upper and Lower Extremities: No clubbing of fingers and toes and cyanosis noted
however. All joints both upper and lower extremities are within normal limits, pain free,
passively and actively.


Neurological Assessment:


a. GCS Eye opening: 4 Verbal Response: Motor Response: Total:            15


b. Deep Tendon Reflex


       Finding: intact sense of smell CN II (Optic): Testing device: newspaper print
Finding: The patient was able to read newspaper print at 14inches distance. CN 111
(Oculomotor): Testing device: pencil to track object in upward and downward movement
Finding: The patient was able to track the object without difficulty. CN IV (Trochlear):
Testing device: pencil to track object in diagonal movements Finding: The patient was
able to track the object. CN V (Trigeminal): Testing device: food for chewing, cotton for
blinking reflex and sensation for face Finding: The patient was able to chew, with
blinking reflex and was able to feel light touch. CN Vi (Abducens): Testing device: pencil
to track object in lateral eye movement Finding: The patient was able to track the object.
CN Vll (Facial): Testing technique: ask the patient to do facial expression and use of
vinegar, salt, sugar and coffee to assess for taste sensation Finding: The patient was
able to smile, frown, grimace and pout. He was able to identify the different tastes. CN
Vlll (Vestibulocochlear): Testing device: Whisper test; Watch tick test. Finding: The
patient was able to repeat the whispered phrase and heard the watch ticking. CN IX
(Glossopharyngeal): Testing device: food for swallowing Finding: The patient was able to
swallow foods and fluids. CN X (Vagus): Testing device: tongue depressor Finding: The
patient gagged after the introduction of tongue depressor to posterior third of the tongue.
CN Xl (Accessory): Testing technique: ask the patient to do shoulder shrug. Finding: The
patient was able to do shoulder shrug with muscle grade of 5/5. CN Xll (Hypoglossal):
Testing technique: ask the patient to move tongue in all directions Finding: Patient was
able to moved tongue in all directions.


2nd Nurse-Patient interaction (Medicine Ward) October 14, 2009
Vital signs: BP: 100/80mmHg Temp: 36.8°C/axilla PR: 88bpm RR: 20bpm 02 Sat: 97%


General Survey: The patient was wearing white t-shirt and shorts and was sited on the
bed. He appears weak witl easy fatigability at times as noted during the interview
(pauses at times during conversation) but oriented a to time, place, name and person.


m. Skin: Has brown complexion, no lesions, cysts or nodules and edema noted. He has
good skin turgor.


n. Head/Scalp: Hair is thin, curly and short with some white hairs generally black in color
equally distributed upon inspection. No pediculosis, dandruff, scratches, lesions, swelling
or depressions. No abnorm^E masses, cysts, nodules and pain felt upon palpation of
scalp.


o. Eyes: Eyebrows and eyelashes are black in color, thin and evenly distributed,
anicteric sclera and pall palpebral conjunctive noted Pupils are equally round and
reactive to light and accommodation. The eye are able to move in cardinal directions and
with ~+) blinking reflex. Upon palpation of the eyeballs, no pail is elicited.


p. Ears: Symmetrical and no abnormal discharges noted. No excess cerumen was
observed in the auditor canal upon inspection. Pain is not felt upon palpation of ears.


q. Nose: No nasal deviation. No nasal discharges, deformities and obstruction noted..
Nasal septum is intac and at the midline.


r. Mouth: With dark colored lips without cracks, dryness and smooth texture. Can purse
lips, with teeth slightly yellow in color without dental caries. Gums are dark in color and
tongue is pink and moist upon inspectior Tonsils are not inflamed and uvula is located at
the midline under lighted penlight upon inspection.


s. Neck: Midline position, no deformities noted. With palpable carotid pulse, with minimal
jugular distensio^l noted. There is no weakness noted on sternocleidomastoid as
evidenced by head turning, neck flexior and extension. No abnormal mass, cysts,
nodules noted upon neck muscle palpation.
t. Chest and Lungs: With symmetrical chest expansion. No lesions and masses noted.


u. Heart: Adynamic precordium and heart rate is of normal rate and rhythm. No murmurs
or abnormal heal sounds heard upon auscultation such as S3 and S4 gallop.


v. Abdomen: Has normal contour, flabby. No lesions, masses, cysts, nodules and
deformities noted. Witl normal abdominal bowel sounds 10-15bowels sounds in all
quadrants, no masses, cysts nodules and tenderness noted upon palpation.


w. Back and Spine: With normal curvature of the back and spinal column is straight. No
report of pain UpOI introduction of direct hit to the costovertebral area.


x. Upper and Lower Extremities: No clubbing of fingers and toes and cyanosis noted
however. All joints both upper and lower extremities are within normal limits, pain free,
passively and actively.


Neurological Assessment:


c.   GCS     Eye opening: 4     Verbal Response:        5    Motor Response:      6   Total:
15


d. Deep Tendon Reflex


       Finding: intact sense of smell CN II (Optic): Testing device: newspaper print
Finding: The patient was able to read newspaper print at 14inches distance.CN 111
(Oculomotor): Testing device: pencil to track object in upward and downward movement
Finding: The patient was able to track the object without difficulty.
CN IV (Trochlear): Testing device: pencil to track object in diagonal movements Finding:
The patient was able to track the object.CN V (Trigeminal):         Testing device: food for
chewing, cotton for blinking reflex and sensation for face Finding: The patient was able
to chew, with blinking reflex and was able to feel light touch. CN Vl (Abducens): Testing
device: pencil to track object in lateral eye movement Finding: The patient was able to
track the object.CN Vll (Facial): Testing technique: ask the patient to do facial expression
and use of vinegar, salt, sugar and coffee to assess for taste sensation
Finding: The patient was able to smile, frown, grimace and pout. He was able to identify
the different tastes. CN Vlll (Vestibulocochlear): Testing device: Whisper test; Watch tick
test.Finding: The patient was able to repeat the whispered phrase and heard the watch
ticking. CN IX (Glossopharyngeal): Testing device: food for swallowing Finding: The
patient was able to swallow foods and fluids. CN X (Vagus): Testing device: tongue
depressorFinding: The patient gagged after the introduction of tongue depressor to
posterior third of the tongue. CN Xl (Accessory): Testing technique: ask the patient to do
shoulder shrug. Finding: The patient was able to do shoulder shrug with muscle grade of
515.CN Xll (Hypoglossal): Testing technique: ask the patient to move tongue in all
directions Finding: Patient was able to moved tongue in all directions.


3rd Nurse-Patient interaction (Medicine Ward) October 14, 2009


Vital signs: BP: 100/80mmHg Temp: 36.7°C/axilla PR: 89bpm RR: 22bpm 02 Sat: 98%


General Survey: The patient was wearing white t-shirt and shorts and was sited on the
bed. He appears weak witl easy fatigability at times as noted during the interview
(pauses at times during conversation) but oriented a! to time, place, name and person.


a. Skin: Has brown complexion, no lesions, cysts or nodules and edema noted. He has
good skin turgor.


b. Head/Scalp: Hair is thin, curly and short with some white hairs generally black in color
equally distribute upon inspection. No pediculosis, dandruff, scratches, lesions, swelling
or depressions. No abnorrna masses, cysts, nodules and pain felt upon palpation of
scalp.


c. Eyes: Eyebrows and eyelashes are black in color, thin and evenly distributed, anicteric
sclera and pall palpebral conjunctive noted. Pupils are equally round and reactive to light
and accommodation. The eye! are able to move in cardinal directions and with (+)
blinking reflex. Upon palpation of the eyeballs, no pail is elicited.
d. Ears: Symmetrical and no abnormal discharges noted. No excess cerumen was
observed in the auditor canal upon inspection. Pain is not felt upon palpation of ears.


e. Nose: No nasal deviation. No nasal discharges, deformities and obstruction noted..
Nasal septum is intac and at the midline.


f. Mouth: With dark colored lips without cracks, dryness and smooth texture. Can purse
lips, with teetl slightly yellow in color without dental caries. Gums are dark in color and
tongue is pink and moist upon inspection. Tonsils are not inflamed and uvula is located
at the midline under lighted penlight UpOI inspection.


g. Neck: Midline position, no deformities noted. With palpable carotid pulse, with minimal
jugular distension noted. There is no weakness noted on sternocleidomastoid as
evidenced by head turning, neck flexio~ and extension. No abnormal mass, cysts,
nodules noted upon neck muscle palpation.


h. Chest and Lungs: With symmetrical chest expansion. No lesions and masses noted.


i. Heart: Adynamic precordium and heart rate is of normal rate and rhythm. No murmurs
or abnormal hear


j. Abdomen: Has normal contour, flabby. No lesions, masses, cysts, nodules and
deformities noted. With normal abdominal bowel sounds 10-15bowels sounds in all
quadrants, no masses, cysts nodules and tenderness noted upon palpation.


k. Back and Spine: With normal curvature of the back and spinal column is straight. No
report of pain upon introduction of direct hit to the costovertebral area


1. Upper and Lower Extremities: No clubbing of fingers and toes and cyanosis noted
however. All jolts of both upper and lower extremities are within normal limits, pain free,
passively and actively


Neurological Assessment:
m. GCS Eye opening: 4 Verbal Response: Motor Response: Total:                  15


n. Deep Tendon Reflex


       Finding: Intact sense of smell CN 11 Optic): Testing device: newspaper print
Finding: The patient was able to read newspaper print at Winches distance. CN 111
(Oculomotor): Testing device: pencil to track object in upward and downward movement
Finding: The patient was able to track the object without difF culty. CN IV (Trochlear)
Testing device: pencil to track object in diagonal movements Finding: The patient was
able to track the object. CN V (Trigeminal): Testing device: food for chewing, cotton for
blinking reflex and sensation for face Finding: The patient was able to chew, with
blinking reflex and was able to feel light touch. CN Vl (Abducens): Testing device: pencil
to track object in lateral eye movement Finding: The patient was able to track the object.
CN Vll (Facial): Testing technique: ask the patient to do facial expression and use of
vinegar, salt, sugar and coffee to assess for taste sensation Finding: The patient was
able to smile frown, grimace and pout. He was able to identify the different tastes. CN
Vlll (Vestibulocochlear): Testing device: Whisper test; Watch tick test. Finding: The
patient was able to repeat the whispered phrase and heard the watch ticking. CN IX
(Glossopharyngeal): Testing device: food for swallowing Finding: The patient was able to
swallow foods and fluids. CN X (Various): Testing device: tongue depressor Finding: The
patient gagged after the introduction of tongue depressor to posterior third of the tongue.
CN Xl (Accessory): Testing technique: ask the patient to do shoulder shrug. Finding: The
patient was able to do shoulder shrug with muscle grade of 515. CN Xll (Hypoglossal):
Testing technique: ask the patient to move tongue in all directions Finding: Patient was
able to moved tongue in all directions.
6. DIAGNOSTICS AND LABORATORY FlNDlNGS

1 . Complete Blood Cou nt (CBC)

   DIAGNOSTIC/          DATE ORDERED(DO)       INDICATION/PURPOSE                  RESULTS     NORMAL       ANALSYS AND
   LABORATORY             DATE DONE (DD)                                                       VALUES     INTERPRETATION
   PROCEDURE           DATE RESULTS IN (DRI)                                                                OF RESULTS
Complete       Blood                           NDICATION/S                   OR
Count                                          PURPOSE'


                                               It   is     an      important
                                               screening t that includes
                                               RBC       cot     hemoglobin,
                                               hematocrit, R indices,
                                               with or without differen
                                               count and platelet count.


Hemoglobin             DO: 10-07-09            Total             hemoglobin 143g/L           140-180g/L   The result is within
                       DD: 10-07-09            measures          amount      of                           normal      values,
                                               hemoglobin present a                                       which indicates that
                       DO: 10-11-09            deciliter (dL or 100mL) 143g/L                             there is adequate
                       DD: 10-11-09            of   wh         blood.   It    is                          oxygen     carrying
                                               indicated for the pati to                                  capacity          of
                            help evaluate iron status                          erythrocytes to be
                            c     oxygen        carrying                       delivered       to     the
                            capacity of R B I                                  different    parts      of
                                                                               the body.


Hematocrit   DO: 10-07-09   It     measures         the 0.40      0.40-0.54    The result is within
             DD: 10-07-09   percentage volume of                               normal          values,
                            packed red blood Cal in                            which indicates that
             DO: 10-11-09   a whole blood sample 0.40                          there is adequate
             DD: 10-11-09   determine               the                        oxygen          carrying
                            percentage RBC's in the                            capacity                of
                            plasma. It indicated for                           erythrocytes to be
                            the patient to h evaluate                          delivered       to     the
                            iron status and ^O^Xy^s                            different    parts      of
                            carrying    capacity      of                       the     body.         This
                            RBC z hydration status                             could    mean         also
                            of the patient.                                    that    there    is    no
                                                                               alteration              of
                                                                               hydration status.


Leukocytes   DO: 10-07-09   The   leukocytes      count 8x109/L   5-10x109/L   The result is within
             DD: 10-07-09   measu the number of                                normal          values,
                             WBC's in a cu millimeter                   which indicates that
                             of blood. It is indical for                there        is        no
                             the patient to detect and                  presence                of
                             evaluate     presence     of               infection               as
                             infection        and      or               evidenced         by   no
                             inflammation and tissue                    signs                  and
                             necrosis.                                  symptoms                of
                                                                        infections such as
                                                                        fever and chills.


