Myocardial Infarction (Heart Attack) : by Rolly M. Policarpio RN

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
AMI/DM
54y/o
yo
51y/o
yo
49y/o
yo
48 y/o
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: 37.5C/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: 36.5C/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
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
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: 36.8C/axilla PR: 88bpm RR: 20bpm 02 Sat: 97%
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
q. Nose: No nasal deviation. No nasal discharges, deformities and obstruction noted..
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,
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.
c.
GCS
Eye opening: 4
Verbal Response:
Motor Response:
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
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: 36.7C/axilla PR: 89bpm RR: 22bpm 02 Sat: 98%
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

e. Nose: No nasal deviation. No nasal discharges, deformities and obstruction noted..
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,
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
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
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)
LABORATORY
DATE DONE (DD)
PROCEDURE
Complete
Blood
DATE RESULTS IN (DRI)
INDICATION/PURPOSE
NORMAL
ANALSYS AND
VALUES
INTERPRETATION
OF RESULTS
NDICATION/S
Count
RESULTS
OR
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
DD: 10-07-09
measures
amount
of
140-180g/L
The result is within

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
oxygen
wh
blood.
It
is
carrying
indicated for the pati to
capacity
of
help evaluate iron status
erythrocytes to be
oxygen
carrying
capacity of R B I
delivered
to
the
different
parts
of
the body.
Hematocrit
DO: 10-07-09
It
measures
the 0.40
0.40-0.54
DD: 10-07-09
percentage volume of
normal
packed red blood Cal in
DO: 10-11-09
a whole blood sample 0.40
there is adequate
DD: 10-11-09
determine
oxygen
the

values,
carrying
percentage RBC's in the
capacity
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
the
capacity
of
RBC z hydration status
could
of the patient.
that
of
body.
This
mean
there
also
is
alteration
no
of
hydration status.
Leukocytes
leukocytes
count 8x109/L
5-10x109/L
DO: 10-07-09
The
DD: 10-07-09
measu the number of
normal
WBC's in a cu millimeter
of blood. It is indical for
there
values,
is
no
the patient to detect and
presence
of
evaluate
presence
of
infection
as
infection
and
or
evidenced
inflammation and tissue
signs
necrosis.
symptoms
by
no
and
of
infections such as
fever and chills.
Lymphocytes
DO: 10-07-09
Lymphocytes produces 0.42
DD: 10-07-09
antibodies
for
0.22-0.37
The result is above
responsible
the normal values,
reaction.
which means that
allergic
Monocytes
have
there
is
phagocytic actions by
inflammation
removing
and
since
cell
cells are denied of
and
adequate 02 and
microorganisms. It was
nutrients leading to
indicated for the patient
hypoxemic
to determine degree of
damage
inflammation.
cellular death and
injured
dead
cells,
fragments
tissue
part
myocardial
causing
necrosis,
of
mechanism
the
is
inflammatory
response.
Lymphocytes,
monocytes
count
are
and
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
LABORATORY
ORDERED(DO)
PROCEDURE
DATE DONE (DD)
INDICATION/PURPOSE
RESULTS
NORMAL
ANALSYS AND
VALUES
INTERPRETATION
OF RESULTS
DATE RESULTS
Creatinine
IN (DRI)
DO: 10-07-09
A routinary exam done 0.9
DD: 10-07-09
upon admission to assess
the normal values,
glomerular filtration and to
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
inadequate renal
do
blood
urea
nitrogen. It has also a

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
0.4-1.4
perfusion.
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
sodium
in
serum
of
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
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
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:
Send sample to the laboratory immediately.
After:
After: Apply direct pressure to the venipuncture site until bleeding stops.
3. Lipid Profile
DIAGNOSTIC/
DATE
INDICATION/S OR
LABORATORY
ORDERED(DO);
PURPOSES
PROCEDURE
DATE DONE
RESULTS
NORMAL
ANALYSIS AND
VALUES
INTERPRETATION OF
RESULTS
(DD); DATE
RESULTS IN
(DRI)
Lipid Profile
Lipid profile measures the

circulating levels of free
cholesterol
cholesterol
and
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
screen for hyperlipidemia.
DD: 10-07-09
Cholesterol,
sterol
5.8 (Increased)
Less than
The result is above the
5.18 mmol/L
normal range. Increased