Lymphocytes   DO: 10-07-09   Lymphocytes produces 0.42      0.22-0.37   The result is above
              DD: 10-07-09   antibodies       responsible               the normal values,
                             for   allergic     reaction.               which means that
                             Monocytes              have                there                   is
                             phagocytic actions by                      inflammation
                             removing      dead      and                since       myocardial
                             injured      cells,     cell               cells are denied of
                             fragments               and                adequate 02 and
                             microorganisms. It was                     nutrients leading to
                             indicated for the patient                  hypoxemic
                             to determine degree of                     damage            causing
                             inflammation.                              cellular death and
                                                                                                                 tissue      necrosis,
                                                                                                                 part       of     the
                                                                                                                 mechanism
                                                                                                                 is       inflammatory
                                                                                                                 response.
                                                                                                                 Lymphocytes,
                                                                                                                 monocytes         and
                                                                                                                 count     are   within
                                                                                                                 normal values.




Nursing Responsibilities: Before:
         Tell the patient that the test requires a blood sample.
         Explain who will perform the yenipuncture and when.
         Explain to the patient that he may feel discomfort from the tourniquet and needle puncture. Instruct the patient need no to
          restrict food and fluids


During:
         Handle the sample gently to prevent hemolysis.
         Send sample to the laboratory immediately.
After:
        Apply direct pressure to the venipuncture site until bleeding stops.

  DIAGNOSTIC/                 DATE            INDICATION/PURPOSE                  RESULTS       NORMAL     ANALSYS AND
  LABORATORY             ORDERED(DO)                                                            VALUES   INTERPRETATION
  PROCEDURE             DATE DONE (DD)                                                                      OF RESULTS
                        DATE RESULTS
                             IN (DRI)
Creatinine             DO: 10-07-09           A routinary exam done 0.9                     0.4-1.4      The result is within
                       DD: 10-07-09           upon admission to assess                                   the normal values,
                                              glomerular filtration and to                               which indicates that
                                              screen for renal damage.                                   the kidneys are
                                              Serum creatinine levels                                    functioning well and
                                              provide a more sensitive                                   there is no apparent
                                              measure of renal damage                                    evidence of
                                              than     do    blood        urea                           inadequate renal
                                              nitrogen. It has also a                                    perfusion.
                                              direct   measurement           of
                                              glomerular filtration rate.
                                              Creatinine     is        excreted
                                              entirely by the kidneys
                                              and therefore is directly
                                              proportional        to      renal
excretory function.
It is indicated to the
patient to evaluate if there
is renal dysfunction
already in which a large
number of nephrons have
been destroyed due to
inadequate renal
perfusion secondary to
decreased cardiac output
as brought about by
decreased contractility of
the heart due to infarction.


It   measures       serum     of
sodium        in   relation   to
amount of water in the
body,    it    reflects   water
balance. It is


lso useful to evaluate
fluid, electrolyte,
Sodium      DO: 10-07-09   ~ hypernatremiat              140.8 mmol/L   135-150 mmol/L   The result is within
            DD: 10-07-09   hyponatremia) and acid-                                       normal range
                           base balance and related                                      which~ii~ the
                           renal and adrenal                                             patient does not
                           functions.                                                    have sodium
                                                                                         excess        or
                           This is indicated to the                                      depletion, more so,
                           patient to determine if                                       no further evidence
                           there is water, electrolyte                                   of acidbase
                           and acid-base balance                                         imbalances as well
                           since the patient is                                          as signs and
                           suffering from pulmonary                                      symptoms of
                           congestion.                                                   hyponatremia
                                                                                         neither
                           It measures serum levels                                      hypernatremia
                           of potassium, a major
Potassium   DO: 10-07-09   intracellular cation that     4.2 mmol/L     3,50-5.5mmol/L   The result is within
            DD: 10-07-09   helps maintain cellular                                       normal limits,
                           osmotic equilibrium;                                          which indicates
                           regulates muscles activity,                                   absence of
                           and aci-base; influences                                      electrolyte
                           renal function                                                imbalance. This
                             also suggests that
It is indicated to the       the kidneys are
patient since with           functioning
myocardial infarction, the   properly. The
necrotic cells become        patient        didn't
electrically inactive and    experience
their membranes become       arrhythmias/
disrupted, such that their
intracellular contents,      dysrhythmias within
including potassium, are     period of
released into the            hospitalization.
surrounding extracellular
fluid. This causes local
areas of hyperkalemia,
which can affect the
resting membrane
potentials of functioning
myocardial cells
which        may
cause
arrhythmias/dysrhythmias.
Nursing Responsibilities:

Before:
        Explain to the patient that the serum creatinine test evaluates kidney function.
        Tell the patient that the test requires a blood sample.
        Explain who will perform the venipuncture and when
        Explain to the patient that he may feel discomfort from the tourniquet and needle puncture. ·
        Instruct the patient need no to restrict food and fluids
During:
        Handle the sample gently to prevent hemolysis.
        Send sample to the laboratory immediately.
After:
        After: Apply direct pressure to the venipuncture site until bleeding stops.




3. Lipid Profile
                      DATE
                 ORDERED(DO);
DIAGNOSTIC/                                                                                         ANALYSIS AND
                   DATE DONE       INDICATION/S OR                                 NORMAL
LABORATORY                                                       RESULTS                        INTERPRETATION OF
                   (DD); DATE          PURPOSES                                    VALUES
PROCEDURE                                                                                              RESULTS
                   RESULTS IN
                      (DRI)



 Lipid Profile                  Lipid profile measures the
                                circulating levels of free
                                cholesterol              and
                                cholesterol    esters;     it
                                reflects the level of the
                                two forms in which this
                                biochemical compound in
                                the body. It is indicated to
                                the patient to assess the
                                risk for Coronary Artery
                                Diasease (CAD) and to
A. Cholesterol   DO: 10-07-09                                   5.8 (Increased)    Less than    The result is above the
                                screen for hyperlipidemia.
                 DD: 10-07-09                                                     5.18 mmol/L   normal range. Increased
                                Cholesterol,    a     sterol                                    cholesterol   level   could
                                found in animal tissue,                                         lead to development of
circulates in the blood in                  atheroma. Once there is
combination              with               endothelial injury excess
triglycerides and protein-                  fats     and     cholesterol
bound          phospholipids.               could assimilate at the
This complex is called a                    injured site together with
lipoprotein.                                monocytes,
                                            macrophages                and
    To assess the risk of
                                            platelets     forming     foam
Coronary Artery Disease
                                            cells.        Foam         cells
(CAD) and evaluation of
                                            engulfed the lipids and
fat metabolism
                                            smooth        muscle       cells
                                            developed.
                                            Consequently,            these
                                            smooth        muscle       cells
                                            reproduce        themselves
                                            and      synthesize         the
                                            connective tissues while
                                            they           subsequently
                                            proliferate             (intimal
                                            proliferation) making the
                                            intima thick, thus, plaque
                                            formation/atheroma
                                Less than
                                                                                        1.26 mmol/L   developed                which
                                                                                                      increases       the    risk    of
   B. Triglycerides   DO: 10-07-09                                    1.54(Increased)
                                                                                                      developing MI.
                      DD: 10-07-09
                                        Serum      triglycerides
                                                                                                      The result exceeds the
                                     provides          quantitative
                                                                                                      normal limits. Increased
                                     analysis of triglycerides,
                                                                                                      triglycerides     level could
                                     the main storage form of
                                                                                                      initiate development           of
                                     lipids,   which    constitute
                                                                                                      atheroma. Injury to the
                                     about 95% of fatty tissue.
                                                                                                      blood     vessel         cause
                                        Indicated to patient to                                       attraction of excess fats
                                     screen for hyperlipidemia                                        and              cholesterol,
                                     and to assess Coronary                                           macrophages,
                                     Artery Disease.                                                  monocytes and platelets
                                                                                                      leading   to foam            cells
                                                                                                      development           that      is
                                                                                                      responsible                    for
                                                                                                      atherogenesis posing the
                                                                                                      risk of MI to occur.



                                                                            29          >35mmol/L
                                        HDL is responsible for
                      DO: 10-07-09                                                                    The result is normal, that
C. High Density
                                     “reverse          cholesterol
                      DD: 10-07-09                                                                    means, at any rate, the
Lipoprotein (HDL)                  transport,” which return                                                HDL could participate in
                                   excess cholesterol from                                                 endothelial    repair    and
                                   the tissues to             the liver                                    decreases formation of
                                   metabolism.               It         also                               thrombosis.      More     so,
                                   participates in endothelial                                             within normal levels or
                                   repair     and            decreases                                     more     importantly     high
                                   thrombosis.                                                             levels of HDL maybe
                                                                                                           more protective for the
                                      It     is        indicated          to
                                                                                                           development                of
                                   patient        to    screen           for
                                                                                                           atherosclerosis than low
                                   hyperlipedemia                 and     to
                                                                                                           levels of HDL.
                                   assess Coronary Artery
                                   Disease.




                                     LDL is responsible for                                                The result is above the
                    DO: 10-07-09                                                  5.67       2.10 – 4.90
 D. Low Density                    the delivery of cholesterol                                             normal      range.       This
                    DD: 10-07-09                                               (Increased)    mmol/L
Lipoprotein (LDL)                  to the tissues. Serum                                                   signifies      that       an
                                   level of LDL are normally                                               increased               serum
                                   controlled           by        hepatic                                  concentration of LDL is a
                                   receptors for LDL that                                                  strong      indicator      of
                                   bind LDL and limit liver                                                coronary      risk.      LDL
                                   synthesis             of             this                               particles are the most
lipoprotein.                          atherogenic since they
                                      play a role in endothelial
   It     is        indicated   to
                                      injury, inflammation, and
patient        to    screen     for
                                      immune responses that
hyperlipedemia           and    to
                                      have been identified as
assess Coronary Artery
                                      being         important     in
Disease.
                                      atherogenesis. More so,
                                      when an excess of LDL
                                      is      produced,          LDL
                                      particles        adhere     to
                                      vulnerable        points    in
                                      arterial         endothelium.
                                      Here           macrophages
                                      ingest them, leading to
                                      formation of foam cells
                                      and     the    beginning    of
                                      plaque formation.           In
                                      addition, elevated levels
                                      of LDL combined with
                                      low     levels     of      HDL
                                      increase the risk for MI.
Nursing Responsibilities:

Before:

        Explain to the patient the purpose of the procedure.
        Tell the patient that the test requires a blood sample. Explain who will perform the venipuncture and when.
        Explain to the patient that he/she may experience slight discomfort from the tourniquet and needle puncture.
        Instruct patient to fast for 12 to 14 hours before the test.
        Notify the laboratory and physician of medications the patient is taking that may affect test results; it may be necessary to restrict
         them.


During:

        Perform a venipuncture and collect the sample in a 5 ml clot-activator tube.
        Send the sample to the laboratory immediately.
        Handle the sample gently to prevent hemolysis.
        Be aware that hemolysis caused by rough handling of the sample may influence test results.
        Be aware that hemolysis may elevate results.
After:

        Apply direct pressure to the venipuncture site until bleeding stop


4. Fasting Blood Sugar (FBS)
                    DATE
                ORDERED(DO)
DIAGNOSTIC/
                ; DATE DONE    INDICATION/S OR                         NORMAL       ANALYSIS AND INTERPRETATION OF
LABORATORY                                               RESULTS
                 (DD); DATE          PURPOSES                          VALUES                         RESULTS
PROCEDURE
                 RESULTS IN
                    (DRI)



Glucose (FBS)   DO: 10-07-09         The       fasting      6.81        4.20 –   The result is above the normal range.
                DD: 10-07-09   blood       sugar   or    (Increased)    6.40     Imbalance    between     coronary     supply       and
                               fasting        plasma                   mmol/L    myocardial demand secondary to coronary
                               glucose test is used                              occlusion will lead to myocardial O2 deficit
                               to measure plasma                                 which causes myocardial damage-death and
                               glucose levels after                              necrosis. The myocardial cells significantly
                               a 12-to 14hour fast.                              release catecholamines and norepinephrine.
                                                                                 Catecholamines       mediate   the     release      of
                                     This is indicated
                                                                                 glycogen, glucose, and stored fat from body
                               to patient to screen
                                                                                 cells. Therefore, plasma concentrations of free
                               for           diabetes
                                                                                 fatty acids and glycerol rise within 1 hour after
                               mellitus, in which
                                                                                 onset   of   acute    myocardial     infarction.    In
                               absence             or
                                                                                 addition, norepinephrine elevates blood sugar
                               deficiency of insulin
                                                                                 levels through stimulation of liver and skeletal
                               allows persistently
                                                                                 muscle cells. It also suppresses pancreatic B
                                        high glucose levels.                               cell activity which reduces insulin secretion and
                                                                                           elevates blood glucose further. Not surprisingly,
                                                                                           hyperglycemia is noted approximately 72 hours
                                                                                           after an acute myocardial infarction. In the case
                                                                                           of the patient, increased glucose was noted on
                                                                                           the 2nd day of hospitalization (05-07-08).




Nursing Responsibilities:

Before:

      Explain to the patient that this test detects disorders of the glucose metabolism and aids in the diagnosis of diabetes.
      Tell the patient that the test requires a blood sample. Explain who will perform the venipuncture and when.
      Explain to the patient that he may experience slight discomfort from the tourniquet and needle puncture.
      Instruct to the patient to fast for 12 hours to 14 hours before the test.
      Notify the laboratory and physician of medications the patient is taking that may affect test results; it may be necessary to restrict
       them.


During:

      Assist in performing a venipuncture and collect the sample in a 5 ml clot-activator tube.
      Send the sample to the laboratory immediately.
After:

        Apply direct pressure to the venipuncture site until bleeding stops.
        Provide a balanced meal or snack.
        Instruct the patient that he may resume his usual medications that were stopped before the test.




5. Troponin (Cardiac T)

                               DATE
  DIAGNOSTIC/             ORDERED(DO);                                                                            ANALYSIS AND
                                                     INDICATION/S OR                                NORMAL
  LABORATORY            DATE DONE (DD);                                           RESULTS                       INTERPRETATION
                                                          PURPOSES                                  VALUES
  PROCEDURE              DATE RESULTS                                                                              OF RESULTS
                              IN (DRI)



Troponin (Cardiac       DO: 10-07-09              The cardiac Troponin T is a      Positive          negative   The resultis positive,
          T)            DD: 10-07-09           protein in striated is extremely                                 though     there    is
                                               specific    cardiac      damage                                  evident increase of
markers that is released into        Creatinine          Kinase
the bloodstream after an injury.     Myocardial      Muscles
Elevation in Troponin T level        (CKMB), troponin T
can be seen within 1 hour of         on the other hand is
myocardial infarction (MI) and       on its normal limits.
will persist for 1 week or longer.   This    signifies     that
                                     there is no significant
  It is indicated to the patient
                                     reinfarction event that
to detect and diagnose acute
                                     happened             since
myocardial      infarction    and
                                     troponin            assays
reinfarction.
                                     (Troponin       I     and
                                     Troponin T) are more
                                     capable of detecting
                                     episodes                of
                                     myocardial
                                     reinfarction.        They
                                     rises   more        slowly
                                     than myoglobin and
                                     maybe       useful     for
                                     diagnosis               of
                                     reinfarction, even up
                                     to 3 to 4 days.
Nursing Responsibilities:

Before:

        Explain to the patient that this test helps assess myocardial injury and that multiple samples may be drawn to detect fluctuations
         in serum levels.
        Tell the patient that the test requires a blood sample. Explain who will perform the venipuncture and when.
        Inform the patient that he need not restrict food and fluids, and instruct him to maintain his prescribed medications and diet
         regimen.
        Explain to the patient that he may experience slight discomfort from the tourniquet and the needle puncture.



During:

        Perform a venipuncture and collect the specimen in a 7-ml clot-activator tube.
        Obtain each specimen on schedule and note the date and collection time one each.



After:

        Apply direct pressure to venipuncture site until bleeding stops.
6. Chest X-ray (Sitting)

                           DATE
                     ORDERED(DO);
 DIAGNOSTIC/                                                                                                       ANALYSIS AND
                       DATE DONE     INDICATION/S                                          NORMAL
 LABORATORY                                                       RESULTS                                     INTERPRETATION OF
                       (DD); DATE    OR PURPOSES                                           VALUES
 PROCEDURE                                                                                                           RESULTS
                       RESULTS IN
                           (DRI)


Chest X-ray AP      DO: 10-07-09
                                       To detect the          1.Atherosclerotic      Chest films show           There                     is
    (Sitting)       DD: 10-07-09
                                    status             of           aorta.           the              bony atherogenesis         at      the
                                    respiratory                                      structures      (ribs, aorta since the patient
                                    system. A chest x-        2. Cardiomegaly        sternum,                has               increased
                                    ray can be used to       with left ventricular   clavicles,              cholesterol level, wherein
                                    define                      prominence.          scapulae          and excess       lipids         could
                                    abnormalities      of                            upper portion of accumulate              within     the
                                    the lungs such as           3. Pulmonary         the     humerus). vessel wall and coalesce
                                    excessive       fluid,       congestion.         The          vertebral into a pool called the lipid
                                    pneumonia,                                       column is visible core              to            form
                                    bronchitis, asthma,                              vertically through atherosclerotic           plaque.
                                    cysts, and cancers                               the middle of the Furthermore,
                                    as well as exact                                 thorax. The two cardiomegaly              with      left
location and size        hemidiaphragms           ventricular     prominence
of the organs such       normally        appear occurred         since      the
as heart.                rounded, smooth patient had infarction, it
                         and             sharply loses its contractility at
   It is indicated to
                         defined; the right some degree because of
the      patient    to
                         hemidiaphragm is lack           of     response     to
determine          and
                         slightly         higher electrical         impulses,
evaluate      if there
                         than the left. The eventually the heart work
is/are
                         junction of the rib hard          to     meet      the
complication(s)
                         cage       and      the demand, it will enlarge
brought about by
                         diaphragm called significantly (hypertrophy
myocardial
                         the     costophrenic of the heart) as well as
infarction.
                         angle, is normally thickening             of       the
                         clearly visible and ventricles             as       a
                         angled.           Heart compensatory
                         tissue     is    dense mechanism.              Moreso,
                         and             appears cardiac                 tissue
                         white      but     less surrounding the area of
                         intensely         white infarction also undergoes
                         than              bone. changes          such      as
                         Normally            the myocardial remodeling, a
                         heart shadow is process                mediated    by
clearly     outlined, angiotensin                II,
extends primarily aldosterone,
on to the left side catecholamines,
of the thorax, and adenosine,                  and
occupies no more inflammatory          cytokines
than one third of which                      causes
the chest width. hypertrophy            of      the
Close observation myocardial         cells     and
shows            the sustained activation of
trachea     in   the neurohormonal
upper        middle compensatory
chest        almost mechanism                 which
superimposed          eventually increases wall
above the cervical stress in the ventricle
and         thoracic and thus to reduce wall
vertebra.        The stress,   the    myocardial
trachea bifurcates cells             hypertrophy
at the level of the (Laplace’s Law). On the
fourth      thoracic other hand, pulmonary
vertebra into the congestion          developed,
left       mainstem since           there        is
bronchi.         The cardiomegaly       imparing
                            pulmonary blood cardiac pumping leading
                            vessels, bronchi, to           decreased       cardiac
                            lymph nodes are output.             In   return,     left
                            located      in     the ventricular      hypertrophy
                            hilum on both the occurred                as           a
                            right     and       left compensatory
                            sides of the mid- mechanism.              The      right
                            thorax.            Lung side     of      the       heart
                            tissue       appears continuously                propel
                            black      on      x-ray blood    to     the     lungs,
                            film.       Vascular thereby, the left ventricle
                            lung       structures is unable to fully eject the
                            are      visible     as returning        blood        to
                            white, thin, wispy systemic               circulation
                            strings         fanning leading to congestion.
                            out       from      the
                            hilum.




Nursing Responsibilities:
Before:

        Make sure the patient has signed an appropriate consent form.
        Explain that the patient will be asked to a deep breath and hold it momentarily during the X-ray.
        Explain that the test takes less than 5 minutes.



During:

        The patient is instructed to sit in front of a stationary radiography machine.
        Post-anterior and left lateral views are obtained.



After:

        Check that no tubes have been dislodged during positioning.
        Whenever possible, place a lead apron over the patient’s abdomen to protect from exposure to radiation.
        To avoid radiation exposure, leave the area or wear lead shielding while the films are being taken.




7. Twelve (12) Lead Electrocardiogram (ECG)

   DIAGNOSTIC/                   DATE             INDICATION/S OR                                 NORMAL            ANALYSIS AND
                                                                              RESULTS
  LABORATORY                ORDERED(DO);             PURPOSES                                     VALUES           INTERPRETATION
  PROCEDURE         DATE DONE (DD);                                                                      OF RESULTS
                     DATE RESULTS
                         IN (DRI)



Twelve (12) Lead    DO: 10-07-09      To determine any           ST-segment                              ST   segment    is
Electrocardiogram   DD: 10-07-09      abnormal pumping             elevation                        elevated since there
     (ECG)                            action of the heart                                           is    alteration    and
                                                              Rate: A: 90/min
                                      and   to     indicate                     Rate:               delay                of
                                                                    V: 90/min
                                      presence           of                     A:60100/min         repolarization      and
                                      arrythmias                                V:60-100/min        depolarization
                                                                                                    properties     of   the
                                                              P: 0.08
                                                                                P:                  heart        due     to
                                                                                less than 0.11      impairement or even
                                                                                sec.                lack of response to
                                                              P-R: 0.20
                                                                                P-R:                electrical    impulses
                                                                                0.12 to 0.20 sec.   secondary            to
                                                              QT:0.36
                                                                                QT:                 prolonged
                                                                                up to 0.42 sec.     ischemia/infarction of
                                                              QRS: 0.06
                                                                                QRS:                the myocardial cells
                                                                                0.04-0.11           including     all   the
                                                                                                    layers of the heart. It
                                                                                                    also signifies that the
                                                                                                             area    of      infarction
                                                                                                             extends to the zone
                                                                                                             of   injury     which   is
                                                                                                             significantly
                                                                                                             developed,       wherein
                                                                                                             ischemic          tissues
                                                                                                             produces                an
                                                                                                             elevation in the ST
                                                                                                             segment. More so,
                                                                                                             there   is    prolonged
                                                                                                             period of decreased
                                                                                                             blood supply to the
                                                                                                             heart    causing        an
                                                                                                             infarction.




Nursing Responsibilities:

Before:

      Check doctor’s order.
      Verify patient’s name in the chart with the actual patient.
      Explain that the procedure is done to detect abnormalities in the electrical activity of the heart.
        Reassure the client that he will not receive any electrical shock or impulses.
        Remove any metal object from the patient (e.g. belt buckle, coins, zipper).



During:

        Provide privacy to the patient.
        Secure electrodes to appropriate locations on chest and extremities.
        Instruct the patient to remain still during the procedure.



After:

        Secure results.
        Write the patient’s name, age and diagnosis in the result and attach it to his chart.
        Document the time and the procedure done.
        Refer results to the physician.
ANATOMY AND PHYSIOLOGY OF THE HEART AND BLOOD VESSEL

SIZE, FORM, and LOCATION of the HEART



        The adult heart is shaped like a blunt cone is approximately the size of a
closed fist. Its larger in physcically active adults than in less active but otherwise
healthy adults, and it generally decreases in size after approximately age 65,
especially in those who are not physically active. The blunt, rounded point of the
cone is the apex: and the larger; flat part at the opposite end of the cone is the
base.




                  Figure 1. Location of the Heart in the Thorax

        The heart is located in the thoracic cavity between the two pleural cavities,
which surround the lungs. The heart, trachea, esophagus, and associated
structures from a midline partition the mediastinum (see figure 1). The heart is
surrounded by its own cavity, the pericardial cavity.

        The heart lies obliquely in the mediastinum, with its base directed
posteriorly and slightly superiorly and the apex directed anteriorly and slightly
inferiorly. The apex is also directed to the left so that approximately two-thirds of
the heart’s mass lies to the left of the midline sternum. (see figure 1.). The base
of the heart is located deep to the sternum and extends to the second
intercostals space. The apex is located deep to the left fifth intercostals space,
approximately 7-9centimeters (cm) to the left of the sternum near the
midclavicular line, which is perpendicular line that extends down from the midline
of the clavicle (see figure 1.).

ANATOMY OF THE HEART

       The heart is surrounded by the pericardial cavity. The pericardial cavity is
formed by the pericardium, or pericardial sac, which surrounds the heart and
anchors it within the mediastinum (see figures 1 and 2). The pericardium consists
of two layers. The tough, fibrous connective tissue outer layer is called the
fibrous pericardium and the inner layer of flat epithelial cells, with a thin layer of
connective tissue, is called the serous pericardium. The portion of the serous
pericardium lining the fibrous pericardium is the parietal pericardium, whereas
the portion covering the heart surface is the visceral pericardium, or
epicardium. The parietal and visceral pericardium are continuous with each
other where the great vessels enter or leave the heart. The pericardial cavity,
located between the visceral and parietal pericardia, is filled with a thin layer of
pericardial fluid produced by the serous pericardium. The pericardial fluid helps
reduce friction as the heart moves within the pericardial sac.

                                                           EXTERNAL ANATOMY




                                                                  The right and left
                                                           atria are locate at the
                                                           base of the heart, and
                                                           the    right   and     left
                                                           ventricles extend from
the base of the heart toward the apex (figure 3). A coronary sulcus extends
around the heart, separating the atria from the ventricles. In addition, two
grooves, or sulci, which indicate the division between the right and left ventricles,
extend inferiorly from the coronary sulcus. The anterior interventricular suclus
extends inferiorly from the coronary sulcus. The anterior interventricular sulcus
extends inferiorly from the coronary sulcus on the anterior surface of the heart,
and the posterior interventricular sulcus extends inferiorly from the coronary
sulcus on the posterior surface of the heart (see figure 3).

                  Figure 3. Anterior and Posterior Surface View of the Heart




       Six large veins carry blood to the heart (see figure 3); the superior vena
cava and inferior vena cava carry blood from the body to the right atrium, and
four pulmonary veins carry blood from the lungs to the left atrium. Two arteries,
the pulmonary trunk and the aorta, exit the heart. The pulmonary trunk, arising
from the right ventricle, splits into the right and left pulmonary arteries, which
carry blood to the lungs. The aorta, arising from the left ventricle, carries blood to
the rest of the body.

Blood Supply to the Heart

Coronary Arteries

       Cardiac muscle in the wall of the heart is thick and metabolically very
active. Two coronary arteries supply blood to the wall of the heart (figure 5). The
coronary arteries originate from the base of the aorta, just above the aortic
semilunar valves. The left coronary artery originates on the left side of the aorta.
It has three major branches: The anterior interventricular artery lies in the anterior
interventricular sulcus, the circumflex artery extends around the coronary sulcus
on the left to the posterior surface of the heart, and the left marginal artery
extends inferiorly along the wall the lateral wall of the left ventricle from the
circumflex artery. The branches of the left coronary artery supply much of the
anterior wall of the heart and most of the left ventricle. The right coronary artery
originates on the right side of the aorta. It extends around the coronary sulcus on
the right to the posterior surface of the heart and give rise to the posterior
interventricular artery, which lies in the posterior interventricular artery, which lies
in the posterior interventricular sulcus. The right marginal artery extends inferiorly
along the lateral wall of the right ventricle. The right coronary artery and its
branches supply most of the wall of the right ventricle.

Cardiac Veins

       The cardiac veins drain blood from the cardiac muscle. Their pathways
are nearly parallel to the coronary arteries and most drain blood into the coronary
sinus, a large vein located within the coronary sulcus on the posterior aspect of
the heart. Blood flows from the coronary sinus into the right atrium (see figure 4).
Some small cardiac veins drain directly into the right atrium.