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 could
bound
phospholipids.
assimilate at the injured
This complex is called a
site
together
lipoprotein.
monocytes,
with
macrophages
To assess the risk of

Coronary Artery Disease
(CAD) and evaluation of
and
platelets
forming
foam
cells.
Foam
cells
engulfed the lipids and
fat metabolism
smooth
muscle
cells
developed.
Consequently,
smooth
muscle
reproduce
and
these
cells
themselves
synthesize
the
connective tissues while

they
subsequently
proliferate
(intimal
proliferation) making the

intima thick, thus, plaque
Less than
B. Triglycerides
DO: 10-07-09
1.54(Increased
DD: 10-07-09
)
Serum triglycerides
1.26 mmol/L
formation/atheroma
developed
increases
which
the
developing MI.
risk
of
provides
quantitative
The result exceeds the
analysis of triglycerides,
normal limits. Increased
the main storage form of
triglycerides
lipids,
initiate development
which
constitute
about 95% of fatty tissue.
level could
of
atheroma. Injury to the

blood
Indicated to patient to
vessel
cause
attraction of excess fats
screen for hyperlipidemia
and
and to assess Coronary
cholesterol,
macrophages,
Artery Disease.
monocytes and platelets

leading
to
development
foam
that
responsible
cells
is
for
atherogenesis posing the

risk of MI to occur.
C. High Density
Lipoprotein (HDL)
DO: 10-07-09
DD: 10-07-09
HDL is responsible for

reverse
cholesterol
29
>35mmol/L
The result is normal, that
transport, which return
means, at any rate, the
excess cholesterol from
HDL could participate in
the tissues to
endothelial
metabolism.
the liver
It
also
repair
and
decreases formation of
thrombosis.
More
so,
participates in endothelial
within normal levels or
repair
more
importantly
levels
of HDL maybe
and
decreases
thrombosis.
more protective for the
It is indicated to
patient
to
screen
hyperlipedemia
and
high
development
for
of
atherosclerosis than low
to
levels of HDL.
assess Coronary Artery

Disease.
D. Low Density
DO: 10-07-09
Lipoprotein (LDL)
DD: 10-07-09
LDL is responsible for

the delivery of cholesterol
5.67
2.10 4.90
(Increased)
mmol/L
The result is above the

normal
range.
to the tissues. Serum
signifies
level of LDL are normally
increased
controlled
concentration of LDL is a
by
hepatic
that
This
an
serum
receptors for LDL that
strong
bind LDL and limit liver
coronary
synthesis
particles are the most
of
this
lipoprotein.
to
risk.
of
LDL
atherogenic since they
It is indicated to
patient
indicator
screen
for
play a role in endothelial

injury, inflammation, and
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,
particles
vulnerable
arterial
LDL
adhere
to
points
in
endothelium.
Here
macrophages
ingest them, leading to

formation of foam cells
and
the
plaque
beginning
formation.
of
In
addition, elevated levels

of LDL combined with
low
levels
of
HDL
increase the risk for MI.

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.
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)
DIAGNOSTIC/
DATE
INDICATION/S OR
LABORATORY
ORDERED(DO)
PURPOSES
PROCEDURE
; DATE DONE
(DD); DATE
RESULTS
NORMAL
ANALYSIS AND INTERPRETATION OF
VALUES
RESULTS
RESULTS IN
(DRI)
Glucose (FBS)
DO: 10-07-09
DD: 10-07-09
The fasting
blood
fasting
sugar
or
plasma
6.81
4.20
(Increased)
6.40
mmol/L
The result is above the normal range.

Imbalance
between
coronary
supply
and
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.
This is indicated
to patient to screen
for
diabetes
mellitus, in which
absence
or
deficiency of insulin
allows
persistently
high glucose levels.
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. In the case
of the patient, increased glucose was noted on

the 2nd day of hospitalization (05-07-08).
Before:
Explain to the patient that this test detects disorders of the glucose metabolism and aids in the diagnosis of diabetes.
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);
LABORATORY
DATE DONE (DD);
PROCEDURE
DATE RESULTS
INDICATION/S OR
PURPOSES
RESULTS
NORMAL
VALUES
ANALYSIS AND
INTERPRETATION
OF RESULTS
IN (DRI)
Troponin (Cardiac
DO: 10-07-09
The cardiac Troponin T is a
T)
DD: 10-07-09
protein in striated is extremely
though
specific
evident increase of
cardiac
damage
Positive
negative
The resultis positive,

there
is
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.