Heart Chambers and Internal Anatomy

       The heart is a muscular pump consisting of four chambers; two atria and
two ventricles (figure 6).
Right and Left Atria

       The right atria of the heart receive blood from veins. The atria function
primarily as reservoirs; where blood returning from veins collects before it enters
the ventricles. Contraction of the atria forces blood into the ventricles to complete
ventricular filling. The right atrium receives blood through three major openings.
The superior vena cava and the inferior vena cava drain blood from most of the
body (see figure 6), and the smaller coronary sinus drains blood from most of the
heart muscle. The left atrium receives blood through the four pulmonary veins
(see figure 6), which drain blood from the lungs. The two atria are separated from
each other by a partition called the interatrial (between the atria) septum.




Right and Left Ventricles

       The ventricles of the heart are its major pumping chambers. They eject
blood into the arteries and force it to flow though the circulatory system. The atria
open into the ventricles, and each ventricle has one large outflow route located
superiorly near the midline of the heart. The right ventricle pumps blood into the
pulmonary trunk, and the left ventricle pumps blood into the aorta. The two
ventricles are separated from each other by the muscular interventricular
(between the ventricles) septum (see figure 6).

       The wall of the left ventricle is thicker than the wall of the right ventricle,
and the wall of the left ventricle contracts more forcefully and generates a greater
blood pressure than the wall of the right ventricle. When the left ventricle
contracts, the pressure increases to approximately 120mmHg. When the right
ventricle contracts, the pressure increases to approximately one-fifth of the
pressure in the left ventricle. However, the left and right ventricles pump nearly
the same volume of blood. The higher pressure generated by the left ventricle
moves blood through the larger systemic circulation, whereas the lower pressure
generated by the right ventricle moves blood through the smaller pulmonary
circulation (see figure 6).
Heart Valves

       The atrioventricular (AV) valves are located between the right atrium
and the right ventricle and the left atrium and the left ventricle. The AV valve
between the right atrium and the right ventricle has thee cusps and is called the
tricuspid valve (see figure 7). The AV valve between the left atrium and left
ventricle has two cusps and is called the bicuspid, or mitral valve (resembling a
bishop’s miter, a two-pointed hat) valve (see figures 7). These valves allow blood
to flow from the atria into the ventricles but prevent it from flowing back into the
atria. When the ventricles relax, the higher the pressure in the atria forces the AV
valves to open and blood flows from the atria into the ventricles (figure 7). In
contrasts, when the ventricles contract, blood flows toward the atria and causes
the AV valves to close (figure 7).




                        Figure 7. Function of the Heart Valves

       Each ventricle contains cone-shaped muscular pillars called papillary
muscles are attached by thin, strong connective tissue strings called chordae
tendineae to the free margins of the cusps of the atrioventricular valves. When
the ventricles contract, the papillary muscles contract and prevent the valves
from opening into the atria by pulling on the chordae tendineae attached to the
valve cusps (see figure 7).

        The aorta and pulmonary trunk posses aortic and pulmonary
semilunar(halfmoon-shaped) valves, respectively (see figure 7). Each valve
consists of three pocketlike semilunar cusps (see figure 7). When the ventricles
relax, the pressure in the aorta is higher than in the ventricles and pulmonary
trunk. Blood flows back from the aorta or pulmonary trunk toward the ventricles,
and enters the pockets of the cusps, causing them to bulge toward and meet in
the center of the aorta or pulmonary trunk, thus closing the vessels and blocking
blood flow back into the ventricles (see figure 7).

        A plate of fibrous connective tissue, sometimes called the cardiac
skeleton, consisting mainly of fibrous rings around the atrioventricular and
semilunar valves, provides a solid support for the valves (see figure 7). This
connective tissue plate also serves as electrical insulation between the atria and
the ventricles and provides a rigid site of attachment for cardiac muscle.

Route of Blood Flow Through the Heart

        The route of blood flow through the heart is depicted in figure 8. Even
though blood flow through the heart is described for the right and then left side of
the heart, it is important to understand that both atria contract at the same time,
and both ventricles contract at the same time. This concept is most important
when the electrical activity, pressure changes, and heart sounds are considered.

        Blood enters the right atrium from the systemic circulation through the
superior and inferior vena cava, and from heart muscle through the superior and
inferior vena cava, and from the heart muscle through the coronary sinus (see
figure 8). Most of the blood flowing into the right atrium flows into the right
ventricle while the right ventricle relaxes following the previous contraction.
Before the end of ventricular relaxation, the right atrium contracts, and enough
blood is pushed from the right atrium into the right ventricle to complete right
ventricular filling.
                      Figure 8: Blood Flow Through the Heart

       Following right atrial contraction, the right ventricle begins to contract.
Contraction of the right ventricle pushes blood against the tricuspid valve, forcing
it closed. After pressure within the right ventricles increases, the pulmonary
semilunar valve is forced open, and blood flows into the pulmonary trunk. As the
right ventricle relaxes, its pressure falls rapidly, and pressure in the pulmonary
trunk becomes greater than in the right ventricle. The back-flow of blood forces
the pulmonary semilunar valve to close.

       The pulmonary trunk branches to form the right and left pulmonary
arteries, which carry blood to the lungs, where carbon dioxide is released and
oxygen is picked up. Blood returning from the lungs enters the left atrium through
the four pulmonary veins (see figure 8). Most of the blood flowing into the left
atrium passes into the left ventricular while left ventricle relaxes following the
previous contraction. Before the end of ventricular relaxation, the left atrium
contracts, and enough blood is pushed from the left atrium into the left ventricle
to complete left ventricular filling.

       Following left atrial contraction, the left ventricle begins to contract.
Contraction of the left ventricle pushes blood against the bicuspid valve, forcing it
closed. After pressure within the left ventricle increases, the aortic semilunar
valve is forced open, and blood flows into the aorta (see figure 8). Blood flowing
through the aorta is distributed to all parts of the body, except to that part of the
lung supplied by the pulmonary blood vessels. As the left ventricle relaxes, its
pressure falls rapidly, and pressure in the aorta becomes greater than in the left
ventricle. The back-flow of blood forces the aortic semilunar valve to close.

Histology of the Heart

Heart Wall

       The heart wall is composed of three layers of tissue: the epicardium, the
myocardium, and the endocardium (figure 9). The epicardium, is also called
visceral epicardium, a thin serous membrane forming the smooth outer surface
of the heart. It consists of simple squamous epithelium overlying a layer or loose
connective tissue and fat. The thick middle layer of the heart, the myocardium,
is composed of cardiac muscle cells and is responsible for the ability of the heart
to contract. The smooth inner surface of the heart chambers is endocardium,
which consists of simple squamous epithelium over a connective tissue. The
endocardium allows blood to move easily through the heart. Each heart valve is
formed by a fold of endocardium which connective tissue between two layers.

       The surfaces of the interior walls of the ventricles are modified by ridges
and columns of cardiac muscle. Smaller muscular ridges are found in portions of
the atria.




                                Figure 9: Heart Wall

Cardiac Muscle

       Cardiac muscles are elongated, branching cells that contain one, or
occasionally two, centrally located nuclei (figure 10). The cardiac muscle cells
contain actin and myosin myofilaments organized to form sacromeres, which are
joined end-to-end to form myofibrils. The actin and myosin myofialments are
responsible for muscle contraction, and their organization gives cardiac muscle a
(branded) appearance. The striations are less regularly arranged and less
numerous than is the case in skeletal muscle.

      Adenosine triphosphate (ATP) provides the energy for cardiac muscle
contraction, and, as in other tissues, ATP production depends on oxygen
availability. Cardiac muscle cells are rich in mitochondria, which produce ATP at
a rate rapid enough to sustain the normal energy requirements of cardiac
muscles. An extensive capillary network provides an adequate oxygen supply to
cardiac muscle cells. Unlike skeletal muscle, however, cardiac muscle cannot
develop a significant oxygen debt. Development of large oxygen debt could result
in muscular fatigue and cessation of cardiac muscle contraction.




                          Figure 10. Cardiac Muscle Cells

      Cardiac muscle cells are organized into spiral bundles or sheets. The cells
are bound end-to-end and laterally adjacent cells by specialized cell-to-cell
contracts called intercalated disks (see figure 10). The membranes of the
intercalated disks are highly folded, and the adjacent cells fit together, greatly
increasing contract between them. Specialized cell membrane structures in the
intercalated disks called gap junctions reduce electrical resistance between
cells, allowing action potentials to pass easily from one cell to adjacent cells. The
cardiac muscle cells of the atria or ventricles, therefore, contract at nearly the
same time. The highly coordinated contractions of heart depend on this
characteristics.

Electrical Activity of the Heart

Action Potential in Cardiac Muscles




        Figure 11: Comparison of Action Potentials in Skeletal and Cardiac Muscle

       Like action potential muscle and neurons, those in cardiac muscle exhibit
depolarization followed by repolarization of the resting membrane potential. In
cardiac muscle, however, the plateau phase. Which is period of slow
repolarization, greatly prolongs the action potential (see figure 11). In contrast to
action potentials in skeletal muscle, which take less than 2 miliseconds (ms) to
complete, action potentials in cardiac muscle take approximately 200 to 500 ms
to complete.
       Unlike in skeletal muscle, action potentials in cardiac muscles are
conducted from cell to cell. Not only does the action potential take longer, but the
rate of conduction in cardiac muscle cells is slower than the rate of conduction of
action potential in skeletal muscle cells and neurons.

       In cardiac muscle each potential consists of a rapid depolarization phase
followed by a rapid, but partial early repolarization phase. Then a longer period
of slow repolarization, called the plateau phase, occurs. At the end of the
plateau phase, a more rapid final repolarization phase takes place. During the
final repolarization phase the membrane potential returns to its resting level (see
figure 11).

       Changes in membrane channels are responsible for the changes in the
permeability of the cell membrane that produce action potentials. The
depolarization phase of the action potential results from three permeability
changes. Voltage-gated sodium channel open, increasing the permeability of the
cell membrane to sodium. Sodium ions then diffuse into cell, causing
depolarization. Voltage-gated potassium channels quickly close, decreasing
the permeability of the cell membrane to potassium. The decreased diffusion of
potassium out the cell also causes depolarization. Voltage-gated calcium
channels slowly open, increasing the permeability of the cell membrane to
calcium. Calcium ions then diffuse into cell and cause depolarization. It is not
until the plateau phase that most of the voltage-gated calcium channels are
opened.

       Early repolarization occurs when the voltage-gated sodium channels close
and a small number of voltage-gated potassium channels open. Diffusion of
sodium into cells stops, and there is some movement of potassium out of the cell.
These changes in ion movement result in an early, but small repolarization.

       The plateau phase occurs as voltage-gated calcium channels continue to
open, and the diffusion of calcium into the cell counteracts the potential change
produced by the diffusion of potassium out of the cell. The plateau phase ends
and final repolarization begins as the voltage-gated calcium channels close, and
many voltage-gated potassium channels open. Diffusion of calcium into the cell
decreases and diffusion of potassium out of the cells increases. These changes
cause the membrane potential to return to resting level.

       Action potentials in cardiac muscle exhibit a refractory period, like that of
action potentials in skeletal muscle and in neurons. The refractory period lasts
about the same length of time as the prolonged action potential in cardiac
muscle. The prolonged action potential and refractory period allow cardiac
muscle to contract and almost complete relaxation to take place before another
action potential can be produced. Also, the long refractory period in cardiac
muscle prevents titanic contractions from occurring, thus ensuring a rhythm of
contraction and relaxation for cardiac muscle. Therefore, action potentials in
cardiac muscle are different from those in skeletal muscle because of the plateau
phase, which makes the action potential and its refractory period last longer.

       The sinoartial (SA) node, which functions as the pacemaker of the heart,
is located in the superior wall of the right atrium and initiates the contraction of
the heart. The SA node is the pacemaker because it produces action potentials
at a faster rate than other areas of the heart. The action potential of the SA node
acts as a stimulus to adjacent areas of the heart. Also, the SA node action
potentials have characteristics that are somewhat different from action potentials
in the rest of the cardiac muscles. The SA node has a larger number of voltage-
gated calcium channels than other areas of the heart. As soon as the resting
membrane potential is reestablished after an action potential, some of the
voltage-gated calcium channels open spontaneously. As they open, Calcium
begin to diffuse into the cell and cause depolarization. The depolarization
stiumulates additional voltage-gated calcium channels to open and voltage-gated
sodium to open. Thus, additional calcium and sodium diffuse into the cell and
cause further depolarization. Quickly, threshold is reached and another action
potential is produced. Drugs called calcium channel blocking agents are used to
treat some types of tachycardia (rapid heart rate) and arrhythmia (abnormal
rhythm) because they block calcium channels and slow the rate of action
potential production.

Conduction System of the Heart

       Contraction of the atria and ventricles is coordinated by specialized
cardiac muscles cells in the wall of the heart that form the conduction system
of the heart (see figure 12). Action potentials originate in the SA node and
spread over the right and left atria, causing them to contract.

       A second are of the heart, called atrioventricular (AV) node, is located in
the lower portion of the right atrium. When action potentials reach the AV node,
they spread slowly through it and then into a bundle of specialized cardiac
muscle called the atrioventricular bundle. The slow rate of action potential
conduction in the AV node allows the atria to complete their contraction before
the action potentials are delivered to the ventricles.




                        Figure 12: Conduction System of the Heart



       After action potentials pass through the AV node, they are transmitted
though the AV bundle, which projects through the fibrous connective tissue plate
that separates the atria from the atria from the ventricles (see figure 12). The AV
bundle then divides into two branches of conducting tissue called the left and
right bundle branches (see figure 12). At the tips of the left and right bundles
branches, the conducting tissue forms many small of Purkinje fibers. The
Purkinje fibers pass to the apex of the heart and then extend to the cardiac
muscle of the ventricle walls. The AV bundle, the bundle branches and the
Purkinje fibers are composed of specialized cardiac muscles fibers that conduct
action potentials more rapidly than do other cardiac muscles fibers.
Consequently, action potentials are rapidly delivered to all cardiac muscle of the
ventricles. The coordinated contraction of the ventricles depends on the
conduction of action potentials by the conduction system.

       Following their contraction, the ventricles begin to relax. After the
ventricles have completely relaxed, another action potential originates in the SA
node to begin the next cycle of contractions.

       The SA node is the pacemaker of the hart, but other cardiac muscle cells
also are capable of producing action potentials spontaneously. For example, if
the SA node is unable to function, another of the heart, such as the AV node,
becomes the pacemaker. The resulting heart rate is much slower than normal.
When action potentials originate in an area of the heart other than the SA node,
the result is called an ectopic beat.
The major events of the cardiac cycle are:

   1. As systole begins, contraction of the ventricles pushes blood toward the
       atria, causing the AV valves to close. When the pressure in the ventricles
       exceeds the pressure in the pulmonary trunk and aorta, the seminulunar
       valves are forced open, and blood is ejected into the pulmonary trunk and
       aorta (see figure 14).
   2. At the beginning of ventricular diastole, the pressure in the ventricules
       decreases. The semilunar valves close and prevent blood from flowing
       back into the ventricles. The pressure continues to decline in the ventricles
       until finally the AV valves open and blood flow directly from the atria into
       the relaxed ventricles. During the previous ventricular systole, the atria
       were relaxed and blood collected in them. When the ventricles relax and
       the AV valves open, blood flows into the ventricles (see figure 14, step 2)
       and fills them to approximately 70% of their volume.
   3. At the end of ventricular diastole, the atria contract and then relax. Atrial
       systole forces additional blood to flow into the ventricles to complete their
       filling (see figure 14, step 3). The semilunar valves remain closed.



       Figure 15. Displays the interval the main events of the cardiac cycle in the
graphic form and should be examined from the top to bottom for each period of
the cardiac cycle. The ECG indicates the electrical events that cause contraction
and relaxation of the atria and ventricles. The pressure graph shows the pressure
changes within the left atrium, left ventricle, and aorta resulting from the atrial
and ventricular contraction and relaxation. The pressure changes on the right
side of the heart are not shown here, but are similar to those in the left side, only
lower. The volume graph presents the changes in ventricular volume as blood
flows into and out of the left ventricle as a result of the pressure changes. The
sound graph records the closing of the valves caused by blood flow. See figure
14 for illustration of the valves and blood flow.
                      Events Occurring During the Cardiac Cycle

Heart Sounds

       A stethoscope was originally developed to listen to the sounds of the
lungs and heart and is now used to listen to other sounds of the body. There are
two main heart sounds. The first heart sound can be represented by the syllable
lubb, and the second heart sound can be represented by dubb. The first heart
sound has a lower pitch than the second. The first heart sound occurs at the
beginning of ventricular systole and results from closure of the AV valves (see
figure 14 step 1 and 15). The second heart sound occurs at the beginning of
ventricular diastole and results from closure of the semilunar valves (see figure
14 step 2 and 15). The valves usually do not make sounds when they open.

       Clinically, ventricular systole occurs between the first and second heart
sounds. Ventricular diastole occurs between the second heart sound and the first
heart sound of the next beat.

       Abnormal heart sounds called murmurs are usually a result of faulty
valves. For example, an incompetent valve fails to close tightly and blood leaks
through the valve makes a swishing sound immediately after closure of the valve.
For example, an incompetent bicuspid valve results in a swishing sound
immediately after the first heart sound.
       When the opening of a valve is narrowed, or stenosed, a swishing sound
precedes closure of the stenosed valve. For example, when the bicuspid valve is
stenosed, a swishing sound precedes the first heart sound.

Regulation of the Heart Function

       Cardiac Output (CO) is the volume of blood pumped by either ventricle of
the heart each minute. Cardiac output can be calculated by multiplying the stroke
volume times the heart rate. Stroke volume (SV) is the volume of blood pumped
per ventricle each time the heart contracts, and the heart rate (HR) is the
number of times the heart contracts each minute.




                     CO      =     SV     X        HR

                  (mL/min)       (mL/beat)      (beats/min)

       Under resting conditions, the heart rate is approximately 72 beats/min (or
bpm) and the stroke volume is approximately 70 mL/beat. Consequently, the
cardiac output is slightly more than 5 L/min:




                     CO      =     SV     X        HR

                             =     70 mL/beat X 72 bpm

                             =     5040 mL/min (approximately 5 L/min)




       The heart rate and the stroke volume vary considerably among people.
Athletes tend to have a larger stroke volume and lower heart rate at rest because
exercise has increased the size of their hearts. Nonathletes are more likely to
have a higher heart rate and lower stroke volume. During exercise the heart in a
nonathelete can increase to 190 bpm and the stroke volume can increase to
115mL/beat. Therefore, the cardiac output increases to approximately 22 L/min:




                     CO     =      SV     X      HR

                            =      115 mL/beat X 190 bpm

                            =      21,850 mL/min (approximately 22 L/min)

This produces a cardiac output that is several times greater than the cardiac
output under a resting conditions. Athletes can increase their cardiac output to a
greater degree than nonathletes.

       The control mechanisms that modify the stroke volume and the heart rate
are classified as intrinsic and extrinsic mechanisms.

Intrinsic Regulation of the Heart

       Intrinsic regulation of the heart refers to the mechanisms contained
within the heart itself. The force of contraction produced by cardiac muscle is
related to the degree of stretch of cardiac muscle fibers. The amount of blood in
the ventricles at the end of ventricular diastole determines the degree to which
cardiac muscle fibers are stretched. Venous return is the amount of blood that
returns to the heart, and the degree to which the ventricular walls are stretched at
the end of diastole is called preload. If venous return increases, the heart fills to
greater volume and stretches cardiac muscle fibers, producing and increased
preload. In response to the increased preload, cardiac muscle fibers contract with
a greater force. The greater force of contraction causes an increased volume of
blood to be ejected from the heart, resulting in resulting in an increased stroke
volume. As venous return increases, resulting in an increased preload, cardiac
output increases. Conversely, if venous return decreases, resulting in a
decreased preload, the cardiac output decreases. The relationship between
preload and stroke volume is called Starling’s law of the heart.
      Because venous return is influenced by many conditions, Starling’s law of
the heart has a major influence on cardiac output. For example, muscular activity
during exercise caused increased venous return, resulting in an increased
preload, stroke volume and cardiac output. This is beneficial because an
increased cardiac output is needed during exercise to supply oxygen to
exercising skeletal muscles.

      Afterload refers to the pressure against which the ventricles must pump
blood. People suffering from hypertension have an increased afterload because
they have an elevated aortic pressure during contraction of the ventricles. The
heart must do more work to pump blood from the left ventricle into the aorta,
which increases the workload on the heart and can eventually lead to heart
failure. A reduced afterload decreases the work the heart must do. People who
have a lower blood pressure have a reduced afterload and develop heart failure
less often than people who have hypertension. The afterload, however,
influences cardiac output less than preload influences it. The afterload must
increase substantially before it decreases the volume of blood pumped by a
healthy heart.




Extrinsic Regulation of the Heart

      Extrinsic regulation refers to the mechanisms external to the heart, such
as either hormonal or nervous regulation (see figure 16). Nervous influences are
carried through the autonomic nervous system. Both sympathetic and
parasympathetic nerve fibers innervate the heart, and have a major effect on the
SA node. Stimulation by sympathetic nerve fibers causes the heart rate and the
stroke volume to increase, whereas stimulation by parasympathetic nerve fibers
causes the heart rate to decrease.
                    Figure 16. Baroreceptors and Chemoreceptor Reflexes

       The baroreceptor reflex plays an important role in regulating the function
of the heart. Baroreceptors are stretch receptors that monitor blood pressure in
the aorta and in the wall of internal carotid arteries, which carry blood to the brain
(see figure 16). Changes in blood pressure result in changes in the stretch of the
walls of these blood vessels. Thus, changes in blood pressure cause changes in
the frequency of action potentials produced by the baroreceptors. The action
potentials are transmitted along nerve fibers from the stretch receptors to the
medulla oblongata of the brain.

       Within the medulla oblongata of the brain is a cardiogulatory center,
which receives and integrates action potentials from the baroreceptors. The
cardioregulatory center controls the action potential frequency in sympathetic and
parasympathetic nerve fibers that extend from the brain and spinal cord to the
heart. The cardioregulatory center also influences sympathetic stiumulation of the
adrenal gland (see figure 16). Epinephrine and norepinenephrine, released from
the adrenal gland increase the stroke volume and heart rate.
         When the blood pressure increases, the barorecptors are stiumulated.
There is increased frequency of action potentials, sent along the nerve fibers to
the medulla oblongata of the brain. This prompts the cardioregulatory center to
increase parasympathetic stimulation and to decrease sympathetic stimulation of
the heart. As a result, the heart rate and stroke volume decrease, causing blood
pressure to decline.

         When the blood pressure decreases, there is less stimulation of the
baroreceptors. A lower frequency of action potentials is sent to the medulla
oblongata of the brain and this triggers a response in the cardioregulatory center.
The cardioreulatory center responds by increasing sympathetic stimulation of the
heart and decreasing parasympathetic stimulation. Consequently, the heart rate
and stroke volume increase. If the decrease in blood pressure is large,
sympathetic stimulation of the adrenal medulla also increases. The epinephrine
and norepinephrine secreted by the adrenal medulla increase the heart rate and
stroke volume, also causing the blood pressure to increase toward its normal
value.

         Emotions integrated in the cerebrum of the brain can influence the heart.
Excitement, anxiety, or anger can affect the cardioregulatory center, resulting in
increased cardiac output. Depression, on the other hand, can increase
parasympathetic stimulation of the heart and an increased cardiac output.

         Epinephrine and small amounts of norepinephrine released from the
adrenal medulla in esponse to exercise, emotional excitement, or stress also
influence the heart’s function (see figure 16). Epinephrine and norepinephrine
bind to receptor molecules on cardiac muscle and cause increased rate and
stroke volume.

         The medulla oblongata of the brain also contains chemoreceptors that are
sensitive to changes in pH and carbon dioxide levels (see figure 6). A decrease
in pH, often caused by an increase in carbon dioxide, results in sympathetic
stimulation of the heart.
       Changes in the extracellular concentration of potassium, calcium, and
sodium, which influence other electrically excitable tissues, also affect cardiac
muscle function. Excess extracellular potassium causes the heart rate and stroke
volume to decrease. If the extracellular potassium concentration increases
further, normal conduction of action potentials through the cardiac muscle is
blocked, and death can result. An excess of extracellular calcium causes the
heart to contract arrythmically. Reduced extracellular calcium cause both the
heart rate and stroke volume to decrease.

Effects of Aging on the Heart

       Gradual changes in the function of the heart are associated with aging.
These changes are minor under resting conditions, but become more obvious
during exercise and in response to age-related diseases.

       By the age 70 cardiac output often decreases by approximately one-third.
Because of the decrease in the reserve strength of the heart, many elderly
people are limited in their ability to respond to emergencies, infections, blood
loss, or stress.

       Hypertrophy (enlargement) of the left ventricle is common age –related
change. This appears to result from a gradual increase in the pressure in the
aorta (afterload) against which the left ventricle must pump. The increased aortic
pressure results from gradual decrease in the elasticity of the aorta, and there is
an increased stiffness of the cardiac muscle. The enlarged left ventricle has a
reduced ability to pump blood out of the left ventricle. This can cause an increase
in left atrial pressure, which can result in increased pulmonary edema.
Consequently, there is an increased tendency for people to feel out of breath
when they exercise strenuously.

       Aging cardiac muscle require muscle requires a greater amount of time to
contract and relax. Thus, there is a decrease in the maximum heart rate. Both the
resting and maximum cardiac output slowly decrease as people age, and by 85
years old, the cardiac output is decreased by 30-60%.
       Age-related changes in the connective tissue of the heart valves occur.
The connective tissue becomes less flexible, and calcium deposits develop in
valves. As a result, there is an increase tendency for the aortic semilunar valve to
become stenosed or incompetent.

       There is an age-related increase in cardiac arrhythmias as a consequence
of a decrease in the number of cardiac cells. In the Sa node and because of the
replacement of cells of the AV bundle.

       The development of coronary artery disease and heart failure also are
age-related. Approximately 10% of elderly people over age 80 have heart
faiulure, and major contributing factor is coronary heart disease. Advanced age,
malnutrition, chronic infections, toxins, severe anemias, hyperthyroidism, and
hereditary factors can lead to heart failure.

       Exercise has many beneficial effects on the heart. Regular aerobic
exercise improves the functional capacity of the heart at all ages, providing there
are no conditions that cause the increased workload of the heart to be harmful
ANATOMY AND PHYSIOLOGY OF THE BLOOD VESSELS

General Features of Blood Vessel Structure

       Arteries are blood vessels that carry blood away from the heart. Blood is
pumped from the ventricles of the heart into the large elastic arteries, which
branch repeatedly to form progressively smaller arteries. As they become
smaller, the arteries undergo a gradual transition from having walls containing
more elastic tissue than smooth muscle to having walls with more smooth muscle
than elastic tissue (figure 17). The arteries are normally classified as (1) elastic
arteries, (2) muscular arteries, or (3) arterioles, although they form a continuum
from the largest to the smallest branches.




                          Figure 17. Blood Vessel Structure

       Blood flows from arterioles into capillaries, where exchange occurs
between the blood and tissue fluid. Capillaries have thinner walls. Blood flows
through them more slowly, and there are far more of them than any other blood
vessel type.

       From the capillaries, blood flows into veins. Veins are blood vessels that
carry blood toward the heart. Compared with arteries, the walls of veins are
thinner and contain less elastic tissue and fewer smooth muscles cells. Going
from capillaries toward the heart, small-diameter veins come together to form
larger diameter veins, which are fewer in number. Veins increase in diameter and
decrease in number as they project toward the heart, and their walls increase in
thickness. Veins are classified as (1) venules, (2) small veins, (3) medium-sized
veins, or (4) large veins (see figure 17).