It is indicated to the patient
to detect and diagnose acute
myocardial
reinfarction.
infarction
and
This
signifies
that
there is no significant
reinfarction event that
happened
since
troponin
assays
(Troponin
and
Troponin T) are more

capable of detecting
episodes
of
myocardial
reinfarction.
rises
more
They
slowly
than myoglobin and

maybe
useful
diagnosis
for
of
reinfarction, even up
to 3 to 4 days.
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.
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)
DIAGNOSTIC/
DATE
INDICATION/S
LABORATORY
ORDERED(DO);
OR PURPOSES
PROCEDURE
DATE DONE
RESULTS
NORMAL
ANALYSIS AND
VALUES
INTERPRETATION OF
RESULTS
(DD); DATE
RESULTS IN
(DRI)
Chest X-ray AP
DO: 10-07-09
(Sitting)
DD: 10-07-09
To detect the
status
of
1.Atherosclerotic
aorta.
respiratory
Chest films show
There
at
is
the
bony atherogenesis
the
structures
(ribs, aorta since the patient
system. A chest x-
2. Cardiomegaly
sternum,
has
ray can be used to
with left ventricular
clavicles,
cholesterol level, wherein
prominence.
scapulae
define
abnormalities
of
the lungs such as

excessive
fluid,
and excess
increased
lipids
upper portion of accumulate
could
within
the
3. Pulmonary
the
humerus). vessel wall and coalesce
congestion.
The
vertebral into a pool called the lipid
pneumonia,
column is visible
bronchitis, asthma,
vertically through atherosclerotic
cysts, and cancers
the middle of the Furthermore,
as well as exact
thorax. The two cardiomegaly
location and size
hemidiaphragms
of the organs such
normally
as heart.
rounded, smooth patient had infarction, it
It is indicated to
and
core
ventricular
appear occurred
to
form
plaque.
with
left
prominence
since
the
sharply loses its contractility at
defined; the right some degree because of
the
patient
determine
evaluate
to
and
if there
hemidiaphragm is lack
slightly
of
response
higher electrical
to
impulses,
than the left. The eventually the heart work
is/are
junction of the rib hard
complication(s)
cage
brought about by
diaphragm called significantly (hypertrophy
myocardial
the
infarction.
angle, is normally thickening
of
clearly visible and ventricles
as
and
to
meet
the
the demand, it will enlarge
costophrenic of the heart) as well as
angled.
tissue
Heart compensatory
is
and
white
the
dense mechanism.
Moreso,
appears cardiac
but
tissue
less surrounding the area of
intensely
white infarction also undergoes
than
bone. changes
Normally
as
the myocardial remodeling, a
heart shadow is process

clearly
such
mediated
outlined, angiotensin
by
II,
extends primarily aldosterone,

on to the left side
catecholamines,
of the thorax, and adenosine,

occupies no more inflammatory
than one third of which
and
cytokines
causes
the chest width. hypertrophy

Close observation myocardial
shows
of
the
cells
and
the sustained activation of
trachea
in
the neurohormonal
upper
middle compensatory
chest
almost mechanism
superimposed
which
eventually increases wall
above the cervical stress in the ventricle

and
thoracic and thus to reduce wall
vertebra.
The stress,
the
trachea bifurcates cells
myocardial
hypertrophy
at the level of the (Laplaces Law). On the

fourth
thoracic other hand, pulmonary
vertebra into the congestion

left
mainstem since
bronchi.
developed,
there
The cardiomegaly
is
imparing
pulmonary blood cardiac pumping leading

vessels, bronchi, to
decreased
lymph nodes are output.

located
in
In
the ventricular
return,
and
left
hypertrophy
hilum on both the occurred

right
cardiac
as
left compensatory
sides of the mid- mechanism.
The
right
thorax.
tissue
Lung side
of
the
appears continuously
black
on
x-ray blood
to
heart
propel
the
lungs,
film.
Vascular thereby, the left ventricle
lung
structures is unable to fully eject the
are
visible
as returning
white, thin, wispy systemic

strings
out
blood
circulation
fanning leading to congestion.