       Blood vessel walls consist of three layers, except in capillaries and
venules. The relative thickness and composition of each layer varies with the
type and diameter of the blood vessel. From the inner to the outer wall of the
blood vessels, the layers, or tunics, are (1) the tunica intima, (2) the tunica
media, and (3) the tunica adventitia, or tunica externa (see figure 17).

       The tunica intima consists of an endothelium composed of simple
squamous epithelial cells, a basement membrane, and a small amount of
connective tissue. In muscular arteries, the tunica intima also contains a layer of
thin elastic connective tissue. The tunica media, or middle layer, consists of
smooth muscle cells arranged circularly around the blood vessel. It also contains
variable amounts of elastic and collagen fibers, depending on the size and type
of the of the vessel. In muscular arteries, there is a layer of elastic connective
tissue at the outer margin of the tunica media. The tunica adventitia composed
of connective tissue. It is a denser connective tissue adjacent to the tunica media
that becomes loose connective tissue toward the outer portion of the blood
vessel wall.

Arteries

       Elastic arteries are the leargest diametr arteries and have the thickest
walls (see figure 13.1a). A greater proportion of their walls is elastic tissue, and a
smaller proportion is smooth muscle compared with other arteries. Elastic
arteries are stretched when the ventricles of the heart pump blood into them. The
elastic recoil of the elastic arteries prevents blood pressure from falling rapidly
and maintains blood flow while the ventricles are relaxed.

        The muscular arteries include medium-sized and small-diameter arteries.
The walls of medium-sized arteries are relatively thick compared with the
diameter. Most of the thickness of the walls results from smooth muscle cells of
the tunica media (see figure 13.1b). Medium-sized arteries are frequently called
distributing arteries because the smooth muscle tissue enables these vessels
to control blood flow to different regions of the body. Contraction of the smooth
muscle in blood vessels, which is called vasoconstriction, decreases blood
vessel diameter and blood flow. Relaxation of the smooth muscle in blood
vessels, which is called vasodilation, increases blood vessel diameter and blood
flow.

        Medium-sized arteries supply blood to small arteries. Small arteries have
about the same structure as the medium-sized arteries, except that small arteries
have a smaller diameter and their walls are thinner. The smallest arteries have
only three of four layers of smooth muscle in their walls.

        Arterioles transport blood from small arteries to capillaries and are the
smallest arteries in which the three tunics can be identified. The tunica media
consists of only one or two layers of circular smooth muscle cells. Small arteries
and arterioles are adapted for vasodilation and vasoconstriction.
B.     BOOK – BASED SYNTHESIS OF THE DISEASE

       1.      Definition of the Disease
       Coronary Artery Disease

       Coronary Artery Disease (CAD) is a broad term that includes stable angina
pectoris and acute coronary syndrome, (Ignatavicius, 2006). Nonetheless, Coronary
Artery Disease (i.e. Coronary Heart Disease, Coronary Atherosclerosis, Ischemic Heart
Disease) results from focal narrowing of large and medium-sized coronary arteries due
to intimal plaque formation (atherosclerosis), (Hargrove-Huttel, 2005). It may also refers
to the diseases of the heart that may result from an impaired blood flow to the
myocardium usually due to accumulation of atherosclerotic plaque (Suddarth and
Brunner, 2008). Coronary Atherosclerosis is also a progressive disease characaterized
by atheroma (plaque) formation, which affects the intimal and medial layers of large and
midsize arteries and results to the occlusion of the coronary arteries (Black, 2005).

       In addition, Coronary Artery Disease is simply atherosclerosis of the coronary
arteries. Atherosclerosis occurs when the arteries become clogged and narrowed,
restricting blood flow to the heart. Without adequate blood, the heart becomes starved of
oxygen and vital nutrients it needs to work properly. When the blood flow is slowed the
heart doesn't get enough oxygen and nutrients. This can cause chest pain called angina.
When one or more of the coronary arteries are completely blocked, the result is a heart
attack (injury to the heart muscle), (Cleveland Clinic, 2008).

Acute Coronary Syndrome

       Acute Coronary Syndromes (ACS) has recently been accepted to describe
spectrum of acute ischemic heart diseases that include unstable angina, non-ST-
segment elevation (non Q wave) myocardial infarction (NSTEMI), and ST-segment
elevation (Q-wave) myocardial infarction (STEMI). Persons with an ACS are routinely
classified as low risk or high risk based on presenting charcterisctics, ECG variables,
serum cardiac markers, and the timing of presentation. Persons with ST-segment
elevation on ECG are usually found to have complete coronary occlusion on
angiography, and many ultimately have Q-wave myocardial infarction. This type of ACS
has been labeled reperfusion elgible acute myocardial infarction(AMI). Persons without
ST-segment elevation or non ST-segment elevation usually represent a group in whom
thrombotic coronary occlusion is subtotal or intermittent, and most experience unstable
angina or are found on the basis of elevated cardiac markers to have non-ST-segment
elevation AMI (Porth, 2007).

         Acute Coronary Syndrome is a term used to describe disorders that include
unstable angina, subendocardial MI, and MI. In acute coronary syndrome, it is believed
that the atherosclerotic plaque in the coronary artery ruptures, resulting in platelet
aggregation (“clumping”), thrombus (clot) formation, and vasoconstriction. The amount of
disruption of the atherosclerotic plaque determines the degree of obstruction of the
coronary artery and the specific disease process (unstable angina or myocardial
infarction [MI]), (Ignatavicius, 2006).

         In addition, ACS is an umbrella term used to cover any group of clinical
symptoms compatible with acute myocardial ischemia, (AHO, 2008), thus include those
whose clinical presentations cover the following range of diagnoses: unstable angina,
non–ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial
infarction (STEMI) (Fenton, 2008).

         In other cases, the blood clot (coronary thrombus) may totally block the blood
supply to the heart muscle (coronary occlusion), causing one three serious conditions,
called acute coronary syndromes: This is actually a name given to three serious
conditions: Forms of acute coronary syndrome may include the following (WebMD,
2008):

    1. Unstable angina: This may be a new symptom or a change from stable angina.
         The angina may occur more frequently occur more easily at rest, feel more
         severe, or last longer. Although this can often be relieved with oral medications, it
         is unstable and may progress to a heart attack. Usually more intense medical
         treatment or a procedure is required to treat this acute coronary syndrome
         (WebMD, 2008).
    2. Non-ST segment elevation myocardial infarction (NSTEMI): This heart attack,
         or MI, does not cause changes on an electrocardiogram (ECG). However,
         chemical markers in the blood indicate that damage has occurred to the heart
         muscle. In NSTEMI, the blockage may be partial or temporary, and so the extent
         of the damage is relatively minimal (WebMD, 2008).
   3. ST segment elevation myocardial infarction (STEMI): This heart attack, or MI,
         is caused by a prolonged period of blocked blood supply. It affects a large area of
         the heart muscle, and causes changes on the ECG and chemical markers in the
         blood (WebMD, 2008).

Myocardial Infarction

         Myocardial infarction, sometimes called as Acute Myocardial Infarction(AMI) or
Myocardial Ischemia is also known as heart attack, coronary occlusion, or simply
“coronary,” which is a life-threatening condition characterized by the formation of
localized necrotic areas within the myocardium (Black, 2005) and occurs when
myocardial tissue is abruptly and severed deprived of oxygen. When blood flow if acutely
reduced by 80% to 90%, ischemia develops. Ischemia can lead to injury and necrosis
(infarction) of myocardial tissue if blood flow is not restored (Ignatavicius, 2006).
Myocardial ischemia develops if the supply of coronary blood cannot meet the demand
of the myocardium for oxygen and nutrients. Imbalances between coronary blood supply
and myocardial demand can result from a number of conditions. The most common
cause of decreased coronary blood flow and resultant myocardial ischemia is the
formation of atherosclerotic plaques in the coronary circulation (Porth, 2007). Often MIs
begin with infarction (necrosis) of the subendocardial layer of cardiac muscle. This layer
has the longest myofibrils in the heart, the greatest oxygen demand, and the poorest
oxygen supply. Around the initial area of infarction (zone of necrosis) in the
subendocardium are two other zones: (1) the zone of injury, tissue that is injured but not
necrotic, and (2) the zone of ischemia, tissue that is oxygen deprived (Ignatavicius,
2006).

TYPES OF MYOCARDIAL INFARCTION AS TO DEPTH OF INFARCTION

   1. Transmural Infarction
   2. Intramural Infarction
   3. Subepicardial Infarction
   4. Subendocardial Infarction


Classification of Myocardial Infarction by Location
       The clients response to an MI also depends on which coronary artery or arteries
were obstructed or arteries were obstructed and which part of the left ventricle wall
damaged:

       1. Posterior (Inferior) MI – Occlusion of Right coronary artery (RCA)
           -Obstruction of the right coronary artery often have inferior wall MIs. Inferior
           wall MIs (IWMIs) account for about 17% of all MIs and have a mortality rate of
           about 10%. Up to 50% of all inferior wall MIs are associated with an occlusion
           of the right coronary artery causing significant damage to the right ventricle
           (Ignatavicius, 2006).

       2. Massive anterolateral MI – Occlusion of Left coronary artery (LCA)
           (Ignatavicius, 2006).
       3. Anteroseptal MI – Occlusion of Left anterior descending artery (LAD)
           -Obstruction of the LAD causes anterior or septal MIs because LAD artery
           perfuses the anterior wall and most of the septum of the left ventricle. Anterior
           wall MIs (AWMIs) account for 25% of all MIs and have the highest mortality
           rate. Clients with anterior MIs are most likely to experience left ventricular
           heart failure and ventricular dysrhythmias because large segment of the left
           ventricle wall may have been damaged (Ignatavicius, 2006).

       4. Lateral MI – Occlusion of Left circumflex coronary artery (LCX)
           -Clients with obstruction of the circumflex artery may experience a lateral wall
           MI (LWMIs) and sinus dysrhythmias since the circumflex artery supplies the
           lateral wall of the left ventricle and possibly portions of the posterior wall or
           the sinoatrial (SA) or atrioventricular (AV) nodes (Ignatavicius, 2006).

ANGINA PECTORIS

       Chest pain resulting from reduced coronary blood flow, which causes a
temporary imbalance between myocardial blood supply and demand. More over, it is a
chest pain resulting from myocardial ischemia (inadequate blood supply to the
myocardium), (Black, 2005).

Patterns of Angina

   1. Stable Angina
   -a.k.a Exertional Angina is stable angina is paroxysmal chest pain or discomfort
   triggered by a predictable degree of exertion (e.g. walking 20feet) or emotion.
   Characteristically, a stable pattern of onset, duration, severity, and relieving
   factors is present, normally stable angina is relieved with rest or nitroglycerin, or
   both (Black, 2005).




2. Unstable Angina
   -a.k.a. Preinfarction angina, crescendo angina or intermittent coronary syndrome)
   is paroxysmal chest pain triggered by an unpredictable degree of exertion or
   emotion which may occur at night. Unstable angina attacks characteristically
   increase in number, duration. And severity over time. If unstable angina occurs, it
   must be treated as a medical emergency with the client receiving immediate
   medical attention (Black, 2005).

3. Prinzmental’s Angina
   -a.k.a Variant Angina, is chest discomfort similar to classic angina but of longer
   duration; it may occur while the client is at rest. These attacks tend to happen
   between midnight and 8 AM. Variant angina results from coronary artery spasm
   and may be associated with elevation of the ST segment on the
   electrocardiogram (ECG) (Black, 2005).

4. Nocturnal Angina
   -Nocturnal Angina is possibly associated with rapid eye movement (REM) sleep
   during dreaming (Black, 2005).

5. Angina Decubitus

   -Paroxysmal chest pain that occurs when the client reclines and lessens

   when the client sits or stands up (Black, 2005).

5. Intractable Angina
   -Is chronic incapacitating angina that is unresponsive to intervention.

6. Postinfarction Angina
          -Pain occurs after MI, when residual ischemia may cause episodes of angina
          (Black, 2005).




          The Killip classification is a system used in individuals with an acute
myocardial infarction (heart attack), in order to risk stratify them. Individuals with a low
Killip class are less likely to die within the first 30 days after their myocardial infarction
than individuals with a high Killip class.

                                Killip Classification of Heart Failure
          Class                                       Description
    I                 Absent crackles and S3
    II                Crackles in the lower half of the lung fields and possible S3
    III               Crackles more than halfway up the lung fields and frequent pulmonary
                      edema
    IV                Cardiogenic Shock
                                                                Source (Ignatavicius, 2006)


2. Non-Modifiable Factors and Modifiable Factors

Non-Modifiable Factors

    1. Increasing Age
                  Age influences both the risk and the severity of CHD. Symptomatic CHD
          appears predominantly in people older than 40 years of age, and four of five
          people who die of CHD are age 65years or older . Angina and MI, however, can
          occur in a person’s 30s and even in one’s 20s. At older ages women who have
          heart attacks are twice as likely as men to die of heart attack (Black, 2005).

    2. Gender (Men develop CAD at an earlier age than women)
                  Coronary heart disease is the number-one killer of both men and women.
          In 1999 mortality from CHD was almost equal for men and women. Although men
          are at higher risk for heart attacks at younger ages, the risk for women increases
          significantly at menopause, so that CHD rates in women after menopause are
          two or three times that of women the same age before menopause. Women with
          an early menopause are also at higher risk than are women with a normal or late
          menopause (Black, 2005).
   3. Family history of coronary artery disease

          Children whose parents had heart disease are at higher risk for CHD. This
   increased risk is related to genetic predisposition to hypertension, elevated lipid
   levels, diabetes, and obesity; all of these conditions increase the risk of CHD (Black,
   2005). In addition, primary or familial dyslipidemia result from genetic defects causes
   abnormalities in lipid-metabolizing enzymes and abnormal cellular lipid receptors
   (MacCance, 2006). In addition, particular genotype patterns also may place
   individuals at risk of CAD/MI. For example, recent studies of a few families with high
   rates of CAD/MI have identified mutations in a gene known as MEF2A, which codes
   for one of the transcription factors known as myocyte enhancer factor-2. In its normal
   expression, this protein is involved in the early stages of vasculogenesis (formation
   of new blood vessels); mutations may compromise its ability to perform this function,
   resulting in increased susceptibility to heart disease (Corwin, 2008).

   4. Race/Ethnicity


          African-American women face the highest risk for death from heart disease,
   and their rate of heart attacks is increasing. (Mortality rates in men do not differ much
   by race.) Native American men have a lower risk for heart disease than Caucasian
   men, and Hispanics have the lowest risk for heart disease of all major American
   population groups.African-Americans face a number of biologic and social dangers to
   their hearts, including; They have a higher prevalence of diabetes and hypertension
   than do Caucasians. They tend to have poorer diets, higher stress levels, and less
   access to health care. Some African-Americans with coronary artery disease appear
   to have a genetic trait that increases the danger of triglycerides, which may be
   particularly hazardous for women (Simon, 2008).

Modifiable Factors

   a. Hyperlipidemia
              An increased serum concentration of LDL is a strong indicator of coronary
      risk. High dietary intake of cholesterol and fats, often in combination with a
      genetic predisposition to accumulations of LDL in the serum (e.g. dysfunction of
      the hepatic LDL receptor), results in high levels of LDL in the bloodstream. The
      term LDL actually describes several types of LDL molecules; the small dense
   LDL, particles are the most atherogenic. LDL oxidation, migration into the vessel
   wall, and phagocytosis by macrophages are key steps in the pathogenesis of
   atherosclerosis. LDL also plays a role in endothelial injury, inflammation, and
   immune responses that have been identified as being important in atherogenesis
   (McCance, 2006).

b. Hypertension
          High blood pressure afflicts nearly 50 million American Adults and
   children. It increases the workload of the heart by increasing afterload, enlarging
   and weakening of the left ventricle over time. As blood pressure increases, the
   risk of serious cardiovascular event escalates. When clients have hypertension,
   obesity, tobacco use, high cholesterol levels and dibetes, the risk of heart attack
   increases significantly (Black, 2005). In addition, it is responsible for a twofold to
   threefold increased risk of atherosclerotic cardiovascular disease. It further
   contributes to endothelial injury, a key step in atherogenesis and causes
   myocardial hypertrophy, which increases myocardial demand for coronary flow
   (McCance, 2006).




c. Cigarette smoking
          Cigarette smoking contributes to the development and severity of CAD in
   the following three ways.

          First, the inhalation of smoke increases the blood carbon monoxide level,
   and hemoglobin, the oxygen-carrying component of blood, combines more
   readily with carbon monoxide than with oxygen (Suddarth and Brunner, 2008).
   More over, carbon monoxide in cigarette smoke reduces the oxygen content of
   arterial blood. Hypoxemia (insufficient oxygen in arterial blood) may promote
   atherosclerosis by deceasing the availability of oxygen to the vessel walls and
   increasing vessel wall permeability. More so, a decreased amount of available
   oxygen may decrease the heart’s ability to pump (McCance, 2006).

          Second, the nicotine stimulates the release of cathecholamines
   (epinephrine and norepinephrine), which increase heart rate and peripheral
   vascular constriction. As a result, blood pressure increases, as do cardiac
   workload and oxygen demand. Elevated catecholamines also stimulate release
   of free fatty acids (McCance, 2006). In addition, the nicotinic acid in cigarette can
   also cause the coronary arteries to constrict. Smokers have a tenfold increase in
   risk for sudden cardiac death. The increase in catecholamines maybe a factor in
   sudden cardiac death (Suddarth and Brunner, 2008). More so, nicotine activates
   platelets and stimulates smooth-muscle-cell proliferation in the arterial walls
   (Black, 2005).

          Third, use of cigarette causes a detrimental vascular response and
   increases platelet adhesion, leading to a higher probability of thrombus formation
   (Suddarth and Brunner, 2008). More so, Cigarette smoking is associated with an
   increase in LDL, a decrease in HDL, and induction of a prothrombotic state, as
   well as increases in inflammatory markers of CAD such as C-reactive protein and
   fibrinogen. In addition, the cadmium in cigarette smoke maybe related to
   elevations in blood pressure.

          In addition, passive smoking from “second-hand smoke” substantially
   reduces blood flow velocity in the coronary arteries of healthy young adults
   (Ignatavicius, 2006).

d. Obesity
          Obesity places an extra burden on the heart, requiring the muscle to work
   harder to pump enough blood to support added tissue mass. In addition, obesity
   increases the risk for CHD because it is often associated with elevated serum
   cholesterol and triglyceride levels, high blood pressure, and diabetes (Black,
   2005). More so, It is estimated that 65% of the adult population in the United
   States is overweight or obese resulting in a much increased risk for CAD and
   stroke. An estimated 47million U.S. residents have a combination of obesity,
   dyslipidemia, and hypertension called the metabolic syndrome, which is
   associated with an even higher risk for CAD events. In addition, abdominal
   obesity has the strongest link with increased CAD risk and is related to insulin
   resistance, decreased HDL, increased blood pressure, and decreased levels of
   recently described cardioprotective protein called adiponectin (McCance, 2006).

e. Physical Inactivity/Sedentary Lifestyle
            The Framingham Study demonstrated an inverse relationship between
     exercise and reduce their risk of CHD because they (1) higher HDL levels; (2)
     lower LDL cholesterol, triglyceride, and blood glucose level; (3) greater insulin
     sensitivity; (4) lower blood pressure; and (5) lower body mass index (Black,
     2005). A sedentary life-style not only increases the risk of obesity but also has an
     independent effect on increasing CAD risk (McCance. 2006). More so, physical
     inactivity may be the most important risk factor for the general population. Less
     active, lest-fit persons have a 30% to 50% greater risk of developing high BP,
     which predisposes to CAD, (Ignatavicius, 2006).

f.   Response to Stress (Occupational Stress)
            A persons’ response to stress may contribute to the development of CHD.
     Some researchers have reported a relationship between CHD risk and stress
     levels, health behaviors, and socioeconomic status. Stress appears to increase
     CHD risk through its effects in major risk factors. (Black, 2005). Severe emotional
     stress cause surge in adrenaline, which causes the blood to clot readily
     increasing the risk of heart attacks. British investigators have shown that chronic
     work stress can produce chronic increases in adrenaline levels, and have related
     those changes to an increased risk of heart disease (Fogoros, 2009). For
     example, some people respond to stress by overeating or by starting or
     increasing smoking. Stress is also associated with elevated blood pressure.
     Although stress is unavoidable in modern life, an excessive response to stress
     can be a health hazard. Significant stressors include major changes in residence,
     occupation, or socioeconomic status (Black, 2005).

g. Diet
            Increased dietary intake of foods high in sodium, fats and cholesterol
     predisposes a person to cardiovascular disoders (Udan, 2005). Engaging in
     eating too much fatty foods (atherogenic diet) could cause increase cholesterol
     level in the blood wherein elevated serum lipid level is one of the four most firmly
     established risk factors for Coronary Artery Disease (Mantitz, 2004).


h. Amphetamine Use
            Young adults who abuse amphetamines may be at greater risk of
     suffering a heart attack. Amphetamine also acts in this way with norepinephrine
     (noradrenaline) and to a lesser extent serotonin. Thus, the physical effects of
     amphetamine could include reduced appetite, dilated pupils, flushing, loss of
     coordination, restlessness, dry mouth, headache, tachycardia, increased
     breathing rate, increased blood pressure, fever, sweating, diarrhea, constipation,
     blurred vision, impaired speech, dizziness,uncontrollable movements, insomnia,
     numbness, palpitations, arrhythmia. In high doses or chronic use convulsions,
     dry or itchy skin, acne, pallor can occur (Ignatavicius, 2006).

             Since amphetamine use releases cathecolamines (norepinephrine and
     epinephrine) it therefore increases peripheral vasoconstriction which increases
     the cardiac workload and oxygen demand. It also stimulates the release of free
     fatty acids.

i.   History of Diabetes Mellitus
             Diabetes Mellitus is an extremely important risk factor for CAD. Diabetes
     is associated with a two-fold increase in the risk for CAD death and up to a
     sixfold risk for stroke. Diabetes and insulin resistance have multiple effects on the
     cardiovascular system through the production of toxic reactive species (ROS)
     that alter vascular cell function. These effects can include endothelial damage,
     thickening of the vessel wall, increased inflammation and leukocyte adhesion,
     increased thrombosis, glycation of vascular proteins, and decreased production
     of endothelial-derived vasodilators such nitric oxide. It is also associated with
     dyslipidemia because of resulting alteration of hepatic lipoprotein synthesis and
     increases in LDL oxidation. Aggressive management of this additional risk factor
     can significantly improve CAD risk in individuals with diabetes (McCance, 2006).

j.   Menopause
             The incidence of CHD markedly increases among women after
     menopause. Before menopause estrogen is thought to protect against CHD risk
     by raising HDL and lowering LDL levels. Epidemiologic studies have shown that
     the loss of natural estrogen as women age may be associated with increase in
     total and LDL cholesterol and a gradually increasing CHD risk. If menopause is
     caused by surgical removal of the uterus and ovaries, the risks of CHD and MI
     increase (Black, 2005).

k.   Behavior Pattern (Type A Personality)
              The type A personality may not be as significant as was once thought;
     evidence of its precise role remains inconclusive. Current predictors of coronary
     events focus on physiologic factors. However, it has been long been recognized
     that emotional stress can lead to release of catecholamines and subsequent
     coronary ischemia. Thus, people with type A traits are advised to alter behaviors
     and responses to triggering events and to reduce risk factors (Suddarth and
     Brunner, 2008).

l.   Inflammatory Response
              A newly identified risk factor currently being researched is the presence of
     any chronic inflammatory state that leads to an increase in body’s production of
     CRP. Too much CRP tends to destabilize plaque inside artery walls. When
     plaque lesions crack or break, a clot is formed and this may lead to heart attack.
     Researchers have discovered that a high CRP is a marker for coronary disease.
     This means that clients with chronic inflammatory diseases, such as arthritis,
     lupus, and autoimmune deficiency, may be at higher risk for heart attack (Black,
     2005).

m. Increase homocysteine Levels
              Hyperhomocysteinemia occurs because of genetic lack of enzyme that
     breaks down homocysteine (an amino acid) or because of a nutritional deficiency
     of folate, cobalamin (vitamin B12), or pyridoxine (vitamin B6). It has been
     identified as a risk factor for CAD, although its significance in CAD and stroke
     continues to be explored. Mechanisms by which it contributes to coronary
     disease include associated increases in LDL, decreases in endogenous
     vasodilators, and an increased tendency for thrombosis. Routine serum
     measurement of homocysteine is not currently recommended and prevention and
     management are focused on increasing the dietary intake of folate and B
     vitamins (McCance, 2006).

n. Infection
              Emerging is evidence that infection may play a role in atherogenesis and
     CAD risks. Studies have found that several microorganisms, especially
     Chlamydia     pneumonae      and   Helicobacter    pylori   are   often   present   in
     atherosclerotic lesions. Serum antibodies to microorganisms have been linked to
       an increased risk for CAD as has the presence of periodontal disease (McCance,
       2006).

3. Clinical manifestations with Rationale

     SIGNS AND SYMPTOMS                                    RATIONALE
                                          Atherosclerosis plaques are initiated by injury to
                                      the coronary artery endothelium. The specific cause
                                      of endothelial dysfunction maybe attributed to the
                                      non-modifiable factors and modifiable factors. Once
                                      the injury occurs the endothelium may become
                                      more permeable and recruit leukocytes. LDLs leak
                                      through the endothelium and into the vessel wall
                                      (insudation) where they are oxidized by endothelial
                                      cells and macrophages. Oxidized lipids are
         Atherosclerosis              damaging to the endothelial and smooth muscle
       (Plaque Formation)             cells, and stimulate the recruitment of macrophages
                                      into the vessel wall where they engulf the lipids.
                                      Lipid-filled macrophages are called foam cells. The
                                      macrophages and foal cells release inflammatory
                                      mediators and growth factors that attract more
                                      leukocytes     and     stimulate   smooth      muscle
                                      proliferation. Excess lipid and debris begins to
                                      accumulate within the vessel wall and coalesce into
                                      a pool called the lipid core. Atherosclerotic plaques
                                      with large lipid cores are fragile and prone to
                                      rupture.

                                          Due to obstruction of blood flow to the coronary
                                      arteries there will imbalance between coronary
                                      supply and demand, as a result myocardial O2
                                      deficit will occur. Since myocardial cells are denied
                                      of adequate O2 and nutrients resulting from
                                      myocardial ischemia (inadequate blood supply to
                                      the myocardium) may result to myocardial cell death
   Angina Pectoris/Chest Pain         which in turn will lead to accumulation of metabolic
                                      acid within ischemia part (necrotic part) of the
                                      myocardium, thus anaerobic metabolism is
                                      established leading to increase production of lactic
                                      acid. Lactic acid causes irritation to the myocardial
                                      fibers/nerve endings thus causing pain along the
                                      chest wall ranging from a sensation of heaviness or
                                      pressure to moderately severe pain.
                                       Prolonged ischemia will lead to myocardial cell
                                  death causing accumulation of lactic acid due to
                                  anaerobic metabolism. Lactic acid causes pain as it
                                  irritates myocardial fibers/nerve endings. Discomfort
       (+) Levine’s Sign          may radiate to the neck, lower jaw, left arm, and left
                                  shoulder or, occasionally, to the back or down the
                                  right arm causing a Levine’s sign (Individuals often
                                  describe the sensation by clenching a fist over the
                                  left sternal border).