from
the
hilum.
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.
to
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 patients 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)
DATE
DIAGNOSTIC/
ORDERED(DO);
LABORATORY
DATE DONE (DD);
PROCEDURE
DATE RESULTS
INDICATION/S OR
PURPOSES
RESULTS
NORMAL
VALUES
ANALYSIS AND
INTERPRETATION
OF RESULTS
IN (DRI)
Twelve (12) Lead
DO: 10-07-09
To determine any
ST-segment
ST segment is
Electrocardiogram
(ECG)
DD: 10-07-09
abnormal pumping
action of the heart
and
to
indicate
presence
of
elevation
Rate: A: 90/min
V: 90/min
arrythmias
P: 0.08
P-R: 0.20
QT:0.36
QRS: 0.06
elevated since there

is
alteration
Rate:
delay
A:60100/min
repolarization
V:60-100/min
depolarization
and
of
properties
and
of
due
the
P:
heart
to
less than 0.11
impairement or even
sec.
lack of response to
P-R:
electrical
0.12 to 0.20 sec.
secondary
QT:
prolonged
up to 0.42 sec.
ischemia/infarction of
QRS:
the myocardial cells
0.04-0.11
including
impulses
to
all
the
layers of the heart. It

also signifies that the
area
of
infarction
extends to the zone

of
injury
which
is
significantly
developed,
ischemic
wherein
tissues
produces
an
elevation in the ST
segment. More so,
there
is
prolonged
period of decreased
blood supply to the
heart
causing
infarction.
Before:
Check doctors order.
Verify patients 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.
an
Secure electrodes to appropriate locations on chest and extremities.
Instruct the patient to remain still during the procedure.
After:
Secure results.
Write the patients 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 hearts 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
sulcus
extends
separating the atria from the
around
ventricles.
coronary
the
heart,
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
bishops 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 voltagegated 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
(mL/min)
SV
(mL/beat)
HR
(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
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
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 Starlings law of the heart.
Because venous return is influenced by many conditions, Starlings 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 hearts 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-STsegment 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,
nonST-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)
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. Prinzmentals 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.
Class
I
II
III
IV
Killip Classification of Heart Failure

Description
Absent crackles and S3
Crackles in the lower half of the lung fields and possible S3
Crackles more than halfway up the lung fields and frequent pulmonary
edema
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 persons 30s and even in ones 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 hearts 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
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 bodys 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
Atherosclerosis
(Plaque Formation)
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
damaging to the endothelial and smooth muscle
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.
Angina Pectoris/Chest Pain
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
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.
(+) Levines Sign
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
may radiate to the neck, lower jaw, left arm, and left
shoulder or, occasionally, to the back or down the
right arm causing a Levines sign (Individuals often
describe the sensation by clenching a fist over the
left sternal border).
Elevated Cardiac Enzymes

(CK-MB, Troponin I, Troponin T,
Myoglobin)
ST-segment elevation, T wave

Inversion,
pathologic Q wave
Dysrhythmias/Arrhythmias
Elevated Glucose Level
Continued ischemia due to coronary obstruction

will cause myocardial cell/tissue necrosis. Necrosis
of myocardial tissue results in the release of certain
intracellular enzymes (CK-MB, Troponin I, Troponin
T, Myoglobin) through the damaged cell 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
occlusion will lead to myocardial O2 deficit which
causes death of the myocyte, Prolonged ischemia
causes myocardial infarction. Since there is death
on myocardium electrical impulses is impaired or
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
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.
causes myocardial damage-death and necrosis.
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.
Increased WBC (Leukocytosis)
Nausea, Vomiting, Epigastric Pain
Cardiomegaly
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
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
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
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 (Laplaces Law). As a result there will
be thickening of the ventricular wall which
contributes to cardiomegaly.
Pallor, diaphoresis, dyspnea, body

weakness/easy fatigability,
headache, sense of impending
doom
Stimulation of SNS
Increased VS
(-)Bowel Movement
O2 needs and demands
Hemoglogbin, hematocrit,
delayed capillary refill time, pallor,

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.
acid will lead to acidosis. In return, myocardial cells
will become sensitive to changes in pH and become
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
impulses, myocardial remodelling and myocardial
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.
Weakness/restlessness, easy
fatigability, fatigue,
Left ventricular hypertrophy

Decrease Ejection fraction
Pulmonary Congestion
Fine crackles on BLF (bibasal

rales), wheezes, S3 gallop
Edema
Jugular Distension
Dyspnea (Difficulty of breathing)
Body Weakness/Easy fatigability
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
failure. As a result, there will be decreased cardiac
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
heart rate or pumping action as a compensatory
mechanism, which leads to left ventricular
hypertrophy eventually hearts 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
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
stimulated increasing heart rate or pumping action
as a compensatory mechanism, which leads to left
ventricular hypertrophy eventually hearts ability to
pump will deteriorate thus leading to moderate left
ventricular failure which decreases ejection fraction.
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.
Cough
Lost of consciousness, dizziness,

fainting, sense of impending doom
Ventricular Aneurysm, Perforation

of the Ventricular Septum
Valve Regurgitation
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
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
supply of O2, the body responds to this event
through loss of consciousness, dizziness, fainting,
sense of impending doom.
causes myocardial damage-death and necrosis. In
return, these there will be scar tissue formation
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, 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. 7 th 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. Harrisons 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. Nurses 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.
.
C. Internet Readings
American Heart Association (AHA), 2009.
http://www.americanheart.org/presenter.jhtml?identifier=3010002, retrieved on 0614-08 at 2:55pm
American Heart Association (AHA), 2009.
http://www.americanheart.org/presenter.jhtml?identifier=4478, retrieved on 06-2609 at 2:56pm.

Myocardial Infarction (Heart Attack) : by Rolly M. Policarpio RN

Transféré par

Informations du document

Description originale:

Titre original

Copyright

Formats disponibles

Partager ce document

Partager ou intégrer le document

Options de partage

Avez-vous trouvé ce document utile ?

Ce contenu est-il inapproprié ?

Droits d'auteur :

Formats disponibles

Myocardial Infarction (Heart Attack) : by Rolly M. Policarpio RN

Transféré par

Droits d'auteur :

Formats disponibles

MYOCARDIAL

In the Philippines. as to the 10 leadings causes of Mortality in the Philippines

perform a comprehensive assessment of the patient with myocardial infarction.

enumerate the signs and symptoms of myocardial infarction

perform appropriate therapeutic interventions for each of the formulated nursing

evaluate the effectiveness of nursing care for myocardial infarction formulate

II. NURSING ASSESSMENT

Mang Undoy is a 51-year-old male patient, a Filipino, and a member of the

Socio - Economic and Cultural Factors

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

3. HISTORY OF PAST ILLNESS

Vital signs: BP: 140/100mmHg Temp: 36.5C/axilla P R: 109bpm R R: 36bpm 02 Sat:

b. Deep Tendon Reflex

Testing device: food for

d. Ears: Symmetrical and no abnormal discharges noted. No excess cerumen was

m. GCS Eye opening: 4 Verbal Response: Motor Response: Total:

n. Deep Tendon Reflex

6. DIAGNOSTICS AND LABORATORY FlNDlNGS

DATE DONE (DD)

DATE RESULTS IN (DRI)

screening t that includes

The result is within

which indicates that

deciliter (dL or 100mL) 143g/L

indicated for the pati to

help evaluate iron status

packed red blood Cal in

which indicates that

a whole blood sample 0.40

The result is within

percentage RBC's in the

plasma. It indicated for

the patient to h evaluate

iron status and ^O^Xy^s

RBC z hydration status

The result is within

measu the number of

which indicates that

of blood. It is indical for

the patient to detect and

inflammation and tissue

Lymphocytes produces 0.42

The result is above

the normal values,

which means that

cells are denied of

indicated for the patient

cellular death and

Nursing Responsibilities: Before:

Tell the patient that the test requires a blood sample.

Explain who will perform the yenipuncture and when.

Handle the sample gently to prevent hemolysis.

Send sample to the laboratory immediately.

Apply direct pressure to the venipuncture site until bleeding stops.

DATE DONE (DD)

A routinary exam done 0.9

upon admission to assess

the normal values,

glomerular filtration and to

which indicates that

screen for renal damage.

the kidneys are