                                      Continued ischemia due to coronary obstruction
                                  will cause myocardial cell/tissue necrosis. Necrosis
  Elevated Cardiac Enzymes        of myocardial tissue results in the release of certain
                                  intracellular enzymes (CK-MB, Troponin I, Troponin
(CK-MB, Troponin I, Troponin T,   T, Myoglobin) through the damaged cell
          Myoglobin)              membranes into the interstitial spaces. The
                                  lymphatics pick up the enzymes and transport them
                                  into the bloodstream, where they can be detected
                                  by serologic tests.

                                     Imbalance between coronary supply and
                                  myocardial demand secondary to coronary
                                  occlusion will lead to myocardial O2 deficit which
                                  causes death of the myocyte, Prolonged ischemia
ST-segment elevation, T wave      causes myocardial infarction. Since there is death
         Inversion,               on myocardium electrical impulses is impaired or
     pathologic Q wave            even lack of response to electrical impulses may
                                  occur causing alteration and delay of repolarization
                                  and depolarization properties of the heart. This is
                                  evidently reflected on ECG (Electrocardiogram)
                                  showing ST-segment elevation, T wave inversion
                                  and pathologic Q wave.

                                     Due to infarcted myocardium, heart loses
                                  contractility and lack of responses to electrical
  Dysrhythmias/Arrhythmias        impulses. This activity of the heart will eventually
                                  lead to dysrhythmias/arrhythmias which is very fatal
                                  to the individual and if not attended immediately
                                  may result to sudden death.
                                      Imbalance between coronary supply and
                                  myocardial demand secondary to coronary
                                  occlusion will lead to myocardial O2 deficit which
                                  causes myocardial damage-death and necrosis.
    Elevated Glucose Level
                                  The     myocardial    cells  significantly   release
                                  catecholamines          and          norepinephrine.
                                  Catecholamines mediate the release of glycogen,
                                  glucose, and stored fat from body cells. Therefore,
                                  plasma concentrations of free fatty acids and
                                    glycerol rise within 1 hour after onset of acute
                                    myocardial infarction. In addition, norepinephrine
                                    elevates blood sugar levels through stimulation of
                                    liver and skeletal muscle cells. It also suppresses
                                    pancreatic B cell activity which reduces insulin
                                    secretion and elevates blood glucose further. Not
                                    surprisingly, hyperglycemia is noted approximately
                                    72 hours after an acute myocardial infarction.

                                        Obstruction of blood flow to the coronary artery
                                    because of occlusion could cause imbalance
                                    between coronary supply and myocardial demand
                                    leading to myocardial O2 deficit. In return,
                                    myocardial cells are denied of with adequate O2
                                    and nutrients leading to O2, glycogen and ATP
 Increased WBC (Leukocytosis)
                                    stores depletion causing irreversible hypoxemic
                                    damage causing cellular death and tissue necrosis,
                                    as part of the response, there will be also
                                    inflammation as evidenced by attraction of
                                    increased WBCs near the injured area.

                                        Infarcted myocardium as brought about by
                                    prolonged ischemia due to imbalance between
                                    coronary supply and myocardial demand stimulates
                                    the vasovagal reflexes affecting the gastrointestinal
Nausea, Vomiting, Epigastric Pain
                                    tract causing nausea and vomiting. These events is
                                    also brought by increased production of lactic acid
                                    which stimulate pain fibers at the vomiting center,
                                    which in turn triggered Medulla Oblongata causing
                                    nausea and vomiting.
                                         When heart loses its contractility and lack of
                                    response to electrical impulses due to myocardial
                                    infarction, the compensatory mechanism of the
                                    heart will work hard to increase its workload.
                                    Eventually, as the heart works hard to meet the
                                    demand, it will enlarge significantly (hypertrophy of
                                    the heart) as well as thickening of the ventricles
                                    resulting to cardiomegaly. In addition, cardiac tissue
                                    surrounding the area of infarction also undergoes
                                    changes such as myocardial remodeling, a process
         Cardiomegaly
                                    mediated      by    angiotensin     II,  aldosterone,
                                    catecholamines, adenosine, and inflammatory
                                    cytokines which causes hypertrophy of the
                                    myocardial cells and sustained activation of
                                    nuerohormonal compensatory mechanism which
                                    eventually increases wall stress in the ventricle and
                                    thus to reduce wall stress, the myocardial cells
                                    hypertrophy (Laplace’s Law). As a result there will
                                    be thickening of the ventricular wall which
                                    contributes to cardiomegaly.
                                           Due to obstruction of blood flow to the coronary
                                         arteries there will imbalance between coronary
                                         supply and demand, as a result myocardial O2
                                         deficit will occur. Since myocardial cells are denied
                                         of adequate O2 and nutrients resulting from
                                         myocardial ischemia (inadequate blood supply to
                                         the myocardium) may result to myocardial cell death
                                         which in turn will lead to accumulation of metabolic
Pallor, diaphoresis, dyspnea, body
                                         acid within ischemia part (necrotic part) of the
    weakness/easy fatigability,
                                         myocardium, thus anaerobic metabolism is
  headache, sense of impending
                                         established leading to increase production of lactic
               doom
                                         acid. Lactic acid causes irritation to the myocardial
                                         fibers/nerve endings thus causing pain along the
                                         chest wall ranging from a sensation of heaviness or
                                         pressure to moderately severe pain. As a result, the
                                         body will respond, thus there will be pallor,
                                         diaphoresis,      dyspnea,    body    weakness/easy
                                         fatigability, headache, sense of impending doom.

                                             Due to obstruction of blood flow to the coronary
                                         arteries there will imbalance between coronary
                                         supply and demand, as a result myocardial O2
                                         deficit will occur. Since myocardial cells are denied
                                         of adequate O2 and nutrients resulting from
                                         myocardial ischemia (inadequate blood supply to
                                         the myocardium) may result to myocardial cell death
                                         which in turn will lead to accumulation of metabolic
                                         acid within ischemia part (necrotic part) of the
                                         myocardium, thus anaerobic metabolism is
       Stimulation of SNS
                                         established leading to increase production of lactic
           Increased VS
                                         acid will lead to acidosis. In return, myocardial cells
       (-)Bowel Movement
                                         will become sensitive to changes in pH and become
     ↑O2 needs and demands
                                         less functionsal leading to conduction system
                                         disorder      decreasing     myocardial    contractility
                                         stimulating the sympathetic nervous system causing
                                         increased vitals signs and no bowel movement and
                                         increased O2 needs and demands. Blood pressure
                                         is increased also because of decreased arterial
                                         pressure due to decreased cardiac output, therby,
                                         stimulating     barorecptors     causing    peripheral
                                         vasoconstriction.

                                             Due      to  myocardial      infarction, different
                                         mechanisms will occur such as heart loses
                                         contractility and lack of response to electrical
   ↓Hemoglogbin, ↓hematocrit,            impulses, myocardial remodelling and myocardial
delayed capillary refill time, pallor,   dysfunction, all of which actions will lead to heart
                                         failure. As a result, there will be decreased cardiac
                                         output leading to decreased systemic circulation
                                         decreasing blood carrying O2 to peripheral parts of
                                       the body hence there will be ↓hemoglogbin,
                                       ↓hematocrit, delayed capillary refill time, pallor.

                                           Due      to   myocardial     infarction, different
                                       mechanisms will occur such as heart loses
                                       contractility and lack of response to electrical
                                       impulses, myocardial remodeling and myocardial
                                       dysfunction, all of which actions will lead to heart
   Weakness/restlessness, easy         failure. As a result, there will be decreased cardiac
       fatigability, fatigue,          output leading to decreased systemic circulation
                                       redirecting of blood away from the skin to major
                                       organs, thus the body feels weakness/restlessness,
                                       easy fatigability, fatigue.

                                           Since there is heart failure, there is also
                                       decreased in cardiac output. As a result,
                                       symphathetic receptors are stimulated increasing
    Left ventricular hypertrophy       heart rate or pumping action as a compensatory
     Decrease Ejection fraction        mechanism, which leads to left ventricular
                                       hypertrophy eventually heart’s ability to pump will
                                       deteriorate thus leading to moderate left ventricular
                                       failure which decreases ejection fraction

                                            Coronary occlusion will lead to ischemia of the
                                       heart muscles (myocardial infarction), one of the
                                       complications of MI is heart failure which
                                       consequently decreases the cardiac output, since
                                       there is apparent decreased in cardiac output as a
                                       compensatory mechanism of the heart, it increases
                                       its pumping action. In return, it will eventually lead to
      Pulmonary Congestion             ventricular failure (left ventricle), the right side of the
                                       heart continuously propel blood to the lungs since
                                       left ventricle is unable to fully eject the returning
                                       blood to the systemic circulation, there will be
                                       pooling of blood to the lungs which consequently
                                       lead to pulmonary congestion.


                                        Heart failure leads to decreased in cardiac
                                    output. As a result, symphathetic receptors are
Fine crackles on BLF (bibasal
                                    stimulated increasing heart rate or pumping action
rales), wheezes, S3 gallop
                                    as a compensatory mechanism, which leads to left
              Edema
                                    ventricular hypertrophy eventually heart’s ability to
         Jugular Distension
                                    pump will deteriorate thus leading to moderate left
  Dyspnea (Difficulty of breathing)
                                    ventricular failure which decreases ejection fraction.
  Body Weakness/Easy fatigability
                                    Still, the right side of the heart continuously propel
                                    blood to the lungs, in return, left ventricle is unable
                                    to fully eject the returning blood to systemic
                                    circulation thus, there will be pooling of blood
                                     resulting to pulmonary congestion. Since there is
                                     congestion, there will be stasis of fluid leading to
                                     formation of exudates in the alveoli and bronchioles
                                     forming consolidation of exudates as manifested by
                                     fine crackles (bibasal rales on BLF), edema, and
                                     jugular distension. As a result of pulmonary
                                     congestion, the body responded by my using
                                     accessory muscles, difficulty of breathing as
                                     compensated by orthopnea, easy fatigability or body
                                     weakness.

                                         Since there is pulmonary congestion, there will
                                     be fluid stasis leading to formation of exudates in
                                     the alveoli and bronchioles. The consolidated
                                     exudates irritate pulmonary sensory receptors and
             Cough
                                     action potentials are carried and conducted to
                                     medulla oblongata, in return, productive cough
                                     reflex is initiated.


                                        Because of heart failure, there is decreased in
                                     cardiac output which eventually leads to inadequate
                                     cerebral perfusion, since the brain is depleted of
 Lost of consciousness, dizziness,
                                     supply of O2, the body responds to this event
fainting, sense of impending doom
                                     through loss of consciousness, dizziness, fainting,
                                     sense of impending doom.


                                        Imbalance between coronary supply and
                                     myocardial demand secondary to coronary
                                     occlusion will lead to myocardial O2 deficit which
                                     causes myocardial damage-death and necrosis. In
Ventricular Aneurysm, Perforation    return, these there will be scar tissue formation
    of the Ventricular Septum        which apparently replaces by new tissues, as a
                                     result, tissues become weak and soft leading to
                                     ventricular aneurysm or perforation of the
                                     ventricular septum.

                                        Lack of O2 supply because of coronary
                                     occlusion could lead to myocardial infarction,
       Valve Regurgitation           complications may include ischemia of the valve
                                     leaflets/papillary muscles leading to valve
                                     regurgitation.
XIV.   BIBLIOGRAPHY

A. Books


Black, Joyce M. and Hawks, Jane Hokanson. Medical-Surgical Nursing Clinical
Management for Positive Outcomes. 7th Edition. Elsevier Saunders, USA, 2005.

Copstead Lee-Ellen C. et.al. Pathophysiology. 3rd Edition. Elsevier Saunders, St.
Louis, Missouri. 2005.

Corwin, E.J. Handbook of Pathophysiology. 3rd Edition. Lippincott Williams and
Wilkins. Philadelphia. 2008

Doenges, Marilynn E., et.al. Nurses Pocket Guide: Diagnoses, Interventions and
Rationales. 8th Edition. F.A. Davis Company. Philadeplhia, U.S.A. 2006.

Doenges, Marilynn E., et.al. Nursing Care Plans: Guidelines for Individualizing
Patient Care Actions Across the Life Span. 7th Edition. F.A. Davis Company.
Philadeplhia, U.S.A. 2006.

Doyle, Rita M., et.al. Nursing 2006 Drug Handbook. 26th Edition. Lippincott Williams
and Wilkins, U.S.A. 2006.

Fauci, Kasper, et.al. Harrison’s Principles of Internal Medicine. 16th Edition. RR and
Donnelley & Sons Inc., U.S.A, 2005.

Gould, Barabara E. Pathophysiology for the Health Professionals. Elsevier Inc.,
U.S.A. 2006.

Ignatavicius, Donna D. and Workman, M. Medical-Surgical Nursing: Critical Thinking
for Collaborative Care. 5th Edition. Elsevier Saunders, St. Louis, Missouri, 2006

Kelly, W.J. et. al. Nurse’s Quick Check: Diagnostic Tests. Lippincott Williams and
Wilkins, U.S.A. 2006.

Kozier, Barbara, et.al. Fundamentals of Nursing: Concepts, Process and Practice.
7th Edition. Pearson Education South Asia PTE LTD, Philippines. 2004.
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C. Internet Readings

American Heart Association (AHA), 2009.
http://www.americanheart.org/presenter.jhtml?identifier=3010002, retrieved on 06-
14-08 at 2:55pm

American Heart Association (AHA), 2009.
http://www.americanheart.org/presenter.jhtml?identifier=4478, retrieved on 06-26-
09 at 2:56pm.

				
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Description: Case study on patient with Myocardial Infarction by Rolly Policarpio RN